Endoscopic Management of Boerhaave Syndrome: Are Outcomes Better Than Surgery? A Case Report and Review of Literature.

Boerhaave syndrome (BS) is a rare clinical diagnosis associated with a high morbidity and mortality rate. Diagnosis of this condition is usually delayed which can lead to a very poor outcome. The timing of presentation and time to management plays a very important role in the prognosis and selection of the management method. With the advances seen in therapeutic endoscopy, many authors have been exploring the possibility of shifting the focus of management from surgery to interventional endoscopy. We present a case report of a patient presenting with BS that was successfully managed endoscopically. We also reviewed the literature on how surgical management compares to endoscopic management and attempted to establish general recommendations from available literature on management of BS.

A Rare Case of a Rectal Gastrointestinal Stromal Tumor (GIST) Discovered During a Routine Colonoscopy.

A gastrointestinal stromal tumor (GIST) is a rare malignancy, accounting for only 0.1% to 3% of all gastrointestinal (GI) malignancies. Although GISTs are the most common mesenchymal tumor of the GI tract, they are primarily found within the stomach, with rectal GISTs rarely reported. They may present with rectal bleeding, constipation, pain, or a palpable mass while some are found incidentally. The incidence of GISTs has been on the rise, possibly due to advancements in diagnostic technology. In this case report, we present a 50-year-old female who presented with intermittent constipation and rectal pain and was found to have a submucosal rectal mass during a routine diagnostic colonoscopy. Further evaluation confirmed the presence of a spindle-cell neoplasm, which was mildly cellular and showed positive expression of CD34 and CD117 on immunohistochemistry, consistent with the diagnosis of GIST of the rectum. This case report emphasizes the importance of routine colonoscopies in the early detection of neoplastic lesions of the colon and highlights the rare incidence of GISTs, their risk factors, pathogenesis, and common sites of occurrence.

Herpes Simplex Virus Type 1 Hepatitis in an Immunocompetent Female After Laparoscopic Cholecystectomy.

We present a rare case of a healthy, non-pregnant, middle-aged and immunocompetent woman who underwent laparoscopic cholecystectomy for acute cholecystitis with a post-operative course complicated by herpes simplex virus type 1 (HSV-1) hepatitis secondary to post-surgical inflammation. Her initial post-operative course was complicated by intermittent fevers, leukocytosis, jaundice, elevated transaminases, and right upper quadrant abdominal pain, and she was subsequently placed on broad-spectrum antibiotics with no improvement. During her hospital course, the patient developed herpes labialis, and HSV-1 hepatitis was confirmed by serology and HSV-1 polymerase chain reaction (PCR), in lieu of a liver biopsy. After this was discovered, the patient was placed on valacyclovir and had a successful response. The importance of this case is to emphasize the possibility of herpes simplex virus (HSV) hepatitis as a post-operative complication and the benefit of early empiric antiviral treatment.

The Effect of Lipopolysaccharide on Ischemic-Reperfusion Injury of Heart: A Double Hit Model of Myocardial Ischemia and Endotoxemia.

INTRODUCTION: Myocardial ischemia may coincide and interact with sepsis and inflammation. Our objective was to examine the effects of bacterial endotoxin on myocardial functions and cell injury during acute ischemia. METHODS: Rabbits were pretreated with incremental doses of E. Coli lipopolysaccharide (LPS) or normal saline. Myocardial ischemia was induced by 50-minute occlusion of left anterior descending artery. S-TNFaR was additionally used to block the effects LPS. RESULTS: Ventricular contractility as it was measured by dp/dt during systole decreased from 2445± 1298 to 1422 ± 944 mm Hg/s, P = .019. Isovolumetric relaxation time as an index of diastolic function was prolonged from 50±18 ms to 102± 64 ms following ischemia. Pretreatment with low concentrations of LPS (<1 µg) had no effect on dp/dt, while at higher concentrations it suppressed both contractility and prolonged IVRT. Cell injury as measured by cardiac troponin I level increased to 15.1± 3.2 ng/dL following ischemia and continued to rise with higher doses of LPS. While blocking TNFa did not improve the myocardial contractility after ischemia, it eliminated additional deleterious effects of LPS. CONCLUSION: Lower doses of LPS had no deleterious effect on myocardial function, whereas higher doses of this endotoxin cause cardiac dysfunction and increased extent of injury.

