As per ICU

1. ONCOLOGICAL EMERGENCIES
DR. VISHAL KR. KANDHWAY
Max Superspeciality Hospital,
Patparganj

2. Complications of Mlignancy
- Upper airway obstruction
- Malignant pericardial tamponade
- Superior vena cava syndrome
- Acute spinal cord compression
- Hypercalcemia
- Hyperviscosity syndrome
- Hyperleukocytic syndrome
- Tumor lysis syndrome
- SIADH
- Adrenal insufficiency / crisis
- Thrombocytopenia / hemorrage
- Immunosuppression / infection

3. TLS
• Metabolic consequenses resulting from sudden release of
potassim, phosphates & purine metabolites from tumor cells
undergoing cell death.

4. Pathogenesis
• Chemotherapy is given to fast growing cells. This lysis causes a
shift of intracellular components into the circulation, affecting
the kidneys and causing dangerous electrolyte imbalances

5. Abnormalities
Hyperuricemia
Hyperkalemia
Hyprephophatemia
Hypocalcaemia
Raised LDH

6. Risk factors
Cancer type- ALL, Burkitts lymphoma
Following chemotherapy,radiation, chemoembolisation
Renal insufficiency
Dehydration

7. Signs & Symptoms
GI: nausea, vomiting, diarrhea
Cardiac: dysrhythmias
GU: flank pain, anuria, cloudy urine
Neuro: seizures, altered mentation, stupor

8. TREATMENT
HYDRATION
• High rate of fluids – 200-300ml/hr
• U.O. to be maintained @ 80-100ml/m2/h
• Urine specific gravity to be maintained <1.01
• Most effective strategy for preventing urate induced obstructive
uropathy
LOOP DIURETICS
• To maintain U.O.
• Contraindicated in hypovolemia or obstructive uropathy

9. URINE ALKALANIZATION
Controversial
Can lead formation of urinary xanthine crystals
May cause urinary obstruction
ALLOPURINOL
• Hypoxanthine analog that competitively inhibits xanthine oxidase
• Dose 600mg/day if uric acid <8mg/dl
• Start prior to chemo
• Caution in renal impairment
• Causes skin hypersensitivity reaction

10. RASBURICASE
• Oxidizes preformed uric acid to allantoin which is highly soluble in
urine
• Used when uric acid level >8mg/dl
• Dose-infusion 0.1-0.2mg/kg/day in 50 ml NS over 30 min for 5
days
• Adverse reaction- anaphylaxis, rash, hemolysis
Hyperkalemia
• Increase excretion: IVF, diuretics, Kaexylate
• Shift back into cells: IV insulin and dextrose
Hypocalemia- Only treat if extremely low.

11. HYPERPHOSPHATEMIA
•Phosphorus binder: aluminum hydroxide, Calcium carbonate,
sevelamer hydroxide, lanthanum carbonate
•Decrease oral intake
HEMODIALYSIS
• Volume overload
• Serum uric acid >10mg/dl
• Rapidly rising phosphorus
• Uncontrolled hyperkalemia

12. Treatment Summary

13. LEUCOSTASIS
• Syndrome associated with high number of immature
leukocytes(blasts) in peripheral circulation
• High & rapidly rising blast counts usually >100,000/ml
Associated malignancy
• AML especially myelomonocytic(M4) & monocytic(M5)
subtypes
• CML in blast crisis
• Rarely in ALL or CLL

14. Pathology:
• Occlusive intravascular aggregates of blasts blocks microcirculation
in multiple organs
Symptoms:
• Usually nonspecific
• SOB
• Headache
• Confusion
• Stupor
• Focal neurologoical deficit

15. TREATMENT
• Hydration
• Hydroxyurea 50-100mg/kg/day in 3 divided doses till blast count>
50,000/ml
• Allopurinol and/or rasburicase
• Leucopheresis till count< 50,000/ml
• Definitive treatment for cancer
Supportive Treatment:
RBC transfusion to be restricted
Correct DIC & thrombocytopenia
Broad spectrum antibiotics

16. Treatment Summary

17. HYPERCALCEMIA
Pathogenesis: 3 mechanisms
• Osteolytic metastases with local cytokine release
• Tumor secretion of parathyroid hormone-related protein (PTHrP)
• Tumor production of calcitriol

18. • Symptoms & Signs usually non-specific
GI:
• Constipation is most common
• Anorexia
• Vague abdominal pain

19. Renal dysfunction:
Nephrolithiasis
– More common in hyperparathyroidism
Nephrogenic diabetes insipidus
– Defect in concentrating ability
– Polyuria and polydipsia
Chronic renal failure
– Longstanding high calcium
Calcifcation, degeneration, and necrosis of tubules

20. Neuropsychiatric:
• Anxiety
• Depression
• Cognitive dysfunction
– Delerium
– Psychosis
– Hallucinations
– Somnolence
– Coma
CVS
• Short QT interval
• Supraventricualr arrhythmias
• Ventricular arrhythmias

21. Osteolytic metastases

22. Treatment

23. SUPERIOR VENA CAVA SYNDROME
• Partial blockage or compression of blood flow in the superior vena
cava results in signs and symptoms of SVC syndrome

