2
Dear Readers,
You now hold the result of the dedicated work of numerous physicians from a wide range of
medical, not only surgical, departments. Each author is deeply committed to facilitating your
orientation within surgical topics and fostering a comprehensive understanding to guide you
effectively toward accurate surgical reasoning and action.
The aim of this work extends beyond merely reflecting the dynamic evolution of the field of
surgery. Above all, it seeks to impart key insights rooted in the rich surgical tradition of Brno – to
authentically highlight the historical significance of what we consider the "crown jewel" of surgery
at the Faculty of Medicine, Masaryk University.
These materials are by no means a substitute for the mandatory and recommended literature;
rather, they serve as an overview and supplement, designed primarily as a guide to assist you in
preparing for questions on the state examinations in surgery (the number of the official state exam
question can be found in brackets after the chapter title).
Finally, we kindly request your feedback – an evaluation of each chapter in terms of both
scope and content. Your input is invaluable and will greatly contribute to the improvement of this
resource. We welcome any suggestions for revisions, proposals for additions or improvements,
whether by condensing or expanding particular sections. Beyond constructive criticism, we are, of
course, equally appreciative of any questions or positive feedback.
Your feedback will be invaluable in guiding this text's further development and refinement.
Please send your thoughts to our email address: chirmuni@group.muni.cz, and we will respond to
each message.
We wish you joy in achieving grown understanding and the creative inspiration it brings as
you use this resource to enhance your surgical knowledge and skills.
The Editors,
Tomáš Ledvina, Jan Ledvina, Petr Krsička, Petra Kurečková and Teodor Horváth
VERSION UPDATED TO 7.1.2025
3
RECOMMENDED LITERATURE:
PAFKO, Pavel. Základy speciální chirurgie. 1. vyd. Praha: Galén, 2008, 385 s.
ISBN 9788072624027.
ŠNAJDAUF, Jiří a Richard ŠKÁBA. Dětská chirurgie. 1. vyd. Praha: Galén, 2005, 395 s.
ISBN 807262329X.
HOCH, Jiří a Jan LEFFLER. Speciální chirurgie: učebnice pro lékařské fakulty. 2. vyd. Praha:
Maxdorf, 2003, 224 s. ISBN 8085912066.
MARKO, Ľubomír a Peter KOTHAJ. Atlas miniinvazívnej chirurgie a chirurgickej endoskopie. 1.
vyd. Banská Bystrica: Marko, 1998, 156 s. ISBN 8096807609.
KABELKA, Miroslav. Dětská chirurgie: učebnice pro lékařské fakulty. 1. vyd. Praha: Karolinum,
1992, 320 s. ISBN 8070665610.
4
TEAM OF AUTHORS
University Hospital Brno - Bohunice:
• Surgical Clinic: MUDr. Cabanová Lucia; MUDr. Csölle Jakub; MUDr. Farkašová Martina;
MUDr. Gregora Jakub; MUDr. Grolich Tomáš, Ph.D.; MUDr. Hlavsa Jan, Ph.D.; doc.
MUDr. Horváth Teodor, CSc.; MUDr. Ivanecká Dominika; MUDr. Jaborník Martin; MUDr.
Konečná Drahomíra; MUDr. Kurečková Petra; MUDr. Mgr. Kysela Petr, Ph.D.; MUDr.
Linhartová Marcela, Ph.D.; MUDr. Marek David; MUDr. Marek Filip, Ph.D.; MUDr. Mitáš
Ladislav, Ph.D.; MUDr. Moravčík Petr; MUDr. Petríková Laura; MUDr. Poláchová
Veronika; MUDr. Pospíšil Jan; MUDr. PharmDr. Potrusil Martin; doc. MUDr. Procházka
Vladimír, Ph.D.; MUDr. Svatoň Roman; MUDr. Svoboda Martin; MUDr. Španková
Markéta; MUDr. Štefela Horváthová Erika; MUDr. Trenz Aleš; MUDr. Vaverka Vítězslav;
MUDr. Vysloužil Pavel; MUDr. Vytešníková Martina; MUDr. Zatloukal Martin
• Clinic of Radiology and Nuclear Medicine: MUDr. Andrašina Tomáš, Ph.D.; MUDr. Bárta
Radek; MUDr. Hanžlová Barbora; MUDr. Matkulčík Peter; MUDr. Rohan Tomáš
• Deparment of Gastroenterology and Internal Medicine: doc. MUDr. Dastych Milan,
CSc., MBA; doc. MUDr. Kroupa Radek, Ph.D.; MUDr. Skutil Tomáš
• Urology Clinic: doc. MUDr. Fedorko Michal, Ph.D., FEBU; MUDr. Kašík Marek; MUDr.
Moravčíková Mária; MUDr. Trinh Tuan; MUDr. Varga Gabriel, Ph.D., FEBU; MUDr.
Wasserbauer Roman
• Clinic of accident surgery: MUDr. Dobiášek Miroslav; doc. MUDr. Krtička Milan, Ph.D.;
MUDr. Rak Václav, Ph.D.; MUDr. Staňa Martin; MUDr. Študent Petr; MUDr. Tručka
Robert Clinic of burns and reconstructive surgery: MUDr. Dubovská Nikola; MUDr.
Ferkodičová Iveta; MUDr. Hokynková Alica, Ph.D.; MUDr. Holoubek Jakub; MUDr. Mager
Radomír, Ph.D.; MUDr. Matysková Dominika; doc. MUDr. Streit Libor Ph.D.; doc. MUDr.
Šín Petr, Ph.D., MBA; MUDr. Topolčaniová Lenka; MUDr. Váňa Vladimír
• Clinic of Neurosurgery: doc. MUDr. Fadrus Pavel, Ph.D.; prof. MUDr. Smrčka Martin,
Ph.D., MBA
• Orthopedic clinic: doc. MUDr. Chaloupka Richard, CSc.; MUDr. Parížek Dominik; MUDr.
Ryba Luděk, Ph.D.
• Institute of Laboratory Medicine - Bacteriology Section: MUDr. Horváthová Beáta
• Hospital Pharmacy - Clinical Pharmacy Section: PharmDr. Musilová Karolína
5
University Hospital Brno - Children's Hospital:
• Clinic of paediatric surgery, orthopedics and traumatology: MUDr. Bibrová Štěpánka,
Ph.D.; MUDr. Doušek Robert; MUDr. Husár Matej; MUDr. Ledvina Jan; MUDr. Mareček
Lukáš; MUDr. Marek Ondřej, Ph.D.; prof. MUDr. Plánka Ladislav, Ph.D.; MUDr. Starý
David, Ph.D., MUDr. Tůma Jiří, CSc.; MUDr. Turek Jakub, Ph.D.; MUDr. Urbášek Karel,
Ph.D.; MUDr. Václav Ondrej
• Clinic of paediatric anesthesiology and resuscitation: MUDr. Klabusayová Eva, DESAIC;
MUDr. Kořínková Bianka; MUDr. Šoltysová Jana; prof. MUDr. Štourač Petr, Ph.D., MBA,
FESAIC
St. Anne’s University Hospital Brno:
• 1st Dept. of Surgery: MUDr. Berková Alena, Ph.D.; MUDr. Glombová Katarína; MUDr.
Hasara Roman; MUDr. Hemmelová Beáta, Ph.D.; MUDr. Chovanec Zdeněk, Ph.D.; MUDr.
Kašpar Michal; MUDr. Konečný Jan, Ph.D.; MUDr. Křenek Adam; MUDr. Musil Tomáš;
doc. MUDr. Penka Igor, CSc.; MUDr. Peštál Adam, Ph.D.; MUDr. Prudius Vadim, Ph.D.,
MUDr. Reška Michal, Ph.D.; MUDr. Urbánek Libor; doc. MUDr. Veverková Lenka, Ph.D.;
MUDr. Vlček Petr, Ph.D.; MUDr. Vojtaník Pavol; MUDr. Vystrčilová Tamara; MUDr. Žák
Jan, Ph.D.
• 2nd Dept. of Surgery: MUDr. Novotný Tomáš, Ph.D.
• Dept. of Neurosurgery: MUDr. Barák Martin; prof. MUDr. Brichtová Eva, Ph.D.
• 1st Dept. of Orthopedic: MUDr. Jindra Jakub; MUDr. Kubíček Marian; MUDr. Liskay
Jakub; MUDr. Mahdal Michal, Ph.D.; MUDr. Martinek Lukáš; MUDr. Nachtnebl Luboš,
Ph.D.; MUDr. Pazourek Lukáš, Ph.D.; doc. MUDr. Tomáš Tomáš, Ph.D.
• Dept. of Plastic and Aesthetic Surgery: MUDr. Bayezid Can Kadir; MUDr. Berkeš Andrej;
doc. MUDr. Dvořák Zdeněk, Ph.D.; MUDr. Janeček Pavel; MUDr. Klabusay Filip, Kubát
Martin; MUDr. Menoušek Jan; MUDr. Streit Libor, Ph.D.
Center for Cardiovascular and Transplant Surgery: MUDr. Fila Petr, Ph.D.; doc. MUDr. Němec
Petr, CSc., MBA
Masaryk Memorial Cancer Institute:
• Department of Surgical Oncology: doc. MUDr. Coufal Oldřich, Ph.D.; doc. MUDr. Fait
Vuk, CSc; MUDr. Gabrielová Lucie; MUDr. Hrabec Roman, FEBU; MUDr. Krésová
Pavlína, Ph.D.; MUDr. Krsička Petr; MUDr. Rothová Veronika; doc. MUDr. Staník Michal,
Ph.D.; MUDr. Šimůnek Radim; MUDr. Zapletal Ondřej; prof. MUDr. Žaloudík Jan, CSc
6
Trauma Hospital in Brno:
• Dept. of Traumatology: MUDr. Kelbl Martin, Ph.D.; MUDr. Pavlacký Tomáš; prof. MUDr.
Veselý Radek, Ph.D.; prof. MUDr. Wendsche Peter, CSc.; MUDr. Zukal Radek
Ivančice Hospital:
• Dept. of Surgery: MUDr. Koloděj Daniel; MUDr. Ledvina Tomáš; MUDr. Majerčák Lukáš;
MUDr. Musilová Zuzana, Ph.D.
University Hospital Ostrava:
• Dept. of Imaging Methods: MUDr. Zavadil Jan
Tábor Hospital, Inc.:
• Dept. of Surgery: MUDr. Laššáková Zuzana
Academican Ladislav Dérer Hospital:
• Surgical Clinic of SZU and UNB: MUDr. Kučera Adam
External Contributors: MUDr. Melichar Jindřich, CSc.
7
GENERAL SURGERY....................................................................................................................................................... 9
Acute gastrointestinal bleeding (25) ......................................................................................................................... 10
Acute appendicitis (26).............................................................................................................................................. 14
Presentation, diagnostic process and management of appendicitis in paediatric, pregnant and elderly patients (38)
................................................................................................................................................................................... 18
Acute (a)calculous cholecystitis, common bile duct stones, jaundice (4) .................................................................. 22
Diverticular disease (36)............................................................................................................................................ 25
Intestinal ischemia (28) ............................................................................................................................................. 28
Peritonitis (27)........................................................................................................................................................... 33
Ileus (29).................................................................................................................................................................... 37
Hernias of the anterior abdominal wall, diaphragmatic hernias (11) ....................................................................... 40
Small bowel and large bowel neoplasms (37)........................................................................................................... 44
Inflammatory diseases of small bowel and their surgical management (34) ........................................................... 48
Inflammatory diseases of large bowel and their surgical management (35)............................................................ 52
Hemorrhoids, anal fissure (2) .................................................................................................................................... 56
Anorectal fistula and abscess, pilonidal sinus disease (1) ........................................................................................ 60
Esophageal surgery, anatomy, approaches, types of operations (20) ...................................................................... 65
Surgery for benign gastric diseases (31).................................................................................................................... 68
Gastroduodenal ulcer diseases (32) .......................................................................................................................... 71
Gastric tumours (33).................................................................................................................................................. 74
Liver surgery – anatomy, approaches, types of operations (3) ................................................................................. 78
Neoplasms of the liver (5) ......................................................................................................................................... 83
Spleen surgery – anatomy, approaches, types of operations (6) .............................................................................. 87
Acute and chronic pancreatitis (7) ............................................................................................................................ 90
Pancreatic neoplasms (9) .......................................................................................................................................... 94
Obstructive jaundice (30) .......................................................................................................................................... 97
Retroperitoneal tumours (10)..................................................................................................................................102
Adrenalectomy - anatomy, approaches, types of operations (8) ............................................................................106
Diagnostic methods in urology . examination, laboratory tests, endoscopic and imaging methods (39) ..............108
Arterial aneurysms (12)...........................................................................................................................................113
Peripheral arterial disease of lower extermities (13) ..............................................................................................117
Acute limb ischemia (14) .........................................................................................................................................122
Treatment of varicose veins (15).............................................................................................................................126
Goitre, surgery of thyroid gland (17).......................................................................................................................128
Gynecomastia, inflammatory disorders of the breasts (16)....................................................................................132
Breast tumors (24)...................................................................................................................................................136
8
Thoracic outlet syndrom, nerve compression syndromes of arm and forearm (21)................................................141
Acute mediastinitis (18)...........................................................................................................................................145
Mediastinal tumors, superior vena cava syndrom (19)...........................................................................................148
Pulmonary abscess, empyema (22).........................................................................................................................151
Lung cancer and mesothelioma (23) .......................................................................................................................155
9
10
ACUTE GASTROINTESTINAL BLEEDING (25)
Majerčák Lukáš, Kysela Petr
Acute gastrointestinal bleeding is part of the acute abdomen group. Gastrointestinal bleeding can be
classified into upper, middle and lower GI bleeding due to the different diagnostic and therapeutic
approaches. Acute bleeding has a sudden onset, often accompanied by haemodynamic instability
(e.g., blood pressure drops and increased heart rate).
Acute Upper GI Bleeding:
The boundary is the Treitz ligament. The most common cause of upper GI bleeding is peptic ulcer
disease of the gastroduodenum. Other sources may include oesophageal varices, Mallory-Weiss
syndrome, or tumours (most commonly adenocarcinoma, typically GIST, less frequently
lymphoma).
The presentation includes haematemesis—vomiting blood, either fresh or digested (resembling
coffee grounds), and melaena, which is stool containing digested blood, typically tarry black,
sticky, and with a characteristic odour. Similar stool discolouration can also occur after consuming
beetroot, blueberries, activated charcoal, or iron supplements, although the stool is usually formed in
these cases. In some cases of massive bleeding with rapid passage, upper GI bleeding can present as
enterorrhagia—the evacuation of red, undigested blood. Depending on the severity of the bleeding,
the patient may develop anaemic symptoms (weakness, pallor, palpitations, dyspnoea), haemorrhagic
shock (centralised circulation, cold sweat, cold extremities), or altered consciousness (collapse,
syncope, often during defecation).
History-taking should include asking about the use of NSAIDs or corticosteroids, which can cause
gastroduodenal ulcers, as well as any coagulopathies or anticoagulant/antiplatelet medication. Ask
about alcohol abuse and signs of liver cirrhosis, which is the most common cause of portal
hypertension and oesophageal varices. The physical examination assesses the patient's overall
condition (consciousness, BP, HR, SpO2) and confirms melaena or enterorrhagia on rectal
examination. Abdominal pain rarely accompanies upper GI bleeding. Blood tests initially show
leukocytosis, followed by anaemia and a drop in haematocrit. In massive bleeding, a drop in
haemoglobin may only appear later, so clinical status should guide management. The definitive
diagnosis and source of bleeding are confirmed by gastroscopy (only if the patient is stabilised). In
peptic ulcer disease, the Forrest classification assesses bleeding severity (I. active bleeding, II. signs
of recent bleeding, III. no signs of bleeding).
11
The main treatment involves monitoring the patient's vital signs in an ICU, stabilising circulation
with fluid replacement, followed by blood transfusion if necessary, discontinuing anticoagulants, and
correcting coagulation (with fresh frozen plasma, clotting factors, etc.). For peptic ulcer bleeding,
proton pump inhibitors (PPIs) are administered. In variceal bleeding, vasoactive agents
(terlipressin, somatostatin) are used. Gastroscopy is key in diagnosing and treating acute upper GI
bleeding. It offers the possibility of controlling the bleeding through local injection (e.g., diluted
adrenaline or ethanol injected around the lesion, then into its centre), thermocoagulation, or
mechanically (applying clips or ligating varices with rubber bands). If endoscopic treatment of
arterial bleeding fails or is impossible, angiography is indicated to selectively embolise the source
(transarterial embolisation - TAE). In cases of endoscopically unmanageable variceal bleeding, one
option is a portosystemic shunt (TIPS), or a Sengstaken-Blakemore tube may be temporarily used
to tamponade the gastric cardia and oesophagus. However, this method is temporary due to the risk
of pressure ulcers. Surgical treatment of upper GI bleeding is rarely needed due to advances in
endoscopy and minimally invasive techniques and is reserved for cases of uncontrollable bleeding.
Surgery includes suturing or excising the ulcer via duodenotomy or gastrotomy (incising the
duodenum or stomach) or, in most cases, resectional surgery (Bilroth I, Bilroth II, or in extreme
cases, total gastrectomy). Every rebleed with circulatory instability after less invasive methods
should be managed surgically.
Acute Middle GI Bleeding:
Bleeding from the small intestine is a diagnostic and therapeutic challenge. The most common cause
in older patients is angiodysplasia. However, other causes can include ulcers due to ectopic gastric
mucosa (typically in a Meckel's diverticulum), bleeding due to portal hypertension after endoscopic
treatment of gastric varices, or GIST, and rarely other malignancies. It's also important to consider
aorto-enteric fistula, particularly in patients with a history of severe retroperitoneal inflammation
(e.g., pancreatitis) or vascular reconstruction on the aorta.
Upper and lower endoscopies are usually performed in a stable patient, which does not reveal the
source. Push-type endoscopy can evaluate up to 160 cm of the jejunum orally and up to 120 cm of
the terminal ileum anally. In cases of recurrent minor bleeding, intestinal ultrasound, enteroclysis,
or CT can be performed. Suspicion of small bowel pathology without detection on CT, US, or
enteroclysis is a typical indication for capsule endoscopy. To exclude ectopic gastric mucosa or
neuroendocrine neoplasia, octreotide scanning from nuclear medicine can be used. Significant
bleeding warrants immediate contrast-enhanced CT. Therapeutically, intervention is usually either
surgical or through endovascular embolisation, with the risk of ischaemia. Surgical resection is
12
usually simple, but localising the bleeding source is difficult, and intraoperative enteroscopy may
be required. In case of the aorta-enteric fistula neither endoscopy nor contrast-enhanced CT usually
confirms the diagnosis. After typical repeated unexplained bleeding, it often manifests with massive
exsanguinating enterorrhagia. In suspected aorto-enteric fistula, urgent surgical revision is indicated.
Acute Lower GI Bleeding:
Lower GI bleeding occurs less frequently than upper GI bleeding. The most common cause is
colonic diverticulosis, followed by anorectal conditions (bleeding haemorrhoids), bowel
inflammation of ischaemic or infectious origin (including Clostridium enterocolitis), and IBD or
malignancies. A specific group includes bleeding after colonoscopy polypectomy or recent bowel
surgery.
Clinically, lower GI bleeding presents as rectal bleeding (rectorrhagia/enterorrhagia). It is important
to determine whether the blood is fresh, clotted, on or within the stool. The fresher the blood on the
stool's surface, the more distal the bleeding source. As with upper GI bleeding, depending on the
severity, the patient's condition may progress to shock and altered consciousness.
History-taking should include asking about family history of malignancies, diagnosed diverticulosis,
IBD, recent colonoscopy or bowel surgery, use of broad-spectrum antibiotics, and again
coagulopathies or anticoagulant medication. The clinical examination focuses on assessing
circulatory stability, abdominal examination, and rectal examination—starting with inspection for
external haemorrhoids, fistulas, fissures, palpation for thrombosed haemorrhoids or tumours, and
then evaluating the stool consistency on the glove. Laboratory tests should focus on blood count (to
assess bleeding severity) and coagulation parameters (normalising coagulation is crucial for
stabilising the patient). Early diagnosis requires anoscopy/proctoscopy, which identifies the source
of bleeding from the rectum or anus, or it may reveal blood coming from higher up.
Again, the cornerstone of treatment is stabilising the patient in an ICU (monitoring vital signs, fluid
therapy, blood transfusion, normalising coagulation parameters etc.). In cases of uncertainty about
the bleeding source and suspected varices/haemorrhoids, somatostatin analogues are also
administered. PPIs do not have a direct therapeutic effect but are given prophylactically as acute
bleeding increases the risk of stress ulcers. In most cases (about 80 %) of acute lower GI bleeding,
spontaneous haemostasis occurs without requiring radiological, endoscopic, or surgical
intervention. Colonoscopy in acute undiagnosed bleeding and an unstable patient is not indicated.
Verifying the bleeding source and possibly its treatment via colonoscopy is possible in a stable
patient after proper orthograde bowel preparation (cleansing with laxatives). In an unstable patient
with enterorrhagia, the source should also be considered in the upper GI tract (see above), and
13
gastroscopy (GFS) should be performed. If haemodynamic instability persists despite initial
treatment, CT angiography is indicated to identify the bleeding source. If found, bleeding can be
stopped radiologically by selective embolisation, with the risk of ischaemia. If radiological
intervention fails and the patient's haemodynamic instability persists, resection surgery is
indicated—either right or left hemicolectomy, depending on the bleeding site, or in extreme cases,
total colectomy.
14
ACUTE APPENDICITIS (26)
Křenek Adam
Introduction:
Acute appendicitis is the most common abdominal emergency requiring surgery. Establishing the
correct diagnosis is a key prerequisite for successful treatment. Acute appendicitis may be the
biggest liar in the field of surgery, because the symptoms described in textbooks are given for typical
forms and for the typical course of acute inflammation of the appendix. Depending on the position of
the appendix, the duration of the inflammation and the age of the patient, inflammation of the
appendix can manifest itself in a wide range of symptoms in each affected individual. When
examining the abdomen, every surgeon must think about this disease.
Academician Arnold Jirásek already stated in 1949: "It is an insidious, insidious and dangerous
disease that causes diagnostic difficulties due to its unpredictable onset and course. We can definitely
say that this statement is still valid today.
Patogenesis:
Although acute appendicitis is the most common acute abdominal emergency, its etiopathogenesis is
still not fully understood.
Obstruction of the lumen of the appendix probably plays the most important role in the pathogenesis
of appendicitis.
According to various authors, obstruction is found in up to 2/3 of cases of acute appendicitis,
especially obstruction of the proximal part of the lumen - fibrous bands from the cecum, lymphatic
hyperplasia, fecoliths, stones, rarely parasites. In the remaining third of cases, no obstruction is
found. In these cases the triggers may include pressure on the appendix from the outside, its length or
a disturbance of the microbial flora caused by frequent use of antibiotics.
Intraluminal pressure causes arterial obstruction and ischemia in the intestinal wall. Intestinal
microorganisms penetrate the damaged mucosa causing intramural inflammation. Depending on the
stage of the inflammation, we distinguish between catarrhal, ulcerative, phlegmonous and the most
severe stage – gangrene. Gangrene is the cause of perforation of the appendix with the development
of circumscript (bounded) or diffuse peritonitis.
If our organism reacts to a perforation or an acutely inflamed appendix by limiting the entire process,
it surrounds the inflamed organ with omentum, small and large intestine, adjacent mesentery - a
periappendicular infiltrate is formed. The infiltrate consists of our tissues, organs, exsudate and
fibrin. Macroscopically, the organs are closely adhered to each other, their preparation is difficult,
with a risk of their injury and bleeding. The rule is that the infiltrate is not treated surgically (of
15
course, only in case the patient's condition is stable), but is treated conservatively - hospitalization,
bed rest, ATB, infusion therapy , analgesic therapy. A periappendicular abscess may develop from
the infiltrate.
Abscess treatment is today the domain of interventional radiology, when a puncture is performed
under CT or US.
Clinical picture:
Typically, the disease begins with pain, periumbilical with subsequent transfer to the right
hypogastrium. The pain is limited, worse when coughing, walking, and moving. Patients usually
describe it as a dull constant pain. If vomiting is present, it develops early after the onset of
abdominal pain. Vomiting before the development of pain rather casts doubt on the diagnosis of
appendicitis.
The clinical picture of appendicitis can be influenced by the atypical position of the appendix or the
patient's altered reaction due to age, pregnancy or the use of drugs - antibiotics, immunosuppressants,
steroids.
Laterocaecal appendicitis - pain in the lateral right hypogastrium and muscle contraction can affect
the lumbar region.
With a long appendix that reaches the subhepatic landscape, it can mimic inflammation of the
gallbladder.
Retrocaecal appendicitis leads to pain and muscle contraction, similar to laterocaecal appendicitis,
with painful extension of the leg in the hip when examining the patient on the left side.
The inflammation located close to the ureter can mimic the picture of renal colic.
Pelvic appendicitis may not cause muscle spasms. The pain is usually close to the symphysis and
the inguinal ligament, internal rotation in the hip is painful. Dysuric problems or diarrhea also occur.
In women, it mimics gynecological disease.
Mesoceliac appendicitis (the appendix lies medially between the loops of the small intestine on the
mesentery) is manifested by poor clinical findings on the abdomen with pain around the navel.
Left-sided appendicitis (a long appendix extends into the left hypogastrium or a normal-length
appendix is located to the left due to situs viscerum inversus) leads to pain and muscle contraction in
the left hypogastrium. Clinically, it can mimic diverticulitis. The situation will often be clarified only
during surgical revision of the abdomen
Appendicitis in children
a) Up to 2 years of age - rare, the appendix opens into the caecum widely, there is no congestion of
the contents in the appendix. Danger due to reduced ability to limit inflammation (low immune
resistance of the organism, poor ability of the peritoneum to form adhesions, short omentum).
16
Manifestations: drowsiness, irritability, tearfulness, loss of appetite. Vomiting, high temperature and
pain occur when the disease progresses
b) Above 2 years of age, the clinical picture practically does not differ from that of adults
Senile appendicitis
Difficult to diagnose, the body's ability to respond to inflammation is reduced, classic symptoms may
not be present, pain is low, muscle contractions are usually absent. The course of the disease itself is
more serious, purulent complications and perforation are frequent
Appendicitis in pregnancy
Symptoms depend on the stage of pregnancy. In the 1st trimester, the clinical picture is not different
from non-pregnant women. During the 2nd and 3rd trimester, the clinical finding is changed by the
dislocation of the cecum with the appendix cranially. The uterus overlaps the area of the
hypogastrium, making the clinical examination difficult and reducing the ability of the omentum to
localize the infection, therefore there is an increased risk of developing diffuse peritonitis in case the
appendix perforates. The mother can thus be at risk of severe intra-abdominal infection and the fetus
from premature birth to death. Therefore, when appendicitis is suspected, it is better not to hesitate
with appendectomy.
Abdominal examination:
Inspection - restriction of the breath wave in the right hypogastrium during inflammatory irritation
of the peritoneum in this place may be present. Auscultation - is of no greater importance for
establishing the diagnosis, in case of diffuse peritonitis we do not hear peristalsis for paralytic ileus.
Percussion - soreness and defensive contraction of the abdominal wall - Pléniés sign. Palpation pain
in the right hypogastrium, Blumberg's sign - pain during decompression of the right
hypogastrium, Rovsing - pain in the right hypogastrium during decompression of the left
hypogastrium Per rectum: bulging of Douglas space, painful indagation.
Laboratory tests: in the tests we look for elevation of inflammatory parameters - Leukocytes, CRP.
Paraclinical examination:
a) Ultrasound examination - can exclude or confirm the diagnosis.
b) X-ray: not contributive in the diagnosis of acute appendicitis, in some cases we can observe the
air fluid levels in the right half of the abdomen.
Given that, as already mentioned in the first paragraph of the chapter, that acute appendicitis can be
manifested by a whole range of symptoms, we always combine and evaluate clinical examination
and paraclinical methods as a whole and in the context of the patient's overall condition. If, despite
all the available examinations, we have diagnostic dilemma, a CT examination of the abdomen or a
diagnostic laparoscopy is performed.
17
Differential diagnosis
Acute mesenteric lymphadenitis, inflammation of Meckel's diverticulum, Crohn's disease,
gallbladder disease (cholecystitis, biliary colic), perforated gastroduodenal ulcer, acute
gastroenteritis, renal colic, ureterocele, ureteral stricture and systemic diseases, e.g. porphyria,
diabetes mellitus.
In women, we always consider gynecological diseases – right-sided adnexitis, ovarian cyst
perforation, ovarian cyst torsion, ruptured ectopic pregnancy
Therapy:
The treatment of appendicitis is primary surgical - appendectomy. Appendectomy can be performed
laparoscopically or from a laparotomy. In the case of appendectomy from laparotomy, we choose
gridiron (McBurney) incision, pararectal or lower median laparotomy. Periappendicular infiltrate is
treated conservatively. In extreme cases, when adequate surgical care is not available, acute
appendicitis can be treated conservatively - ATB, infusion therapy.
Complications of acute appendicitis:
Perforation - perforation can result in:
a) Periappendicular infiltrate - treatment: conservative (hospitalization, bed rest, ATB, infusion
therapy, analgesic therapy)
b) Abscess - treatment: puncture under CT or ultrasound
c) Peritonitis - treatment: surgery
Post-inflammatory adhesions in the postoperative period can be the cause of mechanical ileus.
Pylephlebitis - rarely occurring purulent thrombophlebitis of the portal venous system. Patients tend
to have chills, high temperature, subicterus, and later liver abscesses. This is a rare but serious and
potentially fatal complication
Conclusion:
Appendicitis is a common disease that requires an acute surgical solution. In most cases, the disease
follows a typical course, but we must always think of a different course and different symptoms.
18
PRESENTATION, DIAGNOSTIC PROCESS AND MANAGEMENT OF APPENDICITIS IN PAEDIATRIC,
PREGNANT AND ELDERLY PATIENTS (38)
Poláchová Veronika, Konečná Drahomíra
Acute appendicitis (hereinafter referred to as „AA“) is the most common cause of sudden abdominal
stroke, which can affect the entire population. Issue of AA has been elaborated in detail in a separate
chapter. In this chapter, we will focus on AA in childhood, pregnancy and old age, which are
characterized by elements so specific that they require their their own commentary.
In developed countrie, AA affests 7% of the population with incidence peaking in the 2nd
- 3rd
decade
of life.
I. CHILDHOOD
AA in childhood, especially up to the age of twoo, tends to be a rarity. Considerable experience and
patience on the part of the physician is required due to very limited cooperation from the young
patient. In the early stages, the clinic may manifest itself with tearfulness, irritability and
inappetence. This symptomatology may initially be mistaken for dyspepsia or enterocolitis. Later
vomiting, temperature and pain may follow. As a consequence of this delay, a definitive diagnosis of
AA is more often not made until the later stages, when it is often alredy complicated by perforation
of appendix with peritonitis.
In youth and in adolescence the clinic already resembles more AA of an adult, with problems
such as migratory pain passing within a few hours from the umbilicus to the right lower quadrant,
signs of peritoneal irritation, tachycardia, subfebrile, vomiting may being to appear. Children tend to
take an antalgic posture with the lower limbs flexed. However, in making the diagnosis we must
beware of possible dissimulation on the side of boys and tendency to exaggeration on the side of
girls.
The diagnosis includes: taking a targeted anamnesis, clinical findings, ultrasound of
abdomen, and in case of complications it is possible to perform a CT scan, blood count
(leukocytosis), CRP and urine analysis.
In the differential diagnosis it is necessary to exclude urological causes of difficulties, ovarian
or testicular torsion, mesenteric lymphadenitis, intestinal invagination and ileus.
Children are treated surgically. It consists in appendectomy, which can be performed either
clasically from laparotomy or laparoscopically, whis is preferred treatment for children older than 8
years or it depends on the habit of the body.
II. PREGNANCY
19
The incidence of AA is the same for pregnant women as for non-pregnant woman. It can occur in all
trimesters of gestatin, at birth or in the puerperium, however most often in the second and third
trimesters of pregnancy. Diagnosis of this disease is usually dificult. There may be a more rapid
progression of inflammation, which is associated with additional risks for both the expectant mother
and the fetus. Quickness of diagnosis and interdisciplinary cooperation are therefore very important.
Physiological changes and anatomical distribution of organs caused by a gradually growing uterus
significantly affect the clinical picture. Initial symptoms such as nausea, vomiting, lack of appetite or
unclear laboratory (leukocytosis) are initially attributed to the current pregnancy.
Symptoms and physical examination in the 1st
trimester do not differ significantly from nonpregnant
women. Right lower abdominal tenderness can be a reliable sign of AA.
Diagnostic difficulties occur in the 2nd
and 3rd
trimesters due to atypical localization of pain
caused by relocation of the appendix and cecum to the right subcostal region. Thus, as the pregnancy
progress we can expect the appendix to lodge more cranially. It si important to differentiate the pain
caused by AA, which is constant and localized in the right subcostal region, from possible uterine
contractions, which occur at regular intervals. Others symptoms may include diarrhoea or conversely
cessation of gas and faeces.
During the clinical examination the patient is examined in the classic position on the back.
Especially when it comes tu pregnant women we can apply the examination with rolling the patient
to the left side with constant pressure in the painful area, if the pain persists, it may be appendicitis.
The same examination in revers with rolling over to the right side with pain ileocecally may also to
clarify the diagnosis of AA.
Diagnosis is also difficult durin labour because of persistence of pain even in between
contractions or in the puerperium of labour because of abdominal wall weakness and thus
obscuration of symptoms.
Laboratory testing of blood and urine is not conclusive as a result of leukocytosis caused by
pregnancy, and therefore i tis possible to monitor the dynamics of inflammatory parameters during
possible developing inflammation.
Among imaging methods, ultrasound is the first choice, during which the fetal vitality is of course
also determined. We try to avoid CT scans because of the radiation load, MRI is more expensive
however it is compensanted by zero radiation.
In differential diagnosis, the most important thing is to exclude gynaecological causes of
problems, such as ectopic pregnancy, ovarian cyst, ovarian torsion, miscarriage, adnexitis, and rightsided
hydronephrosis or pyelonephritis.
20
When AA is suspected, even if paraclinicity is not proven, we usually proceed to surgery.
This is due to the lower risk of anaesthesia for mother and child compared to appendicitis without
sergery. At first in the early stage of pregnancy laparoscopic revision is considered, only at a more
later stage of pregnancy, approximately after the third trimester, laparotomy from an alternate
incision is resored to.
III. OLD AGE
10% of patients with acute appendicitis are over 60 years of age. In the old age, due to age,
comorbidities or possible dementia, diagnosis is more difficult. They often underestimate their
symptoms and seek medical attention at more advanced stages of the problem than would be
appropriate. Therefore morbidity and mortality rates are increasing when it comes to patients over 70
in comparison to younger patient.
Only 20% of seniors with AA have typical clinical smyptomatology. Most of them have
history of difficulties longer than 48h at the time of diagnosis of AA. Symptomatology of elders
comes often with a minimal increase in temperature, 25% have no tenderness in the right lower
abdomen, overal discreet local findings. Hence, the risk of complications increases from the more
frequent finding of perforations with peritonitis. In addition, almost in half of the case difficulties
may appear clinically as intestinal obstruction.
In laboratories leukocytosis is mostly absent.
The golden standard in the diagnosis of AA is an ultrasound examination and obdominal Xray
for exclusion of ileus or pneumoperitoneum. CT scan is indicated only in case of atypical
symptomatology or unclear clinical picture with negative ultrasound findings.
In the differential diagnosis we focus on urinary tract infection, bladder retention, perforation
of organs, intestinal ischemia or possible malignancy in the abdominal cavity.
The treatment is surgical, we prefer the laparoscopic appriach, however in advanced stages of
inflammation the laparotomy approach cannot be excluded.
21
Addiss DG, Shaffer N, Fowler BS, Tauxe RV. The epidemiology of appendicitis and appendectomy in the United States. Am J Epidemiol 1990; 132:910 –925
22
ACUTE (A)CALCULOUS CHOLECYSTITIS, COMMON BILE DUCT STONES, JAUNDICE (4)
Glombová Katarína
Cholelithiasis
Introduction and Definition: Cholelithiasis is the presence of stones in the gallbladder
(cholecystolithiasis) or in the bile ducts (choledocholithiasis). It may be asymptomatic, but it can also
lead to serious complications: acute cholecystitis, pancreatitis, cholangitis, or biliary colic.
Gallstones are composed of cholesterol, bilirubin, or a combination of both. The prevalence in
Western countries is around 10–20% in adults. The incidence increases with age, obesity, and certain
genetic factors.
The pathogenesis of stone formation is complex and involves several factors. Cholesterol stones:
result from an excess of cholesterol in the bile, exceeding the ability of bile acids and lecithin to keep
cholesterol in micellar solution. The excess cholesterol crystallizes and forms monohydrate crystals
that aggregate into stones. This process is promoted by bile stasis in the gallbladder (reduced motility
of the gallbladder during pregnancy, obesity, or rapid weight loss). Pigment stones: non-conjugated
bilirubin that precipitates in the presence of calcium. Typically found in patients with chronic
hemolysis, such as those with sickle cell anemia or liver cirrhosis. Increased hemoglobin turnover
leads to overproduction of bilirubin, which does not conjugate and subsequently crystallizes. Mixed
stones: the most common, containing both cholesterol and bilirubin. They form through a
combination of the pathophysiological mechanisms mentioned above.
Risk factors for the development of cholelithiasis: obesity and metabolic syndrome, pregnancy,
rapid weight loss, medications (e.g., fibrates, hormonal contraception, somatostatin), genetic factors.
Cholelithiasis is often asymptomatic and is incidentally discovered during imaging studies performed
for other reasons. Symptoms include: biliary colic - the most common symptom of cholelithiasis. It
is a sudden, intense pain in the right upper quadrant of the abdomen or epigastrium, often radiating to
the back or under the right shoulder blade. Usually occurs after a high-fat meal and lasts 1–5 hours.
On physical examination, the gallbladder is often tender to palpation.
Complications of cholelithiasis:
Acute cholecystitis: occurs in 10% of patients with cholelithiasis. Characterized by persistent pain,
fever, nausea, and vomiting. Clinical examination reveals a tender gallbladder, a positive Murphy's
sign, and sometimes subfebrility. Choledocholithiasis and cholangitis: stones in the bile duct can
cause obstruction leading to cholestasis and cholangitis. The classic symptoms of cholangitis are
Charcot's triad: right upper quadrant pain, fever with chills, and jaundice. Untreated, it rapidly leads
23
to septic shock. Pancreatitis: stones blocking the ampulla of Vateri. Symptoms: sudden abdominal
pain radiating to the back, elevated pancreatic enzymes, inflammatory response, multi-organ failure.
