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

This report describes light and transmission electron microscopy (LM and EM, respectively) studies of kidneys from five cases of hepatorenal syndrome. The kidneys were removed and fixed for LM and EM between 30 and 120 min after death. All patients had progressive renal failure after admission to the hospital. All cases were jaundiced, had ascites, and exhibited features of hepatic encephalopathy. LM study revealed severe acute tubular lesions (ATL) or, more conventionally, acute tubular necrosis (ATN). EM study demonstrated necrosis of the proximal tubules characterized by swelling, disorganization of the cristae and appearance of dark bodies in the mitochondria, coalescence, fragmentation or displacement of the microvilli, loss of plasma membranes, rupture of the basement membranes, and separation of the cells from the basement membranes. Rupture of tubular basement membranes (tubulorrhexis) and mitochondrial dark bodies suggest an ATN due to ischemia or induced by vasoconstrictor substance(s). Glomerular lesions were infrequent (one in five) and therefore, do not seem to have contributed to renal failure. All cases terminally had extremely low urinary sodium (11 mEq/liter), high urinary potassium (50 mEq/liter), a remarkably low urinary sodium/potassium ratio (0.26, normal = 4.27), and a low urinary osmolality (less than 400 mOsm/kg). From this study we conclude that an ATN of variable severity may be associated with the hepatorenal syndrome. Since this ATN developed without preceding shock, sepsis, or hypotension it is possible that this ATN like that in ischemic acute renal failure may be due to reduced renal blood flow and intense cortical vasoconstriction which has been reported in hepatorenal syndrome. Finally, our data imply that low urinary sodium is consistent with this pathologic lesion in this clinical setting.
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PMID:Acute tubular necrosis in hepatorenal syndrome: an electron microscopy study. 714 28

Lactate-buffered peritoneal solution traditionally has been used as dialysate for continuous renal replacement therapy (CRRT) in the United States because no bicarbonate solution is commercially available. Since 1994, the Cleveland Clinic Foundation Dialysis Unit has prepared a bicarbonate solution (sodium 144 +/- 3 mEq/L, HCO3 37 +/- 2 mEq/L, potassium 3 or 4 mEq/L, calcium 3.0 +/- 0.3 mEq/L, and magnesium 1.4 +/- 0.3 mg/dL) replicating the dialysate for chronic intermittent hemodialysis. No solute precipitation, as calcium or magnesium salts, were observed, and several cultures of the solution, performed at various time periods, remained negative. Fifty critically ill acute renal failure patients have been treated with bicarbonate-CRRT. All patients were in multiple organ failure and required mechanical ventilation; 37 were receiving vasopressors. Forty-four continuous venovenous hemodialysis sessions and eight continuous arteriovenous hemodialysis sessions were performed with a mean duration of 7.8 +/- 6.1 days. The mean inflow dialysate rate was 1,249 +/- 225 mL/hr and the mean outflow rate (dialysate plus ultrafiltration) was 1,399 +/- 237 mL/hr; the inflow rate was constantly kept lower or equal to the outflow rate to avoid an enhanced potential for backfiltration. No related fever spikes or sepsis episodes were noted.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Bicarbonate dialysate for continuous renal replacement therapy in intensive care unit patients with acute renal failure. 750 65

The study deals with an animal model for the problems of surgical intensive care patients. Following repeated applications of E. coli endotoxin WO 111:B4 under standard conditions, specific hemodynamic and biochemical (TNF, TXA2, PGI2, IL-6, PAF) and morphological (endothelium of the lung) alterations were detected. ARDS patterns induced by the sepsis were analyzed by high-frequency measurement of pressure and flow (385 measurements per breathing cycle). The role of the intestine in sepsis was investigated by ion-selective monitoring of surface potassium activity comparing mucosa and serosa. Every injection of endotoxin was followed by a selective increase of the potassium activity revealing relative ischemia induced by the endotoxin. The profile of the potassium levels on the surface correlates both with the cardiac output and with the prostacyclin levels. The continuous narrowing of the difference between mucosa and serosa, potassium during the period of investigation can be regarded as evidence for pathologic change in permeability fostering the septic course.
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PMID:[Septic shock and multiple organ failure in surgical intensive care. An animal experiment model on the analysis of pulmonary and intestinal dysfunction]. 769 Jan 6

