Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0036690 (sepsis)
59,461 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The treatment of subarachnoid haemorrhage caused by aneurysm in comatose patients with or without midbrain symptoms is a matter of controversy. The question is, which comatose patients will profit from aneurysm surgery and which will not? In a retrospective study, 573 patients were examined between 1986 and 1992. Of these, 116 were in poor condition (Hunt and Hess Grade IV or V). The following management protocol was used: after computer tomography, a decision was made whether intensive medical treatment was performed or not. The reason for not operating was essentially the severity of the cerebral haemorrhage and poor or absent intracranial filling on angiography. Extracerebral causes were renal failure, sepsis, liver cirrhosis and pulmonary embolism. The direct early aneurysm operation was performed in the clinical deterioration phase in patients with space-occupying haematomas. In dilatation of the ventricle system, external drainage was initially positioned, in the case of bilateral haematocephalus, two-sided drainage was positioned, then intensive medical treatment and angiography were performed. The aneurysm operation was then ruled out if there was no clinical improvement. Aneurysm operation was performed on 57 of the 116 patients; 13 died, 32 showed a good and 12 a poor or fair outcome. 15 patients had mid-brain syndrome, and 5 of them died. Based on our experience, we draw the following conclusion: the Hunt and Hess scale alone is not a sufficient basis for decision taking. Some of the comatose patients, even in mid-brain syndrome, profit from an early operation.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Modulated surgery in the management of ruptured intracranial aneurysm in poor grade patients. 791 32

The annual incidence of acute renal failure (ARF) in the general population seems close to 150 per million inhabitants. For the past 20 years, there has been an increase in ARF of medical origin and a simultaneous decrease in surgical, traumatic and obstetrical ARF. Drug-induced ARF accounts for 20% of total cases. Factors of poor prognosis include a poor previous health status, the presence of oliguria, cardiac or respiratory insufficiency, sepsis, coma, a need for mechanical ventilation and, most importantly, the number of failing organs. The three main severity scoring systems used are SAPS, APACHE II and OSF. The predictive value of these scoring systems seems acceptable provided the data are collected when ARF is diagnosed and not on the patients' admission. After years, the overall survival rate does not exceed 30% to 50%. Full renal recovery is observed in 1/3 to 2/3 of surviving patients and varies according to the type of nephropathy. The social and financial consequences of these results emphasize the importance of preventing ARF, especially in its iatrogenic form.
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PMID:[Epidemiology and prognosis of acute renal insufficiency]. 798 47

Paracetamol poisoning is the most common cause of fulminant liver failure in the United Kingdom. An accurate assessment of prognosis at the time of referral will allow the appropriate application of liver transplantation in this setting. The outcome of 92 patients consecutively admitted to a specialist liver unit with severe poisoning has been examined. In patients who did not have a transplant, a fatal outcome was seen for 26/82 (32%), and was associated with late presentation, coma grade, prothrombin time prolongation, metabolic acidosis, and renal dysfunction. Cerebral oedema, and sepsis were responsible for most deaths. Prognostic criteria defined at King's College Hospital seemed to predict the outcome of patients who did not have a transplant managed on the Birmingham liver unit. Seventeen patients were listed for transplantation, 10 had liver transplantation, and seven of 10 survived. Seven were listed but not transplanted, and one of seven survived. Psychological rehabilitation of patients who had a transplant has not proved difficult. These results suggest a role for liver transplantation in the management of selected patients with paracetamol poisoning.
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PMID:Serious paracetamol poisoning and the results of liver transplantation. 802 Aug 10

Twenty-six patients presenting with 33 episodes of Diabetic Ketoacidosis (DKA) and managed on a protocol oriented system were analysed. Diabetes mellitus was newly diagnosed at presentation in 18% of the 33 episodes. The presenting symptoms were polyuria and polydipsia (58%), nausea and vomiting (52%), change in sensorium (24%), hyperventilation (24%), and abdominal pain (18%). The main clinical findings at admission were dehydration (97%), acidotic respiration (67%), coma and confusion (61%), a clinically detectable source of sepsis (49%), fever (33%) and hypotension (9%). Blood sugar levels at admission ranged between 351 mg/dl and 1200 mg/dl (mean = 633 mg/dl). The mean serum potassium at diagnosis was 5.1 mmol/l and the mean calculated serum osmolality was 320 mOsm/kg. The mean serum osmolality was higher in those with disturbed conscious level. Infections, particularly those of the urogenital tract, were the main precipitating cause for the DKA. Only 12 of the 19 patients with sepsis had fever. Eight of the episodes were attributed to patients' non-compliance with insulin. Four patients died during the 33 hospitalisations, giving a mortality rate of 10%. Death occurred despite glucose control and stabilisation of the ketoacidotic state and was due to uncontrolled septicaemia. The mean duration of hospitalisation was 11 days. The ketoacidosis state was reversed after a mean duration of 9.5 hours, with an average soluble insulin requirement per patient of 52.4 units.
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PMID:Diabetic ketoacidosis--a study of 33 episodes. 815 79

