Modified Triage Method by Pneumonia Severity Index for Patients with Community: acquired pneumonia

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.

Effects of N6-L-phenylisopropyl Adenosine in Rats after Asphyxial Cardiac Arrest

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.

Effect of Steroids on Interleukin-1beta and Tumor Necrosis Factor-alpha Expression due to High Tidal Volume in the Rat Ventilator-induced Lung Injury Model

PURPOSE: Although mechanical ventilation is used to improve oxygenation, this strategy can impose injurious mechanical stress on lung tissue. This is recognized as ventilator-induced lung injury (VILI). Recently, several studies have reported that inflammatory cells and mediators play an important role in the progression of VILI. This study was designed to investigate, in a rat model, the expression of interleukin (IL)-1beta and tumor necrosis factor (TNF)-alpha, as well as the anti-inflammatory activity of steroids in VILI. METHODS: Male Sprague-Dawley rats were divided into 3 groups. The control group received low tidal volume (6ml/kg) ventilation. The second group received high tidal volume (25 ml/kg) ventilation and the third group received high tidal volume (25 ml/kg) ventilation with methylprednisolone (30 mg/kg) treatment. After 60 minutes of mechanical ventilation, the animals in each group were sacrificed. Resected lungs were immunostained with antisera for IL-1beta and TNF-alpha. The stained areas were evaluated with an image analyzer. RESULTS: In the groups that received a high tidal volume, the number of positive pixels in IL-1 beta and TNF-alpha was significantly higher than it was in the low tidal volume group. The high tidal volume group showed greater expression of I L - 1beta and TNF-alpha,but this was significantly decreased by methylprednisolone. CONCLUSION: Our study suggests that an inflammatory response related with IL-1beta and TNF-alpha is involved in the development of VILI. The expression of IL-1beta and TNF-alpha was lessened by treatment with methylprednisolone, which might have contributed to improving lung dysfunction after mechanical ventilation.

Painless Aortic Dissection Presenting as Acute Ischemic Stroke: Administ-ra-tion of Tissue lasminogen Activator

Acute aortic dissection is a catastrophic, often life threatening event that usually presents as a sudden, severe, exquisitely painful, ripping sensation in the chest or back. Painless dissection occurs in approximately 5% of the patients, and the diagnosis may often be delayed. It can be associated with neurologic sequelae, such as ischemic stroke, spinal cord ischemia, ischemic peripheral neuropathy, in as many as one-third of the patients. As an initial manifestation, neurologic deficit is seen in about 20% of patients. The diagnosis of ischemic stroke in patients who present within a 3-hour time window is generally made on clinical grounds before administration of thrombolytic therapy. The etiology of the stroke is not definitely determined until well after the patient has received recombinant tissae plasminogen activator. It is likely that poor outcomes will occur in ischemic stroke resulting from aortic dissection if r-tPA is administered intravenously. Therefore, it is important to clinically recog-nize this possibility. We report the case of a patient who presented with symptoms consistent with acute ischemic stroke and was given r-tPA. Further investigation demon-strated an aortic dissection as the cause of her stroke.

Effects of Continuous Descending Aortic Balloon Occlusion on Brain Ischemia during Cardiopulmonary Resuscitation in Rabbits

PURPOSE: A recent report introduce a new option for cardiopulmonary resuscitation by using of a continuous descending aortic balloon occlusion. The aim of the present study was to evaluate the effect of balloon occlusion of the descending aorta during cardiopulmonary resuscitation on brain ischemia. METHODS: Twelve rabbits were enrolled in this study. A 4 French Swan-Ganz catheter was advanced through the right femoral artery into the descending aorta. Ventricular fibrillation was induced with an AC current delivered through an electrode catheter advanced into the right ventricle. After 3 minutes of untreated ventricular fibrillation, the rabbits were randomized in two groups: (1) chest compression without balloon occlusion (control group) and (2) chest compression with balloon occlusion of the descending aorta (experimental group). The balloon was inflated for 3 minutes during resuscitation. Defibrillation was attempted at 3 minutes after start of chest compression. At 24 hours after return of spontaneous circulation, brain tissues were fixed in 4% paraformaldehyde and stained with hematoxylin eosin. Then, the ischemic cells in the hippocampal CA1 area were counted. RESULTS: There was significant difference in ischemic neuronal cells between the two groups (control group: 41.8 +/-10.9%, experimental group: 16.8+/-6.8%, p < 0.05). In the experimental group, carotid blood flow was better than it was in the control group during chest compression (control group: 2.4+/-1.0 mL/min, experimental group: 7.6+/-1.9 mL /min, p < 0.05). CONCLUSION: These results suggests that balloon occlusion of the descending aorta during resuscitation decreases brain ischemia in rabbits during cardiac arrest.

