1 / 77

Oncological Emergencies

Oncological Emergencies. Özlem Sönmez, MD Yeditepe University Hospital Department of Medical Oncology. Oncological Emergency.

kcurran
Download Presentation

Oncological Emergencies

An Image/Link below is provided (as is) to download presentation Download Policy: Content on the Website is provided to you AS IS for your information and personal use and may not be sold / licensed / shared on other websites without getting consent from its author. Content is provided to you AS IS for your information and personal use only. Download presentation by click this link. While downloading, if for some reason you are not able to download a presentation, the publisher may have deleted the file from their server. During download, if you can't get a presentation, the file might be deleted by the publisher.

E N D

Presentation Transcript

  1. Oncological Emergencies Özlem Sönmez, MD Yeditepe University Hospital Department of Medical Oncology

  2. Oncological Emergency Any acute potentially life threatening event which if not anticipated quickly and not treated effectively may rapidly result in permanent morbidity or the death of the patient.

  3. Metabolic Emergencies • Tumor lysis syndrome • Hypercalcemia • Hyponatremia: Syndrome of inappropriate ADH (SIADH) • Mechanical Emergencies(Organ invasion, distant metastases related) • Superior vena kava syndrome • Spinal cord compression • Brain metastasis • Febrile neutropenia

  4. TUMOR LYSIS SYNDROME

  5. Tumor Lysis Syndrome The rapid killing and lysis of neoplastic cells with the release of large quantities of intracellular products and ions may result in a life threatening metabolic derangements and acute renal failure. Intracellular space Extracellular space K+: 4 mEq/L Phosphate : 4 mEq/L K+: 140 mEq/L DNA RNA Phosphate: 75 mEq/L

  6. Tumor Lysis Syndrome • Hyperkalemia • Hyperphosphotemia • Hypocalcemia • Hyperuricemia Purines  Hypoxanthine  Xanthine Xanthine oxidase Uric acid

  7. Etiology • Mostlyassociated with cytotoxic chemotherapy andradiotherapy • Spontaneous tumor lysis syndrome on presentation : rare, reported particularly inpatients with Burkitt’s lymphoma • After surgical manipulationof large tumor masses. • After hormonal therapy

  8. Tumor Lysis Syndrome • Risk factors: • High grade tumors: high growth fraction, high cell turn-over • Large tumor mass • Chemo- and radiosensitive tumors • Most frequently seen in acute leukemia andhigh grade lymphoma • Rarely; • Small cell lung cancer • Breast cancer • Head and neck cancer • Medulloblastoma

  9. Clinical presentation TLS usually occurs in bulky disease treated with cytotoxic agents. • Progressive oliguria • Uremia • Fluid overload • Hypertension • CHF • Seizure • Cardiac arrythmia: related to acute hyperkalemia and hypocalcemia • Syncope • Sudden death

  10. Tumor Lysis Syndrome Hyperuricemia, Hyperphosphotemia Renal failure Hyperphosphotemia Neuromuscular symytoms, arrhytmia, sudden death HypocalcemiaCramp, tetany, convulsion, arrhytmia

  11. Prevention of TLS • Avoid using drugs that inhibit the tubular reabsorption of urate: Such as salicylates, radiographic contrastdye, ethambutol, probenecid and thiazidediuretic • Hydration: Individuals at risk should have pre-hydration 24-48 hours before therapy (min 3000 cc). • Alkalinization of urine: Ph> 7 NaHCO3 Acetozolomide • Oral Allopurinol (Xanthine oxidase inhibitor) 300-600mg daily should be initiated 48 hours before therapy. • Vigilant metabolic monitoring: q 3-4 hours lab test after institution of therapy.

