Adrenal insufficiency following traumatic brain injury in adults.

PURPOSE OF REVIEW: Hypoadrenalism occurs in approximately 25% of patients soon after traumatic brain injury. Neurosurgeons or critical care physicians should be prepared to diagnose and treat this and other related hormonal deficiencies. RECENT FINDINGS: The severity of traumatic brain injury, location of basilar skull fractures and edema or hemorrhage within the hypothalamic-pituitary axis appear correlated with secondary adrenal failure. Primary hypoadrenalism also may occur due to injury-related systemic inflammation. Hypotension requiring vasoactive drug support, hyponatremia and hypoglycemia may be corresponding clinical signs. Evaluation of either primary or secondary hypoadrenalism should include measurement of basal and post-adrenocorticotropin stimulation cortisol blood concentrations. If the basal cortisol is under 15 microg/dl or increases by over 9 microg/dl after stimulation treatment should be considered. Intravenous hydrocortisone at 50-100 mg every 8 h or by continuous infusion is usually sufficient but may be supplemented with a mineralocorticoid if hyponatremia persists. All patients sustaining severe traumatic brain injury should be tested for endocrine failure (adrenal, thyroid and growth hormone) 3 months after injury. SUMMARY: Adrenal gland failure or the inability to produce adrenocorticotropin and other pituitary hormones may occur early after traumatic brain injury. Acute treatment of either cause of hypoadrenalism may correct associated hypotension, hypoglycemia, or hyponatremia.

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.

Characterization of an aquaporin-2 water channel gene mutation causing partial nephrogenic diabetes insipidus in a Mexican family: evidence of increased frequency of the mutation in the town of origin.

A Mexican family with partial congenital nephrogenic diabetes insipidus (NDI) that resulted from a mutation in the aquaporin-2 water channel (AQP2) was characterized, and the source of this rare mutation was traced to the family's town of origin in Mexico. Affected individuals with profound polyuria and polydipsia were homozygous for an autosomal recessive missense V168M mutation in the AQP2 gene. Expression in oocytes revealed that, although retained in the endoplasmic reticulum (ER) to a great extent, a considerable amount of the partially functional AQP2-V168M was expressed at the plasma membrane, and that its ER retention was less than AQP2-T126M, a functional mutant in severe recessive NDI. None of the affected AQP2-V168M individuals had neurologic deficits, which also suggested a milder form of the disease. The homozygous individuals reported subjective improvement in polyuria and polydipsia with the use of dDAVP (1-desamino-8-D-arginine-vasopressin). When clinically tested, infusion of dDAVP at variable doses produced a partial increase in the urinary osmolality in homozygous individuals and decreased their water intake. Heterozygotes were unaffected when compared with controls. Samples were obtained from the population of the Mexican town of origin of the family; 30% of the population was heterozygous for the V168M AQP2 mutation and 1% was homozygous for the mutation. The high frequency of this rare mutation in the town provides evidence for an important health care problem in the village with consequences for future generations.

Severe reversible dilated cardiomyopathy and hyperthyroidism: case report and review of the literature.

OBJECTIVE: To describe a case of a 46-year-old woman with Graves' disease and reversible low-output congestive heart failure and present a comparative analysis of 23 similar cases reported in the literature. METHODS: A detailed case report is presented. In addition, a review of the pertinent literature published between 1960 and 2002 was performed to identify similar cases of dilated cardiomyopathy and thyrotoxicosis and to assess the findings in these patients. RESULTS: A 46-year-old woman without primary heart disease was admitted to the hospital with Graves' thyrotoxicosis and severe low-output congestive heart failure. Her left ventricular ejection fraction (LVEF) at the time of initial assessment was less than 20%, and her condition was categorized as New York Heart Association (NYHA) functional class III. Nineteen months after she was treated for hyperthyroidism, her LVEF was 49% and her status was NYHA class I. A severe hypotensive episode occurred when b-adrenergic blockade therapy was initiated. The group of 23 similar cases from the literature plus our currently described patient had a mean age of 45 years, a male-to-female ratio of 1:1.2, Graves' disease as the principal cause, and LVEF improvement from 29% to 58%. CONCLUSION: Dilated cardiomyopathy is an unusual manifestation of hyperthyroidism with unclear cause. Clinicians should be aware of this entity because it is treatable and hypotension can occur if b-adrenergic blockade treatment is initiated.

Meningitis bacteriana: características clínicas y valor diagnóstico de los signos de irritación meníngea / Bacterial meningitis: clinical characteristic and diagnodtic value of the signs of meningeal irrigation

Se estudiaron retrospectivamente las características clínicas de mayor frecuencia en un grupo de 67 pacientes adulto con meningitis bacteriana a su ingreso, con el objeto de conocer los signos y síntomas claves que permitan realizar un diagnóstico más rápido y preciso que garantice un mejor pronóstico. Se encontró que los signos y síntomas más frecuentes fueron: Cefalea, fiebre, rigidez de nuca, náuseas y vómitos, alteración del estado de conciencia, signos de Kernig y Brudzinski y cambios de conducta. Igualmente se procedió a determinar la sensibilidad (SE) y especificidad (ES) de los signos de irritación meníngea. Rigidez de nuca (SE= 60,74 por ciento/Es= 55,73 por ciento), signo de Kernig (SE= 34,21 por ciento/ES= 91,80 por ciento) y signo de Brudzinski (SE= 38,16/ES= 91,80 por ciento) para conocer objetivamente su verdadera utilidad clínica en el diagnóstico de meningitis bacteriana

Diabetes mellitus y control metabólico: a propósito de la segunda encuesta epidemiológica "Parque del Este" 13 de noviembre de 1993 / Mellitus diabetes and control matabolic: to propous of the second epidemiology inquiry. \"Parque del Este\" 13 de november de 1993

Décadas de controversias sobre la hipótesis de un buen control metabólico para prevenir o retardar las complicaciones crónicas de la diabetes mellitus llegaron a un final desde que fueron publicados los resultados del diabetes control and complication trial (DCCT). Al menos en pacientes diabéticos tipo 1, el riesgo de complicaciones microvasculares puede reducirse categóricamente por un control de la glicemia en forma excelente. En el contexto del día mundial de la diabetes se realizó la segunda encuesta epidemiológica en el Parque del Este de Caracas. Encontramos 179 casos de diabetes (26,8 por ciento). Los pacientes fueron agrupados de acuerdo al tipo de control metabólico: buen control (- 150 mg/dl) = 76 casos (42,4 por ciento). Control regular (151 -200 mg/dl) = 41 casos (22,9 por ciento). Control malo (201 -250 mg/dl) = 29 casos (16,2 por ciento). Control pésimo ( +250 mg/dl) = 33 casos (18,4 por ciento). Estos resultados expresan que al menos 67 por ciento de los diabéticos evaluados no se encontraban suficientemente bien controlados, lo que traducirse en un mayor esfuerzo de los servicios sanitarios, especialmente de los médicos tratantes, los pacientes diabéticos y sus familiares para profundizar en la búsqueda incansable por el mejor control metabólico posible