Oncologic emergencies

1. Oncologic EmergenciesOncologic Emergencies

2. I. Metabolic EmergenciesI. Metabolic Emergencies
II. Haematologic EmergenciesII. Haematologic Emergencies
III. InfectionsIII. Infections
IV. Neurological EmergenciesIV. Neurological Emergencies
V. Miscellaneous EmergenciesV. Miscellaneous Emergencies

3. I. Metabolic EmergenciesI. 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)

4. 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

5. 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

6. 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)

7. 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

8. Management (Treatment):
3.Treat hyperkalemia – resonium, dextrose-insulin-bicarb, dialyze if
indicated
4.Diuretics
5.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

9. 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

10. II II Haematologic EmergenciesHaematologic Emergencies
1.Hyperleucocytosis
2.Coagulopathy
3.Bone Marrow Depression

11. 1.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

12. 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

13. 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

14. 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

15. III. InfectionsIII. Infections

16. 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.

18. Other ManagementOther 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.

19. 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)

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

21. IV Neurological EmergenciesIV Neurological Emergencies

22. Spinal Cord CompressionSpinal 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

23. 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

24. 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

26. Increased ICP and brain herniationIncreased 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

27. 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)

28. 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.

29. Cerebrovascular accidentCerebrovascular 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.

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

31. VVMiscellaneous EmergenciesMiscellaneous 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.

32. 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)

33. 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 -FP
α
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.

34. 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.

36. 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.