Diagnosis:
Laboratory tests: cholestasis - elevated bilirubin, ALP, GGT; acute cholecystitis - elevated CRP,
leukocytosis. Imaging methods: Ultrasonography, MRCP (magnetic resonance
cholangiopancreatography), ERCP (endoscopic retrograde cholangiopancreatography).
Treatment:
Conservative treatment: Asymptomatic cholelithiasis does not require treatment. Symptomatic –
Ursofalk, spasmolytics, analgesics. Surgical treatment: laparoscopic or open cholecystectomy
(subcostal incision in the right upper quadrant). Endoscopic treatment: ERCP.
Prevention: Healthy lifestyle.
Inflammations of the Gallbladder and Bile Ducts
Inflammations are classified as acute, subacute, and chronic.
Acute cholecystitis: arises due to obstruction of the cystic duct, distension of the gallbladder,
ischemia of the wall, followed by inflammation with the potential for necrosis, perforation, and
development of biliary peritonitis. Cholangitis: obstruction of the bile ducts → increased
intraluminal pressure, bile stasis. Subsequently, bacteria from the GI tract enter the bile ducts →
sepsis, MODS, MOF.
Clinical presentation:
Acute cholecystitis: sudden, intense pain in the right hypochondrium, radiating under the right
shoulder blade (Collins' sign), nausea, vomiting, fever. Positive Murphy's sign (tenderness on
palpation of the right hypochondrium during inspiration), subicterus to jaundice (biliary tract
obstruction, presence of Mirizzi's syndrome). Cholangitis: Charcot’s triad: pain, fever with chills,
and jaundice. In severe cases, Reynolds’ pentad (+ hypotension, mental status changes) can develop.
Diagnosis:
Laboratory tests: leukocytosis, elevated CRP, elevated ALP and GGT, elevated bilirubin.
Imaging methods: Ultrasonography: reveals the presence of gallstones, thickening of the
gallbladder wall (>4 mm), pericholecystic edema. ERCP: allows for stone removal, bile duct
drainage, and stent placement. CT and MRCP: CT is indicated in unclear diagnoses or suspected
complications such as gallbladder perforation. MRCP is a non-invasive method that is highly
sensitive for detecting choledocholithiasis and other bile duct abnormalities.
Treatment:
24
Acute cholecystitis: Conservative treatment: fluids, antibiotics, spasmolytics, analgesics. Surgical
treatment: laparoscopic cholecystectomy within 24–72 hours, urgent cholecystectomy,
cholecystostomy.
Cholangitis: Antibiotic therapy: immediate broad-spectrum antibiotics. In septic shock, intensive
care with circulatory support. Endoscopic treatment: ERCP - bile duct decompression.
Percutaneous transhepatic cholangiography (PTC) if ERCP is contraindicated.
Complications:
Acute cholecystitis: empyema, gangrene, and perforation of the gallbladder, biliary peritonitis, and
septic shock. Chronic cholecystitis: porcelain gallbladder, gallbladder carcinoma.
Cholangitis: septic shock, liver abscesses, secondary biliary cirrhosis, and pancreatitis, MODS,
MOF, death.
Jaundice: clinical syndrome characterized by yellowing of the skin, sclera, and mucous membranes
due to elevated bilirubin levels.
Classification:
Prehepatic (hemolytic): overproduction of unconjugated bilirubin during hemolysis leading to liver
overload. Hepatic (liver-related): due to liver cell damage, caused by viral hepatitis, cirrhosis,
alcoholic liver disease, drugs, or toxins. Posthepatic (obstructive): caused by obstruction of bile
flow from the liver – stones, tumors, strictures, or pancreatitis.
25
DIVERTICULAR DISEASE (36)
Ledvina Tomáš, Marek Filip
Diverticulosis of the digestive tract is a condition, when pouches or pockets are formed on the
digestive tube, most often on the colon in the region of the colon descendens and sigmoideum, but
they can be found throughout the whole range, e.g.: esophageal diverticula, parapapillary diverticula
of the duodenum, Grasser's diverticula of the jejunum or Meckel's diverticulum of the small
intestine. On the basis of the aetiology, we distinguish between congenital (=right) diverticula,
whose wall is formed by all layers of the digestive tube, and acquired (=false, pseudo) diverticula,
whose wall is formed only by mucosa and serosa (see figure).
Esophageal diverticula are most often formed by the entire thickness of the wall. According to their
location in the oesophagus, diverticula are divided into parapharyngeal diverticula (=Zenker's
diverticulum), located just below the pharyngeal to oesophageal transition, thoracic diverticula in the
middle part of the oesophagus and epiphrenic diverticula located just above the diaphragm.
Diverticula close to the sphincters (parapharyngeal and epiphrenic) are caused by a malfunction of
these sphincters, leading to an increase in intraluminal pressure in the oesophagus and bulging of the
weakened oesophageal wall – the diverticulum is formed. Thoracic diverticula are most commonly
caused by an inflammation in the mediastinum, the inflammation process pulls out the affected part
of the oesophagus and form a diverticulum. Clinically, oesophageal diverticula are manifested by
swallowing disorders, coughing, foetor ex ore, heartburn, recurrent pneumonia, but they can also be
asymptomatic for a long time and manifest only when large in size by pressure on the surrounding
organs. Diagnosis is based on contrast X-ray/CT passage through the oesophagus, gastroscopy and
manometry to exclude achalasia. In surgical treatment, we choose different surgical procedures
according to the type of diverticulum. For Zenker's diverticulum, we choose endoscopic management
- diverticulotomy with laser or stapler disection. If endoscopic intervention is not possible, we
choose the cervical incision approach at the inner edge of the m. sternocleidomastoideus, we perform
cricopharyngeal myotomy (to release the tension of oesophageal sphincter) and resection of the
diverticulum (e.g. with a stapler), be careful of a damage to the n. laryngeus recurrens. For thoracic
diverticula, we choose the thoracotomy approach or the less invasive VATS - VideoAssisted
Thoracoscopic Surgery. For epiphrenic diverticula, we again choose the thoracotomy / VATS
approach, or we can choose the laparoscopic approach from the abdominal cavity.
Meckel's diverticulum (MD) is the most common congenital defect of the gastrointestinal tract. It is
a true diverticulum that arises from imperfect closure of the omphaloenteric duct, lying 20-100cm
from the ileocecal transition on the small intestine. Inside of the MD, we can find heterotopic tissue
26
(gastric mucosa, pancreatic tissue, angiodysplasia), which may be the cause of patient´s difficulties.
MD is mostly asymptomatic, it manifests only in form of complications, which may be acute
gastrointestinal bleeding, ileus, invagination, nausea and vomiting (mimicking gastroenteritis),
diverticulitis, tumour (most often GIST - GastroIntestinal Stromal Tumour or carcinoid). The main
diagnostic methods are double contrast CT scan of the abdomen and laparoscopy. MD can be an
incidental finding during laparoscopic surgery, e.g.: appendectomy. Surgical treatment consists of
resection of the MD, the extent of the procedure is determined by its pathology. The minimal
procedure is a wedge resection, in larger lesions is necessary to perform resection of the bowel with a
part of the hinge, this applies mainly in tumor involvement to preserve radicality.
Diverticular disease of the colon can occur in its entire length, most commonly in the colon
descendens and colon sigmoideum. It is predominantly a false diverticulum, and its incidence
increases with age (in 70% of people over 80 years of age). The cause is increased intraluminal
pressure on the basis of a low-fibre diet, which causes mucosal extrusion between the weakened
muscular layer and the formation of false diverticula. Diverticula are mostly asymptomatic and
manifest only when complications occur (inflammation, bleeding, abscess, fistula, stenosis,
perforation). CT scan of the abdomen and colonoscopy are the standard diagnostic procedures. The
treatment of diverticulosis consists of adherence to a high-fiber diet. In symptomatic uncomplicated
diverticulosis, cyclic administration of rifaximin (secondary prophylaxis) has been used in recent
years.
Diverticulitis is an inflammation of the diverticula affecting the entire wall of the intestine and
extending into the surrounding area. It is caused by stagnation of stool in diverticula, which is
leading to multiplication of pathogens, pressuring of the intestinal wall and creation of decubital
necrosis of the mucosa. Diverticulitis manifests by pain in the left lower abdomen sometimes even
by peritoneal irritation, there may be a palpable cylindrical infiltrate. Other symptoms include fever,
chills, nausea, vomiting, cessation of gas and stool output, blood in stool can be observed Laboratory
findings include leukocytosis, elevated CRP. Abdominal CT will give us a definitive answer.
Differential diagnosis includes tumor, IBD, renal colic, adnexitis. We treat uncomplicated
diverticulitis with parenteral antibiotics and restriction of p.o. intake with gradual transition to a lowresidue
diet followed by a fiber-rich diet. In case of recurrent inflammation or complications abscess,
perforation, obstruction, fistula - surgical treatment is necessary. Abscess requires drainage
in addition to systemic antibiotics. In case of perforation, fistula or obstruction, acute resection of the
affected part of the intestine is necessary, followed by restoration of the intestinal passage in a
second period with an interval of at least 6 months. In the area of the sigmoid colon, we should
consider resection of the sigmoid colon according to Harmann (closure of the aboral part of the
27
intestine with a stapler and construction of the terminal descendentostomy / sigmoidostomy). In the
case of the small bowel lesion, resection with primary anastomosis may be considered. In case of
bleeding, a conservative approach with administration of haemostatic agents and blood derivatives is
the first choice. In case of failure of conservative therapy we choose surgical resection. In patients
with recurrent deiverticulitis or post inflammatory stenosis, we consider resection with primary
anastomosis at the time of calming of the inflammation (minimum interval of 8 weeks from the last
attack).
28
INTESTINAL ISCHEMIA (28)
Svatoň Roman
Intestinal (bowel) ischemia is defined as an acute or chronic, absolute or relative disorder of arterial
blood supply or venous drainage of the intestine, resulting in hypoxic damage to the cells of the
intestinal wall. Ischemic damage can vary from reversible microscopic damage to the mucosal
epithelium to irreversible complete transmural necrosis with all its consequences. Intestinal
infarction due to arterial occlusion (80–90 %) is significantly more common than that due to venous
occlusion (10–20 %). Despite advances in diagnosis and treatment, the mortality rate for this
condition remains high (30–80 %).
CLASSIFICATION
According to etiology:
Occlusive: 85 % of all cases arise from arterial or venous mesenteric occlusion or stenosis but
also due to external compression in strangulation, volvulus, or intussusception.
Non-occlusive: 15 % of all cases occur as a result of intestinal hypoperfusion and hypoxia in
shock states, sepsis, hypovolemia, cardiac failure, acute myocardial infarction, arrhythmias,
respiratory insufficiency, high doses of vasopressors, or rarely as a complication of tubeadministered
enteral feeding.
According to course:
Acute: due to arterial mesenteric embolism in atrial fibrillation (AF) or endocarditis, arterial
thrombosis due to atherosclerosis, or venous mesenteric thrombosis in congenital or acquired
thrombophilic states. Acute intestinal ischemia can also occur in aortic or mesenteric artery
dissection or strangulation.
Chronic: arterial stenoses or chronic collateralized occlusions due to atherosclerosis, less
commonly due to vasculitis, fibromuscular dysplasia, or external compression (e.g., Dunbar
syndrome – celiac artery compression syndrome caused by the median arcuate ligament).
CLINICAL SYMPTOMS
Acute Intestinal Ischemia: a sudden onset of intense abdominal pain, which may be accompanied
by nausea and vomiting. In some cases, enterorrhagia occurs, or a characteristic stool with a
"raspberry jelly" appearance related to the sloughing of ischemic mucosa. In the initial stages of this
disease (< 6 hours), a relatively common clinical presentation is the contrast between intense, almost
shock-like, subjectively perceived abdominal pain and minimal findings on physical and paraclinical
examination. This persists until the development of irreversible changes in the intestinal wall and the
onset of certain complications, such as ileus, perforation, peritonitis, or sepsis.
29
Chronic Intestinal Ischemia: cramp-like abdominal pain occurring 15–45 minutes after eating
(abdominal angina), nausea, vomiting, diarrhea, or constipation, weight loss, malnutrition with
cachexia, and fear of eating. Chronic intestinal ischemia often develops due to atherosclerosis,
causing stenoses in the abdominal aorta and its branches, with systolic murmurs heard in their
course.
DIAGNOSIS
CT with intravenous contrast and CT angiography (CTA) is the gold standard in diagnosing acute
and chronic intestinal ischemia. Stenoses or occlusions in visceral arteries or veins are detected.
Hypoperfusion of the intestinal wall manifests on CT as reduced or absent enhancement of the
affected segment by contrast agent. In venous thrombosis, edema of the wall occurs due to venous
congestion. More advanced findings, indicating irreversible changes, include the presence of gas in
the intestinal wall (pneumatosis intestinalis) (Fig. 1) or gas in the portal system (Fig. 2). In cases of
intestinal perforation, pneumoperitoneum and fluid in the abdominal cavity are detected. If CTA is
contraindicated (allergy to iodine contrast or renal insufficiency), an alternative is to perform
angiography using magnetic resonance imaging (MRA). Digital subtraction angiography (DSA) is
currently not used as a primary diagnostic method but remains reserved as an imaging method
employed in therapeutic endovascular interventions. Endoscopic methods such as colonoscopy and
enteroscopy allow for macroscopic and biopsy assessment of mucosal changes in the intestine. X-ray
and US examinations of the abdomen, used as first-line imaging methods for patients with suspected
acute abdominal emergencies (AAE), do not allow direct evidence of intestinal ischemia. Rather,
they demonstrate indirect signs, which typically develop only after a delay, often in the period of
irreversible changes in the intestinal wall or as a result of complications (vascular ileus, perforation).
Doppler ultrasound can detect occlusion or stenosis of major visceral vessels in habitually favorable
patients.
In biochemical tests, we search for increases in markers of tissue hypoxia, cellular damage,
thrombosis, and inflammation. Elevations may be seen in lactate, pH, amylase, transaminases
(AST, ALT), alkaline phosphatase, D-dimers, leukocytosis, interleukin-6, procalcitonin, intestinal
fatty acid-binding protein (I-FABP) and ischemia-modified albumin (IMA). Unfortunately, no
biomarker allows for early prediction of intestinal ischemia with sufficient sensitivity and specificity.
TREATMENT
Acute Occlusive Arterial Intestinal Ischemia: this is a condition requiring urgent intervention. The
goal of surgical treatment is early revascularization and resection of irreversibly damaged (necrotic)
parts of the intestine, with sanitation of peritonitis. In the case of irreversible changes, we perform
30
bowel resection, followed by stoma creation or anastomosis construction. This procedure is always
associated with the risk of developing subsequent complications, such as short bowel syndrome. Not
always is the ischemic boundary clearly defined during the primary operation. Intraoperative
fluorescent examination using indocyanine green (ICG) (Fig. 3) or a second-look operation 24–48
hours later can be used to assess bowel viability. The operation may also include a procedure on the
mesenteric arteries, such as direct or indirect (using a Fogarty catheter) embolectomy or
thrombectomy.
Today, depending on availability and the patient's condition, endovascular treatment of arterial
occlusion using endovascular mechanical (crushing of the embolus or thrombus) and aspiration
embolectomy or thrombectomy can precede the operation. Another non-surgical option for
revascularization is local intra-arterial thrombolysis with recombinant tissue plasminogen activator
(rtPA). If atherosclerotic stenosis is identified, it can be treated with balloon percutaneous
transluminal angioplasty (PTA), possibly with stent implantation. An alternative to the
aforementioned procedures is a hybrid approach, combining open surgery with endovascular
treatment of the arterial occlusion in a single procedure.
Acute Mesenteric Venous Thrombosis: in patients with mild clinical symptoms and no signs of
complications, the mainstay of treatment is low-molecular-weight heparin (LMWH). In cases of
clinical deterioration, selective endovascular treatment using mechanical or local thrombolysis can
be considered. Severe cases – shock, sepsis, peritoneal irritation, necrosis with perforation, as well as
CT signs of irreversible changes – are indications for surgical revision. Fluid resuscitation,
correction of electrolyte imbalances, decompressive nasogastric intubation (NGS), and broadspectrum
antibiotics (ATB) are integral parts of therapy for all acute intestinal ischemias.
Chronic Occlusive Intestinal Ischemia: conservative treatment is applicable for oligosymptomatic
patients or as an adjunct to endovascular and surgical therapy. It involves dietary adjustments (lowresidue
diet), management or compensation of factors and diseases contributing to atherosclerosis
(smoking, diabetes, hypertension, hyperlipidemia), antiplatelet therapy (acetylsalicylic acid,
clopidogrel) primarily for arterial involvement, anticoagulant therapy (LMWH, direct oral
anticoagulants – DOAC, vitamin K antagonists) primarily for venous involvement, vasodilator
therapy (nitrates, pentoxifylline), and immunosuppressive therapy in vasculitis.
Endovascular therapy in the form of balloon PTA, possibly with stent or stent-graft implantation, is
indicated for symptomatic patients. There has been a shift away from primary surgical treatment.
Endovascular approaches show fewer complications compared to surgical treatment, albeit with
shorter long-term patency of revascularization.
31
Surgical treatment is currently indicated in cases of failure or infeasibility of endovascular
treatment. Procedures performed include bypass surgery (connection between the abdominal aorta or
common iliac artery and the SMA using a venous graft or prosthesis), endarterectomy (direct
removal of atherosclerotic plaques) with mesenteric artery patching, and surgical interruption of the
arcuate ligament in Dunbar syndrome.
Non-Occlusive Intestinal Ischemia: the basis of therapy for non-occlusive intestinal ischemia is the
removal or compensation of the underlying cause. In shock states, fluid resuscitation and oxygen
therapy are needed; in sepsis, infection source control and ATB; in respiratory insufficiency,
mechanical ventilation. Local intra-arterial infusion of vasodilators (nitrates, prostaglandins,
papaverine) has been successfully used to treat peripheral vasospasm. Supportive therapy includes
anticoagulant and vasodilator therapy. In cases of bowel perforation, peritonitis, or poor overall
condition, surgical intervention is indicated.
COMPLICATIONS
Vascular ileus, necrosis of the intestinal wall, sometimes to an extent incompatible with long-term
survival, disruption of the mucosal barrier with translocation of bacteria and toxins into the
bloodstream and abdominal cavity, bowel perforation, peritonitis, sepsis, multiorgan failure, and
death. Short bowel syndrome, chronic fibrosis of the intestinal wall with the development of
strictures and intestinal fistulas, and recurrence of acute intestinal ischemia.
32
FIGURES:
Fig. 3: Absence of jejunum enhancement during ICG fluorescence examination
Fig. 1: Pneumatosis intestinalis, CT
(Albrecht HC, Trawa M, Gretschel S. Nonocclusive mesenteric
ischemia associated with postoperative jejunal tube feeding:
Indicators for clinical management. J Int Med Res.
2020;48(8):300060520929128. doi:10.1177/0300060520929128)
Fig. 2: Portal venous gas, CT
(Ko S, Hong SS, Hwang J, Kim HJ, Chang YW, Lee E. Benign
versus life-threatening causes of pneumatosis intestinalis:
differentiating CT features. Rev Assoc Med Bras (1992).
2018;64(6):543-548. doi:10.1590/1806-9282.64.06.543)
33
PERITONITIS (27)
Vystrčilová Tamara
Peritonitis is an inflammation of the peritoneum, the tissue that lines the inner wall of the abdomen
and covers and supports most of the abdominal organs. Localised or diffuse peritonitis is caused by:
Bacteria: G+ (pneumo-, gono-, streptococci – mainly primary peritonitis), G– (colibacillary –
mainly secondary peritonitis)
Chemically toxic substances: stomach contents, blood, pancreatic juice, bile, urine, chyle
Types of Peritonitis:
By origin:
1) Primary – Haematogenous or lymphogenous (e.g., pneumonia, tonsillitis), more common
in immunosuppressed individuals or via ascending infections through female genitalia,
mostly G+ mono-infection (i.e. without primary involvement of an intra-abdominal organ).
Spontaneous bacterial peritonitis (SBP) can develop from ascites and is rarely
haematogenous. It occurs commonly in patients with decompensated cirrhosis, especially in
ascites with a protein content < 10 g/l. Bacteria from the intestine are the most common
cause, with Escherichia coli being predominant.
2) Secondary – Due to transition from an inflamed organ (e.g., complications of intraabdominal
disease or injury):
a) Per continuitatem (by continuity - peritonitis from neighbouring spread) – mesenteric
occlusion, ileus, toxic megacolon
b) Perforation – e.g., appendicitis, cholecystitis, diverticulitis, gastric or duodenal ulcer,
bowel perforation, trauma
c) Chemical – Sterile peritonitis (due to bile, blood, etc.) that is clinically indistinguishable
from bacterial peritonitis; the treatment is the same.
3) Postoperative – E.g., anastomotic leakage (the most common postoperative cause); for
elective procedures, incidence should be below 2%.
4) Special types – TB peritonitis, plastic peritonitis (after irradiation), dialysis-related
peritonitis, and spontaneous peritonitis (from ascites infection).
* Some authors accept the term “tertiary peritonitis” – occurring after removal of the organ
causing secondary peritonitis or after abscess rupture.
By causative agent:
1) Microbial
2) Aseptic
34
By anatomical boundaries:
1) Circumscribed peritonitis (peritonitis circumscripta)
2) Diffuse peritonitis
By time course:
1) Acute peritonitis
2) Chronic peritonitis (e.g., intra-abdominal abscesses, tuberculosis, plastic peritonitis)
Pathology: Peritonitis is most often sero-fibrinous, purulent, or stercoral.
Pathophysiology:
The peritoneum is a large surface area allowing the absorption of bacterial toxins and secretion of
inflammatory exudate with fibrinogen, leading to fluid leakage into the third space (resulting in
hypovolaemia and electrolyte imbalance) and formation of localised inflammatory foci.
In response to bacterial, chemical, or traumatic damage to the peritoneum, vasoactive substances are
released, causing vasodilation and exudation, fibrin plaque formation, and the containment of
inflammation. However, this also leads to the absorption of exo- and endotoxins, triggering a
systemic inflammatory response (with TNF and IL produced by the liver). This process increases
capillary permeability, reduces peripheral vascular resistance, enhances blood coagulation, and
negatively affects the function of vital organs, potentially leading to MODS (multiple organ
dysfunction syndrome).
Inflammation peaks on the third day after perforation; without treatment, the patient typically dies
within a week from cardiorespiratory failure due to sepsis and toxaemia.
The mortality rate of diffuse bacterial peritonitis is reported to be 10–30%.
Clinical examination:
Local symptoms:
Somatic-type pain with guarding; sudden onset in cases of perforation, gradual in other cases.
Pain may radiate to the shoulder (phrenic symptom – pneumoperitoneum, subphrenic
abscess).
Palpable tenderness and muscle guarding (may lessen later); abdominal distension with
dilated bowel loops (ileus).
Plenies, Blumberg, and Rovsing signs (peritoneal irritation signs).
Absent respiratory movement and bowel sounds (paralytic ileus – "dead silence" in the
abdomen).
Rectal tenderness and sphincter relaxation.
35
A temperature difference of more than 1°C between the axilla and rectum (Lennander's sign).
General symptoms:
Nausea, vomiting (initially reflexive, then due to bowel paralysis), absence of stool and gas.
Decreased BP, increased HR, increased temperature, tachypnoea, oliguria/anuria (shock
symptoms), pallor, sweating, dry tongue.
In severe cases, late-stage symptoms may include facies Hippocratica (sunken eyes, sharp
nose, sunken cheeks, sticky sweat) and septic encephalopathy (delirium).
Diagnostics:
Medical history and clinical examination.
Laboratory tests: Full Blood Count - FBC (↑leucocytes, ↑CRP), liver function tests - LFTs
(↑bilirubin and transaminases), amylase, acid-base imbalances (e.g., metabolic acidosis,
respiratory alkalosis, ↑lactate, ↓pO2, ↓pCO2).
Imaging:
Ultrasound: Free fluid in the abdomen or abscess, with ultrasound-guided puncture for
microbiological and biochemical analysis.
X-ray: Pneumoperitoneum (indicative of perforation).
CT scan: The gold standard method for evaluating acute abdomen conditions.
Endoscopy: For suspected perforated ulcers if clinical and X-ray findings are unclear.
Treatment:
Four main principles:
Control the source of infection.
Eliminate bacteria and toxins.
Maintain organ function.
Control the inflammatory response.
Specific interventions include:
Venous access with infusion (Hartmann’s solution).
Stabilisation of vital functions (maintain urine output > 0.5 ml/kg/hour).
Broad-spectrum antibiotics, later adjusted based on sensitivity testing (take a swab or blood
culture perioperatively).
NG tube and urinary catheter (or puncture epicystostomy if needed).
Special procedures (e.g., NPWT for temporary abdominal closure if repeated access is
needed).
36
Early enteral feeding and immune support for prolonged septic symptomatology.
Surgical intervention:
The indication is developing clinical symptomatology – worsening pain and defences, ↑ TF
and ↓ BP despite intensive therapy, X-ray evidence of pneumoperitoneum, ultrasound
evidence of free fluid with exclusion of ascites in liver cirrhosis and AP.
It includes laparotomy or laparoscopy for infection source control (e.g., appendectomy,
cholecystectomy, ulcer repair, resection of the stomach and hemicolectomy in perforated
malignancies, resection of the small intestine, e.g. in Crohn's disease, Hartmann resection in
perf. diverticulitis, etc.), suture perforation (GD ulcer, bowel perforation,...), stoma
construction, especially in colon malignancies, necrectomy, lavage and drainage in AP.
Complications of Peritonitis:
Possible complications include dehydration, ileus, hepatorenal syndrome, sepsis, septic shock,
multiple organ failure, and death.
37
ILEUS (29)
Csölle Jakub
1. Definition
Ileus, or intestinal obstruction, is a form of acute abdomen where the passage of contents through the
gastrointestinal tract is halted. This condition can be mechanical or functional. In mechanical ileus, a
physical blockage occurs in the intestinal passage, while in functional ileus, the movement of
intestinal content is impaired due to a disruption in intestinal motility.
2. Classification and Causes of Ileus States: Ileus conditions can be divided into three categories:
Mechanical Ileus:
Adhesions (scar tissue): Formation of fibrous adhesions or bands between the intestines or other
organs and structures within the abdominal cavity can cause narrowing or strangulation of the
intestine. Adhesions typically arise after surgeries or inflammation within the abdominal cavity. This
is the most common cause of small bowel obstruction.
Tumors: Benign or malignant tumors obstructing the intestinal lumen. The most common cause of
obstruction in the large intestine.
Hernias: Intestinal loops may become strangulated in hernia openings, leading to ileus.
Volvulus: Twisting of an intestinal loop around its axis, causing mechanical blockage.
Intussusception: Part of the intestine telescopes into itself, often due to a polyp being pulled by
peristalsis.
Gallstone Ileus: A large gallstone enters the gastrointestinal tract through bile ducts or erodes from
the gallbladder into the intestinal lumen via a chronic biliodigestive fistula.
Swallowed Foreign Objects.
Neurogenic Ileus: No physical obstruction is present, but the intestine cannot perform normal
peristalsis.
Paralytic (functional) Ileus: Absence of peristalsis, which may occur after surgeries, infections,
injuries, or metabolic disturbances such as electrolyte imbalances.
Spastic Ileus: A pathological spasm of the intestine, a rare form of ileus, seen in conditions affecting
the CNS or lead poisoning.
Vascular Ileus: Occurs due to ischemic bowel disease, where blood circulation in mesenteric vessels
is impaired. This can be caused by:
Thrombosis or Embolism of Mesenteric Vessels: A blood clot blocks the arteries supplying the
intestine, leading to an interruption of blood flow.
Insufficient Blood Flow: Caused by shock, heart failure, dehydration, or septic states.
38
3. Pathophysiology Significantly depends on the type of ileus and the location of the blockage.
Small Bowel Ileus: The bacterial colonization of the small bowel is typically low. With impaired
passage, bacterial overgrowth occurs, leading to hypersecretion from the mucosa and increased blood
flow to the intestinal wall. Even with significant small bowel dilation, the intestinal wall’s blood
flow remains intact.
High Small Bowel Ileus: The obstruction is in the jejunum. The patient is primarily at risk of severe
fluid and electrolyte loss, leading to hypovolemia and electrolyte imbalance.
Low Small Bowel Ileus: The obstruction is in the ileum. Stagnation of intestinal contents leads to
bacterial overgrowth, mucosal hypersecretion, disruption of the mucosal barrier, and subsequent
bacterial translocation. Systemic inflammatory response syndrome (SIRS) and organ dysfunction
develop.
Large Bowel Ileus: Significant distension of the large bowel, with increasing intraluminal pressure,
leads to impaired blood supply to the bowel wall, ischemia, and eventually perforation. Unlike small
bowel ileus, mucosal hypersecretion and bacterial translocation do not play a major role.
Bowel Ischemia: Rapidly progresses to gangrene of the entire intestinal wall, followed by the
development of SIRS and multi-organ failure (MOF).
4. Clinical Symptoms
Abdominal Pain: Usually colicky, more common in mechanical ileus. In paralytic ileus, the pain
may be less pronounced.
Abdominal Distension and Bloating: Intestinal content accumulates, causing tension in the
abdominal wall. In high small bowel ileus, distension may not be evident.
Vomiting: Common, especially with obstructions in the upper gastrointestinal tract. It may become
fecal in prolonged obstruction. In large bowel ileus with a competent Bauhin’s valve, vomiting may
be absent.
Absence of Stool and Gas: A typical sign, indicating halted bowel activity. In cases of obstruction
in the proximal bowel, stool passage may continue until the large intestine is emptied.
Deterioration of General Condition: Dehydration, electrolyte imbalances, hypotension,
tachycardia, and shock may occur in untreated ileus.
5. Diagnosis The diagnosis of ileus conditions is complex and involves various methods:
Clinical Examination: Identifying typical symptoms (see above). Auscultation of the abdomen may
reveal hyperactive bowel sounds in mechanical ileus or absent sounds in paralytic ileus. Key history
elements include previous abdominal surgeries, malignancies, or inflammatory bowel diseases.
39
Imaging Methods:
Abdominal X-ray: Shows dilated bowel loops and fluid levels.
CT Scan: The most accurate method for determining the level of obstruction and, often, its cause.
Contrast-enhanced CT is not always necessary.
Ultrasound: Mainly used in unclear cases and in children.
Laboratory Tests: Blood tests can reveal dehydration, electrolyte imbalances, or signs of
inflammation.
6. Treatment Treatment of ileus conditions depends on the cause and severity:
Conservative Treatment: Mainly for functional ileus, involving bowel rest (nothing by mouth),
nasogastric tube decompression, fluid and electrolyte replacement, and medications to stimulate
peristalsis (for paralytic ileus).
Surgical treatment: If a mechanical obstruction is present, surgery is often necessary, but the
indication must be carefully considered, for example, in patients after multiple abdominal operations,
where any further intervention may result in the development of significant complications, up to
abdominal catastrophe. The type of surgical procedure depends on the etiology of the ileus, which is
often only discovered during the procedure itself. Among the most common are: Adhesiolysis release
of adhesions. Resection of a part of the intestine that is obstructed, for example, by a tumor, a
chronic inflammatory process, or is affected by irreversible ischemic changes. Based on the patient's
current condition and intraoperative findings in the abdominal cavity, it is necessary to decide
whether the procedure will be performed with the restoration of GIT continuity (anastomosis) or with
the establishment of an intestinal outlet (stomy). Volvulus derotation, reposition of the invaginated
part of the intestine, hernia reposition. Bowel opening - Enterotomy/colotomy, with extraction of an
obstruction blocking the passage, eg bulky gallstone, swallowed foreign body. The surgical approach
is in most cases openly from laparotomy. Exceptionally, especially in patients without a history of
numerous abdominal surgeries, a minimally invasive laparoscopic approach can be used.
8. Prognosis The prognosis for patients with ileus depends on the speed of diagnosis and treatment.
Mechanical ileus often requires urgent surgery to prevent irreversible changes. In paralytic ileus, the
prognosis is generally favorable unless complications like aspiration and ARDS arise.
40
HERNIAS OF THE ANTERIOR ABDOMINAL WALL, DIAPHRAGMATIC HERNIAS (11)
Prudius Vadim
Hernia is a condition in which an organ (or organs) pathologically shifts from its natural position.
Etiology. The most common causes of hernias include increased intra-abdominal pressure, prostate
hyperplasia, hormonal changes associated with menopause and andropause, excessive physical
exertion, abdominal surgeries, congenital defects, and other genetically determined conditions.
Symptomatology. A patient with a hernia may not feel any discomfort (asymptomatic hernia), or may
experience a wide range of symptoms (symptomatic hernia). The most common reason for seeking
medical attention is the sensation of pressure and burning at the site of the hernia. Other symptoms
may include pain, itching at the site of the hernia, digestive issues, and psychosocial factors (cosmetic
defects, sexual dysfunction). A patient with an asymptomatic hernia may live without any issues for
several years. However, the risk (and potential complication) of any hernia is
incarceration(incarceratio). Incarceration is considered an acute surgical condition and falls under the
category of acute abdominal emergencies. It is characterized by severe pain, a hard, extremely painful
mass at the hernia site, and in cases involving a portion of the digestive tract, symptoms like bowel
obstruction, vomiting, and other signs related to an ileus condition (see the relevant chapter). Caution!
In elderly patients, an incarcerated hernia may present without typical symptoms due to reduced pain
sensitivity. The first signs may instead be symptoms of a developed ileus condition.
Diagnosis. Most abdominal wall hernias can be diagnosed through a clinical examination of the
abdomen. A key diagnostic maneuver is the Valsalva maneuver. Naturally, a thorough medical history
is essential, particularly for educating the patient and preventing recurrence. Ultrasound also plays an
important role, especially in unclear cases and for confirming femoral, recurrent, and incisional
hernias. Standard imaging methods like CT and MRI are typically not used for diagnosing inguinal
and umbilical hernias. However, CT scans may be used for large ventral hernias to assess the
abdominal wall defect and the technical feasibility of its repair (discussed further in the section on
preparation for surgery).
Differential Diagnosis. In the differential diagnosis of femoral hernias, it is important to consider
lymph node syndromes, especially in elderly women. Inguinal hernias need to be distinguished from
tumors, most commonly lipomas. Small umbilical hernias should be differentiated from inflammatory
processes or small lipomas. The primary tools for differentiation are ultrasound and, if necessary, CT
scans. For diaphragmatic hernias, conditions like achalasia or esophageal tumors (including MALT
lymphomas) should also be considered.
Classification of Hernias. By location: External, Internal. By origin: Congenital hernias (herniae
41
congenitae). Acquired hernias (herniae acquisitae). By the presence of a sac: True hernias (with a
hernial sac present), false hernias (without a hernial sac). By reducibility: Freely reducible (hernia
libera), Irreducible, Incarcerated hernia (hernia incarcerata), Elastic incarceration (incarceratio
elastica), Fecal incarceration (incarceratio stercoracea), Incarceration "in W", Adhesions between the
sac and hernia contents (hernia accreta). Large hernia (hernia permagna). Richter's hernia –
Incarceration of part of the intestinal wall while preserving bowel passage (temporarily). Littre's hernia
– Incarceration of Meckel's diverticulum. By location: Abdominal hernias: Inguinal/scrotal,
umbilical, epigastric/supraumbilical, supravesical, femoral, obturator, perineal, sciatic, incisional,
parastomal
Diaphragmatic hernias: Sliding, paraesophageal (including upside-down stomach), Bochdalek hernia,
Lorei's hernia. Post-traumatic (after thoracic and cardiac surgeries). Internal hernias
Cassification. In herniology, the classification system of the European Hernia Society is commonly
used today.
Worldwide incidence of hernias. Inguinal hernias: 75% (♂:♀ 7:1), of which 75% are indirect.
Umbilical hernias: 5-14%. Incisional hernias: 10%. Femoral hernias: 3-5%.
Anatomy of hernias. Hernial opening, hernial sac, hernial contents.
Patient preparation for surgery. For the vast majority of small hernias, standard preoperative
preparation is sufficient. Special preparation is required for large ventral hernias, for which we use CT
scans, as mentioned above. In cases of fistulization in the area of the hernial defect with the presence
of mesh from previous surgery, an MRI is advisable. This is mainly to measure the amount of free
tissue needed to close the defect. For obese patients, weight reduction is recommended, which
decreases intra-abdominal volume and increases the amount of usable tissue for closing the defect
(altering the ratio between abdominal wall area and intra-abdominal volume). In many centers, Botox
is used for this purpose, applied to the abdominal muscles under ultrasound guidance.
Hernia surgery. The effectiveness of each procedure is evaluated based on recurrence rates and
postoperative complications. Minimally invasive procedures are preferred today, as they have lower
recurrence rates and fewer complications compared to traditional methods. Patients also tolerate them
better, and they shorten hospital stays.
Inguinal hernia surgery. Traditional methods. Without mesh (McVay, Shouldice, Bassini). With mesh
(Lichtenstein). Minimally invasive methods. Laparoscopic - TEP (totally extraperitoneal approach),
TAPP (transabdominal preperitoneal approach), TOM (transabdominal onlay mesh, rarely used
today).
To choose the correct approach for a patient, factors such as age, physical activity, comorbidities,
previous surgeries, and prostate issues in men should be considered. For younger, otherwise healthy
42
patients, a minimally invasive transabdominal approach like TAPP or TEP is often advantageous.
Statistically, TEP has a slightly lower incidence (a difference of just a few per mille) of postoperative
and perioperative complications but does not allow for simultaneous correction of bilateral inguinal
hernias or abdominal organ revision, unlike TAPP. For larger defects, a traditional approach, most
often Lichtenstein, is preferred. In case of inguinal hernia recurrence, the next step depends on the type
of the previous surgery. For example, if the first surgery was traditional, a laparoscopic approach is
preferred for recurrence and vice versa.
Femoral hernia. In femoral hernias, abdominal or pelvic organs pass beneath the inguinal ligament
through the femoral canal. This type of hernia occurs far less frequently than inguinal hernias, at a
ratio of 1:30. It is very rare in children and young adults, affecting primarily older women. About 50%
of patients with femoral hernias present with incarceration, often with a parietal strangulation
(Richter's hernia). For elective procedures, TAPP is preferred, while in emergency situations,
laparoscopy is considered to assess the viability of the bowel loop, or the procedure is performed via
traditional surgery.
Umbilical hernia: typically appears after the third decade, predominantly in women (80%). They
account for about 5-10% of all hernias. Most are small defects, so, as mentioned, Mayo repair is
primarily used. For hernias larger than 4 cm or recurrent umbilical hernias, procedures such as MILOS,
eMILOS, or eTEP may be considered.
