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

Bleeding from hemorrhagic erosions in the stomach or duodenum of seriously ill patients is associated with a high mortality. While the pathogenesis of such lesions is by no means certain, it is known that they are universal after shock, sepsis or severe burns. Fiberoptic endoscopy has become the most valuable means of diagnosis. This should be preceded by gastric irrigaiton, which usually sufficies to control bleeding caused by acetylsalicylic acid or alcohol, or both. Neutralization of gastric acidity is essential. The histamine HI-receptor antagonist, cimetidine, was used in 27 patients with erosive gastritis, and bleeding ceased in 24. There is a prospect that sugh agents will obviate the necessity of total gastrectomy in the occasional resistant cases in favour of conservative surgery.
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PMID:Symposium on intensive care: 3. Upper gastrointestinal bleeding in the intensive care unit. 2 13

The restraint model and other models for the production of experimental stress ulcers have been reviewed. The mechanism of experimental stress ulcers appears to depend on an interaction between the presence of acid, changes in mucosal circulation, an increase in the excretion of glycoproteins in the mucus, and a decrease in mitotic activity of the mucosal lining of the stomach. Factors enhancing ulceration are cold, starvation, increased acidity, burns, reflux of bile, endotoxin, adrenalectomy, and hemorrhage. Factors inhibiting ulceration are vagotomy, anticholinergics, elemental diets, vitamin A, antacids, prevention of bile reflux, corticosteroids, epinephrine and norepinephrine, serotonin antagonists, and immediate replacement of blood loss with low molecular weight dextran. The role of sepsis is unclear and more work is needed in this area. Ulcers from intracranial injury are usually associated with the hypersecretion of gastric acid. Stimulation of the hypothalamus, directly or indirectly, with resultant vagal stimulation is thought to be the responsible mechanism for the increase in acid.
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PMID:Experimental stress ulcers: a review. 110 3

Vibrio vulnificus is an extremely invasive gram-negative bacillus that causes bacteremia and shock. It should be suspected in any patient who is immunocompromised or has liver disease or hemochromatosis. Reduced gastric acidity may also increase the risk of infection if a patient presents with a history of ingesting raw shellfish (especially oysters) or trauma in brackish waters and skin lesions. Patients most commonly present with one of three clinical syndromes: primary septicemia, wound infection, or gastroenteritis. Treatment includes aggressive wound debridement, antibiotic therapy, and supportive care. Rapidly diagnosing and promptly initiating therapy are critical because V vulnificus infection is rapidly progressive and mortality approaches 100% if septic shock occurs.
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PMID:Vibrio vulnificus. Hazard on the half shell. 177 90

One of the major unanswered questions regarding the presence of Listeria monocytogenes in foods is how many cells must be ingested in order to cause illness. To answer this question, studies were undertaken by using Macaca fascicularis (cynomolgus monkey) as an animal model. Healthy nonhuman primates were dosed with various concentrations of L. monocytogenes suspended in sterile whole milk. Final concentrations of 10(5), 10(7), and 10(9) total cells of the organism were used; a control was also included. Blood samples, as well as fecal and nasal specimens, were taken at various time intervals. Only animals that received 10(9) cells of L. monocytogenes became noticeably ill, with symptoms of septicemia, irritability, loss of appetite, and occasional diarrhea. Monkeys that received 10(7) and 10(9) cells shed L. monocytogenes in the feces for approximately 21 days. In monkeys that received the dose of 10(9) cells, severe lymphopenia and neutrophilia occurred within 48 h. In a separate trial, monkeys received Maalox to reduce the gastric acidity of the stomach. However, no substantial differences were observed between Maalox-treated and control monkeys.
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PMID:Feeding trials of Listeria monocytogenes with a nonhuman primate model. 177 70

Critically ill patients are prone to stress-induced ulcerations in the upper gastrointestinal tract, which might lead to life-threatening bleeding. Therefore, an effective stress ulcer prophylaxis is absolutely indicated and H2-blocking agents, anticholinergics, antacids, sucralfate, enteral nutrition and prostaglandin E analoges are recommended. H2-blocking agents seem to provide effective prophylaxis, but severe side effects seem to limit their application. Most of all, as they are less effective as antacids and as they cause considerable costs. Additionally H2-blocking agents elevate gastric pH, thereby favouring microbic colonisation of gastric juice. Microorganism from gastric juice may reach the tracheobronchial system and lead to nosocomial pneumonias. The contaminated gastric juice may also be considered as endogenous source for sepsis and entero-colitis. The anticholinergic agent pirenzepine does not increase gastric pH and seems to be effective in neurological and neurosurgical intensive care patients. Antacids are effective in stress ulcer bleeding prophylaxis, but favour bacterial overgrowth, are badly tolerated by patients and cause a high amount of nursing time. Sucralfate seems to be as effective as antacids, is better tolerated and does not elevate gastric pH. The remaining acidity of gastric juice blocks bacterial contamination. After all, the smallest costs of effective stress ulcer prophylaxis, makes sucralfate to the medicament of first choice. However, in severely ill patients, a combined stress ulcer prophylaxis with two or more agents seems to be necessary.
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PMID:[Prevention of stress ulcer in intensive care patients]. 288 1

Stress ulcer is a condition seen after major trauma and surgery, sepsis, shock and extensive burns so its prevention is very important. Cimetidine and antacids are the drugs most often administered for prevention. Sometimes these drugs are insufficient and complications and side-effects appear. In order to prevent stress ulcers, experimental administration of intragastric glucose has been tested. A 30% dextrose solution given intragastrically decreased both luminal acidity and mean ulcer index. Similar results were obtained with intragastric 0.9% NaCl. The results showed that a luminal factor, not identified in this experiment, is present.
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PMID:Prevention of stress ulcer by intragastric glucose. An experimental study. 292 73