  12. Hyperkalemia • Fatique • Neuromuscular abnormalities • Arrythmia • ECG: tall tented T wave, flat P wave,increase P-R interval and widening of QRS complex, sine-wave patern, asystole or ventricular arrythmia Potassium levels and ECG findings

  13. An Electrocardiographic Sine Wave in Hyperkalemia Petrov DB. N Engl J Med 2012;366:1824-1824.

  14. Treatment of hyperkalemia • Avoid drugs that cause hyperkalemia, NSAIDS, Beta blocker, ACE inhibitor, K+ sparing diuretic • IV 10 ml calcium gluconate 10% over 2 minutes (This provides cardioprotection) • IV 20 units soluble Insulin + 50ml of glucose 50% ( Insulin moves K+ into the cell) • Nebulized Salbutamol 2.5mg also moves K+ into the cell. • Dialysis

  15. Hyperphosphatemia (>4.5 mg/dl) • Treatment • Hydration: 2-4 lt/day • IV 20 units soluble Insulin + 50 ml of glucose 50% ( Insulin moves K+ into the cell) • Aliminium hydroxate 4x 30-60 ml • Dialysis

  16. Hyperuricemia • Precipitation in renal medulla, distal tubules • Treatment • Hydration • Alkalinization of urine pH 7-7,5 NaHCO3 Acetozolamide 250-500 mg • Dialysis

  17. Hypocalcemia • Treat only if tetany develops • Treatment Ca gluconate or Ca chloride

  18. HYPERCALCEMİA

  19. Hypercalcemia • Cancer is the 2nd most common cause of hypercalcemia after primary hyperparathyroidism. • Cancer associated hypercalcemia is due to an imbalance between bone resorption and calcium excretion. • Most common malignancy associated hypercalcemia include: • Non small cell lung cancer (squmous cell ) • Breast cancer • Renal cell cancer • Multiple myeloma and lymphoma • Head and Neck cancers

  20. Pathogenesis • Direct bone destruction • Humoral factors • PTH • PTH-related protein - squamous cell ca, renal cell ca • Prostoglandins(PGE) • Vit D (1-25 DHKK)-lymphoma • Cytokines IL-1, IL-6, EGF, TNF-B, TGF-, PDGF

  21. Tumors not associated with hypercalcemia • Small cell lung cancer • Prostate ca • Colorectal ca

  22. Clinical Presentation • General: Dehydration, weakness, fatigue. • CNS: Hyporeflexia, mental status changes, seizure, proximal neuropathy, coma. • GIS: Weight loss, nausea, vomiting, constipation, ileus, dyspepsia, pancreatitis. • Genitourinary: Polyuria • Cardiac: Bradycardia, short QT interval, wide T wave, Prolong PR interval, arrythmia, arrest.

  23. Laboratory Findings • Serum Ca, P, albumin • Serum alkalen phosphatase (HyperPTH, metas) • Electrolytes, BUN, Creatinine • ECG • Radiology • PTH, PTH-RP Corrected Ca (mg/dl): 0.8x [(4-Albumin)+Measured Ca]

  24. Treatment All patients with hypercalcemia of malignancyshould be actively treated. • Hydration with normal saline and diuretic: • 250-300 ml/hr 48-72 hours with adequate K+ • Furosemide: Forceful diuresis increase calcium excretion. • Biphosphonates: • IV Pamidronate or zolendronate is effective in 70-90%. • Maximum effectachieved within 72 hours after treatment.

  25. Treatment 3. Calcitonin and Corticosteroids: • Are used in combination, effective in lowering theserum calcium.They have rapid mode of action andno toxicity when used in short term. • Salmon calcitonin is given SC or IM at 4units/kg 12 hourly • Oral prednisolone: 40mg/day.

  26. Treatment • Mithramycin, 25 gr/kg • Gallium nitrate, 100-200 mg/m2 • PG inhibitors • Steroids • Dialysis

  27. Hyponatremia: Syndrome of inappropriate ADH (SIADH)

  28. ADH secretion • Increased osmolality Plasma osmolality: 2xNa+K+BUN/2.8+Glukoz/18 Normal: 280-290 mOsm/kg • Decreased plasma volume

  29. Inappropriate ADH secretion • Hypotonic plasma • Hyponatremia • Urine not maximally diluted

  30. Etiology • Tumor • Lung cancer (esp. Small cell) • Mesothelioma • CNS disease (mass, bleeding, infection) • Pulmonary infection (pnemonia, tbc, abcess) • Hyponatremic agents • Vincristine, cyclophosphamide • Chlorpropamide (sulfonylurea) • Carbamazepine • IV narcotics • Psychotropic agents: Amitriptilin, Thioridazine

