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Query: UMLS:C0036690 (sepsis)
 59,461 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In a 3-month period (January to March, 1992), patients with rectal temperature below 35 degrees C detected by an electrical rectal thermometer (Diatek, Inc, San Diego, CA) were enrolled. In addition to treatment of the underlying diseases, the patients were rewarmed with either a heating lamp (core temperature > 32 degrees C) or warm fluid intravenous infusion and/or gastric lavage (core temperature < 32 degrees C). Patients' vital signs, serum potassium, pH, initial temperature, mean weather temperature, underlying disease and outcome were recorded and compared between survivors and non-survivors. We collected 23 cases with mean age of 71.6 years and mean core temperature, 33.32 degrees C (29.4-34.9 degrees C). The diagnosis included hypoglycemia in 7 cases, sepsis in 3 cases, active TB in 2 cases, HHNK in 1 case, DKA in 1 case, UGI bleeding in 1 case, parkinsonism in 1 case, intracerebral hemorrhage in 1 case, urinary tract infection in 1 case, brain tumor post operation in 1 case, arrhythmia in 1 case, senile dementia in 1 case, COPD in 1 case and lung CA in 1 case. 12 (52%) cases died during admission. No significant difference in clinical parameters was noted between survivors and non-survivors. In conclusion, although in subtropic area, the hypothermic patients in our country cannot be overlooked. As patients are usually elder and have other diseases, the prognosis is correlated with the severity of the underlying disease. Alert, intensive care, prevention and treatment of the complications that arouse, and careful rewarming are necessary for management of such patients.
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PMID:[Hypothermia in the patients of emergency department]. 828 89

Eighty patients underwent open-heart surgery from March 1990 to March 1993. We used combined aortic root (antegrade)/coronary sinus (retrograde) perfusion for cardioplegia delivery as a means of myocardial protection. The special retroplegia cannula was introduced to the coronary sinus (CS) in 67 patients by the transatrial (blind intubation) after one cannula cava insertion; the CS was cannulated under direct vision by right atriotomy after bicaval cannulation in 13 patients. Varied and prolonged cardiac procedures were done using cooled crystalloid cardioplegia (4 centigrades + potassium) except in one patient with severe ventricular damage in whom warm blood cardioplegia was infused. There was no CS or cardiac vein damage or disruption. There was no A-V blockade. The CS was intubated easily in all cases and cardioplegia solution readily infused. Coronary sinus pressure never exceeded 40 mm Hg. Overall hospital mortality (30 days postoperative) was 3.75% (3 cases). Sepsis was the cause of death in 2 patients and stroke in one. Inotropes were used in few cases as a means of renal protection. We conclude that the combined antegrade/retrograde cardioplegia delivery can be used routinely in most patients undergoing open-heart surgery.
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PMID:[The versatility of anterograde/retrograde cardioplegia in heart surgery]. 829 27

A substantial increase in pulmonary vascular resistance is associated with sepsis and its sequelae (sepsis syndrome and septic shock). It is postulated that increased resistance may result from sepsis-induced endothelial cell injury or altered vasoreactivity secondary to pulmonary hypertension. We, therefore, tested the hypothesis that sepsis causes endothelial cell injury and that increased pulmonary pressure alters vascular reactivity. Young swine (15-25 kg) were anesthetized and ventilated. Septic animals received a 1-hr infusion of live Pseudomonas aeruginosa (n = 11), and the control cohort received 0.9% NaCl (n = 7). All animals were studied for 300 min following the infusion. Postmortem branches of peripheral pulmonary arteries were prepared and tested in a vessel myograph. Ring segments were set to 90% of the circumference the vessels would have at pressures of 20, 30, 40, or 50 mmHg (L90), corresponding to varying pulmonary pressures observed in sepsis. A high dose of potassium was used to obtain maximum possible contraction. Prostaglandin was used to precontract the vessels before testing endothelial cell responses to acetylcholine or bradykinin. Sodium nitroprusside was added at the end of each experiment to obtain maximum possible smooth muscle relaxation. No differences in contraction or relaxation were observed when vessels were set to different pressures (i.e., 20 vs 50 mmHg). Maximum possible contraction to KCl was significantly decreased after 300 min of sepsis compared to control. No differences between groups were found in contractility to prostaglandin. Bradykinin-induced EDRF/NO production, mediated by BK2 receptors, was not altered in Pseudomonas sepsis (97-98% of total relaxation control and 91-95% septic cohort). Response to acetylcholine was significantly decreased after sepsis (89-95% of total relaxation control and 51-61% of septic cohort relaxation). Decreased response to acetylcholine could not be attributed to decreased smooth muscle sensitivity to nitric oxide because the response to bradykinin plus sodium nitroprusside was not altered following sepsis. Vessel reactivity was not altered by increasing pressure settings reflective of changing pulmonary pressure in vivo. These results strongly suggest a sepsis-induced alteration in pulmonary artery endothelial cell receptor sensitivity to acetylcholine, independent of changing pulmonary arterial pressures. This is the first time this decrease has been shown in pseudomonas sepsis.
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PMID:Pulmonary artery endothelial cell function in swine pseudomonas sepsis. 859 13

