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I. METABOLIC EMERGENCIES Tumour Lysis Syndrome Introduction Tumour lysis syndrome • massive tumour cell death with rapid release Characterised by: hyperuricemia of intracellular metabolites, which exceeds hyperkalemia the excretory capacity of the kidneys leading hyperphosphatemia with to acute renal failure. Can occur before associated hypocalcemia chemotherapy is started. • more common in Iymphoproliferative tumours with abdominal involvement (e.g. B cell/ T cell Iymphoma, leukaemias and Burkitt’s Iymphoma) Hyperuricaemia • release of intracellular purines increase uric acid Hyperkalaemia • occurs secondary to tumour cell Iysis itself or secondary to renal failure from uric acid nephropathy or hyperphosphotaemia. Hyperphosphotaemia with associated hypocalcaemia Most commonly occurs in Iymphoproliferative disorders because Iymphoblast phosphate content is 4 times higher than normal lymphocytes. Causes: • tissue damage from CaPO₄ precipitation. Occurs when Ca X PO4 > 60 mg/dl. Results in renal failure, pruritis with gangrene, eye and joint inflammation • hypocalcaemia leading to altered sensorium, photophobia, neuromuscular irritability, seizures, carpopedal spasm and gastrointestinal symptoms Renal failure Multifactorial: • uric acid, phosphorus and potassium are excreted by kidneys • the environ of the collecting ducts of the kidney is acidic coupled with lactic acidosis due to high leucocyte associated poor perfusion will cause uric acid crystallization and then uric acid obstructive nephropathy. Usually occur when levels > 20 mg/dl. • increased phosphorus excretion causing calcium phosphate precipitation (in vivo solubility dependant on Ca X P = 58) in microvasculature and tubules. • risk increases if renal parenchymal is infiltrated by tumour e.g. lymphoma or ureteral/venous obstruction from tumour compression (lymph nodes).
Table 1. Risk factors for Tumour lysis syndrome Bulky disease Rapid cellular turnover. Tumour which is exquisitely sensitive to chemotherapy Elevated LDH / serum uric acid Depleted volume Concentrated urine or acidic urine Poor urine output
(Intracellular potassium 30 . • Hydration: Double hydration . alveolar rhabdomyosarcoma. Therefore may hyperkalaemia may develop after chemotherapy.4%) into IV fluids to keep urine pH 7. This can only be done if HCO₃ in the blood is below normal range.200 mmol/m²/day (3 mls/kg/day NaHCO₃ 8. Monitor urine pH and VBG 8 hourly.0 . then management is directed to correct the high phosphate . Hypercalcaemia • associated with Non Hodgkin lymphoma. • Alkalization of urine: Adding NaHCO₃ at 150 . Management (Treatment) • treat hyperkalaemia – resonium. Ensure adequate urine flow once hydrated. consider increasing NaHCO₃ infusion.0 7. PO₄. Hodgkin lymphoma.5. • diuretics • hypocalcaemia management depends on the phosphate level: . uric acid. Consider dialysis. Otherwise.125ml/m²/hr or 3000ml/m²/day. No added potassium.if hypocalcaemia is refractory to treatment. Use diuretics with caution. It can also cause precipitation of calcium phosphate if pH >8. • Allopurinol 10mg/kg/day.if phosphate is normal or if child is symptomatic.BUSE.if phosphate is raised. Other Metabolic Emergencies: Hyponatraemia • usually occurs in acute myeloid leukaemia (AML) • treat as for hyponatraemia. dextrose-insulin. Peritoneal dialysis is not effective in removing phosphates. Ca²⁺. • Close electrolyte monitoring. • may have to delay chemotherapy until metabolic status stabilizes. bicarbonate • Strict I/O charting. Haemodialysis most efficient at correcting electrolyte abnormalities. creatinine. max 300mg/day. exclude associated hypomagnesaemia • dialysis if indicated.Management (Prevention): To be instituted in every case of acute leukaemia or Iymphoma prior to induction chemotherapy. rhabdoid tumours and others. Management • hydration.40 X times higher than extracellular potassium). then give replacement IV calcium . Avoid over alkalinization as this may aggravate hypocalcemia and cause hypoxanthine and xanthine precipitation. Hypokalaemia • common in AML • rapid cellular generation leads to uptake of potassium into cells. • oral phosphate • IV frusemide (which increases calcium excretion) • mithramycin HAEMATO-ONCOLOGY 221 . If urine pH < 7. have to accept that some patients just cannot alkalinise their urine.