25. Etiology:
• Lung Cancer 80%
• Lymphoma 10%
• Other Malignancy 5%
• Benign causes 5%
(e.g. aneurysm, goitre, fibrosis, infection etc.)
 Thrombosis
 Indwelling central venous catheters
 Subcutaneous tunneled catheters have fewer thrombotic and
infectious complications

26. Symptoms & Signs
As the obstruction develops venous collaterals are formed
Symptom onset depends on speed of SVC obstruction onset
Shortness of breath is the most common symptom
Facial swelling or head fullness
– exacerbated by bending forward or lying down
Cough
Arm edema
Cyanosis

27. Physical findings:
Venous distension
– neck
– chest wall

28. DIAGNOSIS
Radiographic studies:
• Most patients have an abnormal chest x-ray at presentation
• Most common findings are
– Mediastinal widening
– Pleural effusion

29. CT Chest
• Preferred choice
• IV contrast
– defines the level of obstruction
– Maps out collateral pathways
– Can identify underlying cause of obstruction

30. Venography:
• Bilateral upper arm venograpy
– superior to CT to define site of obstruction
– Does not define cause unless thrombosis is solely responsible

31. MRI:
Can be useful in patients with IV contrast allergies

32. Treatment

33. SPINAL CORD COMPRESSION
• Neoplastic invasion of the space between vertebrae and spinal
cord (epidural invasion)
– Usually from bone metastases
Causes
• Metastatic tumor from any primary site
• Prostate, breast, and lung carcinoma
– 15-20% of cases
• Renal cell, non-Hodgkin’s lymphoma, or myeloma
– 5-10% of cases

34. Spinal Locations:
• Thoracic spine: 60%
• Lumbosacral spine: 30%
• Cervical spine: 10%

35. Clinical Features
Pain:
• Usually first symptom
– 80-90% of the time
• Usually precedes other neurologic symptoms by several weeks
– Increases in intensity
• Severe local back pain
• Aggravated by recumbency
– Distension of venous plexus
• May become radicular

36. Motor:
• Weakness: 60-85%
• At or above conus medularis
– Extensors of the upper extremities
• Above the thoracic spine
– Affects flexors in the lower extremities
• Patients may be hyperreflexic below the lesion and have extensor
plantars
• Weakness tends to be symmetrical
• Progressive weakness is followed by loss of gait function then paralysis
• The severity of weakness is greatest with thoracic metastases

37. Sensory:
• Less common than motor findings
• Still present in majority of cases
• Ascending numbness and parathesias

38. Bowel & Bladder:
• Loss is late finding
• Autonomic neuropathy presents usually as urinary retension
– Rarely sole finding

39. Radiological investigations:
• CT myelography involves a lumbar puncture
– Contraindicated in brain metastases, thrombocytopenia, or
coagulopathy
– Can diagnose leptomeningeal metastases
• MRI
Images whole spine
High detail
Spares lumbar puncture
Patients in pain must lie still

40. MRI of epidural spinal cord compression in a women with past
history of breast cancer.

41. Pain management:
• Corticosteroids
– Decrease edema
• Opiates
– Needed to decrease pain for comfort and examination purposes

42. Radiation therapy:
• Relieves pain in most cases
• Post-neurological function usually determines response
• Response most associated with tumor type and radiosensitivity; eg.
lymphoma

43. Surgery:
• Changing role
• Recent controlled trial comparing aggressive surgery followed by
radiation vs. radiation alone
• Improvement in surgery + radiation therapy

44. Chemotherapy:
• Can be successful in chemosensitive tumors
– Hodgkin’s lymphoma
– Non-Hodgkin’s lymphoma
– Neuroblastoma
– Germ cell
– Breast cancer (hormonal manipulation)
– Prostate cancer (hormonal manipulation)

45. Treatment Summary

46. HYPERVISCOSITY SYNDROME
• Refers to the clinical sequelae of increased blood viscosity.
• Increased serum viscosity results from increased circulating serum
immunoglobulins and can be seen in diseases like multiple
myeloma.
• HVS can also result from increased cellular blood components in
hyperproliferative states such as leukemia, polycythemia &
myloproliferative disorders.

47. Clinical Presentation: consists of triad of mucosal bleeding, visual
changes & neurologic symptoms.
Pathophysiology:
• Viscosity is a property of liquid & is described as the resistance that
a liquid exibits to the flow of 1 layer over another.
• As serum proteins or cellular components increase, the blood
becomes more viscous. Vascular stasis & resultant hypoperfusion
then lead to clinical symptoms of HVS.
• HVS is associated most commonly with plasma cell dyscrasias & is
due to the large size of IgM.

48. Labs:
• Elevated serum viscosity (normal 1.4-1.8 centipoises)
• CBC- rouleaux formation
• WBC- 100,000/uL or greater
• TP & albumin
• Electrolytes: hypercalcemia, hyperphosphotemia & hyperkalemia
• Coagulation profile
• CXR, CT brain, MRI

49. Treatment:
• Plasmapheresis is the treatment of choice for initial management
& stablization.
• Other options are leukapheresis, plateletpheresis & phlebotomy

50. THANK YOU