  31. Diagnosis • Symptoms and Signs : • Lethargy, nausea, anorexia, fatigue, confusion, convulsion, coma • Laboratorary findings: • Serum electrolite, creatinin, BUN, Ca, P, glukoz, T. protein, TG • Urine Na • Chest X-ray • Urine and serum osmalality • If signs of Endocrine hypofunction: • TFT, Adrenal function tests, hypophysis function tests

  32. Diagnostic Criteria • Hyponatremia + inappropriately low BUN (<10 mg/dl) • No intravascular volume deficit Urine Na > 30 mEq/L • Absence of abnormal fluid retention • Normal renal function • Serum hypotonicity along with urine that is not maximally diluted • Serum osmo: <260 mOsm/kg • Urine osmo: >75-100 mOsm/kg (Urine SG >1003)

  33. Treatment • Severe hyponatremi (Na <110 mEq/L) • Lower plasma volume  prox. tubule Na absorp • IV %3 NaCl, 1 lt every 6-8 hours • Furosemide 40-80 mg, every 6-8 hr • Na correction must be <12 mEq/L/d (<2 mEq/4 hours) • Moderately severe hyponatremi (Na >110 mEq/L) • Fluid restriction • If Na <125: 500-750 cc/d • If Na >125: 1000 cc/d • Demeclocycline: 4x150-300 mg PO • Induces renal resistance to ADH • Major toxicity: Azotemia • Lithium

  34. SUPERIOR VENA CAVA OBSTRUCTION (SVCO)

  35. SVCO • Superior vena cava: • Drain head, neck, upperextremities and upper thorax • The superior vena cava is located in the middlemediastinum surrounded by trachea, (R)bronchus,aorta, pulmonary artery and perihilar andparatracheal lymph nodes. • Obstruction of SVC may be due to: • Extrinsiccompression • Direct invasion by disease process • Thrombosis. • >90% SVCO: Due to malignant process.

  36. Etiology • Malignancy • Lung cancer: 67-82% (small cell cancers) • Lymphomas: 5-15% • Thymomas • Germ cell tumor • Metastatic disease: 3-20% ( Breast cancer most common) • Benign Causes • Fibrous mediastinitis from granulomatous disease include histoplasmosis, tuberculosis, syphilis. • Thrombosis due to central line catheter • Behçet’s diseases

  37. Clinical presentation Usually incidious in onset. • Dyspnea • Facial swelling • Neck, chest and upper extremity edema • Facial and head fullness • Dizziness, Fatigue • Visual disturbance • Cough • Hoarseness of voice • Chest pain • Dysphagia • Neurological findings: (2-22%) • Due to increase intracranial pressure • Agitation, Confusion, Seizure

  38. Physical Findings • Venous distention in the neck and chest. • Facial edema, Plethora • Cyanosis • Arm and hand edema • Telangiectasis of chest and upper back • Tachypnea • Stridor • Papilloedema

  39. Diagnosis • The diagnosis is usually obvious clinically but atthe time of presentation less than 50% ofpatients have a known diagnosis of cancer. • The diagnostic approach should begin with leastinvasive procedure.

  40. Imaging study Chest Radiograph: • Usually abnormal in majority of cases. • Show mediastinal mass or widening. • Some have right hilar mass or pleural effusion. CT Scan thorax: • Further define the anatomy of intrathoracic structures and pathologic lesions. • Level of SVC obstruction. • Superimposed SVC thrombosis. • Collateral circulation. • Mediastinal adenopathy or masses. MRI

  41. Histological diagnosis • Sputum cytology • FNAC • Bronchoscopy • Thoracocentesis • Lymph node biopsy • Bone marrow biopsy • Mediastinoscopy

  42. Treatment • The aim of treatment is to relieve the symptomand to cure. Emergency measures: • Life threatening cerebral or laryngeal edema requireimmediate radiation therapy without a firm tissuediagnosis.

  43. General measures: • Bed rest with head elevated • Diuresis • Reduce sodium intake • Corticosteroid • Anticoagulant

  44. Specific measures: • Radiation therapy is the primary treatment. • Chemotherapy alone may be beneficial forchemosensitive tumors i.e, • SCLC (small cell lung cancer) • NHL • Germ cell tumors • Relief from signs and symptoms usually occurswithin 7-10 days. • Evidence of benefit within 24 hours in somecases.

More Related