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

Both acute and chronic hepatic insufficiency can result in lactate accumulation and lactic acidosis; data from both types of patients were compared. In the chronic group, an acute precipitating event was identified in seven of nine subjects. Four had sepsis and three had gastrointestinal hemorrhage. In these patients, results from most tests of hepatic function were not altered dramatically. There were no long-term survivors in this group. In contrast, patients with acute hepatic failure had striking alterations in their results of hepatic function tests. Notable prolongation of the prothrombin time was always present initially and antedated other abnormalities of hepatic function. Three of seven patients in this group survived. Hypoglycemia was seen in both groups and in two subjects with acute hepatic insufficiency, glucose administration alone resulted in rapid lowering of lactate levels.
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PMID:Lactic acidosis and liver disease. 50 18

The hyperdynamic circulation characteristic of severe sepsis is not likely due to peripheral arteriovenous shunts since in skeletal muscle, at least, capillary blood flow is increased and varies directly with cardiac index. The finding that flow is normal in some septic patients who are severely ill and close to death suggests that blood flow can no longer be considered the critical factor explaining the death of the septic patient. Clearly, the commonly accepted sequence of low blood flow, tissue hypoxia, lactacidosis, and death does not apply to all patients dying from shock. The hyperdynamic circulatory state and the metabolic changes associated with severe sepsis may be related. Skeletal muscle capillary blood flow was increased in fasting normal subjects and septic postoperative patients, both of whom were catabolic. Therefore, elevated blood flow, which is characteristic of severe sepsis, may be a response to the catabolism of body protein required for energy production. If this concept of sepsis is accepted, it follows that treatment which heretofore has been aimed at increasing blood flow and blood pressure should be redirected to therapy which provides energy substrates and alters hormonal patterns to favor anabolism.
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PMID:Cardiovascular changes in sepsis. 78 54

Lactic acid is generated as the end product of anaerobic metabolism of glucose and is disposed by gluconeogenesis or oxidation. Changes in the lactate pyruvate ratio are not necessarily indicative of tissue hypoxia. The plasma lactate concentration is the result of lactate production and lactate removal (hepatic and renal gluconeogenesis; oxidation by muscle, liver and kidney). Lactic acidosis is defined as a state of metabolic acidosis (arterial pH less than 7.3) due to an increase in the blood concentration of lactate (greater than 2 mEq/l). Lactic acidosis may occur with evidence of tissue hypoxemia (type A) or in its absence (type B). Lactic acidosis has been described in association with phenformin therapy, hereditary enzymatic defects, hematological malignancy, prolonged fasting, shock with or without septicemia and occasionally without any underlying disease ("idiopathic" lactic acidosis). The therapy of lactic acidosis consists of administration of sodium bicarbonate and restoration of adequate tissue perfusion; hemodialysis may be helpful to control sodium excess and possibly to remove phenformin. The effectiveness of methylene blue, glucose and insulin are not yet established.
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PMID:Lactic acidosis. 87 61

There was little dispute that endotoxin treatment of experimental animals could recreate the O2 extraction defect that had been observed in critically ill patients. The remaining question was whether or not this necessarily signified pervasive tissue hypoxia. Some limitation to O2 diffusion in the tissues had been postulated because of known effects of endotoxin that ultimately result in damage to endothelium. We were unable to alter the critical DO2 or 0(2)ER in endotoxic dogs by manipulating the arterial PO2. This tended to rule against there being a diffusion limitation created by the endotoxin as a result of endothelial disruption or microvascular dysfunction. The results of the DCA and dopexamine experiments served to remind us that arterial lactate measurements may or may not indicate widespread tissue hypoxia. Sepsis, as emulated by endotoxin infusions, is also a metabolic disease that can cause inactivation of PDH and thus cause lactacidosis without tissue hypoxia. Regional measurements of lactate flux indicated that gut was hypoxic in spite of DO2 above critical because of maldistribution of blood flow between muscularis and mucosa. The questions persist of how much tissue hypoxia is caused by sepsis or endotoxin when DO2 is supported at supposedly adequate levels and whether there are marked regional differences. Such questions still await answers. Newer technological advances that permit assessment of tissue oxygenation by noninvasive methods, such as near infrared spectrophotometry or nuclear magnetic resonance measurement of tissue energy potential, may soon be feasible in critically ill patients. This kind of information will be of vast importance in designing the most effective therapeutic regimen.
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PMID:Oxygen supply dependency in the critically ill--a continuing conundrum. 128 44

Severe sepsis is characterized by increased oxygen demand, alteration of oxygen extraction, and a diminution of myocardial contractility. The importance of each of these three factors is directly related to the severity of the sepsis. The combination of these factors may lead to tissue hypoxia, which is the shortest route to development of multiple organ failure (MOF). The presence of tissue hypoxia should be suspected in the presence of lactic acidosis. The phenomenon of dependence on oxygen consumption (VO2) in relation to oxygen transport (DO2) is detectable where there is a rise in DO2 induced by perfusion of liquids or administration of vasoactive agents. Study of the relationship between cardiac flow and oxygen extraction is a simple means of studying the relations between VO2 and DO2 at the patient's bedside.
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PMID:[Septic syndrome: cardiocirculatory assessment]. 160 82