Ventral hernia surgery. For smaller defects, the patient's own tissues are preferred. The most commonly
used method is Mayo repair. However, the defect often cannot be closed without tension using only
native tissues. In such cases, mesh or extensive plastic surgery using the tissues of the anterior
abdominal wall is used. Component separation of the anterior abdominal wall is not uncommon. The
procedures can be divided into anterior and posterior approaches. In practice, anterior separation means
separating the subcutaneous tissue, fascia, and oblique muscles, while posterior separation involves
separating the peritoneum, posterior sheath of the rectus muscles, and transverse muscles. A
combination of separation and the use of xenograft materials is also possible.
Anterior component separation: Ramirez’s procedure is a typical example of anterior separation, used
to close defects after “open abdomen” or in recurrent large ventral hernias. Currently, traditional
Ramirez anterior component separation is being replaced by the minimally invasive eACS (endoscopic
anterior component separation).
Posterior component separation: TAR (Transversus Abdominis Muscle Release) has two main
variants: Novitsky’s operation, which gradually separates the transverse fascia from the subcostal
space caudally, or reverse TAR (Spanish TAR). This procedure is primarily aimed at enlarging the
43
area of the anterior abdominal wall. It can be performed openly, minimally invasively (eTAR), or
robotically (rTAR). It is often combined with Rives-Stoppa surgery.
Rives-Stoppa operation uses posterior separation with mesh and is chosen for recurrent ventral hernias,
incisional hernias, or multiloculated hernias along the midline.
MILOS surgery for large umbilical hernias or recurrent ventral hernias is a minimally invasive
alternative to ventral repair with mesh. It has been gaining popularity due to a lower recurrence rate
(2.2-2.4%). The improved version, eMILOS, is the endoscopic variant.
eTEP has almot the same indications as MILOS surgery but uses a completely endoscopic approach
with three or more ports, usually positioned in the lower abdomen.
Robotic hernia surgeries: Recently, large abdominal wall defects, including parastomal and hiatal
hernias, are increasingly being addressed robotically in Europe.
Traction methods: This procedure involves intraoperative traction of the abdominal wall defect edges.
Traction time varies from 10 to 30 minutes, and the total force ranges from 8 to 18 kg. It is intended
for closing large ventral defects and is usually combined with the Rives-Stoppa procedure.
Internal hernias: occur when abdominal organs are pushed into preformed recesses on the posterior
wall of the peritoneal cavity, mesentery, or mesocolon. They are not true hernias, as the hernial sac
does not protrude outside the abdominal wall. Internal hernias are rare and are most commonly
diagnosed during surgeries for bowel obstruction or incidentally during open abdominal surgeries.
Diaphragmatic hernia. Hiatal hernia occurs when part of the stomach passes through the diaphragm
into the chest, most often the cardia (upper stomach) through the esophageal hiatus. In extreme cases,
the entire stomach may enter the chest. If only the stomach passes without a hernial sac and the angle
of His is absent, it is called a sliding hernia. The main complication is gastroesophageal reflux. If the
hernial sac is formed and the gastroesophageal junction remains in the abdominal cavity, it is a
paraesophageal hernia. Complications include venous stasis with bleeding, ulcers of the distal
esophagus, necrosis with perforation due to strangulation, obstruction with passage disorder (high
ileus), and compression of intrathoracic structures (heart, lungs).
44
SMALL BOWEL AND LARGE BOWEL NEOPLASMS (37)
Svoboda Martin, Grolich Tomáš, Procházka Vladimír
Small bowel tumours are rare and occur in less than 10% of all GIT tumours. The majority of small
bowel tumours are benign tumours including adenomas, lipomas and haemangiomas. They are
usually asymptomatic and manifest most often with ileus, intussusception or bleeding, which is
either acute or chronic, expressed by anaemia. Although CT scanning is the method of choice (e.g.,
in the case of obstruction, the radiologist will describe the so-called transition zone on the bowel
where the dilated section transitions to the collapsed section and, in the best case, the possible
etiology of the obstruction), if the neoplasia causes anemia, the diagnosis is difficult and the CT scan
may be equivocal. Small bowel examination is generally difficult and capsule endoscopy or small
bowel endoscopy can be used for diagnosis. Symptomatic lesions are treated by resection of the
affected section with construction of an anastomosis. Malignant tumours of the small intestine are
rare, diagnosed late and usually manifest with obstruction. The following 4 types of tumors are
responsible for 99% of small bowel malignancies. Adenocarcinoma is more common in the jejunum
than in the ileum. Patients with m. Crohn's disease (CD), celiac disease, familial adenomatous
polyposis (FAP) are more likely to be affected. Clinically, it manifests either by obstruction,
invagination, anaemia or acute bleeding. The prognosis is poor, especially in patients with CD, due
to late diagnosis, because of similar clinical manifestations. The method of treatment is surgical
resection of at least 5 cm on each side of the tumor, including the appropriate section of the relevant
part of the mesentery where the lymph nodes are located. For terminal ileal tumours, ileo-cecal
resection or right-sided haemicolectomy is an adequate procedure. Neuroendocrine tumors (NETs,
carcinoids) occur most frequently in the appendix, then in the ileum. Metastases to the lymph nodes
may be larger than the primary tumor, which is usually small. NETs produce vasoactive peptides,
most commonly serotonin. Liver metastases may manifest with carcinoid syndrome because the
vasoactive substances are not filtered through the liver and enter the systemic circulation.
Radiopharmaceuticals - somatostatin analogues - are used to image NETs (NETs often have
receptors for somatostatin), and chromogranin A is detected in plasma, which can be used to monitor
recurrence and prognosis. Surgical resection of NETs is usually sufficient; tumours are not sensitive
to chemotherapy and radiotherapy. Patients with carcinoid syndrome (diarrhea, bronchospasm, flush,
palpitations) are given somatostatin analogues during surgery to prevent carcinoid crisis. NETs grow
slowly, and even patients with metastatic disease may live for several years. Small bowel
lymphomas are most often secondary to systemic lymphoma. They are more common in patients
with CD and immunodeficiency. They present with pain, weight loss, inappetence, fatigue, diarrhea,
45
tenesmus and acute conditions. They often occur in the region of the ileo-cerebral transition
(Burkitt's lymphoma). Chemotherapy is the method of treatment. Surgical treatment is performed in
the case of an acute condition of obstruction, perforation, hemorrhage, or the need for histological
verification not otherwise obtainable. Gastrointestinal stromal tumors (GISTs) are mesenchymal
tumors and the distinction between malignant and benign is difficult even on histopathological
examination. Malignant potential is determined by tumor size and the degree of
immunohistochemical c-kit (CD117) staining. They are most commonly found in the stomach. It is
often asymptomatic and is diagnosed incidentally. It presents with fatigue, pain, nausea,
haematemesis or melena. GIST is resistant to radiotherapy and conventional chemotherapy. Surgery
is the most effective method of treatment and its principle is to remove the lesion without breaking
its wall and without the need for lymphadenectomy or extensive resection. The tyrosine kinase
inhibitor imatinib (Glivec) is used in adjuvant therapy.
Colorectal cancer (CRC) includes adenocarcinoma of the colon and rectum. The incidence in the
Czech Republic is around 7000 cases per year and half die from it. Despite the established screening,
there is still a very high proportion of patients diagnosed in the later stages of the disease (stages III
and IV), which reduces the chances of a good treatment outcome and decreases survival. Hereditary
forms include Lynch syndrome and FAP. Sporadic occurrence of up to 90% predominates. One of
the important molecular characteristics of CRC is the detection of microsatellite instability (MSI) of
the tumor (in about 15% of CRC), determined by immunohistochemistry from biopsy.
Immunotherapy can be used in MSI tumours, which allows significant regression of the tumour, or
its complete disappearance (up to 90%) with avoidance of surgery and its possible complications.
From the point of view of CRC management, it is necessary to strictly divide tumours into tumours
of the colon and rectum. Appendiceal tumours are usually detected incidentally on histological
examination and occur in 1% of appendixes removed. The most common tumours are epithelial
adenocarcinomas, mucinous neoplasms and neuroendocrine tumours. Because of the oncological
radicality, it is often necessary to perform a right-sided hemicolectomy after appendectomy. Patients
with mucinous neoplasms are at risk of developing pseudomyxoma of the peritoneum; for this
reason, during appendectomy when a mucinous tumor is suspected (mucocele), the mucin must not
leak into the free abdominal cavity (dissemination). Colon tumors manifest differently depending on
the localization. Up to 20 % of them present acute abdomen (obstruction, perforation, bleeding).
Right-sided tumours usually do not present with obstruction, but more often with anaemia because
the tumour grows long and bleeds slowly. On the other hand, left-sided tumours often present with
ileus. In acute conditions, the priority is to save the patient's life, remediate sepsis and allow a good
recovery after surgery for subsequent oncological treatment. Perforation leads to peritonitis
46
(mortality up to 65%) and the most common solution is to perform resection of the perforated colon
with stoma creation. The construction of an anastomosis is very risky in the field of severe sepsis due
to dehiscence. In case of left colonic obstruction, Hartmann's operation (resection with terminal
colostomy), axial colostomy derivation or endoscopic stent insertion is possible. The last two options
are based on resolving the ileus at the first time (simple procedure to stabilize a patient) and planning
a radical resection with a few days' interval at the second time. Obstruction of the right colon is more
often resolved by primary resection with ileo-transverse anastomosis. Before elective surgery, each
patient must be properly examined (staging). Colonoscopy is used for biopsy, to exclude
synchronous lesions and to localize the tumor (tattooing). High levels of oncomarkers (CEA) tend to
be present in metastatic disease. CT of the abdomen, pelvis and chest is the primary imaging
modality to exclude metastases, which occur in up to 20% of patients. The liver is most commonly
affected (17%), followed by the peritoneum, lungs and lymph nodes (LU). Colonoscopic removal is
sufficient for early pTis cancers, but only if risk factors are not present in pT1 (vascular invasion,
grade 3, tumour budding > 1 - risk of lymph node metastasis). Treatment is sequenced as tumour
resection followed by adjuvant therapy, neoadjuvant therapy is not routinely used for colon tumours.
The goal of surgical treatment is radical resection (removal of the tumor) with lymphadenectomy,
i.e. R0 resection. The basic principles include resection of the tumor with sufficient resection
margins (at least 10 cm), respecting the vascular and lymphatic supply of the columns. For tumors of
the right colon, a right-sided hemicolectomy is performed (resecting the terminal ileum and the oral
third of the colon transversum, ligating the a. ileocolica, a. colica dextra, and the right branch of the
a. colica media at the origin) with construction of an ileo-transverso anastomosis. In tumors of the
hepatic flexure and the oral part of the transversum, an extended right-sided hemicolectomy can be
performed. In tumors of the middle part of the transversum, segmental resection with ligation of the
a. colica media with a colic-colic anastomosis is performed. In the case of tumors of the left colon,
ligation of the a. mesenterica inferior is performed; in the case of tumors of the colon sigmoideum,
the a. mesenterica inferior can be ligated distally to the a. colica sinsitra to leave a blood supply for
the colon descendens. A descendento-rectal anastomosis is performed. Removal of the entire colon
leaving the rectum is called subtotal colectomy (e.g. in FAP) and proctocolectomy is removal of the
colon including the rectum. Continuity is restored by ileo-pouch anal anastomosis, the pouch being a
reservoir formed from the ileum. Colorectal surgery is burdened with a high morbidity rate of up to
40 % and a mortality rate of 5 %. The most feared complication is anastomotic leak, the
disintegration of the anastomosis. It occurs several days after surgery and can result in peritonitis and
sepsis.
47
Tumours of the rectum are often manifested by bleeding or a change in the pattern of defecation. In
addition to the above diagnostic methods, rectoscopy is used and MRI of the pelvis is an essential
imaging method to determine the exact extent of the tumour and other risk factors: whether the
tumour extends into the mesorectal fascia (MRF), whether there is involvement of the nodes,
invasion of the mesorectal vessels. The treatment strategy depends on the height of the tumor in the
rectum and the presence of risk factors on staging MRI. In case of acute obstruction, the first
procedure is a derivation stoma. For oral rectal tumors (10-15 cm from the anus), primary resection
is usually performed (they are treated more like colonic tumors). For tumours of the mid (5-10 cm)
and distal rectum (0-5 cm), neoadjuvant treatment (NAT) is often started on the basis of staging,
which includes chemoradiotherapy (usually 5 weeks) or in combination with additional
chemotherapy (usually 18 weeks). This is followed by radical resection of the rectum with total
mesorectal excision (TME). The aim of TME is to remove the rectum with the surrounding
mesorectum containing the LU in their entirety without disturbing the MRF. If the MRF and
mesorectum are damaged during surgery there is a higher risk of local recurrence in the pelvis. If the
tumor infiltrates the sphincters, rectal amputation is usually indicated. Sometimes, however, these
patients may experience tumour disappearance after NAT, a so-called complete response. These
patients are then closely monitored (Watch and Wait strategy) with repeated MRI, rectoscopy and
p.r. examinations and may be spared radical resection. Standard rectal resection is performed
laparoscopically, robotically and possibly transanally. Because of inferior blood supply to the anus,
AL often occurs after rectal resection when the tract is connected to the anal canal. For this reason, in
rectal resection after the construction of a low-lying anastomosis in the pelvis, a protective ileostomy
with diversion of the passage is performed to allow the anastomosis to heal and the consequences of
AL are not severe. In addition to the complications described above, another specific feature of rectal
tumors is the possibility of perioperative damage to the nerves of the bladder, sphincters and genital
organs and the resulting postoperative dysfunction. Adjuvant therapy is administered only selectively
according to the results of definitive histology. The entire management of rectal cancer is decided by
a multidisciplinary team.
48
INFLAMMATORY DISEASES OF SMALL BOWEL AND THEIR SURGICAL MANAGEMENT (34)
Vlček Petr
Surgical Inflammations of the Small Intestine
Introduction - Inflammatory diseases of the small intestine, including its diverticula, represent a
smaller group of pathological conditions of various etiologies, but they can lead to serious
complications such as obstruction, perforation, or peritonitis.
1. Crohn's Disease
Etiology and Pathophysiology - Crohn's disease is a chronic disease that belongs to the group of
non-specific inflammatory bowel diseases. It can affect any part of the gastrointestinal tract, most
commonly the ileum. The exact etiology is unknown, but it is believed to involve genetic
predisposition, systemic immune dysfunction, and environmental factors.
Clinical Presentation - Crohn's disease presents with a wide range of symptoms, including
abdominal pain, chronic diarrhea, weight loss, and anemia. A typical finding is segmental
granulomatous inflammation throughout the entire thickness of the bowel wall, which can lead to
strictures, fistulas, and abscesses.
Diagnosis - Diagnosis is based on medical history, clinical examination, and endoscopy,
supplemented by histopathological examination. Imaging methods such as magnetic resonance
enterography (MRE) or CT enteroclysis are useful for assessing the extent and activity of the disease,
often showing characteristic skip lesions.
Surgical Treatment - Surgery is indicated for complications like obstruction, perforation, abscesses,
or fistulas. The most common procedure is resection of the affected bowel segment with primary
anastomosis. Surgical treatment should be coordinated with gastroenterologists. Abscesses are often
best treated by interventional radiology, followed by resection after infection treatmentl. The most
common surgery is ileocecal resection, primarily for stenosis resistant to conservative therapy. A
laparoscopic approach with intracorporeal or extracorporeal anastomosis is preferred. A wide sideto-side
anastomosis is favored, and stapling devices are not contraindicated. Recently, the KONO-S
anastomosis, a wide end-to-end anastomosis using colonic (entero)plastic techniques, has become
popular. Robotic systems are useful for performing this procedure intracorporeally. Strictureplasty
can be used for additional skip lesions.
2. Ischemic Enteritis
Etiology and Pathophysiology - Ischemic enteritis occurs due to inadequate blood supply to the
small intestine, leading to reactive changes. The most common causes include embolism, mesenteric
vessel thrombosis, low cardiac output, or hypotension.
49
Clinical Presentation - Patients typically present with sudden, severe abdominal pain. Other
symptoms may include diarrhea, bloody stools, and fever. Advanced ischemia can lead to bowel
necrosis and perforation.
Diagnosis - Fast diagnosis is crucial for successful treatment. Key diagnostic tools include CT
angiography to detect mesenteric vessel occlusions and laboratory tests showing elevated
inflammatory markers and lactate levels.
Surgical Treatment - If bowel necrosis occurs, immediate surgery is required, usually involving
resection of the affected segment with anastomosis. If diagnosed early, revascularization procedures
such as embolectomy or bypass may be considered to restore bowel blood flow.
3. Radiation Enteritis
Etiology and Pathophysiology - Radiation enteritis arises as a complication of radiation therapy,
where ionizing radiation damages intestinal mucosal cells, leading to inflammation, fibrosis, and
strictures. Chronic radiation enteritis can develop months to years after radiotherapy.
Clinical Presentation - Symptoms include chronic abdominal pain, diarrhea, nausea, weight loss,
and bleeding in the stool. In severe cases, bowel obstruction or fistula formation may occur.
Diagnosis - Diagnosis of radiation enteritis involves endoscopy, which can reveal inflammatory
changes, strictures, and ulcerations. Imaging techniques like CT or MRI are helpful in assessing the
extent of damage.
Surgical Treatment - Surgery is indicated for bowel obstruction, perforation, or fistula formation.
Resection of the affected bowel segment with anastomosis is the most common procedure, though
surgery can be complicated by adhesions.
4. Acute Infectious Enteritis
Etiology and Pathophysiology - Acute infectious enteritis is caused by infection of the intestinal
mucosa by various pathogens, including bacteria (e.g., Salmonella, Shigella, Campylobacter), viruses
(e.g., Norovirus, Rotavirus), and parasites (e.g., Giardia lamblia). Mucosal inflammation leads to
malbsorption and fluid secretion, leading to diarrhea.
Clinical Presentation - Symptoms include the acute onset of diarrhea, abdominal pain, vomiting,
fever, and dehydration. Some patients may develop severe complications such as toxic megacolon or
bowel perforation.
Diagnosis - Diagnosis is typically based on clinical symptoms and laboratory tests, such as stool
cultures or pathogen detection via PCR. In severe cases, imaging (CT or X-ray) is recommended to
rule out complications like perforation.
50
Surgical Treatment - Surgery is generally only indicated for severe complications like perforation
or toxic megacolon. In such cases, resection of the affected bowel segment with temporary diversion
or laparostomy with a provisional abdominal wall closure is necessary.
5. Diverticulitis
Diverticula of the small intestine are rare, but inflammation can lead to serious complications such as
perforation, bleeding, or bowel obstruction. Diagnosis is often difficult due to their rarity, which can
worsen the clinical picture.
Etiology and Pathophysiology - Diverticula of the small intestine are divided into congenital (true)
and acquired (false).
Congenital diverticula involve all layers of the intestinal wall (mucosa, submucosa, and muscle
layer) and most often arise from developmental anomalies during embryogenesis. An example is the
Meckel's diverticulum which occurs in the ileum and is differentially diagnostic associated with
appendicitis.
Acquired diverticula result from increased intraluminal pressure, causing mucosa and submucosa to
push through the weakened muscle layer of the bowel wall. These diverticula are common in older
patients, particularly in the duodenum near the ampulla of Vater.
Clinical Presentation - Most diverticula are asymptomatic and are often discovered incidentally
during imaging or surgery for other reasons. When symptomatic, complications include:
Diverticulitis: Inflammation, presenting with abdominal pain, often localized to the epigastrium or
mesogastrium, fever, nausea, and vomiting. Symptoms can mimic acute appendicitis or cholecystitis.
Perforation: Leads to acute peritonitis, with sudden, severe abdominal pain, abdominal wall rigidity,
and sepsis, requiring immediate surgery.
Bleeding: Can cause melena or hematochezia, sometimes leading to anemia. Meckel's diverticulum
is the most common source of painless lower gastrointestinal bleeding in children.
Bowel Obstruction: May be caused by inflammation, lumen narrowing from recurrent inflammation,
or diverticular torsion. Symptoms include abdominal pain, vomiting, distension, and absence of stool
and gas passage.
Diagnosis - Diagnosing small bowel diverticula can be challenging due to non-specific symptoms,
often resembling other abdominal conditions. Diagnosis typically relies on a combination of clinical
presentation and imaging:
Endoscopy: Duodenal diverticula can often be diagnosed by endoscopy, especially if located in the
proximal duodenum. Meckel's diverticulum is rarely identifiable endoscopically.
Imaging: CT and MRI are the most commonly used imaging methods, detecting diverticula and their
complications. CT angiography may be useful for localizing bleeding sources.
51
Surgical Treatment - Surgery is indicated for symptomatic diverticula or complications. Procedures
vary based on diverticulum location and type:
Meckel's Diverticulum: If symptomatic, resection of the diverticulum or segmental bowel resection
with anastomosis is usually performed. Even asymptomatic diverticula found during other surgeries
may be prophylactically resected.
Duodenal Diverticula: Surgical resection is indicated for symptomatic or complicated diverticula.
These surgeries can be technically challenging due to the duodenum's proximity to the pancreas and
bile ducts.
Jejunal and Ileal Diverticula: Resection of the affected bowel segment with anastomosis is the
standard approach, particularly for complications such as perforation or obstruction.
Prognosis and Complications - The prognosis for small bowel diverticula depends on timely
diagnosis and management of complications. Asymptomatic diverticula generally have a good
prognosis, while complicated cases may have high morbidity and mortality. Perforation or severe
bleeding can be life-threatening if not treated promptly and adequately.
Conclusion - Inflammatory diseases of the small intestine and its diverticula are clinically significant
conditions that require a comprehensive diagnostic and therapeutic approach. Surgical treatment is
often necessary in the presence of complications such as obstruction, perforation, or fistulas. Correct
diagnosis and timing of surgical intervention are crucial.
52
INFLAMMATORY DISEASES OF LARGE BOWEL AND THEIR SURGICAL MANAGEMENT (35)
Marek David, Grolich Tomáš
Inflammatory bowel diseases encompass a diverse group of conditions characterized by
inflammation of the large intestine. These include acute and chronic appendicitis (discussed in
Chapter 26 Acute Appendicitis), acute diverticulitis (discussed in Chapter 36 Diverticulosis of the
Gastrointestinal Tract), infectious colitis, idiopathic inflammatory bowel diseases (ulcerative
colitis and Crohn's disease), pseudomembranous colitis, and ischemic colitis (discussed in Chapter
28 Intestinal Ischemia). Each of these conditions has its own unique etiology, pathogenesis,
symptomatology, course, and treatment.
CROHN´S DISEASE is an idiopathic chronic transmural inflammation that can affect any part of
the gastrointestinal tract from the oral cavity to the rectum, most commonly the ileum and the
adjacent cecum. Typical are segmental "skip" lesions, where multiple parts of the gastrointestinal
tract are affected simultaneously. The exact cause is unknown, however, a genetic predisposition
and the influence of environmental factors such as diet and the immune response to the microbial
flora are assumed.
Symptoms include abdominal pain, usually in the right lower quadrant, chronic diarrhea, weight
loss, or fever. Extraintestinal symptoms may include ocular and skin manifestations, arthritis, and
involvement of the liver, kidneys, or pancreas.
Laboratory tests may show elevated inflammatory parameters, anemia, thrombocytosis,
hypoalbuminemia, positive ASCA antibodies, and a non-specific elevation of fecal calprotectin.
The method of choice in the non-acute phase is endoscopy with typical "skip" lesions, focal
aphthous ulcers, or linear ulcers. On abdominal ultrasound, MRI, or CT enterography, we can
see a thickened intestinal wall (most often the terminal ileum), abscesses, fistulas, or typical multiple
involvement of so-called "skip" lesions. Complications typically include the formation of fistulas
(enteroenteric, enterocolic, enterovesical, rectovaginal, rectoperineal), as well as the formation of
abscesses (interloop, pelvic, retroperitoneal) and strictures, which can lead to ileus. Malnutrition,
anemia, or malignant transformation in chronic inflammation must not be neglected.
Treatment is managed by gastroenterologists and consists of administering aminosalicylates,
corticosteroids, immunosuppressants, or biological agents in several consecutive lines. Surgical
treatment involves managing acute and chronic complications, in case of failure of conservative
therapy, and often involves multiple surgical procedures in the course of recurrent disease. The most
common type is ileocecal resection with ileo-ascending anastomosis. Stricturoplasties (longitudinal
incision of the stricture with transverse suture) are also performed if the stenotic lesion cannot be
53
treated endoscopically with balloon dilatation. Other procedures may include segmental resection,
right hemicolectomy with ileo-transverse anastomosis, subtotal colectomy with ileo-rectal
anastomosis, or proctocolectomy with ileostomy and management of perianal fistulas. In general,
during surgery for IBD, we resect only the affected segment of the intestine without
lymphadenectomy, trying to preserve the maximum length of the gastrointestinal tract.
ULCERATIVE COLITIS is an idiopathic chronic inflammatory disease affecting the mucosa of
the colon and rectum, with a typical location in the rectosigmoid segment. The inflammation spreads
continuously in an oral direction. The cause, like in Crohn's disease, is unknown, with the influence
of environmental and genetic factors.
Gastrointestinal symptoms include diarrhea with blood and mucus, cramping abdominal pain
associated with defecation, tenesmus, and weight loss. Extraintestinal manifestations are less
common than in Crohn's disease.
Positive ANCA antibodies are found in 70% of patients, otherwise, the laboratory diagnosis is
identical to Crohn's disease, including fecal calprotectin. In the case of endoscopy, which is also the
method of choice here, we observe a hemorrhagic mucosa and diffuse inflammation. In biopsy
specimens, typical crypt abscesses are found in the microscopic image.
The most common acute complications include decompensated pancolitis, toxic megacolon
(significant distension of the colon with impaired motility, bacteria and toxic products begin to
penetrate through the intestinal wall into the abdominal cavity when intestinal contents accumulate)
and perforation. Chronic complications include the development of colorectal cancer (after 50 years
in 40% of patients).
Treatment is managed by gastroenterologists and involves the use of aminosalicylates,
corticosteroids, immunosuppressants, or biological agents. In acute cases with decompensation of the
disease and failure of conservative therapy, a total colectomy with a terminal ileostomy is performed,
leaving the rectal stump. In chronic courses or after sanitation of an acute condition in patients who
do not respond adequately to conservative therapy, an operation is planned in two or three stages
based on the severity of the inflammation. First, a colectomy is performed with the creation of a
terminal ileostomy. In patients with a good colon finding, a proctocolectomy and the immediate
creation of an ileal pouch (J-shaped reservoir) with an axial ileostomy is possible in the first stage,
which is often constructed in the second stage. In the final stage, the continuity of the gastrointestinal
tract is restored by removing the protective axial ileostomy.
Prognosis depends on the severity and stage of compensation of the underlying disease.
54
INFECTIOUS COLITIS is an inflammatory condition caused by infection with bacterial, viral, or
parasitic agents. They can occur from insufficiently heat-treated food, expired food, or fecal-oral
transmission in a collective.
They manifest as abdominal pain, fever, nausea, and frequent diarrhea, which may also contain
mucus and blood, leading to dehydration and ion imbalance.
Laboratory tests show elevated inflammatory parameters, hypokalemia, elevated renal parameters,
and hematocrit. On an abdominal X-ray, there may be distension of the colon, and on ultrasound,
thickening of the intestinal wall and possibly complications. In clinically severe cases, we often
supplement with an abdominal CT scan, while colonoscopy is contraindicated. To confirm the agent,
a swab is taken from the rectum for obligatory intestinal pathogens and it is also necessary to rule out
Clostridium difficile colitis.
Most infections have a short course and require only outpatient treatment in the form of dietary
measures, adequate oral hydration, and possibly antibiotic therapy. More severe forms, especially in
older polymorbid patients, may require hospitalization for rehydration, correction of the internal
environment, and antibiotic therapy. A serious complication is the development of sepsis.
Surgical treatment is exceptional here and mainly represents the management of complications
associated with colitis, such as uncontrollable sepsis, intestinal perforation, and toxic megacolon.
Prevention is adequate hygiene and heat treatment of food, and possibly vaccination (e.g., against
rotavirus).
A specific example is PSEUDOMEMBRANOUS COLITIS. This is an acute inflammatory disease
of the large intestine characterized by the formation of pseudomembranes on the intestinal mucosa. It
is often caused by an overgrowth of the bacterium Clostridium difficile after disruption of the
intestinal microflora.
It most often occurs after the administration of broad-spectrum antibiotics, not infrequently as a
nosocomial infection. Older people are more susceptible to development, as well as
immunosuppressed individuals, for example, after chemotherapy or immunosuppressive therapy.
Other factors may include PPIs, which reduce stomach acidity and can thus increase the risk.
The manifestation is typical of watery diarrhea (in numbers of 10-15 per day). It usually has an
acute onset and can have a mild to severe course.
Diagnosis includes, among other things, the detection of Clostridium difficile toxin in the stool.
Even after successful treatment, pseudomembranous colitis may recur, especially with repeated use
of antibiotics.
55
Early diagnosis is important! Treatment includes discontinuation of broad-spectrum antibiotics, if
possible. Metronidazole is used for less severe forms, Vancomycin is preferred for more severe cases
or recurrences, or Fidoxamicin as a newer antibiotic with high efficacy and a low rate of recurrence.
Rehydration therapy, including electrolyte substitution, is important: Probiotics can help restore the
intestinal microflora and reduce the risk of recurrence. In the progression of the disease, a total
colectomy with a terminal ileostomy is performed with high morbidity, usually without a plan for
destomization in a polymorbid elderly patient.
Prognosis depends on early diagnosis and treatment. In more severe cases, serious complications can
occur that can be fatal, especially in elderly and immunosuppressed patients.
Prevention means the judicious use of antibiotics and, together with them, the administration of
probiotics, which can reduce the risk of developing Clostridium difficile colitis. Prevention of spread
is thorough hand washing and isolation of patients (barrier care regimen).
DIFFERENTIAL DIAGNOSIS is challenging in the most severe clinical conditions, and from a
surgical standpoint, it's more about ruling out acute complications based on a combination of clinical
findings (appendicitis), signs of inflammation, and imaging studies (contrast-enhanced CT scan
when ischemia is suspected). This information is used to decide whether to proceed with surgical
intervention or initiate empirical conservative treatment (antibiotics, intravenous fluids), often
without knowing the exact etiology of the inflammation. In cases with milder courses, by
supplementing with cultures, endoscopy, and laboratory tests, we can arrive at a diagnosis within a
week, allowing us to target treatment specifically.
In the initial diagnostic process of sudden abdominal events with similar histories and clinical
findings, it is essential to consider other conditions such as pyelonephritis, urinary tract infections,
acute pancreatitis, gastroenteritis, gynecological infections, or colorectal cancer.
56
HEMORRHOIDS, ANAL FISSURE (2)
Berková Alena
HAEMORRHOIDS
Definition: Hemorrhoids are dilated, coiled blood vessels in the wall of the anal canal. Hemorrhoidal
disease is a very common problem in both women and men. Hemorrhoidal plexuses are anatomical
and physiological structures of the anal canal. The hemorrhoidal plexus is significantly involved in
the continence of stool.
Pathophysiology: Currently, the pathogenesis of hemorrhoidal disease is based on two main
pathological factors:
mechanical factor: in which, most often due to aging or chronic irritation, degenerative processes
occur in the connective tissue of the hemorrhoidal plexus. This results in a prolapse of the mucosa
with venous plexuses in the wall of the anorectum.
vascular factor: when, during prolonged strenuous defecation, the circulation in the capillaries of the
arterio-venous junctions is blocked, resulting in abnormal dilatation of the cavernous tissue.
Etiology: The etiopathogenesis of hemorrhoids is multifactorial. The most common causes of
hemorrhoids include defecation disorders, prolonged sitting, certain sports activities, pregnancy, use
of hormonal contraceptives, constitutional predisposition, hypercholesterolemia, hyperlipidemia, and
abnormalities in collagen quality in Ehlers-Danlos syndrome.
Classification: Anatomically, according to the relationship to the linea dentata, we distinguish:
internal haemorrhoids (nodi haemorrhoidales interni) are located above the linea dentata
external haemorrhoids (nodi haemorrhoidales externi) located below the linea dentata.
intermediate haemorrhoids are found directly in the submucosal part of the anal canal between the
linea dentata and the anocutaneous passage.
Internal hemorrhoids are most commonly classified into four stages according to Goligher:
Stage I: minimal nodules without laceration, hemorrhoidal nodules are visible only by anoscope.
They are usually asymptomatic, but may present with bleeding or discomfort in the anorectal area;
Stage II: during defecation, the nodes prolapse but spontaneously recollapse. Symptomatic patients
complain of bleeding, itching, "wet anus" sensation or discharge;
Stage III: the nodes prolapse, and manual repositioning is necessary. In addition to bleeding and
discomfort, there is often spotting;
Stage IV. submucosal prolapse, which is already fixed, without the possibility of repositioning, often
accompanied by prolonged discomfort, pain, bleeding and some degree of incontinence.
57
Clinical signs and symptomatology:
Problems associated with internal haemorrhoids are usually chronic and last for several weeks or
months. These include discomfort in the anorectal area, foreign body sensation, itching, prolapse;
bleeding that can lead to secondary anaemia, irritation of the perineum, itching. Pain can be caused
by complications such as thrombosis, ischemia or inflammation, acute prolapse of internal
hemorrhoids.
External hemorrhoids are very prone to thrombosis, which is accompanied by extreme pain. After
healing of the perianal thrombosis, skin folds, so-called mariscs, which are oriented radially, are
formed around the anocutaneous transition.
Diagnosis: History and clinical examination and per rectum examination are essential. In addition,
an anoscopy or a rectoscopic examination is performed – typical localization of internal hemorrhoids
is at number 3, 7, 11. Colonoscopic examination is indicated in all patients with past or present
bleeding to exclude other pathological conditions of the rectum and colon
Therapy:
Conservative therapy: this includes regimen measures and reduction of risk factors, regular
defecation and training of defecation reflex, diet rich in fiber. Physical activity is important, or
weight reduction in case of obesity.
Local therapy: includes sitting baths, which are antiseptic, antiphlogistic and analgesic. Another
option is the administration of suppositories, ointments and creams.
Systemic therapy: includes the administration of venoactive substances so-called flavonoids, which
improve the tone of blood vessels. As a result, the permeability of the blood vessels is reduced, and
the circulation is accelerated.
Obliteration methods are methods in which the haemorrhoidal node is obliterated and fibrosed and
blood flow is restricted. These include Barron's elastic ligature, sclerotherapy, laser therapy, infrared
photocoagulation, and bipolar or monopolar diathermy.
Surgical therapy: is indicated for symptomatic grade III-IV hemorrhoids in which conservative
treatment does not provide relief. It is performed under general or spinal anaesthesia, in the jack
knife or gynaecological position, after preoperative preparation of the rectum with an infusion. The
classical methods include the Whitehead operation – in this procedure a circular resection of the
mucosal prolapse is performed. Or preparation of individual haemorrhoidal nodes with vascular
pedicle ligation according to Milligan-Morgan or Ferguson is performed.
Miniinvasive methods include stapler haemorrhoidopexy according to Longo or stapler
haemorrhoidopexy – TST (tissue selecting therapy) – selective resection of haemorrhoidal tissue.
58
Differential diagnosis: malignant diseases: colorectal cancer, anal carcinoma, Bowen's disease;
CAVE: Behind every rectal bleeding can be a tumor!
perianal thrombosis, mariscus, anal fissure, perianal eczema;
hypertrophic anal papilla ("anal polyps", "cat's teeth");
inflammatory bowel disease, anal abscess, anal fissures and fistulas;
rectal polyps;
prolapse of the rectum and ulcus recti;
Condylomata acumtnata (HPV infection) Condylomata lata (syphilis).
FISSURA ANI
Definition: An anal fissure is caused by an injury to the mucous membrane in the anal canal. It is
manifested by pain and bright red bleeding.
Etiopathogenesis: Relative ischemia and traumatization of the mucosa during defecation may play a
role. Chronic increased anal sphincter tone leads to fibrosis of the muscle and the formation of a
fissure.
Often there is a history of constipation, anal sexual practices, perineal infections, perianal area,
Sexual transmitted diseases – STD, other anorectal diseases – hemorrhoids, cryptitis and Crohn's
disease.
Chronic fissure is associated with spasm of the smooth muscle of the internal sphincter, resulting in
impaired blood supply to the base of the fissure and complicated healing.
Classification:
acute fissure – a minor mucosal injury that heals quickly and rarely requires treatment.
chronic fissure – persisting for several weeks.
Clinical picture: Symptom is severe sharp pain with each defecation localized at the site of the
fissure and pelvic pain persisting hours after defecation, probably due to spasm in the pelvic floor
muscles. Burning and itching of the rectum. Bleeding is not pronounced, as it originates only from
the mucosal margins.
Diagnosis: History, clinical examination and per rectum examination are essential. Digital rectal
examination can be difficult as the area is sensitive and the anus is closed by sphincter spasm.
Usually the lower edge of the fissure can be seen by gently separating the buttocks. Next, anoscopy
or rectoscopic examination should be performed. Usually the fissure is located in the posterior
midline of the anal verge, but it may be located in the anterior midline. In a chronic fissure, a firm
rim with a protrusion at the outer edge called a guarding bump develops and there is overgrowth of
59
the nearest anal papilla. Further investigation includes colonoscopic examination, exclusion of
inflammatory bowel diseases – IBD, exclusion of Sexual transmitted diseases –STD in multiple
fissures or fissures in lateral positions.
Therapy:
Conservative therapy: includes treatment of constipation and 6-week application of glyceryl trinitrate
suppositories and ointment. Glyceryl trinitrate causes relaxation of the smooth muscles of the
internal sphincter. The therapy may also include injection of botulinum toxin into the sphincter area.
Surgical therapy: is indicated mainly in chronic fissures where conservative therapy fails. Excision of
the fissure may be performed. Histological examination of the lesion is always necessary to exclude
malignancy. Another option is to perform an anus divulgation. Lateral sphincterotomy is nowadays
only rarely performed for extensive findings.
When sphincter spasm is significant and outpatient examination is not possible, the fissure can be
diagnosed and treated under general anesthesia and other important differential diagnoses, such as
abscess or fistulation, can be excluded if necessary.
Differential diagnosis:
- malignant disease of the perianal area, anus and rectum;
- perianal fistulations and abscesses;
- haemorrhoids;
- sexual infections, condylomata acuminata (HPV infection) condylomata lata (syphilis).
60
ANORECTAL FISTULA AND ABSCESS, PILONIDAL SINUS DISEASE (1)
Trenz Aleš
Perianal and periproctal fistulas
Fistulation in this area is defined as pathological communication between the lumen of the anal canal
or the rectum and the skin of the perianal area or perineum.
