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As COVID-19 continues to cause an increasing number of deaths worldwide, it is important that providers stay abreast with new research related to the pathophysiology of COVID-19 disease presentation states and clinical management. It is now well recognized that COVID-19 affects extrapulmonary organs, particularly the cardiovascular system. For example, cardiogenic shock has been increasingly observed in patients with COVID-19, owing to the various mechanisms involved and the affinity of the SARS-CoV-2 virus to cells comprising the cardiovascular system. In this review, we have briefly discussed the link between the cardiovascular system and COVID-19 infection, focusing on underlying mechanisms including but not limited to cytokine storm, direct virus-induced myocarditis, and ST-elevation myocardial infarction leading to cardiogenic shock. We have highlighted the cardiovascular risk factors associated with disease prognostication in COVID-19 patients. We have also briefly discussed vasopressors and inotropes used for treating shock and presented their mechanism of action, contraindications, and side effects in the hopes of providing a quick reference to help the provider optimize management of COVID-19 patients presenting with cardiovascular complications such as shock.
Assuntos
COVID-19 , Doenças Cardiovasculares , Sistema Cardiovascular , Miocardite , COVID-19/complicações , Síndrome da Liberação de Citocina , Humanos , Miocardite/terapia , SARS-CoV-2 , Choque CardiogênicoRESUMO
A typical presentation of septic arthritis (SA) includes pain, swelling, and erythema in the affected joint. Often, patients complain of inability to bear weight on the affected limb. However, some patients may present with subtle symptoms of pain and no fever or obvious swelling of the affected limb thus making the initial suspicion of SA low. Especially, patients with rheumatoid arthritis (RA) may present with polyarticular joint pain and initial synovial fluid analysis from an infected joint not consistent with overt septic arthritis. In such situations, the diagnosis of septic arthritis could be missed on delayed. In this case report, we present a 79-year-old female with a history of RA who presents with polyarticular pain, most notably in her right knee. SA was not initially suspected because of her history of RA and her current presentation with polyarticular pain. The initial synovial analysis did not suggest SA as well. However, cultures of synovial fluid from her right knee confirmed SA. Thus, we have highlighted that physicians should have a high suspicion for SA when addressing joint pain in RA patients.
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The pathophysiology of coronavirus disease 2019 (COVID-19) involves multi-organ dysfunction, particularly involving the respiratory, cardiovascular and hematological systems. This dysfunction is partly due to systemic inflammation causing a wide array of pathological sequelae thus posing a significant challenge to management despite the advances in treatment made thus far. In this report, we present a COVID-19 patient who developed a transient complete heart block and was temporarily paced as a complication of a saddle pulmonary embolus (PE). The mechanism of complete heart block is unclear, may be related to strain, ischemia, or vagal response. We believe that this is a unique sequence of events in a COVID-19 patient and, to our knowledge, is the first of its kind to be reported.
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COVID-19-associated coagulopathy (CAC) is a feature of COVID-19 that can lead to various thrombotic complications and death. In this review, we briefly highlight possible etiologies, including direct cytotoxicity caused by the SARS-CoV-2 virus, and the activation of proinflammatory molecules such as cytokines, underlying coagulopathy. Endothelial dysfunction has been highlighted as pivotal, irrespective of the mechanism involved in CAC. Specific features of CAC distinguishing it from disseminated intravascular coagulopathy and sepsis or ARDS-associated coagulopathy have been discussed. We have also highlighted some hematological parameters, such as elevated d-dimers and partial prothrombin and prothrombin times prolongation, which can guide the use of anticoagulation in critically ill patients. We conclude by highlighting the importance of prophylactic anticoagulation in all COVID-19 hospitalized patients and reiterate the need for institution-specific guidelines for anticoagulation COVID-19 patients since individual institutions have different patient populations.
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Transtornos da Coagulação Sanguínea , COVID-19 , Anticoagulantes/efeitos adversos , Transtornos da Coagulação Sanguínea/tratamento farmacológico , Transtornos da Coagulação Sanguínea/etiologia , Produtos de Degradação da Fibrina e do Fibrinogênio , Humanos , SARS-CoV-2RESUMO
Congenital lobar emphysema (CLE) is a developmental anomaly of the lower respiratory tract characterized by hyperinflation of one or more pulmonary lobes in the absence of extrinsic bronchial obstruction. We present a case of a 24-year-old male, nonsmoker who presented with shortness of breath and severe left sided chest pain. A chest x-ray was significant for a very large left-sided pneumothorax and chest CT showed lobar emphysematous changes. Video assisted thoracoscopic surgery (VATS) and lobectomy was subsequently performed after persistence of pneumothorax despite chest tube insertion and conservative management. Surgical pathology of resected specimen showed chronic emphysematous changes with patchy chronic organizing pneumonitis. Histology showed advanced emphysematous changes of pulmonary parenchyma consistent with congenital lobar emphysema. This finding combined with features seen on computed tomography of the chest led to the diagnosis of congenital lobar emphysema. This case demonstrated that CLE can be a cause of tension pneumothorax in adults in rare cases.
