Oncologic emergencies

Oncologic Emergencies

I. Metabolic Emergencies II. Haematologic Emergencies III. Infections IV. Neurological Emergencies V. Miscellaneous Emergencies

I. Metabolic Emergencies
A. Tumour Lysis Syndrome
Massive tumour cell death with rapid release of intracellular metabolites, which exceeds the
excretory capacity of the kidneys leading to acute renal failure. Can occur before chemotherapy is started.
More common in:
Iymphoproliferative tumours with abdominal involvement (e.g. B cell/ T cell Iymphoma, leukaemias and Burkitt's Iymphoma)

Characterized by : ↑ Uric acid ↑ K+ ↑ PO4 with associated ↓ Ca++ Risk factors for tumour Iysis syndrome: • Bulky disease • Rapid cellular turnover. • Tumour which is exquisitely sensitive to chemotherapy. • ↑↑ LDH / se uric acid • Depleted volume • Concentrated urine or acidic urine. • Poor urine output

a. Hyperuricaemia :
Release of intracellular purines increase uric acid
b. Hyperkalaemia
Occurs secondary to tumour cell Iysis itself or secondary to renal failure from uric acid nephropathy or ↑↑ PO4.
c. Hyperphosphotaemia (↑PO4) with associated ↓Ca++)
Most commonly occurs in Iymphoproliferative disorders because Iymphoblast PO4 contents is 4 times higher than normal lymphocytes.
Causes:
Tissue damage secondary to CaPO4 precipitation. Occurs when Ca X PO4 > 60 mg/dl. Results in renal failure, pruritis with gangrene and inflammation of the eyes and joints.
Hypocalcaemia leading to altered sensorium, photophobia, neuromuscular irritability, seizures, carpopedal spasm and GIT symptoms

d. Renal failure
Multifactorial:
Uric acid, phosphorus and potassium are excreted by kidneys
The environment of the collecting ducts of the kidney is acidic coupled with lactic acidosis due to high leukocyte associated poor perfusion – uric acid crystallizes causing uric acid obstructive nephropathy. Usually occur when levels > 20 mg/dl.
Increased phosphorus excretion causing calcium phosphate precipitation in microvasculature and tubules.
Risk increases if renal parenchymal is infiltrated by tumour eg: lymphoma or ureteral/venous obstruction from tumour compression (lymph nodes)

Management (Prevention):
To be instituted in every case of acute leukaemia or Iymphoma prior to induction chemotherapy.
Hydration: 3000 ml/m2/day (i.e. double hydration) No potassium should be added.
Alkalization of urine: Adding NaHCO3 at 150-200 mmol/m2/day (3 mls/kg/day NaHCO3 8.4%) into IV fluids to keep urine pH 7.0 - 7.5. Avoid over alkalinization. (Aggravate hypocalcemia and cause hypoxanthine and xanthine precipitation, also precipitation of calcium phosphate in pH >8)
Allopurinol 10mg/kg/day, max 300mg/day.
KIV delay chemotherapy until metabolic status stabilizes
Close electrolyte monitoring- BUSE, Ca2+, PO4 2-, uric acid, creatinine, bicarbonate.
Strict I/O charting. Make sure urine is flow is adequate once hydrated. Usediuretics with caution

Management (Treatment):
Treat hyperkalemia – resonium, dextrose-insulin-bicarb, dialyze if indicated
Diuretics
Hypocalcaemia management depends on the PO4 level:
• If PO4 is ↑, then management is directed to correct the ↑PO4
• If PO4 is normal OR if child is symptomatic, then IV Ca++ replacement is given.
• And if hypocalcaemia is refractory to treatment, associated
hypomagnesaemia (Mg2++) is to be excluded
4. Dialysis if indicated. Haemodialysis most efficient at correcting electrolyte abnormalities, peritoneal dialysis ineffective in removing phosphates

B. Other Metabolic Emergencies
a. Hyponatraemia (↓ Na+)
Usually occurs in AML. Treat as for hyponatraemia.
b. Hypokalaemia (↓ K+)
Common in AML. Rapid cellular generation leads to uptake of K+ into cells. (Intracellular K+ is 30 - 40 X higher than extracellular K+). Therefore may develop ↑ K+ after chemotherapy.
c. Hypercalcaemia (Ca++)
Associated with Non Hodgkin and Hodgkin Lymphoma, alveolar rhabdo, rhabdoid tumours, etc.
Management:
1. Hydration.
2. Oral PO4
3. IV Lasix (which increases Ca2- excretion)
4. Mithramycin

