Emergencies in cancer patients
Jiří Vyskočil
ICU/HDU
Medical Outpatient Unit
Overview
• Cancer related
• Treatment related
• Medical emergencies
• Surgical emergencies
• Unrelated to cancer, though with increased
incidence in cancer patients
Cancer related
• Local (mechanical) effect of cancer
– Vena cava syndrome
– Intracranial hypertension
– Compression of pericardium/airways
– Effusions – pericardial, pleural, ascites
– Spinal cord compression
• Metabolic
– SIADH, hypercalcemia, hyperviscosity syndrom, refeeding
syndrome, diabetes decompensation due to
cancer/treatment, spontanious tumor lysis syndrom
• Thrombembolic disease - PE
Treatment related and medical
emergencies
• Febrile neutropenia/neutropenic sepsis
• Thrombocytopenia
• Tumor lysis syndrome
• Chemotehrapy associated diarrhea – colitis
• AKI (acute kidney injury)
– Cisplatin, TLS, posterenal, dehydration, interstitial nephritis)
• Liver failure
• Congestive heart failure (acute, deterioration of chronic HF)
– Tachyarhytmias due to side effects/electrolyte imbalance
• Acute coronary artery disease (5-FU, cDDP)
• Alergic reactions/anaphylaxis
• Increased risk of PE
• Deterioration of medical conditions
Surgical
• GI obtsruction, urinary tract obstruction
(postrenal AKI)
• Pneumothorax – spontanious/complication of
procedures (central line, tapping effusions)
• Cancer bleeding– melanoma, GI cancers, lungs
cancer..
• Acute abdominal
• Spinal cord compression
Neutropenic sepsis
febrile neutropenia
Introduction
• FN definition – TT >38.5°C* or 2 episodes of
TT >38.0°C for 2h** and ABC count <0.5 ×
109/l or expected fall < 0.5 × 109/l
• Potential lifethreatening condition
* or 38,3 pending source
** or 1 hour pending source
Risk factors
• MASCC (symptoms of underlying disease, COPD, age,
hematol. Malignancies, mycotic infection, dehydration,
BP<90, inpatinet onset)
• https://www.qxmd.com/calculate/calculator_134/mas
cc-febrile-neutropenia-risk
• Time of neutropenia
• GIT toxicity
• Other medical conditions (CHF, CAD, DM, CKD, COPD)
• Known colonisation with MRSA/VRE/ESBL
• Onset during G-CSF profylaxis
Management
• C/E incl. PR
• ECG
• Lung X ray +/- abdomen
• BC+coag, electrolytes, RFT, LFT, CRP,
prokalcitonin
• BC– central line + peripheral line, urine,
(C. diff, stool, throat, tonsills…)
Management
• Broad spectre antibiotics incl. anti
pseudomonas aeruginis activity
• History of MRSA/VRE/ESBL?
• Up front G-CSF up are not generally
recommended
• Antimycotics – pending of mycotis infection
risk
Management
• Tazocin (piperacilin/tazobactam) 4,5g i.v. a 6 h
till neu >1,0, then a 8h
• Gentamycin 240-320mg in septic patients
• Antimycotics – pending on mycotic infection
risk
• Metronidazol in pts with S/O collitis
• G-CSF up front in pts with pneumonia, GI
toxicity and severe comorbidities (CHF, CAD,
DM, CKD, COPD)
Vena Cava Syndrome (VCS)
• Superior vena cava obstruction account
for 99 % of VCS cases
– Anatomy of the mediastinum + Thin-walled vein filled
at relatively low pressure  any significant
compression can result in obstruction to blood flow
• External compression by tumour or lymphadenopathy
• Internal compression by thrombosis or catheter
• The severity of the resulting syndrome depends on the
rapidity of onset and level of the obstruction
• Despite the sometimes dramatic and distressing
clinical picture, VCS is usually not lethal complication
Vena Cava Syndrome (VCS)
• Symptoms and Signs
– Cough and dyspnea
– Facial, cervical and arms edema
– Venous dilatations (chest and upper extremities)
– Headache
– Dysphagia
– Symptoms worse by bending or lying down
Vena Cava Syndrome (VCS)
• Causes
– Malignant (85 – 95 %)
• Lung cancer, Non-Hodgkins lymphoma, Germ cell neoplasms,
Metastatic breast cancer, Oesophageal carcinoma, others
– Non-Malignant
• Mediastinal fibrosis, VC thrombosis, Indwelling central lines
(catheters), Sarcoidosis, TBC, others
• Differential diagnosis: Heart failure,
Cardiac tamponade
• Diagnosis
– Chest X-ray (mediastinal widening, mass, pleural effusion,
… normal X-ray in < 20 %)
– CT of the thorax with contrast or CT/MRI venography
Vena Cava Syndrome (VCS)
• Management
– Immediate management
• Corticosteroids (DXM 8mg p.o. 2-3 times a day) + Diuretics
• Stent placement
– The most rapid relief  in the presence of cerebral edema or
disabling symptos or in the case of chemo/radio-resistant disease
• Thrombolysis (if thrombus is documented)
• Surgery (bypass or thrombectomy, primarily in pts with good
prognosis or in benign causes of VCS)
– Treatment of the uderlying malignancy
• Chemotherapy (SCLC, lymphoma, germ cell tumours)
• Radiotherapy (for non-chemosensitive disease)
– Prognosis dependent on the type of cancer and the
patients general condition. VCS commonly relapses.
