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 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*

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

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: Reperfusion of ischemic myocardium has been postulated to result in a specific oxygen radical mediated tissue injury. Iron may liberate during ischemia and we hypothesized that administration of the iron chelator, deferoxamine during ischemia would result in improved recovery after postischemic reperfusion. PURPOSE: To test whether iron-catalyzed processes contribute to myocardial necrosis during ischemia and reperfusion, deferoxamine was administered to block iron catalyzed hydroxyl radical formation in rabbits. METHODS: Eleven rabbits were divided into two groups: control group (n=5) and deferoxamine pretreatment group (n=6). the left circumflex coronay artery was ligated for 30 minutes and reperfused for 180 minutes. Area at risk (AR) was measured by non-stained area with ethylene blue injection into left atrium after left circumflex coronary artery ligation. Infarct size was measured by weighing after tripheyltetrazolium chloride staining. Heart rate was measured using electrocardiographic recording and systemic blood pressure was monitored by pressure transducer connected to the catheter in the left ventricle. RESULTS: 1. There was no significant difference of heart rate and blood pressure in deferoxamine pretreatment group compared with control group. 2. There was significant decrease of serum iron concentration after continuous infusion of deferoxamine compared with serum iron concentration before ligation of coronary artery (P<0.05). 3. There was no significant difference of area at risk between control and deferoxamine pretreatment group. 4. Area at necrosis to area at risk was significantly reduced in deferoxamine pretreatment group compared with control group (P<0.05) The results suggest that deferoxamine infusion prior to coronary artery occlusion has a significant benefit in reducing infarct size in this model.
Arteries ; Blood Pressure ; Catheters ; Coronary Vessels ; Deferoxamine* ; Electrocardiography ; Heart Atria ; Heart Rate ; Heart Ventricles ; Hydroxyl Radical ; Iron ; Ischemia ; Ligation ; Myocardial Infarction* ; Myocardium ; Necrosis ; Oxygen ; Rabbits ; Reperfusion ; Transducers, Pressure

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

BACKGROUND: This study evaluated the inhibitory effects of N-acetylcysteine(NAC) and methylprednisolone on lung injury in the paraquat-poisoned rat model. METHODS: Sixty rats were divided into four groups(n=15 in each group) accordingly to the drug administered : group I, only intraperitoneally injected paraquat (20 mg/kg); group II, intraperitoneally injected paraquat and NAC(300 mg/kg); group III, intraperitoneally injected paraquat and methylprednisolone(60 mg/kg); and group IV, intraperitoneally injected paraquat, NAC(300 mg/kg), and methylprednisolone(60 mg/kg). On the 7th day after injection, the survival rate of experimental rats and the positive area of collagen fiber in the injured lung stained by Masson's trichrome were evaluated. RESULTS: 1. There were no differences in the 7-day survival rates for the four groups. 2. The percent of collagen fiber for group II(6.3+/-4.7%) was significantly decreased in comparison with that for group I (14.4+/-9.7%). 3. The percent of collagen fiber for Group III(13.2+/-5.9%) was not significantly different from that for group I(14.4+/-9.7%). 4. The percent of collagen fiber for Group IV(6.9+/-4.6%) was significantly decreased in comparison with that for group I, but was not different from that for group II. CONCLUSION: These results suggest that NAC protects against pulmonary fibrosis in paraquat-poisoned rats whereas methylprednisolone does not protect against pulmonary fibrosis.
Acetylcysteine* ; Animals ; Collagen ; Lung Injury* ; Lung* ; Methylprednisolone* ; Models, Animal* ; Paraquat ; Pulmonary Fibrosis ; Rats* ; Survival Rate

BACKGROUND: Flood is the most common natural disaster in our country. Lots of victims occurred during the period of flood in the northern territory of Kyoungkido on August 5, 1998. We tried to describe the characteristics of the flood-related injury and illness, management and medical requirements. METHODS: We interviewed the patients admitted to 8 hospitals in Ujungbu and reviewed medical records from aug 5 to Aug 14, 1998. RESULTS: There were total 102 patients, male were 52%and women were 48% Most of patients were between 30's and 60's. Most of them were minor, and less than 3%of them needed critical care. The diagnosis were laceration(39.2%, contusion(22.5%, fracture(13.7%, infectious disease(7.8%, ligament rupture(7.8%, aggravation of chronic illness(5.9%, dermatitis(2.0% and traumatic hyphema(1.0%. The laceration occurred in the foot(37.9%, lower leg(27.0%, thigh(16.2%, hand(10.8% and head(8.1%. The location of ligament injury were achilless tendon(62.5%, hand(25% and knee(12.5%. The 67.5%of flood-related laceration patients progressed cellulitis, especially in sutured wound and a typical tetanic patient was developed. Of hospitalized patients, 2 patients showed evidence of post-traumatic stress disorder(PTSD). CONCLUSION: During flood, civils have better to be educated about prevention of injury, such as wearing of shoes and clothes. Although laceration was minor, lacerated wounds should be thoroughly irrigated, debrided the margin and considered delayed closure, tetanus immunization. Reportedly, there is an increased prevalance of PTSD and depression after disasters. Therefore mental health care will be required in the future.
Cellulitis ; Critical Care ; Depression ; Diagnosis ; Disasters ; Female ; Gyeonggi-do ; Humans ; Immunization ; Lacerations ; Ligaments ; Male ; Medical Records ; Mental Health ; Northern Territory ; Shoes ; Stress Disorders, Post-Traumatic ; Tetanus ; Wounds and Injuries

BACKGROUND: Hepatic necrosis after acetaminophen overdose results from the increased formation of a highly toxic intermediatc(N-acetyl-p-benzoquinoneimine), produced by acetaminophen metabolism through the cytochrome P450 mixed function oxidase system. N-acetyl-p-benzoquinoneimine is normally detoxified by endogenous glutathione, but the increased production induced by an acetaminophen overdose may depletc glutathione stores, allowing the intermediate to react with and to destroy hepatocytes. METHOD & MATERIAL: We have estimated the hepatoprotective effects of 4-methylpyrazole(500mg/kg and 50mg/kg), inhibitor of cytochrone P450 isoenzyme, when given at two hours after single oral overdose of acetaminophen(2,000mg/kg) in rats. RESULTS: As far as overall protective effect of 4-methylpyrazole on hepatic necrosis score concerned, seam transaminase(AST, ALT) level were found to be decreased in 4-methylpyrazole-treated group compared to untreated group after acetaminophen overdose. No consistent difference in hepatoprotective effect was demonstrated between rats with high dose of 4-methylpyazole(500mg/kg) and rats with lower dose of 4-methylpyrazole(50mg/kg). CONCLUSION: We concluded that oral administration of 4-methylpyrazole apperas to protect hepatotoxicity effectively to acetaminophen overdose.
Acetaminophen* ; Administration, Oral ; Animals ; Cytochrome P-450 Enzyme System ; Glutathione ; Hepatocytes ; Metabolism ; Models, Animal* ; Necrosis ; Oxidoreductases ; Rats*