A unique case of Miller Fisher-Guillain-Barré overlap syndrome in a liver transplant recipient.

Guillain-Barré syndrome (GBS) is an ascending demyelinating polyneuropathy often associated with recent infection. Miller Fisher syndrome represents a variant with predominant facial and cranial nerve involvement, although Miller Fisher and Guillain-Barré overlap syndromes can occur. Guillain-Barré spectrum syndromes have been thought to be rare among solid organ transplant recipients. We describe an immunocompromised patient with a liver transplant who presented with ophthalmoplegia and bulbar deficits. His symptoms rapidly progressed to a state of descending paralysis involving the diaphragm; he then developed acute respiratory failure and eventually developed quadriparesis. Electromyography and a nerve conduction study demonstrated a severe sensorimotor axonal polyneuropathy consistent with Miller Fisher variant Guillain-Barré syndrome. Despite several negative nasopharyngeal swabs for COVID-19 polymerase chain reaction, a serology for SARS-CoV-2 IgG was positive. He was diagnosed with Miller Fisher-Guillain-Barré overlap syndrome with rapid recovery following treatment with plasma exchange. Although Guillain-Barré is a rare complication in solid organ transplant recipients, this case highlights the importance of rapid diagnosis and treatment of neurologic complications in transplant patients. Furthermore, it demonstrates a possible case of neurological complications from COVID-19 infection.

Another Role for Angiotensin II?: Vasopressin-Refractory Shock After Pheochromocytoma Resection: A Case Report.

A patient presented with multiple unrelated tumors and was found to have a small but functional adrenal pheochromocytoma. After pheochromocytoma resection, shock developed unresponsive to vasopressin in recommended doses (0.04 U/min infusion plus repeated 1-U boluses) but responded dramatically to an angiotensin II infusion (20 ng/kg/min) with a mean arterial pressure >100 mm Hg. The patient's blood pressure was maintained for 42 hours postoperatively with an infusion rate that ranged from 2 to 38 ng/kg/min. Because vasopressin may not always be effective for postresection shock in people with pheochromocytomas, angiotensin II may prove to be an effective alternative.

The association of preoperative haemoglobin A1c with 30-day postoperative surgical site infection following non-cardiac surgery.

Diabetes has been shown to be associated with postoperative infections; however, the association of haemoglobin A1c (HbA1c) with postoperative surgical site infections (SSI) is unclear. All HbA1c data from patients receiving general, vascular, or orthopaedic surgeries between 1 January 2014 and 1 December 2016 were identified from hospital records. The primary outcome was 30-day SSI. Multivariable logistic regression was performed to determine if HbA1c was associated with infection. The cohorts assessed were: (1) HbA1c < 6.5% (reference group); (2) greater than or equal to 6.5% and less than 8.0%; (3) greater than or equal to 8.0% and less than 10.0%; and (4) greater than or equal to 10.0%. There were 3064 patients included in the final analysis. The overall rate of 30-day SSI was 2.42%. After adjusting for confounders, when compared to the reference group, HbA1c ≥ 8.0% and less than 10.0% (OR 2.4, 95% CI 1.2-4.7, p = 0.015) and HbA1c ≥ 10.0% (OR 3.0, 95% CI 1.2-7.3, p = 0.016) had increased odds ratio for 30-day SSI. A HbA1c of 8.0% or higher significantly increased the odds ratio of developing postoperative SSI (p < 0.05). This may aid in the development of guidelines for optimising diabetic patients.

Postoperative mortality and morbidity following non-cardiac surgery in a healthy patient population.

PURPOSE: Perioperative mortality ranges from 0.4% to as high as nearly 12%. Currently, there are no large-scale studies looking specifically at the healthy surgical population alone. The primary objective of this study was to report 30-day mortality and morbidity in healthy patients and define any risk factors. METHODS: Using the American College of Surgeons National Surgical Quality Improvement Program (NSQIP) dataset, all patients assigned an American Society of Anesthesiologists physical status (ASA PS) classification score of 1 or 2 were included. Further patients were excluded if they had a comorbidity or underwent a procedure not likely to classify them as ASA PS 1 or 2. Multivariable logistic regression was performed to identify predictors of the outcomes, in which odds ratios (OR) and 95% confidence intervals (95% CI) were reported. RESULTS: There were 687,552 healthy patients included in the final analysis. Following surgery, 0.7, 7.0, and 0.7 per 1000 persons experienced 30-day mortality, sepsis, and stroke or myocardial infarction, respectively. Healthy patients greater than 80 years of age had the highest odds for mortality (OR 17.7, 95% CI 12.4-25.1, p < 0.001). Case duration was associated with increased mortality, especially in cases greater than or equal to 6 h (OR 3.0, 95% CI 2.0-4.5, p < 0.001). CONCLUSIONS: Thirty-day mortality and morbidity is, as expected, lower in the healthy surgical population. Age may be an indication to further risk stratify patients that are ASA PS 1 or 2 to better reflect perioperative risk.

Macrophage-produced IL-12p70 mediates hemorrhage-induced damage in a complement-dependent manner.

Hemorrhage and hemorrhagic shock instigate intestinal damage and inflammation. Multiple components of the innate immune response, including complement and neutrophil infiltration, are implicated in this pathology. To investigate the interaction of complement activation and other components of the innate immune response during hemorrhage, we treated mice after hemorrhage with CR2-fH, a targeted inhibitor of the alternative complement pathway and assessed intestinal damage and inflammation 2 h after hemorrhage. In wild-type mice, CR2-fH attenuated hemorrhage-induced, midjejunal damage and inflammation as determined by decreased mucosal damage, macrophage infiltration, leukotriene B4, IL-12p40, and TNF-[alpha] production. The critical nature of intestinal macrophage infiltration and activation in the response to hemorrhage was further determined using mice pretreated with clodronate-containing liposomes. The absence of either macrophages or IL-12p70 attenuated intestinal damage. These data suggest that complement activation and macrophage infiltration with IL-12p70 production are critical to hemorrhage-induced midjejunal damage and inflammation.

Hemorrhage-induced intestinal damage is complement-independent in Helicobacter hepaticus-infected mice.

With more than half of the world population infected, Helicobacter infection is an important public health issue associated with gastrointestinal cancers and inflammatory bowel disease. Animal studies indicate that complement and oxidative stress play a role in Helicobacter infections. Hemorrhage (HS) induces tissue damage that is attenuated by blockade of either complement activation or oxidative stress products. Therefore, we hypothesized that chronic Helicobacter hepaticus infection would modulate HS-induced intestinal damage and inflammation. To test this hypothesis, we examined HS-induced jejunal damage and inflammation in uninfected and H. hepaticus-infected mice. Helicobacter hepaticus infection increased HS-induced midjejunal mucosal damage despite attenuating complement activation. In addition, infection alone increased chemokine secretion, changing the HS-induced neutrophil infiltration to a macrophage-mediated inflammatory response. The HS-induced macrophage infiltration correlated with increased secretion of tumor necrosis factor-α and nitric oxide in the infected mice. Together, these data indicate that Helicobacter infection modulates the mechanism of HS-induced intestinal damage and inflammation from a complement-mediated response to a macrophage response with elevated tumor necrosis factor-α and nitric oxide. These data indicate that chronic low-level infections change the response to trauma and should be considered when designing and administering therapeutics.