Acute respiratory alkalosis (hyperventilation) occurs in clinical settings associated with electrolyte-induced complications such as cardiac arrhythmias (such as myocardial infarction, sepsis, hypoxemia, cocaine abuse). To evaluate the direction, magnitude and mechanisms of plasma potassium changes, acute respiratory alkalosis was induced by voluntary hyperventilation for 20 (18 and 36 liter/min) and 35 minutes (18 liter/min). The plasma potassium response to acute respiratory alkalosis was compared to time control, isocapnic and isobicarbonatemic (hypocapnic) hyperventilation as well as beta- and alpha-adrenergic receptor blockade by timolol and phentolamine. Hypocapnic hypobicarbonatemic hyperventilation (standard acute respiratory alkalosis) at 18 or 36 liter/min (delta PCO2-16 and -22.5 mm Hg, respectively) resulted in significant increases in plasma potassium (ca + 0.3 mmol/liter) and catecholamine concentrations. During recovery (post-hyperventilation), a ventilation-rate-dependent hypokalemic overshoot was observed. Alpha-adrenoreceptor blockade obliterated, and beta-adrenoreceptor blockade enhanced the hyperkalemic response. The hyperkalemic response was prevented under isocapnic and isobicarbonatemic hypocapnic hyperventilation. During these conditions, plasma catecholamine concentrations did not change. In conclusion, acute respiratory alkalosis results in a clinically significant increase in plasma potassium. The hyperkalemic response is mediated by enhanced alpha-adrenergic activity and counterregulated partly by beta-adrenergic stimulation. The increased catecholamine concentrations are accounted for by the decrease in plasma bicarbonate.
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PMID:Plasma potassium response to acute respiratory alkalosis. 773 Nov 49

Experimental data suggest an association between hypomagnesaemia and hypokalaemia, and also with hypophosphataemia, but there have been few large studies using clinical results to study the prevalence of hypophosphataemia and/or hypokalaemia in patients with hypomagnesaemia. Our results show a two-fold increase in the prevalence of hypophosphataemia (plasma phosphate concentration < or = 0.80 mmol/l) in patients with hypomagnesaemia (plasma magnesium level < or = 0.70 mmol/l) compared with patients without this condition, and a six-fold increase in hypokalaemia (plasma potassium < or = 3.5 mmol/l). A triology consisting of hypomagnesaemia, hypophosphataemia and hypokalaemia is also described, which was found in 8% of patients with hypomagnesaemia and 17% of patients with severe hypomagnesaemia (plasma magnesium < or = 0.50 mmol/l). Patients most susceptible to this phenomenon include those in intensive therapy, post-operative patients, those with sepsis being treated with aminoglycosides, and oncology patients receiving chemotherapy.
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PMID:Hypophosphataemia and hypokalaemia in patients with hypomagnesaemia. 784 32

We have previously reported differential impairment of pulmonary and systemic vascular contractility in hyperdynamic sepsis. The objectives of this study were (1) to determine whether the magnitude of this phenomenon depends on the control group chosen for comparison, and (2) to examine the role of nitric oxide (NO) in this altered vascular contractility. Rats were randomized to sepsis induced by cecal ligation and perforation (CLP) or to one of two control procedures. The Sepsis group had a jugular venous line for fluid administration, laparotomy, and CLP. Control group 1 (Control) had only a jugular venous line inserted, while group 2 (Sham) had a jugular venous line inserted and an abdominal incision. All rats were killed 24 h after surgery. Vascular contractility of small pulmonary arterial and thoracic aortic rings was assessed in vitro by obtaining cumulative dose-response curves to the contractile agonists potassium chloride (KCl), phenylephrine (PE), and prostaglandin F2 alpha (PGF2 alpha). Pulmonary vessels from animals in the Sepsis and Sham groups exhibited significant attenuation of the contractile responses to KCl, PE, and PGF2 alpha compared with the Control group. In contrast, contractility of the aortic rings to KCl, PE, and PGF2 alpha was not significantly different in the three groups studied. Incubation of pulmonary and aortic vessels with NG-nitro-L-argine methyl ester (L-NAME, 10 microM) caused an increase in the response to KCl, PE, and PGF2 alpha in pulmonary vessels in Sepsis and Sham rats but not in Control rats.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Vascular reactivity in sepsis: importance of controls and role of nitric oxide. 788 60

