Endoscopic nasogastric-jejunal feeding tube placement in critically ill patients.

BACKGROUND: Historically, placement of small bowel nasoenteric feeding tubes in the critically ill patient has been difficult because of lack of bedside fluoroscopy, inadequately designed endoscopic tubes, or failure of the tube to spontaneously pass into the duodenum following placement. METHODS: We followed-up 54 consecutive critically ill patients who had a combined nasogastric-jejunal feeding tube placed at the bedside using a new endoscopic, nonfluoroscopic method of placement. Data were obtained on the placement procedure, outcomes, and complications that followed. RESULTS: Tubes were successfully placed in 94% of the patients in an average time of 12 minutes. Negative outcomes included the following: inadvertent removal by patient or staff (21%), intolerance to tube feeding (14%), clogging (9%), kinking (6%), and cracking at the tube adapter (11%). The duration of the tube following placement ranged from 1 to 42 days, with an average of 9 days. CONCLUSION: The combined tubes were easy to place endoscopically. The endoscopic, nonfluoroscopic method of placing feeding tubes can be performed at the bedside and allows for gastric decompression and enteral feeding to be rapidly and efficiently achieved, which is particularly useful for intubated patients in an intensive care setting. Negative outcomes should decrease by avoidance of inadvertent tube removal and by improved tube maintenance and materials.

Small flat adenoma: important in colon carcinogenesis?

The risk for development of colonic carcinoma increases with increasing size of the polyp. Endoscopists have focused attention on large polyps. Small flat adenomas are sessile polyps that measure less than 1 cm; they are nearly flat, and they have a slight depression in the center. They have a high incidence of cancer in situ. Adenomatous polyps follow the adenoma-carcinoma sequence. Small flat adenomas do not appear to follow this sequence, but they may be precursors of so called de novo colonic carcinoma. The genetics of small flat adenomas are not fully elucidated. Small flat adenomas may not be identified during standard colonoscopy due to the small size of the lesion. Chromoendoscopy may increase the rate of detection.

Nutrition support in pancreatitis.

Nutrition support in patients with pancreatitis has created a challenge for clinicians. Because the pancreas is normally stimulated by the ingestion of food, particularly fat, patients are often denied oral nutrition. This reduction in the ingestion of food, together with the increased metabolic demands of this disease, often results in a negative energy balance and occasionally undernutrition or malnutrition. This review summarizes the etiologies and methods for staging pancreatitis, the physiology of pancreatic exocrine secretion and the response of the pancreas to different methods of nutrition support. The results of clinical trials, which examine both parenteral and enteral nutrition in animals and humans with this disease, are reviewed. Recommendations for nutrition management of patients with acute and chronic pancreatitis and areas for future research are discussed.

Lactic acidosis and acute ethanol intoxication.

Ethanol intoxication has been widely reported as a cause of lactic acidosis. To determine the frequency and severity of ethanol-induced lactic acidosis, patients who presented to an emergency department with a clinical diagnosis of acute ethanol intoxication and a serum ethanol concentration of at least 100 mg/dL were studied. Arterial blood was sampled for lactate and blood gas determinations. A total of 60 patients (mean age, 41 years) were studied. Twenty-two patients sustained minor trauma. Ethanol concentrations ranged from 100 to 667 mg/dL (mean, 287 mg/dL). Lactate concentrations were abnormal (> 2.4 mmol/L) in seven patients (11.7%). In all cases, blood lactate was less than 5 mmol/L. Of the patients with elevated lactate, other potential causes for lactic acidosis, including hypoxia, seizures, and hypoperfusion, were also present. Only one case with elevated blood lactate concentration had associated acidemia. Significant elevations of blood lactate are uncommon in acute ethanol intoxication. In patients with ethanol intoxication who are found to have lactic acidosis, other etiologies for the elevated lactate level should be considered.