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A National Survey of Burnout and Depression Among Fellows Training in Pulmonary and Critical Care Medicine: A Special Report by the Association of Pulmonary and Critical Care Medicine Program Directors

Sharp, Michelle; Burkart, Kristin M; Adelman, Mark H; Ashton, Rendell W; Daugherty Biddison, Lee; Bosslet, Gabriel T; Doyle, Stephen T; Eckmann, Thomas; Khurram S Khan, Malik M; Lenz, Peter H; McCallister, Jennifer W; O'Toole, Jacqueline; Rand, Cynthia S; Riekert, Kristin A; Soffler, Morgan I; Winter, Gretchen R; Zaeh, Sandra; Eakin, Michelle N
BACKGROUND:The prevalence of burnout and depressive symptoms is high among physician trainees. RESEARCH QUESTION/OBJECTIVE:What is the burden of burnout and depressive symptoms among fellows training in pulmonary and critical care medicine (PCCM) and what are associated individual fellow, program, and institutional characteristics? STUDY DESIGN AND METHODS/METHODS:We conducted a cross-sectional electronic survey of fellows enrolled in pulmonary, PCCM, and critical care medicine training programs in the United States to assess burnout and depressive symptoms. Burnout symptoms were measured using the Maslach Burnout Index two-item measure. The two-item Primary Care Evaluation of Mental Disorders Procedure was used to screen for depressive symptoms. For each of the two outcomes (burnout and depressive symptoms), we constructed three multivariate logistic regression models to assess individual fellow characteristics, program structure, and institutional polices associated with either burnout or depressive symptoms. RESULTS:Five hundred two of the 976 fellows who received the survey completed it-including both outcome measures-giving a response rate of 51%. Fifty percent of fellows showed positive results for either burnout or depressive symptoms, with 41% showing positive results for depressive symptoms, 32% showing positive results for burnout, and 23% showing positive results for both. Reporting a coverage system in the case of personal illness or emergency (adjusted OR [aOR], 0.44; 95% CI, 0.26-0.73) and access to mental health services (aOR, 0.14; 95% CI, 0.04-0.47) were associated with lower odds of burnout. Financial concern was associated with higher odds of depressive symptoms (aOR, 1.13; 95% CI, 1.05-1.22). Working more than 70 hours in an average clinical week and the burdens of electronic health record (EHR) documentation were associated with a higher odds of both burnout and depressive symptoms. INTERPRETATION/CONCLUSIONS:Given the high prevalence of burnout and depressive symptoms among fellows training in PCCM, an urgent need exists to identify solutions that address this public health crisis. Strategies such as providing an easily accessible coverage system, access to mental health resources, reducing EHR burden, addressing work hours, and addressing financial concerns among trainees may help to reduce burnout or depressive symptoms and should be studied further by the graduate medical education community.
PMID: 32956717
ISSN: 1931-3543
CID: 4770662

Management of nontuberculous mycobacterial pulmonary disease

Adelman, Mark H; Addrizzo-Harris, Doreen J
PURPOSE OF REVIEW/OBJECTIVE:To highlight recent original research and specialty society guidelines regarding the diagnosis and treatment of nontuberculous mycobacterial (NTM) pulmonary disease. RECENT FINDINGS/RESULTS:The prevalence of NTM pulmonary disease has risen in recent years. The prevalence of individual NTM species varies geographically, although Mycobacterium avium complex (MAC) and Mycobacterium abscessus complex (MABC) remain among the most commonly encountered in many regions. Diagnosis and treatment of NTM pulmonary disease can be complex but guideline-based recommendations have been published. However, adherence to guideline recommendations is poor. Drug susceptibility testing plays a role with important caveats for treatment. Alternative therapies are being explored with older antimycobacterial drugs like clofazimine, which has demonstrated efficacy and tolerability for treatment-refractory NTM infections, and a novel formulation of amikacin for inhalation which may be better tolerated than parenteral administration. Several studies have shown that patients will have recurrences as high as 48%, and that these are not solely relapses but many cases are reinfections with a new organism. United States and European research registries of patients with non-cystic fibrosis bronchiectasis are expected to provide needed data on clinical characteristics of patients at risk for NTM pulmonary disease. SUMMARY/CONCLUSIONS:The evidence base for optimal management of NTM pulmonary disease is expanding but notable gaps in the literature remain.
PMID: 29470253
ISSN: 1531-6971
CID: 2963842

Severe thrombocytopenia induced by vancomycin-dependent anti-platelet antibodies [Meeting Abstract]

