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Emergencies In Oncology
The document outlines various emergencies in oncology, including neutropenic fever, superior vena cava syndrome, malignant pericardial tamponade, hypercalcemia, and tumor lysis syndrome. It details their causes, clinical presentations, diagnostic methods, and treatment guidelines. The information targets oncological complications, emphasizing symptoms and management strategies critical for patient care.
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Emergencies In Oncology
- 1.
- 2. 1. Neutropenic fever 2.SVCO 3. Malignant pericardial tamponade 4. Hypercalcemia 5. Tumour lysis syndrome 6. Cord compression 7. Brain metastases 8. Pain
- 3.
- 4. • Fever • Singlereading >38.3ºC • Sustained (> 1 h) reading >38ºC • Neutropenia • ANC <500 cells/uL (pedantic) • ANC 500 to 1000 cells/uL with a predicted nadir of <500 (pragmatic) • Risk is inversely proportional to ANC
- 5. high index ofsuspicion • Signs of inflammation may be absent • Erythema, induration, pus • Pulmonary infiltration • Pyuria • Pleocytosis • Fever is not always present • Elderly, pts receiving steroids • May present with hypothermia and hypotension
- 6. Most common causes •Majority are bacterial in origin • 30% have bacteremia • 80% are endogenous • Gram (-) used to predominate • Gram (+) are on the rise
- 7. Bacterial infection • Gram(-) • E coli • Klebsiella • Pseudomonas • Enterobacter • Gram (+) • Staphylococcus species • Streptococcus species • Enterococcus • Corynebacterium
- 8. Anaerobic infection • Represents3.4% of cases • Routine cover is not necessary • Except for special sites • Oral and sinus infections • Intra-abdominal or pelvic infection • Perirectal infection • Anaerobic becteremia
- 9. Fungal infection • Usuallya secondary infection • Prolonged neutropenia • Prolonged antibiotic use • Candida and Aspergillus species • One-third of febrile neutropenic pts who fail to respond after 7 days of antibiotic have systemic fungal infection
- 10. Viral infection • Predominantlyin BMT and hematologic cancer patients • Predominantly herpesviruses (HSV, VZV, CMV, EBV) • Sometimes respiratory viruses • There is usually no indication for empiric anti-viral therapy without evidence of viral infection
- 11. Treatment • evaluation forsubtle signs & symptoms of infection • Full blood count • Liver and renal panels • CXR • Blood and urine cultures
- 12. Treatment • Perform bloodculture from ALL PORTS and the peripheral vein • Start antibiotic therapy IMMEDIATELY!
- 13. Monotherapy • Broad spectrumb-lactams with anti-pseudomonal coverage • Ceftazidime 2 g q8 hrly • Cefepime 2 g q8 hrly • Imipenam 500 mg q6 hrly • Meropenam 1 g q8 hourly • Tazocin 4.5g q8 hourly
- 14. Two-drug therapy • Theaddition of an aminoglycoside to • Tazocin • Ceftazidime or Cefepime • Imipenam or Meropenam • Synergistic against gram (-) bacilli with less risk of emergence of resistance • Indicated when severe sepsis, septic shock, high prevalence of multi-drug resistance gram (-) bacilli
- 15. ? Vancomycin • Additionto initial empiric antibiotic regimen has not been shown to decrease mortality • Considered when • Clinically suspected serious catheter related infection • Known MRSA colonization • Gram (+) bacteremia • Hypotension
- 16. CVC-related infection • Classification •Exit wound infection • Tunnel infection • CVC-associated bacteremia • Septic thrombophlebitis
- 17. CVC-related infection • Mostcommonly • Coagulase-negative staph • S aureus • Less commonly • Gram (+) bacilli (Corynebacterium and bacillus specie) • Candida • Mycobacteria
- 18. Catheter removal • Tunnelinfection • Septic thrombophlebitis • Septic emboli • Culture (+) after 72 hrs of therapy
- 19. Catheter removal • Selectedpathogens • Corynebacterium • Bacillus • S aureus • VRE • Candida • Mycobacterium
- 20. Typhlitis • Neutropenic enterocolitis •? when neutropenia + “appendicitis” • Distended cecum, edematous cecal wall, pneumatosis intestinalis on CT • Typically pseudomonas + clostridium • Primary treatment: antibiotics! • Surgery if with bowel complications
- 21. Treatment • No localizablefocus • No s/s of systemic infection other than fever • ANC > 500/ mm3 • Cancer responding to treatment • No significant co-morbidity • No recent hospitalization • Age <60 • Stable patient
- 22. Treatment • Oral Augmentin+ Ciprofloxacin x 5 days • Follow up with Doctor in ≤3 days • Trace preliminary culture results O/A
- 23. Colony-stimulating factor • toshorten duration of neutropenia • Can reduce neutropenia-related morbidities • Use of antibiotics • Cost of management
- 24.
