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The value of hepatobiliary scans in fasted patients receiving total parenteral nutrition
Abstracts From the Literature-Surgery Selected Nutritional Patients
World
Support in Surgical
J Surg
11:194,
by A. Craig
in the Management of Critically Intensive Care. Streat SJ, Hill
Ill
CL.
1987.
Nutritional support is given to many patients in surgical intensive care after major trauma and serious sepsis but rarely after major elective surgery. We have quantified the changes in body composition that occur in these patients and have found that serious losses of body protein still occur after trauma and sepsis despite nutritional support. Correct nutritional management of critically ill patients in surgical intensive care depends on an understanding of the underlying physiology, drainage of sepsis, a high standard of general intensive care measures, and appreciation of sound principles of administration of intravenous nutrition. (Reprinted with permission.) The Value of Hepatobiliary Scans in Fasted Patients Receiving Total Parenteral Nutrition. Warner BW. Hamilton FN,
Silberstein
EB, et a/. Surgery
102:595,
1987.
Hepatobiliary scanning is considered to be a highly accurate method for the diagnosis of acute cholecystitis. Falsepositive scans (failure to visualize the gallbladder in the absence of cholecystitis) have been reported to occur in fasted patients receiving total parenteral nutrition (TPN). To determine the prevalence of false-positive scans in this patient population and identify factors that might be associated with scan outcome, hepatobiliary imaging was performed in fasted patients receiving TPN and without clinical evidence of acute cholecystitis. Gallbladder nonvisualization occurred in 18 of 50 (36%) patients. In the group whose gallbladders did not visualize, a significantly higher male to female ratio (15:3 versus 17:15; p = 0.016), alkaline phosphatase (346 f 84 IU/L versus 212 k 32 IU/L, p < 0.04), total bilirubin (1.7 _+ 0.3 mg/dl versus 1.0 k 0.2 mg/dl, p < 0.02), and lower serum albumin (2.4 * 0.01 gm/dl versus 2.8 r 0.2 gm/dl, p < 0.02) levels were noted. In 18 patients, gallbladder ultrasonography was also performed, and the presence of sludge or a thickened gallbladder wall did not correlate with scan outcome. The prevalence of false-positive hepatobiliary scans in fasted patients receiving TPN is significant and does not always correlate with a syndrome of acute gallbladder inflammation. The results of such scans must therefore be interpreted with caution in these patients. (Reprinted with permission.) The Fundamental Gastric “Stress
RW, Bulkley 1987.
Hemodynamic Mechanism Underlying Ulceration” in Cardiogenic Shock. Bailey
GB. Hamilton
SR, et al. Ann
Surg
205:597,
Acute hemorrhagic ulceration of the gastric mucosa is seen frequently in patients with hypovolemic or cardiogenic shock. Although such lesions clearly are related to regional gastric ischemia, little attention has been directed at the underlying mechanism(s) mediating the ischemia itself. To this end, anesthetized pigs were subjected to sustained cardiogenic shock (mild hemorrhage and pericardial tamponade) such
Journalof
CriticalCare,
Vol 3, No 2 (June),
1988:
pp 151-160
Eddy
and
Charles
Rice
that cardiac output was reduced to 38 t 1% of the baseline level for 4 hours, followed by release of the tamponade, reinfusion of the shed blood, and resuscitation for 2 hours. During the period of shock, there was profound regional gastric ischemia, resulting from severe and disproportionate gastric vasoconstriction. “Blinded” gross and microscopic evaluation of the stomachs removed after the experiment revealed severe mucosal ischemic necrosis, hemorrhage, and ulceration, whereas sham-operated pigs showed no lesions. The characteristics of this model therefore mimic the essential features of the gastric “stress ulceration” syndrome. Prior confirmed total alpha-adrenergic blockade with phenoxybenzamine failed to alter these features significantly. In contrast, prior ablation of the renin-angiotensin axis, whether by angiotensin-converting enzyme inhibition with teprotide or by bilateral nephrectomy, significantly and substantially ameliorated the ischemia, vasospasm, and mucosal injury. In this model of cardiogenic shock, acute gastric mucosal “stress ulceration” is caused by a disproportionately severe regional gastric ischemia resulting from selective splanchnic vasospasm that is unaffected by sympathetic blockade but abolished by prior ablation of the renin-angiotensin axis. Like nonocclusive small bowel ischemia, ischemic colitis, and the “shock liver” syndrome, gastric “stress ulceration” is yet another component of the multiple splanchnic organ failure syndrome that appears to be mediated primarily by the remarkable sensitivity of the splanchnic vascular bed to the renin-angiotensin axis. (Reprinted with permission.) Comparison Hemorrhagic
43:52,
of Approaches to Stress Ulcer Prophylaxis Shock. Ephgrave KS, Horton JW. J Surg
in
Res
1987.
