Serum levels of Selenium and C-reactive protein in comatose patients with severe traumatic brain injury during the first week of hospitalization: case-control study.

INTRODUCTION: Mortality and morbidity related to traumatic brain injuries still remain high in patients. Many authors reported the importance of Selenium in maintaining the integrity of brain functions. This fact is supported by clinical evidence that therapy with selenium supplementation could help patients suffering from brain disorders like neurodegenerative diseases. The aim of our study was to assess the relationship between Selenium concentration in serum and evolution of comatose patients with severe traumatic brain injury, in the first week of admission, and the correlation between selenium and C-reactive protein. METHODS: This case-control study was conducted with 64 comatose patients with TBI, in the Department of Anesthesiology and Reanimation, IbnSina University Hospital and Hospital of specialties in Rabat-Morocco, and healthy volunteers recruited in Blood transfusion center of Rabat. Blood sampling was collected from TBI patients, in the first week (3h after admission and each 48h during one week), and from healthy volunteers one time. Concentration of Se in serum was determined by electrochemical atomic absorption spectrometry. Statistical analysis was performed using Statistical software (SPSS) and the cases and controls were compared using the Mann-Whitney U test. A P-value < 0.05 was considered to be statistically significant. RESULTS: Comparison selenium concentration in the first day (D0), third day (D2) and fifth day according to the death and survival statue in patients did not show statistical significance (p > 0.05). Selenium concentration of D0 in patients and Selenium concentration in control group also did not show statistical significance (p > 0.05). Similarly, we did not report a correlation between selenium and C-reactive protein. CONCLUSION: According to our data selenium and CRP may not play a role in progression of coma state in patients with severe traumatic brain injury.

[Hypercalcemic crisis and hypocalcemic tetany]. / Hyperkalzämische Krise und hypokalzämische Tetanie.

A serum calcium level >3.5 mmol/l together with clinical symptoms such as muscle weakness, fatigue, nausea, vomiting, pancreatitis or even coma are characteristic for a hypercalcemic crisis (HC). Primary hyperparathyroidism (1HPT) and malignancy-associated hypercalcemia are the most frequent causal diseases for a HC. The analysis of serum levels for calcium, phosphorous, intact parathyroid hormone, electrophoresis and renal function parameters indicate which further radiological, scintigraphic or serum diagnostic steps are adequate to identify the cause of the patient's acute situation (i. e. most frequently 1HPT or malignant disease with bone involvement, e. g. myeloma) and thus to initiate the required surgical or oncological intervention. However, the primary goals in the treatment of HC include correcting dehydration and improving kidney function, lowering calcium levels and decreasing osteoclastic bone resorption. The goals are accomplished by volume repletion, forced diuresis, antiresorptive agents and hemodialysis on an intensive care unit. Hypocalcemic tetany (HT) is the consequence of severely lowered calcium levels (<2.0 mmol/l), usually in patients with chronic hypocalcemia. The causal disease for hypocalcemic tetany is frequently a lack of parathyroid hormone (PTH), (e. g. as a complication of thyroid surgery) or, rarely, resistance to PTH. HT due to severe and painful clinical symptoms requires rapid i. v. calcium replacement by central venous catheter on an intensive care unit. For the treatment of chronic hypocalcemia oral calcium and 25OH-vitamin D or even 1,25(OH)2-vitamin D3 and magnesium supplements may be necessary to achieve the desired low normal calcium levels. Thiazides are useful to reduce renal calcium loss and to stabilize the calcium levels. Some patients continue to exhibit clinical symptoms despite adequate calcium levels; in these cases s. c. parathyroid hormone 1-84 should be considered to stabilize calcium levels and to lower the dosage of calcium and vitamin D supplements.

[Ethanol, water, salt and coma]. / Alkohol, Wasser, Salz und Koma.

We report on a 52-year-old woman with liver cirrhosis who suddenly fell into deep coma after correction of an intercurrent hyponatremia. After exclusion of the commonest causes of coma, the MRI showed a symmetrical osmotic demyelination of both thalami. The newest epidemiological data, the pathophysiology of osmotic demyelination, the threats of the treatment of a prolonged severe hyponatremia as well as the therapeutic options in face of osmotic demyelination are discussed.