Two patients aged 37 and 44 years developed life-threatening lactic acidosis following abdominal surgery and a period of about 3 weeks of total parenteral nutrition. Septicaemia and hypoxia were excluded as possible causes. Conventional treatment including high doses of buffer agents was unsuccessful. Thiamine (vitamin B1) depletion was suspected as the cause of the metabolic acidosis, and two doses of 400 mg thiamine were given. In both patients, the lactic acidosis improved immediately, and it disappeared following the second dose of thiamine. Both patients were subsequently discharged as symptom-free. As part of the pyruvate-dehydrogenase (PDH) complex, thiamine was capable of improving the life-threatening situation.
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PMID:[Thiamine deficiency as a cause of life threatening lactic acidosis in total parenteral nutrition]. 181 18

This review article examines the pathophysiology of septic shock, with special attention to the concept of supply-dependent consumption and the implications this concept has for therapy. Patients with septic shock require higher levels of oxygen delivery (DO2) to maintain aerobic metabolism. When DO2 is inadequate, peripheral tissues switch to anaerobic metabolism and oxygen consumption decreases. The lactic acidosis that occurs is a reasonable clinical marker of supply dependency and inadequate tissue perfusion. Maximizing DO2 is an important part of the hemodynamic resuscitation of patients with septic shock. To achieve this goal, intravascular volume must be restored and the myocardial depression associated with sepsis must be treated to optimize cardiac output. The normalization of arterial lactate concentration is a reasonable goal of resuscitative efforts.
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PMID:Oxygen consumption in sepsis and septic shock. 202 29

Two patients, 37 and 44 years old, respectively, developed severe metabolic acidosis after abdominal surgery which was followed by three weeks of total parenteral nutrition. Septicaemia, peritonitis or hypoxia were excluded as possible causes. Both patients had very high serum lactate concentrations (24.3 and 22.8 mmol/l, respectively). Conventional treatment with buffer agents was unsuccessful. Because vitamin B1 deficiency was suspected, two doses of 400 mg thiamine were administered. In both patients the extreme lactic acidosis disappeared immediately after the injections. Both patients were later discharged without any symptoms.
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PMID:[Life-threatening lactic acidosis during total parenteral nutrition. Successful therapy with thiamine]. 210 78

We studied the effect of mechanical ventilation on systemic oxygen extraction and lactic acidosis in peritonitis and shock in rats. Sepsis was induced by cecal ligation and perforation. After tracheostomy, rats were randomized to spontaneous breathing (S) or mechanical ventilation with paralysis (V). Five animals were studied in each group. The V animals were paralyzed with pancuronium bromide to eliminate respiratory effort. Mechanical ventilation consisted of controlled ventilation using a rodent respirator with periodic adjustment of minute ventilation to maintain PaCO2 and pH within normal range. Arterial and central venous blood gases and thermodilution cardiac output were measured at baseline before abdominal surgery, and sequentially at 0.5, 3.5, and 6 h after surgery. At 6 h, cardiac output was 193 +/- 30 ml/kg.min in S animals and 199 +/- 32 ml/kg.min in V animals (NS). The central venous oxygen saturation was 27.4 +/- 4.7% in S animals and 30.0 +/- 6.4% in V animals (NS). Systemic oxygen extraction was 70 +/- 5% in S animals and 67 +/- 6% in V animals (NS). Arterial lactate was 2.4 +/- 0.4 mmol/L in S animals and 2.2 +/- 0.5 mmol/L in V animals (NS). The S animals developed lethal hypotension at 6.6 +/- 0.4 h compared to 6.8 +/- 0.4 h in V animals (NS). These data suggest that mechanical ventilation does not decrease systemic oxygen extraction or ameliorate the development of lactic acidosis during septic shock.
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PMID:Effect of mechanical ventilation on systemic oxygen extraction and lactic acidosis during early septic shock in rats. 229 71

It is assumed that the development of metabolic acidosis during sepsis is secondary to lactic acidosis. We assessed the composition of the anion gap during severe sepsis induced by cecal perforation in rats. In the first experiment, cardiac output, arterial blood gases, and arterial lactate were measured over a 6 hr interval in five septic rats and in five rats serving as sham-operated controls. The cardiac output decreased from 331 +/- 32 to 172 +/- 9 ml/kg/min (P less than 0.01) in the septic rats. Although the arterial lactate was increased to 2.1 +/- 0.2 mEq/L in septic rats compared to 0.8 +/- 0.1 mEq/L in sham rats (P less than 0.01), the HCO3- was decreased to 16.5 +/- 0.6 mEq/L in septic rats versus 23.8 +/- 1.10 mEq/L in sham rats (P less than 0.01). We further investigated this bicarbonate deficit in a second study in which arterial blood was sampled at 6 hr for blood gases, and plasma Na+, K+, Cl-, HCO3-, lactate, pyruvate, beta-hydroxybutyrate, acetoacetate, citrate, creatinine, albumin, and amino acids in five septic and five sham rats. The serum anion gap was calculated as [(Na(+) + K+) - (Cl(-) + HCO3-)]. The anion gap was 21.6 +/- 1.6 mEq/L in the septic animals as compared to 13.2 +/- 0.5 mEq/L in the sham animals (P less than 0.01). There were no differences in the concentration of pyruvate, beta-hydroxybutyrate, acetoacetate, citrate, creatinine, albumin, or amino acids.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Unmeasured anion during severe sepsis with metabolic acidosis. 231 Dec 1


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