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*

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

Rectus sheath hematoma of the abdominal wall is a well-recognized, but uncommon condition, caused by a tear in an epigastric vessel and characterized by sudden onset of severe abdominal pain and palpable mass. In most cases, a precipitating cause can be demonstrated. Causes include external trauma, strenuous activities, coughing, lifting, sneezing, vomiting, straining while urinating or defecating, golfing, pregnancy and the puerperium, anticoagulation therapy, infection, chronic diesase, arteriosclerosis, hypertension, prior paracentesis or laparotomy, inadequate hemostasis or excessive retraction in surgery, and idiopathy. Unfortunately, the correct diagnosis often is missed, and the hematoma is found only during an exploratory laparotomy. Treatment should be conservative in most instances. Although the mortality rate for patients with rectus sheath hematoma is low, the condition may be fatal if the volume of the hemorrhage is large and if treatment is delayed. Hence, it should be included in the differential diagnosis of any patient who presents to the emergency department with acute onset of abdominal pain. Our purpose is to familiarlize emergency physicians with the pathophysiology, the diagnosis, and the treatment of rectus sheath hematoma. We describe a patient with fatal rectus sheath hematoma presenting to the emergency department and give a review of the literature.
Abdominal Pain ; Abdominal Wall ; Arteriosclerosis ; Cough ; Diagnosis ; Diagnosis, Differential ; Emergencies ; Emergency Service, Hospital ; Golf ; Hematoma* ; Hemorrhage ; Hemostasis ; Humans ; Hypertension ; Hypovolemia* ; Laparotomy ; Lifting ; Mortality ; Paracentesis ; Postpartum Period ; Pregnancy ; Shock* ; Sneezing ; Vomiting

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*

BACKGROUND: Intestinal ischemia remains a devastating event despite improvements in clinical recognition and in diagnostic and therapeutic modalities. The ischemic bowel diseases encompass a wide clinical spectrum from mild, reversible disease to severe, irreversible injury. The clinical picture is characterized initially by poorly localized whether an increased serum lactate level is a recognized danger signal marker for intestinal ischemia in patients who present at the emergency department because of abdominal complaints. METHODS: Patients who came to our emergency department with abdominal pain and the risk factors of intestinal ischemia between Apr. 1999 and Nov. 1999 were included in this study. The data analysis included age, sex, final diagnosis, pathogenesis of bowel ischemia, and serum lactate level. RESULTS: The serum lactate level in the intestinal ischemia group was 28.54+/-22.51mg/dl; in non-ischemia group, it was 15.49+/-22.52mg/dl. This difference between the two groups was significatn(p<0.05). An increased serum lactate level had a sensitivity of 88.2% and specificity of 59.2%, a positive likelihood ratio of 4.92, and a negative likelihood ratio of 0.47 as a marker of bowel ischemia. These results do not represent a very meaningful revision of bowel ischemic provability, but may make a small contribution to management of the disease, depending upon their magnitude and the clinical context in which they are applied. CONCLUSION: In patients with abdominal complaints, an increased serum lactate level is usually a useful aid as a diagnostic marker of bowel ischemia.
Abdominal Pain ; Diagnosis ; Early Diagnosis* ; Emergency Service, Hospital ; Humans ; Ischemia* ; Lactic Acid* ; Risk Factors ; Sensitivity and Specificity ; Statistics as Topic