Dual effects of tumor necrosis factor alpha on myocardial injury following prolonged hypoperfusion of the heart.

OBJECTIVE: To examine the dose response of TNFα in an ex vivo rat model of myocardial ischemia reperfusion. METHODS AND RESULTS: Seventy-two rat hearts were mounted on Langendorff apparatus and perfused with oxygenated Krebs-Henseleit solutions. Ischemia was induced by reducing the perfusate flow rate. During reperfusion, incremental doses of recombinant TNFα were infused as a part of perfusate. TNFα was blocked with monoclonal TNFα antibody. Myocardial function was measured by dP/dT and relaxation time (IVRT). Cellular injury was assessed by released myoglobin and tissue concentration of malondialdehyde activity of the heart homogenates. Baseline +dP/dT was 1645 ± 125 mmHg/sec, -dP/dT was 945 ± 73 mmHg/sec and IVRT was 65 ± 5 msec. At the conclusion of reperfusion period, lower doses of TNFα increased +dP/dT and lowered IVRT. In contrast, the higher doses of TNFα decreased +dP/dT and prolonged IVRT. Pretreating the hearts with monoclonal TNFα antibody completely abolished the effects of TNFα on myocardial contractility and relaxation comparable to ischemia controls. CONCLUSION: Low dose TNFα improved myocardial function and decreased resultant cellular injury while high dose TNFα decreased myocardial function and increased myocardial injury following ischemia and reperfusion.

The comparative myocardial protection by propofol and isoflurane in an in vivo model of ischemia reperfusion.

BACKGROUND: Anesthetic Agents protect the heart from ischemic injury during perioperative period. We evaluated the protective effects of 2 anesagents on myocardial ischemia -reperfusion injury in rabbit models. METHODS: 58 anesthetized and mechaniventilated rabbits randomly received isoflurane (ISO) 2%, propofol (PRP), or were observed as the control group for 15 minutes. We applied vascular tourniquet around the left anterior descending artery (LAD). Myocardium was reperfused for 4 hours. Derivative of pressure over time (dP/dT(max)), left ventricular pressure (dLVP), isovolumetric relaxation time (Tau), and segment shortening (SS) were measured over the ischemic and non-ischemic regions of left ventricle (LV). Cardiac troponin I (cTnI), tissue concentrations of tumor necrosis factor á (TNFá), myeloperoxidase activity assay (MPO), and tissue malonyl dialdehyde (MDA) concentrations were measured as indices of cellular injury and inflammatory response. RESULTS: dP/dT(max) values significantly decreased during ischemia. Following reperfusion, dP/dT(max), dLVP, and Tau remained depressed in the control animals. Both PRP and ISO restored the function of the myocardium globally. CONCLUSION: Only ISO improved the recovery of the ischemic myocardium during reperfusion. The effects of PRP were global in nature and involved compensatory hypercontractile state in nonischemic regions of the myocardium. Implication. PRP and ISO protect the heart against an ischemic injury, but only ISO preserves the function of the myocardium at the ischemic region. The survival rate of the PRP-treated group versus the ISO-treated group supports the claim that PRP has smaller contribution to recovery from myocardial ischemia.

Reversibility of hepatic encephalopathy after liver transplantation.

Until the advent of Liver transplantation, it was widely believed that Hepatic Encephalopathy (HE) was usually reversible. The exceptions were the so called "Acquired Hepatocerebral Degeneration cases" which were considered irreversible. Paradoxically, it seems, with liver transplantation, we have seen cases that contradict these rules. Whether the "residual effects" of HE, degenerative brain injury or independent neurological insults are causing post transplant neurological deficits is not easy to discern. As more emphasis is being put on maintaining brain 'status' after liver transplantation, we are finding confirmation of the largely reversible nature of HE. But, enough important exceptions to this rule are occurring to make further research on this topic mandatory.