- 25. Superior vena cava •Drains venous blood from head, neck, upper limbs and thorax • Surrounded by relatively rigid structures • Thin walled, low pressure and easily compressible • Completely encircled by chains of lymph nodes that drain the whole right and lower left thorax
- 26. Causes • Lung (65%) •Lymphoma (8%) • Other cancers (10%) • Nonmalignant (12%) • Undiagnosed (5%)
- 27. Clinical Presentations • Mostcommon symptoms • Dyspnoea (63%) • Facial swelling (50%) • Head fullness (24%) • Most common signs • Venous distension of neck (66%) • Venous distension of chest wall (54%) • Facial edema (46%)
- 28. complications • Cerebral edema •Laryngeal edema
- 29. Imaging studies • CXR •CT scan is often diagnostic • Upper extremity venography seldom needed
- 30. CXR findings Findings Patients(%) Sup mediastinal widening 64 Pleural effusion 26 (R) hilar mass 12 Bilateral infiltrates 7 Cardiomegaly 6 Calcified paratracheal LNs 5 Ant mediastinal mass 3 Normal 16
- 31. Treatment • Raise theupper body • Transfer iv access to lower limbs • Supplemental oxygen • Mist morphine 5-10 mg q4-6 hrly • Furosemide 20-40 mg om • Hydrocortisone 100 mg q6-8 hrly
- 32. Treatment • Treat underlyingcancer • Radiation therapy • Chemotherapy • Re-establish patency • Thrombolytic therapy • Endovascular stenting • Bypass surgery
- 33.
- 34. Causes • Often (butnot always) a preterminal event • Occurs in about 10-15% of advanced cancer pts • Lung and breast cancer make up 75% of all the cases
- 35. Clinical Presentations • Symptomssimilar to CCF • Signs • Kussmaul’s sign • Pulsus paradoxus • Distant heart sounds
- 36. imaging studies • CXR •Water-bottle silhouette • Echocardiography • Echo separation • RA or RV collapse • CT chest
- 37. Treatment • IV fluids •Supplemental O2 • Morphine for SOB • Inotropic support • Pericardiocentesis
- 38. Treatment • Pericardial window •Pericardial sclerosis • Radiotherapy • Treat underlying cancer
- 39.
