Introduction Although COVID-19 is transmitted via respiratory droplets, there are multiple gastrointestinal and hepatic manifestations of the disease, including abnormal liver-associated enzymes. However, there are not many published articles on the pathological findings in the liver of COVID-19 patients. Methods We collected the clinical data from 17 autopsy cases of COVID-19 patients including age, sex, BMI, liver function test (ALT, AST, ALP, direct bilirubin and total bilirubin), D-dimer and anticoagulation treatment. We examined histopathologic findings in postmortem hepatic tissue, immunohistochemical (IHC) staining with antibody against COVID spike protein, CD68 and CD61, and electron microscopy. We counted the number of megakaryocytes in liver sections from these COVID-19 positive cases. Results Abnormal liver-associated enzymes were observed in 12/17 cases of COVID-19 infection. With the exception of three cases that had not been tested for D-dimer, all 14 patients’ D-dimer levels were increased, including the cases that received varied doses of anticoagulation treatment. Microscopically, the major findings were widespread platelet-fibrin microthrombi, steatosis, histiocytic hyperplasia in the portal tract, mild lobular inflammation, ischemic-type hepatic necrosis and zone 3 hemorrhage. Rare megakaryocytes were found in sinusoids. COVID IHC demonstrates positive staining of the histiocytes in the portal tract. Under electron microscopy, histiocyte proliferation is present in the portal tract containing lipid droplets, lysosomes, dilated ribosomal endoplasmic reticulum (RER), micro-vesicular bodies and coronavirus. Conclusions The characteristic findings in COVID-19 patients’ liver include numerous amounts of platelet-fibrin microthrombi as well as various degrees of steatosis and histiocytic hyperplasia in the portal tract. Possible mechanisms are also discussed.

Surgeons write 1.8% of all prescriptions and 9.8% of all opioid prescriptions. Of a total of 180 patients (median age 63 years), 127 did not receive opioids; 53 were prescribed opioids against protocol. The operating surgeon was the only variable independently correlated with protocol adherence. Ambulatory breast surgery patients tolerated a nonopioid pain regimen well. Surgeons' decisions, rather than patient characteristics, primarily drove the choice of pain management in our study.

A B S T R A C T Stercoral ulcer perforation (SUP) was first described in 1894. Fewer than 150 cases have been reported in the literature. Historically, stercoral ulcers (SU) are mostly seen in older patients. However, in recent years younger patients have presented with this condition. Stercoral ulcers are caused by impacted feces, which result in loss of bowel wall integrity due to chronic pressure necrosis. This can lead to perforation and fecal peritonitis. It is a deadly but rare complication of chronic constipation. The case of a 78-year-old woman with a history of chronic constipation who presented to the emergency department (ED) with diffuse abdominal pain is described. Initial imaging studies revealed severe fecal impaction, most significant in the sigmoid and rectum. The patient was admitted for observation with serial abdominal exams, however, during the hospital course her clinical status deteriorated over a 12-hour period. Abdominal x-ray demonstrated free air under the diaphragm, and the patient was taken to the operating room (OR) for emergency exploratory laparotomy. Colorectal perforation was discovered and repaired. The patient tolerated the surgical intervention, but unfortunately died during the post-operative period. The patient's history of chronic constipation, immobility, and opioid use for pain management after knee surgery most likely precipitated the stercoral ulceration and colonic perforation.In this study, a systematic review was conducted to assess the epidemiology, presentation, diagnosis, management, complications, and clinical implications associated with stercoral ulcers.

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