Accurate information on short-term prognosis is needed to help patients, their doctors, and society to make appropriate decisions concerning starting dialysis. We sought to develop a clinically applicable prognostic scoring system to aid in the prediction of death within 6 months of starting maintenance dialysis. Factors potentially predictive of early death were examined retrospectively in an inception cohort of all 325 patients starting dialysis for irreversible renal failure between 1980 and 1991 at a single tertiary care center. The overall mortality rate was 22% at 6 months. Age, cardiac failure, ischemic heart disease, dysrhythmia requiring therapy, severe peripheral vascular disease, advanced neoplasia, ventilator dependency, coma, systemic sepsis, and hepatic failure were independent, significant, prognostic indicators for early death. Multivariate models were used to suggest weights for these variables in a simplified scoring system. Patients with scores < or = 4 (N = 201) had a 6-month mortality rate of 4%, whereas those with a score higher than 9 (N = 21) had a 6-month mortality rate of 100%. Thus, when age and multiple comorbid illnesses were taken into account, it was possible to identify with 100% accuracy 29% of the patients who died within 6 months of starting maintenance dialysis therapy, accounting for 6.5% of the cohort studied. A larger prospective study is warranted to validate this scoring system.
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PMID:Advance prediction of early death in patients starting maintenance dialysis. 820 66

Some clinical manifestations of severe malaria resemble those of sepsis and there may be mediators of the host response that are common to both sepsis and malaria. Phospholipase A2 (PLA2), a proinflammatory enzyme whose expression is induced by tumor necrosis factor (TNF), has been implicated in the pathogenesis of complications of the sepsis syndrome. We examined levels of circulating PLA2 in Plasmodium falciparum malaria and studied the association of PLA2 with disease severity. Plasma PLA2 and TNF were measured in 75 Malawian children with P. falciparum malaria. The mean (SD) plasma PLA2 activity in children with acute malaria was 53,804 (37,256) units/ml as compared with 424 (349) units/ml in 34 healthy controls (P < 0.00001). The mean PLA2 activity in 45 convalescent patients was 2,546 (7,372) units/ml (P < 0.00001). In 48 patients with pretreatment PLA2 activity less than 60,000 units/ml, mortality was 8.3%, while in 27 patients with pretreatment PLA2 levels greater than 60,000 units/ml, mortality was 33.3% (P = 0.008). There were significant correlations between PLA2 and TNF (r = 0.471, P < 0.01), density of parasitemia (r = 0.443, P < 0.0001) and a decrease in hematocrit (r = 0.352, P < 0.005). These data show that P. falciparum malaria is associated with a markedly increased circulating PLA2, especially in patients with severe disease, as manifested by high parasite burden, anemia, coma, and death.
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PMID:Increased serum phospholipase A2 activity in Malawian children with falciparum malaria. 821 74

Tumor necrosis factor-alpha (TNF-alpha) has been implicated in several late consequences of trauma such as sepsis, multiple organ failure, and ischemia-reperfusion injury. However, no data are available to indicate whether TNF-alpha is involved in the initial pathophysiologic response to trauma. To address this issue, serum TNF-alpha was determined (by ELISA) longitudinally (first blood sample on admission) in 100 randomly selected trauma patients admitted to the emergency department and trauma division at Jefferson Medical Center, Philadelphia. The TNF-alpha levels were detectable at one or more time points in 35 patients. Mean values tended to be elevated (50.3 +/- 11.5 pg/mL) during the first 5 days, but this trend did not differ statistically from that in healthy controls (n = 12) and did not correlate with the severity of injury (Injury Severity Score and Glasgow Coma Scale score). The TNF-alpha response was not dependent on the mechanism and site of injury, the presence of shock (systolic blood pressure < 90 mm Hg), and the need for emergent surgery. Also, serum TNF-alpha levels were not significantly elevated in patients who subsequently developed multiple organ failure (n = 4), septic shock (n = 5), or both (n = 3). Taken together, these data do not support a role for circulating TNF-alpha in the initial acute inflammatory response to trauma.
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PMID:Serum tumor necrosis factor-alpha profile in trauma patients. 823 Mar 32