Stress ulceration can be prevented clinically by prophylaxis with antacids or sucralfate, while hyperosmolar glucose and prostaglandins have prevented gastric mucosal injury in experimental models. We compared these four agents’ effectiveness in gastric mucosal protection as well as their interaction with the pathophysiology of hemorrhagic shock. Gastric mucosal injury was produced in a canine model with the insults important in clinical situations: intragastric acid, intragastric bile, and gastric mucosal ischemia. Hypotension was maintained at a constant level for 3 hr, during which one of the prophylactic treatments or vehicle (H,O) was given hourly intragastrically. The stomachs were harvested for quantification of gastric mucosal injury after return of shed blood. The percentage of gastric area damaged was significantly decreased to 1 .O t 0.7% by antacids but was increased to 43.5 t 4.9% by 16.16-dimethyl prostaglandin E, (16,16dmPGE,), in comparison to vehicle treatment which caused 28.4 + 4.7% lesioned mucosa. Additionally, hemodynamic function differed between treatment groups after 1 hr of shock. Irrespective of treatment group, parameters reflecting volume status and hemodynamic function correlated significantly with the amount of gastric mucosal injury measured in individual animals. lntragastric treatments did not variably affect systemic pH or systemic glucose, and neither of these parameters was related to gastric mucosal injury. In conclu-
151
World
Support in Surgical
J Surg
11:194,
by A. Craig
in the Management of Critically Intensive Care. Streat SJ, Hill
Ill
CL.
1987.
Nutritional support is given to many patients in surgical intensive care after major trauma and serious sepsis but rarely after major elective surgery. We have quantified the changes in body composition that occur in these patients and have found that serious losses of body protein still occur after trauma and sepsis despite nutritional support. Correct nutritional management of critically ill patients in surgical intensive care depends on an understanding of the underlying physiology, drainage of sepsis, a high standard of general intensive care measures, and appreciation of sound principles of administration of intravenous nutrition. (Reprinted with permission.) The Value of Hepatobiliary Scans in Fasted Patients Receiving Total Parenteral Nutrition. Warner BW. Hamilton FN,
Silberstein
EB, et a/. Surgery
102:595,
1987.
Hepatobiliary scanning is considered to be a highly accurate method for the diagnosis of acute cholecystitis. Falsepositive scans (failure to visualize the gallbladder in the absence of cholecystitis) have been reported to occur in fasted patients receiving total parenteral nutrition (TPN). To determine the prevalence of false-positive scans in this patient population and identify factors that might be associated with scan outcome, hepatobiliary imaging was performed in fasted patients receiving TPN and without clinical evidence of acute cholecystitis. Gallbladder nonvisualization occurred in 18 of 50 (36%) patients. In the group whose gallbladders did not visualize, a significantly higher male to female ratio (15:3 versus 17:15; p = 0.016), alkaline phosphatase (346 f 84 IU/L versus 212 k 32 IU/L, p < 0.04), total bilirubin (1.7 _+ 0.3 mg/dl versus 1.0 k 0.2 mg/dl, p < 0.02), and lower serum albumin (2.4 * 0.01 gm/dl versus 2.8 r 0.2 gm/dl, p < 0.02) levels were noted. In 18 patients, gallbladder ultrasonography was also performed, and the presence of sludge or a thickened gallbladder wall did not correlate with scan outcome. The prevalence of false-positive hepatobiliary scans in fasted patients receiving TPN is significant and does not always correlate with a syndrome of acute gallbladder inflammation. The results of such scans must therefore be interpreted with caution in these patients. (Reprinted with permission.) The Fundamental Gastric “Stress
RW, Bulkley 1987.
