ABSTRACT
A 21-year-old male trauma patient presented after a motor vehicle crash, witnessed massive aspiration and sustained traumatic brain injury. On postinjury day 3, the patient progressed to adult respiratory distress syndrome (ARDS) refractory to all conventional therapies, prompting the use of extracorporeal membrane oxygenation (ECMO). After 5 days of ECMO support and 3 thrombosed oxygenators, systemic anticoagulation was initiated. After 20 days of ECMO, 15 of which required systemic anticoagulation, the patient was decannulated and transferred to a rehabilitation facility. The patient is currently home without any neurological deficits. Although controversial, ECMO may serve a role as a rescue therapy in ARDS when conventional therapies fail in the brain-injured patient.
Subject(s)
Brain Injuries/therapy , Extracorporeal Membrane Oxygenation , Respiratory Distress Syndrome/therapy , Accidents, Traffic , Anticoagulants/therapeutic use , Brain Injuries/complications , Extracorporeal Membrane Oxygenation/adverse effects , Humans , Male , Respiratory Distress Syndrome/etiology , Thrombosis/drug therapy , Thrombosis/etiology , Young AdultABSTRACT
BACKGROUND: Thyroid hormones are important determinants of energy expenditure, and in rodents, adipose tissue affects thyroid hormone homeostasis via leptin signaling. The relationship between thyroid hormones and nutritional status in humans has been assessed primarily in drastic dietary or bariatric surgery interventions, while limited information is available on serial assessment of this axis during moderate, prolonged dietary restriction. METHODS: To evaluate the effects of moderate dietary restriction on thyroid hormone homeostasis, 47 subjects with a body mass index (BMI) of 25-45 kg/m(2) were enrolled in a longitudinal intervention study; 30 nonoverweight volunteers were also enrolled as controls. Overweight and obese subjects underwent a 12-month individualized dietary intervention aimed at achieving a 5-10% weight loss. RESULTS: The intervention resulted in a 6.3±0.9 kg (6.5±1.0%) weight loss. At baseline, thyrotropin (TSH) and T3 concentrations correlated significantly with fat mass (R=0.257, p=0.024 and R=0.318, p=0.005, respectively). After weight loss, T3 decreased significantly (from 112.7±3.1 to 101.8±2.6 ng/dL, p<0.001) in the absence of significant changes in TSH or free T4 (fT4). The decrease in serum T3 correlated with the decrease in weight (R=0.294, p<0.001). The T3:fT4 ratio decreased significantly (p=0.02) in individuals who lost >5% body weight. CONCLUSIONS: T3 concentration closely correlates with individual nutritional status, and moderate weight loss results in a decrease in T3 with minimal changes in other thyroid hormone homeostasis parameters. The data suggest that a decrease in peripheral conversion of the prohormone T4 into its hormonally active metabolite T3 is at least in part responsible for the observed changes in thyroid hormone homeostasis.