Forty-six patients with severe nonpenetrating brain injury [Glasgow Coma Scale (GCS) 4-7] were randomized to standard management at 37 degrees C (n = 22) and to standard management with systemic hypothermia to 32 to 33 degrees C (n = 24). The two groups were balanced in terms of age (Wilcoxon's rank sum test, p > 0.95), randomizing GCS (chi-square test, p = 0.54), and primary diagnosis. Cooling was begun within 6 h of injury by use of cooling blankets. Metocurine and morphine were given hourly during induction and maintenance of hypothermia. Rewarming was at a rate of 1 degree C per 4 h beginning 48 h after intravascular temperature had reached 33 degrees C. Muscle relaxants and sedation were continued until core temperature reached 35 degrees C. There were no cardiac or coagulopathy-related complications. Seizure incidence was lower in the hypothermia group (Fisher's exact text, p = 0.019). Sepsis was seen more commonly in the hypothermia group, but difference was not statistically significant (chi-square test). Mean Glasgow Outcome Scale (GOS) score at 3 months after injury showed an absolute increase of 16% (i.e., 36.4-52.2%) in the number of patients in the Good Recovery/Moderate Disability (GR/MD) category as compared with Severe Disability/Vegetative/Dead (SD/V/D) (chi-square test, p > 0.287). Based on evidence of improved neurologic outcome with minimal toxicity, we believe that phase III testing of moderate systemic hypothermia in patients with severe head injury is warranted.
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PMID:A phase II study of moderate hypothermia in severe brain injury. 825 39

Infection is one of the major complications of severe head trauma in children. To assess whether intravenous immunoglobulin (IVIg) decreases the incidence of secondary infection after head injury in children, a randomized, double-blind trial was performed. Thirty-three children (mean age, 6.67 years; mean injury severity score, 32.8; mean Glasgow coma score, 6.1) with severe head injuries were enrolled; 1 child was excluded, 18 received IVIg, and 14 received the placebo preparation. Four hundred milligrams per kilogram of IVIg or albumin placebo was administered within 48 hours of admission. IgG levels were obtained before the infusion and then 1 week later. Patients were monitored for evidence of infection for the next 21 days. There was a 66% increase in mean IgG levels in the treatment group compared with 45% in the control group (P = .057). One death occurred in the IVIg group and two in the placebo group. No significant differences in the incidence of pneumonia, sepsis, presumed sepsis, or any other type of infection was noted. There was no difference in the number of days on mechanical ventilation or in number of hospital days. There were no side effects. It is concluded that prophylactic administration of commercial IVIg at a dose of 400 mg/kg, although safe, had no effect on the incidence of secondary infections in children with severe head injuries.
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PMID:Safety and efficacy of intravenous immunoglobulin prophylaxis in pediatric head trauma patients: a double-blind controlled trial. 830 58

Patients with fulminant hepatic failure have severe circulatory disturbances which may be due to fibrin and cellular plugs in micro-vessels which are a consequence of intravascular coagulation and which can lead to multiorgan failure. Since antithrombin III supplementation has been shown to be beneficial in animal models of septic shock with disseminated intravascular coagulation, a controlled study was performed to investigate the effect of antithrombin III supplementation in fulminant hepatic failure. Twenty-five patients in grade III or IV coma were selected on the basis of evidence of sepsis, intravascular coagulation and a high risk of developing multiorgan failure. Thirteen patients received 3000 units of antithrombin III (Kybernin P; Behringwerke), followed by a further 1000 units every 6 h. Antithrombin III activity increased from 0.26 +/- 0.04 SE U/ml to 0.82 +/- 0.07 U/ml at 3 h post infusion (normal range 0.80-1.20 U/ml) and remained greater than 0.80 U/ml throughout the study without any apparent increase in the frequency of bleeding. However, survival was not improved and markers of intravascular coagulation remained similar between the two groups. Thus, although the antithrombin III deficiency in fulminant hepatic failure can be corrected by supplementation with antithrombin III concentrate, its use in the prevention of intravascular coagulation and to avoid microvessel plugging needs to be studied at an earlier stage in the disease.
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PMID:Controlled trial of antithrombin III supplementation in fulminant hepatic failure. 831 61


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