II Haematologic Emergencies
Hyperleucocytosis
Coagulopathy
Bone Marrow Depression

Hyperleukocytosis
Occurs in acute leukaemia
TWBC ≥ 100 000
Associated in
• ALL with high risk of tumour Iysis
• AML with leucostasis (esp monocytic)
• Affecting the lungs causing SOB, hypoxaemia and RV failure
• Affecting the CNS causing headaches, papilloedema, seizures,haemorrhage or infarct.
• Others: renal failure, priapism, dactylitis
Mechanism:
Excessive leukocytes form aggregates and thrombi in small veins
⇒ obstruction; worsens when blood is viscous.
Excessive leukocytes compete for oxygen and damage vessel wall
⇒ bleeding

Management of Hyperleukocytosis
Hydration
• to facilitate excretion of toxic metabolites
• to reduce blood viscosity
Avoid ↑ blood viscosity.
• Cautious use of blood transfusion and diuretics.
During induction in hyperleukocytosis, keep platelet >20 000 and coagulation profile near normal
Exchange transfusions and leukopheresis should not be used alone as rapid rebound usually occur. Concurrent drug treatment should therefore be initiated soonest possible

2. Coagulopathy
AML especially M3 associated with an initial bleeding diathesis secondary to consumptive coagulopathy
Due to release of a tissue factor with procoagulant activity from cells
Management
Platelet transfusions – 6units/m2
- should increase platelets by 50,000/ml3.
FFP or cryoprecipitate
Vitamin K
+/- heparin therapy (10u/kg/hr)
- controversial

3. Depression of bone marrow activity
Depression of normal bone marrow activity results in anaemia, thrombocytopenia, and neutropenia.
Best treated with supportive care, regardless of their etiology
Supportive care often includes transfusion of individual blood components

III. Infections

A. Febrile neutropaenia
Febrile episodes in oncology patients MUST be treated with urgency especially if associated with neutropenia.
Nearly all episodes of bacteraemia or disseminated fungal infections occur when the absolute neutorphil count (ANC) <500.
Risk increases maximally if ANC < 100 and greatly reduced if the ANC > 1000.

Other Management
1. If central line present, culture from central line from both lumens, add anti Staph cover e.g.cloxacillin.
2. Repeated P/E to look for new clues and signs and symptoms of possible sources.
3. Close monitoring of patient’s well-being – vital signs, perfusion, BP, I/O.
4. Repeat cultures if indicated
5. Investigative parameters, FBC, CRP, BUSE as per necessary .
6. In presence of oral thrush or other evidence of candidal infection, start antifungals.
7. Try to omit aminoglycoside and vancomycin if on Cisplatinum - nephrotoxic and ototoxic. If required, monitor renal function closely.

B. Typhilitis
Necrotizing colitis localised to the caecum occuring in neutropenic patients.
Pathophysiology:
Bacterial invasion of mucosa causing inflammation. Can lead on to full thickness infarction and perforation.
Organisms: Clostridium, Pseudomonas
X-ray shows non specific thickening. At the other end of the spectrum, there can be presence of pneumatosis intestinalis +/- evidence of free gas
Management
Usually conservative (unless surgically indicated) with broad spectrum antibiotics covering
Gram negative organisms and anaerobes (metronidazole), mortality 20-100%
Criteria for surgical intervention :
• Persistent GI bleed despite resolution of neutropenia and thrombocytopenia and correction of coagulation abnormalities.
• Evidence of perforation
• Clinical deterioration suggesting uncontrolled sepsis (controversial)

C. Shock
Common causes of shock in child with cancer
Management:
Ascertain cause and treat accordingly.

IV Neurological Emergencies

Spinal Cord Compression
Pathophysiology.
The most common scenario for cord compression is the direct extension of a metastatic lesion from the vertebrae into the epidural space.
Although metastatic lesions are more common, cord compression may be the initial presentation of the tumor.
Half of the metastatic lesions are due to lung, breast, or prostate cancer.
The most common site of compression is the thoracic spine (70%). The lumbar spine 20%, cervical spine 10%.
Intradural: Spinal cord tumour

Prolonged compression leads to permanent neurologic sequelae.
Epidural extension: Iymphoma, neuroblastoma and soft tissue sarcoma
Presentation:
Back pain-localized or radicular, aggravated by movement, straight leg raising, neck flexion.
Later – weakness, sensory loss, incontinence.
Diagnosed by CT myelogram/MRI