The proinflammatory cytokines have been implicated in mediating myocardial dysfunction associated with myocardial infarction, severe congestive heart failure, and sepsis. We tested the hypothesis that cytokine levels are elevated after uncomplicated coronary artery bypass grafting and associated with episodes of postoperative myocardial ischemia and dysfunction. Coronary artery bypass grafting was performed under general anesthesia with moderate systemic hypothermia and cold-blood potassium cardioplegic solution. Tumor necrosis factor-alpha and interleukin-6 levels were determined by bioassays, and interleukin-8 levels were measured by a sandwich enzyme-linked immunosorbent assay. Myocardial function and ischemic episodes were assessed by intraoperative transesophageal echocardiography and perioperative 12-channel Holter monitoring. A total of 22 patients were studied, with no deaths or complications. Arterial tumor necrosis factor-alpha rose in a bimodal distribution, peaking at 2 and 18 to 24 hours after the operation (at 20.2 +/- 6.4 pg/ml, [mean +/- standard error of the mean]) and 5.8 +/- 1.6 pg/ml, respectively; before cardiopulmonary bypass: 0.90 +/- 0.20 pg/ml, p < 0.001 for both peaks) then progressively declined to levels before bypass. Arterial interleukin-6 was maximally elevated immediately on termination of cardiopulmonary bypass and peaked again 12 to 18 hours after cardiopulmonary bypass (at 7520 +/- 2439 pg/ml and 6216 +/- 1928 pg/ml, respectively; before bypass: 746 +/- 187 pg/ml, p < 0.0001 for both peaks). Arterial interleukin-8 levels were more variable but followed a similar pattern, peaking in the early period after cardiopulmonary bypass and again at 16 to 18 hours after the operation (at 4110 +/- 1403 pg/ml and 1760 +/- 1145 pg/ml, respectively; before bypass: 461 +/- 158, p < 0.05 for both peaks). By multivariate analysis, the aortic crossclamp time was independently predictive of postoperative cytokine levels. Left ventricular wall motion abnormalities were associated with both interleukin-6 and interleukin-8 levels, worsening scores being associated with increasing levels (for interleukin-6, p = 0.003; for interleukin-8, p = 0.05). Postoperative myocardial ischemic episodes were associated with interleukin-6 levels, six of seven (85%) patients with episodes of myocardial ischemia after a peak in interleukin-6 concentrations (p < 0.01). We conclude that proinflammatory cytokines are elevated after uncomplicated coronary revascularization and may contribute to postoperative myocardial ischemia and segmental wall motion abnormalities.
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PMID:Relationship of the proinflammatory cytokines to myocardial ischemia and dysfunction after uncomplicated coronary revascularization. 793 95

