ABSTRACT
During the COVID-19 pandemic, many patients are hospitalized, and those suffering from in-hospital cardiac arrest (IHCA) have been previously reported to have poor outcomes. This is a single-center, retrospective, observational study conducted at the Veterans Affairs Medical Center, Washington, DC, USA. The inclusion criteria were: patients admitted to the hospital with a diagnosis of COVID-19 who underwent cardiopulmonary resuscitation (CPR) for IHCA. Patients were labeled as COVID-19 positive based on a laboratory-confirmed positive polymerase chain reaction test. Patients with do-not-resuscitate (DNR) orders, those who were made comfort care, or enrolled in hospice were excluded. The study was approved by the hospital's institutional review board. A total of 155 patients with COVID-19 infection were admitted; 145/155 (93.5%) admitted to the medical floor and 10/155 (6.5%) to the medical intensive care unit (MICU). 36/145 (24.8%) floor patients were upgraded to MICU. Of the 46 patients treated in MICU, 17/46 (36.9%) were excluded for DNR status. From the remaining 29/46 (63.1%) patients, 19/29 (65.5%) patients survived, and 10/29 (34.5%) patients had IHCA. All 10/10 (100%) died after CPR without return of spontaneous circulation (ROSC). The initial rhythm was non-shockable in all patients, with pulseless electrical activity (PEA) in 7/10 (70%) and asystole in 3/10 (30%) patients. Patients with COVID-19 infection who had an IHCA and underwent CPR had a 0% survival at our hospital. Discussions on advanced care options, especially CPR, with COVID-19 patients and their families, are important as the overall prognosis after CPR for IHCA is poor.
ABSTRACT
The novel SARS-CoV-2 virus (severe acute respiratory syndrome coronavirus 2) is now known to cause acute respiratory distress, cytokine storm, and coagulopathy. Multiple other manifestations have been published in recent literature. Rhabdomyolysis is a syndrome of muscle damage, with release of intracellular contents into circulation. It is characterized by marked elevations of creatinine kinase levels and myoglobinuria. In this article, we describe a series of 5 cases who were admitted with COVID-19 pneumonia and had severe muscle injury, as demonstrated by significant elevation (>5 times upper limit of normal) of creatinine kinase levels likely secondary to SARS-CoV-2 virus. The median age for these patients was 65 years, and most of them suffered from diabetes and hyperlipidemia. All patients were hypertensive males. Four out of 5 patients had preserved kidney function at baseline and were chronic kidney disease (CKD) stage 2 or better. However, most of them suffered significant kidney injury and at the time of discharge one patient was CKD stage 2 or better, 2 were CKD stage 3 or worse, and 2 patients had renal failure and died due to complications of SARS-CoV-2 infection.
Subject(s)
COVID-19/complications , Rhabdomyolysis/virology , Aged , COVID-19/therapy , Creatine Kinase/blood , Diabetes Mellitus, Type 2/complications , Hospitalization , Humans , Hypertension/complications , Male , Middle Aged , Renal Insufficiency, Chronic/complications , Renal Insufficiency, Chronic/physiopathology , Rhabdomyolysis/blood , SARS-CoV-2ABSTRACT
Context. Anaplastic thyroid cancer (ATC) is an aggressive tumor with a median survival of 3 to 9 months, a 1-year survival of less than 10% and without definitive therapies. Recently, in BRAF V600E mutated ATCs, new targeted therapy using a combination of a BRAF inhibitor, dabrafenib (Dab), with a mitogen-activated extracellular protein kinase (MEK) inhibitor, trametinib (Tram), has shown significant promise. Case Description. We report a case of aggressive ATC with 5 sequence mutations: BRAF V600E (mutation fraction [MF] 34%), TERT E441del (MF 37%), RET N579K (MF 55%), EZH2 D154E (MF 60%), and CDK4 S259L (MF 48%). The patient had a dramatic response to the Dab/Tram combination with near complete resolution of his lung, bone, hepatic, and splenic lesions soon after starting therapy. Unfortunately, intolerable side effects (grade 2-3) on this regimen required tapering and discontinuation of the treatment. He had a quick resurgence of disease after stopping the combination therapy. The patient died approximately 3 months after discontinuing Dab/Tram. Autopsy revealed an atrophic thyroid gland with microscopic subcapsular focus of well-differentiated papillary thyroid carcinoma. There was extensive lymphatic spread of the tumor throughout bilateral lungs with fibrosis. No other metastatic site was identified. Conclusion. We report a unique case of ATC with 2 new mutations of EZH2 D154E and CDK S529L. This case exemplifies the significant promise Dab/Tram therapy holds, the potential side effects that limit their use, and autopsy findings status post use of this combination therapy.
Subject(s)
CDC2 Protein Kinase/genetics , Enhancer of Zeste Homolog 2 Protein/genetics , Molecular Targeted Therapy , Proto-Oncogene Proteins B-raf/genetics , Thyroid Carcinoma, Anaplastic/genetics , Thyroid Neoplasms/genetics , Aged , Autopsy , CDC2 Protein Kinase/antagonists & inhibitors , Enhancer of Zeste Homolog 2 Protein/antagonists & inhibitors , Fatal Outcome , Humans , Imidazoles , Male , Mutation , Oximes , Positron Emission Tomography Computed Tomography , Protein Kinase Inhibitors/therapeutic use , Proto-Oncogene Proteins B-raf/antagonists & inhibitors , Pyridones , Pyrimidinones , Thyroid Carcinoma, Anaplastic/drug therapy , Thyroid Neoplasms/drug therapyABSTRACT
In this study we investigate the diagnostic value of pleural fluid procalcitonin (PCT) in distinguishing infectious and noninfectious etiologies of pleural effusion. We reviewed the medical records of 75 hospitalized patients who underwent thoracentesis between 2011 and 2012. Data on pleural fluid lactate dehydrogenase (LDH), protein, albumin, cell count and differential, pH, Gram stain and culture, cytology, triglyceride, cholesterol, amylase, and PCT were collected. Data on serum LDH, protein, albumin, prothrombin time, normalized, and blood culture were also collected. Pleural effusions were classified into 2 groups, infectious and noninfectious. There were 18 infectious pleural effusions (IPE) and 57 noninfectious pleural effusions (NIPE). Median pleural fluid PCT was 1.088 ng/mL (0.312-2.940 ng/mL) in IPE and 0.123 ng/mL (0.05-0.263 ng/mL) in NIPE, with a P value < 0.0001. Pleural fluid PCT > 0.25 ng/mL had a sensitivity of 77.78% and specificity of 74.14% for diagnosing an IPE. A subgroup analysis of PCT in exudative infectious effusions versus exudative noninfectious malignant/paramalignant effusions showed higher levels in the former. PCT is a novel biomarker for diagnosing infectious pleural effusion, and it would be worthwhile to investigate the role of pleural PCT in assessing severity of illness, risk stratification, and antibiotic stewardship in hospitalized patients with pleural effusions. Journal of Hospital Medicine 2016;11:363-365. 2016 Society of Hospital Medicine.