RESUMO
We present a patient who presented with diabetic ketoacidosis and severe rhabdomyolysis-induced acute kidney injury. The patient developed generalized edema, nausea, and vomiting, and his kidney function deteriorated, necessitating renal replacement therapy, despite the successful treatment of his initial conditions. A comprehensive evaluation was conducted to determine the underlying cause of the severe rhabdomyolysis, including autoimmune myopathies, viral infections, and metabolic disorders. A muscle biopsy revealed necrosis and myophagocytosis but no significant inflammation or myositis. The patient's clinical and laboratory results improved with appropriate treatment, including temporary dialysis and erythropoietin therapy, and he was discharged to continue his rehabilitation with home health care.
RESUMO
Surgical left atrial appendage occlusion (LAAO) is being used increasingly in the setting of atrial fibrillation but has been associated with procedural complications. This systematic review and meta-analysis compared the outcomes of surgical LAAO with those of no LAAO and the use of direct oral anticoagulants (DOACs) and vitamin K antagonists (VKAs) using the PRISMA guidelines. A literature search was undertaken for relevant studies published between January 1, 2003, and August 15, 2021. Primary clinical outcomes were all-cause mortality, embolic events, and stroke. Secondary clinical outcomes included major adverse cardiac events (MACE), postoperative atrial fibrillation, postoperative complications, reoperation for bleeding, and major bleeding. There was a statistically significant 34% reduction in incidence of embolic events (odds ratio [OR] 0.66, 95% confidence interval [CI] 0.57-0.77, p < 0.001) and a significant 42% reduction in risk of MACE (OR 0.58, 95% CI 0.38-0.88, p = 0.01) in patients who underwent LAAO.Surgical LAAO has the potential to reduce embolic events and MACE in patients undergoing cardiac surgery for atrial fibrillation. However, complete replacement of DOACs and warfarin therapy with surgical LAAO is unlikely despite its non-inferiority in terms of minimizing all-cause mortality, embolic events, MACE, major bleeding, and stroke in patients on oral anticoagulation therapies.
RESUMO
Since the beginning of the coronavirus disease 2019 (COVID-19) pandemic, many cases of arrhythmias have been reported in patients with COVID-19 infection. We present the case of a 66-year-old female with no known cardiovascular history who presented with worsening shortness of breath and productive cough and tested positive for COVID-19 infection in the ED. The patient had a recent hospitalization for COVID-19 infection during which she was treated with dexamethasone and remdesivir therapy and her course remained uncomplicated at that time. Following this, she developed worsening shortness of breath at home for which she presented to the ED. During this hospitalization, she was treated with dexamethasone, remdesivir, and supplemental oxygen. On day six of hospitalization, the patient became tachycardic and had palpitations. Cardiac monitor and EKG showed evidence of new-onset atrial fibrillation (NOAF). Initially patient received metoprolol and diltiazem, both of which failed to achieve adequate rate control. Following this, the patient was started on carvedilol 30 mg every six hours, which attained good rate control. Her CHA2DS2-VASc (congestive heart failure, hypertension, age ≥75 (doubled), diabetes, stroke (doubled), vascular disease, age 65 to 74, and sex category) score was 4 for which she was started on apixaban 5mg twice daily. The patient was discharged on the same medications. Despite increasing reported incidences of NOAF in COVID-19 infection, only little is known about the optimal management strategies and possible etiopathology. The aim of our review is to highlight the possible mechanisms triggering atrial fibrillation in COVID-19 infection and go over the management strategies while reviewing the available literature.
