Outcomes of COVID-19 in hospitalized solid organ transplant recipients compared to a matched cohort of non-transplant patients at a national healthcare system in the United States.

Data describing outcomes of solid organ transplant (SOT) recipients with coronavirus disease 2019 (COVID-19) are variable, and the association between SOT status and mortality remains unclear. In this study, we compare clinical outcomes of SOT recipients hospitalized with COVID-19 between March 10, and September 1, 2020, to a matched cohort of non-SOT recipients at a national healthcare system in the United States (US). From a population of 43 461 hospitalized COVID-19-positive patients, we created a coarsened exact matched cohort of 4035 patients including 128 SOT recipients and 3907 weighted matched non-SOT controls. Multiple logistic regression was used to evaluate association between SOT status and clinical outcomes. Among the 4035 patients, median age was 60 years, 61.7% were male, 21.9% were Black/African American, and 50.8% identified as Hispanic/Latino ethnicity. Patients with a history of SOT were more likely to die within the study period when compared to matched non-SOT recipients (21.9% and 14.9%, respectively; odds ratio [OR] 1.93; 95% confidence interval [CI]: 1.18-3.15). Moreover, SOT status was associated with increased odds of receiving invasive mechanical ventilation (OR [95% CI]: 2.34 [1.51-3.65]), developing acute kidney injury (OR [95% CI]: 2.41 [1.59-3.65]), and receiving vasopressor support during hospitalization (OR [95% CI]: 2.14 [1.31-3.48]).

Post transplant renal vein thrombosis, with successful thrombectomy and review of the literature.

INTRODUCTION: Renal vein thrombosis post kidney transplant is a rare but graft threatening event. RVT is reported in 0.3-4.2% of kidney transplants. When occurring early post transplant, prior to development of collateral venous outflow, may be catastrophic with loss of the allograft or even death. Anatomic abnormalities or technical problems during surgery are common causes. Early diagnosis and urgent treatment are necessary but often unsuccessful. PRESENTATION OF CASE: We report a patient with residual function in a failing allograft who developed RVT in a living donor preemptive kidney transplant. DISCUSSION: We review the literature regarding renal vein thrombosis following kidney transplant. CONCLUSION: Prompt diagnosis and immediate surgicathrombectomy after ex-planting allograft with subsequent re-implanting the allograft was successful.

Total pancreatectomy for the treatment of chronic pancreatitis: indications, outcomes, and recommendations.

Total pancreatectomy (TP) for chronic pancreatitis (CP) has not gained widespread acceptance because of concerns regarding technical complexity, diabetic complications, and uncertainty with respect to long-term pain relief. Records of patients having TP from 1997 to 2005 were reviewed. Patient presentation, etiology of disease, and the indication for TP were examined. Operative results were analyzed. Long-term results were critically assessed, including narcotic usage and the need for re-admission. Postoperative quality of life (QOL) was assessed by the SF-36 health survey. During the study period, 7 patients with CP had TP, and 28 had other operations. The etiology of CP was alcohol in four and hereditary pancreatitis in three. The indication for surgery was pain and weight loss. Preoperatively, all patients used narcotics chronically and two had insulin-dependent diabetes. Four had TP after failed previous surgical procedures. Endoscopic retrograde cholangiopancreatography and computed tomography demonstrated small ducts and atrophic calcified glands. The mean length of the operation was 468 minutes, and only two patients required transfusion. There were no biliary anastomotic complications. The mean length of stay was 14 days. Major morbidity was limited to a single patient with a leak from the gastrojejunal anastomosis. Thirty-day mortality was zero, with one late death unrelated to the surgical procedure or diabetes. The mean length of follow-up was 46 months. All patients remained alcohol and narcotic free. No patient was readmitted with a diabetic complication. When compared with the general population, QOL scores were diminished but reasonable. We conclude that TP is indicated in hereditary pancreatitis and in those with an atrophic, calcified pancreas with small duct disease; that TP is technically arduous but can be completed with very low morbidity and mortality; and that on long-term follow-up, pain relief and abstinence from alcohol and narcotics was excellent with an acceptable QOL.

Cerebral activation of mitogen-activated protein kinases after circulatory arrest and low flow cardiopulmonary bypass.

