Elevated S100B level in cerebrospinal fluid could predict poor outcome of carbon monoxide poisoning.

OBJECTIVE: S100B is a calcium-binding protein produced by astroglia in the brain and has been used as a marker of neuronal damage after brain trauma. We investigated the utility of S100B in cerebrospinal fluid (CSF) measured during the early phase of carbon monoxide (CO) poisoning in predicting the subsequent clinical course. METHODS: The study included 31 patients who were admitted to the hospital with loss of consciousness following CO poisoning. S100B levels were measured by enzyme-linked immunosorbent assay in CSF, and serum samples collected simultaneously within 24 hours and on the fourth day after CO exposure. All patients were followed for at least 3 months and divided into 3 groups based on the clinical course: persistent vegetative state (PVS), delayed encephalopathy (DE), and complete recovery with no complications (NC). RESULTS: During the 3-month period, 3 patients developed PVS, 5 developed DE, and 23 were classified as NC. The mean S100B levels in the CSF within 24 hours after CO exposure were higher in the PVS group (9.25 ng/mL) than in the DE (2.03 ng/mL) and NC groups (1.86 ng/mL). However, the mean serum S100B levels were not elevated in the 3 groups (0.21, 0.59, and 0.16 ng/mL, respectively). CONCLUSION: Early elevation of S100B in CSF after CO poisoning could be a suitable predictor of subsequent development of PVS.

Severe carbon monoxide poisoning complicated by hypothermia: a case report.

It is proposed that the significant elevation of interleukin-6 (>400 pg/mL) in cerebrospinal fluid during the early phase of carbon monoxide poisoning may be a predictive biomarker for the development of delayed encephalopathy. A 52-year-old man presented to the emergency department with severe carbon monoxide poisoning. On arrival, the patient was comatose with decorticate rigidity (Glasgow Coma Scale, E1V1M3). His core body temperature, measured in the urinary bladder, was 32.4°C. Laboratory blood analysis revealed elevated CO-Hb (36.0%) and metabolic acidosis with elevated lactate (pH 7.081; base excess [BE], -19.2 mmol/L; HCO3, -9.8 mmol/L; lactate, 168.8 mg/dL). After treatment with hyperbaric oxygen and several different rewarming techniques, he became alert and his core body temperature increased to normal. Interleukin-6 in cerebrospinal fluid at 5.5 hours after his last exposure to carbon monoxide was significantly elevated (752 pg/mL). However, he did not develop delayed encephalopathy. In this case, hypothermia in the range of therapeutic hypothermia (32°C to 34°C) may have suppressed formation of reactive oxygen species and subsequent lipid peroxydation, preventing the development of delayed encephalopathy. Therapeutic hypothermia initiated soon after the last exposure to carbon monoxide may be an effective prophylactic method for preventing the development of delayed encephalopathy.

[Acute alcoholism and clinical examination].

Acute alcoholism causes consciousness disorder. It should be suspected when expired air smells of alcohol on arrival, or laboratory data suggest hyperosmolarity. In addition, an increase in the osmotic pressure gap suggests the possibility of acute alcoholism. The blood alcohol level can be estimated from the value.

Gastric stenosis in severe corrosive gastritis: prognostic evaluation by endoscopic ultrasonography.

INTRODUCTION: Endoscopic ultrasonography can provide high-resolution images of the gastric wall. CASE REPORT: A 24-year-old woman with severe corrosive gastritis following massive ingestion of an alkaline household chemical was examined with endoscopic ultrasonography using a 20-MHz probe. Endoscopic ultrasonography disclosed diffuse thickening of the entire gastric wall and lack of demarcation of the muscular layer in the antrum. Several weeks after the ingestion, stenosis developed in the antrum and was treated with laparoscopic gastrectomy. DISCUSSION: Endoscopic ultrasonography can provide accurate evaluation of depth of lesions in corrosive gastritis and may be useful in predicting gastric stenosis.

Intermittent complete atrioventricular block after long term low-dose carbamazepine therapy with a serum concentration less than the therapeutic level.

After twelve months of low dose carbamazepine therapy (200 mg daily) for temporal lobe epilepsy, a 66-year-old woman presented to the hospital complaining of frequent episodes of sudden dizziness. Because Holter monitoring documented intermittent complete atrioventricular block, the patient was admitted to the hospital when the serum concentration of carbamazepine was 4 microg/mL. After discontinuation of carbamazepine, the patient returned to normal sinus rhythm. The present case suggests that complete atrioventricular block may occur long after initiation of carbamazepine therapy in an older woman even if the daily dosage or the serum concentration of carbamazepine is low.