Data were analyzed on 290 children admitted consecutively to the pediatric intensive care unit (PICU) of the Postgraduate Institute of Medical Education and Research in Chandigarh, India, in 1993 to examine the frequency, severity, risk factors, and mortality of hypokalemia (3.5 mEq/l serum potassium) and the efficacy of treatment. 43 (14.8%) children had 54 episodes of hypokalemia. Most (68.6%) episodes were moderate. Predisposing factors were the nature of primary disease (renal disease 19%, septicemia 19%, acute diarrhea 14%, and heart disease with congestive failure and meningoencephalitis 12% each), malnutrition (weight for age 80% in 72%), and treatment with drugs (diuretics 20%, beta-agonists 13%, and corticosteroids 11%). Diagnoses most common in hypokalemia cases were acute renal failure (25%), septicemia (22.8%), and acute severe bronchial asthma (20%). The most important predisposing factor for hypokalemia prior to hospitalization was poor oral intake (i.e., inability to replace adequate potassium) (27%). All 43 children received 4-6 mEq potassium/100 ml of intravenous fluids. Clinicians administered an infusion of 0.3 mEq potassium/kg/hour to 7 children (9 episodes) who had ECG changes of hypokalemia until the ECG became normal. Potassium levels returned to normal in all 9 episodes requiring rapid correction and in 40 of 45 episodes requiring slow correction. PICU patients with hypokalemia were more likely to die than PICU patients with no hypokalemia (25.6% vs. 10.9%; p 0.05; odds ratio = 2.34). Hypokalemia patients who received slow correction therapy were more likely to die than those who received rapid correction therapy (31% vs 0; p 0.05). Mortality was lower in PICU patients whose hypokalemia was corrected than in PICU patients whose hypokalemia was not corrected (13.5% vs. 100%; p 0.05). Based on these findings, regular monitoring and rapid correction are recommended to improve the outcome of hypokalemia.
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PMID:Hypokalemia in a pediatric intensive care unit. 877 44

Thirty-one patients (26 males, 5 females) with mean age 35 +/- 19 years (range 8 to 85 years) were diagnosed as non-traumatic rhabdomyolysis by clinical findings and elevation of serum creatine kinase (CK) between January 1989 and December 1993. Causes, laboratory measures, clinical courses, and outcome were reviewed retrospectively. Drug abuse, seizure, and excessive activity are the most common etiologies for non-traumatic rhabdomyolysis. Twelve patients presented with muscular pain and seven patients with muscle weakness. Twenty eight patients had urinalysis and five of them (18%) had negative orthotolidine dipstick test. Only seven patients (25%) were detected positive orthotolidine test without microscopic hematuria. Patients with acute renal failure had higher levels of potassium and uric acid. The patients who developed acute renal failure after admission had significantly higher levels of uric acid. The peak levels of CK did not correlate with development of acute renal failure. There was no episode of hyercalcemia. Seventeen patients (55%) had acute renal failure. Hemodialysis was required in nine cases. All survivors recovered with normal renal function except one who needed maintenance hemodialysis after two months follow-up. Two patients died of multi-organ failure and sepsis.
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PMID:Non-traumatic rhabdomyolysis and acute renal failure. 893 69