The effect of two ranitidine intravenous infusion regimens on intragastric pH was studied in 134 critically ill patients admitted to 15 intensive care units. Intragastric pH was determined hourly for 30 hours. Those patients whose intragastric acidity fell below pH 4.0 for 3 or more of the first 6 hours were considered 'at risk' of developing stress-related gastric lesions and randomized to receive a 50 mg bolus of ranitidine together with a continuous intravenous infusion of either 0.125 or 0.25 mg kg-1 h-1 ranitidine for 24 hours. The maximal elevation in intragastric pH was achieved within 12 hours. The median intragastric pH for the last 20 hours of the infusion period was 5.9 for the higher dose group and 5.6 for the lower dose group. The increase in intragastric pH achieved by the two dosage regimens did not differ significantly throughout the 24 hour period. Patients having two or more of five major risk factors (head injury, major trauma, sepsis, respiratory failure/insufficiency and major surgery) had better overall control of intragastric pH on the higher dose of ranitidine than those receiving the lower dose. The majority of intensive care patients are likely to receive satisfactory treatment with the lower dosage regimen that was tested (0.125 mg kg-1 h-1). Those with multiple risk factors may, however, require treatment with higher doses of ranitidine (0.25 mg kg-1 h-1).
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PMID:A comparison of two ranitidine intravenous infusion regimens in critically ill patients. 297 34

The problem of gastric secretory and mucosal injury response was evaluated in 19 patients who had suffered a severe head injury. Fifteen of 19 patients had some evidence of gastrointestinal hemorrhage. In 7 cases, this was marked. The mean volume of gastric secretions ranged from 36.4 ml/hour on Day 1 to 47.6 ml/hour on Day 6. The mean value of titratable acidity ranged from 3.4 meq/hour on Day 1 to 3.9 meq/hour on Day 6. Possible risk factors were analyzed as a means of predicting specific subgroups of severely injured patients who would be more prone to have gastrointestinal complications. During the first 6 days after injury, there was no significant association (correlation coefficient not significant at the 0.05 level of significance) of the presence of an intracranial mass lesion, elevated intracranial pressure, brain stem dysfunction or prior episodes of hypotension or hypoxia, sepsis, shock, or the requirement for pressor agents with elevated gastric acid output, mucosal erosion, or hemorrhage. Because no specific risk factor or factors could be identified, all severely brain-injured patients should be on some form of therapy for the prevention of gastrointestinal complications.
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PMID:Gastric secretory and mucosal injury response to severe head trauma. 683

One hundred forty-four critically ill patients admitted to an intensive care setting were randomly assigned to cimetidine or antacid treatament groups. Gastric pH was monitored hourly. One hundred twenty-three (85%) patients demonstrated a fall in pH to less than 4 and were considered to require prophylaxis. Prophylaxis was considered adequate if the measured pH could then be maintained at greater than or equal to 4. Fifty-eight patients received antacids alone, the average requirement being 41 cc/hour. Sixty-five patients received cimetidine. Seventeen (26%) of the cimetidine prophylaxis patients failed to raise their pH and were than placed on hourly administration of antacid with successful elevations of pH to greater than or equal to 4 in all cases on an average supplementary dose of 53 cc/hour. Risk factors, including sepsis, hypotension, head injury, respiratory failure, degree of trauma, and age, were not statistically different in the two treated groups. Using these same criteria, responders to cimetidine could not be differentiated from nonresponders. All patients were protected from significant stress bleeding while on this study. Significant complications of either treatment were minimal. Antacids offered consistent protection against gastric acidity and were 100% effective. A routine schedule of 300 mg every six hours of cimetidine was effective in only 47% of patients, and the maximum dose of cimetidine was effective in only 74% of patients. Hourly measurement of intragastric pH is required for monitoring the response to prophylaxis of stress bleeding in severely ill patients.
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PMID:Randomized prospective evaluation of cimetidine and antacid control of gastric pH in the critically ill. 740 71

A peptic ulcer is a lesion in which acid and pepsin are essential components of pathogenesis. Regardless of the type of patient or the setting in which the ulcer presents, the basic pathogenetic scheme is the same. The primary event is disruption of mucosal integrity. In the presence of acid and pepsin, such disruption of integrity leads to an ulcer. While rarely sufficient by itself to cause ulceration, the presence of acid is a necessary cofactor. The causes of disruption of mucosal integrity include nonsteroidal anti-inflammatory drugs (NSAIDs), Helicobacter pylori and critical illness. With the latter, tissue ischaemia may be the primary event, leading to back-diffusion of H+ ions through increased membrane permeability. Impaired mucosal buffering then leads to intramural acidosis and cell death. Risk factors for bleeding peptic ulcer in the intensive care unit (ICU) include severe trauma, sepsis, respiratory failure, and coagulopathy. Potential roles for decreasing gastric acidity in the treatment of bleeding peptic ulcer include cessation of active bleeding, prevention of rebleeding in hospital and primary prevention of bleeding. Most published studies dealing with the first two situations suggest no benefit with antisecretory therapy. However, the optimal pH for clot and platelet function may be > or = 7.0. Can such pH levels be maintained with antisecretory agents such as the proton pump inhibitors? Are the published trials adequate to demonstrate any benefit from antisecretory agents? Primary prevention of bleeding ulcer in the outpatient setting includes avoidance of NSAIDs, use of antisecretory agents and eradication of H. pylori.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:The role of acid in upper gastrointestinal haemorrhage due to ulcer and stress-related mucosal damage. 749 42


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