Background Acute treatment of cerebral edema and elevated intracranial pressure is a common issue in patients with neurological injury. Practical recommendations regarding selection and monitoring of therapies for initial management of cerebral edema for optimal efficacy and safety are generally lacking. This guideline evaluates the role of hyperosmolar agents (mannitol, HTS), corticosteroids, and selected non-pharmacologic therapies in the acute treatment of cerebral edema. Clinicians must be able to select appropriate therapies for initial cerebral edema management based on available evidence while balancing efficacy and safety. Methods The Neurocritical Care Society recruited experts in neurocritical care, nursing, and pharmacy to create a panel in 2017. The group generated 16 clinical questions related to initial management of cerebral edema in various neurological insults using the PICO format. A research librarian executed a comprehensive literature search through July 2018. The panel screened the identified articles for inclusion related to each specific PICO question and abstracted necessary information for pertinent publications. The panel used GRADE methodology to categorize the quality of evidence as high, moderate, low, or very low based on their confidence that the findings of each publication approximate the true effect of the therapy. Results The panel generated recommendations regarding initial management of cerebral edema in neurocritical care patients with subarachnoid hemorrhage, traumatic brain injury, acute ischemic stroke, intracerebral hemorrhage, bacterial meningitis, and hepatic encephalopathy. Conclusion The available evidence suggests hyperosmolar therapy may be helpful in reducing ICP elevations or cerebral edema in patients with SAH, TBI, AIS, ICH, and HE, although neurological outcomes do not appear to be affected. Corticosteroids appear to be helpful in reducing cerebral edema in patients with bacterial meningitis, but not ICH. Differences in therapeutic response and safety may exist between HTS and mannitol. The use of these agents in these critical clinical situations merits close monitoring for adverse effects. There is a dire need for high-quality research to better inform clinicians of the best options for individualized care of patients with cerebral edema.
Pneumocephalus (PNC) is a condition in which when air is trapped inside the intracranial vault. The causes are varied, but include trauma and intracranial surgery. Treatment of PNC typically consists of augmenting patient oxygenation with the attempt of washing out pulmonary nitrogen, creating a gradient in which nitrogen in the intracranial air bubble diffuses out of the lungs via the blood. Though several high flow methods have been tested, the ideal mode of oxygenation has not fully been investigated. Here we present 3 cases of post-operative PNC who we felt were symptomatic from PNC. With administration of high-flow nasal cannula (HFNC), all patients improved both clinically and radiographically within a few hours, faster than in both anecdotal experience and published trials. Due to its steady FiO2 administration, positive pressure, comfort, and low side-effect profile, HFNC may be the ideal mode of oxygen delivery in PNC. We present a review of the physiology of PNC and the characteristics of several oxygen delivery systems to build a case for HFNC in this disease process.
Neurological deterioration is prevalent in the NICU population. Although hourly neurological examinations may be beneficial in the acute phase of neurological injury, prolonged use may be paradoxically harmful due to sleep deprivation.
Hyperammonemia is a rare complication of lung transplant with a high mortality rate. It presents as encephalopathy and progresses to seizures, status epilepticus, coma, cerebral edema, and brain death. Multiple treatments have been documented including administration of medications, gut decontamination, and dialysis. However, no definitive treatments exist and mortality remains between 67% and 75%. We present the case of a 65-year-old male with idiopathic pulmonary fibrosis who developed refractory status epilepticus secondary to hyperammonemia following lung transplant. The patient presented on postoperative day 7 with super-refractory status epilepticus and normal computed tomography scan of the head. Hyperammonemia was suspected due to refractory seizures and confirmed with peak ammonia level >1000 μmol/L. Despite aggressive treatment, the patient developed global cerebral edema and died. Postmortem investigations revealed that the patient was positive for Ureaplasma parvum. Additional studies are needed to elucidate the exact mechanism of disease and investigate successful treatment options.
The active nocturnist APP model was associated with an approximately 10% reduction in SAH mortality (P = .54). This supports the hypothesis that APPs can provide noninferior care as the previous model. Further studies are needed to demonstrate the effects of both nocturnist and APP-driven models.
Patients with cirrhosis are at high risk for sepsis and sepsis-related mortality. Aggressive treatment aimed at avoidance of hypoperfusion and prompt identification and treatment of the causative organism can improve patients' survival. Fluid administration is the first-line treatment to improve perfusion to vital organs; however, care should be taken to assess true intravascular volume status. In patients with adequate intravascular volume, vasopressors are then added to support blood pressure. Complications of cirrhosis often worsen in the setting of sepsis. Portosystemic encephalopathy, pulmonary complications, renal complications, adrenal insufficiency, malnutrition, and insufficient glucose control all must be considered and treated to support a patient with cirrhosis through sepsis. The quality of care that these patients receive ultimately influences their survival.
Hypertriglyceridemia is infrequently reported as a cause of suboptimal delivery of dialytic therapy in critically ill patients. We report the case of a critically ill liver transplant patient in the Intensive Care Unit who was found to have recurrent filter clotting during continuous renal replacement therapy (CRRT). The patient had increased serum triglycerides (TGs), which was identified approximately 2 weeks into hospitalization and initially believed to be due to prolonged propofol use. The patient's elevated TGs ultimately caused her blood to become lipemic, causing the dialytic circuit to become nonfunctional and placed the patient in imminent danger due to hyperkalemia and metabolic acidosis. Therapeutic plasma exchange was emergently used to lower TG levels, and renal replacement therapy was resumed without any other issues. The patient's persistent hypertriglyceridemia was attributed to a combination of adverse effect of medications and liver graft failure. The high TG level and abnormal liver functions improved after a repeat liver transplantation.
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