Although a linkage between aerobic glycolysis and sodium-potassium transport has been demonstrated in diaphragm, vascular smooth muscle, and other cells, it is not known whether this linkage occurs in skeletal muscle generally. Metabolism of intact hind-leg muscles from young rats was studied in vitro under aerobic incubation conditions. When sodium influx into rat extensor digitorum longus (EDL) and soleus muscles was facilitated by the sodium ionophore monensin, muscle weight gain and production of lactate and alanine were markedly stimulated in a dose-dependent manner. Although lactate production rose in both muscles, it was more pronounced in EDL than in soleus. Monensin-induced lactate production was inhibited by ouabain or by incubation in sodium-free medium. Preincubation in potassium-free medium followed by potassium re-addition also stimulated ouabain-inhibitable lactate release. Replacement of glucose in the incubation medium with pyruvate abolished monensin-induced lactate production but exacerbated monensin-induced weight gain. Muscles from septic or endotoxin-treated rats exhibited an increased rate of lactate production in vitro that was partially inhibited by ouabain. Increases muscle lactate production in sepsis may reflect linked increases in activity of the Na+, K+-ATPase, consumption of ATP and stimulation of aerobic glycolysis.
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PMID:Linkage of aerobic glycolysis to sodium-potassium transport in rat skeletal muscle. Implications for increased muscle lactate production in sepsis. 894 58

We tested the hypothesis that expression of inducible nitric oxide synthase (NO-synthase) in response to endotoxin (lipopolysaccharide) produces activation of potassium channels. Contraction of the rat thoracic aorta in response to phenylephrine was measured in vitro after treatment in vivo for 15 hr with vehicle (control) or lipopolysaccharide (10 mg/kg i.p.). Impaired contraction in response to phenylephrine was used as an index of inducible NO-synthase expression, and activation of potassium channels was examined with specific inhibitors. Contraction in response to 10(-5) M phenylephrine (expressed as a percentage of contraction in response to 85 mM KCI) was markedly impaired in lipopolysaccharide-treated rats, compared with control (15 +/- 5% vs. 131 +/- 10%, P < .05, mean +/- S.E.). Expression of inducible NO-synthase mRNA in the vessel wall in lipopolysaccharide-treated rats was confirmed using reverse transcription-polymerase chain reaction. Contraction of the aorta in lipopolysaccharide-treated rats was restored to normal by 0.3 mM aminoguanidine (an inhibitor of inducible NO-synthase). Contraction of the aorta in response to phenylephrine, which was inhibited by lipopolysaccharide, was not affected by glibenclamide (an inhibitor of ATP-sensitive potassium channels) but was increased 2-fold (P < .05) by iberiotoxin (50 nM), an inhibitor of Ca(+2)-dependent potassium channels. Relaxation of the aorta in response to sodium nitroprusside, an exogenous donor of nitric oxide, and 8-bromo-cyclic GMP was also inhibited by iberiotoxin. These findings suggest that nitric oxide produced by vascular expression of inducible NO-synthase activates calcium-dependent potassium channels and that this mechanism may contribute to impaired vasoconstrictor responses during sepsis.
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PMID:Vascular expression of inducible nitric oxide synthase is associated with activation of Ca(++)-dependent K+ channels. 896 77

This study was carried out to compare the efficacy of a cereal based ORS (prepared with 50 G of sagodana (cereal), 3.5 G/L sodium chloride, 1.5 G/L potassium chloride, 2.9 G/L trisodium citrate) with rice based oral rehydration solution (using same amounts of rice and electrolytes) for treatment of diarrhoea. One hundred and twelve children aged 3 months to 2 years with watery diarrhoea of less than 5 days duration with mild to moderate dehydration and no sepsis, were included in the study. The amount of ORS intake, stool volume and frequency were similar in both groups. Clinical success was seen in 79% of rice ORS group and 81% in sagodana group. Both can be used as a cereal based ORS in the management of acute diarrhoea in communities where it is culturally accepted and used as a weaning diet.
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PMID:Sagodana based verses rice based oral rehydration solution in the management of acute diarrhoea in Pakistani children. 905 31