Hemodynamic Mechanism Underlying Ulceration” in Cardiogenic Shock. Bailey
GB. Hamilton
SR, et al. Ann
Surg
205:597,
Acute hemorrhagic ulceration of the gastric mucosa is seen frequently in patients with hypovolemic or cardiogenic shock. Although such lesions clearly are related to regional gastric ischemia, little attention has been directed at the underlying mechanism(s) mediating the ischemia itself. To this end, anesthetized pigs were subjected to sustained cardiogenic shock (mild hemorrhage and pericardial tamponade) such
Journalof
CriticalCare,
Vol 3, No 2 (June),
1988:
pp 151-160
Eddy
and
Charles
Rice
that cardiac output was reduced to 38 t 1% of the baseline level for 4 hours, followed by release of the tamponade, reinfusion of the shed blood, and resuscitation for 2 hours. During the period of shock, there was profound regional gastric ischemia, resulting from severe and disproportionate gastric vasoconstriction. “Blinded” gross and microscopic evaluation of the stomachs removed after the experiment revealed severe mucosal ischemic necrosis, hemorrhage, and ulceration, whereas sham-operated pigs showed no lesions. The characteristics of this model therefore mimic the essential features of the gastric “stress ulceration” syndrome. Prior confirmed total alpha-adrenergic blockade with phenoxybenzamine failed to alter these features significantly. In contrast, prior ablation of the renin-angiotensin axis, whether by angiotensin-converting enzyme inhibition with teprotide or by bilateral nephrectomy, significantly and substantially ameliorated the ischemia, vasospasm, and mucosal injury. In this model of cardiogenic shock, acute gastric mucosal “stress ulceration” is caused by a disproportionately severe regional gastric ischemia resulting from selective splanchnic vasospasm that is unaffected by sympathetic blockade but abolished by prior ablation of the renin-angiotensin axis. Like nonocclusive small bowel ischemia, ischemic colitis, and the “shock liver” syndrome, gastric “stress ulceration” is yet another component of the multiple splanchnic organ failure syndrome that appears to be mediated primarily by the remarkable sensitivity of the splanchnic vascular bed to the renin-angiotensin axis. (Reprinted with permission.) Comparison Hemorrhagic
43:52,
of Approaches to Stress Ulcer Prophylaxis Shock. Ephgrave KS, Horton JW. J Surg
in
Res
1987.
Stress ulceration can be prevented clinically by prophylaxis with antacids or sucralfate, while hyperosmolar glucose and prostaglandins have prevented gastric mucosal injury in experimental models. We compared these four agents’ effectiveness in gastric mucosal protection as well as their interaction with the pathophysiology of hemorrhagic shock. Gastric mucosal injury was produced in a canine model with the insults important in clinical situations: intragastric acid, intragastric bile, and gastric mucosal ischemia. Hypotension was maintained at a constant level for 3 hr, during which one of the prophylactic treatments or vehicle (H,O) was given hourly intragastrically. The stomachs were harvested for quantification of gastric mucosal injury after return of shed blood. The percentage of gastric area damaged was significantly decreased to 1 .O t 0.7% by antacids but was increased to 43.5 t 4.9% by 16.16-dimethyl prostaglandin E, (16,16dmPGE,), in comparison to vehicle treatment which caused 28.4 + 4.7% lesioned mucosa. Additionally, hemodynamic function differed between treatment groups after 1 hr of shock. Irrespective of treatment group, parameters reflecting volume status and hemodynamic function correlated significantly with the amount of gastric mucosal injury measured in individual animals. lntragastric treatments did not variably affect systemic pH or systemic glucose, and neither of these parameters was related to gastric mucosal injury. In conclu-
151