Heme-Onc Emergencies Workshop Management of the Hospitalized Patient San Francisco, CA November 2013 J. Ben Davoren, MD, PhD Clinical Professor of Medicine, UCSF Division of Hematology/Oncology This session will be an interactive, cased-based discussion of the diagnosis and management of important hematologic or oncologic emergencies that the hospitalist may need to manage. We will work through the cases to cover the objectives for this discussion including: • Diagnosis and management of suspected spinal cord compression • Diagnosis and management of suspected brain metastasis • Management of hypercalcemia with or without renal failure • Management of febrile neutropenia • Differentiating causes of rapid onset thrombocytopenia • Identifying and managing clinical versus laboratory tumor lysis syndrome • Acute management of very high white blood cell counts Handouts with additional information and answers will be provided at the session. In addition, participants are encouraged to present their own diagnostic dilemmas and real life cases for discussion. Suggested Real-time Reference Sources: Internet Free: Emedicine.medscape.com (reference section) www.merckmedicus.com (includes Harrison’s online & Hospital Medicine online) Internet Cost: UpToDate (www.utdol.com) MDConsult (www.mdconsult.com) Mobile Device Applications (Free): Medscape (Diseases & Conditions) Clinical Care Options Oncology inPractice (Freter & Haddadin Oncologic Emergencies section)
CASES 1. A 56 year old man with established castrate-resistant prostate cancer presents with new motor weakness but intact bowel and bladder function. You are concerned about spinal cord compression. a. What evaluation is needed to make the diagnosis? b. While waiting for definitive therapy, what is the right empiric dose of dexamethasone to administer and on what schedule? 2. The same patient receives radiation therapy for suspected cord compression and clinically improves over the first two days, but then deteriorates. a. What else do you need to think about? b. Who else besides you needs to know? 3. A 51 year- old man with no past medical history presents with altered mental status, weight loss, pancytopenia, and baseline emergency room labs show a high calcium and low albumin. What is the first thing you need to do? a. 80 mg IV furosemide b. 2L Normal Saline c. IV pamidronate 30-90 mg d. IV/ SQ calcitonin e. IV Solumedrol f. Something else 4. A similar patient presents with a high calcium and renal insufficiency, a CrCl less than 30 ml/min. a. How does that limit your options in treating hypercalcemia? 5. A 77 year old woman with stable Chronic Lymphocytic Leukemia is admitted for dehydration, fatigue, and anemia. On hospital day 2, a differential reveals a neutrophil count of 400 cells/mm3 just as the nurse calls that the patient has a temperature of 100.8F a. What is the first thing you need to do? b. Does that change if she has a permanent indwelling catheter? c. Should you administer filgrastim (G-CSF) to stimulate neutrophils? 6. You have just received signout on a 51 year old female admitted with community- acquired pneumonia. She has yet to ‘turn the corner’ clinically. Before you see her, you get a stat page from the lab saying that her CBC shows a platelet count of 14,000/mm3. What do you want to know right now this minute? a. PT/PTT/fibrinogen to rule out DIC b. Yesterday’s platelet count to see how far it’s fallen c. Is the patient bleeding? d. Has this patient received heparin in any form in the last week? e. LDH to rule out TTP
7. If Heparin-Induced Thrombocytopenia (HIT) is the leading diagnosis in this patient, how long should she receive warfarin anticoagulation after the platelet count has normalized with a thrombin inhibitor? a. If no clot, stop; If clot, 3 months b. If no clot, 3-4 weeks; If clot, 3 months c. If no clot, 3-4 weeks; If clot, indefinite (at least 6 months) 8. If Thrombotic Thrombocytopenic Purpura (TTP) is the leading diagnosis in this patient, how soon should there be clinical improvement with plasma exchange (apheresis)? How long should plasma exchange be continued? 9. If Disseminated Intravascular Coagulation (DIC) is the leading diagnosis in this patient, when should heparin be considered in addition to supportive care? a. Once FFP, cryo and platelets given, give heparin to prevent further rise in PT/INR b. When there is definite evidence of thromboembolism c. When factor/platelet replacement are ongoing but DIC labs are still abnormal d. When factor/platelet replacement are ongoing, DIC labs are abnormal, but only if patient having clotting/bleeding 10. How would the possible diagnosis change if the patient were post-cardiac catheterization and had received antiplatelet therapy with a gpIIb/IIIa inhibitor? 11. A previously healthy 64 year old man is admitted with fatigue, confusion, SOB, and easy bruising for 5 days, associated with a WBC count of 128,000 cells/mm3, Hgb of 6.8 g/dL, platelets of 22,000/mm3, a plasma creatinine of 3.4 mg/dL, uric acid of 9 mg/dL and plasma potassium of 5.6 mmol/l, with a tentative diagnosis of Acute Myeloid Leukemia. What do you want to do first? a. Evaluate for DIC / Transfuse platelets b. Check tumor lysis labs and start allopurinol c. Give antibiotics for functional neutropenic fever & sepsis d. Call Renal to initiate dialysis for hyperkalemia e. Call IR for central catheter for leukapheresis f. Give chemotherapy to reduce WBC count 12. Medical Oncology decides to treat the patient above and begins fluids and allopurinol to prevent tumor lysis syndrome. a. What should you watch for while you are on duty and the oncologist is away at the race track? b. What is the role of empiric rasburicase to bring down the uric acid level and what are the risks of using it?