In Pennsylvania, a 29-year-old woman was admitted to Temple University Health Sciences Center in Philadelphia with hypotension (100/80 mmHg), fever (105.3 degrees Fahrenheit), and a diffuse, nondesquamating erythroderma. Five weeks earlier, she had delivered her last child vaginally. Three days before admission, she had undergone endotracheal intubation so surgeons could perform a laparoscopic tubal ligation with Falope Rings. Two days before the tubal ligation, she had had a sore throat. She experienced no surgical complications and was discharged the same day as the operation. The day before her latest admission, she experienced nausea, vomiting, diarrhea, fever, chills, and diffuse abdominal pain. Upon admission, her surgical incisions were clean and dry and had no erythema. Her pulse rate was 140 beats/minute. Her respiration rate was 20/minute. The white blood cell count was 15,200 cells/cu. m (71% neutrophils, 23% band forms, 2% lymphocytes, and 4% monocytes). Her potassium level was 3.2 mmol/l. The anion gap was 22. All blood and urine cultures were negative. She experienced mild uterine tenderness. Upon admission, physicians administered ticarcillin-clavulanate and vancomycin for suspected postoperative pelvic infection. After learning that cervical and pharyngeal cultures were positive for Streptococcus pyogenes, physicians changed to ampicillin, 1 g intravenously every 6 hours. On the 6th day, she was discharged and prescribed 500 mg oral amoxicillin every 8 hours for 2 weeks. Within 2 weeks, she felt fine, had a normal physical examination, no fever, and no rash. The major signs and symptoms indicated a toxin-mediated illness. Both mucosal surfaces colonized by S. pyogenes were manipulated during laparoscopy and manipulation may have caused minor tissue injury and hyperemia with subsequent dissemination of streptococcal toxin. In conclusion, the patient had a S. pyogenes toxin-induced toxic shock-like syndrome that mimicked a pelvic wound infection with gram-negative septicemia.
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PMID:Streptococcal toxic shock-like syndrome as an unusual complication of laparoscopic tubal ligation. A case report. 799 32

The aetiology of hyponatremia in tetraplegic patients is multifactorial and includes not only general factors such as the use of diuretics and the intravenous infusion of hypotonic fluids, but also certain mechanisms which operate in the spinal cord injured: decreased renal water excretion due to both intrarenal and arginine vasopressin dependent mechanisms (resetting of the osmostat), coupled with habitually increased fluid intake, and the ingestion of a low salt diet. Between 1984 and 1993 we treated 28 episodes of hyponatremia in 19 patients (males: 10; females: 9). Fourteen were tetraplegic and five paraplegic (thoracic lesion in four and lumbar lesion in one). Six patients were asymptomatic during seven episodes of hyponatremia which were detected during routine blood tests. Seven patients were suffering from an acute chest infection, three had an acute urinary tract infection, one had an infected ischial pressure sore and a 69 year old paraplegic patient had bronchopneumonia as well as sepsis from a gangrenous pressure sore in the supraanal region. The time interval between the onset of paralysis and occurrence of the first episode of hypnoatremia was less than a month in only four of the patients. The lowest plasma sodium level observed was less than 100 mmol/l in two, between 100 and 110 mmol/l in four, between 111 and 120 mmol/l in eight patients, and between 121 and 128 mmol/l in 14 cases. Six patients also had hypokalemia (K+ < 3 mmol/l). Only one patient had and elevated plasma creatinine (201 umol/l). Treatment of sepsis and fluid restriction were the mainstay of treatment with only two patients receiving hypertonic saline. All patients with underlying sepsis were treated with antibiotics, usually administered intravenously. The outcome was good in 26 of the 28 episodes. Two patients died: a 68 year old tetraplegic patient with consolidation of the left lung, cystadenocarcinoma of both ovaries and squamous cell carcinoma of the forehead who presented with generalised oedema, with a plasma sodium level of 118 mmol/l, and potassium of 2.4 mmol/l and who was treated with 2 N saline + potassium + frusemide; she died 1 day later. The only other death was that of a 78 year old female tetraplegic patient who 2 days after sustaining cervical trauma developed hyponatremia because of intravenous infusion of hypotonic fluids given at another hospital, presumably to correct hypotension. She recovered from hyponatremia with fluid restriction, but 3 days later she succumbed to bronchopneumonia and respiratory insufficiency. No patient developed central pontine myelinolysis.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:A retrospective study of hyponatremia in tetraplegic/paraplegic patients with a review of the literature. 799 39

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


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