- 40. • Elevated levelsof ionized calcium in the blood • Corrected calcium = measured calcium + 0.02 x (40 – measured albumin) mmol/L • Normal 2.2 – 2.6 mmol/L • Symptomatic > 3.0 mmol/L
- 41. Causes • The 2most common causes are cancer and hyperparathyroidism
- 42. Causes • The mostcommon malignancies are • Multiple myeloma • Breast • NSCLC • RCC • Hypercalcemia is the most common life-threatening metabolic oncologic disorder
- 43. Clinical presentation • General •Dehydration, fatigue, lethargy, pruritis • Neuromuscular • Confusion, psychosis, obtundation, seizure • Proximal myopathy, hyporeflexia • GIT • Nausea, emesis • Dyspepsia • Pancreatitis • Constipation, ileus
- 44. Clinical manifestations • Renal •Polyuria, ARF • Cardiac • Bradycardia, prolonged PR, shortened QT, widen T, arrhythmia
- 45. Treatment • Forced diuresis •Saline 4-6 L over 24 hr • Urine output 150-200 ml/h • Volume re-expansion • Calciuresis • Loop diuretic • Calciuresis • may worsen dehydration • Those at risk of hypervolemia
- 46. Treatment • Pamidronate 60-90mg IV over 2-4 hr • Inhibits osteoclasts • Commence when diuresis is achieved • Calcitonin 2-8 U/kg SC or IM q6-12 hrly • Inhibits osteoclasts • Fast, safe but short • Severe symptomatic hypercalcemia before the onset of bisphosphonate
- 47. Treatment • Hydrocortisone 250-500mg q8 hrly • Inhibits osteoclasts • Helpful in MM, lymphoma, some breast cancers • No value in most solid tumours
- 48. Treatment • Hemodialysis canbe considered in those with severe symptomatic hypercalcemia who are unable to tolerate forced diuresis
- 49. Watch for: • Fluidstatus • Hemodynamic status • Metabolic status • Hypomagnesemia • Hypokalemia
- 50. Supportive Treatment • Avoiddrugs that may worsen hypercalcemia or those that are nephrotoxic • Decrease intestinal absorption by restricting dietary calcium intake or with the use of oral phosphate (1-3 g/day) • Ensure early mobilization
- 51.
- 52. ATLS • Rapid lysisof malignant • Release of intracellular products • Exceeds renal excretory capacity • Resulting in life-threatening metabolic derangements
- 53. Usual presentation • Usuallyduring 1st cycle chemotherapy • Anticipated event • Treatment is primarily PROPHYLACTIC
- 54. • Hyperkalemia (3.5-4.5mmol/L) • Hyperphosphatemia (0.8-1.45 mmol/L) • Hypocalcemia (2.12-2.65 mmol/L) • Hyperuricemia (M < 420; F < 360 umol/L) • Acute renal failure
- 55. Prophylaxis • Identify whois at risk • Hydration 3 L/m2/day • Don’t add potassium • Keep urine flow 150-200 ml/ hr • Alkalinization • 50-100 mEq Na(HCO3)2 • Keep urine pH 6.5 to 7 • Allopurinol 300 mg/day • Institute these measures 24-48 hr before chemotherapy for treatment of cancer at risk of ATLS
- 56. High risk: • Hematologicalcancers • Aggressive lymphomas • Acute leukemias • Chemosensitive solid cancers • Small cell lung cancer • Germ cell tumour
- 57. • Bulky disease •Abdominal disease • LDH >1500 U/L • Pre-existing volume depletion • Pre-existing renal dysfunction • Post-treatment ARF • Concentrated urine • Acidic urine
- 58. Treatment • Same measuresas those for prophylaxis • Correct electrolyte derangements but don’t try to correct the hypocalcemia • Urate oxidase (Rasburicase) • Coverts UA to highly soluble allantoins • Rapid onset of action • Very expensive • Hemodialysis
- 59.