Although it is a problem in a lot related to some systemic diseases - see below, the first diagnostic
and treatment steps are the domain of the surgical department. Thus, the surgeon must always bear in
mind the possible multidisciplinary overlap, even if apparently small and localized lesions, especially
in patients with recurrence of such problems.
In the prevalence data, we observe a significant prevalence of the disease in the male population,
almost twice as much (the overall average for the population is approx. 8.5/100000).
Etiology can be traced to an infectious inflammation of one of the anal glands. These are a typical
anatomical structure under the mucosa near the linea dentata in the number of 10-15, mostly on the
dorsal side. The infection is further complicated by the formation of a abscess, which breaks through
into the anal canal, thus giving rise to wider communication with the intersphincteric space. We call
this sequence of overlapping pathologies the "cryptoglandular theory" of the formation of fistulas,
and only about 10-20% of cases in which the origin can be determined in another pathology, for
example, in IBD, deviate from traumatization of the area, cancers,
actinomycotic/TBC/chlamydial/STD/etc. infections, post-radiation conditions, pelvic sepsis and
other - rather rarer - conditions.
An unpleasant and often smelly discharge or suppuration, soreness or pruritus will bring the patient
to the doctor. They can even be associated with subfebrile.
Anamnestically, one can often find a history of non-surgically resolved abscesses, sometimes
intermittently and spontaneously emptying with varying lengths of remission. Other reported
systemic symptoms such as diarrhea, abdominal pain, and weight loss should not escape our
attention.
Diagnosis by clinical examination usually does not cause difficulties and includes, in addition to the
aspect and determination of the location and size of the lesion, also determination of the nature of the
secretion, palpation of the extent of induration, examination per rectum with not obvious possible
verification of the internal orifice. But this is usually confirmed by anoscopy which i salso necessary.
It is possible to try a gentle probing and thereby better map the course of the fistula tract or inject
peroxide or with a colored solution, to make it leak visualise.
61
Optionally, paraclinical methods are added - typically NMR (gradually displaced CT, fistulography
with contrast solution and TRUS - TransRectalUltraSonography), colonoscopy.
In the differential diagnosis, we think of a fistula from the Bartholin's gland in women, advanced
hidradenitis, pilonidal cyst, osteomyelitis of the pelvic bones, secreting skin affections, etc. In a
simplified and general way, we can say that it is not a mistake to delegate a patient with a typical
lesion in the perianal area to a follow-up and examination to a surgical department.
Before starting and choosing a specific treatment modality - the solution is surgical - it is necessary
to determine the type of fistula in more detail. The aim is always to preserve the sphincter function.
Generally accepted and known is the classification according to the dominant course of the tract.
1) submucosal
2) intersphincteric (most common, runs between the internal and external sphincter)
3) suprasphincteric (arises from supralevator abscesses)
4) extrasphincteric (the rarest, runs outside the sphincters and pierces the rectum above the level
of the levator ani muscle).
Furthermore, it is determined whether the fistula has an internal orifice and is therefore not/complete.
In the case of uncomplicated, low and complete fistulas, we proceed to fistulotomy or fistulectomy,
the fistula tract towards the surface is widely opened, or even excided into healthy tissue.
The technique according to Seton is suitable for high complete fistulas and involves cutting the
external orifice of the fistula, thus inserted an elastic fiber along the entire course of the tract, leading
it out through the anal canal and creating a closed circuit of the fiber. Its elastic pull causes a gradual
cutting of the tissues with the simultaneous formation of a fibrous scar. As the thread progresses and
loosens, it is necessary to tighten it periodically. In this way, with the correct execution and
indication, fistulas can be cut or cut through to the outside in 6-8 weeks.
For practically all types of fistulas, except for very low subcutaneous fistulas, the surgical method
can be used by moving the mucosal flap through the excised internal orifice. Alternatively, the
remaining tract and external orifice can be excochleated, cut out or filled with tissue glue, etc. In
certain situations, the use of tissue glue can be considered as the method of choice even on its own.
There are other less commonly used treatment modalities, such as "patch" the fistula with artificial
biogenic material or ligation of the tract in the intersphincteric space using a fistuloscope. The
choice between individual methods is finally determined by the experience of the practicing
workplace. Properly indicated, they may be interchangeable in their effectiveness.
Periproctal and perianal abscesses
Perianal and periproctal abscesses are similar in their pathological and pathophysiological origin to
the first described fistula and often follow each other in time/progressively. The developing tuber in
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the area of the infected anal gland is usually formed by coliform flora and can be emptied early in the
intraluminal direction, which does not cause major clinical difficulties for the patient and the
condition resolves spontaneously. Less often, it spreads in the form of phlegmon to the surrounding
area and a diffuse inflammation occurs, which must be widely incised immediately, treated with
local antiseptics and immediately covered with antibiotics - empirically at first and targeted as soon
as possible. Rapidly progressing or insufficiently early and aggressively treated phlegmon can result
in putrefactive perianal involvement with irreversible damage to sphincter function and pelvic sepsis.
By far, the process is bounded in the form of an abscess collection, the spontaneous regression of
which is not possible. Therefore, the abscess grows and, left untreated, prolapses until it finally
perforates into the rectum, anal canal or perineal skin. We recognize 6 groups of abscesses
depending on their location, again reflected in the name itself.
1) submucosal
2) intersphincteric
3) transsphincteric
4) ischiorectal
5) pelvirectal
6) subcutaneous (=perianal)
The diagnosis is based on a typical anamnesis of short-lasting pains, problems with emptying,
possible IBD present (up to 90% of all patients with Crohn's disease are treated surgically at least
once in their life), often with a short-term febrile state, etc. Follow-up clinical examination is usually
sufficient to finish diagnosis and indicate incision and evacuation of the abscess under general
anesthesia. We find painful induration and inflammation in varying degrees.
Due to the usual high pain, we retreat from anoscopy, which is preferably completed only in CA at
the same time as remediation of the deposit (incision, evacuation, lavage, possibly drainage) in
order to rule out the presence of fistula into the rectum. If this is present, we mark it by inserting a
ligature, see above. There is no alternative to conservative therapy here either. A mutually beneficial
approach to the procedure under general anesthesia during hospitalization is the promise of thorough
treatment without compromises that we would otherwise be forced to make due to the pain so typical
in the given location. We always supplement surgical therapy with the introduction of ATB
(empirical -> targeted).
Pilonidal sinus
Focal disease of the soft tissues in the sacrococcygeal region is typical for the young but adult
generation, significantly more often in obese men with a higher degree of pubic hair. The hormonal
influence of adolescents on the sebaceous and sweat glands - men - has also been proven.
63
Anamnestically, patients frequently report a sedentary occupation/lifestyle. It is for this phenomenon
that the disease was previously known under the eponym "jeep disease" (young soldiers-drivers in
WWII.).
The manifestation is either in the form of a secreting sinus or as its complication - an acute abscess in
the sacrococcygeal region. The base of the lesion consists of inverted tissue of the skin adnexa
containing hairs, granulomatosis and fibrosis, which distinguishes it from a simple soft tissue abscess
in other areas. There are also asymptomatic forms.
Diagnosis is based on anamnestic and clinical examination supplemented by probing with a small
probe through possible fistulas. US and CT is a very exceptional paraclinical modality of choice
reserved for differentially diagnostically complicated cases with an unclear connection with the
pelvic space, skeleton, suspicion of a tumor process. The examiner thinks about such conditions in
the differential diagnosis, as well as hidradenitis, manifestation of cleft defects, pyoderma
granulosum, carbuncle, etc.
The introduction of regimen measures is an integral part of the treatment of all stages of the disease.
In addition to motivating the patient for thorough hygiene, we also explain the importance of
depilation of the area and the choice of clothing made of natural materials - "absorbent". In the case
of asymptomatic or calmed fistulizing disease without secretion, such a procedure supplemented
with dispensary can be considered sufficient.
Other treatment options are already instrumental/operative.
The simplest method for small and unbranched sinuses is the instillation of phenol, which causes
limited tissue destruction, scarring and closure. The method can be applied repeatedly depending on
the effectiveness.
More extensive surgical therapy is divided into 3 basic groups
1) incision and drainage (in the acute phase of an abscess, other methods may follow
after
2) calming down)
3) 2) excision and secondary healing (rather for smaller foci, lower risk of
recurrence, without risk of
4) early abscesses)
5) 3) excision and primary closure (rather smaller and medium deposits, less
requirements for
6) compliance patient, risk of surgical site infection, the need for longer
hospitalization)
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4) excision with reconstruction by displaced skin flap (sec. Limberg /
Karydakis)
Although the last 2 mentioned methods are better tolerated by the patient due to the "immediately
visible result", the level of risk of the primary suture is not negligible due to the typically significant
bacterial colonization in the given location and therefore the risk of early infection incl. anaerobic. It
is therefore advisable to hospitalize the patient for longer (depending on the case, even for 7 days)
with simultaneous covering by ATB and directed positioning in bed. Any failure of the suture or
infection leads to a sometimes unacceptable cosmetic effect of the wound.
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ESOPHAGEAL SURGERY, ANATOMY, APPROACHES, TYPES OF OPERATIONS (20)
Jaborník Martin, Marek Filip
Introduction:
The esophagus, derived from the Greek words "oiso" meaning "to carry" and "phagos" meaning "to
eat," is a muscular tube that transports food and liquids from the pharynx to the stomach. Due to its
anatomical location anterior to the spine in the neck and posterior mediastinum, it was historically
difficult to access for both clinical examination and surgical intervention. However, significant
advancements in diagnostic and therapeutic techniques occurred in the 1970s and 1980s, leading to
standardized procedures. Today, minimally invasive techniques have become the gold standard.
Anatomy:
The esophagus is a muscular tube approximately 25-30 cm in length. It begins at the level of the C6
vertebra, connecting to the lower part of the pharynx, and ends in the region of T11, where it joins
the cardia of the stomach. Based on its course, the esophagus can be divided into three topographic
parts: cervical, thoracic, and abdominal. Both ends of the esophagus are equipped with sphincters:
the upper esophageal sphincter (UES) or cricopharyngeal sphincter, and the lower esophageal
sphincter (LES). As an organ of the digestive tract between the pharynx and stomach, it ensures the
passage of food and secretions between these organs.
Unlike the rest of the gastrointestinal tract, it is composed of only three histologically defined layers,
lacking a serosa except for a short intra-abdominal portion. The mucosa is lined with stratified
squamous epithelium, except for the distal 1-2 cm, known as the Z-line, where there is a transitional
zone with columnar epithelium. The mucosa is the strongest part of the esophagus, and therefore, its
perfect suturing is crucial during surgical procedures. The muscularis externa of the esophagus is
composed of striated muscle in the upper third, which gradually transitions to smooth muscle in the
middle third, with the lower third being entirely composed of smooth muscle. The muscle fibers are
arranged in an outer longitudinal and inner circular layer.
The blood supply to the esophagus is provided by several arteries. The cervical portion is supplied by
the inferior thyroid artery. The thoracic portion is supplied by the intercostal arteries, branches of the
thoracic aorta, and bronchial arteries. The abdominal portion is supplied by the left gastric artery and
inferior phrenic arteries. Venous drainage occurs from the submucosal plexus to the superficial
plexus, and then to the surrounding veins: inferior thyroid veins, intercostal veins, azygos and
hemiazygos veins, and left gastric vein.
The innervation of the esophagus is provided by both parasympathetic and sympathetic nerve fibers.
Parasympathetic innervation originates from both branches of the vagus nerves. This innervation
66
stimulates peristalsis and secretion. Sympathetic innervation originates from the thoracic sympathetic
trunk. This innervation generally has an inhibitory effect on peristalsis and increases the tone of the
sphincters. Nerve fibers branch on the surface of the esophagus and form plexuses: the submucosal
plexus of Meissner, located in the submucosa, regulates gland secretion; and the myenteric plexus of
Auerbach, located between the muscle layers, controls peristalsis.
Surgical approaches to different levels of the esophagus:
1/ Cervical: Left-sided approach behind the sternocleidomastoid muscle. 2/ Thoracic: Right-sided
thoracotomy or thoracoscopy; see Figure 2. 3/ Abdominal transhiatal: Upper midline laparotomy
or laparoscopy; see Figure 1.
List of surgical procedures:
Heller's Cardiomyotomy
Indications:
Esophagogastric achalasia - a functional disorder of the entire esophagus, characterized by decreased
or absent esophageal peristalsis, progressive esophageal dilation, and impaired relaxation of the
lower esophageal sphincter.
Diagnosis:
Gastrofibroscopy, esophageal barium swallow, distal esophageal endosonography (to rule out
pseudoachalasia), esophageal manometry
Procedure description:
Historically performed via a transabdominal approach (upper midline laparotomy), today it is
performed laparoscopically. An extramucosal longitudinal myotomy is performed approximately 2
cm distal and 6 cm proximal to the gastroesophageal junction. It is usually supplemented with a
fundoplication to prevent postoperative reflux. Intraoperative endoscopy is recommended to assess
the integrity of the mucosa and control the extent of the myotomy.
Anti-reflux Surgery
Indications:
Gastroesophageal reflux disease (GERD) is a condition where the contents of the stomach flow back
into the esophagus. The cause may be functional or morphological. If the esophagus reacts
pathologically to reflux, we speak of gastroesophageal reflux disease. Conservative therapy in the
form of lifestyle changes and proton pump inhibitors is fully sufficient for about 80% of patients. In
the remaining cases, anti-reflux surgery should be considered, especially in patients with significant
regurgitation and extra-esophageal symptoms of reflux, Barrett's esophagus, or as an alternative to
long-term PPI therapy.
67
Diagnosis:
Gastrofibroscopy, 24-hour pHmetry, manometry
Procedure description:
Laparoscopy is the standard approach. The principle is to create a cuff around the distal esophagus
using the wall of the gastric fundus in various modifications: Nissen-Rossetti procedure - complete
360° wrap, incomplete 270° wrap according to Toupet, and others. The procedure is performed with
a thick calibration probe introduced orally into the esophagus, which is then removed after the
procedure.
Esophagectomy
Indications:
Esophageal cancer, with squamous cell carcinoma being most common in the upper two-thirds and
adenocarcinoma being typical for the distal esophagus and gastroesophageal junction. Other
indications include Barrett's esophagus unresponsive to conservative treatment and esophageal injury
associated with mechanical or chemical insult.
Diagnosis:
Endoscopy with biopsy, oncological staging (CT of the chest and abdomen, tumor markers),
multidisciplinary team.
Procedure description:
In the gastroesophageal junction area, classical resection procedures vary depending on the tumor
location. The Siewert classification of tumors is used. For type II (cardial) and III (subcardial)
tumors, total gastrectomy with resection of the terminal esophagus and reconstruction of the passage
using a Roux-en-Y loop is a radical solution. The surgical approach is laparotomy (upper midline
laparotomy or transverse supraumbilical). For adenocarcinoma from Barrett's esophagus (type I
adenocarcinoma of the gastroesophageal junction), due to the risk of submucosal spread of the tumor
orally, as well as for other tumors in the intrathoracic esophagus, subtotal esophagectomy is
indicated. The esophagus can be approached either through laparotomy - transhiatal approach or
through right thoracotomy, both of which can also be performed as minimally invasive procedures.
Subsequently, two approaches can be used to construct the esophageal anastomosis: cervical from
the left or from the right hemithorax. There are several options for replacing the resected esophagus.
The most commonly used is a tubulized stomach, other options include coloplasty or a small bowel
segment.
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SURGERY FOR BENIGN GASTRIC DISEASES (31)
Chovanec Zdeněk
Anatomy: the stomach is divided into cardia, fundus, corpus, antrum and pylorus. It is fixed in the
abdominal cavity by the lig. gastrophrenicum, hepatogastricum, gastrolineale and gastrocolicum.
The arterial supply is provided by a. gastrica dextra (a. hepatica propria - tr. coeliacus), supplying
the lesser curvature, a. gastrica sinistra (tr. coeliacus) supplying the lesser curvature and fundus, a.
gastroepiploica dextra (a. gastroduodenalis - a. hepatica communis - tr. coeliacus) supplies the
greater curvature, a. gastroepiploica sinistra (a. lienalis - tr. coeliaous) supplies the greater curvature
and aa. gastricae breves (a. lienalis - tr. coeliacus) supplies the gastric fundus. The veins are marked
like the arteries, draining into the v. portae. Besides, they have connections through the rr.gastricae
breves to the lesser curvature and through the v. linealis and vena coronaria ventriculi to the
esophageal veins (portocaval anastomosis). In portal hypertension, esophageal varices may arise via
this route.
Lymphatic drainage is divided into 4 groups. There is a connection to the hepatic, suprapancreatic,
linear, mesenteric, mediastinal, celiac and paraaortic lymph nodes, and lymph drains through the
ductus thoracicus and angulus venosus into the venous system.
Sympathetic innervation is provided via the gl. coeliacum, parasympathetic innervation via the n.
vagus.
The surgical approach can be classical, through laparotomy (transverse, longitudinal) or miniinvasive
(laparoscopic, robotic).
Indications: Benign and malignant tumors, distal stomach obstruction, therapy of gastroduodenal
ulcer disease, therapy of complications of ulcer disease (perforation, bleeding, penetration),
treatment of GERD, bariatric surgery, provision of nutrition, drainage of gastric secretions and
creation of a neoesophagus after subtotal esophagectomy.
Total gastrectomy is resection of the entire stomach.
Subtotal gastrectomy is the removal of a portion of the stomach, leaving the remaining portion to
restore the GIT. The types of subtotal resection depending on how much of the stomach is removed,
and what type of GIT reconstruction is performed. Both the distal part of the body of the stomach
with antrum and pylorus can be resected, as well as the proximal part in the form of resection of the
cranial part of the body, fundus and cardia of the stomach.
Reconstruction of the GIT after total gastrectomy can be performed by creating a Roux-en-Y
anastomosis, interposition of the jejunum, or creation of an esophago-duodenal anastomosis.
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The principle of the Roux-en-Y anastomosis is to connect a long ileum, approximately 40 cm, to the
esophagus (to ensure the passage of food from the esophagus to the intestine) and then to connect the
dislocated part of the duodenum (to ensure the drainage of bile and pancreatic juices) to the
esophagus. GIT reconstruction consists of the creation of an espohagojejuno-anastomosis
(connection options are end-to-side, end-to-end, manual, mechanical or semi-mechanical) and an
entero-entero (end-to-side, side-to-side) anastomosis. The jejunum can be routed both anterocolically
and retrocolically.
Billroth I (B I) resection is the removal of the lower part of the stomach up to the pylorus and the
connection of the remaining part of the stomach directly with the duodenum (terminal
gastroduodeno-anastomosis, end-to-end or end-to-side) is indicated in the treatment of complications
of peptic ulcers (perforation, penetration, bleeding), the disadvantage is duodeno-gastric reflux. B I
can be modified by interposition of a discarded segment of jejunum (the operation is functionally
favorable for physiological food transport), there is no blind-loop syndrome and afferent-loop
syndrome.
Billroth II (B II) resection is the removal of the lower part of the stomach up to the pylorus and the
connection of the remaining part of the stomach to the jejunal branch (gastroentero-anastomosis,
connection of the gastric stump to the jejunum), retrocolically or antecolically with the exclusion of
the blindly closed duodenum, in modification with Braun's enteroentero-anastomosis (omega loop)
or in combination with Roux-en-Y anastomosis. Complications of the omega loop can be afferent
loop (congestion in the feeding loop, colonization by bacteria and stasis of pancreatic and biliary
secretions), efferent loop syndrome (gastric emptying is reduced by narrowing of the anastomosis or
invagination of the draining loop), blind loop syndrome (colonization of the blind loop by intestinal
bacteria, deconjugation of bile acids and consumption of vit. B12).
Pyloroplasty is a surgical enlargement of the pylorus to improve the passage of food (longitudinal
stretching of the pylorus with its transverse suture). It is usually performed in combination with
vagotomy to avoid complications from excessive gastric retention.
Vagotomy is the severing of the vagus nerves innervating the stomach to reduce the production of
stomach acid. 1) truncal vagotomy is the interruption of the main trunks of the vagus nerves, 2)
selective vagotomy is the interruption of the gastric-specific branches of the vagus nerves, and 3)
proximal selective vagotomy is the interruption of only the fibers leading to the parietal cells, with
minimal impact on gastric motility.
Simple suture of a perforated gastric ulcer, sealing with omentum. Suture of a bleeding gastric ulcer
with a puncture ligature after gastrotomy in case of impossibility to treat the bleeding by endoscopic
means. Suture of a penetrating ulcer e.g. into the pancreas.
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Fundoplication consists of wrapping the fundus of the stomach around the lower esophageal
sphincter to prevent reflux of gastric contents into the esophagus and simultaneously restore the
angle of His. There are countless modifications of this operation, however the most common is
Nissen fundoplication (complete 360° wrapping of the fundus around the esophagus).
Sleeve gastrectomy is a bariatric operation for weight reduction in obese patients, tubulisation of the
stomach is performed, the principle is to reduce the volume of the stomach.
Gastric bypass is also a bariatric operation that combines reduction of the stomach and alteration of
the digestive tract (the stomach is divided into two parts, the cranial smaller part is connected to the
jejunum, continuity is restored by Roux Y anastomosis, and the caudal larger part remains connected
to the duodenum.
Antrectomy is the removal of the antrum of the stomach (distal portion), often performed in
ulcerative diseases or in patients with gastrin (e.g., Zollinger-Ellison syndrome).
Gastrostomy is a surgical procedure used to insert a tube, often referred to as a "G-tube", through
the abdomen and into the stomach. Gastrostomy is used to provide a route for tube feeding if needed
for four weeks or longer, and/or to vent the stomach for air or drainage.
The tubulated stomach can also be used as a non-intact stomach in case of sub-total esophagectomy.
71
GASTRODUODENAL ULCER DISEASES (32)
Petríková Laura
Definition : A peptic ulcer is an open sore found on the lining of the stomach or duodenum caused
by an imbalance between protective and aggressive factors acting on the mucosal layer. An ulcer
extends into the submucosal layer and deeper. It´s a disease characterized by the appearance of one
or more ulcers in the wall of the stomach or duodenum. Most often they are localized on the small
curvature of the stomach and the bulb of the duodenum.
The most common causes of peptic ulcers include Helicobacter pylori infection, long term use of
ulcerogenic drugs, imbalance between protective and aggressive factors acting on the mucosal layer.
Protective factors include gastric mucus, mucosal regenerative ability, prostaglandins, and
physiological microcirculation of the stomach. Aggressive factors include overproduction of
Hydrochloric acid ("no acid no ulcer"), H.pylori infection, gastric motility disorders,
microcirculation disorders, ulcerogenic drugs – anti-inflammatory drugs, corticosteroids, cytostatics;
smoking, alcohol, caffeine.
Diagnosis: Begins with a comprehensive physical exam which can reveal pain in the epigastric
region. Gastrointestinal endocsopy with biopsy allows us to diagnose peptic ulcer disease and to
examine the mucous lining of the upper GIT. Testing for H.pylori infection includes urea breath
tests, serologic testing, blood tests ,stool antigens and biopsy. In case of positivity, eradication with
antibiotics is necessary.
Clinical findings in gastric ulcer are burning pain sensation in the upper abdominal region after
food, lack of appetite, pyrosis, vommiting, weight loss and foetor ex ore. Antacids usually do not
bring any relief. The most common symptoms of a duodenal ulcer are waking up at night with
upper abdominal pain. The pain usually improves with eating or after taking antacids. The
occurrence is rather seasonal in younger patients.
Special types of ulcers include: Cushing's ulcer – produced by elevated intracranial pressure
caused by tumors or lesions of the CNS, overstimulation of the vagus causes higher secretion of HCl.
Curling's ulcer – gastric erosion resulting as a complication from severe burns when reduced
plasma volume leads to ischemia and cell necrosis of the gastric mucosa. Zollinger-Ellison
syndrome - in connection with endocrinally active gastrin - producing tumors - gastrinomas, most
often localized in the pancreas, resulting in overproduction of HCL. Stress ulcer - ischemia +
disturbance of microcirculation in the mucosa.
Complications and treatment: acute bleeding from an ulcer lesion, clinically manifested by
hematemesis (bright red blood/coffee ground vomitus ), melena (dark stool), anemia, hypotension. In
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patients with GIT bleeding, PPI´s are administered intravenously. Acute endoscopy is performed , it
allows us to stop the bleeding with endoscopic ligation, metallic clamps or sclerotherapy.
Classification: during endoscopic examination, the bleeding ulcer lesion can be evaluated according
to Forrest classification - I (active bleeding) Ia: active spurter, arterial bleeding, Ib: active oozing
venous bleeding from the base of the ulcer. IIa: a visible, gaping vessel at the base of the ulcer, IIb:
adherent clot, IIc: flat pigmented haematin on ulcer base. III: clean- based ulcer.
Surgical management is indicated in unstable patients with endoscopically untreatable bleeding. A
puncture of the bleeding vessel at the base of the ulcer may be performed through
gastrotomy/duodenotomy, possibly followed by ligation of the supplying artery, suturing the
gastro/duodenotomy. To prevent ileus in case of significant narrowing of the duodenum due to ulcer
punctures, gastroenteroanastomosis should be performed. In extreme cases of bleeding from a gastric
ulcer that cannot be resolved by puncture, a partial gastrectomy may be performed.
Another complication is perforation into the abdominal cavity, most often the anterior wall of the
duodenal bulb or the prepyloric area of the stomach, presenting as sudden, severe pain - patients
assume a typical bent-forward position, in a state of shock.
Initially, iv. therapy is recommended, surgery is necessary if pneumoperitoneum is demonstrated (Xray/CT
scan). Surgical therapy involves suturing or omental plugging, biopsy to exclude perforated
gastric tumour. Another complication is penetration of the ulcer through the stomach or duodenum
into another nearby organ, most often the head of the pancreas. There is a risk of bleeding from large
vessels. Any non-healing ulcer with established PPI therapy is highly suspicious for malignancy.
Stenosis occurs as a result of scarring of a chronic ulcer, the surgical treatment is
gastroenteroanastomosis or resection of the stenotic part of the stomach (according to Billroth).
Conservative therapy includes regimen measures - smoking ban, restriction of irritating food,
alcohol, coffee and NSAIDs. In the presence of H.pylori infection, eradication with the combination
of Omeprazole, Amoxicillin and Clarithromycin is necessary for at least one week. Medical therapy
and prevention include proton pump inhibitors - inhibiting HCl secretion ( Omeprazole, Pantoprazole
). Also H-2 blockers and antacids, which neutralize the pH of the stomach. Endoscopy is used for
biopsy, locating the ulcer and possibly treating the source of bleeding. Vagotomy was once
commonly performed to treat and prevent peptic ulcer disease, however now acid secretion control
can be achieved with medication.Today, endoscopically intreatable complications of the peptic ulcer
disease are addressed surgically.
Conservative treatment is most commonly used to treat gastroduodenal ulcer disease. PPI therapy
significantly reduces the incidence of complications. In case of endoscopically untreatable
complications, surgical treatment is indicated.
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74
GASTRIC TUMOURS (33)
Chovanec Zdeněk
Epidemiology: gastric cancer is the fifth most common malignancy worldwide and the third most
common cause of cancer death. The highest incidence is recorded in East Asia, especially in Japan,
South Korea and China, whereas in Europe and North America the incidence has been declining in
recent years, probably due to reduced consumption of salts and canned foods and eradication of
infection caused by Helicobacter pylori. In the Czech Republic, the incidence of gastric cancer is
also declining, with an 18% decrease in incidence between 2006 and 2016, and according to
available data, 9.16 women/15.09 men per 100 000 population will have the disease in 2021. The
prognosis of patients with gastric cancer depends mainly on the stage of the disease at the time of
diagnosis. Early gastric cancer has a very good prognosis, with a five-year survival rate of up to 90
%. For patients with locally advanced cancer, the 5-year survival ranges is between 30-60 %,
depending on the extent of lymph node involvement and the locoregional findings.
Etiology: is multifactorial, involving environmental and genetic factors. In non-cardia
adenocarcinoma, increased salt intake, canned foods, low fruit and vegetable intake, smoking and
Helicobacter pylori infection leading to chronic gastritis followed by metaplasia and dysplasia are
risk factors. Other risk factors are Epstein-Barr virus infection, previous gastric surgery, pernicious
anemia, bile acid reflux, and blood type A. For cardia (proximal type), obesity with gastroesophageal
reflux disease (GERD) leading to chronic irritation of the mucosa is a risk factor. Genetic
predispositions include hereditary diffuse gastric cancer (HDGC), familial adenomatous polyposis,
hereditary non-polyposis colorectal cancer, BRCA 1, BRCA 2, Li-Fraumeni syndrome, PeutzJeghersen
syndrome, and more recently gastric adenocarcinoma and gastric adenocarcinoma multiple
polyposis syndrome (GAPPS).
Diagnosis: clinical symptoms of gastric cancer are non-specific and especially late. Usually it is the
so-called small symptom syndrome (lack of appetite, aversion to meat, weakness, anaemia, weight
loss). Esophagogastroduodenoscopy (EGD) has the highest sensitivity and specificity with the
simultaneous possibility of biopsy. Endosonographic examination (EUS) specifies the depth of
invasion (which is used to classify the TNM category T). Computed tomography (CT) of the chest,
abdomen and pelvis is the standard examination for staging (N, M). Positron emission tomography
(PET) is used to detect distant metastases. Diagnostic laparoscopy with peritoneal lavage is indicated
for locally advanced carcinoma with suspected peritoneal spread, with the possibility of
cytoreductive surgery followed by hyperthermic intraperitoneal chemotherapy (HIPEC). Tumour
marker determination is not a diagnostic or screening method, but is a standard part of monitoring
75
disease progression and treatment effect. The most commonly used tumour markers are
carcinoembryonic antigen, CEA, CA 19-9, and CA72- 4.
Histology. The basic division is into benign and malignant tumours. Benign gastric tumours include
polyps (most often inflammatory and hyperplastic), less frequently occurring leiomyomas, lipomas,
fibromas, neurinomas and hemangiomas. The most common malignant tumour is adenocarcinoma
(about 90 %). It is divided into intestinal type (tubular and papillary), diffuse type (poorly cohesive)
and unclassified type, which includes tumours that cannot be clearly classified according to the
previous categories. Mixed carcinoma contains multiple components of these types and often only
one component is diagnosed, complicating the accuracy of diagnosis. There are also lymphomas
(MALT lymphoma), neuroendocrine neoplasia (NET) - (gastrinoma, somatostatinoma and
enterochromaffin cell carcinoid) and mesenchymal tumours - gastrointestinal stromal tumour
(GIST).
Surgical treatment remains the mainstay of therapy for gastric cancer, especially in early and
locally advanced stages. The success of surgical treatment depends on early detection, accurate
diagnosis and careful surgical technique. The TNM classification of gastric cancer allows accurate
determination of the extent of the disease and is essential for the choice of therapeutic approach.
For localised tumours (stage I - III), the basic therapeutic approach is to perform a total
gastrectomy, with an anastomosis between the oesophagus and the small intestine (usually Roux-enY
reconstruction). Subtotal gastrectomy (preservation of the proximal part of the stomach) can also
be performed for distally located tumours of smaller size, but it is not suitable for diffuse carcinomas.
D2 lymphadenectomy is the standard procedure, dissecting the lymph nodes along the a. hepatica
communis, a. gastrica sin., truncus coeliacus and a. lienalis up to the splenic hilum. The goal is to
achieve a resection (R0) with histologically negative margins and at least 15 lymph nodes removed.
Peroperatively, jejunostomy is indicated to provide postoperative enteral nutrition. Splenectomy or
resection of the pancreatic duct is not a standard part of the procedure, but it can be performed if the
radicality of the operation requires it.
For early stage I carcinoma (TIS, T1a, T1b), tumour resection can be performed using endoscopic
technique, in the form of endoscopic mucosal resection (EMR) for T1a less than 2 cm or
endoscopic submucosal dissection (ESD) for T1b without lymph node involvement. Surgical
resection is indicated for early tumors with a higher risk of lymphatic metastasis (T1b) or when
endoscopic resection is not feasible, namely subtotal or total gastrectomy with D2
lymphadenectomy.
In locally advanced T2-4 or N+ M0 disease, the standard procedure is the application of
perioperative chemotherapy aimed at shrinking the primary tumor and eradicating micrometastases.
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Laparoscopic and robotic-assisted approaches offer patients the advantages of less postoperative
pain, faster recovery, and lower complication rates without compromising the oncologic radicality of
the procedure.
In patients with advanced gastric cancer with metastases (stage IV), surgical treatment is rarely
curative. In these cases, palliative surgery is often performed to relieve symptoms caused by the
tumor, such as gastric obstruction or bleeding. Palliative gastrectomy may be indicated for patients
with localised symptoms, such as an obstruction in the pyloric region that prevents the passage of
food. This procedure helps to improve the patient's quality of life, although it does not lead to
prolonged survival. Bypass surgery is in cases where resection cannot be performed,
gastrojejunostomy or other bypass surgery can be performed to allow food passage and relieve
obstructive symptoms.
A multimodal approach combining surgery with chemotherapy, radiotherapy and targeted therapy is
increasingly being advocated. The goal of neoadjuvant therapy is to shrink the primary tumor and
eradicate micrometastases. Adjuvant therapy aims to improve overall survival and reduce the risk of
disease recurrence.
In conclusion, gastric cancer remains a serious health problem in the Czech Republic, mainly due to
the high mortality associated with late diagnosis. Despite the decline in incidence, treatment remains
challenging, with surgical resection playing a key role in therapy, especially in early and
intermediate stages of the disease. More effective screening and early detection are key factors in
improving the prognosis of patients with this disease. Therapy should always be assessed by a
multidisciplinary medical team. After gastrectomy, lifelong vitamin B12 replacement is required.
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STAGES OF GASTRIC CANCER AND CORRESPONDING TREATMENT
Stage Description Treatment
Stage 0 (Tis, N0,
M0)
Intraepithelial tumor
(carcinoma in situ), limited to
the mucosa without lymph node
involvement or metastases.
EMR/EDS
Regular follow up is important
Stage I (T1,
N0/N1, M0)
Tumor limited to the mucosa or
submucosa (T1), with
involvement of 0–2 regional
lymph nodes, no distant
metastases
Subtotal or total gastrectomy with D1
lymphadenectomy
Early tumors limited to the mucosa may be
treated with endoscopic therapy (EMR/ESD)
Often no neoadjuvant or adjuvant therapy is
required if complete resection is achieved
Stage II (T2/T3,
N0-N2, M0)
Tumor invades the muscular
layer (T2) or serosa (T3), with
involvement of 0–6 regional
lymph nodes, no distant
metastases
Total or subtotal gastrectomy with D2
lymphadenectomy
Neoadjuvant chemotherapy is often indicated to
reduce tumor size and improve prognosis
Adjuvant chemotherapy/radiotherapy postresection
based on histopathological findings
Stage III (T3/T4,
N0-N3, M0)
Tumor invades the serosa (T3)
or adjacent organs (T4), with
involvement of more than 7
lymph nodes, no distant
metastases
Total gastrectomy with D2 lymphadenectomy
Neoadjuvant chemotherapy (or
chemoradiotherapy)
Adjuvant chemotherapy post-resection
Sometimes palliative resection if curative
surgery is not possible
Stage IV (any T,
any N, M1)
Any primary tumor with lymph
node involvement and distant
metastases (M1).
Surgery is usually palliative to relieve
symptoms like obstruction, bleeding, or
perforation
Palliative chemotherapy and radiotherapy
aimed at improving quality of life
Bypass surgery or stenting in cases of gastric
outlet obstruction
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LIVER SURGERY – ANATOMY, APPROACHES, TYPES OF OPERATIONS (3)
Penka Igor
Liver surgery focuses on focal liver involvement. The liver itself is located in the area of the right
subphrenium, where it is partially fixed by suspension apparatuses, which are represented by the
falciform ligament (ligamentum falciforme) and coronary ligament (lig. coronarium), including their
duplications and round ligament of the liver (lig. teres hepatis), which divides the anatomically liver
parenchyma into the left and right lobes. However, this anatomical classification does not correspond
to the surgical anatomical classification. The division of the two lobes (right and left) is an imaginary
line principal fissure (fissura principalis), or Rex-Cantlie line, which runs from the fundus of the
gallbladder through the convexity of the liver to the middle of the inferior vena cava and thus
surgically divides the right and left liver lobes. This line is essential from a surgical point of view
and corresponds to the intraparenchymal course of the middle hepatic vein. Each lobe is further
divided into hepatic segments, each of which has its own portal triad, which includes the hepatic
artery, portal vein and bile duct for each segment so that each hepatic segment has its own "hilus"
(also known as hilus, the inferior surface where major blood vessels, lymphatics, and ducts enter or
exit the organ). The division into individual segments is determined by the imaginary lines of the, at
first glance, invisible intraparenchymal course of the liver veins.
The left lobe consists of three segments (segments II, III, and IV, which are further divided into
segments IVa and IVb), and the right lobe contains four segments V, VI, VII, and VIII.
The caudate lobe, or segment I, is located posteriorly. It has an exceptional position because it has a
different vascular supply, including venous and bile drainage. This Couinaud’s classification of
liver segments allows surgical resections to be performed.
From a surgical point of view, the anatomy of the hepatic hilum – the place where the main
vascular and bile structures enter the liver parenchyma on the visceral surface of the liver - is also of
great importance. At the site of the hepatic hilum, the hepatic artery, portal vein and the main bile
duct enter the liver via the hepatoduodenal ligament. The hepatic artery itself sends a separate right
and left branch to both lobes shortly before the hepatic hilum. The common hepatic bile duct also
divides into a right and left branch in the area of the hepatic hilum, similar to the portal vein, and
forms the main right and left portal triad. Since the purpose of liver surgery is to remove a
pathological hepatic focus, it is necessary to identify the main structures, i.e. the relevant hepatic
artery, portal vein and bile duct, treat them with a ligature – or ligate and intersect them. However, it
is equally important to treat and cancel venous drainage into the inferior vena cava, where the venous
blood of the hepatic vein gradually forms the main right, middle and left branches. The
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corresponding liver parenchyma supplied by the above-mentioned magistral structures is then
gradually removed by transparenchymal resection.
In this way, entire lobes (right or left) or individual segments (1st – 8th) are removed. Of course, it is
possible to remove more segments during one surgery or to perform the extended liver resection,
where the entire 4th segment is removed together with the right lobe (extended right-sided
hemihepatectomy) or with the left lobe (enlarged left-sided hemihepatectomy).