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Klippel-Trenaunay syndrome (KTS) is a rare genetic condition defined by capillary malformation, venous malformation, and soft tissue and bony overgrowth. Due to venous malformations, individuals are predisposed to intravascular coagulopathy leading to thrombosis and thromboembolism. However, anticoagulating these patients long-term remains a challenge because of the presence of capillary malformations that increase bleeding risk. We present a rare case of a 30-year-old Caucasian male with KTS and history of gastrointestinal bleeding who has been on anticoagulation since the age of 7 and has had three different inferior vena cava filters placed during his lifetime. At presentation, he had dyspnea with stable vital signs. His prothrombin time/international normalized ratio was 37.3 and 3.2, respectively and chest computed tomography showed bilateral segmental pulmonary embolism (PE). He was treated with heparin drip and his home anticoagulation was switched from warfarin to apixaban at the time of discharge for better anticoagulation optimization. KTS is a condition associated with venous thromboembolic complications that can be difficult to manage. PE should remain on the top of the list of differential diagnoses in patients with KTS presenting with dyspnea even if laboratory findings suggest an alternate diagnosis.
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Chest pain (CP) is a common reason for visits to the emergency department (ED). The underlying etiology of a good number of cases of CP can be diagnosed with adequate history taking and routine laboratory testing. However, atypical presentations of CP, in the settings of other causes of CP such as gastroesophageal reflux disease (GERD), can sometimes be tricky to diagnose with only routine lab tests and electrocardiogram (EKG). Herein, we present a 73-year-old male with a history of GERD and coronary artery disease who presented to our ED complaining of postprandial CP unaffected by exertion or rest. Initially, his symptoms were thought to be GERD-related but other heart-related causes of CP were considered due to the persistence of his CP postprandially. A cardiac stress test was subsequently done to rule out possible cardiac causes of his CP. His stress test was abnormal prompting heart catheterization that showed almost complete occlusion of his left anterior descending (LAD) and left circumflex (LCx) arteries. His symptoms resolved post-catheterization/stenting of his LAD and LCx arteries. He was later discharged unconditionally. His presentation highlights the required vigilance physicians must maintain when interrogating CP, even when other non-cardiac-related causes seem more plausible.
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BACKGROUND: Bronchopleural fistulas (BPF) are abnormal sinus tracts connecting the bronchi and pleural cavity and form after surgical resection of a lung lobe. It is a complication with potentially disastrous sequelae including, failure of the bronchial stump to heal, ischemia of the affected area, and/or infection of the stump. Bronchopleural fistulas caused by surgical intervention most commonly present on the right side and within 7-12 days post-operatively, i.e., subacutely. While the fistula may initially be asymptomatic, they carry a mortality rate of 25-71% in the absence of other comorbidities. CASE PRESENTATION: A 60-year-old female developed a BPF more than seven months after a left lower lobe lung lobectomy for non-small cell adenocarcinoma is presented. She was seen at our hospital on multiple occasions after her lobectomy with no evidence of a developing fistula on chest computer tomography (CT) during those visits. During her most recent presentation, roughly 7 months postoperatively, she was noted on imaging to have a new left-sided bronchopleural fistula. Bronchoscopy with lavage and culture of the fistula grew Pseudomonas Aeruginosa, for which she received appropriate treatment. Further surgical interventions were deferred due to poor prognosis. Her presentation differed from the typical BPF presentation in that it was left-sided and occurred out of the window of its usual occurrence. CONCLUSION: Late-onset BPF is an important diagnosis to consider in patients who have undergone lung resection, regardless of the type of surgery or postoperative duration, especially when patients are known to have multiple predisposing factors.
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Damage to the liver or kidney can occur through direct toxic effects; however, damage can also be drug-induced immune-mediated. Levamisole-adulterated cocaine (LAC) is known to cause antineutrophil cytoplasmic antibody- (ANCA-) associated vasculitis and glomerulonephritis leading to acute kidney injury and end-stage renal disease. It remains unclear whether LAC is associated with hepatic duct damage. Here, we report a case with biopsy-proven evidence of intrahepatic duct damage months after being diagnosed with ANCA-associated crescentic and sclerosing glomerulonephritis caused by LAC use. This case represents the first report of LAC-induced ANCA-associated hepatic duct cholestasis in the setting of previous LAC-induced ANCA-positive glomerulonephritis.