Vena Cava Syndrome (VCS)
Vena Cava Syndrome (VCS)
A men with VCS before and after stenting
Tumour Lysis Syndrom (TLS)
– TLS is a group of metabolic complications arising
from treatment of a rapid proliferating neoplasm.
Occasionally TLS can occur prior to the initiation of
the treatment.
– Cancer therapy (ischemia)  cell death / lysis 
release of intracellular product into the circulation
• Hyperuricaemia
– Purine nucleic acid breakdown  hypoxanthine xanthine 
(xanthine oxidase)  uric acid  kidney  precipitation in
the tubules  URATE NEPHROPATHY  ARF
• Hyperphosphataemia
– Phosphate + calcium  precipitation  Acute Renal Failure (ARF)
• Hyperkalaemia ( K+  fatal arrrhythmias)
• Hypocalcaemia (precipitation with phosphate in kidney, skin…)
• Uraemia (consequence by TLS)
Tumour Lysis Syndrom
(TLS)
• Clinical signs
– Hyperuricaemia
• Haematuria, flank pain, acute obstructive nephrophaty (AON) (anuria /
oligouria)
– Hyperphosphataemia
• Nausea, vomitin, diarrhoea, seizures, hypocalcaemia, AON
– Hyperkalaemia
• Nausea, vomiting, diarrhoea, cramps, weakness, paraesthesiae,
arrhythmias, sudden death
– Hypocalcaemia
• Muscle cramps, spasms, tetany, arrhythmias, confusion, hallucinations,
seizures
– Uraemia
• Lethargy, anorexia, nausea, vomiting, confusion, encephalopathy,
perciarditis, acidosis, oedema, hypertension
Tumour Lysis Syndrom (TLS)
– Clinical TLS
• Creatinin > 1,5x upper limit of normal
• Cardiac arrhytmia / sudden death and/or seizure
– Cairo-Bishop laboratory definition
• Uric acid > 476 umol/l or 25 % increase from baseline
• K > 6,0 mmol/l or 25 % increase from baseline
• Phosphate > 1,45 (2,1 children) mmol/l or 25 % increase
from baseline
• Ca < 1,75 or 25 % decrease from baseline
TLS – treatment:
• Correction of the electrolyte imbalances and
optimazing renal function
– Hyperuricaemia: Intravenous fluids and loop diuretics, rasburicase
(urate oxidase)
– Hyperkalaemia: Aovid IV or p.o. K supplements. Calcium gluconate (10
ml of 10 % iv over 2 min) as a cardioprotectant, if K+ > 6,0  Actrapid
insulin 10 units plus 50 ml of 50 % dextrose over 30 min iv infusion,
Calcium resonium 15g p.o. 3-4x daily, correct acidosis (50-100 ml 8,4
% NaHCO3 via central line)
• Haemodialysis may be needed for:
– K > 7 mmol/l
– Symptomatic ureamia (tremor, seizures, confusion, pericarditis,
coma)
– Metabolic acidosis (arterial pH< 7,1, [HCO3] < 12 mmol/l
– Fluid overload unresponsive to diuretics
TLS - identification of high risk patients:
• Patient-releated factors
– decreased urine output,
– pre-existing renal impairment or hyperuricaemia,
– dehydratation
– acid urine
• Tumour-releated factors
– high proliferative rate
– high tumour burden
– high sensitivity to cytotoxic agents
– ALL, High grade NHL, CLL, Myeloma,
– testicular cancer, SCLC, breast cancer
TLS – prevention:
• Vigorous hydratation (app. 3l/m2/d) with a urine
output of > 100 ml/m2/h
• Allopurinol 300 mg daily increasing 600-900 mg in
2-3 doses. Start allopurinol 24 h before the first
chemotherapy treatment
• High risk patients: Rasburicase (200 ug/kg once
daily for up to 7 days according to plasma uric acid
concentration.