Management:
The goal of therapy is to decompress the spinal cord
1. Laminectomy urgently (If deterioration within 72 hours).
2. Once paralysis have been there longer than 72hours, chemotherapy might be the
better option if tumour is chemosensitive especially for lymphoma. This avoids vertebral damage. Other chemosensitve tumour include neuroblastoma and Ewing’s with an onset of action similar to radiotherapy.
3. Prior IV Dexamethasone 0.5mg/kg 6 hourly to reduce oedema
4. +/- Radiotherapy

Increased ICP and brain herniation
Cause : brain tumours e.g. astrocytoma, PNET, usually infratentorial and block the 3rd or 4 th ventricle.
Signs and symptoms vary according to age/site.
Infant; vomiting, lethargy, regression of milestones, seizures, symptoms of obstructive hydrocephalus.
Older: early morning recurrent headaches with or without vomiting.
Cerebellar: ipsilateral hypotonia and ataxia
Herniation of cerebellar tonsil – head tilt and neck stiffness

Tumours near 3rd ventricle – cranio, germinoma, optic glioma, hypothal and pit tumours- visual loss, increased ICP and hydrocephalus - obstruction of aqueduct of Sylvius due to pineal tumour – raised ICP and Parinaud’s synd (impaired upward gaze, convergence nystagmus and altered pupillary response)

Management:
1. Assessment of vital signs, look for focal neurological deficit.
2. Look for evidence of raised ICP (bradycardia, hypertension and apnea) and
3. Look for evidence of herniation (changes in respiratory pattern, pupil size and reactivity.
4. Dexamethasone 0.5 mg/kg (tp decrease edema)
5. Urgent CT to determine cause
6. Prophylactic antiseizures
7. LP is contraindicated
8. Decompression- ie shunting +/- surgery.
-Because of their multiple nature, surgical resection of intracerebral metastases is usually not a therapeutic option.

Cerebrovascular accident
Direct or metastatic spread of tumour, antineoplastic agent, haematologic abnormality.
L-Asparaginase associated with venous or lateral and sagittal sinus thrombosis caused by rebound hypercoagulable state
AML especially APML associated with DIVC and CVA. Due to release of procoagulant.

Management
Suportive
Use of anticoagulant potentially detrimental
In L-Aspa induced, recommended BD FFP

V Miscellaneous Emergencies
A. Superior Vena Cava Obstruction
Common in NHL/Hodgkin Lymphoma/ALL .
Rarely: malignant teratoma, thymoma, neuroblastoma, rhabdo or Ewing’s may present with anterior or middle mediastinal mass and obstruction.
50% associated with thrombosis.
Presentation: shortness of breath, facial & upper body edema , headache, nausea, dizziness, vision changes, hoarseness, cough, dysphagia or syncope.

Stridor and dyspnea, especially when the patient is supine, are associated with airway obstruction.
Physical examination is often remarkable for neck vein distention, facial edema, and trunk and upper extremity swelling.
Enlarged, dilated, cutaneous vessels in the anterior chest and upper abdomen provide evidence for collateral blood flow.
Plethora and tachypnea may also be noted.
In later stages, papilledema, lethargy, mental status changes, seizures, and coma may develop (dt. Cerebral edema & increase ICP)

Management:
1) Tissue diagnosis is important but should be established by the least invasive measure available. Circulatory collapse or respiratory failure may occur with sedation.
a) BMA
b) Biopsy of superficial LN under local anaesthesia.
c) Measurement of serum markers eg α-FP
If tissue diagnosis is unobtainable, empiric treatment may be necessary based on the most likely diagnosis. Both chemo and radiotherapy may render histology uninterpretable within 48 hours, therefore biopsy as soon as possible.

2) Interim therapeutic measures such as elevation of the head, diuretics, and supplemental oxygen may be instituted for symptomatic relief.
3) Dexamethasone may be used in patients with evidence of intracerebral edema.
4) In patients with highly chemosensitive tumors, lymphoma, germ cell carcinoma, and small cell carcinoma of lung, chemotherapy plays a significant role in treatment.
5) However, in most patients, radiotherapy is the cornerstone of therapy.
6) Balloon angioplasty and stent placement can be used to relieve the obstruction.

B. ATRA (all-trans retinoic acid) syndrome
Characterised by: fever, respiratory distress, respiratory failure, oedema, pleural/pericardial, effusion, hypotension
Pathophysiology:
Respiratory distress due to leukocytosis associated with ATRA induced multiplication and differentiation of leukaemic promyelocytes.
Treatment:
Dexamethasone 0.5 – 1mg/kg/dose BD.

Oncologic emergencies

by Mohd Hanafi on Apr 14, 2011

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