Randomized trial to evaluate nutritional status and absorption of enteral feeding after brain death.

CONTEXT: Catecholamines and inflammatory mediators, with elevated levels after brain death, are associated with reduced function and survival of transplanted organs. Enteral nutrition reduces tissue damage and may benefit organs. OBJECTIVE: To evaluate the effects of immunomodulating enteral nutrition in organ donors. DESIGN: Prospective, randomized, open-label study. SETTING: Intensive care unit. PATIENTS: Thirty-six brain-dead organ donors. INTERVENTIONS: Donors were randomized to receive enteral nutrition containing omega-3 polyunsaturated fatty acid, antioxidants, and glutamine or standard care (fasting). Donors received hormonal replacement therapy of corticosteroid, levothyroxine, dextrose, and insulin. MAIN OUTCOME MEASURES: Gastrointestinal assimilation (measured by 13 carbon-labeled uracil breath analysis), quantity of organs recovered, resting energy expenditure, urine level of urea nitrogen, and serum levels of albumin, prealbumin, interleukin 6, tumor necrosis factor-α, and C-reactive protein were evaluated. RESULTS: Thirteen patients (36%) assimilated 13C-labeled uracil. Resting energy expenditure was significantly higher than predicted between 10 and 14 hours after baseline in 33 donors (P= .007). Other measures were not conclusively different between fed and fasting groups. No adverse events occurred that were related to the enteral feeding. CONCLUSIONS: About 30% of donors metabolized 13C-labeled uracil, although no difference in oxidation rate was found between fasting and fed donors. Corticosteroid administration lowers plasma levels of interleukin 6 and most likely contributes to greater than predicted resting energy expenditure. Thus energy needs may not be met during fasting if hormones are given. Consequences of this possible energy deficit warrant further study.

Thrombocytosis in the NICU.

An elevated platelet count may occur during care of neurology/neurosurgical patients and is usually due to reactive or secondary thrombocytosis (ST) caused by inflammation or infection. Primary (clonal) thrombocythemia or essential thrombocythemia associated with myeloproliferative disorders is usually known before or during early patient assessment. Rarely, paraneoplastic causes of thrombocytosis may be discovered. Although no single test differentiates primary from secondary etiologies, laboratory tests that show increased acute phase responses, such as C-reactive protein, fibrinogen, erythrocyte sedimentation rate, and interleukin-6, may be useful in diagnosing ST. Thrombosis due to ST is rare in any platelet count. ST, however, should be considered within the overall risk assessment for thromboembolism in any patient. If treatment is initiated, low-dose aspirin is sufficient.

Endocrine failure after traumatic brain injury in adults.

OBJECTIVE: To review histopathological and clinical data linking endocrine failure to traumatic brain injury (TBI) during acute neurosurgical treatment and rehabilitation. METHODS: A focused search of the Medline (PubMed) medical literature database and the authors' files were used to identify selected publications. RESULTS: Endocrine failure may produce clinically important consequences during acute and convalescent care after TBI, and may be caused by direct injury to the hypothalamic- pituitary axis (HPA), neuroendocrinological effects from catecholamines and cytokines, or from systemic infection/inflammation that produces primary gland failure. Autopsy evidence of hemorrhage or ischemia in the HPA is common soon after TBI. The estimated incidence of acute hormone reduction is adrenal 15%, thyroid 5 - 15%, growth hormone 18%, vasopressin 3 - 37%, and gonadal (25 - 80%). Hyperprolactinemia occurs in more than 50% of patients. Inappropriate secretion of antidiuretic hormone (SIADH) and the euthyroid sick syndrome are common. Acute adrenal failure, central hypothyroidism, SIADH, and diabetes insipidus (DI) may cause poor neurological outcomes including death, hypo/hypernatremia, hypotension, and increased vasoactive drug requirements. Treatment of those conditions is warranted. Delayed diagnosis of hypopituitarism is often mistaken for symptoms of residual head injury. Some chronic hormone deficiency occurs in 30 - 40% of selected patients after TBI, more than one deficiency in 10 - 15%, growth hormone in 15 - 20%, gonadal hormones in 15%, and hypothyroidism in 10 - 30%. Chronic adrenal failure and DI are reported over a wide incidence. Prolactin is elevated in 30%. All clinical symptoms respond favorably to replacement therapy. CONCLUSIONS: Severe TBI associated with basilar skull fracture, hypothalamic edema, prolonged unresponsiveness, hyponatremia, and/or hypotension is associated with a higher occurrence of endocrinopathy. Greater awareness of this possible complication of TBI and appropriate testing are encouraged.

Counteracting the effects of anticoagulants and antiplatelet agents during neurosurgical emergencies.

OBJECTIVE: Emergent neurosurgery may be precipitated or complicated by previous or concomitant administration of anticoagulants, thrombolytic medications, or antiplatelet agents. Recommendations are presented to reverse or counteract the effects of those drugs before or during neurosurgical interventions. METHODS: Directed literature review. RESULTS: Evidence-based data specific to neurosurgery are limited. CONCLUSION: Other clinical experience based on mechanisms of drug action within the coagulation process confirm that single or combined administration of platelet transfusions, fresh frozen plasma, cryoprecipitate, vitamin K, protamine, desmopressin, and recombinant activated factor VII can treat coagulopathies caused by warfarin, heparin, aspirin, adenosine diphosphate-receptor antagonist, glycoprotein IIb/IIIa receptor blocking agents, and thrombolysis. Specific interventions and recommended dosages are reviewed.

Factors during donor care that may affect liver transplantation outcome.

Publications are reviewed that identify factors during donor care and characteristics of the donor liver that may be associated with outcome following liver transplantation. The procurement coordinator has the opportunity to influence cold ischemia time, blood pressure, the serum sodium concentration and, perhaps, liver glycogen reserves. These variables may significantly affect postimplantation graft performance and graft or recipient survival. Summaries of those publications comprising this database are presented, and several limitations in their interpretation are discussed.