All these resection procedures, where we interrupt the main vascular supply and bile duct, are called
anatomical resections. Because the pathological lesion itself is removed together with the
surrounding liver (usually healthy) parenchyma, these resections are referred to as non-sparing
parenchyma. Unlike the non-anatomical resections, which are referred to as sparing parenchyma
because they remove only the pathological focus of the liver and only a minimum of the surrounding
liver parenchyma with the safety margin. Non-anatomical resections do not respect the segmental
arrangement of the liver parenchyma. Treatment of individual segmental structures is unnecessary
since only individual small vascular and bile structures in the resection line of the parenchyma
around the pathological focus are interrupted. Essential for the possibility of performing
extraanatomical resection is the favourable – mostly marginal – peripheral location of the
pathological lesion and, of course, the nature of the lesion (primary tumour, secondary tumour,
benign lesion). No structure of the magistral triad of the left liver parenchyma should be damaged,
which would lead to subsequent serious complications (necrosis, abscess etc.). A classic example of
extraanatomical resection is the wedge-shaped resection: wedge resection.
The basic surgical approaches in liver surgery are similar to those in other issues. We choose either
an open laparotomy approach or a minimally invasive laparoscopic approach followed by minilaparotomy
to extract the resected liver parenchyma. The most frequent types of laparotomies in liver
surgery are – subcostal laparotomy on the right and transverse bilateral subcostal laparotomy or
supplemented with a longitudinal incision towards the gladiolus in the midline. In some cases, it is
possible to choose a median laparotomy from the gladiolus towards the symphysis. The laparoscopic
approach means the establishment of a capnoperitoneum with the introduction of a camera and
working ports. The following dissection techniques are currently used for resection of the liver
parenchyma – crushing of the liver tissue using fingers (finger fracture technique) or peans (Kelly
fracture technique) with the treatment of individual vascular-biliary structures with clips or
ligatures. Modern dissection devices are also used for resection of the liver parenchyma: harmonic
scalpel, CUSA (Cavitron Ultrasonic Surgical Aspirator) aspirator, Water-Jet, Radiofrequency
Ablation (RFA), Microware Ablation (MWA, Thunder-beat, Ligasure, Argon spray, etc. The use of
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local haemostatic drugs, including Tachosil, Gelaspon, fibrin adhesives and many other local agents,
is also advantageous.
Indications for liver resection
Primary liver tumours (hepatocellular carcinoma, cholangiocellular carcinoma), secondary
malignant tumours (metastases mainly of colorectal cancer, but also of mamma carcinoma, renal
cell carcinoma and possibly others), benign tumours (mainly liver adenomas, only very large
hemangiomas are a relative indication), cysts and parasitic cysts. Associated liver resections (for
primary biliary tract tumours, ingrowth of tumours from the surrounding area into the liver
parenchyma etc.) Liver injury is a separate chapter.
Each of these nosological units has its specific aetiology, anamnesis, symptomatology and specifics
for the diagnostic and therapeutic process. In general, it should be noted that depending on the nature
of the basic diagnosis, each indication for liver resection must be a multidisciplinary decision of the
participating specialists such as radiologists, medical oncologists, gastroenterologists, pathologists,
radiation oncologists, anaesthesiologists, infectologists, and haematologists. Anamnesis and clinical
examination play a crucial role in diagnosis, which in themselves must lead to an initial working
diagnosis, which is then only refined by imaging methods and supplemented by laboratory
examination. The most important imaging methods are ultrasound examinations and contrast
ultrasound examinations. An essential preoperative standard is a current contrast CT examination of
the liver. To exclude extrahepatic metastases, a PET/CT examination is necessary, which is
sometimes suitable to refine the character of the liver focus. An important role is played by the
volumetry of the liver parenchyma, which provides us with preoperative information on how much
functionally fit liver parenchyma remains after the resection procedure – the residual liver
parenchyma (future liver remnant – FLR). On average, 60-70 % of liver tissue can be removed, but
only in the case of a functionally fit parenchyma. It is obvious that in the affected parenchyma
(hepatocellular carcinoma most often in the field of cirrhosis, conditions after chemotherapy),
functional liver parenchyma cannot be assumed (see Fig. Child-Pugh classification), and the extent
of the resection must be significantly smaller. Insufficient FLR value can be increased by
embolisation of the main branch of the portal vein, which leads to hypertrophy of the non-embolized
liver parenchyma. Interventional radiology plays an important role not only in preoperative but also
in the case of postoperative complications (embolisation in bleeding, angiointervention in ischemia,
percutaneous transhepatic drainage – PTD with the possibility of dilatation of stenoses and insertion
of stents in biliary tract obstruction, percutaneous CT-guided drainage of liver abscesses and
perihepatic collections, etc.).
81
Treatment:
In oncological indications, radical anatomical resections are preferred in primary tumours. In
secondary malignant tumours – metastasis of colorectal carcinoma (the most common indication for
surgical resection of the liver in our conditions), on the other hand, parenchyma-sparing nonanatomical
resections are performed, if possible. In general, in cancer patients, the optimal timing of
the resection procedure in connection with the ongoing oncological treatment is crucial so that the
benefit from the surgical procedure is maximal, and therefore, a commission interdisciplinary
agreement is absolutely necessary – see above.
For benign tumour lesions, surgical removal of adenoma with its potential for malignancy is
indicated. Treating parasitic cysts is in the full competence of infectious medicine, and the surgeon
acts as a consultant after the cyst has been treated. In addition to imaging methods, immunological
examination with the detection of specific serum antibodies (ELISA) plays a crucial role in the
diagnosis. Treatment of non-parasitic symptomatic cysts – usually very voluminous, which cause
the patient difficulties due to compression of neighbouring organs with pressure pain – is performed
in most cases by laparoscopic fenestration of the cyst into the free abdominal cavity and biopsy of
the cyst wall for histological examination. Liver abscesses are indicated for surgical treatment quite
exceptionally. The originally exclusive position of the surgeon in the treatment of these lesions has
been completely replaced by interventional radiology and the possibilities of CT-guided drainage
with antibiotic treatment.
Complication: After liver resection therapy, the following complications may occur: Bleeding,
biliary leakage, infection and liver abscess, subphrenic abscess, abdominal abscess, pleural effusion,
wound infection – laparotomy. Serious complications include hepatic insufficiency due to a lack of
functionally fit liver parenchyma (future liver remnant – FLR). Late postoperative complications
include the formation of a hernia in the area of the scar. General complications occurring after any
major intra-abdominal procedure (pulmonary embolism, heart failure, myocardial infarction, stroke,
thrombosis of the lower limbs and others) are understandable.
Liver injury is a separate chapter. Most often, it is a blunt, non-penetrating trauma in high-energy
injuries (traffic injuries, falls from heights). Intra-abdominal organs in high-energy injuries can also
injure the spleen, pancreas, GIT, or the suspension apparatus of the intestine or large blood vessels.
Patients should be transported from the field by emergency medical assistance (EMS) to the
emergency departments of hospitals. The circulatory stability of the injured person and the state of
consciousness are essential for further progress. If an abdominal (liver) injury is suspected, it is
necessary to perform a bedside ultrasound examination urgently. In more severe traumas, a wholebody
CT scan will provide us with immediate information about the condition of the body
82
cavities. In the most severe cases of circulatory instability, urgent surgical revision is necessary. To
evaluate the extent and severity of liver parenchyma injuries, there are many classification schemes
according to which the next steps are determined. The most serious are deep fissures with injuries to
the main vascular and bile trunks. During an urgent surgical revision, laparotomy is used to treat
bleeding liver according to the principles of Damage Control Surgery (DCS) – performing lifesaving
procedures with the aim of circulatory stabilisation of the patient. The primary requirement is
to stop bleeding. For this purpose, we most often perform liver tamponade using abdominal drapes
or packing the liver using a mesh. After the operation, the patient is usually transferred to the
Anesthesiology and Resuscitation Department, where further treatment occurs. In the case of
persistent bleeding, interventional radiology can significantly help us by using methods of selective
embolisation of bleeding vessels. In the postoperative period, CT-guided drainage is performed in
the development of perihepatic collections and Percutaneous Transhepatic Drainage (PTD) in bile
leakage.
83
NEOPLASMS OF THE LIVER (5)
Farkašová Martina
Primary - benign x malignant
Secondary - metastasis
Symptoms - 1/ Asymptomatic in early stages 2/ Pain in the right upper quadrant 3/ Icterus 4/
Fatigue and weakness, weight loss
Diagnosis – 1/ Laboratory tests, including oncomarkers (AFP, CEA, CA 19-9), 2/ Imaging
(ultrasound, contrast-enhanced ultrasound, CT, MRI) 3/ Biopsy 4/ Assessment of functional reserve
of liver parenchyma (e.g. ICG - indocyanine green clearance)
Treatment – 1/Surgical 2/ Radiofrequency ablation and embolization 3/ Chemotherapy,
radiotherapy, immunotherapy
Surgical procedures – 1/ Fenestration 2/ Extra-anatomical resection 3/ Segmentectomy 4/
Hemihepatectomy 5/ Extended hemihepatectomy 6/ Liver transplantation
Resectability
• Removability of the tumor lesion (R0: no microscopically visible tumor residue, R1:- with
microscopically positive resection margin, R2: with macroscopically visible tumor residue
left in the patient's body)
• Up to 70-80% of liver parenchyma can be removed without liver failure. However, in case of
liver parenchyma involvement (e.g. liver cirrhosis) the functional reserve of liver tissue
decreases.
• Preservation of the arterial and portal supply is necessary
• Preservation of venous and biliary drainage is essential
• Most important is the relationship to critical anatomical structures (inferior vena cava, hepatic
veins, portal vein, hepatic artery, surrounding organs - stomach, colon, and diaphragm).
Benign tumors
Haemangiomas - They are the most common benign lesions of the liver. These are mesenchymal
lesions that consist of cavities of varying sizes filled with blood. They can occur at any age and are
usually diagnosed incidentally in adulthood. Women are affected 5 times more often than men. In
diagnosis, ultrasound in healthy people is sufficient. If the lesion is found in patients with cancer, it is
necessary to supplement MRI, CT or contrast-enhanced ultrasound, to exclude metastasis. Treatment
is conservative and regular follow-up is not necessary. Surgical treatment is indicated only in case of
symptomatic lesions.
84
Focal nodular hyperplasia - This is the second most common benign tumor of the liver. It is
conditioned by proliferation of hepatocytes as a hyperplastic response to congenital arteriovenous
malformation. It occurs more in women aged 30-40 years. It is usually asymptomatic, typically less
than 5cm in size and 80% solitary. It is diagnosed incidentally on ultrasound examination. There is
no malignant relapse or increased risk of bleeding, therefore no therapy is required.
Adenomas - Relatively rare benign tumors arising from hepatocytes. Etiology is associated with
hormonal contraception, anabolic steroid use, obesity, DM, hepatic steatosis, and inborn errors of
metabolism such as glycogenosis and galactosemia. They most commonly affect women of
reproductive age, but rarely occur in men, children or elderly patients. The course is usually
asymptomatic. Abdominal pain is occasionally observed, especially in the case of larger adenomas.
Diagnosis relies on imaging. The most sensitive method of diagnosis is liver MRI. Complications
include bleeding and malignant reversal.
Clinically significant are 4 main subtypes of adenomas:
Inflammatory (35-40%)
• Women with high BMI (steatosis), alcohol
• Higher risk of bleeding (>30%).
HNF-1alpha mutated
• More in women (contraceptive).
B-catenin activated
• Risk of malignant transformation
• Men,
• Glycogenosis,
• Anabolic steroids,
• Familial adenomatous polyposis
Unclassified
• Diagnosis by exclusion method
Treatment is conservative, but there are criteria for which resection is indicated. Men, adenoma
larger than 5cm, B-catenin activated, inflammatory and adenomas that do not shrink in women after
discontinuation of hormonal contraceptives. In these cases, there is a high risk of malignant reversal.
In the case of adenoma bleeding, the method of choice is adenoma feeding artery embolization,
which is performed by an interventional radiologist.
Adenomatosis of the liver
85
It is defined by the presence of 10 or more adenomas in the liver. Treatment is conservative. Surgical
treatment is indicated in some cases for lesions larger than 5cm, smaller lesions are regularly
monitored by imaging. Exceptionally, liver transplantation is performed.
Liver cysts - They are divided into congenital and acquired. Congenital occur either as solitary or as
polycystic. Solitary arise from a malformation of the bile ducts. They tend to be small and
asymptomatic. If growth and associated symptoms occur, laparoscopic fenestration is performed.
Polycystosis is an autosomal inherited disease where 10 or more cysts are present. It is associated
with polycystic kidney disease. Complications include bleeding, portal hypertension, liver failure and
infection. Treatment is pharmacological and surgical, combining resection procedures with
fenestrations. Transplantation is performed in exceptional cases.
Acquired cysts include mainly echinococcal cysts. This is a parasitic disease caused by larvae of
tapeworms of the genus echinococcus. Infestation can occur after ingestion of contaminated fruit,
vegetables, water or direct contact with an infectious animal (dogs, sheep, rodents). They are divided
into two forms:
Alveolar form - E. Multilocularis
• Ultrasound, MRI, serology
• Primarily affects the liver
• Invasive growth
• Satellite foci (brain, lungs)
• albendazole therapy during one year and resection after metastatic lesions are excluded
Cystic form - E. Granulosus
• Liver, brain, lung, bone
• Typical appearance of a cyst
• Albendazole, resection
Malignant tumors
• Hepatocellular carcinoma
• Cholangiocellular carcinoma
• Epithelial hemangioendothelioma
• Hepatoblastoma
• Neuroendocrine neoplasia (NEN)- carcinoid
• Lymphoma
• Sarcoma - angiosarcoma, embryonal sarcoma, rhabdomyosarcoma, leiomyosarcoma,
• Teratoma
86
• Yolk sac tumor
Hepatocellular carcinoma (HCC) - It is the most common primary malignant tumors of the liver
arising from hepatocytes. It accounts for up to 80% of primary malignant tumors. It is mainly
associated with cirrhosis of the liver and chronic hepatitis B and C. More recently, it has also been
associated with non-alcoholic fatty liver disease (NAFLD). HCC is usually clinically silent and small
tumors are picked up in screening or as an incidental finding. Clinical symptoms such as abdominal
pain and pressure, fatigue, abdominal distension or weight loss are more common in advanced
stages. Sometimes the tumor will manifest itself by distant metastases. Laboratory findings include
elevated liver function tests and AFP. Fibrolamellar HCC is a separate entity. It occurs in young
individuals around 20-30 years of age. These are patients without chronic liver disease. There is no
elevated liver file in the laboratory and the AFP level is normal. At the time of diagnosis, 80% are
advanced. Treatment is surgical (resection, transplantation), radiofrequency ablation for small foci,
chemoembolization, systemic therapy for advanced inoperable tumors.
Cholangiocellular carcinoma (CCC) - It is a primary malignant tumor of the biliary tract. It is
divided into intrahepatic (from the intrahepatic bile ducts) and extrahepatic, which affects the large
bile ducts. A special category is the hilar type, which is known as Klatskin's tumor (65% of all
CCCs).
Hepatoblastoma - It is the most common liver tumor of childhood. It is a highly malignant
embryonal tumor. About 90% of cases occur before the 5th year of life of the child. The tumor is
most commonly found as a painless palpable mass in the right upper quadrant in the poorly thriving
child. Laboratory values tend to include anemia, thrombocytosis, coagulopathy, and elevated alphafetoprotein
levels. Diagnosis is based on CT and MRI scans, which are important for assessing the
operability of the tumor. If technically feasible, radical resection is performed. If it is not possible,
chemotherapy is administered, which may shrink the tumor and allow radical resection. In some
cases, liver transplantation is performed. If curative treatment is not possible, locoregional treatment
(radiofrequency ablation, chemoembolization, radiotherapy) can be used to prolong the patient's life.
The 5-year survival rate is more than 75% in children.
Secondary tumors - They account for 90% of all malignant liver tumors. Colorectal, pancreatic,
breast or gastric cancers are the most common to metastasize to the liver. Metastases can be
synchronous (detected at the same time as the primary tumor) or metachronous (with a varying time
lag from the diagnosis of the primary tumor). Diagnosis relies on a combination of imaging methods.
CT has a sensitivity of 73% for liver metastases, PET CT 93.9%. Treatment includes: surgical
resection, radiofrequency ablation, stereotactic radiotherapy, chemotherapy or immunotherapy.
87
SPLEEN SURGERY – ANATOMY, APPROACHES, TYPES OF OPERATIONS (6)
Vytešníková Martina., Španková Markéta
The spleen is the organ filling the left diaphragmatic vault. It is covered by the 9th to 11th ribs, the
so-called splenic ribs. It is normally not palpable, weighs about 120 to 160 grams, measures 12 x 7 x
4 cm, and is commonly compared to the shape of a coffee bean.
The vascular supply is secured by the lienal artery, which branches off from the truncus coeliacus. A.
lienalis divides into several segmental branches in the hilum of the spleen, each supplying one of the
4-6 segments of the spleen. Part of the vascular supply is provided by aa. gastricae breves in the
gastrolienal ligament. Blood is drained through the lienalis vein to the portae vein.
The suspensory apparatus of the spleen consists of lig.phrenicolienale, lig. pancreaticolienale and
already mentioned lig. gastrolienal. The spleen is adjacent to the cauda of the pancreas, the stomach,
the left kidney and adrenal gland, and the lienal flexure of the colon. Sometimes there are also
smaller accessory spleens in the abdominal cavity, the so-called splenuncles, most often in the
vicinity of the spleen itself. Their presence should be excluded using imaging methods (CT) before
splenectomy from the hematological indication.
The spleen is part of the immune system with the production of lymphocytes, its other function is the
absorption and destruction of old and non-functional erythrocytes, it also has the function of a blood
reservoir, around 250 ml; in the prenatal period it is one of the organs of erythropoiesis.
Types of surgeries and their indications:
Splenectomy, or removal of the spleen, is indicated, for example, in case of injury to the spleen
(injury passing through the hilum, larger fissures and untreatable bleeding from the parenchyma).
Trauma to the spleen can result in massive bleeding with hemorrhagic shock immediately after a
traumatic stroke, if it occurs delayed, this is a so-called two-stage rupture of the spleen. It arises on
the basis of a subcapsular hematoma of the spleen, which gradually increases in size, as a
hyperosmolar agent it binds fluid from the surroundings, thereby increasing its volume even more.
Subsequently, without further trauma after approx. 10 to 14 days after the original stroke, under the
pressure of the hematoma, the capsule can burst and bleed.
Another indication for splenectomy can be splenomegaly unresponsive to systemic treatment in a
malignant lymphoproliferative disease (lymphoma, leukemia,...), or hematological indications (sickle
cell anemia, hereditary spherocytosis...), infection of the spleen.
A special chapter is represented by cysts and pseudocysts of the spleen. They tend to be parasitic
(e.g. Echinococcal pseudocyst) and non-parasitic (often post-traumatic). With a larger size, they can
88
cause discomfort and pressure in the left subclavian, or pressure on the surrounding structures. When
malignancy is ruled out, cysts up to 4 cm can only be observed,
above 4 cm in diameter, splenectomy or fenestration of the cyst is considered (does not apply to
Echinococcosis, where fenestration is not possible due to the risk of the parasite spreading to the
abdominal cavity and the risk of anaphylaxis).
Splenectomy is also performed as part of an oncosurgical procedure, when tumors of the surrounding
structures either directly infiltrate the spleen and its vascular structures, or can spread to the lymph
nodes in the splenic hilum. E.g. tumor of the stomach, pancreas, lienal flexure colon...
Another type of procedure is a partial splenectomy - more rare, e.g. in children's patients, when it is
important to preserve at least part of the spleen as part of the development of immunity.
Operational approaches
Splenectomy can be performed laparoscopically or as an open abdominal procedure. A limitation for
laparoscopic surgery is a bulky spleen, the assumption of adhesions in the abdominal cavity in a
patient who has already been operated on several times, or the urgency of the procedure due to a
traumatological indication, when we assume reduced visibility in the abdominal cavity in the case of
massive hemoperitoneum.
In the case of both approaches, dissection of the suspensory apparatus of the spleen and interruption
of the supply and drainage vessels is required. Advantageously, the lienal artery is ligated/clipped
first to stop the blood flow to the spleen, followed by the lienal vein. In the case of laparoscopy, the
spleen is extracted from the abdominal cavity, either through one of the ports, when the spleen is
previously crushed in an endobag. We choose this type of extraction if we do not need to preserve
the spleen in its entirety for histopathological analysis (e.g. for a hematological indication). If the
spleen needs to be preserved intact (due to oncological indication), we perform the extraction
through a separate incision
Complications
As with any surgery, complications can occur during a splenectomy. Most often, there is bleeding,
injury of the surrounding structures, especially the cauda of the pancreas, and complications resulting
from the patient's internal comorbidities or the underlying hematological disease. A feared
complication is OPSI (overwhelming postsplenectomy infection), when a serious immune disorder
after splenectomy can result in life-threatening, rapidly progressing sepsis in the case of infection
caused mainly by encapsulated agents (pneumococci, meningococci, haemophilus inf. B). Therefore,
post-splenectomy patients should be vaccinated against pneumococci, meningococci, hemophilus
influenzae type B, and other vaccinations are also recommended, e.g. against influenza. In the case
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of a planned procedure, it is advisable to ensure some vaccinations before the operation through
infectious medicine.
Conclusion:
Indications for spleen surgery can be hematological, oncological or traumatological. After
splenectomy, it can disrupt immune processes in the body, therefore it is necessary to observe
measures to prevent the development of life-threatening sepsis either by vaccination or early
initiation of ATB therapy immediately upon suspicion of symptoms of a developing infection.
90
ACUTE AND CHRONIC PANCREATITIS (7)
Glombová Katarína
Pancreatitis
Inflammatory disease of the pancreas that can occur acutely or chronically. Both types of pancreatitis
have distinct pathophysiology, clinical presentations, diagnostic approaches, and treatment strategies.
1. Acute Pancreatitis
Definition: Acute pancreatitis is a sudden inflammatory disease with varying degrees of severity—
from mild interstitial pancreatitis to severe necrotizing pancreatitis with multi-organ failure. The
primary mechanism is the premature activation of pancreatic digestive enzymes, especially trypsin,
leading to autodigestion of pancreatic tissue and a subsequent inflammatory process.
Pathophysiology:
Initiation: Obstruction of the pancreatic duct (e.g., by gallstones) or toxic damage to pancreatic cells
(e.g., alcohol). Obstruction leads to the accumulation of digestive enzymes, which become activated
within the pancreas, while alcohol promotes oxidative stress and disruption of lysosomal and
zymogen membranes, leading to trypsin activation. Autodigestion: Activation of trypsin triggers a
cascade of other enzymes, including elastase and phospholipase A2, which destroy acinar cells and
cause pancreatic necrosis. The inflammation can spread to surrounding tissues, leading to pancreatic
edema, necrosis, and pseudocyst formation. Systemic inflammatory response: Release of
inflammatory mediators (e.g., TNF-α, IL-6, IL-8) into the systemic circulation, which can result in
multi-organ failure, including acute respiratory distress syndrome (ARDS), renal failure, and septic
shock.
Causes:
Biliary pancreatitis: The most common in Europe, caused by obstruction of the pancreatic duct by a
gallstone. Associated with sudden onset of abdominal pain and a high risk of complications.
Alcoholic pancreatitis: Long-term alcohol consumption is the second most common cause and can
trigger acute pancreatitis, particularly after the abuse of large amounts of alcohol. Idiopathic
pancreatitis: In about 10–20% of cases, no clear cause is identified. It is suspected that these cases
may be related to microlithiasis or genetic factors. Other causes: Hypertriglyceridemia,
hypercalcemia, medications (e.g., azathioprine, thiazides), infections (e.g., mumps), trauma, ERCP
(endoscopic retrograde cholangiopancreatography), and genetic factors (e.g., CFTR mutations).
Clinical manifestations:
Abdominal pain: Sudden, intense pain in the epigastrium radiating to the back, nausea, vomiting. In
biliary pancreatitis, jaundice may be present. Systemic symptoms: Fever, tachycardia, hypotension,
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and signs of hypovolemic shock are common in severe forms. Patients with necrotizing pancreatitis
may show signs of peritoneal irritation (Cullen’s and Grey-Turner’s signs), indicating the presence of
retroperitoneal bleeding.
Diagnosis:
Laboratory tests: Elevated serum levels of amylase and lipase, with lipase being more specific.
Elevated liver enzymes (ALT, AST, ALP) and bilirubin may indicate a biliary etiology. CRP is a
useful marker of inflammation severity. Imaging: Abdominal ultrasound is the initial method of
choice to detect biliary stones. Contrast-enhanced CT is recommended to assess the extent of
pancreatic necrosis and identify complications such as pseudocysts or abscesses. MRCP and ERCP
can be used for the diagnosis and treatment of biliary pancreatitis.
Treatment: Mild acute pancreatitis can be managed conservatively (hospitalization, intravenous
fluids, analgesia with opioids, and possibly antibiotics). Fasting is recommended until symptoms
improve. For biliary pancreatitis, urgent ERCP is appropriate. In complicated cases with necrosis or
abscess, surgical intervention, such as necrosectomy or drainage, may be necessary. In severe
pancreatitis with multi-organ failure, intensive care is critical, including monitoring of vital signs,
respiratory support, dialysis in renal failure, and prevention of DIC (disseminated intravascular
coagulation).
Complications:
Local: Pancreatic necrosis, abscesses, pseudocysts, obstruction of the pancreatic duct or bile ducts.
Systemic: SIRS (systemic inflammatory response syndrome), multi-organ failure, septic shock, and
ARDS (acute respiratory distress syndrome).
Prognosis: Mild pancreatitis has a good prognosis, while severe necrotizing pancreatitis is
associated with high mortality. Prevention of recurrences includes addressing the underlying cause
(e.g., cholecystectomy, alcohol abstinence).
2. Chronic Pancreatitis
Chronic pancreatitis is a long-term, progressive inflammation of the pancreas, leading to permanent
structural changes, fibrosis, and loss of both exocrine and endocrine function. Repeated
inflammation results in gradual destruction of acinar and ductal tissue, replaced by fibrotic tissue,
leading to loss of pancreatic function and complications such as diabetes mellitus and malabsorption.
Pathophysiology:
Oxidative stress: In alcoholic pancreatitis, oxidative stress caused by alcohol metabolites damages
pancreatic cell membranes and activates inflammatory cascades. Obstruction of pancreatic
ducts: Strictures or calcifications lead to increased pressure within the ducts, causing atrophy and
necrosis of acinar tissue. Genetic factors: Mutations in genes like CFTR (cystic fibrosis
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transmembrane conductance regulator), PRSS1 (encoding cationic trypsinogen), and SPINK1 (serine
protease inhibitor) contribute to disease development.
Main causes:
Alcohol consumption: Up to 70% of cases in the Czech Republic. Genetic factors: Conditions like
cystic fibrosis and hereditary forms linked to mutations in genes like PRSS1, which cause premature
activation of trypsin within the pancreas. Obstructive causes: Obstruction of the pancreatic duct by
a tumor, stricture, or lithiasis. Autoimmune pancreatitis: A rare form, chronic inflammation of the
pancreas often associated with diffuse enlargement of the gland and elevated IgG4 levels, responds
well to corticosteroid treatment.
Symptoms:
Abdominal pain: Recurrent or persistent pain in the epigastrium that may radiate to the back, often
worsened by eating. Exocrine insufficiency: Loss of exocrine function leads to malabsorption,
steatorrhea (fatty, bulky stools), and weight loss. Steatorrhea occurs when exocrine function is
reduced to less than 10% of normal capacity.
Endocrine insufficiency: Development of diabetes mellitus, known as pancreatic diabetes or type
3c, characterized by low insulin production and increased risk of hypoglycemia.
Diagnosis:
Laboratory tests: Measurement of pancreatic elastase-1 in stool. Low levels indicate exocrine
insufficiency. Abnormal glucose levels are common with endocrine insufficiency.
Imaging: Ultrasound and CT may show calcifications, ductal dilation, and structural changes in the
pancreas. ERCP provides direct visualization of the pancreatic ducts, revealing strictures, dilations,
or calcifications, and allows for treatment. MRCP is a non-invasive method that is highly sensitive
for detecting ductal changes and provides detailed assessment of pancreatic anatomy.
Treatment: Aimed at symptom relief, complication prevention, and improving the patient’s quality
of life.
Conservative management: Alcohol abstinence, glycemic control, dietary modifications with fat
restriction, and pancreatic enzyme supplementation. Pharmacological treatment: Analgesics
(NSAIDs, tramadol, or opioids). Endoscopic interventions: Dilation of strictures, stone removal, or
stenting of pancreatic ducts. Surgical procedures: Resection of the affected part of the pancreas
(e.g., Whipple procedure) or drainage procedures (e.g., Puestow procedure) in patients with severe
pain unresponsive to conservative treatment.
Complications:
Pancreatic diabetes (type 3c): Common complication, resistant to insulin treatment, requiring
careful glycemic control. Malabsorption: Due to exocrine insufficiency, leading to nutrient
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malabsorption, especially fats, resulting in weight loss and nutritional deficiencies such as fat-soluble
vitamin (A, D, E, K) deficiency. Pancreatic pseudocysts: Fluid-filled formations that may become
infected or rupture. Increased risk of pancreatic adenocarcinoma: Especially in patients with
long-standing alcoholic pancreatitis.
Prognosis: Chronic pancreatitis prognosis depends on its etiology, the extent of pancreatic damage,
and the patient's adherence to the treatment regimen, particularly alcohol abstinence. Long-term
complications can significantly reduce the quality of life and increase mortality risk. Prevention
includes alcohol abstinence, early diagnosis, and treatment of predisposing factors, and regular
monitoring of patients at risk for developing chronic pancreatitis.
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PANCREATIC NEOPLASMS (9)
Moravčík Petr, Zatloukal Martin, Hlavsa Jan
1. PRIMARY PANCREATIC TUMOURS
1.1 Ductal adenocarcinoma of the pancreas
It is the most common pancreatic tumour - it accounts for more than 90% of all pancreatic cancers. It
is the most frequently surgically treated and also the most aggressive pancreatic cancer. Its incidence
is increasing in a long-term trend. In 2018, this disease was the 7th most frequently diagnosed
neoplasm in the Czech republic. The mortality rate is very similar to the incidence rate. In the year
2018, pancreatic adenocarcinoma was the 3rd most common cause of cancer death in the Czech
Republic. It mostly affects patients over 60 years of age. The majority of tumors are diagnosed late at
clinical stage III and IV, which is closely related to the unfavorable prognosis of this disease.
Clinical symptoms are non-specific - abdominal pain, lack of appetite, weight loss, back pain, and in
the case of most common localization of the tumour - in the head of the pancreas - typically painless
jaundice. Computed tomography (CT) play a key role in diagnosis. The typical CT image for the
tumor lesion in the head of the pancreas is double duct sign - dilatation of the bile duct and the
pancreatic duct before tumor obstruction.
Complementary examinations are: magnetic resonance imaging (MRI) - better for the evaluation of
cystic lesions, to assess the biliary tract and pancreatic duct. It has a higher sensitivity to detect liver
metastases. Also PET CT/MR - for detection of distant metastatic disease and assessment of disease
recurrence. EUS - endoscopic ultrasonography - good visualization of the pancreas, has higher
sensitivity in lesions below 2 cm, increases the accuracy of the assessment of resectability, in
indicated cases allows targeted fine needle aspiration biopsy FNAB.
Surgical resectability of a tumour is defined by its anatomical relationship to the surrounding
structures, especially blood vessels. In case of infiltration of surrounding arteries or larger vein
infiltration, the tumor is evaluated as locally advanced and the treatment of choice is neoadjuvant or
palliative systemic cancer therapy. In the case of a resectable tumour, resection of the tumour
without prior oncological treatment is currently indicated in a patient in good clinical condition and
with favourable oncomarker levels (CEA, CA 19-9).
The extent of the resection procedure depends on the tumor localization. The goal is complete
macroscopic and microscopic removal of the tumor - RO resection and adequate lymphadenectomy.
Most commonly, 3 types of procedures are performed - see operation diagrams below. For tumours
in the head of the pancreas (but also of distal bile duct and the Vater's papilla) we perform proximal
pancreatectomy – also called hemipancreatoduodenectomy (HPDE) or Whipple's surgery. Distal
95
pancreatectomy (splenopancreatectomy) is done for tumors in the body or in the tail of the pancreas.
Total duodenopancreatectomy is a possible option for multiple pancreatic lesions or for inferior
tissue of the remaining pancreas that does not allow reimplantation into the gastro-intestinal tract.
Pancreatic procedures are characterized by high postoperative morbidity of up to 40% and a nonnegligible
5% mortality.
1.2 Cystic tumours of the pancreas
The detection of pancreatic cystoid tumors has been increasing in recent years with the spread of
imaging techniques. Cystic lesions are often diagnosed incidentally during examinations performed
for other reasons.
Four types of cystic pancreatic tumors are encountered in clinical practice:
Serous cystadenoma: it is benign, affecting more often women (in 75%). It can be localized
throughout the pancreas. If large in size or located in the head of the pancreas, it may be
symptomatic. Patients with asymptomatic tumors are only followed up. Surgical management is
indicated only for symptomatic and tumors.
Mucinous cystic adenoma: usually localized in the body and tail (95%), surgical management is
indicated due to malignant potential. It typically affects females (>95%), in the 4th-5th decade.
Intraductal papillary mucinous neoplasia (IPMN): grows from the main duct or its branches. It
has malignant potential. Surgical resection may be beneficial in certain cases. Communicates with
the pancreatic ductal system. May present with epigastric pain with frequent irradiation to the back.
Solid pseudopapillary tumor (Frantz tumor): The specificity of this type of cystic tumor is the
diagnosis at a young age. It typically affects women, less so men of the 2nd and 3rd decennia.
Rarely, it can occur in adolescents. Surgical resection is always indicated for malignant potential.
1.3 Neuroendocrine tumours
Neuroendocrine cells are diffusely distributed in various organ systems (GIT, lung, nervous tissue,
etc.) and like other cells can undergo neoplasia or malignancy. They are divided - according to the
degree of differentiation - into NET G1, G2, G3 and neuroendocrine carcinomas (NEC). The degree
of dysplasia corresponds to the aggressiveness of the tumor and the prognosis of the patient. The
most common localization of NETs is the gastrointestinal tract, including the pancreas.
Neuroendocrine tumours of the pancreas
They account for about 2-5% of all pancreatic tumors. They are hormonally active in 70-85%. They
arise from islet cells of Langherhans. According to the cell type and their hormonal production, they
have corresponding clinical manifestations. In general, they have a better prognosis than ductal
adenocarcinoma. Hormonally non-functional tumours are usually found incidentally, or, when they
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progress in size, they manifest themselves by oppression of surrounding structures or non-specific
manifestations - abdominal pain, weight loss, lack of appetite.
Hormonally active (functional) syndromes resulting from hormonal overproduction (Whipple's trias,
Zollinger Ellison syndrome, ..)
Insulinoma: is the most common endocrine tumor of the pancreas. It is mostly benign.
Manifestations result from hypoglycaemia due to overproduction of insulin - weakness, confusion,
tremor, sweating to unconsciousness. Diagnostically, the so-called Whipple's triad is demonstrated
(hypoglycaemia during fasting, glycaemia below 2 mmol/l during an attack, resolution of symptoms
after glucose administration).
Gastrinoma: most often located in the duodenum or pancreas, secreting gastrin causing
hypersecretion of gastric acid with severe ulcer disease and reflux - Zollinger-Ellison syndrome.
Other hormonally active tumors ( VIPoma, glucagonoma, somatostatinoma) are very rare.
Hormonal inactive pancreatic neuroendocrine tumors often grow inaparentally. They are often
discovered incidentally during an examination indicated for another reason (e.g. CT scan for
nephrolithiasis). Histological verification by EUS FNAB is always necessary to determine malignant
potential. Tumours up to 2cm in diameter with low malignant potential can only be followed up.
Larger tumours are usually indicated for resection. In contrast to pancreatic cancer, where metastatic
liver involvement is considered a contraindication to resection of the primary tumour, resection can
be considered for PNET even in the case of metastatic liver involvement, provided that all metastatic
lesions are completely removed.
2. SECENDARY PANCREATIC TUMOURS
Metastases of tumours of other origin.
They represent 2-5% of all pancreatic malignancies. They do not have a predilection site. Most often
they are solitary metastasis, but multiple metastasis are not an exception. The most common primary
origin of metastases is renal cell carcinoma (RCC), followed by lung adenocarcinoma, melanoma,
colorectal cancer, breast cancer and sarcomas. Secondary pancreatic tumours are only about 30%
synchronous (occurrence of metastasis at the same time as the primary tumour), so metachronous
metastases (occurring later) are more common. Late metastases are a specific feature - typically in
RCC, where 10% of patients develop metastases up to 10 years after treatment of the primary
tumour. Secondary tumors of the pancreas do not have a typical characterization on imaging
methods, so differentiation from primary tumours can be difficult in the absence of biopsy
confirmation of the diagnosis. Resection is indicated in patients with a good prognosis of the primary
tumour (e.g. meta RCC, meta breast).
97
OBSTRUCTIVE JAUNDICE (30)
Žák Jan
Objectives
This is an elevated serum bilirubin level due to biliary obstruction. Icterus is clinically manifested at
levels above 35μmol/l.
The metabolism of bilirubin
The production of unconjugated bilirubin is 250-300 mg/day. It is produced by the breakdown of Hb
by the reticuloendothelial system, predominantly in the spleen. Unconjugated bilirubin is waterinsoluble
and is transported by albumin in the bloodstream. It is taken into the liver by active
transport and conjugated to glucuronide in hepatocytes. Conjugated bilirubin is water soluble and can
be excreted in the urine as bilirubinuria. When excreted into the duodenum, bilirubin is bound to
cholesterol, lipids and bile salts as micelles. In the terminal ileum, conjugated bilirubin is converted
to urobilinogen by bacterial proteases. 90 % of urobilinogen is oxidised to stercobilinogen and
excreted in the faeces. The portal system reabsorbs 10 % and is finally excreted by the urine.
It is taken into the liver by active transport and conjugated to glucuronide in hepatocytes.
Obstructive icterus is manifested by conjugated hyperbilirubinemia, dark urine with bilirubin
present, and pale stools due to decreased stercobilinogen. ALP > ALT. PT is prolonged but
correctable with vitamin K.
Classification of biliary obstruction according to aetiology:
- intraductal
- mural
- extra ductal
Aetiology:
1. Intraductal
• choledocholithiasis – loosening of the gallbladder stone – the most common cause
• tumours
• strictures (90 % of iatrogenic, postlithiatic strictures)
• parasites (roundworms, liver flukes, bile flukes)
• AIDS-related cholangiopathy, possible involvement of opportunistic pathogens such as
CMV, crypto spores
• biliary tuberculosis
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• sump syndrome – a complication of side-to-side choledochojejuno anastomosis - due to
stagnation of sludge distal to the anastomosis
2. Mural abnormalities of the biliary tract
• biliary stricture – intra-/extrahepatic
• primary sclerosing cholangitis – males between 20-40 years, cause unknown, association
with IBD, mainly ulcerative colitis
• chronic cholangitis
• primary biliary cirrhosis
• iatrogenic, traumatic disabilities
• tumours (cholangiocarcinoma, periampullary, pancreatic tumours)
• congenital atresia
1. Extraductal – tumours, pancreatitis, pseudocyst, lymphadenopathy
Differential diagnosis of icterus:
In the differential diagnosis, excluding other types of icterus is necessary.