PURPOSE: Cardiac arrest and resuscitation produce global cerebral ischemia and reperfusion injury to the brain, which lead to high mortality and delayed neuronal death. Adenosine has been suggested as an endogenous neuroprotective molecule, acting through multiple potential mechanisms. We investigated the possible neuroprotective effects of adenosine on cerebral recovery following global ischemia induced by asphyxial cardiac arrest. METHODS: Twenty-four rats were randomized into three groups. Group I, II, and III had anesthesia, procedures, and asphyxia for 7 minutes and then survived to 72 hours. Group I(n=8) was not administered N6- L - phenylisopropyl adenosine(L-PIA). Group II(n=8) was administered LPIA(0.8 mg/kg), and group III(n=8) was administered LPIA(1.5 mg/kg) after spontaneous circulation. The dosedependent neuroprotective effects of L-PIA were compared to the control by using a histopathological method. RESULTS: Histological observations of CA1 showed a more significant reduction of neuronal cell loss in groups II and III than in group I(p<0.05). Histological observations of CA2 and CA3 didn't show a significant reduction of neuronal cell loss in groups II and III compared to group I. CONCLUSION: These results show that post-ischemic administration of adenosine protected against delayed neuronal damage in the hippocampal CA1 area following a 7-min asphyxial cardiac arrest in rats.
Adenosine* ; Anesthesia ; Animals ; Asphyxia ; Brain ; Brain Ischemia ; Heart Arrest* ; Ischemia ; Mortality ; Neurons ; Neuroprotective Agents ; Rats* ; Reperfusion Injury ; Resuscitation

PURPOSE: Considerable variation exists in hospital admission rates for patients with community-acquired pneumonia (CAP). The objective of this study was to evaluate whether the pneumonia severity index (PSI) could be applied to patients with CAP as a method for triage in an emergency medical center. METHODS: A total number of 110 patients admitted with community-acquired pneumonia between January 1997 and September 2001. Their medical records were reviewed, with pneumonia severity index, and other risk factors, the time to resolution, and the results of treatment being evaluated. RESULTS: The pneumonia severity index accurately identified the patients with community-acquired pneumonia. Factors we evaluated were related to significant differences statistically, including such as PaCO2, WBC count, suffered lobe count, hypoxic index (PaO2/ F i O2), diabetes, hypertension, number of coexisting illness, period of admission and intravenous antibiotic therapy, and aggravated PaO2. If body temperature was less than 38.5 degrees C, it was considerable for outpatients clinics in Class I and II. CONCLUSION: The pneumonia severity index was a useful screening tool for patients with community-acquired pneumonia. Admission and an active therapeutic plan could be recommended for patients assigned to Class III. Inappropriate admissions were reduced to 27.3% by modified triage algorithm.
Body Temperature ; Emergencies ; Humans ; Hypertension ; Mass Screening ; Medical Records ; Outpatients ; Pneumonia* ; Risk Factors ; Triage*

BACKGROUND: A major pathway leading toward neuronal injury following ischemia-reperfusion of the brain involves elevation of extracellular glutamate and activation of glutamate receptors, with a subsequent increase in intracellular calcium, resulting in a generation of free radicals. Oxygen free radicals cause brain injury following resuscitation from cardiac arrest. Oxyradicals produce strand breakage in DNA, which triggers energy-consuming DNA repair mechanisms and activates the nuclear enzyme poly(ADP-ribose) synthetase(PARS). However, excessive PARS activation leads to energy depletion and exacerbation of neuronal damage in cerebral ischemia. METHODS: We investigated the effect of a potent, free-radical scavenger, N-acetylcysteine(NAC), on hippocampal neuronal death in an asphyxial cardiac arrest model of rats. The effect of NAC on hippocampal neuronal death was studied in 32 rats which were subjected to asphyxial cardiac arrest for 7 minutes, followed by resuscitation. The animals were divided into four group(8 rats in each group) as follows: Group I was saline treated for 3 days, Group II was NAC treated for 3 days, Group III was saline treated for 6 days, and Group IV was NAC treated for 6 days. In the NAC-treated groups, NAC(150 mg/kg) was intravenously injected after return of spontaneous circulation. The coronal sections with hippocampus levels were stained with hematoxylin-eosin(H-E) and PARS antibodies at 3 and 6 days after survival. In addition, the levels of myeloperoxidase(MPO) and malondialdehyde(MDA) were determined in the brains of each group. RESULTS: The results are as follows: 1. MPO and MDA levels were significantly lower in the NAC-treated groups, II and IV, than in the saline-treated groups, I and III. 2. The histologic damage score(HDS), as determined by H-E staining, was significantly lower in the NAC-treated groups, II and IV, than in the saline-treated groups, I and III. 3. In PARS immunohistochemical staining, the HDS was significantly lower in the NAC-treated groups, II and IV, than in the saline-treated groups, I and III. CONCLUSION: These results suggest that a free-radical scavenger, N-acetylcysteine, may effectively prevent neuronal damages after reperfusion from asphyxial cardiac arrest in rats. Further studies will be required to examine both the mechanism of the action and the clinical application of NAC in patients with cardiac arrest.
Acetylcysteine* ; Animals ; Antibodies ; Brain ; Brain Injuries ; Brain Ischemia ; Calcium ; DNA ; DNA Repair ; Free Radicals ; Glutamic Acid ; Heart Arrest* ; Hippocampus ; Humans ; Neurons ; Neuroprotective Agents* ; Oxygen ; Poly Adenosine Diphosphate Ribose ; Rats* ; Receptors, Glutamate ; Reperfusion ; Reperfusion Injury ; Resuscitation

