Pentobarbital Induced Hypokalemia: A Worrying Sequela.

INTRODUCTION: Intracranial hypertension that is not responsive to other therapies can be managed through the use of a barbiturate induced coma. Although potentially effective, there are known complications associated with this treatment, and as such it is typically reserved for the most severe cases. One such sequela of barbiturate induced coma therapy is refractory hypokalemia and subsequent rebound hyperkalemia. PRESENTATION OF CASE: This case report discusses a patient who experienced hypokalemia during pentobarbital induced coma for unmanageable elevations in intracranial pressure and was treated conservatively to avoid rebound hyperkalemia depicting successful deployment of permissive hypokalemia. DISCUSSION: It is vital that clinicians understand the possible adverse effects associated with barbiturate induced coma therapy, and that a careful balance be struck between hypokalemia and potassium supplementation to avoid rebound hyperkalemia. CONCLUSION: Given that the risk of rebound hyperkalemia is of significant concern in patients who experience hypokalemia on barbiturate induced coma therapy, permissive hypokalemia can be a viable treatment option achieved by lowering the potassium replacement target threshold in such patients.

Varicella Pneumonia: Case Report and Review of a Potentially Lethal Complication of a Common Disease.

Varicella zoster virus causes varicella (chickenpox). It can be reactivated endogenously many years later to cause herpes zoster (shingles). Although varicella is usually a benign disease in healthy children, it resulted in over 11 000 hospitalizations and over 100 deaths every year, in all ages, in the United States. Morbidity was considerably worse in older teenagers and adults. Between 5% and 15% of cases of adult chickenpox will produce some form of pulmonary illness. Progression to pneumonia risk factors include pregnancy, age, smoking, chronic obstructive pulmonary disease, and immunosuppression. Typically, pulmonary symptoms occur 1 to 6 days after varicella zoster infection. They often include cough, fever, and dyspnea. Treatment is a 7-day course of intravenous acyclovir for varicella pneumonia. Early intervention may modify the course of this complication. This review illustrates practical features with a case of a 34-year-old female with severe varicella pneumonia. Despite the lack of significant past medical history and absence of immunosuppression, her pneumonia worsened and by using continuous positive airway pressure mask, intubation was avoided. More important, the radiographic progression of severe varicella pneumonia is shown. This highlights how a common disease of varicella can progress in an adult and manifest with significant organ malfunction.

Near-fatal kinking of mammary graft due to emphysematous lung disease.

Left internal mammary artery grafting is commonly used in elective coronary artery bypass graft surgery. We report a near-fatal case with graft kinking upon sternal closure due to distended, emphysematous lungs impinging on the mammary graft. After the sternum was closed, the patient suffered a severe hemodynamic deterioration. Surgical examination revealed kinking of his left internal mammary artery upon sternal closure due to distended, emphysematous lungs impinging on the mammary graft. Using an off-bypass technique, the kink in the mammary graft to the left anterior descending artery was removed by moving the origin of the left internal mammary artery to a hooded graft of a saphenous vein graft instead. In this position, the graft no longer was impinged upon by the distended emphysematous lungs. Subsequently, the patient's sternum was closed without hemodynamic impingement. Although chronic obstructive pulmonary disease is well described to increase complications in coronary artery bypass graft surgery, it has not been previously associated with the kinking of a left internal mammary artery. This report highlights another contribution that chronic obstructive pulmonary disease can make to increased morbidity following coronary artery bypass graft surgery and alerts readers to watch for this complication in susceptible patients.

A sphingosine-1 phosphate agonist (FTY720) limits trauma/hemorrhagic shock-induced multiple organ dysfunction syndrome.

BACKGROUND: Trauma/hemorrhagic shock (T/HS) is one of the major consequences of battlefield injury as well as civilian trauma. FTY720 (sphingosine-1-phosphate agonist) has the capability to decrease the activity of the innate and adaptive immune systems and, at the same time, maintain endothelial cell barrier function and vascular homeostasis during stress. For this reason, we hypothesize that FTY720, as part of resuscitation therapy, would limit T/HS-induced multiple organ dysfunction syndrome in a rodent T/HS model. METHODS: Rats subjected to trauma/sham shock (T/SS) or T/HS (30 mm Hg × 90 min) were administered FTY720 (1 mg/kg) post-T/HS during volume resuscitation. Lung injury (permeability to Evans blue dye), polymorphonuclear leukocyte (PMN) priming (respiratory burst activity), and red blood cell (RBC) rigidity were measured. In addition, lymph duct-cannulated rats were used to quantify the effect of FTY720 on gut injury (permeability and morphology) and the biologic activity of T/HS versus T/SS lymph on PMN-RBC and RBC deformability. RESULTS: Trauma/hemorrhagic shock-induced increased lung permeability, PMN priming, and RBC rigidity were all abrogated by FTY720. The systemic protective effect of FTY720 was only partially at the gut level, because FTY720 did not prevent T/HS-induced gut injury (morphology or permeability); however, it did abrogate T/HS lymph-induced increased respiratory burst and RBC rigidity. CONCLUSIONS: FTY720 limited T/HS-induced multiple organ dysfunction syndrome (lung injury, red cell injury, and neutrophil priming) as well as T/HS lymph bioactivity, although it did not limit gut injury.