Swanenberg, I; Bhalla, S; Altshuler, D; Adelman, M; Colon, L; Sloane, M
INTRODUCTION: Vancomycin has been implicated uncommonly in the development of immune-mediated thrombocytopenia. We present the case of a patient who developed severe thrombocytopenia after receiving vancomycin that was refractory to several therapies. CASE PRESENTATION: A 69-year-old woman with metastatic breast cancer, atrial fibrillation (on coumadin) and CKD stage III was admitted after a fall. She was treated for pneumonia with ceftriaxone and azithromycin. On hospital day 2, the patient became encephalopathic, hypotensive and required endotracheal intubation for hypercapneic respiratory failure. Antibiotics were broadened to vancomycin and piperacillin/tazobactam. On hospital day 3, the platelet count abruptly dropped from 168x103/mL to 1x103/mL with initially stable hemoglobin and WBC count. Labs and peripheral smear did not suggest a microangiopathic hemolytic process or worsening coagulopathy. The patient developed small-volume hemoptysis and extensive ecchymoses. Druginduced thrombocytopenia was suspected and vancomycin was discontinued. Notably, the patient was not exposed to any heparin products as her INR was therapeutic. She received prothrombin complex concentrate and plasma to reverse her coagulopathy, along with a total of 8 units of platelets and 2 units of pRBCs. Intravenous immunoglobulin was given but the platelet count never recovered. The patient developed worsening hypoxic respiratory failure and died in hospice on hospital day 7. Labs subsequently confirmed the presence of vancomycin-dependent anti-platelet IgM and IgG antibodies. DISCUSSION: Thrombocytopenia induced by vancomycin exposure is thought to be due to the synthesis of IgG and IgM antibodies that interact with the glycoprotein IIb/IIIa receptor on the platelet surface in a vancomycin dependent manner, with subsequent platelet activation and destruction. Thrombocytopenia typically occurs after several days of exposure to vancomycin but platelet counts can drop precipitously in patients who have been previously exposed. We suspect this patient had prior vancomycin exposure given the rapid drop in platelet count. The degree of thrombocytopenia induced by vancomycin can be very severe and platelet transfusion is often ineffective. Cessation of vancomycin is essential, which results in normalization of the platelet count in most patients. Intravenous immunoglobulin and plasmapheresis have been used to neutralize or remove the vancomycin-dependent antibodies. Delayed clearance of vancomycin from renal failure can delay the recovery of platelet counts, which was likely a factor for our patient. CONCLUSIONS: Our case highlights drug-induced thrombocytopenia as a rare but life-threatening complication of vancomycin administration. Immediate discontinuation of vancomycin is paramount; however, platelet destruction may be so rapid and refractory to treatment that clinical consequences can be dire
ISSN: 1931-3543
CID: 2860192

Diffuse Alveolar Hemorrhage Due to K2 Inhalation [Meeting Abstract]

Adelman, Mark; Thorp, Michael; Smith, Robert
ISSN: 0012-3692
CID: 2572132

Rapidly progressive disseminated MSSA: Septic emboli causing quadriplegia [Meeting Abstract]

Sternschein, R; Adelman, MH; Mahmoudi, M; Chitkara, N
INTRODUCTION: We present a case of disseminated MSSA infection causing devastating ischemic sequelae of septic emboli. CASE PRESENTATION: The patient is a 66 year-old man presenting to the ER after he fell off his couch and could not get up. He had chronic back pain and weakness and swelling of both legs. His medical history included recent dental work, acupuncture for shoulder pain, and ORIF for bilateral wrist fractures. On presentation, he was febrile, tachycardic, tachypneic, and hypoxemic, with 4/5 muscle strength throughout. Chest X-ray showed lower lobe infiltrates. Urinalysis suggested infection. He was given broad-spectrum antibiotics and IV fluids. He was transferred to the medical ICU for hypotension. His weakness rapidly progressed to quadriplegia, with shallow, labored breathing. He was intubated for hypoxemic respiratory failure and septic shock requiring vasopressors. CT imaging of the head, cervical and thoracic spine was negative. Lumbar puncture retrieved purulent CSF with a neutrophilic pleocytosis and gram-positive cocci. Dexamethasone was added for bacterial meningitis. A cervical spine MRI showed C3-C7 cord signal abnormality of the central gray matter, concerning for spinal cord infarction. MSSA grew from blood, urine and CSF cultures. Antibiotics were narrowed to nafcillin. A chest CT showed peripheral septic emboli in the lungs. A transthoracic echocardiogram showed large, shaggy aortic and tricuspid valve vegetations. The patient developed massive upper GI bleeding. Endoscopy revealed diffuse ischemic ulcerations, requiring radiologically-guided embolization for hemostasis. His mental status remained depressed; he intermittently answered questions by blinking. He did not regain any neurologic function. He developed progressive multiorgan system failure. After discussion with his family, in keeping with his known wishes in the case of a terminal condition, the patient was palliatively extubated and expired soon thereafter. DISCUSSION: Our patient represents an uncommon case of widely disseminated MSSA infection due to infective endocarditis of the tricuspid and aortic valves. The sequelae included a descending UTI, septic emboli to the lungs, and septic emboli causing ischemic ulceration of the duodenal mucosa, vertebral artery occlusion, and cervical spinal cord infarction resulting in quadriplegia. The patient's MSSA infection was likely due to bacteremia resulting from acupuncture treatments for shoulder pain. He was hyperglycemic on admission, his HbA1c was 6.7%. Impaired glucose tolerance or uncontrolled undiagnosed diabetes mellitus likely predisposed the patient to dissemination of MSSA infection. CONCLUSIONS: This case illustrates rapidly progressive MSSA infective endocarditis, with ischemic injury from septic emboli contributing to multiorgan system failure and devastating neurologic injury
ISSN: 0012-3692
CID: 1476492


Adelman, Mark H; Iturrate, Eduardo
ISSN: 1525-1497
CID: 1268422