RESUMO
Ischemic colitis is one of the most common ischemic pathologies of the gastrointestinal system and can be divided into non-gangrenous and gangrenous forms. The pathophysiology involves restricted blood supply to the colonic mucosa. Several risk factors have been implicated in the development of ischemic colitis. Lactulose, one of the mainstay therapies for the treatment of hepatic encephalopathy in patients with cirrhosis, has been rarely reported as a cause of ischemic colitis. To the best of our knowledge, there has been only one case report associating lactulose use with the development of ischemic colitis. The exact pathophysiology is unknown but might be associated with the fermentation of lactulose by intestinal bacteria, causing gaseous distention and increasing the intraluminal pressure. We present the case of a 77-year-old African American male, a known case of non-alcoholic liver cirrhosis with portal hypertension and esophageal varices, brought in by his family to the emergency department for altered mental status, non-bilious vomiting, abdominal distension, and pain for one day. On physical examination, the patient had upper extremity asterixis and was alert but disoriented to place and person. Diagnostic paracentesis was performed, which revealed leukocytosis, predominantly neutrophils. The patient was admitted for spontaneous bacterial peritonitis and hepatic encephalopathy with decompensated liver cirrhosis. The patient was started lactulose with a goal of three to four bowel movements per day. Despite adequate treatment, the patient continued to develop worsening mental function and abdominal distension. This was later followed by a bloody bowel movement. Laboratory assessment showed an elevated white blood cell count, worsening kidney function, and high anion gap metabolic acidosis. CT scan revealed dilated loops of bowel with air and fluid along with submucosal wall edema, findings suggestive of ischemic colitis. Given the poor prognosis and the patient's condition, colonoscopy was deferred. Lactulose was discontinued, as it was thought to be a contributing cause of the patient's ischemic colitis. His condition continued to deteriorate, and he passed away on Day 18 of admission.
RESUMO
Stent thrombosis (ST) is a frequently reported complication in cardiac patients with percutaneous coronary intervention (PCI) that adversely impacts their prognostic outcomes. Medical literature reveals several baseline characteristics of PCI patients that may predict their predisposition to ST and its potential complications. Our systematic review and meta-analysis aimed to determine the diagnostic significance of these baseline parameters in terms of determining the risk of ST among adult patients with PCI. We statistically evaluated 18 baseline characteristics of more than 15,500 PCI patients to delineate their stent thrombosis attribution. We included a number of articles focusing on baseline parameters in-stent thrombosis-related PCI scenarios. We explored the articles of interest based on inclusion/exclusion parameters across PubMed, JSTOR, Cochrane library, Google Scholar, and Embase. Medical subject headings (MeSH) words included "stent thrombosis," "percutaneous coronary intervention," and "coronary stenting." We extracted the research articles published between 2005 and 2021 on April 20, 2021. The included studies also focused on procedures and clinical factors concerning their association with PCI-related ST. Our findings ruled out the progression of abnormal left ventricular ejection fraction (LVEF)-related stent thrombosis in PCI patients (odds ratio {OR}: 9.68, 95% CI: 1.88-49.90, p=0.007). We found an insignificant clinical correlation between stent thrombosis and PCI in the setting of acute coronary syndrome (ACS). Our study outcomes further revealed the absence of stent thrombosis in PCI patients with antiplatelet prescription (OR: 32.42, 95% CI: 21.28-49.39). The findings affirmed the absence of ST in PCI patients receiving aspirin therapy (OR: 32.77, 95% CI: 18.73-57.34; OR: 4.59, 95% CI: 1.97-10.73). The majority of the included studies negated the clinical correlation of stent thrombosis with diabetes mellitus in the setting of PCI (OR: 0.49, 95% CI: 0.06-3.78). Our study did not reveal statistically significant results based on stent thrombosis in PCI patients with drug-eluting stents (OR: 2.91, 95% CI: 0.35-24.49). The findings also did not reveal the impact of cardiac biomarker elevation on stent thrombosis in PCI patients (OR: 8.42, 95% CI: 2.54-27.98, p=0.0005). Eight studies revealed a statistically insignificant correlation between myocardial infarction and stent thrombosis in PCI scenarios (OR: 2.69, 95% CI: 0.89-8.11, p=0.08). The clinical correlation between PCI and stent thrombosis/major bleeding in the setting of hypertension also proved statistically insignificant at 0.67 (OR: 1.31, 95% CI: 0.38-4.51, p=0.97). The study findings did not correlate mean body mass index and multivessel coronary artery disease with ST in PCI scenarios (OR: 1.98, 95% CI: 0.02-239.58, p=0.78; OR: 1.09, 95% CI: 0.58-2.04, p=0.80). Only two studies revealed statistically significant results confirming stent thrombosis in PCI patients with a prior history of PCI (OR: 0.49, 95% CI: 0.23-1.06; OR: 0.33, 95% CI: 0.02-5.59; p=0.03). Our findings question the clinical significance of baseline characteristics in terms of predicting stent thrombosis in PCI patients. The results support the requirement of future studies to investigate complex interactions between procedural, medicinal, genetic, and patient-related factors contributing to the development of stent thrombosis in PCI patients.