Phenobarbital is a long-acting barbiturate causing generalized depression of neuronal activity in the brain. Its effect is primarily achieved through enhanced GABA-mediated synaptic inhibition. Its use as an antiepileptic agent was first described in 1912. Before the introduction of phenytoin, phenobarbital is used as sedative-hypnotics. It is used for the treatment of epilepsy and status epilepticus. All barbiturates, including phenobarbital, have a high potential far abuse. They were frequently used for suicide attempts in the past, but they have in large part been replaced by benzodiazepines. the onset of symptoms depends on the drug and the route of administration. Mild to moderate barbiturate intoxication resembles ethanol inebriation with slurred speech, ataxia, and lethargy. Severe acute barbiturate intoxication is life threatening. Early deaths are generally cardiovascular-related. Hypotension, shock, pulmonary edema, and cardiac arrest that occurs with large doses are caused by depression of central sympathetic tone and as well as by direct depression of cardiac contractility. The potentially fatal oral dose of phenobarbital is 6-l0g. We describe an 23-year-old woman with pulmonary edema and cardiac arrest after ingestion of 18 grams of phenobarbital. She was completely recovered by successful cardiopulmonary resuscitation and hemoperfusion. We report a case with literature review.
Ataxia ; Barbiturates ; Benzodiazepines ; Brain ; Cardiopulmonary Resuscitation ; Depression ; Eating ; Epilepsy ; Ethanol ; Female ; Heart Arrest* ; Hemoperfusion ; Humans ; Hypotension ; Lethargy ; Neurons ; Phenobarbital* ; Phenytoin ; Pulmonary Edema* ; Shock ; Status Epilepticus ; Suicide ; Young Adult

Isoniazid(Isonicotinic acid hydrazide) is an antimicrobial drug used since 1952 as a fast line agent for the prophylaxis and treatment of tuberculosis. Isoniazid is well known for problems in population having a high prevalence of isoniazid use for prophylaxis or treatment of tuberculosis. But intentional or accidental isoniazid overdose is uncommon. The ingestion of toxic amounts of isoniazid causes recurrent seizures, profound metabolic acidosis, coma and even death. In adults, toxicity can occur with the acute ingestion of as little as 1.5g of isoniazid. Doses larder than 30mg per kg often produce seizures. When ingested in amounts of 80-150mg per kg or more, isoniazid can be rapid fatal. 40-year-old woman having previous pulmonary tuberculosis ingested 7 gram of isoniazid(140mg/kg) to attempt suicide approximately 30 minutes prior to visit to our emergency medical center. She had recurrent generalized tonicclonic seizures and metabolic acidosis. We report one patient treated with pyridoxine, which was equivalent to the amount of isoniazid ingested and administered as a intravenous dose and oral dose.
Acidosis ; Adult ; Coma ; Eating ; Emergencies ; Female ; Humans ; Isoniazid* ; Prevalence ; Pyridoxine ; Seizures* ; Suicide ; Tuberculosis ; Tuberculosis, Pulmonary