ABSTRACT
BACKGROUND: Trauma increases risk for venous thromboembolism (VTE) and obesity is a known independent risk factor for VTE development. Currently, no consensus on an optimal prophylactic dosing strategy for morbidly obese trauma patients exists. The objective of this study is to evaluate the effectiveness and safety of a BMI-stratified dosing strategy for VTE prophylaxis in morbidly obese trauma patients. METHODS: This was a single center, retrospective cohort study of adult major trauma patients with a body mass index (BMI) of ≥40 kg/m2 admitted to the surgical-trauma intensive care unit from April 2014 to July 2020. Patients included were those who received enoxaparin 40 mg subcutaneously (SQ) every 12 hours (Q12H) for BMI of 40 to 49.9 kg/m2 or 60 mg SQ Q12H BMI ≥ 50 kg/m2 (per protocol), or enoxaparin 40 mg SQ Q12H for BMI of 40 to 49.9 kg/m2 (non-protocol). The primary endpoint was confirmed incidence of VTE. Secondary endpoints included occurrence of deep vein thrombosis (DVT) or pulmonary embolism (PE) during hospitalization, bleeding events, intensive care unit (ICU) and hospital length of stay (LOS) and hospital mortality. RESULTS: One hundred forty-five morbidly obese major trauma patients were included, with 123 patients (84.8%) in the per-protocol group. The primary outcome of in-hospital VTE did not occur in any patients in this group. Bleeding events occurred in 3 patients (2.7%) with a BMI of 40 to 49.9 kg/m2 and in 2 patients (16.7%) with a BMI of ≥50 kg/m2 (P = .064). Twenty-two patients in the non-protocol group were reviewed. One VTE event (4.5%) and no bleeding events occurred in this group. Median ICU LOS was 5 days, and hospital LOS was 11 days for the entire study group. CONCLUSIONS: Administration of enoxaparin 40 mg SQ Q12H to morbidly obese major trauma patients with a BMI of 40 to 49.9 kg/m2 and enoxaparin 60 mg SQ Q12H in those with a BMI of ≥50 kg/m2 resulted in low rates of VTE and bleeding events in the current study. However, future larger studies using this BMI-stratified dosing strategy are necessary to confirm these findings.
ABSTRACT
Hereditary coproporphyria (HCP) is a rare disorder caused by a deficiency of an enzyme, coproporphyrinogen oxidase, in the heme synthetic pathway. This disease has a highly variable clinical presentation with acute attacks of neurologic symptoms that can last from days to months. Rarely, it and other acute porphyrias may cause ascending paralysis, which is difficult to distinguish from Guillain-Barré syndrome (GBS). Acute attacks can be triggered by factors that increase the synthesis of heme, such as hormonal changes, certain medications, dietary changes, and infections. We report a 26-year-old female with HCP who presented with acute ascending flaccid paralysis and respiratory failure after coronavirus disease 2019 (COVID-19) infection and was initially misdiagnosed and treated for GBS. She was transferred to our neurosciences intensive care unit, where the diagnosis of acute porphyria was established. Initial improvement occurred during treatment for several weeks with hemin (Panhematin®) and continued with givosiran (Givlaari®), which was recently introduced for the prevention of acute attacks. We suggest that acute porphyria should be part of the differential diagnosis when GBS is suspected. To our knowledge, this is the first report of an attack of acute hepatic porphyria (AHP) that developed after a COVID-19 infection and the first with advanced paresis to be treated with givosiran. Her response suggests that givosiran may contribute to recovery from advanced neurological manifestations of acute porphyrias.