Pre-hepatic icterus is hemolytic, with increased red blood cell breakdown. Unconjugated
hyperbilirubinemia, normal-coloured stools and urine, and no bilirubin in the urine manifest it.
Its aetiology is most commonly:
• haemolytic anaemia
• congenital abnormalities of the structure of red blood cells (spherocytosis, sickle cell
anaemia)
• transfusion reactions
• drug reactions
Hepatic icterus results from failure of bilirubin conjugation in hepatocytes, with enzyme deficiency
or failure of uptake. There are elevated levels of mainly conjugated bilirubin. Mixed jaundice is
manifested by dark urine and normal stools. Elevated ALT > ALP levels are seen in the laboratory.
PT is elevated and not correctable with vitamin K.
Most common aetiology:
• cirrhosis
• infection: viral (hepatitis A/B/C, eBV, CMV); bacterial (liver abscess); parasitic (amoebic)
• Crigler-Najjar syndrome – congenital inability to conjugate bilirubin due to enzyme
inhibition
• Gilbert syndrome – inhibition of conjugation and defective uptake by hepatocytes,
exacerbated by concomitant disease
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• sepsis
• medications (excess paracetamol, amiodarone, diclofenac, fluconazole)
• non-infectious hepatitis (alcohol-related)
• liver tumours (malignant and benign)
Diagnosis of obstructive icterus
• Anamnesis should include key features to obtain a list of likely differential diagnoses.
Important questions include family history of blood disorders, recent travel abroad,
medications, gallstones, alcohol, weight loss, recent infections, and colour and consistency of
urine and stool.
• Similarly, the clinical examination and presentation depend on the cause, but it usually
includes yellowing of the sclera and skin, dark urine, and pruritus.
• Examination findings such as spider nevi, xanthomas, and hepatosplenomegaly should be
sought, and these may suggest an underlying pathophysiology.
• Pruritus - its cause is not clear. It may be related to the deposition of bile acids in the skin or
to the release of endogenous opioids. Excoriation of the skin indicates a long-standing course
of icterus.
The investigation of jaundice should focus on elucidating the underlying cause, and the history and
clinical examination should guide such investigation.
Painful versus painless jaundice?
To further diagnose and treat obstructive icterus, it is necessary to determine whether jaundice is
painful or painless.
Collinson sign – radiating pain under the right scapula is present in biliary colic.
It is important to differentiate simple biliary colic from acute cholecystitis. In simple colic, there is
no temperature or peritoneal irritation, and the pain is visceral, nonspecific, and poorly localisable.
Charcot's triad – icterus, abdominal pain and fever are manifested in acute cholangitis of various
etiologies (carcinoma, Mirizzi syndrome, ascending cholangitis, acute pancreatitis, biliary ileus).
The painless manifestation of obstructive icterus is associated with carcinoma of the pancreatic
head and biliary tract. It requires first investigation as an ultrasound/CT with assessment of local
findings and staging.
Blood tests:
KO including differential, liver function tests, coagulation, Coombs test (hemolytic disorders),
reticulocyte count, hepatitis screening, EBV, CMV, ferritin, α1-antitrypsin, immunoglobulins,
smooth muscle antibodies (chronic active hepatitis), antimitochondrial antibodies (primary biliary
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cirrhosis), autoantibodies, AFP, copper (Wilson), tumour markers in suspected underlying
malignancy.
Urinalysis: presence or absence of bilirubin, urobilinogen. As in hepatic icterus, only conjugated
haemoglobin leaks into the urine. Paper tests are extremely sensitive, and sometimes bilirubinuria
can be detected before serum bilirubin takes time to make icterus.
Imaging methods:
• Ultrasonography: excludes the presence of extrahepatic obstruction and can identify the
underlying pathology
• MRCP: more sensitive to identify underlying lesions as the cause of biliary obstruction
• CT: cross-sectional imaging may be useful depending on the cause
• EUS: micro lithiasis, lesions in the head of the pancreas
• Liver biopsy: for suspected hepatitis and cirrhosis
Treatment
In general, treatment of acute obstructive icterus depends on the underlying cause.
As part of the basic treatment, the following is needed:
• Hydration and adjustment of the internal environment
The patient with obstructive icterus is often dehydrated. Fluid balance must be monitored, and
caution is required in patients with pre-existing or suspected liver disease.
• Treat sepsis with antibiotic therapy.
• Adjustment of coagulation - administer vitamin K 10 mg if PT is prolonged.
• Nutritional assessment if parenteral/enteral nutrition is provided.
Specific treatment for obstructive icterus is mechanical biliary decompression to help:
• ERCP and sphincterotomy with extraction of choledocholithiasis, and possible stent
placement (plastic or expanded metal). It also allows biopsies and cytology to be performed
when malignancy is suspected
• Percutaneous transhepatic cholangiogram (PTC) – injection of bile ducts under X-ray control.
It allows, among other things, the insertion of a stent and temporary external drainage of the
blocked biliary tree, including tissue collection for histology.
• Surgical treatment:
- cholecystectomy with bile duct revision (conventional, laparoscopic, robotic)
- drainage and/or surgical resection (chronic pancreatitis, pancreatic and biliary tumours)
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Complications of obstructive icterus:
• Infection: cholangitis is typically caused by gram-negative bacteria (Escherichia coli,
Pseudomonas).
• Hepatorenal syndrome is caused by a combination of dehydration, underlying sepsis and high
bilirubin levels with toxic effects on the kidneys. High associated mortality in patients over
65 years of age
• coagulopathy – decreased synthesis of vitamin K-dependent coagulation factors (II, VII, IX,
X) and impaired platelet function
• Immunosuppression - hyperbilirubinemia predisposes to opportunistic systemic infection and
poor wound healing due to decreased protein synthesis
Poor prognosis is associated with risk factors such as:
• Age>65 years.
• Elevated serum urea
• bilirubin in the serum >200 g/L.
• underlying malignancy
• sepsis and multi-organ failure
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RETROPERITONEAL TUMOURS (10)
Hrabec Roman, Staník Michal, Šimůnek Radim
1/ Definition
Retroperitoneal tumours are tumours that arise in the retroperitoneum, which is defined ventrally by
the posterior layer of the peritoneum and dorsally by the transversal fascia located on the posterior
abdominal wall (back muscles, vertebrae). Cranially, the boundary of the retroperitoneum is the
diaphragm, and caudally, it gradually transitions into the subserous space of the pelvis (for more
details, see the respective question on retroperitoneal anatomy). Retroperitoneal tumours are
extremely rare. They are classified as malignant or benign. Malignant tumours represent 0.1-0.2% of
all malignant tumours. Tumours originating from organs within the retroperitoneum are not
considered retroperitoneal tumours, as they are the subject of other discussions.
2/ Etiology
Retroperitoneal tumours are classified as primary or secondary.
Primary tumours originate from the soft tissues of the retroperitoneum and are very rare, often
reported as case studies. They arise from mesenchymal and nerve tissue and embryonic remnants of
the urogenital system, known as extragonadal germ cell tumours. Among mesenchymal tumours,
both benign and malignant, the most common benign tumours are myolipomas or lipomas, followed
by fibromas, hemangiomas, lymphangiomas, etc. Among malignant variants (up to 80% of all
mesenchymal tumours), the most common are liposarcomas, followed by leiomyosarcomas,
fibrosarcomas, high-grade sarcomas SFT (solid fibrous tumours). There are more than 50
histological subtypes of sarcomas. Neurogenic tumours most commonly include neurinomas
(schwannomas), ganglioneuromas, neuroblastomas (in children), and their malignant variants.
Primary extragonadal germ cell tumours are very rare but highly aggressive. Their development is
explained by the persistence of gonadal cells in the retroperitoneum that remained after the descent
of the testes, with histological types primarily including seminomas and teratomas.
Secondary tumours in the retroperitoneum are much more common than primary ones. These
tumours metastasise to the retroperitoneum (most commonly to the retroperitoneal lymph nodes) or
invade by contiguity (urological, gynaecological, or gastrointestinal tumours). Systemic tumors such
as lymphomas also occur in the retroperitoneum.
3/ Pathogenesis
Due to the varied histological findings, it is difficult to specify the mechanisms and causes of
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retroperitoneal tumours. In some cases, a history of prior radiation therapy, especially for childhood
cancer, can be traced. In these patients, the risk of developing retroperitoneal tumours is up to 11
times higher than in the healthy population. Another risk factor is a genetic predisposition; in
families with a history of cancer, the risk of developing tumours in the retroperitoneum increases in
subsequent generations. The occurrence of some tumours is also associated with genetic disorders.
For example, patients with neurofibromatosis type 1, retinoblastoma, or tuberous sclerosis have a
higher incidence of retroperitoneal sarcomas. In general, primary malignant tumours most commonly
affect people between 50-80 years of age, with an equal distribution between genders.
4/ Clinical symptoms and assessment
a) Clinical symptoms: Due to their location, retroperitoneal tumours do not show specific symptoms
in the early stages, making clinical diagnosis very challenging. However, as the tumour grows, it
may cause a heterogeneous group of symptoms. The most common initial symptoms include
pressure discomfort, a palpable mass in the abdomen, or even abdominal wall bulging. The tumour
may compress the spinal roots if located near the spine, causing corresponding irritation or paretic
symptoms. The upper urinary tract is often affected, with ureter compression leading to dilatation of
the renal collecting system. Other possible symptoms include vague back pain, digestive disorders,
ileus, loss of appetite, constipation, and cachexia. Tumours may also compress major blood vessels,
potentially leading to oedema and varicosities in the lower limbs or thrombotic complications.
Retroperitoneal tumours should be considered in cases of unclear abdominal symptoms.
b) Paraclinical assessment – blood test, imaging, and biopsy: Laboratory abnormalities associated
with retroperitoneal tumours are mainly due to their expansive growth. In cases involving the upper
urinary tract, renal insufficiency may develop. Depending on the tumour's location and its
radiological characteristics, the adrenal function should be assessed (as retroperitoneal tumours are
often mistaken for adrenal tumours), and tumour markers for testicular tumours should be evaluated.
So, as in the clinical and ultrasonographic assessment of testes in men, A differential blood count can
help identify lymphoproliferative diseases. Specific tumour markers for retroperitoneal tumours are
currently under research. Imaging modalities are crucial for diagnosing retroperitoneal tumours. The
first choice is a CT scan, which provides basic information about the tumour's position, size, contact
with surrounding structures, and blood supply. More accurate imaging is achieved with MRI,
especially indicated before surgical treatment. PET/CT is often used to exclude tumour
generalisation, which provides higher sensitivity. If a primary retroperitoneal tumour or an atypical
appearance of a tumour in retroperitoneal organs is suspected, a critical step for solid tumours is
performing a needle biopsy, preferably under CT guidance. Pathological examination of biopsy
104
samples can help determine the exact histological nature of the tumour, guiding the oncological team
towards a more precise treatment plan.
5/ Prognosis
The essential condition for prognosis is the histological type of the tumour. This is a heterogeneous
group of tumours, varying from benign to semi-malignant and even extremely aggressive forms. It
greatly depends on tumour differentiation (grading), size (diameter in cm), and distant metastases.
6/ Differential diagnosis
When assessing pathological lesions of the retroperitoneum, pseudotumors may also be encountered,
most commonly cystic formations. These arise due to inflammatory diseases of certain
retroperitoneal organs (e.g., pancreas, kidney) or after injuries (bleeding into the retroperitoneal
space). Treatment is surgical. A rare disease of unclear aetiology is idiopathic retroperitoneal
fibrosis, also known as Ormond's disease. It involves the development of pathological fibrous tissue
of unclear aetiology around large vessels, nerves, and especially ureters, which gradually thickens
and most commonly leads to ureteral compression with the development of renal failure. Treatment
is challenging and includes corticosteroids and immunosuppressants. In advanced stages, surgical
treatment is performed to release the ureters from the infiltrate and perform their peritonealization.
7/ Treatment
Due to the rarity and heterogeneity of this group of tumours, studies have demonstrated better
treatment outcomes for patients when managed at specialised oncology centres.
The retroperitoneal tumour treatment and prognosis depend on the histological form of the tumour;
that is why the primary biopsy is crucial and essential.
In some types of retroperitoneal tumours can, primary chemotherapy be a curative option, i.e.
lymphomas in retroperitoneum and Ewing sarcoma.
Other types can be used, such as radiotherapy or chemotherapy before operation (neoadjuvant
radiotherapy, neoadjuvant chemotherapy). The objective of this pretreatment is downsizing and
downstaging the tumour. This can make the operation easier and shrink the amount of the resection
needed to achieve a complete resection – R0 resection. Due to the rarity of these diseases, the rules
of neoadjuvant treatment are still not clearly stated.
In many retroperitoneal tumours, the only curative option is radical surgical resection; the margins of
the resection depend on the histological type of the tumor.
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The most extensive resections are needed in retroperitoneal liposarcomas. In these cases, according
to worldwide recommendations is necessary to resection of all organs in contact with the tumor. It
means left hemicolectomy, nephrectomy adrenalectomy, splenectomy, distal pancreatectomy and
resection of the psoas muscle in left-site located tumours. In right-site located tumours then: right
hemicolectomy, nephrectomy, adrenalectomy and psoas muscle resection.
For extragonadal tumours, a so-called template resection is performed, where not only the
pathological finding is removed but also the entire lipo lymphatic tissue on the corresponding side of
the major vessels (paracaval, inter-aortocaval, and paraaortic lymph nodes).
Unfortunately, the primary diagnosis of these tumours often comes in the distant metastatic stage.
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ADRENALECTOMY - ANATOMY, APPROACHES, TYPES OF OPERATIONS (8)
Cabanová Lucia, Španková Markéta
Anatomy
The adrenal glands are a pair of endocrine organs that lie on the upper poles of the kidneys. They are
placed retroperitoneally at the level of Th11. Due to the lower position of the right kidney, the right
adrenal gland is also located lower. The right adrenal gland is pyramid-shaped and lies dorsal to the
liver, the left is crescent-shaped and lies dorsal to the stomach and in close proximity to the spleen.
The vascular supply of the adrenal glands is important. It consists of three arteries - superior
suprarenal artery (branch of the inferior phrenic artery), middle suprarenal artery (branch directly
from the abdominal aorta) and inferior suprarenal artery (branch of renal artery). Further, the arteries
in the adrenal gland branch and form a plexus in the cortex of the gland, from which they flow into
the veins of the medulla. The veins from the right adrenal gland join into the right suprarenal vein
that flows directly into the inferior vena cava, on the left side the veins join into the left suprarenal
vein that flows into the left renal vein.
Adrenal function disorders
The adrenal gland consists of cortex and medulla. The cortex produces glucocorticoids and
mineralocorticoids, while the medulla produces catecholamines. The hormonal secretion regulated
by the adrenal cortex is ensured by ACTH from the adenohypophysis. The medulla is formed by
postganglionic sympathetic neurons.
Cortical pathology - hyperfunction includes several syndromes. Conn's syndrome or primary
hyperaldosteronism, is manifested by hypertension and mineral imbalance (hypokalemia and
hypernatremia). Furthermore, Cushing's syndrome is overproduction of glucocorticoids and it
manifests as centralized obesity, a crescent-shaped face, skin changes, especially purple striae and
easy formation of hematomas, the development of osteoporosis and a variety of other symptoms.
Another cortical pathology - hypofunction includes Addison's disease which means reduced
production of aldosterone and cortisol. The symptoms include fatigue, weight loss, diarrhea,
hypotension due to sodium loss and potassium accumulation.
The pathology of the adrenal medulla is pheochromocytoma, which is a rare neuroendocrine tumor.
The tumor realeses hormones that can cause various symptoms such as hypertension, palpitations,
headache and other systemic manifestations. It can also occur in hereditary MEN II syndromes that
cause tumors in various endocrine glands (medullary carcinoma of the thyroid gland, often bilaterall
pheochromocytoma, primary hyperparathyroidism or mucosal neuromas).
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Diagnostics
Adrenal tumor is often detected as an incidental finding on imaging during the investigation of
another disease. We refer to these findings as so-called incidentalomas. Due to the development and
availability of imaging methods, their incidence is increasing. It is mostly an unilateral pathology.
The basic imaging method is nativ CT or MR. When detecting an incidentaloma, malignancy must
always be excluded first. Smaller benign tumors without hormonal activity do not need further
follow up. Borderline CT findings with normal hormone levels are indicated for CT follow-up. If the
CT findings show malignancy or the tumor is hormonally active, then the adrenalectomy is indicated.
Hormonal examination includes assessment of cortisol level, aldosterone level in the blood and
possibly examination of metanephrines.
Adrenalectomy
The surgical procedure of the adrenal gland is either unilateral, bilateral or partial adrenalectomy.
Indication for the surgical treatment is made by an endocrinologist. The pathologies that are
indicated for adrenalectomy include: CT tumors suspected of malignancy, findings that increase in
size within a few months and hormone-producing findings. Another pathology of the adrenal glands
can be metastases of other tumors, e.g. breast cancer, kidney cancer, or bronchogenic cancer.
Today the gold standard is laparoscopic adrenalectomy. An open approach is indicated for bulky
tumors and tumors with signs of local invasion.
Complication
Like any surgical operation, adrenalectomy has its complications. The complications include for
example, the wound infection, bleeding, or intraoperative injury to surrounding organs. Other
complications may be related to the patient's internal comorbidities, or they may be directly related
to the function of the adrenal glands such as hormonal imbalance, arterial hypertension or
hypotension. A serious complication is an adrenal (Addisons) crisis, adrenal insufficiency with
manifestation of symptoms as heart rhythm disorders, hypotension, tachycardia, abdominal pain,
vomiting, weakness, dehydration.
Conclusion
Adrenal tumors can cause abdominal discomfort, pressure pain in case of larger tumors or systemic
symptoms depending on the hormones produced in hormonally active findings. Some adrenal tumors
are detected incidentally on imaging examinations. If the indication criteria are met, an
adrenalectomy is performed by the surgeon. Monitoring of patients with adrenal pathology is further
done by endocrinologists.
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DIAGNOSTIC METHODS IN UROLOGY . EXAMINATION, LABORATORY TESTS, ENDOSCOPIC AND
IMAGING METHODS (39)
Trinh Tuan, Fedorko Michal
Basic evaluation of a patient involves taking a detailed history and performing a physical
examination.
1. Anamnesis
Anamnesis (previous illnesses) entails a basic medical history. Emphasis is placed on the urological
history, where we document information related to urological diseases and operations.
2. Clinical examination of the patient
A complete and thorough physical examination is an essential part of the evaluation of patients with
urological diseases. Correct execution helps to choose the appropriate diagnostic examination. The
visual examination of the patient provides a general overview. We notice the colour of the skin
(icterus, pallor), nutritional status (cachexia as a frequent symptom of malignancy, obesity as a
possible manifestation of a hormonal disorder). This is followed by examinations focused in urology,
typically on the abdomen, pelvis and genitals.
2.1 Examination of the kidneys
With the patient lying on his back, we perform the so-called bimanual palpation of the kidneys
(Israeli´s sign). Palpating the kidneys in men can be difficult due to the resistance of the back and
abdominal muscles and a more fixed position than in women. Tapotement of the kidneys is an
examination in which the doctor taps the kidney area with the edge of the palm. A positive finding
(pain reported by the patient) is a symptom of inflammatory kidney disease or renal colic.
2.2 Examination of the bladder
The bladder can be felt or identified by percussion if it is filled with at least 150 ml. At a filling of
around 500ml, the filled bladder is visible in slim patients as an oval bulge in the lower abdomen.
Bimanual examination of the bladder is performed under general anaesthesia and is part of the
examination to determine the extent of bladder tumours or other pelvic tumours (in men, we palpate
the bladder between the abdominal wall and the rectum, in women between the abdominal wall and
the vagina).
2.3 Examination of the male genitalia
When examining the penis, we retract the foreskin (if the patient is not circumcised) and examine the
entire glans to exclude a tumour or balanoposthitis. If it is not possible to retract the foreskin, we
recommend surgical correction (dorsal slit or circumcision). We note the position of the urethral
orifice (hypospadia, epispadias) and changes on the penis (herpes simplex, condylomata, ulceration,
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fibrous plaques in Peyronie's disease). Symmetrical enlargement of the scrotum may correspond to
swelling due to anasarca or lymphedema in the case of lymphatic obstruction (e.g. after operations in
the small pelvis, in endemic parasitic filariasis). Asymmetrical enlargement may be caused by
involvement of the testis, epididymis or spermatic cord. It could be a hydrocele or a cyst of the
epididymis, if it is outside the scrotum, it is necessary to think of a scrotal hernia. In a patient with
epididymitis, it is difficult to distinguish between the testicles and the epididymis
(orchioepididymitis), there is usually a painful induration, and the skin of the scrotum on the affected
side is red and tense.
Resistance of the spermatic cord can be caused by funiculocele (hydrocele of the spermatic cord) or
varicocele (dilated veins of the pampiniform plexus).
A life-threatening condition is an infection of the soft tissues of the perineum, perianal area and
external genitalia, the so-called Fournier's gangrene (necrotizing fasciitis), manifested by painful
swelling on the genitals with necrotic areas of the skin and surrounding redness. Any solid resistance
on the testis should be considered a malignant tumour until it is excluded. Resistances on the
epididymis are almost always benign.
2.4 Examination of the genitals and pelvis in a woman
It is performed in the standard lithotomy position with abduction of the lower limbs. Evaluate the
external genitalia and introitus (atrophic changes, erosion, discharge, condylomas). On the urethra,
we can identify caruncles, cysts, urethral prolapse or a tumor. Furthermore, we can evaluate the
severity of stress incontinence (Marshall and Froevis test).
2.5 Rectal examination
Digital rectal examination (DRE) is a basic examination method and the only way to examine the
prostate, it is an integral part of a man's urological examination. It should be done for men over the
age of 40. We perform a DRE at the end of the clinical examination after instructing the patient and
with his consent. The most suitable is the standing position, when the patient bends over the edge of
the examination bed with legs slightly apart, or the position on the knees and elbows. The normal
prostate has the shape and size of an edible chestnut, with a groove in the midline, is elastic, smooth
and painless. The consistency is similar to a contracted thenar. Of patients with prostate biopsy due
to suspected DRV, 18% have prostate cancer. Any suspicious finding (hard nodule, asymmetrically
harder lobe, prostate stone) on the prostate is an indication for biopsy. In inflammatory diseases, the
prostate is palpably painful and boggy or is a palpable fluctuation in the presence of an abscess.
3 Laboratory examination
3.1 Examination of urine
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Physical (color, turbidity, specific gravity, osmolality, pH) and qualitative chemical examination of
urine are among the basic examinations. A fresh midstream urine sample must be collected after
genital hygiene (or disinfection) into a clean container. A urine sample can also be obtained by
catheterization, it is routinely performed mainly in women, in some indicated cases in men. A urine
dipstick test is a quick way to evaluate urine (pH evaluation, presence of blood, proteins, leukocytes,
nitrites, glucose, etc.).
Urinalysis is a laboratory test involves chemical and microscopic analysis of urine sample, it is a
more accurate examination. In a urological patient, we notice pH values do not depend only on the
nature of the diet and individual metabolism, the physiological pH range of urine is between 4.5-7.0.
For example, in the case of urinary infection with ureolytic bacteria, the pH of the urine is above 7.0.
The specific gravity of urine indicates the ability of the kidneys to concentrate urine, a low value of
the specific gravity (hyposthenuria) can be a sign of altered kidney function. In the sediment
examination, we mainly evaluate the presence of erythrocytes and leukocytes. An abnormal amount
of erythrocytes may indicate a higher permeability of the glomerular membrane, or bleeding in the
urinary tract. The number of leukocytes with relation to the patient's dysuria symptoms indicates a
possible inflammation of the urinary tract.
Microbiological examination of urine is an integral part of diagnostics. In the collected material, the
microbiologist identifies the infectious agent and determines the pathogen's sensitivity to antibiotics,
the so-called antibiogram. Prostatic secretion, ejaculate, urethral or any purulent discharge can also
be sent for microbiological examination. For cytological examination of the urinary tract, urine can
be obtained by spontaneous voiding or catheterization, or from the upper urinary tract during an
endoscopic procedure. We use cytological examinations especially in the diagnosis or follow-up of
uro-oncological patients.
3.2 Prostate-specific antigen (PSA) testing
PSA is a protein produced in the prostatic tissue, is released from the prostatic epithelia and can be
found in ejaculate and blood serum. Physiologically, PSA occurs in very small amounts in the blood.
PSA is organ-specific, not tumour-specific. It increases with benign enlargement of the prostate or
with prostate tumours. Values can be altered in case of urinary infections or when a urinary catheter
is inserted. The level of PSA in the blood increases with age. PSA determination is used to detect the
risk of prostate cancer early (typically in men aged 50-70 years) and to evaluate the effectiveness of
treatment. Patients with a PSA value above 3ug/l should undergo an examination to rule out prostate
cancer.
4. Endoscopic examination
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Endoscopy in urology enables the visualization of the urinary tract, from the external meatus to the
renal calyces. Endoscopy requires irrigation fluid, a light source, and an endoscope.
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4.1 Urethrocystoscopy (UCSK)
Endoscopy of the lower urinary tract is the most common procedure in urology. It is performed
under both local and general anaesthesia, allowing examination of the urethra and bladder. The most
common indications for UCSK are microscopic or macroscopic hematuria, recurrent urinary tract
infections, persistent dysuria problems, urinary incontinence or urethral stricture. During the
examination, flushing cytology, biopsies for histological examination, or retrograde
ureteropyelography (UPG) and insertion of a ureteral stent can be performed. Another routine
indication is the monitoring of patients diagnosed with non-invasive urothelial bladder cancer.
4.2 Examination of the upper urinary tract
The most common indications for examination of the upper urinary tract are management of
urolithiasis, ureteral obstruction and the diagnosis of a tumour of the renal pelvis and ureter. It is
performed using a ureterorenoscope (URS) exclusively under general anesthesia. Endoscopes have a
working channel enabling the introduction of instruments, e.g. extraction forceps, laser fibers,
ultrasonic or electrohydraulic lithotriptors. Nephroscopy is a percutaneous examination of the renal
collecting system. Nephroscopy is used for treatment of large kidney stones over 2 cm (percutaneous
nephrolithotripsy - PCNL).
5. Imaging examination
Ultrasonography (US) is a basic imaging method in urology. With ultrasound, a urologist most often
examines the kidneys, bladder, prostate and scrotal organs. A whole range of interventions are
performed using ultrasound (e.g. introduction of nephrostomy, puncture and drainage of cysts or
abscesses, introduction of epicystostomy, prostate biopsy, etc.). Non-contrast CT of the urinary tract
is the method of choice when renal colic is suspected, if we want to confirm or rule out the presence
of urolithiasis. CT urography (with the administration of an iodine contrast agent) is mainly used to
investigate hematuria, recurrent infections and tumours of the kidneys or urinary tract. Another
option is magnetic resonance imaging. At present, the most common indication for magnetic
resonance imaging is prostate examination, in the case of suspicious findings, the patient is indicated
for targeted fusion biopsy of the prostate. Other imaging tests include urethrocystography, retrograde
or antegrade pyelography and nuclear medicine scans (phase scintigraphy of the kidneys, bone
scintigraphy). State-of-the-art PET/CT or PET/MR are reserved for uro-oncological indications,
mostly within the re-examination and follow-up of patients with prostate cancer.
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ARTERIAL ANEURYSMS (12)
Novotný Tomáš
1/ definition
An arterial aneurysm is an enlargement of the diameter of an artery by at least 50% of its normal
size. It can affect any artery, but there are predilection sites: the abdominal aorta (up to 8% of the
population of age 65+) and its main branches, the popliteal artery, the visceral arteries (most
commonly the splenic artery), and the large intracranial arteries (Intracranial aneurysms are not the
subject of this chapter). In other arteries, aneurysms occur sporadically.
2/ etiology
The etiology is multifactorial. The strongest risk factors are genetic risk, hypertension, dyslipidemia,
smoking, atherosclerosis (but it is not a pathogenetic factor), age, male sex, race, infection, arterial
injury, and hereditary connective tissue disorders.
3/ pathogenesis
The vast majority of aneurysms are of degenerative type. The pathogenesis is a complex process, and
little is known about its details. In general, there is a progressive disruption of the structure and
function of the layers of the vascular wall, especially the media, and adventitia. The consequence of
the loss of wall strength is a gradual progressive widening of the given arterial segment. Other types
of aneurysms with different pathogenesis are less common.
4/CLINICAL MANIFESTATION
a) clinical symptoms and signs
The vast majority of aneurysms are asymptomatic and are discovered accidentally. Lean individuals
may find a pulsating mass in the abdomen or limb. In a small group of patients, manifestations may
be due to the pressure of the aneurysm on the surrounding area, e.g. pain, and swelling. Other
symptoms are usually caused by aneurysm complications.
Signs depend on the location and size of the aneurysm. Abdominal aortic aneurysms can be palpated
in thinner individuals, usually as a pulsatile resistance to the left of the umbilicus. In obese
individuals, they are not so easily palpated. An aneurysm of the popliteal artery is also usually
palpable, but again with the limitation in overweight patients. Visceral aneurysms are difficult to find
during physical examination.
b) paraclinical investigations - laboratory, imaging, and functional testing
Of the paraclinical examinations, imaging is the main one used for accurate diagnosis and decisionmaking.
Ultrasonography is an inexpensive, radiation-free examination that can confirm the
aneurysm in most patients. Often, aneurysms are detected during examinations indicated for other
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diseases. CT angiography is the gold standard for treatment decisions. This imaging modality
provides the most accurate morphological information. The contribution of magnetic resonance
imaging for the diagnosis and management of vascular disease is lower - the examination is more
expensive, less accessible, and has numerous artifacts. Digital subtraction angiography might be
limited for the diagnosis of aneurysms by the presence of an intraluminal thrombus, so the aneurysm
may not be visualized at all on the scan.
5/ course of the disease
Most aneurysms develop during a lifetime, with their formation and enlargement taking place over a
period of years, and therefore usually affect older patients. A large proportion of them remain
asymptomatic throughout life. However, some patients develop complications.
6/ complications
Rupture of the aneurysm and life-threatening bleeding is the most serious and common complication.
It is a typical complication of aneurysms located in the abdominal and thoracic cavity. The usual
symptom triad for abdominal aortic aneurysm rupture is abdominal pain, pulsatile abdominal mass,
and shock. Bleeding from visceral aneurysms manifests similarly, except that these aneurysms are
usually not palpable.
Peripheral embolization is another complication. It is typical for limb aneurysms - mainly aneurysms
of the popliteal artery. This aneurysm rarely ruptures and bleeds, but its early treatment is necessary
because of the risk of successive embolization into the tibial arteries and its subsequent closure with
limb loss. Embolization as a complication of abdominal aortic or pelvic artery aneurysm is less
common. The clinical manifestation varies from asymptomatic to acute lower extremity necrosis to
chronic critical limb-threatening ischemia or acute limb ischemia.
Aneurysm thrombosis may be a separate complication where major arteries remain patent distally to
the aneurysm or final thrombotic closure of the aneurysm in the absence of outflow after its closure
by emboli. The clinical picture may vary from asymptomatic, through variable chronic ischemic
symptoms, to acute ischemia of the limb.
7/ prognosis
The prognosis of the disease is determined by the size of the aneurysms, the location, and especially
the complications. Small asymptomatic aneurysms with no or minimal intraluminal thrombus usually
do not develop complications. Large aneurysms and aneurysms with intraluminal thrombus, on the
other hand, represent serious diseases with a high risk of life-threatening bleeding or possible lower
limb loss.
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8/ differential diagnosis
In the differential diagnosis, tumors at intra-abdominal localization should be considered in the first
place in clinically diagnosed pulsatile resistance. In popliteal aneurysms, the Baker's cyst should be
considered. Ultrasonography or CT angiography as the main diagnostic method will safely
differentiate the conditions.
9/ TREATMENT
Small aneurysms that are not treated by intervention are monitored at regular intervals using imaging
methods (ultrasonography, CT), usually annually. There is no drug treatment for the disease. Risk
factor modification such as treatment of hypertension, treatment of dyslipidemia, and smoking
cessation is recommended.
Interventions are performed based on indication criteria that are specific to each site.
Abdominal aortic aneurysm
The indication margin for elective intervention for abdominal aortic aneurysm is an aortic diameter
of 55 mm. When this size is reached, the patient's health status should be considered in terms of
perioperative risks and aneurysm repair may be offered. Recent data show that the risk of aneurysm
rupture below this threshold is up to 3 times higher in women than in men. Therefore, in women,
intervention can be considered as early as 50 mm in diameter. However, it must also be taken into
consideration that aortic aneurysm interventions in women are associated with twice the mortality
rate according to the available evidence. The available data do not allow analysis of the cause, but it
is suggested that age may be a factor, as aortic aneurysms in women reach a clinically relevant size
at an older age.
The treatment options are: 1) open surgery - resection of the aneurysm and aortic replacement with
an artificial vascular prosthesis, 2) endovascular surgery - implantation of an aorto-iliac stent graft.
Only in a few centers in the world, resections are performed laparoscopically or robotically.
Open surgery is burdened with slightly higher periprocedural mortality and morbidity, but it is a
better method in terms of long-term results (a large number of stent graft complications occur 8-10
years after implantation). Therefore, recent guidelines from the European Society for Vascular
Surgery recommend that open surgery should be preferred in patients with a life expectancy of more
than 10-15 years and endovascular surgery in older patients with a life expectancy of less than 10
years. Patients with a short life expectancy of less than 2 years (terminal stages of cancer, etc.)
should be managed conservatively.
Planned procedures in asymptomatic patients should ideally be performed within 2 months of
indication, as recommended. Symptomatic patients are managed acutely after the necessary
preoperative preparation. Patients with aneurysm rupture are operated urgently.
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Aneurysm of the popliteal artery
The indication threshold for elective surgery is a diameter of 2 cm (to prevent thromboembolic
complications and limb loss). In high-risk patients, surgery may be delayed up to 3 cm in diameter.
However, if an intraluminal thrombus is present, the aneurysm should always be treated, even if the
diameter is less than 2 cm. Surgical management has two options: 1) replacement of the popliteal
artery with a venous graft or exclusion of the aneurysm (ligation of the inflow and outflow arteries)
and venous bypass. Endovascular options for treatment are very limited in this aneurysm. In case of
acute ischemia, the procedure is urgent (see Acute arterial occlusions).
Aneurysms of visceral arteries
The indication thresholds for visceral aneurysms are not supported by strong evidence. Generally
accepted indication margins are 3 cm for splenic and renal artery aneurysms and 2 cm for other
visceral arteries. The approach is individual according to morphology and is performed using an
open procedure or endovascularly. Ruptures of visceral aneurysms are managed as acute abdomen.
10/ prevention
Prevention options are very limited due to the unknown pathogenesis. Prevention and treatment of
risk factors is recommended. In some European countries, screening for abdominal aortic aneurysms
at the age of 65 years and older has been introduced.
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PERIPHERAL ARTERIAL DISEASE OF LOWER EXTERMITIES (13)
Kysela Petr
Introduction: There are roughly 1/3 of people dying of malignant tumours and nearly 2/3 (i.e.
twofold more) of cardiovascular diseases in the civilised world. The peak incidences of both diseases
fall in the same age group – above 65 years.
Aetiology and risk factors: Peripheral arterial disease (PAD) comprises the occlusive and the nonocclusive
diseases. Solution to non-occlusive ischaemia can be tricky with unpredictable outcomes.
The non-occlusive group contains namely A-V fistulas (steal, high output heart failure), aneurysms
(thrombi formation, embolisation, rupture), medial sclerosis (inability to open collaterals) and
compression syndromes (TOS, popliteal artery entrapment). The occlusive diseases comprise
atherosclerosis in more than 90 %, cystic adventitial degeneration (i is not to be treated
endovascular), vasculitides (including Buerger´s one related to tobacco abuse), fibromuscular
dysplasia of the external iliac artery in sportsman (bikers), vasoneuroses (vibrating tools, back pain),
and Raynaud´s syndrome (known underlying disease) or Raynaud´s phenomenon (not known
underlying illness). It is atherosclerosis that causes the occlusive ischaemia the most often. It
develops due to vessel wall trauma by high blood pressure and sharp pulses, leading to vessel wall
inflammation. That is why it affects mainly arterial forks and mechanically traumatised parts of
arteries (heart ligaments, Hunter´s canal orifice). In addition, blood pressure in the lower extremities
is higher by 20%. Their diameter is also larger on top of that. It leads to much higher wall tension
(i.e. trauma). Risk factors include (in their significance order) smoking, diabetes, hypertension,
hyperlipoproteinemia, thrombophilia, and increased CRP. PAD revascularisation thus needs no
one but diabetics and smokers. Conventional smoking is even more harmful as it blocks the
binding capacity of Hb to O2 due to irreversible poisoning with CO.
Epidemiology: The incidence of lower limb ischaemia is estimated at 50-100 / 100.000 per year. Its
prevalence symptomatic is around 12 %. 50 % of patients suffering from critical limb ischaemia
survive less than 6 years (quite a malignancy). Similarly, cerebral stroke incidence reaches about 195
/ 100.000 in Europe, being the 2nd most frequent cause of death after myocardial infarction – 1.1
million a year in Europe. Cerebral haemorrhage is to be blamed in 10 – 20 %10 – 20 % Mesenteric
ischaemia comes out in 3-9 / 100.000 a year. However, its mortality reaches 93 %.
Symptoms: Pain upon strain is the main sign of ischaemia. In the case of, for example, diabetic
neuropathy, pain needn´t be expressed. If this is the case, pain is substituted with weakness/loss of
function upon strain or development of necroses. Differential diagnosis is VERY complex.
Symptoms of ischaemia arise due to the depletion of energetic sources (glycogen consumption and
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lack of glucose) and toxic waste gathering, rather than the absence of oxygen. The purvey of glucose
is fundamental to maintaining the Krebs cycle, which breaks down and stops the neutralisation of
free oxygen radicals.
Examination: Medical history of worsening claudications – i.e. blunt pain or weakness and loss of
function of the affected region upon constant dynamic strain. On the contrary, entrapment of the
popliteal artery leads to pain upon static foot plantar flexion. Neuropathic hot and sharp pain usually
appears during the night.