- 60. Spinal cord compression •Overall frequency about 5% • 2nd most common cancer neurological complication • Definition broaden to include • Conus medullaris • Cauda equina • All can be caused by secondaries to the spine
- 61. Causes of SpinalCord Compression • Breast 29% • Lung 17% • Prostate 14% • Lymphoma 5% • Myeloma 4% • Renal 4%
- 62. Clinical Manifestations: • Pain •Most common initial symptom (90%) • Almost always antedate (days - months) • Local pain almost always present • by coughing, neck flexion or straight leg raising • when lying down (c.f. disc disease) • Radicular pain (nerve root)
- 63. • Weakness • Secondmost common symptom • Most evident with proximal LL • Can progress rapidly • Autonomic symptoms • Occurs late • Poor prognosis
- 64. • Classically, spasticparalysis with sensory level • But if in cord shock, can present with absent motor, sensory, reflex and autonomic function
- 65. Conus medullaris • Saddleanaesthesia (S3-5) • Early sphincter involvement (S4-5) • Impotent (S2-4) • Spares the lower limbs (spares S1)
- 66. Cauda equina • Radicularpain • Asymmetrical sensory loss • Asymmetrical flaccid paralysis • Relative autonomic sparing
- 67. Level involved • Thorax70% • Lumbosacral 20% • Cervical 10%
- 68. Extent • Single level(46%) • Multiple non-contiguous levels (28%) • Multiple contiguous levels in about (26%)
- 69. Imaging • Plain XRAY(+): 70-80% when either back pain or signs present • MRI is the modality of choice • CT myelography if MRI unavailable • Bone scan indicates the presence of spinal metastases but does not diagnose cord compression
- 70. Predictor of recovery •The most single most powerful predictor of treatment outcome is the pretreatment neurologic status Pre-treatment Recovery after RT Ambulatory 98% Paraparetic 60% Paraplegic 11%
- 71. Management • Pain control •Preserve spinal stability • Relieve cord edema • Relieve autonomic dysfunction • Confirm diagnosis • Surgical decompression/stabilization • Treat the bone mets
- 72. management • Mist morphine •Bedrest • Dexamethasone 8 mg q6 hrly • Bladder catherization • MRI spine • Refer spine team • Radiation therapy
- 73. Surgical indication: • Needhistology • Retropulsed bone fragment • Spinal instability • Previous RT or progression on RT • Single level • Rapid progression
- 74.
- 75. Cerebral metastases • Occursin 20-40% of cancer patients • Majority are from lung and breast • Majority are supratentorial (80%) • Majority are multiple (70%)
- 76. causes • Metabolic suchas hypoglycemia • Cerebrovascular • Infective • Nutritional • Paraneoplastic
- 77. Features that needsclose monitoring • Massive lesion • Haemorrhage • Extensive edema • Mass effect • Hydrocephalus • Posterior cranial fossa
- 78. management • Dexamethasone 8mg Q8 hourly • Restrict fluids • Anticonvulsant only if symptomatic • Refer neurosurgeon if worrisome features present
- 79.
- 80. Pain in acancer • Concepts of pain • Physical pain • Clinical pain • Total suffering
- 81. Physical pain • Itis an unpleasant sensory and emotional experience associated with actual or potential tissue damage
- 82. Pathophysio classification • Nociceptive •Soft tissue pain • Bone pain • Visceral pain • Neuropathic • Psychogenic
- 83. • Inadequate analgesiae.g. undertreated, poor compliance • Breakthrough pain • Disease progression • Acute complication e.g. tumour rupture, pathological fracture
- 84. • Opioid: mostpains • Steroid: inflammatory pains, raised ICP • NSAID: bone pains • Antispasmodic: colicky pains • Anticonvulsants: “shooting’’ pains • Antidepressants: “burning” pains • Anxiolytics: muscle pains
- 85. Analgesics • Opioid naïvestart 5 mg PO • Scheduled doses q4-6h strictly • Breakthrough doses 5 mg q2h prn • Increase dose by 25-50% • Caution in elderly, liver failure and renal failure
- 86. doses • IV Morphine10 mg (x 1) • TD Fentanyl 0.1 mg (x 100) • IV Pethidine 75 mg (x 0.13) • PO Methadone 20 mg (x 0.5) • PO Oxycodone 20 mg (x 0.5) • PO Morphine 30 mg (x 0.33) • PO Tramadol 120 mg (x 0.08) • PO Codeine 240 mg (x 0.04)
- 87. Titration of morphinedose • For controlling severe pain • i.v. morphine 1 mg • Every 1 min until pain relief or drowsy • Cumulative dose given = dose per 4h • Calculate dose needed for 24h and run as a continuous infusion
- 88. • Source: Google Medscape Harrison’s Oxford Old notesin Medical School http://crisbertcualteros.page.tl