Gastric pneumatosis is the presence of air within the wall of the stomach. It represents a spectrum of conditions ranging from benign disease to septic shock and death. Etiopathologically, it can be classified into emphysematous gastritis or gastric emphysema (GE). Along with hepatoportal venous gas (HPVG), it was considered as an ominous radiological sign and warranted an emergent surgical exploration; however, with widespread use of computerized tomographic (CT) scan, an increasing number of benign causes of GE and HPVG have been reported in the literature, where patients can be managed by noninvasive and conservative measures. We hereby describe a case where recurrent episodes of vomiting led to development of GE and HPVG and the patient was managed successfully by conservative measures.
Paxlovid (nirmatrelvir/ritonavir) is a game changer in the fight against COVID-19 due to its ease of administration and significant benefits of reducing progression to severe COVID-19, hospitalization, and death. Cardiac adverse events such as bradycardia and syncope are not known with this medication. We report a case of a 71-year-old patient who developed symptomatic bradycardia, syncopal episodes, and sinus pause after taking Paxlovid. Discontinuing medication and intravenous atropine helped to reverse the bradycardia and symptoms promptly. She did not require a pacemaker. We would like to report this possible association between Paxlovid and bradycardia. Until further information or studies are available, it is advised to promptly discontinue Paxlovid after any evidence of bradycardia and closely monitor for at least 40 hours in a hospital setting. The reported half-life (t 1/2) of the medication is 6.05 ± 1.79 hours and using 8 hours as a reference for the upper limit of t 1/2, around 97 % of the medication should be cleared off in about 40 hours (five half-lives).
Vitamin B12 deficiency-induced pseudo-thrombotic thrombocytopenic purpura (pseudo-TTP) is a rare condition. In reported literature, most cases were due to pernicious anemia (confirmed by the presence of anti-parietal cells or anti-intrinsic factor antibodies). Nutritional vitamin B12 deficiency causing pseudo-TTP is a much rarer entity. Differentiating thrombotic thrombocytopenic purpura (TTP) cases from pseudo-TTP (from any cause) should be done as soon as possible since the etiology, treatment, and outcome are different. Hematological findings from pseudo-TTP (when associated with vitamin B12 deficiency) respond to B12 replacement but do not respond to plasmapheresis. Neurological symptoms are one of the criteria for TTP, and altered mentation or psychosis in these cases is presumed secondary to either TTP or vitamin B12 deficiency. However, neurological symptoms are more characteristic of TTP rather than pseudo-TTP. In the rarer subsets of patients concerned with nutritional deficiency and neuropsychiatric symptoms, prompt consideration of concomitant vitamin B1 deficiency and Wernicke encephalopathy is essential. Immediate empiric treatment with high-dose IV thiamine should be started. If unrecognized and left untreated, thiamine deficiency can cause rapid progression to irreversible neurological symptoms, coma, and death, despite hematological improvement with B12 replacement. We report a rare case of concomitant vitamin B12 and vitamin B1 deficiency presenting with confusion, severe hemolytic anemia, acute renal failure, diarrhea, and thrombocytopenia mimicking TTP.
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