Physical examination contains palpation of pulsations and auscultation of all main arteries. The
presence of pulsations at the very periphery completely excludes significant occlusive disease. The
murmurs do not correspond to the significance of stenoses. Skin colour changes represent late
symptoms and need not correspond to ischaemia. Open skin collaterals may belay the chronic
mainstream arteries occlusion. There is vasoconstriction in healthy skin.
According to the blood tests, the D-dimer (DD) elevation may point to ongoing acute thrombosis.
There is no other specific marker to prove acute ischaemia. Lactate and acidosis are late signs of a
generally bad medical condition (shock). Chronic elevation of CRP and ANCA supports the
diagnosis of possible vasculitis if it fits the clinical appearance.
The first choice imaging method should be the Doppler ultrasound (US), with a sensitivity of 88 %
and specificity of 96 %. It provides information about the location and degree of stenoses and
visualises A-V fistula or dissection. US measures ankle pressure or toe pressure and ankle-brachial
index (ABI). CT angiogram is necessary whenever one thinks of some revascularisation (sensitivity
of 90 %). MR angiogram is mandated in patients allergic to iodine contrast medium. Digital
subtraction angiography (DSA) usually serves as a treatment method.
Therapy: 1.) Lifestyle rearrangements in all patients and as prevention: Absolute smoking
cessation is necessary, including alternative ways (VAP, heated tobacco) due to the direct toxic
effect of nicotine on the endothelium and vessel wall. These means include an appropriate diet, more
aerobic exercises – 30 minutes of active walking daily and fighting hypertension and diabetes (mind
gluconeogenesis blocking agents which may worsen existing diabetic ulcers).
2.) Pharmacotherapy in all symptomatic patients: Antiplatelet drugs – acetylsalicylic acid (ASA) is
the cornerstone of the treatment. Addition (dual antiplatelet therapy) or switching to ADP P2Y12
receptor blockers (clopidogrel, ticagrelor), GP IIb/IIIa inhibitors (fibans, abciximab) in case of drug
resistance or specific cases, may be indicated. Vasodilating agents and rheologics can be offered to
highly symptomatic, non-revasularizable patients, along with beta-blockers withdrawal (due to their
vasospastic effect). These include pentoxifylline, naftidrofuryl, nicotinic acid (niacin) or capillary
antithrombotic agents like sulodexide, namely in diabetic microangiopathy. Critical chronic limb
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ischaemia can improve after a series of intravenous prostaglandin E1 as salvage therapy in patients
with rest pain without necroses. Hypolipidemic drugs are used as a secondary prevention. Blood
thinning medication is not routinely indicated in PAD. An angiologist is responsible for the
treatment.
3.) Endovascular treatment: Seldinger access to vessels through well-compressible arteries
(common femoral, radial or cubital arteries) inserts a sheath as a way for catheters and other
instruments. It is possible to perform local thrombolysis, mechanical thromboaspiration and
percutaneous balloon transluminal angioplasty (PTA). Placement of stents may sometimes be
necessary. Drug-eluting balloons and stents (DEB, DES) can be used when re-des are needed or in
very tiny arterioles (paclitaxel, everolimus). An interventional radiologist or interventional
angiologist is in charge here. Thorough antiplatelet medication is required after procedures. It is very
often dual (ASA + clopidogrel). Endovascular methods should be favoured in treating the aortic arch
and its branches, intracranial and visceral arteries, and small arteries at the very periphery of limbs.
Carotid artery stenting (CAS) is not deemed the treatment of choice and should be limited to specific
cases. CAS must always use distal protection to prevent cerebral embolisation.
4.) Surgical revascularisation: A vascular surgeon performs it after gaining direct access to target
vessels according to underlying pathology. He may do a thrombectomy, direct or indirect. Plaque
removal can be achieved either directly or distantly. The narrow part of an artery can be enlarged
with a patch, i.e. arterioplasty. However, the typical is bypass surgery. According to the material
used, we recognise autologous (great saphenous vein), allogenic (aortoiliac graft) or artificial (část or
knitted) bypasses. Anatomic bypasses accompany bypassed arteries, whereas non-anatomic ones
connect naturally directly not connected arteries. Nearly all surgical procedures on vessels start with
a shot of heparin (100 IU/kg of body weight) and may but needn´t be terminated with protamin. As
its effect is anticoagulation, it must not be administered excessively.
Combining the endovascular and open approach at once may bring about certain advantages – socalled
hybrid procedures. They are better to be performed in the hybrid operating theatres.
5.) Sympathectomy as additional therapy: It is the upper thoracic sympathectomy or alternatively
US-guided stellate ganglion blockade on the upper extremities. One can perform CT-guided coeliac
ganglion lysis in cases of visceral ischaemia. We can offer retroperitoneal lumbar sympathectomy or
CT-guided sympathetic blockade on the lower extremities. It is of little effect in diabetic patients.
6.) Hyperbaric oxygen therapy is not indicated
Classification: As elsewhere, any classification should mirror either treatment or prognosis. The
invasivity of treatment is chosen according to clinical classification according to Fountain or
Rutherford (the letter developed two classifications – one for acute and one for chronic ischaemia).
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The higher the clinical stage, the shorter the survival rate. Morphologic TASC (TransAtlantic
interSociety Consensus) criteria guide decision-making between endovascular and open approaches.
Carotid artery endarterectomy (CAE) is the only surgery that is also indicated according to the
complication rate of the particular surgeon. Asymptomatic stenoses can be intervened, given the
complication rate below 1.5 %. If the complication rate falls between 1.5 and 3,0 %, it is allowed to
operate on symptomatic stenoses only. If the rate is 3.0 – 4.5 %, only both-sided stenoses on the
symptomatic side can be treated. If you have more than 4.5 % of complications, you should not
operate on carotid arteries at all. The indisputable indication of CAE is represented by symptomatic
stenosis of more than 70 % or even asymptomatic one of more than 60% if the plaque is
unstable/risky. The ABCD2 score gives timing.
Treatment of ischaemic wounds is guided by the WIFI score (Wound, Ischaemia, Foot Infection).
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Modified Font ain's clinical classification
Class Symptoms Ultrasound
I N symptoms ABI usually > 1,0
II a
b
c
Claudication more than 200 m ABI 0,8 - 1,0
20 – 200 m ABI 0,5 - 0,8
less than 20 m
III Rest pain – non-critical Ankle pressure 50 mm Hg
Rest pain - critical Ankle pressure 50 mm Hg
IV a
b
Necrosis – non-critical Toe pressure mm Hg
Necrosis - critical Toe pressure 50 mm Hg
Classification of cerebral ischaemia
Transitory ischemic attack TIA Symptoms disappear within 24 hours –no detectable
ischaemia on CT or MRI
Minor stroke National Institute of Health Stroke Scale <= 3
Completed stroke Detectable ischaemia, more than 24 hours
Stroke in evolution Symptoms progressively worsen over time
Crescendo TIA Periods between two following TIAs get shorter, or
symptoms get worse
ABCD2 Risk of Stroke after TIA Timing of carotid endarterectomy after TIA
Age >60 1 ABCD2 7-days risk of stroke
BP >140/90 1 6 24 – 31 %
Clinical Paresis 2 5 12 %
Fatic imp. 1 4 1-9 %
Duration 10min-1h 1 3 0 %
More 1h 2 6-7 2-days risk of stroke = 8-10 %
D2 = DM 1 ABCD 0-3 delayed, ABCD 4-5 early,
Sum A + B + C + D + D2 = ABCD2 ABCD 6-7 acute surgery.
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ACUTE LIMB ISCHEMIA (14)
Novotný Tomáš
1/ definition
Acute arterial occlusion is the blockage of flow through a peripheral artery, resulting in ischemia of
the supplied body part. The subject of this chapter is acute occlusions of the large arteries of the
systemic circulation, of which the most common are acute occlusions of the limb arteries, especially
in the lower. Acute occlusions of organ arteries are a separate topic.
2/ etiology
The cause of arterial occlusion may be embolism, thrombosis, or injury (including iatrogenic).
3/ pathogenesis
In embolism, the artery is occluded by a piece of material (embolus). The most common embolus is a
thrombus, the source of which is usually the heart. Other possibilities are atherosclerotic masses from
feeding arteries, tumor fragments, amniotic fluid, or foreign bodies (including, e.g. broken-off
instrument parts). The embolus is carried by the bloodstream to a point where its size no longer
allows further movement and it occludes the artery at this point. Arterial thrombosis most often
occurs at the site of an atherosclerotic lesion due to reduced blood flow or plaque complications. The
risk increases dehydration, hypercoagulable states, or shock. However, it can be caused by other
arterial pathologies such as aneurysms, vasculitis, etc. In trauma (including iatrogenic), the arteries
might be transected or their internal layers are injured with subsequent dissection and closure. The
consequence is impaired blood supply to the tissues, anaerobic metabolism, and tissue necrosis.
When blood flow is restored after a prolonged period, reperfusion injury adds to the ischemic
damage.
4/ CLINICAL MANIFESTATION
a) clinical symptoms and signs
The patient's complaints are variable, ranging from asymptomatic to symptoms of severe acute
ischemia. It depends on several factors: the size of the artery, the size of the area supplied, and the
collateral circulation. In symptomatic ischemia, patients complain of pain and coldness of the limb,
tingling or numbness of the limb, and later the inability to walk.
Objectively, the limb is cold and pale, peripheral pulses are absent, and there is a gradual impairment
of the sensory and motor function of the periphery of the limb (numbness and motor dysfunction of
fingers, then the same at the ankle level, etc.). However, sensory and motor dysfunction may affect
larger limb parts if the arterial closure is proximal to the groin.
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The clinical picture can be memorized using the so-called 'six Ps': 1) Pain, Pulselessness - absence of
peripheral pulses, Pallor - initially with insufficient blood flow but may progress to cyanosis,
Poikilothermia - coldness, Paresthesia - tingling (gradually changes to anesthesia progressing from
the periphery of the limb), Paralysis - impaired movement, inability to control the limb (the disability
progresses from the periphery of the limb towards center too).
Acute limb ischemia is classified into grades according to Rutherford classification (Table 1).
b) paraclinical investigations - laboratory, imaging, and functional testing
When acute occlusion of a limb artery is suspected, potassium levels are important among laboratory
tests, as well as creatine kinase and myoglobin levels. Creatine kinase is not as specific as
myoglobin, so we usually determine both values at the initial stage. Creatine kinase alone can be
used later while treating reperfusion syndrome (lab test is cheaper).
Among imaging methods, ultrasonography may be used. However, CT angiography is always the
main imaging modality in acute limb ischemia. This examination is performed in virtually all
patients except those with aortic thrombosis and sometimes in clinically highly probable cases of
embolism, especially in the upper limbs. The examination will provide the most accurate diagnostic
information to choose the correct management. It should also be mentioned that, due to the aging of
the population, patients with embolism tend to have concomitant atherosclerosis, which may
influence the choice of adequate treatment. Other imaging modalities are rarely used in the diagnosis
of acute ischemia.
5/ course of the disease
The course of the disease in symptomatic patients varies depending on the collateral vessel and the
localization and type of occlusion. It generally takes place within a few units of hours. It begins with
pain and coldness of the limb, which is gradually joined first by impaired sensory function and then
by impaired motor function. In the most severe forms, immediate treatment is required, as
revascularization within 6 hours of the onset of ischemia is needed to save the limb and its function.
6/ complications
The most severe complication of acute limb ischemia is loss of life or limb because of late or
inadequate treatment. Most affected patients are polymorbid.
The typical complication in prolonged ischemia (more than 6 hours) is the postoperative
development of compartment syndrome. It occurs after successful revascularization (usually within
hours). The only possible solution is to perform decompressive fasciotomy. For more details, see the
chapter Compartment syndrome.
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After prolonged ischemia and revascularization, reperfusion syndrome should be expected. It is
caused by the washout of potassium, myoglobin, toxic metabolites, inflammatory mediators, and
oxygen radicals from the ischemic limb. It leads to metabolic acidosis as well.
7/ prognosis
The prognosis is given by the extent and severity of ischemia as well as the patient's medical
condition and comorbidities. In the most severe cases, the patient might lose the limb or die (usually
because of reperfusion syndrome or due to other complications).
8/ differential diagnosis
In the differential diagnosis, we try to differentiate clinically between embolism and thrombosis. In
embolism, the onset of ischemia is usually sudden, patients tend to be younger, have a known
potential source of embolism, have no history of lower limb ischemia and peripheral pulsations are
usually present in the contralateral extremity. In thrombosis, the onset is more gradual, the patients
are older, have no known source of embolism, have a history of claudication, and pulsations are
absent even on the unaffected limb. However, it must be said that in reality, cases of embolism may
occur in patients with peripheral arterial disease of the lower limbs and thrombosis can also occur in
patients without a history of ischemia and with cardiac arrhythmia. Therefore, the distinction is often
not easy. Among other diseases, the possibility of vertebrogenic disorders should be considered.
9/ TREATMENT
Initially, full anticoagulation is appropriate unless contraindicated. Unfractionated heparin should be
preferred and applied as early as possible to prevent the progression of thrombosis. Other measures
are supportive - painkillers, oxygen therapy, and hydration.
Conservative management is possible only in a minimum of cases, and most often when a patient
refuses care. Treatment options can be divided into surgical and endovascular. The timing of the
procedure must correspond to the severity of the ischemia. Stages I and IIa should be treated within
hours. For stage IIb, immediate revascularization is necessary. In irreversibly affected limbs, only
amputation is possible.
The surgical methods used are embolectomy or thrombectomy with a Fogarty catheter. In this
procedure, a long catheter with a balloon at the end is introduced into the exposed artery in the groin
or other access site. If we can pass the catheter through the site of the artery occlusion, we then
inflate the balloon and use it to remove thrombi and emboli from the arteries as we pull out the
catheter. If this procedure is not successful, we choose other revascularization options endarterectomy
(removal of the plaque at the site of the occlusion), or bypass (creating a new path
for blood over the occlusion with a vein or vascular prosthesis). In trauma, we use the same
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reconstructive methods with the specificity of using artificial implants only as a last resort because of
the risk of infection.
Among endovascular methods, intra-arterial thrombolysis is possible. This involves the injection of a
thrombolytic agent (usually alteplase) into the blood clot using a microcatheter inserted into the
artery. Systemic thrombolysis is not effective for limb occlusions. This procedure is possible in
patients with ischemia I and IIa (the usual time required for clot dissolution is 24-48 hours) and
needs judicious indication when the outflow tract distally to the occlusion is patent. The procedure
may be complicated by peripheral embolization of dissolved clots, which is subsequently difficult to
manage. An endovascular method that is adequate in speed to surgical revascularization is aspiration
or mechanical thrombectomy. Its use is limited mainly by the availability of equipment and
interventionalists outside working hours.
Reperfusion syndrome treatment should be considered a part of the management. Potassium levels
(dialysis may help) and myoglobin levels must be monitored. The only way to get myoglobin out of
circulation (and prevent kidney damage) is forced diuresis. The patient is given continuous
furosemide and infusions to achieve a urine production of about 250mL/hr.
10/ prevention
Prevention of embolism is provided by proper medical management of patients with a known source
of embolism. Prevention of thrombosis in patients with peripheral arterial disease is by medication
(antiplatelet therapy, statins). Treatment of patients with coagulation disorders is also prevention.
Prevention of traumatic ischemia is ensured by general injury prevention at all social, occupational,
and other levels.
Grade Prognosis Sensory
function
Motor
function
Doppler signal
– arterial
Doppler signal
– venous
I Viable limb + + + +
IIa Limb marginally threatened
– prompt treatment
+/- + +/- +
IIb Limb immediately threatened
– immediate treatment
- +/- - +
III Limb irreversibly damaged - - - Table
1. Acute Limb Ischemia Classification (adapted from Rutherford RB. Clinical Staging of
Acute Limb Ischemia as the Basis for Choice of Revascularization Method. 2009)
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TREATMENT OF VARICOSE VEINS (15)
Vaverka Vítězslav, Štefela Horváthová Erika
Varicose veins of the lower limbs represent a common condition, in which the superficial veins
(epifascial) become dilated, predominantly on the lower limbs. These veins, as part of the capacitive
bloodstream, are often visibly enlarged, twisted and protrude above the surface of the skin, often
with a blue-violet discoloration.
Etiology: the most common cause of varicose veins is an insufficiency of venous valves, which
under normal circumstances prevent blood from flowing backwards (reflux). If the valves do not
function properly, blood accumulates in the veins and causes their expansion. Other important causes
include pressure transfer from the deep venous system localised at so-called junctions and
hydrostatic pressure. The main risk factors are genetic disposition, prolonged standing, obesity,
pregnancy and hormonal changes. With increasing age and sedentary lifestyle, the risk of developing
varicose veins increases. The incidence increases with age, while in younger adults (20-30 years) the
incidence can be 5-10%, in people over 60 it can be up to 50% and more. Women are more prone to
developing varicose veins than men, the incidence in women is estimated at 25-33%, while in men it
is 10-20%. In developing countries, the incidence is generally lower.
Division of the venous systems of the lower limbs: proper understanding of the varicose veins
problematic requires knowledge of the venous systems of the lower limbs, which are divided into a
superficial system, a deep system and their connection (perforators), which are direct and indirect.
The superficial venous system is located just under the skin and drains about 10% of venous blood
from the lower extremities. The main veins are the great saphenous vein (vena saphena magna,
VSM), which originates at the medial ankle and runs along the inside of the leg to the groin, where it
flows through the saphenofemoral junction (SFJ) into the deep system. The small saphenous vein
(vena saphena parva, VSP) begins at the lateral ankle and continues along the back of the calf to the
region of the popliteal fossa, where it empties into the deep system via the saphenopopliteal junction
(SPJ). The deep venous system drains approximately 90% of the venous blood and includes veins
such as vena femoralis (the main vein of the thigh), vena poplitea (vein in the popliteal fossa), vena
tibilais anterior and posterior (veins of the lower leg) the vena peronea (vein running along the calf
bone). The connector veins (perforators) are veins that connect the superficial and deep venous
systems and ensure the one-way flow of blood from the superficial to the deep system. The most
known perforators are Dodd's (in the thigh), Boyd's (in the knee area) and Cockett's perforators (in
the lower leg).
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Classification of varicose veins: varicose veins are classified using the CEAP classification
(Clinical, Etiological, Anatomical, Pathophysiological). C0: no visible or palpable signs of venous
disease. C1: spider veins (telangiectasia) or reticular varicose veins. C2: true varicose veins. C3:
swelling of the lower extremities without skin changes. C4: skin changes caused by chronic venous
insufficiency (pigmentation, eczema, lipodermatosclerosis). C5: healed ulcer. C6: active venous
ulcer.
Varicose veins are further divided into primary and secondary: primary varicose veins arise
independently, without connection to another disease. They are most often caused by congenital
weakness of the vein wall or valves, while prolonged standing, pregnancy and obesity contribute to
their development. Secondary varicose veins are result of another condition, such as chronic venous
insufficiency or deep vein thrombosis. In these cases, the venous system is damaged, which leads to
the development of varicose veins. Morphologically, varices can be of different shapes and sizes.
Some are fine and thin (reticular), while others can be large, coarse, and prominent. Changes in the
vein wall include thinning of smooth muscle layer, loss of elasticity, and changes in connective
tissue.
Treatment: treatment of varicose veins can be conservative or invasive. Conservative treatment
includes wearing compression stockings to improve venous return and reduce swelling. Lifestyle
changes such as increased physical activity, weight reduction and avoidance of prolonged standing,
venotonics are also recommended. Invasive treatment includes various surgical and non-surgical
methods. A high-quality ultrasound examination and mapping of the pathology is very important.
Traditional surgical treatment, such as crossectomy of the saphenofemoral/-popliteal junction, or
possibly another source of reflux (perforator) and stripping (removal of the vein), is now often
beeing replaced by less invasive procedures such as laser and radiofrequency ablation or
sclerotization, in which the lumen of the affected veins is injected with a substance causing damage
to the endothelium and resulting in its closure.
Prevention: Varicose vein prevention is key, especially for those at increased risk. Regular exercise,
avoiding prolonged standing and sitting, wearing compression stockings and maintaining a healthy
weight are recommended. Maintaining an active lifestyle and weight control can make a significant
contribution to preventing and delaying the development of varicose veins, especially in people with
genetic predispositions.
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GOITRE, SURGERY OF THYROID GLAND (17)
Ivanecká Dominika, Linhartová Marcela
The thyroid gland is an endocrine gland. Thyroid cells produce the hormones triiodothyronine (T3),
tetraiodothyronine, i.e. thyroxine (T4) and calcitonin, produced by parafollicular cells. The diagnosis
of functional disorders is dealt with by the branch of internal medicine, endocrinology. Functional
disturbances caused by inflammation or neoplasia then lead to morphological changes in the thyroid
gland, especially its volume increase. The enlargement of the thyroid gland is called a goiter. The
indication of a patient for thyroid surgery is therefore dependent on close collaboration between the
endocrinologist and the surgeon. A fully examined patient is indicated for surgery by the
endocrinologist, the final procedure is then modified by the surgeon according to the perioperative
findings. The basic examination consists, in addition to the history and clinical examination, in the
determination of thyroid hormone levels and ultrasound examination. If the ultrasound shows the
presence of nodules or diffuse volumetric enlargement of the thyroid gland, further investigation is
indicated. For suspicious nodules, the endocrinologist performs a needle aspiration biopsy with the
aim of cytological examination of the collected sample. Cytological findings are then evaluated
according to the Bethesda classification, which establishes diagnostic categories, their risk of
malignancy and recommends algorithms for further therapeutic management. In the case of large
goiter extending retrosternally, the addition of a native CT scan of the chest is necessary. At the time
of surgery, the functional thyroid disorder must be medically compensated to normal (eufunction).
According to the size, there are 4 grades of goiter (Bavarian classification): 0: neither visible nor
palpable, enlargement is only demonstrated on ultrasound, I: palpable, visible only when the head is
tilted, II: visible enlargement, III: goiter oppressing the surrounding organs.
Depending on the cause of thyroid enlargement we distinguish goiter: 1. endemic - caused by iodine
deficiency in the diet, 2. thyrotoxic - caused by an autoimmune disease M. Basedow, 3. malignant caused
by tumor 4. inflammatory.
According to morphology, goiter is divided into diffuse (homogeneous parenchymatous
enlargement) and nodular.
Indications for thyroid surgery are:
Polynodous eufunctional goiter - caused by iodine deficiency in the diet. The earliest diffuse
enlargement gradually progresses to nodular remodeling. Initially asymptomatic, with increase in
volume oppression of surrounding structures occures, especially the trachea, manifested by
dyspnoea, hoarseness and swallowing disorders. If the enlarging thyroid gland propagates to the
mediastinum, we speak of retrosternal goiter.
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Functional disorders:
Hyperfunction:
Graves-Basedow disease is an autoimmune disease caused by the production of stimulatory
autoantibodies against TSH receptors, resulting in increased production of thyroid hormones and
volumetric enlargement of the gland. Typical symptoms of Merserburg's triad are: tachycardia, goiter
and exophthalmos. The mainstay of treatment is thyreostatics, in the case of tachycardia betablockers.
If conservative treatment is unsuccessful, thyroidectomy is indicated.
Toxic adenoma - a nodule of the thyroid gland, which produces hormones at an increased rate. It
does not manifest with exophthalmos, otherwise symptoms and treatment are similar to GravesBasedow
disease
Hypofunction: treated with hormone replacement, not an indication for surgical intervention
Inflammation:
Acute - bacterial or viral, surgical intervention only in case of abscess
Chronic
Hashimoto's goiter - an autoimmune disease caused by antibody production resulting in lymphocytic
infiltration of the gland, clinically manifested by hypofunction. Indicated for thyroidectomy only
when oppressed, represents a risk factor for carcinoma.
Riedl's goiter - fibrous transformation of the gland with signs of compression
Malignant goiter - Tumors of the thyroid gland:
Benign tumors - adenomas, may be eufunctional, manifesting as oppression, or may be toxic
adenomas, inducing a state of hyperthyroidism. Surgical treatment is indicated if they grow or
cytological examination shows cellular atypia.
Malignant tumours - 99% of malignant tumours are carcinomas
Differentiated carcinomas - have preserved iodine uptake capacity. This can be used in adjuvant
radioiodine therapy after total thyroidectomy. At the same time, suppressive thyroxine therapy is
administered postoperatively. Differentiated tumors have a good prognosis, with long-term survival
of 90% of patients.
Papillary carcinoma - typical of childhood and adulthood. Metastasizes to lymph nodes
Follicular carcinoma - is more common between the ages of 50-60, in women, invades the
surrounding area and blood vessels
Undifferentiated carcinomas - have no ability to uptake iodine, are aggressive, grow rapidly and
metastasize early. They have a poor prognosis.
Anaplastic carcinoma - occurs in older people, significantly poor prognosis
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Medullary carcinoma - a carcinoma of parafollicular cells (C cells) that produce calcitonin. As a
result of its elevated levels, bone tissue resorption and disturbances in calcium and phosphate
metabolism occur. It is typical of MEN 2A and MEN 2B multiple endocrine neoplasia syndrome
Surgical procedures on the thyroid gland
Correspond to the anatomical part of the gland that is removed. Complete removal of the thyroid
gland is called total thyroidectomy. For benign diagnoses, only one of the lobes can be removed, in
which case we speak of lobectomy (right-sided or left-sided), or only the isthmus can be removed
(isthmectomy). The surgical approach is provided by a collar incision 2 cm above the jugule (Kocher
incision). Current trends in minimally invasive surgery can also be applied in thyroid surgery by
video-assisted transoral endoscopic thyroidectomy (TOETVA).
Complications of surgical procedures on the thyroid gland are based on its anatomical localization.
The most feared complication is injury to the n. laryngeus recurens, which innervates the vocal cords
and is responsible for their proper mobility. In case of bilateral injury, the vocal cord ligaments
become paresed and remain in a relaxed position, obstructing airflow through the trachea and the
patient is unable to ventilate spontaneously (inspiratory stridor). The surgical technique is therefore
focused on a thorough investigation of this nerve, its visualization and verification by
neurostimulation.
Another dreaded complication is bleeding. The anatomical space of the neck is a constricted area
with many vital structures; therefore, even a small bleed will cause great compression of the
surrounding structures, especially the trachea. If a postoperative hematoma is suspected, immediate
dissolution of the wound at the patient's bedside is necessary to reduce the pressure in the cervical
compartment.
Hypoparathyroidism is a risk in case of manipulation of the parathyroid glands or their complete
removal in case of intraparenchymal placement.
Less common complications: lymphorea (in lymphadenectomy, especially left-sided), pneumothorax
(in large retrosternal stroma), wound complications (keloid).
Parathyroid glands
The parathyroid glands are endocrine organs producing parathyroid hormone. Usually four, they are
normally located on the posterior surface of the thyroid gland. Their localization is variable. It is not
unusual that one of the glands may be located in the upper mediastinum. Parathyroid hormone
regulates the levels of calcium and phosphorus in the blood. Its increased level is called
hyperparathyroidism, decreased hypoparathyroidism.
Hyperparathyroidism
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Primary - caused by an adenoma of the parathyroid gland. Manifestations are general, caused by
high levels of calcium in the blood. Typical symptoms include gastrointestinal discomfort,
arhythmia, nephrolithiasis, osteodystrophy, joint and muscle pain, psychological disorders. Therapy
is surgical, involving removal of the hyperfunctioning gland. Parathyroid carcinoma is a rare but
serious cause of primary hyperparathyroidism. It is a slow-growing tumor with infiltrative growth
into the thyroid gland, blood vessels, muscles, and esophagus.
Primary hyperthyroidism is often the first manifestation of multiple endocrine hyperplasia (MEN)
syndromes. These include 3 syndromes whose typical presentations are endocrine gland tumors.
These are autosomal dominant diseases. MEN 1 syndrome is characterized by parathyroid adenoma,
pancreatic neuroendocrine tumors such as insulinoma or gastrinoma, and pituitary adenomas. MEN
2A syndrome includes trias medullary thyroid carcinoma, parathyroid adenoma and
pheochromocytoma. MEN 2B syndrome includes trias medullary thyroid carcinoma,
pheochromocytoma and mucinous neuromas.
Secondary - high parathyroid hormone levels are due to feedback in low blood calcium levels, most
commonly in renal disease
Tertiary - autonomic parathyroid hyperplasia in dialysis patients
Hypoparathyroidism
Low parathyroid hormone levels lead to hypocalcemia and hypophosphatemia, primarily treated by
endocrinologists. However, it can be induced by the surgeon as a complication of thyroid surgery.
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GYNECOMASTIA, INFLAMMATORY DISORDERS OF THE BREASTS (16)
Berková Alena
Gynaecomastia
Definition: Abnormal enlargement of the breast in men due to hypertrophy of the gland or pathology
of the reproductive tissue. It can occur unilaterally but also bilaterally. Physiological gynecomastia is
seen in newborns, at puberty and in old age. Pseudogynecomastia is lipid deposition in obesity
(lipomastia) or may be caused by tumors (e.g. lipomas).
Etiology: In 50% of cases, it is idiopathic gynecomastia. It may also be hormonal or metabolic or
medically conditioned. Gynecomastia as a paraneoplastic manifestation is found in bronchial
carcinoma, Basedow's disease, myotonic dystrophy. Gynecomastia can be associated with abuse of
alcohol, cannabis, heroin, and anabolic steroids in athletes (bodybuilding).
Classification:
- Stage I - mild gynecomastia - no excess breast skin
- Stage II - moderate gynecomastia - mild excess breast skin
- Stage III - severe gynaecomastia - significant excess breast skin
Clinical findings: Manifested by concentric enlargement of breast tissue unilaterally/bilaterally, may
be associated with tenderness and galactorrhea may be present.
Diagnosis: The basic history and clinical examination is based on examination of both breasts and
both axillae, examination of the genitalia - testes, checking the type of pubic hair. Genetic
examination of the sexes. Laboratory determination of hormones - mainly levels of estrogen,
testosterone, prolactin, LH, alpha-fetoprotein (AFp), β - hCG, thyroid hormones and liver tests.
Sonography is needed to exclude cysts, nodules and tumours. To exclude tumors (pituitary, lung,
adrenal glands) perform CT or MRI. To exclude breast cancer, mammography, breast ultrasound +
core-cut biopsy, abdominal sonography/CT, X-ray/CT lung staging, multidisciplinary team is
needed.
Therapy: Gynecomastia in newborns, adolescents and the elderly is physiological and requires no
therapy.For pathological conditions, treatment may be:
1. Conservative: androgen replacement in cases of proven hypogonadism with testosterone
deficiency, in medicamentous origin it is advisable to change the medication.
2. Surgical: usually elective surgery (psychological or cosmetic reason). The types of procedures
vary according to the size of the excess skin. One can choose liposuction, open excision with or
without reduction of excess skin. The removed tissue must always be sent for histological
examination to exclude carcinoma.
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Differential diagnosis:
-fibromas, fibroadenomas, lipomas, retromammary angiomas
- male breast cancer (unilateral enlargement !histology required!)
- obesity (lipomastia) = pseudogynecomastia
Inflammations of the breast
Definition: Mastitis affects women exclusively in most cases. The predisposing age is between 20-
30 years and between 50-60 years. It is primarily caused by local transfer of infection most
commonly from injury to the mamilla. Inflammatory breast cancer, which may manifest similarly to
mastitis, should always be considered.
Pathophysiology of mastitis: The production of excessive amounts of keratin leads to the formation
of keratin plugs and obstruction of the ducts of the mammary gland. Infection with bacteria leads to
subareolar abscess formation and continued bacterial colonization. Further spread of inflammation to
the surrounding area is predominantly via the lymphatic route. Infection can also spread per
continuitatem most commonly from the injured mamilla, areola and breast skin. Here
Staphylococcus aureus is most commonly present, rarely Proteus, Bacteroides, E.Coli or mixed
infection, mycoses. Tuberculosis or parasites can also spread hematogenously, but these infections
are very rare.
Etiology of mastitis: From the etiological point of view, mastitis is classified into:
1. Puerperal mastitis - 70% of all mastitis. Infection is caused by ragades on the mamilla, further
aggravated by milk retention, lack of hygiene during breastfeeding, transmission of pathogens from
the nasopharynx of the newborn.
2. Non-peripheral mastitis - arises from injury to the breasts, nipples, for example, during nipple
piercing. Or in eczematous changes in the area of mamilla and areola. It can also occur in men.
Clinical picture: Mastitis manifests as a palpable, painful, firm infiltration of the skin and
subcutaneous tissue. Redness, heat of the affected skin is present. Swelling extending to the axillary
region and enlarged axillary nodes may be present. Of the general symptoms, subfebrile to febrile
and chills are typical. Periductal mastitis causes retraction and inversion of the nipple. In puerperal
mastitis, patients complain of painful breastfeeding.
Diagnosis of mastitis: History and clinical examination of both breasts and axillae is essential. In
addition, sonography of the breast, laboratory examination of the blood count, CRP, hormonal
examination - prolactin are performed. When pus is evacuated, microbiological examination is
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recommended to perform. In case of suspicion of a tumor, it is necessary to analyze the tumor
marker Ca 15-3, do mammography and core-cut biopsy of the lesion.
Therapies:
Thelitis
This is an isolated inflammation of the mamilla. Treatment is conservative, topical agents with an
antiseptic or antibiotic in the form of a solution or ointment are used.
Puerperal mastitis
As part of the treatment, it is therefore recommended to continue breastfeeding, which is safe.
Abrupt weaning of the baby is likely to worsen the course of the inflammation. As part of the general
therapy, it is recommended to administer anti-inflammatory drugs, antibiotics (most common
penicillin) for 7-10 days. Surgical therapy is indicated in case of abscess formation, see below.
Non-peripheral mastitis
Conservative therapy is based on the administration of anti-inflammatory drugs and antibiotics.
Antibiotics should cover anaerobic bacteria and gram-negative microbes (e.g. amoxicillin +
metronidazole combination). Surgical therapy is indicated if an abscess develops, see below. If a
fistula is present, extirpation with histological verification is recommended. In case of early
recurrence, resection of the retroareolar duct is recommended.
Complications of mastitis:
Subcutaneous (preglandular) abscess, intramammary (glandular) abscess, paramammary abscess,
retromammary abscess, subpectoral cellulitis, MONTGOMERY abscess - furuncle of Montgomery's
gland of the glandula areolaris, and last but not least, necrosis of the mammary gland.
Breast abscess
It can occur in lactational but also non-lactational mastitis. A pus-filled cavity develops in the
mammary gland.
Clinical picture: febrile, induction of skin and subcutaneous fluctuations. A yellowish purulent
secretion from the nipple may also be present.
Diagnosis: see above
Therapy: in small abscess cavities, aspiration of the contents with a needle can be performed,
preferably under ultrasound guidance. If the abscess cavity is larger and mature, incision and
drainage should be performed as part of acute treatment, preferably under short general anaesthesia.
If necrosis is present, the procedure is supplemented by necrectomy. If malignancy is suspected,
histology should be taken. Surgical therapy is always supplemented by general therapy, i.e.
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administration of anti-inflammatory drugs and antibiotics preferably according to bacteriological
culture.
Other less common mastitis
Tuberculous mastitis
It is very rare, the causative agent is Mycobacterium tuberculosis. This form of mastitis is
characterized by a stiff, bumpy induction with abscess formation and fistulation. It most often
originates from the pulmonary form of tuberculosis, spreading haematogenously or per continuitatem
from the affected ribs and soft tissues. The mainstay of therapy is antituberculous drugs and abscess
therapy as mentioned above.
Granulomatous mastitis
A rare unilateral, chronic, breast disease with the possibility of recurrence. Affects young women of
childbearing age (28-40 years). It arises from an autoimmune background. Diagnosis is by histology
from core-cut biopsy or surgical excision. Therapy is based on the administration of corticosteroids.
Surgical therapy is indicated only in case of abscess development.
Malignant tumours of the mammary gland associated with manifestations of infection
Outside of adenocarcinoma of the breast, the following can manifest as mastitis:
- inflamatory (inflammatory) carcinoma. It is manifested by enlargement of the breast, reddening of
the skin. Early metastasis.
- Paget's carcinoma is a rare subtype of ductal carcinoma, it grows around the nipple, resembling a
non-healing boil in the nipple area.
These forms are associated with numerous abscesses but only mild overall signs of inflammation.
Early biopsy and histological verification contribute to the diagnosis. Treatment is complex
oncological.
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BREAST TUMORS (24)
Coufal Oldřich, Krésová Pavlína, Gabrielová Lucie, Krsička Petr
Breast tumours can be classified as benign, malignant, or tumours of uncertain biological nature.
Benign tumours
The most common is fibroadenoma (FA). It occurs mainly in young women and may regress later
in life. It is usually a solitary unilateral lesion, but occasionally, it occurs as multiple lesions in one or
both breasts (fibroadenomatosis). Macroscopically, it is usually a smooth and oval lesion; however,
sometimes, it has a lobular shape. Tumours larger than 5 cm are called "giant fibroadenoma". On
clinical examination, FA manifests as a palpable lump, but it is sometimes an impalpable lesion,
which is diagnosed as an incidental finding on ultrasonography (US). A US-guided core-needle
biopsy (also called tru-cut or core-cut biopsy) is recommended in that case.
FAs usually do not require surgical resection if they are asymptomatic and have a stable size. The
question of the necessity of dispensary and repeated US examinations is debatable.
We consider surgery, especially in the case of more rapid growth (over 3 cm) or if tumours is
symptomatic, palpable and painful. Surgical treatment consists of extirpation, which usually does not
cause breast deformity. Surgery is performed in general anaesthesia.
Intraductal papilloma usually occur centrally in larger ducts and sometimes cause nipple discharge.
In these cases, breast ductography can show filling defects in the contrast-filled duct or ductal
dilatation, ductal irregularity, and abrupt cut-off. Most of the intraductal abnormalities on
ductography are identified as forms of filling defects. Extirpation (resection with a clear margin) is
recommended due to both possible symptoms and the possibility of cellular atypia or transition to
papillocarcinoma. Macroscopically, it tends to be soft and friable, and it is necessary to resect with a
margin of surrounding tissue. Ductal papillomatosis means multiple papillomas, usually of
microscopic dimensions in the central or peripheral ducts. It also slightly increases the risk of breast
cancer. However, if the process is not limited to a smaller area, the surgical solution would have to
consist of a total mastectomy, which may be considered too mutilating in this situation, so all that
remains is to monitor the patient more carefully. Other benign breast tumours (e.g. lipoma, etc.) are
uncommon.