• Urinary alcalization
Hyperviscosity
• Viscosity pending on a number of blood cells, total
amount of proteins, hydratation, temperature…
Symptoms
• impaired blood suplly (headache, fatigue, dizziness),
dysopnea, cough, heart failure, AKI, bleeding…)
• Polyglobulia, leucostasis (AML, ALL, CML), monoclonal
gamapathies (MM, Waldeström)
Management:
• fluids + aferesis (erythrocyto, leukocyto, plasma)
Hypercalcemia
• 10% pacients, 30-day mortality 50%
• PTHrP tumour related, osteolytic MTS, hyperproduktion of vit D, ectopic
production of PTH
Symptoms
• nausea, vomiting, fatigue, depression, constipation, AKI, coma,
heart arrest
• EKG: short QT, ST depression
• Lab: increased Ca i Ca2+, highPTHrP a low/normal PTH
Management
– Fluids - saline +/- furosemide
– Steroids
– Bisfosfonates
– Hemodialysis
– Phosphate supl - later
Neurological
• Malignant extradural spinal cord
compression
• Raised intracranial pressure
• Leptomeningeal metastases
Spinal cord compression
• Important medical emergency, treatment must begin
within hours, to maximize the chance of neurological
recovery
• 5-10 % of all patients with a known diagnosis of
malignancy: breast, lung, prostate, uknown primary,
myeloma, rencal, other
• May be the first presentation of malignancy (up to 20 %):
prostate, breast, myeloma
• Site of compression: thoracic (60 %), lumbar (30 %),
cervical (10 %)  30 % multiple sites
Spinal cord compression
• Causes
– Expanding metastases to the vertebral body
– Vertebral pathological fracture with posterior
displacement of bony fragments
– Paraspinal mass gains access to the epidural space
via neural foramina
– Epidural metastases
• Two phases of compression
– Reversible: obstruction of venous plexus and
vasogenic oedema  demyelinisation
– Ireversible: ischemic damage and cord infarction
Spinal cord compression
Symptoms:
Pain - usually the first symptom, localized and radicular
Neurological:
- weakness of the legs  paralysis
- sensory loss
- bladder dysfunction (urinary retention  incontinence),
- bowel dysfunction (constipation  incontinence),
- impotence
Spinal cord compression
Spinal cord compression
Raised intracranial pressure
• Result of brain oedema due to either primary brain
tumour or metastases
Symptoms:
• Hypertension, bradykardia, headache, nausea or
vomiting without nausea, meningeal symptoms,
confusion…coma
Management
• Manitol 1,5g/kg/day 3 day, tapering aftewards
• Dexamethason 24mg/day
Thrombembolic disease (TED)
• frequent complication of cancer
• PE is often succesive leading to PH
• 20% of new PE is dg in CA pts.
• PE risk is 6-7x higher
• CTPA
TED - risk factors
• direct procoagulation effect: tissue f. expresion, releasing TF
bearing microparticles, cancer procoagulant
• indirect effect: increased NETS production (neutrophil
extracelullar traps), pro infamatory
• ‚normal‘ risk factors + surgery, sepsis, CVL, lymphedemas
• pancreatic cancer, gastric cancer, lung cancer, myeloma,
lymphomas, gynaecologic cancers, prostate cancer
• chemotherapy, G-CSF, EPO, platelets infusions, tamoxifen,
steroids
TED - prophylaxis and treatment
Prophylaxis
• LMWH in all cancer inpatients
• If LMWH not possible: intermitent pneumatic compression +/-
stockings
• In pts after major surgery 28 days
Treatment
• LMWH (dalteparin, enoxaparin, fondaparinux)
• Chronic:
• In catheters-related 3 months
• Others: lifetime in pts with active disease/ on treatment
Coronary artery disease /
ischaemic heart disease
• Chemotherapy
– 5-FU (vasospasm), capecitabin (vasospasm), cisplatine (both vasospasm +
endoth. dysfuction), etoposide, taxanes (arhytmias), vinca alkaloids (spasm)
• Thoracic irradiation
• Targeted treatment
– bevacizumab, TKI
• Hormonal treatment
– Aromatise inhibitors (Ca prsu, prostaty)
• Change of lifestyle
– Weight gain, lack of physical activity, thyroid gland impairment (TKI)
Heart failure I
• Chemotherapy
– antracyclines, mitoxantron
– CAD inducing drugs – cisplatine, 5-FU
– Arrhytmogennic drugs – taxanes
– Alkylating agents – cyclophosphamide, ifosphamide,
busulfan, mitomycinC
• Radiation therapy (involving thorax)
– O2 radicals- endothel. dysfunction – CAD –
hypoperfusion – fibrotisation of myocardium
Heart failure II
• Targeted treatment
– trastuzumab (breast Ca)
– TKI (kidney, liver, CML, GIST…)
Heart failure III
• developement possibly during years post treatment
• subacute onset after anthracycines within a year
• Acute – within days - after anthracyclins
• Weeks to months – after targeted therapy
• Prevention:
– Follow RF (age, diabetes, hypertension, CKD, prior RT, lipids)
– Follow cumulative anthracycline doses
– ECHO monitoring – anthracyclines, antiHER2 therapy, TKI
Heart failure IV
• Late onset:
– Hematological malignancies
– Childhood cancer
– Breats cancer
– Testicular cancer
• standard management of heart failure