Compared with patients in the forced-air warming group, patients receiving routine thermal care had lower core temperatures, a greater degree of peripheral vasoconstriction, higher norepinephrine concentrations, and higher arterial blood pressures in the early postoperative period. These findings suggest a possible mechanism for hypothermia-related cardiovascular morbidity in the perioperative period.
The indications, methods, and complications of nutritional support of 90 patients admitted with a primary complaint of dysphagia were reviewed. Patients were divided into two groups based on etiology of dysphagia (central neurologic vs local mechanical dysfunction). All patients on admission exhibited marked malnutrition with an average weight loss of 12 +/- 9.8% body weight, serum transferrin 165 +/- 60.1 mg/dl, and albumin 3.2 +/- 0.85 mg/dl. All patients were placed on either enteral (63%) or parenteral (37%) nutrition. Twenty-seven percent of all patients suffered a complication of nutritional therapy. Patients with nasoenteric tubes had a 10% complication incidence (aspiration or endotracheal placement of tube) resulting in a 30% mortality rate; significantly higher (p less than 0.05) than seen with other modalities. Any form of upper enteric feeding (nasoenteric or gastrostomy) was associated with significantly increased (p less than 0.01) risk of aspiration pneumonia. It is concluded that patients admitted to hospital with dysphagia as the major complaint suffer from severe malnutrition, and that upper gastrointestinal intubation should not be employed for feeding until the dysphagia has resolved.
One hundred and forty silicone catheters were inserted in 127 patients for long-term intravenous access with a cumulative follow-up time of 21,125 catheter-days (58 patient-years). Fifty-six patients had acquired immunodeficiency syndrome (AIDS); 44 were not AIDS patients and were receiving ambulatory home parenteral nutrition, whereas the remaining 27 did not have AIDS and were receiving home antibiotic therapy. Patients had a mean of 1.1 catheters inserted, and the rate of Hickman catheter-related sepsis was 0.18 per 100 catheter days or 0.6 septic episodes per patient year of treatment. Catheter-related sepsis was higher in AIDS patients (p < .01) and in patients receiving parenteral nutrition (p < .05) compared with those receiving antibiotic therapy. Prior catheter infection and AIDS were the most significant predictors of catheter infection (p < .01). Staphylococcus aureus was the most commonly isolated pathogen (61%) in AIDS patients. Fever (p < .001) and relative leukocytosis (p < .02) were the most common signs of infection. Only 14 infected catheters (37.8%) were salvaged by antibiotic therapy after the initial infection episode, and 6 of these catheters (42.9%) had recurrent multiple infections. In addition, inflammatory bowel disease was found to be a risk factor for venous thrombosis (p = .018). We conclude that because immunocompromised patients have a high risk of infection, catheter-related sepsis in these patients should be treated by catheter removal and antibiotics.
generalized reduced vascular resistance.1,2 The reasons for Portal hypertension (PHT) is characterized by splanchnic the decreased vascular resistance include exaggerated endohyperemia due to a reduction in mesenteric vascular resisthelial function with enhanced synthesis and/or release of tance. The reasons for the decreased resistance include an vasoactive substance (such as prostacyclin and nitric oxide) increased responsiveness to a vasodilator substance. Because and altered vascular responsiveness to vasoconstrictor subthe activation of an inhibitory guanine nucleotide regulatory stances (such as vasopressin, angiotensin, norepinephrine, (Gi) protein can result in endothelium-dependent relaxation, and methoxamine). [3][4][5][6][7][8] Nitric oxide (NO), a potent endothewe tested the hypothesis that exaggerated Gi-protein induced lium-derived relaxing factor, is one of the major vasoactive relaxation via a nitric oxide (NO)-dependent pathway partly substances implicated in the pathogenesis of the reduced reflects the enhanced Gi-protein expression in PHT vessels.vascular resistance in PHT. [7][8][9][10] The altered vascular respon-PHT was created in Sprague-Dawley rats by a partial portalsiveness and circulatory abnormalities of PHT can be partially vein ligation. Control animals were sham operated. Using corrected following the inhibition of NO synthase (NOS) isolated vascular rings in the absence or presence of an intact with specific NOS inhibitors. [10][11][12][13][14][15] This suggests that enhanced endothelium, N G -nitro-L-arginine methyl ester (L-NAME), and NO production is a major modulator of the exaggerated vaspertussis toxin, dose response relationships for sodium fluocular response in PHT. ride (NaF; range, 0. 1-4 mmol/L), a Gi protein activator, wereAlthough the exact etiology of the enhanced NO response determined in a cumulative manner. Gi-protein expression in PHT remains unclear, it is possible that an overproduction was determined by Western blotting. NaF caused a doseof NO is not a primary but is a secondary event to enhanced dependent relaxation in both sham and portal hypertensive endothelial shear stress, pressure, or endotoxemia. [15][16][17][18] Most pre-contracted vessels, an effect that was significantly inhibstudies to date have been unable to detect endotoxemiaited by pertussis toxin, endothelial denudation, and L-NAME.induced NOS expression in PHT animal models which do not Concentrations of NaF greater than 4 mmol/L caused contracinvolve any hepatic parenchymal dysfunction 19-21 ; however, tions, an effect that was unaffected by L-NAME. The NaFinduced NOS expression has been demonstrated in cirrhotic induced relaxation response was significantly greater in PHT models of PHT, particularly with ascites. [22][23] In prehepatic vessels as compared with sham concomitant with increased models of PHT, basal calcium-dependent endothelial NOS Gi-protein expression in PHT vessels. These data suggest that (eNOS) activity is significantly increased in hypertensive vesthe enhanced endothelia...
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