Tumours of uncertain biological nature
Phyllodes tumours are similar to FA; they histologically consist of epithelial and stromal
components but have a higher cellularity. Based on histological characteristics (cellularity, atypia,
mitotic activity, nature of growth into the surrounding tissue), they can be divided into benign,
borderline and malignant forms. Histological diagnosis is challenging as it presents a morphologic
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continuum from benign to malignant tumour, and the nature of the tumour can sometimes only be
established from its biological behaviour over time. Compared to FA, they occur in middle-aged
women (over 35 years of age). Macroscopically, they tend to be rather pink to greyish, but they are
mainly characterised by rapid growth. In extreme cases, they can reach the size of a soccer ball
within weeks to months. This is also why rapidly growing FA should be surgically resected, as it
could also be FN. Differentiation based only on clinical examination is impossible, and core-cut
biopsy must always be performed. Surgical treatment consists of resection, ideally with a resection
margin of 10 mm. However, this is not always possible, and it is challenging to achieve. Large
tumours can only be treated with a total mastectomy, even if the tumour is benign. The dispensary is
required after surgery, as malignant forms (also called cystosarcoma phyllodes) may return in the
form of either local recurrence or rarely distant metastases, thus clinically resembling sarcomas. On
the other hand, the behaviour of benign variants may not be very different from FA, so even
unjustified extensive surgical radicality may not always be appropriate. Fortunately, FNs are
relatively rare, accounting for less than 1% of all breast tumours.
Malignant tumours
The most common and clinically important malignant tumour of the breast is breast cancer, and it is
the most common malignancy in women, apart from skin tumours. The lifetime risk for a woman in
the general population is reported to be in the range of 6-10%. Since 2002, a screening program has
also been introduced in the Czech Republic consisting of mammography (MG) assessment of
asymptomatic women from the age of 45 in two-year intervals. The majority of cancers develop as
sporadic cancers; however, some cancers occur due to hereditary genetic predisposition, which can
be diagnosed by genetic testing. The most well-known are mutations in the BRCA1 and BRCA2
genes. A positive family history or the occurrence of cancer at a young age will draw attention to the
possibility of a predisposition. In women diagnosed with those mutations, bilateral prophylactic
mastectomy can be considered.
Approximately half of the cancers in our population are screen-detected; the others are
symptomatic, manifested by clinical symptoms, most often palpable painless breast lump. Less
often, it is diagnosed based on skin or nipple changes, skin retraction or infiltration, deformity or
stiffness of the breast. Rarely, the first symptom of breast cancer is a painless enlarged palpable
axillary node.
The most aggressive form of breast cancer is inflammatory carcinoma (stage T4d), associated with
redness and lymphoedema of the skin, which can imitate orange peel (peau d'orange). This can
affect a larger part of the breast or even the entire breast, which may look similar to inflammation
disease.
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Breast cancer diagnosis is based on two pillars:
1 Histological verification – US-guided core-cut biopsy, less often stereotactic biopsy on
mammogram or MRI. A larger amount of tissue can be removed with a vacuum biopsy (VAB) in
case of diagnostic discrepancy. When pathologists report the biopsy findings, they include these
features: the histological type of the tumour (e.g. invasive ductal, lobular, or other subtypes of breast
cancer), tumour grading, expression of oestrogen and progesterone receptors (steroid receptors),
HER2-neu expression and proliferation index (Ki67 index), which together form the tumour
"phenotype".
2 Assessment of the extent of the disease - in the local-regional site (breast + axillary nodes)
and distant organs (most frequently bones, lung, liver, GI tract, or brain). This is described using the
TNM classification. The assessment consists of bilateral MG in two basic projections - a
mediolateral oblique (MLO) view and a craniocaudal (CC) view - and bilateral US of breast and
axilla. In some cases, we also request magnetic resonance imaging (MRI), which has high sensitivity
but low specificity, so it often leads to additional biopsies, frequently reported as "false positives".
MRI is recommended, especially for invasive lobular cancer (ILC), which is characterised by
infiltrative growth that increases the risk of multicentric contralateral disease. Consequently, the
estimation of the extent of the disease in ILC using basic methods (US and MG) is often
underestimated and requires MRI. The staging assessment should be detailed based on the tumour
stage (How detailed the staging assessment should be based on the tumour stage) and the availability
of a particular imaging method. The minimum for staging of early breast cancer is a Chest X-ray and
US of the liver. Compared to bone scans, CT chest, abdomen and pelvis or even PET/CT scans in
advanced disease. Additionally, in early breast cancer, the finding of synchronous distant metastases
at the diagnosis is fortunately rare.
The treatment strategy is based on the phenotype and extent of the disease. For the reason that breast
cancer is considered a systemic disease, treatment is always multimodal, a combination of surgery,
systemic treatment, and radiotherapy.
Primary surgery is mainly applied in the phase of the absence of signs of distant metastases in
localised disease. Timing of surgery can be either primary - systemic treatment and radiotherapy
follows surgery), or surgery follows neoadjuvant (systemic) chemotherapy (NACT). In cases where
its administration can improve the conditions for surgery, NACT is used. NACT is frequently
recommended in patients with more aggressive phenotypes ("triple-negative" and "HER-positive",
high grade, high Ki67), large tumours or involved axillary nodes. Treatment should never be
decided by the surgeon alone but in collaboration with collaborating specialities in a
multidisciplinary team (MDT), also called a "breast committee."
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The surgery itself then consists of resection of the breast tumour and the lymph node removal. The
goal is to resect the primary tumour with a negative resection margin, which can be achieved through
partial mastectomy (also called wide local excision) for smaller solitary or multifocal lesions, while
for larger or multicentric tumours, the entire breast must be removed (total mastectomy). The
decision on the scope of the operation cannot be standardised; it is individual, often difficult, and
based on the competence of the surgeon and the patients should agree. Modern breast surgery
incorporates oncoplastic techniques, enabling the removal of larger tumours while minimizing
cosmetic deformity.
A prerequisite for partial mastectomy in uncertainly palpable tumours is the use of one of the
intraoperative localisation techniques, e.g. iodine or magnetic seeds. Partial mastectomy must always
be supplemented with adjuvant radiotherapy (RT), while after total mastectomy, RT is only indicated
for more locally advanced tumours. Surgery on the lymph nodes aims to determine the level of their
involvement by histological examination. The therapeutic effect of lymphadenectomy is not as
noticeable as it was assumed in the past, and a clear trend is the reduction of surgical radicality in
the axilla. The traditional Axillary Lymph Node Dissection (ALND), burdened with the risk of
iatrogenic secondary lymphedema, can now be avoided in most women. Conservative procedures
such as Sentinel Lymph Node Biopsy (SLNB) and, in recent years, the Targeted Axillary Dissection
(TAD), consisting of removing the most prominent initially pathological node if it regressed during
adjuvant chemotherapy, dominate. Here, too, the use of localisation techniques is necessary.
Surgery is usually followed by adjuvant treatment, systemic or RT, depending on the phenotype and
stage of the tumour.
After a total mastectomy, suitable candidates can consider breast reconstruction, either immediate
(immediately at the time of the mastectomy) or delayed. A breast substitute can be created using
your own tissue (typically an abdominal flap) or using foreign material (mammary implant). It is
always a demanding one-stage or multi-stage operation burdened with the risk of complications, so
not all patients are suitable candidates. Also, the availability of breast reconstruction in the Czech
Republic is generally lower than most patients would like.
Ductal carcinoma in situ (DCIS) is worth mentioning, often asymptomatic and presenting on MG
with the image of "microcalcifications". Histopathologically, it is preceded by atypical ductal
hyperplasia (ADH), which can thus be described as a typical "precancer". DCIS is considered a
direct precursor to invasive carcinoma and requires surgical treatment. If invasion is not
demonstrated even during the histological examination of the surgical resection, no adjuvant
treatment is often necessary. On the other hand, lobular carcinoma in situ (LCIS) is more of an
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indicator of an increased risk of invasive cancer in the future (anywhere in the breast), so a surgical
approach is not so clearly defined.
Other malignant breast tumours are rare. In addition to the already described malignant variant of
FN, it is worth mentioning an extremely rare but even more aggressive (secondary) angiosarcoma
arising as a late side effect of adjuvant radiotherapy, which develops many years after treatment.
Primary breast sarcomas, or metastases of other malignancies (e.g. melanoma) to the breast, are rare.
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THORACIC OUTLET SYNDROM, NERVE COMPRESSION SYNDROMES OF ARM AND FOREARM (21)
Topolčaniová Lenka, Váňa Vladimír, Ferkodičová Iveta, Holoubek Jakub
Introduction
Entrapment syndromes are conditions characterized by localized damage to peripheral nerves caused
by compression at anatomically defined narrow and rigid passageways. This compressive neuropathy
typically occurs in areas where nerves pass through bony, muscular, or fibrous structures. The most
common entrapment syndromes include carpal tunnel syndrome (CTS) and cubital tunnel syndrome,
while less frequent ones are Guyon’s canal syndrome, anterior interosseous nerve syndrome,
pronator syndrome, supinator syndrome, and thoracic outlet syndrome (TOS).
The etiology of entrapment syndromes is multifactorial. It can be caused by anatomical factors, such
as congenital anomalies or abnormal structures. Inflammatory conditions, such as rheumatoid
arthritis and tenosynovitis, can lead to swelling of the surrounding tissues and subsequent nerve
compression. Other causes include metabolic disorders, such as diabetes, postoperative states,
trauma, tumors, iatrogenic damage during medical procedures, and various external factors, such as
repetitive pressure or overuse. In some patients, the exact cause cannot be determined, and the
condition is classified as idiopathic. Pathophysiologically, nerve compression leads to damage to the
myelin sheath, axons, and disruption of the nerve's blood supply (vasa nervorum). This results in
demyelination and, in more severe cases, axonal injury.
The clinical manifestations of these syndromes include pain, often localized at the site of
compression, which may radiate to the area innervated by the affected nerve. Patients frequently
report sensory disturbances such as paresthesia (tingling or numbness) and hypesthesia (reduced
sensitivity). Night pain is also characteristic and can wake the patient from sleep. As the condition
progresses, motor disturbances occur, leading to muscle weakness in the muscles innervated by the
affected nerve. Symptoms often worsen after physical exertion or repeated strain on the affected
area.
Carpal Tunnel Syndrome (CTS)
CTS is caused by compression of the median nerve in the area of the so-called carpal tunnel beneath
the transverse carpal ligament. CTS is the most common peripheral neuropathy, accounting for up to
90% of all entrapment syndromes of the upper extremity. It is more frequently seen in women and in
individuals engaged in manual labor. The syndrome manifests as pain in the wrist area, paresthesia in
the sensory innervation area of the median nerve (affecting the thumb, index, middle, and half of the
ring finger), deterioration of fine motor skills, and in advanced stages, atrophy of the thenar muscles
and limitation of thumb opposition. Paresthesia and pain often awaken the patient at night in the later
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stages. Diagnosis involves taking a thorough history and conducting provocative tests, such as
Tinel's sign (tapping on the site of compression leads to paresthesia in the fingers) and Phalen's test
(flexing the wrist for 60 seconds leads to paresthesia). Additionally, electromyographic (EMG)
testing is necessary during the diagnostic phase; a positive result indicates the need for surgical
intervention. Treatment for mild cases can be conservative (nighttime static splinting, vitamin B
supplementation, corticosteroid injections), but in most cases, open or endoscopic surgical solutions
are required, which involve cutting the transverse carpal ligament under local anesthesia. During the
surgical procedure, the ligament cutting is often supplemented by epineurotomy and release of the
fascicles of the median nerve. Rehabilitation begins on the fifth postoperative day.
Cubital Tunnel Syndrome
Compression of the ulnar nerve behind the medial epicondyle of the humerus, leads to cubital tunnel
syndrome. It is the second most common entrapment syndrome, accounting for up to 9% of all upper
extremity entrapment syndromes, with men being affected more frequently. Typical symptoms
include paresthesia or hypesthesia and motor disturbances in the area innervated by the ulnar nerve,
along with atrophy of the hypothenar muscles. In advanced cases, muscle atrophy may occur in the
interosseous muscles and the adductor pollicis, resulting in a claw-like deformity of the hand.
Diagnosis is based on clinical symptoms, a positive Tinel's sign, and EMG examination. Mild cases
can be managed conservatively with lifestyle modifications or steroid injections. In severe cases,
surgical decompression of the ulnar nerve is necessary, involving cutting the Osborn ligament, or
anterior transposition of the nerve. Endoscopic in situ neurolysis has shown the best results and is the
recommended approach.
Ulnar Tunnel Syndrome
In ulnar tunnel syndrome, the nerve is compressed in Guyon's canal between the pisiform and
hamate bones, beneath the ulnar part of the flexor retinaculum, above the transverse ligament. Due to
the branching of the nerve within the canal, the clinical symptoms depend on whether the trunk is
compressed before branching or only one of the branches. This may manifest as a motor deficit in the
hypothenar region and the adductor pollicis muscle or as a sensory deficit in the palmar innervation
area of the nerve; when the trunk is compressed, a combination of both symptoms can occur. Unlike
cubital tunnel syndrome, there is never a sensory deficit in the ulnar nerve innervation area on the
dorsum of the hand. Diagnosis involves EMG, and possibly ultrasound (US) and magnetic resonance
imaging (MRI). Treatment typically involves surgical decompression of the nerve in combination
with epineurotomy.
Pronator syndrom
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In cases of compression of the median nerve in the proximal forearm between the two heads of the
pronator teres, a very rare condition known as pronator syndrome can occur. This syndrome is
characterized by pain on the volar side of the forearm and paresthesia in the innervation area of the
median nerve. Depending on the location of the branch for the pronator teres, there may be weakness
and pain during resisted pronation. The compression is primarily due to hypertrophy of the muscle
from professional overuse, leading to nerve compression (long-term pronation and finger flexion).
Diagnosis includes a clinical examination to identify painful pronation against resistance or palpation
over the pronator teres muscle. EMG can confirm our hypothesis and determine the extent of nerve
involvement. Treatment typically consists of conservative measures, such as limiting the strain on
the forearm and applying anti-inflammatory medications; in rare cases, surgical intervention for
decompression may be necessary.
Anterior Interosseous Nerve Syndrome (AINS)
AINS is a very rare isolated involvement of the motor branch of the median nerve. This branch
innervates the flexor pollicis longus (FPL), flexor digitorum profundus (FDP) for the second and
third fingers, and the pronator quadratus (PQ). Clinically, it presents with pain and paresis of the
affected muscles without sensory symptoms, which distinguishes AINS from other entrapment
syndromes. The patient is unable to pinch the tips of the thumb and index finger together to form an
"O" shape, which is a key diagnostic sign known as the "pinch sign." Instead, during attempts to
perform this movement, a flat grip is formed. Diagnosis is made clinically, and EMG confirms the
diagnosis. Treatment is primarily conservative, involving lifestyle modifications and antiinflammatory
medications. Surgical treatment consists of nerve decompression.
Thoracic Outlet Syndrome (TOS)
TOS refers to a group of disorders caused by the compression of blood vessels (subclavian
artery/vein, axillary artery/vein) or the brachial plexus in the area of the upper thoracic aperture.
Anatomical structures in this region, such as the scalene muscles, clavicle, first rib, cervical rib,
subclavius muscle, pectoralis minor muscle, and others, contribute to this condition. Thoracic outlet
syndrome (TOS) can be classified into neurogenic (95%), arterial (3-5%), or venous (2%) types. The
syndrome presents with weakness, pain, thermoregulatory disturbances, and paresthesia throughout
the entire upper limb, with worsening symptoms when the limb is elevated above shoulder level. In
cases of vascular compression, symptoms may include claudication, cyanosis, and swelling of the
limb. Diagnosis involves clinical examination using maneuvers such as Adson's, Kelley's, or
hyperabduction (Wright's) maneuver. Imaging methods such as CT scans, angiography, and
ultrasound are also utilized. Treatment is primarily conservative, involving posture correction,
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lifestyle modifications, and physical therapy. If conservative measures fail, surgical decompression is
indicated, most commonly through complete resection of the first rib via an axillary approach.
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ACUTE MEDIASTINITIS (18)
Peštál Adam
Nosology a)
Concept - Acute mediastinitis is a severe purulent inflammatory involvement of the mediastinal
space
Etiology - the infection arises from the spread of purulent inflammation from the head, neck or
transfer of infection from the organs of the mediastinum, primarily the esophagus and airways in
association with perforating involvement. A less frequent cause is the occurrence of infection in
connection with direct injury to the mediastinum - penetrating injuries (stab wounds, gunshot
wounds,...). A specific etiology is infection associated with sternotomy after cardiac surgery.
Pathogenesis - along the deep cervical fascia, spine, esophagus and trachea, the infection spreads
through the mediastinum. Given the anatomical conditions, the organism does not have the ability to
prevent the spread of infection in the mediastinal space and contain the infection. The mediastinal
pleura is a certain anatomical barrier, but this is subject to early necrosis. The mediastinal pleura
prevents the spread of infection only initially, when it limits the spread to the pleural spaces, but
minimally prevents the spread of infection in the craniocaudal direction. Despite the macroscopically
intact mediastinal pleura, secondary empyema collections soon arise in the pleural cavities. Acute
mediastinitis is usually accompanied by pneumonia. The infectious microbiological agents are
varied, and culture examination is necessary, including examination for anaerobes. However, it is
always necessary to initiate intensive broad-spectrum antiobiotic therapy immediately at the
beginning of treatment.
Nosology b)
Clinical symptoms: the development of acute mediastinitis is often rapid. From "full health" the
patient goes into progressive severe septic shock. High fever, tachycardia, hypotension, dyspnoea,
dysphagia, neck pain, headache, chest tightness, anxiety and respiratory failure are the main clinical
manifestations of the disease. In case of perforation of the oesophagus, airway, or gas formation in
the context of ongoing infection, subcutaneous emphysema may be palpated. This may not always be
expressed, but together with skin redness and oedema is a prognostically important factor.
Laboratory tests: to diagnose and monitor the course of treatment, we determine serum levels of
CRP, lactate, procalcitonin, examine KO and specific indicators of MODS - Astrup's test, U,
creatinine, JT, coagulation parameters, CB, prealbumin...
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Imaging methods: the most beneficial is the CT scan, this is performed in both native and contrast
imaging. Contrast agent is administered both parenterally and per os to exclude or confirm
oesophageal perforation. In the case of an intubated patient, an aqueous iodine solution is injected
via a probe behind the sphincter of Kilian. According to CT findings, fibroscopic examination of the
oesophagus or airways is indicated.
Treatment: it is always combined, it is surgical, antibiotic and sepsis treatment in ICU or ARO. The
principle of surgical therapy is the basic rule of surgical treatment of infection, i.e. "ubi pus ibi
evacua". It is therefore the opening and sanitation of the mediastinal space. According to the extent
of the inflammation and its etiology, determined on the basis of CT, from the cervical or pleural
space, combined approaches are common. The cervical approach is the jugular incision in the
jugulus, in the case of ENT etiology of inflammation extended also by bilateral approach along the
clavicles. In collaboration with ENT, rehabilitation of these foci is necessary, and it is not
infrequently necessary to establish a tracheostomy. The intrathoracic approach is VATS or
thoracotomy. The principle of surgical treatment in the pleural cavity is longitudinal intersection of
the mediastinal pleura from the tip to the diaphragm with evacuation of purulent secretions, purulent
masses and necrotic tissue of the mediastinum, with introduction of a lavage drainage system into the
mediastinal space. In a minority of cases, if the mediastinitis is confined to the upper mediastinum,
then revision of the caudal portion of the mediastinum is not necessary. Very often it is also
necessary to resuscitate the accompanying empyema in the pleural cavities. Repeated dressings
under general anesthesia, both in the ENT area with necrectomy and repeated revisions of the
mediastinal space in the subsequent period by transthoracic route are common practice. Lavage
drains, Penrose drains or modern treatment methods in the sense of NPWT are essential. Regular
follow-up of the local findings with CT scanning is necessary. In case of persistent purulent foci,
surgical revisions and targeted drainage are indicated. In case of perforating etiology of mediastinitis,
suturing of the esophagus, trachea or bronchus can be considered in the initial phase. Tissue viability
and anatomical location should be assessed. Another solution is to bridge the perforation with a stent.
In case of oesophageal perforation, endosponge with active suction is also possible. In the case of
extensive necrosis of the oesophagus, resection and blinding or complete extirpation is necessary.
For the future, the patient is referred to enteral nutrition, which is most often applied through a
nutritive jejunostomy. In a certain percentage of cases, esophageal replacement may be attempted
with the passage of time, usually several months. Early recognition of the emerging acute
mediastinitis and its urgent active intensive treatment has a higher probability of treatment success as
well as a reduction in the number and severity of late complications.
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Nosology c)
Complications - early complications of acute mediastinitis are presented by all manifestations of
advanced sepsis, i.e. MODS, ARDS, DIC,... which often lead to death. In the case of advanced
fulminant mediastinitis, mortality is reported to be more than 50%. Late complications include those
associated with subsequent scarring of the mediastinum, e.g. mediastinal fibrosis with dysphagic
manifestations. Dyspnoeic problems are possible, also in connection with tracheal stenosis after
tracheostomy. Complications may also arise in connection with artificial nutrition or the condition
after pneumonia.
Prevention - sufficient attention when eating and drinking, proper chewing of food (swallowing
bones, solid morsels), prevention of accidental ingestion of acid or lye, it is desirable to avoid the
risk of swallowing foreign bodies. Prevention also includes dental care with emphasis on possible
complications associated with the VIIIth tooth, as well as treatment of tonsillitis and other infections
in the ENT area. Specific prevention includes adequate sparing of instrumentation such as OT
intubation and flexible and rigid examination of the esophagus and airway.
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MEDIASTINAL TUMORS, SUPERIOR VENA CAVA SYNDROM (19)
Tomáš Ledvina, Jan Ledvina, Teodor Horváth
Mediastinal neoplasms represent miscelaneous group of diseases with manifold symptomatology
corelating with their site in the – anterosuperior, medial or posterior compartments – and with the
biological character of the illness. They include benign and malignant findings too, both primary or
metastatic.
I
In the anterosuperior compartment occur
A Thymic lesions
1/ Thymic lymphoid hyperplasia usually causing the enlargement of the gland is related to
myasthenia gravis. 2/ Thymomas – the tumours created with epithelial cells of thymus are infiltrated
with various amount of reactive lymphocytes. 3/ Thymolipomas are rare soft and pliant tumours.
They do not affect adjoining structures, therefore they grow up to considerable size. 4/Thymic cysts
are commonly asymptomatic. They are quite often of no consequence. But as thymic cyst can be
present as e.g. Hodgkin lymphoma. 5/ Thymic carcinoid can be asymptomatic or may cause
symptoms because of compression of adjanced tissues. They are malignant and benign forms. They
can be a part of multiple endocrine neoplasia (MEN) 6/ Germ cells neoplasms (GCN). The males
tend to develop malignant GCN, while in females these tumours tend to be benign.
B Mediastinal goiter is in most cases benign. Quite large thyroid gland enlargement causes
dyspnea, hoarseness, dysphagia and/or superior vena cava syndrome.
C The lymphadenopathy in the anterosuperior mediastinum is most often caused by
lymphoma or metastatic adenopathy.
D There are sporadically to be found miscellaneous tumours – benign: ectopic parathyroid
gland adenoma, cystic hygroma, hemangioma, lipoma,, further rare neuroendocrine paraganglioma
and out of malignancies liposarcoma.
II
In the middle part of the mediastinum
arise 1/ enlargement lymphadenopathy based on sarcoidosis, lymphoma, metastatic lung or other
carcinomas or Casstleman disease 2/ primary tumours of the trachea, 3/ bronchogenic cysts localised
frequently in the region of main carina, commonly with mucous content. They communicate with
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central airways rarely 4/ Mesothelial pericardial cysts. Both last-mentioned are suitable for fineneedle
CT guided aspiration, diagnostic and/or therapeutic.
III
The posterior compartment
can contain 1/ neurogenic tumours of peripheral nerves – neurofibroma; neurilemmoma (benign
Schwannoma); neurogenic sarcoma (malignant Schwannoma); They usually arise of intercostal
nerves, seldom of phrenic or vagal nerve. Their expansion into intervertebral foramina threat of
perinterventional injury of spinal nerves. 2/ Gastroenteric (Duplication) cysts can be lined by
nonkeratizing squamous, cilliated collumnar, gastric, or small intestinal epithelium. Communication
with upper GIT is uncommon. 3/ Paravertebral masses are the demonstration of primary or
metastatic tumours of vertebrae, or these can be simulated under the cover of spondylodiscitis.
The role of surgery is important for diagnosis and treatment in this space.
There are used these approaches:
1/ Cervical mediastinoscopy – The entrance to anterosuperior mediastinum represents jugular
incission for diagnosis and treatment of enlarged lymphatics Recent options a) videoassisted
mediastinoscopy b) extended cervical (video)mediastinoscopy access subaortic space c) open
transcervical procedure for extended mediastinal lymphadenectomy.
2/ The parasternal mediastinotomy through the parasternal bed of second or third rib, or their
intercostal spaces both left and right sides, for the purpose of surgical biopsy of the retrosternal mass.
3/ The subxiphoidal access represents way to get to overwhelming majority of the spaces of anterior
mediastinum. Using this way enables the formation of pericardial window into the peritoneal cavity.
4/ Thoracoscopic right- or left-hand sided according to the location of the tumours of posterior
mediastinum or for the formation of pericardial window opened to interpleural space for prevention
of cardiac tamponade in patients with malignancies metastasizing into pericardium.
5/ Through median sternotomy or its partial modifications to the structures of the anterior or
through lateral thoracotomy to the pathology of middle and /or posterior mediastinum.
Superior vena cava syndrome (VCS)
The term evaluating consequences of the compression or infiltration of superior vena cava. VCS is
caused by lung cancer, metastatic lymphadenopathy, lymphoma, rarely by sarcoma. Other causes are
represented by retrosternal goiter, mediastinitis, aneurysm of the thoracic aorta, or postradiation
changes. They give rise to increasing of blood pressure (take care of hemoptysis) and decreasing of
venous return to the right atrium. Slow down of venous return participates onto edema of soft tissues
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of head and neck and causes phlebothrombosis of superior vena cava. They are formed venous
collaterals caused the decompression. Surgical intervention on the congestive region, even though
diagnostic, is usually at high risk or contraindicated. Causal treatment is aimed onto the illness and
diseased region. Supportive or palliative therapy ameliorates the difficulties and swelling using
diuretics, corticotherapy, analgetics / NSAIDs, oxygen, and in advanced cases anodyne.
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PULMONARY ABSCESS, EMPYEMA (22)
Prudius Vadim
Empyema of the chest refers to the accumulation of infected fluid in the pleural cavity, most
commonly pus. It remains a serious condition worldwide, with a reported mortality rate of 4-10%,
with a median of about 8%. In centers specializing in thoracic surgery, mortality is around 4%.
Causes of Empyema:
- Pneumonia and parapneumonic effusions
- Pleural effusion (usually due to repeated punctures of chronic effusions)
- Mediastinitis, esophageal injury
- Iatrogenic causes (previous thoracic surgeries)
Clinical Symptoms of Empyema:
- Shortness of breath
- Dry, irritating cough
- Fever (CAVE: patients receiving pneumonia treatment may have minimal symptoms)
- Chest pain during breathing
- Loss of appetite
- Clinical signs of sepsis
Patient Examination:
- Medical history: usually linked to a previous pneumonia, chronic pleural effusion, thoracic surgery,
or trauma (including hemothorax)
- Pharmacological history: prolonged antibiotic use can lead to an oligosymptomatic or latent course
until stage 3
- Auscultation: weakened breathing on the affected side
- Chest X-ray
- Laboratory tests: CBC, CRP, lactate, urea, creatinine, electrolytes, coagulation; IL-6 in septic cases
- Ultrasound (mandatory for empyema, as septated effusions may not be visible on CT)
- Chest CT for stage II-III empyema
- MRI (rarely used, for suspected fistulas into adjacent organs, spinal cord involvement, etc.)
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Stages of the Disease:
1. Stage I (exudative, acute):** Thin pleural effusion with low cellular content develops. Duration:
1-2 weeks.
2. Stage II (fibropurulent, transitional):** The effusion thickens, containing many
polymorphonuclear cells. Fibrin deposits form a membrane encasing the effusion. Duration: from the
2nd-3rd week to the 5th-6th week of the disease.
3. Stage III (organizing, chronic):** Capillaries and fibroblasts grow into the empyema cavity. The
pleural effusion is thick and contains up to 75% sediment. Occurs 4-6 weeks after the disease onset.
The condition of a trapped lung gradually develops.
Treatment:
- Stage I:** Drainage with a large-bore drain (Ch 24-32, preferred Ch 28). Targeted antibiotic
therapy and symptomatic treatment.
- Stage II:** VATS (video-assisted thoracoscopic surgery) debridement, evacuation of empyema
masses, and intraoperative lavage of the pleural cavity. Targeted antibiotic therapy.
- Stage III:** VATS revision, pleural cavity debridement, decortication. If decortication cannot be
performed technically, conversion is done. Postoperative lavage of the pleural cavity (preferably with
a 3% betadine solution or Prontosan). A primary goal of surgery is complete re-expansion of the lung
parenchyma.
Surgical Approaches:
- VATS: Multi-portal, bi-portal. Although the uniportal procedure is possible, its benefits are
unclear.
- Thoracotomy: Dorso-lateral or anterolateral approach.
Currently, the preferred initial procedure is a VATS revision. For stage III empyema, conversion to
thoracotomy is not uncommon to complete decortication or manage intraoperative complications. In
cases where empyema is combined with other conditions such as bronchopleural fistula, phlegmon,
or necrotizing fasciitis of the chest wall or lung necrosis, a primary thoracotomy revision is
preferred.
Alternative options: Robotic-assisted thoracic surgery (RATS) allows chest debridement and
decortication. However, experiences are still limited globally, including in the Czech Republic, and
the benefits over VATS have not been proven yet.
Postoperative Management:
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- Monitoring in the ICU for at least 12 hours postoperatively
- Antibiotic therapy according to sensitivity
- Pleural cavity lavage with 3% betadine solution at a rate of 8-10 ml/h
- Flutter valve and rehabilitation
- Chest X-ray
- Follow-up chest ultrasound 48-96 hours postoperatively
- Follow-up chest CT 2-4 weeks postoperatively
Postoperative Complications:
- Incomplete lung re-expansion: A risk factor for empyema recurrence.
- Prolonged postoperative air leak: Managed by attaching a Heimlich valve to the chest drain. If
unsuccessful, a chest revision, usually via thoracotomy, may be required.
- Relapse of empyema: Small collections can be managed with CT-guided drainage, while full
relapse necessitates VATS/thoracotomy revision.
- Postoperative bleeding and hemothorax: Commonly occur after decortication, often requiring
revision and lavage of the affected hemithorax.
- Lung necrosis, thoracostomy, and similar complications are rare today.
• Lung Abscess:
A lung abscess is a pathological cavity in the lung parenchyma, surrounded by a pyogenic membrane
and filled with pus (infected secretions). It may communicate with the bronchus. It typically
develops from necrosis of lung tissue due to severe infectious inflammation. Lung abscesses are
relatively rare in the Czech Republic today.
• Causes of Lung Abscess:
- Complicated pneumonia (especially in immunocompromised patients)
- Aspiration pneumonia (including aspiration during anesthesia induction)
- Advanced lung tumors (central necrosis and tumor breakdown)
- Septic pulmonary embolism
- Pulmonary infarction
Clinical Symptoms of Lung Abscess:
- Shortness of breath
- Cough with sputum production
- Fever or high fever
- If the abscess ruptures into the bronchus, massive expectoration of purulent sputum can occur
within hours or days, often providing temporary relief.
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- Chest pain (usually when the infection spreads beyond the focus)
- Loss of appetite, nausea
Patient Examination:
- Medical history (previous surgeries, ENT area diseases)
- Auscultation: Weakened breathing on the affected side in larger abscesses
- Chest X-ray
- Blood tests: CBC, CRP, lactate, urea, creatinine, electrolytes, coagulation. Sputum culture for
microbiological and cytological examination.
- Bronchoscopy
- Chest CT
Treatment:
- CT-guided drainage for smaller peripheral abscesses.
- Surgical revision and lung resection: For small abscesses, an atypical lung resection may be
performed. For larger or centrally located abscesses, lobectomy is preferred, usually performed via
thoracotomy. For smaller abscesses under 5 cm, VATS resection may be considered.
- Targeted antibiotic therapy
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LUNG CANCER AND MESOTHELIOMA (23)
Pospíšil Jan
Lung tumors are the most frequently occurring tumor of the respiratory system. Histologically,
bronchogenic carcinoma predominates. It is the most common tumor in men over 40 years of age
and the maximum incidence is between 55 and 65 years. It is also very common in women and ranks
3rd in incidence among them. Bronchogenic carcinoma ranks second overall among all malignant
tumors and accounts for about 1/3 of all deaths from malignant oncological diseases.
Classification
Benign lung tumors
Primary lung tumors
The primary lung tumor is bronchogenic carcinoma, which can be divided according to histological
classification into - non-small cell (squamous cell carcinoma, adenocarcinoma, large cell
carcinoma), small cell and lung carcinoid
Secondary lung tumors
These are metastases of other tumors to the lungs
Etiology
The influences that cause bronchogenic carcinoma can be divided into endogenous and exogenous.
Endogenous influences are, for example, increased activity of cytochrome P450 (increased, for
example, in smokers) or mutation of the P53 gene. The most significant exogenous influence is
smoking. 90% of lung cancer occurs in smokers. Passive smoking also poses an increased risk. Other
exogenous influences are e.g. increased exposure to radon, asbestos, inorganic compounds of
arsenic, sulphur, chromium, nickel or PVC compounds and ionizing radiation.
Symptomatology
Symptomatology can be of different types
Intrathoracic - Cough (initially dry, irritating, then may be productive), hemoptysis, stridor (with
narrowing of major airways), bronchopneumonia (with bronchus obstruction), superior vena cava
syndrome (as a result of pressure from enlarged lymph nodes), Horner's triad, hoarseness (when
oppressing the recurring laryngeal nerve), shortness of breath and chest pain (for example, when
growing into nerve plexuses)
Extrathoracic - neurological (in the case of metastasis to the CNS), bone marrow function disorders,
possibly pathological fractures (in the case of metastasis to the bones), hepatobiliary
symptomatology (in the case of metastasis to the liver), weight loss, loss of appetite
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Paraneoplastic manifestations - they are very common in bronchogenic carcinoma, they can also
be the first manifestation of the disease. These are, for example, hypercalcemia with
hypophostatemia (with ectopic secretion of parathyroid hormone), hyponatremia (with inadequate
secretion of ADH), Cushing's syndrome with hypokalemia (with ectopic secretion of ACTH). It can
also be skin (dermatomyositis), neurological (peripheral neuropathy, muscle myopathy), muscle and
hematological symptoms.
Diagnostics
Clinical examination
Less extensive tumors may be clinically silent. In the case of a more extensive impairment, there is
usually an auditory finding with the occurrence of secondary phenomena - especially whistling or
wheezing. Alternatively, listening to breathing is absent and the percussion is shortened, which
indicates a pleural effusion or atelectatic changes caused by non-airy parenchyma in the case of
obstruction of the bronchus by tumors. It is necessary to palpate the lymph nodes - supraclavicular,
axillary and cervical. Also, if we palpate the enlarged liver, it may already be metastatic.
Imaging methods
Among the basic imaging methods in the diagnosis of lung tumors are X-ray - back-front and side
projections, CT - lungs and mediastinum, EBUS (endobronchial ultrasonography), as well as PET,
possibly scintigraphy. A less important method is MRI - suitable for diagnosing Pancoast tumor
(tumor growing into the subclavicular space where it can affect nerve fibers and vascular bundle).
Histological sample collection
Among the methods of sampling are in particular - Bronchoscopy (using a brush and forceps),
Video-assisted thoracoscopy (VATS) - biopsy/resection of part of the lung parenchyma, or
transparietal biopsy - under X-ray/CT control (mainly for peripheral lesions).
If it is not possible to perform a sampling examination for the patient, we can cytologically examine
sputum (3-5 doses) or pleural effusion.
Therapy
Small cell carcinoma
Small cell carcinomas have a short doubling time, a high growth fraction and a tendency towards
early regional and distant metastasis. Therefore, surgical treatment of these tumors is rare.
Chemotherapy and radiotherapy targeting the tumor and metastases are indicated, as well as
preventive brain irradiation. Surgical treatment is indicated only in very limited cases and must
always be followed by systemic treatment
Non-small cell carcinoma
Therapy depends on the clinical stage (which is determined according to the TNM classification)
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Stage I – III a – primarily surgical treatment – resection procedure, followed by systemic treatment
Stage IIIB and IV inoperable – systemic treatment + chest RT.
Surgical treatment
Resection procedures for lung tumors are possible from thoracotomy or minimally invasive - videoassisted
(VATS), or robotically. According to the extent of the tumor, its location and possibly
affecting important structures, various types of performance can be performed. Part of the procedure
also includes the removal of lymph nodes - mediastinal lymphadenectomy. The main types of
performance are
Lobectomy - one or two lobes of the lung organ are removed. This method is often used in patients
with an early stage lung tumor, when the tumor is limited to the area of one or two lung lobes.
Lobectomy makes it possible to remove the affected part of the lung and minimize the loss of healthy
tissue.
Pneumonectomy – the entire wing of the lung is removed. This method is used in patients with a
more extensive tumor, possibly growing into the lung hilum, which cannot be removed by
lobectomy. A pneumonectomy is a major operation and may have a greater risk of complications,
Segmentectomy - sublobar resection - involves the removal of 1 lung segment. This procedure is
used in patients with small tumors or those who cannot undergo a lobectomy because of medical
problems or limited lung function.
A wedge resection is another type of sublobal resection in which a small wedge-shaped piece of the
lung with the tumor is removed with a smaller border of healthy tissue. This procedure may be
suitable for patients with small tumors, metastases, or patients with limited lung function. It is also
one possibility to collect a sample for histological verification of the tumor.
Malignant mesothelioma
Mesothelioma is a tumor arising from the mesothelium (the lining of body cavities originating from
the coelomic epithelium). The biological nature of mesothelioma can be benign or malignant
(malignant mesothelioma is characterized by implantation metastases - dissemination through the
serosa (the so-called diffuse malignant mesothelioma). Plate-like thickening of the visceral and
parietal serous sheet occurs, and the tumor invasively grows into the body wall and internal organs).
The localization of mesotheliomas is mainly – pleura, pericardium, peritoneum, possibly.
periorchium
Malignant mesothelioma of the pleura is an occupational disease - it is usually related to many
years of exposure to asbestos. Symptoms include chest pain, shortness of breath, and pleural
effusion. It usually takes up to several decades (even more than 50 years) from exposure to the
formation of a tumor. Therapy is primarily systemic treatment and chemotherapy. Surgical treatment
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is possible only in the case of localized tumors penetrating into the parenchyma, possibly the surgical
procedure is used to take a biopsy from the pleura.
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