BACKGROUND: The improved technique for cardiopulmonary resuscitation(CPR) has resulted in the survival of many patient who experienced cardiac arrest. However, mortality in resuscitated patients is high, and the survival rate without brain damage is very low. Various neurological examination models, neuro-imaging techniques, electrophysiological procedures, and biochemical tests have been studied with respect to the detection of cerebral damage and outcome, but an early, reliable prediction of individual outcomes is still uncertain. METHODS: We studied twenty patient who had been in a coma for more than 24 hours after CPR, Somatosensory evoked potentials(SEP) were measured within the first three days after CPR. RESULTS: Of the twenty patients, seven patients(35%) had a good outcome, and thirteen patients(65%) had a bad outcome. Of the eleven patients with loss of the cortical evoked potential's N20 peak, all had a bad outcome. CONCLUSION: SEPs are of great benefit in prognostic evaluation after CPR.
Brain ; Cardiopulmonary Resuscitation* ; Coma* ; Evoked Potentials, Somatosensory* ; Heart Arrest ; Humans ; Mortality ; Neurologic Examination ; Survival Rate

BACKGROUND: Doxylamine succinate(DS) is an antihistamine commonly used as an over-the-counter medication to relieve insomnia and frequently involved in overdoses. Its overdoses are dominated by anticholinergic effect. Recently it was revealed that DS had a direct effect on muscle, while its exact mechanism is not clear yet. We evaluated the patients with rhabdomyolysis induced by DS overdose for patients disposition based upon clinical decision, especially by creatinine phosphokinase(CPK). METHODS: We reviewed retrospectively the medical records of patients admitted by DS overdose from Jan. 1998 to Oct. 1999. Seventy and nine cases of DS overdose were evaluated with respect to age and sex distribution, amount ingested, clinical symptomatology, time from ingestion to visit, pattern of CPK, amount of bicarbonate used as therapy, complication and prognosis, especially in patients complicated rhabdomyolysis. RESULTS: Rhabdomyolysis, diagnosed as more than 1,000I. U/L of CPK, has been noted in 25(31.6%) of 79 cases of DS overdose visited to our emergency department(ED). In patients diagnosed rhabdomyolysis, the number of man was 10 cases(40%) and the number aged between 20 and 40 years was 22 cases(88%). The average time from DS ingestion to ED visit was 459 minutes. The amount of DS ingested was 500-5,000mg(mean, 1,980mg). 13(52%) cases ingested less than 2,250mg of DS. The initial levels of CPK(range, 48-14900I. U/L; normal range, 26-200I. U/L) after admitting to our emergency department were normal in 15 cases(60%) of rhabdomyolysis patients. The range of peak CPK levels after ingestion was 607 to 412,500I. U/L(mean, 33,550I. U/L). Its peak time was 6 to 96 hours(mean, 28.96 hours). In 14 cases(67%) of 21 visiting within 24 hours after ingestion, peak time of CPK ranged 12 to 24 hours after ingestion. The amount of bicarbonate used as therapy of rhabdomyolysis ranged 100 to 2,740mEq(mean, 656mEq) and all patients was discharged after improvement without other complication including acute renal failure. CONCLUSIONS : Although patients ingested less than 2,250mg of DS, emergency physicians should observe them more than 24 hours after DS ingestion with CPK follow-up after gastric irrigation and charcoal administration.
Acute Kidney Injury ; Charcoal ; Creatinine ; Doxylamine* ; Eating ; Emergencies ; Emergency Service, Hospital ; Follow-Up Studies ; Gastric Lavage ; Humans ; Medical Records ; Prognosis ; Reference Values ; Retrospective Studies ; Rhabdomyolysis* ; Sex Distribution ; Sleep Initiation and Maintenance Disorders ; Succinic Acid*

No abstract available.
Hemangioma* ; Ligation*

Sinus venosus is a rare cardiac defect, which may lead to an interatrial shunt. Diagnosis on echocardiography may be difficult requiring an evaluation by a board-certified cardiologist. We report a case of a 41 year-old male who presented with recurrent episodes of hemiparesis (first left sided, second right sided). Surgical correction of sinus venosus led to resolution of his symptoms.
Heart Septal Defects, Atrial