in acute lymphoblastic leukaemia (ALL) with high risk of tumour Iysis . priapism.affects the lungs due to pulmonary infiltrates. .II.to facilitate excretion of toxic metabolites . May cause dyspnoea.affects the central nervous system causing headaches. Coagulopathy AML especially M3 is associated with an initial bleeding diathesis from consumptive coagulopathy due to release of a tissue factor with procoagulant activity from cells.excessive leukocytes form aggregates and thrombi in small veins causing obstruction. Concurrent drug treatment should therefore be initiated soonest possible. hypoxaemia and right ventricular failure . papilloedema. keep platelet >20 000/mm³ and coagulation profile near normal • exchange transfusions and leukopheresis should not be used alone as rapid rebound usually occurs. dactylitis • mechanism: .controversial Other haematological energencies • thrombocytopenia • severe anaemia HAEMATO-ONCOLOGY 222 . HAEMATOLOGICAL EMERGENCIES Hyperleucocytosis • occurs in acute leukaemia. seizures. worsens when blood is viscous.in AML with leucostasis (esp monocytic) .000 / mm³ • fresh frozen plasma (FFP) or cryoprecipitate • vitamin K • +/.heparin therapy (10u/kg/hr) . Defined as TWBC > 100 000 / mm³ • associated . .cautious in use of packed cell transfusion and diuretics. .to reduce blood viscosity • avoid increasing blood viscosity. Management • platelet transfusions – 6 units / m² should increase platelets by 50. haemorrhage or infarct. However the use of all-trans retinoic acid (Atra) has circumvented this complication. damages vessel wall causing bleeding Management • hydration .excessive leukocytes competes for oxygen.other complications: renal failure. • during induction in hyperleukocytosis.
IV. Risk increases maximally if ANC < 100 /mm³ and greatly reduced if the ANC > 1000 /mm³. facial swelling. cloxacillin Streptococcus pneumonia • repeated physical examination to look for new Escherichia coli clues. Aspergillus • repeat cultures if indicated • investigative parameters. • close monitoring of patient’s well-being Klebsiella spp. start antifungals.nephrotoxic and ototoxic.BMA . add anti-Staph cover e.aggravate SVC obstruction. • primary mode of treatment is with steroids } if pathology due to Non-Hodkin • chemotherapy. FBC. } Lymphoma • +/. BUSE as per necessary.III. monitor renal function closely. I/O.measurement of serum markers e. • presentation: shortness of breath. • try to omit aminoglycoside and vancomycin if on cisplatinum . 223 HAEMATO-ONCOLOGY .biopsy of superficial lymph node under local anaesthesia.DXT. rhabdomyosarcoma or Ewing’s may present with anterior or middle mediastinal mass and obstruction. thymoma. SUPERIOR VENA CAVA OBSTRUCTION Superior Vena Cava (SVC) Obstruction • common in Non Hodgkin Lymphoma / Hodgkin Lymphoma / ALL . Both chemotherapy and DXT may render histology uninterpretable within 48 hours. alpha-fetoprotein If tissue diagnosis is not obtainable. INFECTION Febrile neutropaenia Febrile episodes in oncology patients must be treated with urgency especially if associated with neutropenia.bleeding due to increased intravascular pressure . • rarely: malignant teratoma. neuroblastoma.g. Nearly all episodes of bacteraemia or disseminated fungal infections occur when the absolute neutorphil count (ANC) <500 /mm³. • 50% associated with thrombosis. therefore biopsy as soon as possible. Risk of circulatory collapse or respiratory failure may occur with general anesthesia or sedation.g. perfusion. BP. empiric treatment may be necessary based on the most likely diagnosis. CRP. • in presence of oral thrush or other evidence of candidal infection. culture from central line Staphyylococus epidermidis (both lumens). syncope. Management (Follow Algorithm in Figure 1) Febrile neutropenia other considerations: Common organisms Staphylococcus aureus • if central line is present. Candida spp – vital signs. signs and symptoms of possible sources Pseudomonas spp. Management • recognition of symptoms and signs of SVC obstruction and avoidance of sedation and general anaesthesia Tissue diagnosis is important but should be established by the least invasive measure available. . If required. . • avoid upper limb venepunctures .
• bacterial invasion of mucosa causing inflammation . Approach to a patient with febrile neutropenia Febrile Neutropenia History and examination to identify possible source(s) Septic Work-up (FBC. chest X-ray. bacterial and fungal cultures.evidence of free gas Management • usually conservative with broad spectrum antibiotics covering gram negative organisms and anaerobes (metronidazole). Change antibiotics Still febrile after 4 daynti• look for possible sites of infection • repeat X-ray • repeat cultures • Echo. wound) Site unknown Broad spectrum antibiotics (e. central venous line.can lead on to full thickness infarction and perforation • usual organisms are Clostridium and Pseudomonas • X-ray shows non specific thickening of gut wall. . CXR. cephalosporin. urine. CRP. CRP. At the other end of the spectrum. Typhilitis • a necrotizing colitis localised to the caecum occuring in neutropenic patients. aminoglycoside and nystatin) Site identified • specific antibiotics • proper specimen collected Temperature settles in 3 days Remains febrile after 2 days Reculture.Figure 1. full blood count. ultrasound • consider add antifungals • consider changing antibiotics HAEMATO-ONCOLOGY Continue Treatment Stop Treatment after 1 week Observe Abbrevations. CXR. stool.persistent gastrointestinal bleeding despite resolution of neutropenia and thrombocytopenia and correction of coagulation abnormalities. CVL. C-reactive protein. FBC.clinical deterioration suggesting uncontrolled sepsis (controversial) 224 .evidence of perforation .blood. there can be presence of pneumatosis intestinalis +/. Mortality 20-100% • criteria for surgical intervention: .g.