OBJECTIVES: Mitogen-activated protein kinases (MAPK) are important intermediates in the signal transduction pathways involved in neuronal dysfunction following cerebral ischemia-reperfusion injury. One subfamily, extracellular regulated kinase 1/2, has been heavily implicated in the pathogenesis of post-ischemic neuronal damage. However, the contribution of extracellular regulated kinase 1/2 to neuronal damage following deep hypothermic circulatory arrest and low flow cardiopulmonary bypass is unknown. We attempted to correlate the extent of neuronal damage present following deep hypothermic circulatory arrest and low flow cardiopulmonary bypass with phosphorylated extracellular regulated kinase 1/2 expression in the cerebral vascular endothelium. METHODS: Piglets underwent normal flow cardiopulmonary bypass (n=4) deep hypothermic circulatory arrest (n=6) and low flow cardiopulmonary bypass (n=5). Brains were harvested following 24 h of post-cardiopulmonary bypass recovery. Cerebral cortical watershed zones, hippocampus, basal ganglia, thalamus, cerebellum, mesencephalon, pons and medulla were evaluated using hematoxylin and eosin staining. A section of ischemic cortex was evaluated by immunohistochemistry with rabbit polyclonal antibodies against phosphorylated extracellular regulated kinase 1/2. RESULTS: Compared to cardiopulmonary bypass controls, the deep hypothermic circulatory arrest and low flow cardiopulmonary bypass piglets exhibited diffuse ischemic changes with overlapping severity and distribution. Significant neuronal damage occurred in the frontal watershed zones and basal ganglia of the deep hypothermic circulatory arrest group (P<0.05). No detectable phosphorylated extracellular regulated kinase 1/2 immunoreactivity was found in the cardiopulmonary bypass controls; however, ERK 1/2 immunoreactivity was present in the cerebral vascular endothelium of the deep hypothermic circulatory arrest and low flow cardiopulmonary bypass groups. CONCLUSIONS: Our results indicate that phosphorylated extracellular regulated kinase 1/2 may play a prominent role in early cerebral ischemia-reperfusion injury and endothelial dysfunction. The pharmacologic inhibition of extracellular regulated kinase 1/2 represents a new and exciting opportunity for the modulation of cerebral tolerance to low flow cardiopulmonary bypass and deep hypothermic circulatory arrest.

Sleeve resection of a transcarinal bronchial carcinoid after laser debulking.

We report a case of a bronchial carcinoid tumor extending from the right upper lobe into the left mainstem bronchus in a 30-year-old woman. Diagnosis was established by preoperative bronchoscopy and biopsy. After extensive debulking with seven sessions of bronchoscopic neodymium:yttrium-aluminum-garnet laser therapy, the tumor was resected by right upper-lobe sleeve lobectomy. Final pathology revealed a typical carcinoid tumor with surgical margins and all lymph nodes free of tumor.

Blockade of the extracellular signal-regulated kinase pathway by U0126 attenuates neuronal damage following circulatory arrest.

OBJECTIVES: The extracellular signal-regulated kinase pathway of the mitogen-activated protein kinase signal transduction cascade has been implicated in the neuronal and endothelial dysfunction witnessed following cerebral ischemia-reperfusion injury. Extracellular signal-regulated kinase is activated by mitogen-activated protein kinase/extracellular signal-regulated kinase 1/2. We evaluated the ability of a mitogen-activated protein kinase/extracellular signal-regulated kinase 1/2-specific inhibitor (U0126) to block extracellular signal-regulated kinase activation and mitigate ischemic neuronal damage in a model of deep hypothermic circulatory arrest. METHODS: Piglets underwent normal flow cardiopulmonary bypass (control, n = 4), deep hypothermic circulatory arrest (n = 6), and deep hypothermic circulatory arrest with U0126 (n = 5) at 20 degrees C for 60 minutes. The deep hypothermic circulatory arrest with U0126 group was given 200 microg/kg of U0126 45 minutes prior to initiation of bypass followed by 100 microg/kg at reperfusion. Following 24 hours of post-cardiopulmonary bypass recovery, brains were harvested. Eleven distinct cortical regions were evaluated for neuronal damage using hematoxylin and eosin staining. A section of ischemic cortex was further evaluated by immunohistochemistry with rabbit polyclonal antibody against phosphorylated extracellular signal-regulated kinase 1/2. RESULTS: The deep hypothermic circulatory arrest and deep hypothermic circulatory arrest with U0126 groups displayed diffuse ischemic changes. However, the deep hypothermic circulatory arrest with U0126 group possessed significantly lower neuronal damage scores in the right frontal watershed zone of cerebral cortex, basal ganglia, and thalamus (P < or =.05) and an overall trend toward neuroprotection versus the deep hypothermic circulatory arrest group. This neuroprotection was accompanied by nearly complete blockade of phosphorylated extracellular signal-regulated kinase in the cerebral vascular endothelium. CONCLUSIONS: In this experimental model of deep hypothermic circulatory arrest, U0126 blocked extracellular signal-regulated kinase activation and provided a significant neuroprotective effect. These results support targeting of the extracellular signal-regulated kinase pathway for inhibition as a novel therapeutic approach to mitigate neuronal damage following deep hypothermic circulatory arrest.