BACKGROUND: The goal of successful resuscitation is not only to stop the process of ischemia as soon as possible but also to overcome the secondary injury process after resuscitation, which involves a complex interplay of mechanisms. Brain damage accompanying cardiac arrest and resuscitation is frequent and devastating. Cells die by one of two mechanisms: necrosis or delayed neuronal death. Delayed neuronal death may require protein synthesis. Neurons in the CA1 subfield of the hippocampus are selectively vulnerable to death after injury by ischemia and reperfusion. Death of these neurons occurs after an interval of 1 or 2 days. We assessed the effects of a protein synthesis inhibitor, cycloheximide(CHX), on hippocampal neuronal death of rats by using the ventricular fibrillation cardiac arrest(VFCA) model. METHODS: The effect of CHX(3mg/kg, s.c.) on hippocampal neuronal death was studied in two groups of 18 rats each, one group being subjected to a 2-min VFCA and the other to a 3-min VFCA. Each group was divided into three subgroups: control(group I,II) without subcutaneous injection of CHX, 'exp-12' of group I/II treated with CHX 12 hours after return of spontaneous circulation (ROSC), and 'exp-24' of group I/II treated with CHX 24 hours after ROSC. The coronal sections of the hippocampus levels were stained with hematoxylin-eosin after 72 hours of survival. The histologic damage score(HDS) was used to assign a score to the total number of damaged neurons counted in each of the hippocampal CA1 subfields. RESULTS: 1. There were not significan differences in heart rates, blood pressures, blood sugar, and blood gas in group I & II during the pre-arrest steady state or at 5 min and 30 min after ROSC. 2. In group I & II, the HDS, were significantly reduced in rats(I exp-12, 1.1+/-0.6; I exp-24, 1.3+/-0.5; II exp-12, 1.4+/-0.7; and II exp-24, 1.8+/-0.8) treated with CHX 12 hours or 24 hours after ROSC than control rats(I, 2.5+/-0.9, II, 2.9+/-0.8)(p<0.05). CONCLUSION: These results suggest that delayed hippocampal neuronal death from ischemic insult after ventricular fibrillation cardiac arrest followed by resuscitation can be prevented by a protein synthesis inhibitor, CHX. Further experimental studies of the action mechanism of protein synthesis inhibitors to delayed neuronal death and clinical applications are required.
Animals ; Blood Glucose ; Brain ; Heart Arrest* ; Heart Rate ; Hippocampus ; Injections, Subcutaneous ; Ischemia ; Necrosis ; Neurons* ; Protein Synthesis Inhibitors ; Rats* ; Reperfusion ; Resuscitation ; Ventricular Fibrillation*

No abstract available.
HLA Antigens* ; Humans

No abstract available.
Headache*

No abstract available.
Headache*

No abstract available.
Forearm* ; Free Tissue Flaps* ; Male ; Penis*

Purpose: To demonstrate the clinical features and natural course of chronic retinal detachment-associated neovascular glaucoma. Methods: Ten patients, diagnosed with chronic retinal detachment-associated neovascular glaucoma during 2007-2016 were retrospectively investigated. Besides chronic retinal detachment, no patients had any neovascular glaucoma-predisposing conditions, such as carotid artery disease. Retinal perfusion status was evaluated from the fundus fluorescein angiography images. Results: The mean age of patients was 57.5 years (range, 22-78 years). Complete retinal reattachment was achieved in three eyes, while partial or total chronic retinal detachment persisted in seven eyes. Wide-angle fundus fluorescein angiography revealed peripheral retinal capillary obstruction and severe nonperfusion. Neovascular glaucoma developed 213.4 months (range, 17-634 months) after retinal detachment. Three eyes received Ahmed valve implantation, while five eyes received intravitreal bevacizumab injection. Intraocular pressure was controlled in 10 eyes. Two eyes developed phthisis bulbi during follow-up. Conclusions In eyes with a chronic retinal detachment history, iris neovascularization and neovascular glaucoma can develop due to retinal capillary obstruction and chronic retinal ischemia, even after achieving retinal reattachment. We suggest regular follow-up examinations for patients with chronic retinal detachment, particularly for eyes with retinal nonperfusion, as detected on fundus fluorescein angiography.