RESUMEN
Hypodysfibrinogenemia-related thromboembolic disorder is a rarely encountered clinical entity. We present such a case of a 34-year-old lady with no known co-morbidities presenting to the accident and emergency unit with left-sided pleuritic chest pain associated with non-productive cough and breathlessness. Laboratory tests revealed fibrinogen level of 0.42 g/l (1.5-4g/l) with prolonged prothrombin time (PT), activated partial thromboplastin time (aPTT) along with elevated d-dimer, N-terminal pro-B-type natriuretic peptide (NT-proBNP), and troponin. CT pulmonary angiogram (CTPA) found bilateral pulmonary embolism with right heart strain. Functional/antigenic fibrinogen ratio was 0.38. Genetic testing eventually revealed a heterozygous missense mutation in exon 8-p.1055G>C; p.Cys352Ser in the sequencing of the fibrinogen gene FGG (gamma chain) confirming the diagnosis of dyshypofibrinogenemia. She was treated with anticoagulants with fibrinogen replacement therapy and later discharged on apixaban.
RESUMEN
INTRODUCTION: As researchers and academics around the world scramble ahead to dissect and analyse every aspect of the SARS-CoV2 virus, one such study explored the various underlying electrolyte abnormalities that were precipitated in patients suffering from a confirmed COVID-19 infection. A significant proportion of such patients were noted to be hypokalemic. Hypokalemia can be life threatening as it is known to cause cardiac arrhythmia. CASE PRESENTATION: Our encounter with said presentation was incidental. The on-call medical team was involved in a cardiac arrest call for a 74-year -old gentleman who developed torsades de pointes, Retrospective analysis of the clinical picture pointed out the fact that he was found to be persistently hypokalemic and bradycardic solely triggered as a result of COVID-19. CONCLUSION: Although initially thought to be a pulmonary disease but along with time extra-pulmonary manifestations of Covid-19 has demonstrated significant consequences. Electrolyte abnormalities and cardiac dysfunction are examples of such extra-pulmonary pathologies. Therefore, it is important to keep close monitoring for such abnormalities otherwise could lead into life threatening arrythmias.
RESUMEN
Severe Acute Respiratory Syndrome Coronavirus 2 (SARS-COV-2), a novel coronavirus, originated as an epidemic respiratory illness in Wuhan, China. COVID-19 eventually spread to almost all countries and has now been declared a global pandemic disease by the World Health Organisation. A plethora of research has explored the dynamics of different clinical entities related to SARS-COV-2, in particular, COVID-19 associated coagulopathy. A large scale of patients have been reported to have developed pulmonary embolism without any other standard triggers or risk factors, leading to speculation that COVID-19 is an independent risk factor for venous thromboembolism. In addition to the development of thromboembolic complications such as pulmonary embolism, COVID-19 has also been reported to have triggered disseminated intravascular coagulation (DIC); however, it is unclear whether pulmonary embolism was due to COVID-19-induced thrombosis or a result of coagulopathy secondary to DIC. We describe a unique case of a COVID-19 associated coagulopathy in a patient with confirmed pulmonary embolism along with an overt DIC. Following diagnosis, the challenge was to identify the appropriate treatment modality for this unique situation. The patient was treated with anticoagulants and steroids along with blood products. The patient's condition markedly improved and was clinically stable on discharge.