• infant . regression of milestones. symptoms of obstructive hydrocephalus and increased OFC.vomiting.later: weakness. aggravated by movement. fungal Management Ascertain cause and treat accordingly V. astrocytomas and ependymomas. • epidural extension: Iymphoma. bacterial.early morning recurrent headaches +/.g. • if paralysis present > 72 hours. Signs and symptoms vary according to age/site. This avoids vertebral damage. • older . lymphoma. Common causes of shock in children with cancer Distributive Hypovolaemic Cardiogenic Sepsis Haemorrhage Myopathy haemorrhagic cystitis anthracycline Anaphylaxis gastrointestinal bleeding high dose cyclophosphamide etoposide ulcers radiation therapy L-asparaginase typhilitis anti-thymocyte globulin Cardiac tamponade massive haemoptysis cytosine intracardiac tumour carboplatin Pancreatitis intracardiac thrombus blood products pericardial effusion Addisonian crisis amphotericin B constrictive pericarditis Intractable vomiting Veno occlusive disease Metabolic Diabetes mellitus hyperkalaemia. seizures. lethargy. neuroblastoma and Ewing’s tumour. sensory loss. hypokalaemia Diabetes insipidus hypocalcaemia Hypercalcaemia Myocarditis viral. poor school performance • cerebellar: ipsilateral hypotonia and ataxia 225 HAEMATO-ONCOLOGY . loss of bladder and bowel continence • diagnosed by CT myelogram/MRI Management • laminectomy urgent (if deterioration within 72 hours). • prior IV Dexamethasone 0. neck flexion .vomiting.Radiotherapy Increased Intracranial Pressure (ICP) and brain herniation Cause : Infratentorial tumours causing blockage of the 3rd or 4th ventricles such as medulloblastomas.5mg/kg 6 hourly to reduce oedema • +/. Onset of action of chemotherpay is similar to radiotherapy. chemotherapy is the better option if tumour is chemosensitive. straight leg raising. e.Shock Table 2 lists the common causes of shock in child with cancer Table 2. neuroblastoma and soft tissue sarcoma • intradural: Spinal cord tumour • Presentation .back pain: localized or radicular. NEUROLOGICAL COMPLICATIONS Spinal Cord Compression • prolonged compression leads to permanent neurologic sequelae.
e. • look for evidence of raised ICP (bradycardia. respiratory distress. due to the release of procoagulant Management • supportive • use of anticoagulant potentially detrimental • in L-Asparaginase induced. hypertension and apnea) • look for evidence of herniation (respiratory pattern. maximum dose 20mg bd. altered pupillary response) Management • assessment of vital signs. oedema. Parinaud’s syndrome (impaired upward gaze. ATRA (all-trans retinoic acid) syndrome • characterised by: fever. convergence nystagmus.5 – 1mg/kg/dose bd. recommended FFP bd VI. germinoma. look for focal neurological deficit. Careful examination plus measurement of serum amylase and ultrasound abdomen.aqueduct of Sylvius obstruction due to pineal tumour: raised ICP. respiratory failure. hypotension • pathophysiology: respiratory distress due to leukocytosis associated with ATRA induced multiplication and differentiation of leukaemic promyelocytes • treatment: dexamethasone 0. pupil size and reactivity) • dexamethasone 0.visual loss.5 mg/kg QID • urgent CT to determine cause • prophylactic antiepileptic agents. optic glioma. pleural/ pericardial effusion. 226 . hypothalamic and pituitary tumours . antineoplastic agent or haematological abnormality • L-Asparaginase associated with venous or lateral and sagittal sinus thrombosis caused by rebound hypercoagulable state • AML especially APML is associated with DIVC and CVA. shunting +/. increased ICP and hydrocephalus .surgery. Cerebrovascular accident (CVA) • can result from direct or metastatic spread of tumour.HAEMATO-ONCOLOGY • herniation of cerebellar tonsil – head tilt and neck stiffness • tumours near 3rd ventricle – craniopharyngima . MISCELLANOUS EMERGENCIES Pancreatitis Should be considered in patients on L-Asparaginase and steroids and complaining of abdominal pain. • lumbar puncture is contraindicated • decompression – i.
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