Neuroprotective Effect of N-acetylcysteine in an Asphyxial Cardiac Arrest Model of Rats

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.

Effects of N-acetylcysteine and Methylprednisolone on Lung Injury in a Paraquat-Poisoned Rat Model

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.

Inhibition of Apoptosis Following Transient Forebrain Ischemia in Gerbils by Intraischemic Mild Hypothermia

BACKGROUND: A brief episode of global forebrain ischemia produces selective and often extensive neuronal loss in several vulnerable brain structures. This cell death does not occur immediately, but is delayed for hours to days. This process is termed delayed neuronal death (DND). Recently, several reports have suggested that an apoptotic process may be involved in DND. The most effective treatment at present is intraischemic hypothermia. Thus, we designed this study to investigate whether intraischemic mild hypothermia could inhibit apoptosis following transient forebrain ischemia in gerbils. METHODS: Twenty-four gerbils were divided into two groups based on intraischemic rectal temperature: 34 degrees C(n=12) and 37 degrees C(n=12). Two additional gerbils underwent a sham operation. Cerebral ischemia was produced by occluding both carotid arteries for 10 minutes. The DNA fragmentation in the gerbil hippocapal CA1 area was determined by using the TUNEL method, and the results for the normothermic and the hypothermic groups were compared at 1, 3, and 7 days following 10-min transient ischemia (n=4 for each time point, respectively). RESULTS: 1. Percent dead hippocampal neurons were significantly decreased in the hypothermic group compared with the normothermic group at 1, 3, and 7 days following transient ischemia (p<0.05). 2. In the intraischemic normothermic group, TUNEL positive cells were first detected in the hippocampal CA1 at 3 days (1.9+/-0.6 cells/section), and the number was larger at 7 days following transient ischemia (127.8+/-16.3 cells/section). 3. In the intraischemic hypothermic group, no TUNEL positive cells were detected in the hippocampal CA1 at 1, 3, and 7 days following transient ischemia. CONCLUSION: The data suggest that delayed neuronal death following transient ischemia is, in part, apoptotic and that intraischemic mild hypothermia affords significant neuronal protection and prevents DNA fragmentation.

Usefulness of Blood Cultures in Acute Pyelonephritis

BACKGROUND: Routine cultures of blood in febrile patients being hospitalized with uncomplicated pyelonephritis are parts of accepted management and are advocated in several textbooks of medicine and in several review articles. For a better understanding of the importance of blood cultures for patients admitted with pyelonephritis, we did a retrospective chart review of patients admitted to a medical center over a 2-year period. METHODS: To evaluate the usefulness of blood cultures in patients admitted with pyelonephritis, we conducted a retrospective chart review of patients who were admitted to hospital from 1998 through 1999 with a primary discharge diagnosis of uncomplicated pyelonephritis. RESULTS: Among the 329 patients admitted, 177 patients were included in the study. Sixteen(9.0%) were men, and 161(91%) were women. The mean age was 52.24+/-18.08. The most common precipitating factor was diabetes mellitus (19.2%). Urinalysis results showed E.coli as the causative agent in 155 patients(87.6%). Positive blood culture results were be seen in 67 patients with a 37.9% sensitivity. The usefulness of blood cultures in acute pyelonephritis was statistically significant only in the case of fever(P=0.003). CONCLUSION: In the setting of uncomplicated pyelonephritis in the adults, if urine cultures can be obtained, blood cultures are not usually necessary. Settings where blood cultures might be appropriate include immunosuppressed patients, patients in whom the diagnosis is not clear, patients in whom bacteremic seeding of the kidney is suspected, and patients who have a prior history of urinary tract infection.