Effects of electrical cervical spinal cord stimulation on cerebral blood perfusion, cerebrospinal fluid catecholamine levels, and oxidative stress in comatose patients.

OBJECTIVES: Electrical spinal cord stimulation (SCS) is used to treat of chronic pain, obstructive arterial-related ischemia, and anginal pain. This study investigated cerebral blood perfusion, cerebrospinal fluid (CSF) catecholamine levels, and oxidative stress before and after cervical SCS in comatose patients. METHODS: We evaluated cerebral blood perfusion, catecholamine (dopamine, norepinephrine, and epinephrine) levels, and oxidative stress in 20 comatose patients before and after SCS. After SCS for six months, cerebral blood perfusion (SPECT index, 2.293 +/- 0.255 vs. 2.779 +/- 0.209, p < 0.001), dopamine (49.0 +/- 12.1 vs. 198.9 +/- 62.6, p = 0.025), and norepinephrine (197.6 +/- 62.9 vs. 379.6 +/- 52.6, p = 0.021) but not epinephrine were significantly increased. Moreover, superoxide free radicals in whole blood were significantly decreased (210,079 +/- 47,763 vs. 109,212 +/- 20,086, p = 0.011) after SCS. Nine patients recovered from the consciousness within 71-287 days. CONCLUSIONS: Increase of cerebral blood perfusion and catecholamines (dopamine and norepinephrine) in CSF after SCS was observed, whereas epinephrine level was unchanged. The superoxide free radicals were decreased after SCS. The results suggest that SCS increases cerebral blood perfusion, attenuates oxidative stress and increases biogenic amines in comatose patients.

Transferrin saturation and recovery from coma in cerebral malaria.

To determine if the elevated transferrin saturations found in some patients with severe malaria are associated with an adverse outcome in cerebral malaria, we retrospectively measured baseline saturations in stored serum samples from 81 Zambian children with strictly defined cerebral malaria. The children had been treated with quinine, sulfadox-ine-pyrimethamine, and intravenous infusions of either placebo (n = 39) or the iron chelator, desferrioxamine B (n = 42), in a previously reported trial (Gordeuk et al, N Engl J Med 327:1473, 1992). More than one-third of children in both the placebo- and iron chelator-treated groups had transferrin saturations exceeding 43%, which is 3 standard deviations above the expected mean for age. Among children receiving quinine and placebo, those with elevated transferrin saturations had a delayed estimated median time to recover full consciousness (68.2 hours) compared with those with saturations < or = 43% (25.4 hours; P = .006). The addition of iron chelation to quinine therapy in children with high saturations appeared to hasten recovery (P = .046). We conclude that increased transferrin saturations may be associated with delayed recovery from coma during standard therapy for cerebral malaria and that serum iron and total iron binding capacity should be measured in future studies.

Circadian profile of plasma cortisol and aldosterone in post-traumatic comatose patients under high-dose dexamethasone treatment.

Six comatose patients hospitalized in an intensive care unit immediately following an acute trauma with severe brain injury (road or industrial accident) were examined through out three consecutive 24-h cycles in the first week after trauma, when receiving intramuscularly 12 mg daily of dexamethasone-21-phosphate. Intravenous or enteral nutrition was supplied continuously. Plasma cortisol and aldosterone were measured on blood samples drawn at 4-h intervals. Data were analyzed both by conventional chronograms and by rhythmometric analysis according to the Cosinor procedures. A normally-synchronized circadian pattern of plasma cortisol was recognizable in all cases in the face of the lack of consciousness and of the pharmacological administration of dexamethasone. Acrophase was located at 08:56, with a 95% confidence region vastly overlapping the corresponding region of the controls. By contrast, the circadian pattern of plasma aldosterone appeared to be disrupted; irregular fluctuations were recorded along the entire day. The Cosinor analysis did not detect a significant rhythm of plasma aldosterone during the examined 24-h cycles. Data obtained with the present investigation demonstrate that comatose patients within a few days after severe head injury and given high-dose corticoid treatment do maintain the normal circadian organization of the plasma cortisol, whereas loose that of the plasma aldosterone. Our findings are compatible with the concept that glucocorticoid rhythmicity is particularly resistant to acute injury; the mineralocorticoid rhythmicity appears more labile probably as a consequence of the plurifactorial modulation.