The diagnosis of a pustular dermatosis occurring during the first months of life is usually based on clinical findings. However, some cases may require simple investigations including microscopic examination of pustular content, cultures, and skin biopsies. The main benign transient neonatal types of pustulosis include erythema toxicum neonatorum, infantile acropustulosis, transient neonatal pustular melanosis, and neonatal acne. The most common causes of infectious pustular skin lesions include bacterial infections, which may be initially localized (Staphylococcus aureus) or septicemic (with Listeria monocytogenes as the leading causitive agent); viral infections (herpes simplex, varicella-zoster, and cytomegalovirus infections); fungal infections (candidiasis); or parasitic disorders (scabies). The main objective of this article is to propose a systematic approach to pustular eruptions in the neonate. The need for investigating every neonate with pustules for an infectious disease is emphasized. The Tzanck smear, the Gram's stain, and a potassium hydroxide preparation are the most important quick diagnostic tests. The Tzanck smear is a very easy, rapid, and sensitive test for detection of a herpetic infection (multinucleated giant cells) as well as noninfectious pustular eruptions (eosinophils, neutrophils). Therefore the Tzanck smear should be the first test performed. Moreover, a Gram's stain and potassium hydroxide preparation should be performed in cases of neonatal pustular disorders to detect bacterial and fungal infections. The goal of this diagnostic approach is to spare a healthy neonate with a benign transient condition an invasive evaluation for sepsis, potentially harmful antibiotic therapy, and prolonged hospitalization, with its own inherent morbidity.
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PMID:Diagnosis and treatment of pustular disorders in the neonate. 914 1

The mechanism underlying smooth muscle relaxations of cerebral arteries in response to nitric oxide is still not completely understood. The present study was designed to determine the role of soluble guanylate cyclase in the relaxations to a nitric oxide/nucleophile complex, diethylaminodiazen-1-ium-1,2-dioate (DEA-NONOate). Rings of canine middle cerebral arteries without endothelium were suspended in Krebs-Ringer bicarbonate solution for isometric tension recording. The levels of guanosine 3',5'-cyclic monophosphate (cyclic GMP) were measured by radioimmunoassay technique. During contractions to uridine 5'-triphosphate (UTP), DEA-NONOate (10(-10) to 10(-5) M) caused concentration-dependent relaxations. Measurements of cyclic GMP levels in cerebral arterial wall demonstrated that DEA-NONOate is a potent stimulator of guanylate cyclase and subsequent formation of cyclic GMP. Increasing concentrations of a selective soluble guanylate cyclase inhibitor, 1H-[1,2,4]-oxadiazolo[4,3-a]quinoxalin-1-one (ODQ), caused concentration-dependent reduction of both cyclic GMP production and relaxations to DEA-NONOate. Interestingly, in the presence of the highest concentration (3 x 10(-6) M) of ODQ, production of cyclic GMP in response to 10(-6) M of DEA-NONOate was abolished, whereas the same concentration of DEA-NONOate caused almost complete relaxation, suggesting that mechanisms independent of cyclic GMP production may mediate relaxing effect of high concentration of a nitric oxide donor. A selective Ca2+-activated potassium channel blocker charybdotoxin (CTX) significantly reduced relaxations to DEA-NONOate resistant to ODQ, supporting the idea that in cerebral arteries nitric oxide may activate potassium channels independently of cyclic GMP. The results of our study suggest that under physiological conditions, guanylate cyclase is a key mediator of cerebral arterial relaxations to nitric oxide. However, under pathological conditions associated with induction of nitric oxide synthase and increased biosynthesis of nitric oxide (e.g., cerebral ischemia, inflammation, sepsis), mechanisms other than formation of cyclic GMP may be activated.
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PMID:The effect of 1H-[1,2,4]oxadiazolo[4,3-a]quinoxalin-1-one (ODQ) and charybdotoxin (CTX) on relaxations of isolated cerebral arteries to nitric oxide. 952 59


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