Effect of Pentoxifylline on the Cerebral No-reflow Phenomenon after Cardiac Arrest in Rat

BACKGROUND: Successful resuscitation of the brain requires unimpaired blood recirculation. However, unfortunately there are several factors against the successful recirculation. No-reflow phenomenon, characterized by a lack of reperfusion after cerebral ischemia, is the most important pathogenic factor during the early period of spontaneous circulation(ROSC). This study addresses question that pentoxifylline(PTX) ameliorates no-reflow phenomenon after cardiac arrest. METHODS: Fourteen rats were divided three group ; Sham group(n=2), 12 minutes cardiac arrest group without PTX(group I, n=6), and 12 minutes cardiac arrest group pretreated with PTX(group II, n=6). Group II were premedicated by intravascular injection of 5mg/kg PTX into the external jugular vein before 5minutes of the arrest-induction. We induced cardiac arrest with endotracheal clamping and muscle relaxant. And then, resuscitation was initiated. Arterial blood samples were drawn at the femoral artery before 5 minutes of arrest-induction and at the 5 minutes after restoration of ROSC. Reperfusion of brain was visualized by injection of 0.3g/kg of 15% FITC-albumin at 5 minutes after restoration of ROSC, and the animals were decapitated 2 minutes later. The left hemisphere was fixed with 4% formalin, and coronal sections of 200um thickness at three different standard levels of the rat brain were investigated with fluorescence microscopy. Density of microvasular filling were identified and calculated. RESULTS: Our observation demonstrated that 1. There were no significant differences of blood pressures, heart rates, and results of blood gas analysis between group I and II during the prearrest steady state. 2. There were no significant differences of blood pressures, heart rates, and results of blood gas analysis between group Iand II at 5minutes after ROSC. 3. Group II premedicated with PTX, showed significant increased capillary refiling(0.310+/-0.035)than group I without PTX(0.181+/-0.040). CONCLUSIONS : The results showed that during the prearrest steady state, premedication of PTX ameliorated the no-reflow phenomenon in the rat model of the asphyxial arrest. Further experimental studies are required to focus on the effects of postarrest infused PTX, The neurologic outcome, and the clinical applications.

Rhabdomyolysis in Doxylamine Succinate Overdose

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.

Usefulness of Serum Lactate in the Early Diagnosis of Intestinal Ischemia

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.

Spontaneous Rectus Sheath Hematoma with Hypovolemic Shock

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.

Effects of a Protein Synthesis Inhibitor on Hippocampal Neuronal Damage of Rats in the Ventricular Fibrillation Cardiac Arrest Model

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.

Prognostic Value of Somatosensory Evoked Potentials in Comatose Patients after Cardiopulmonary Resuscitation

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.

Effect of Pentoxifylline on Ischemia-Reperfusion Injury of Brain Following Cardiac Arrest in Rats

BACKGROUND: Two major events occurring in the cerebral hemodynamics after successful resuscitation from cardiac arrest are reactive hyperemia and postischemic hypoperfusion. In this study, we examined the effect of Pentoxifylline(PTX) on the rat brain following cardiac arrest. METHODS: Fourteen rats were anesthetized and artificially ventilated. Cardiac angst was produced by chest compression and clamping of tracheal tube far 3 minutes in ketamine anesthetized rats. Circulation was restored by standard cardiopulmonary resuscitation methods. In 7 rats, PTX 10mg/kg was infused at 10min after cardiac angst(PTX group). In the other 7 rats, same amount of normal saline was infused(control group). RESULTS: In both groups, hemodynamic variables, neurologic deficit(ND) score and histopathologic findings of hippocampal CA1 neurons were observed. Hemodynamic variables and ND score were not significandy different between two groups. Delayed ischemic neurons of hippocampal CA1 were decreased in PTX group(2.2+/-2.4%) compared with control group(9.1+/-1.2%). CONCLUSIONS : We conclude that PTX prevented development of delayed ischemic neurons in hippocampal CA1 after cardiac arrest. PTX may be useful in emergency situations following cardiac arrest.

A Case of Recurrent Seizure following Overdose of Isoniazid

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.

A Patient with Pulmonary Edema and Cardiac Arrest after Phenobarbital Overdose

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.

Effect of 4-Methylpyrazole for Acetaminophen Hepatotoxicity in a Rat Model

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.

A Clinical Analysis of Hospitalized Patients During the Period of Flood in Ujungbu

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.