Selected references: Corticosteroid dose in spinal cord compression http://www.ncbi.nlm.nih.gov/pubmed/18420159 Lancet Neurol. 2008 May;7(5):459-66. doi: 10.1016/S1474-4422(08)70089-9. Metastatic epidural spinal cord compression. Cole JS, Patchell RA. Abstract Metastatic epidural spinal cord compression (MESCC) occurs when cancer metastasises to the spine or epidural space and causes secondary compression of the spinal cord. MESCC is a common complication of malignancy that affects almost 5% of patients with cancer. The most common symptom is back pain. MESCC is a medical emergency that needs rapid diagnosis and treatment if permanent paralysis is to be prevented: the diagnosis of MESCC is best made with MRI; and corticosteroids, radiation therapy, and surgery are all established treatments. Future research will focus on prevention, improving detection, and the development of new treatments. PMID: 18420159 Hypercalcemia and pamidronate in renal insufficiency http://www.abstracts2view.com/endo/view.php?nu=ENDO12L_SAT-366 [SAT-366] Safety of Intravenous Pamidronate for Bone Hyperresorption in Patients with Chronic Critical Illness (CCI) and Chronic Kidney Disease (CKD) Rifka C Schulman, Chenbo Zhu, James H Godbold, Jeffrey I Mechanick. Objective: Chronic critical illness (CCI) occurs in survivors of acute critical illness remaining ventilator- dependent via tracheostomy. Pamidronate reduces bone hyperresorption in patients with CCI (1), but its use has been limited due to concerns about nephrotoxicity. The purpose of this study is to determine the safety of intravenous (IV) pamidronate on renal function in patients with CCI and CKD. Methods: A retrospective case series of patients admitted to The Mount Sinai Hospital Respiratory Care Unit from 2006-2010, identified patients who received IV pamidronate, administered for 24 hour urine N- telopeptide (NTx) ≥ 70 nmol BCE/mmol Cr or serum NTx > 40 nMBCE/L. Pamidronate 30 -90mg was infused intravenously over 4 hours. Patients in both groups received calcium carbonate, ergocalciferol and calcitriol. Changes in glomerular filtration rate (GFR), estimated by the MDRD formula, and creatinine were tabulated for 4 CKD groups for those who did (N=115) and did not (N=200) receive pamidronate, respectively: no or mild CKD up to stage 2 (N=83, N=121), stage 3 CKD (N=13, N=28), stage 4 (N=3, N=30), and stage 5 on hemodialysis (N=16, N=21). Results: None of the pamidronate groups or doses showed significant reductions in GFR ≥ 25% immediately after, or at 7 or 14 days post-infusion. Median changes in GFR from baseline to 7 days per CKD group were 0% (P<0.0001), -4% (P=0.29), -4% (P=1) and -9% (P=0.02) after pamidronate, and 0%, 0%, 6% and 6%, in the control groups (P<0.05), respectivel y. Patients with increases in creatinine ≥ 0.5 or ≥ 1.0 mg/dl (for baseline creatinine < or ≥ 1.4 mg/dl, respectively) were 0%, 4.4%, 6.7% and 18.2%, in the pamidronate groups, and 0.8%, 2.4%, 8.8%, and 20.8%, in the control groups, respectively. Differences in creatinine change between the groups did not reach statistical significance (P=0.17, 0.06, 0.39, 0.78, respectively). Discussion: IV pamidronate was not associated with significant worsening of renal function, irrespective of CKD stage. Small fluctuations in renal function in this cohort of patients with multiple comorbidities were not noted to be significant in the pamidronate group compared to the general CCI population. Conclusion: Pamidronate was not associated with short-term nephrotoxicity in patients with CCI, with or without CKD. It is hoped that these results will remove barriers to more aggressive management of metabolic bone disease in CCI, which may have salutary downstream effects on morbidity and mortality.
Recommend
More recommend