RESUMO
Small cell lung cancer (SCLC) accounts for less than 15% of the cases of lung cancer. Epidermal growth factor receptor (EGFR) mutations are rarely reported in association with SCLC. EGFR tyrosine kinase inhibitors (TKI) are approved as the first-line therapy for metastatic non-small cell lung cancer (NSCLC). The clinical effect of EGFR mutations and its response to osimertinib are unknown in SCLC. We report a case of EGFR-positive metastatic SCLC in a 63-year-old female who was treated with the third-generation TKI, osimertinib.
RESUMO
Marginal zone lymphoma (MZL) is a relatively uncommon subtype of non-Hodgkin lymphoma consisting of extranodal, nodal, and splenic MZL. Mucosa-associated lymphoma constitutes the majority of extranodal MZL including but not limited to the stomach, lung, salivary gland, ocular adnexa, skin, and thyroid. Depending on the site of origin, maltoma may present with different symptoms. Here we present a patient who presented to the pulmonary clinic for further evaluation of a right middle lobe consolidation. She was treated with a course of antibiotics empirically with no interval change in imaging. She underwent bronchoscopy with biopsy. Pathology was remarkable for extensive lymphoid infiltrates consisting of mixed B and T lymphocytes. Positron emission tomography (PET) CT demonstrated mild uniform uptake in consolidation with no evidence of PET avid distant metastasis. CT-guided biopsy was consistent with extranodal marginal zone lymphoma. She underwent right middle lobectomy with no complications. As mentioned in our case, bronchoscopy is usually nondiagnostic and a lung biopsy is needed in pulmonary maltoma. Treatment is based on the tumor location and extent of the disease. Prognosis is good with an 86-95% five-year survival.
RESUMO
Macrophage activation syndrome (MAS) is a subset of hemophagocytic lymphohistiocytosis (HLH) described in patients with rheumatological disorders. Some triggers of MAS and HLH include infection, malignancy, rheumatological disease, HIV, and rarely medications such as immunosuppressants. In recent medical literature, biologic agents are increasingly recognized as a potential trigger, but the mechanism behind this remains poorly understood. We describe the case of a patient who developed MAS after initiating adalimumab and propose a potential pathophysiological link between biologics and this syndrome.
RESUMO
Diabetic ketoacidosis is typically associated with type I diabetes mellitus, but it can be associated with type II diabetes mellitus under the conditions of extreme stress or as a presenting manifestation of ketosis-prone type II diabetes mellitus. A 38-year-old prediabetic male presented to the emergency room with hyperglycemia six weeks after recovery from coronavirus disease 2019 (COVID-19) pneumonia. Laboratory results showed severe hyperglycemia, metabolic acidosis, positive ketones in urine and blood, and elevated fasting C- peptide level. COVID-19 polymerase chain reaction (PCR) was negative, and immunoglobulin G (IgG) antibodies were positive. The workup was completely unremarkable for acute infection. Hemoglobin A1C increased from 6.1% to 10.8% within six weeks. The mechanism by which COVID-19 infection may trigger the onset of full-blown diabetes mellitus remains unknown. Viral infection may cause the direct destruction of pancreatic beta cells or trigger the changes in the body that induce the state of insulin resistance. Antibodies against severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection may cross-react or interfere with the functioning of endogenous insulin. The association between type II diabetes and COVID-19 infections needs additional investigations to ascertain the exact mechanism by which COVID-19 infection triggers the onset of full-blown diabetes mellitus.