Cerebral energy metabolism during transient hyperglycemia in patients with severe brain trauma

Abstract

Critical Care 2003, 7(Suppl 2):P001 (DOI 10.1186/cc1890) Studies on head injury-induced pituitary dysfunction are limited in number and conflicting results have been reported. To further clarify this issue, 29 consecutive patients (24 males), with severe (n = 21) or moderate (n = 8) head trauma, having a mean age of 37 ± 17 years were investigated in the immediate post-trauma period. All patients required mechanical ventilatory support for 8-55 days and were enrolled in the study within a few days before ICU discharge. Basal hormonal assessment included measurement of cortisol, corticotropin, free thyroxine (fT4), thyrotropin (TSH), testosterone (T) in men, estradiol (E2) in women, prolactin (PRL), and growth hormone (GH). Cortisol and GH levels were measured also after stimulation with 100 µg human corticotropin releasing hormone (hCRH) and 100 µg growth hormone releasing hormone (GHRH), respectively. Cortisol hyporesponsiveness was considered when peak cortisol concentration was less than 20 µg/dl following hCRH. TSH deficiency was diagnosed when a subnormal serum fT4 level was associated with a normal or low TSH. Hypogo-nadism was considered when T (males) or E2 (women) were below the local reference ranges, in the presence of normal PRL levels. Severe or partial GH deficiencies were defined as a peak GH below 3 µg/l or between 3 and 5 µg/l, respectively, after stimulation with GHRH. Twenty-one subnormal responses were found in 15 of the 29 patients (52%) tested; seven (24%) had hypogonadism, seven (24%) had cortisol hyporesponsiveness, five (17%) had hypothyroidism, and two patients (7%) had partial GH deficiency. These preliminary results suggest that a certain degree of hypo-pituitarism occurs in more than 50% of patients with moderate or severe head injury in the immediate post-trauma period, with cortisol hyporesponsiveness and hypogonadism being most common. Further studies are required to elucidate the pathogenesis of these abnormalities and to investigate whether they affect long-term morbidity. To investigate cortisol reserve in head trauma, 35 consecutive patients (30 men) with a mean age of 36 ± 16 years were studied 5-60 days after physical injury. Patients were enrolled in the study within a few days before ICU discharge. First, a morning blood sample was obtained to measure baseline cortisol, and ACTH plasma levels. Subsequently, 1 µg synthetic ACTH was injected intravenously and, 30 min later, a second blood sample was drawn to determine stimulated plasma cortisol. Patients having stimulated cortisol levels below 18 µg/dl were defined as nonresponders to the low-dose stimulation test (LDST). Mean (± SD) values for ACTH, baseline, and stimulated cortisol concentrations were 49 ± 27 pg/ml, 19.7 ± 5.5 µg/dl and 23.6 ± 6.7 µg/dl, respectively. Six of the 35 patients (17%) failed the LDST. Nonresponders were similar to responders with regard to age, gender, and severity of head injury. However, nonresponders more frequently required vasopressors (6/6 vs 14/29, P = 0.02) and for a longer time interva...

Hyperglycemia in pediatric head trauma patients: a cross-sectional study

“…The explanation would be that these patients have a more important metabolic response to injury due to the effects of cortisol, glucagon and epinephrine release, causing intrac-pediatric head trauma: hyperglycemia Melo et al ellular acidosis, lactate accumulation, high blood glucose levels and neuronal injury 6,[19][20][21] . Therefore, our data are in accordance with the results from other authors who correlate the head trauma severity and the metabolic response to trauma, particularly higher blood glucose levels 7,22,23 . Some studies show that hyperglycemia is associated with a worse outcome, regardless of injury characteristics 24 .…”

Treating Intracranial Hypertension in Patients with Severe Traumatic Brain Injury during Neurointensive Care

“…Production of lactate decreases brain tissue pH which may deactivate various enzymes, activate destructive intracellular cascades and energy-consuming pumps, thereby impairing functional and structural integrity of the brain in face of its limited energetic reserves even further. As suggested by the recently published results by the group of Christian Nordström only hyperglycemic values > 15 mmol/l are associated with a moderate increase in interstitial lactate levels [120].…”

Intensive Versus Conventional Insulin Therapy in Critically Ill Neurologic Patients

“…Other stroke studies also confirm worse functional outcome with persistent hyperglycemia [7,8]. In moderate to severe TBI studies, higher initial and postoperative glucose levels were associated with high intracerebral lactate levels and worse outcome, especially with a blood glucose level of greater than 160-200 mg/dl [9][10][11][12]. The question of whether hyperglycemia is simply a marker of more severe disease or actually causes worse outcome has not been definitively answered.…”