Stress ulceration

Always address the need for stress-ulcer prophylaxis, deep vein thrombosis (DVT) prophylaxis, anemia prophylaxis, and nutrition support... 

Adjunctive therapies nutrition, deep vein thrombosis prophylaxis, stress ulcer prophylaxis, and sedation for mechanically ventilated patients. 

Stress ulcer prophylaxis is recommended in septic patients. Patients at greatest risk for stress ulcers are coagulopathic, mechanically ventilated, and hypotensive. Histamine-receptor antagonists are more efficacious than sucralfate, and proton pump inhibitors have not been compared to histamine-receptor antagonists. However, they do demonstrate equivalence in the ability to increase gastric pH.24... 

Peptic ulcer disease (PUD) refers to a group of ulcerative disorders of the upper GI tract that require acid and pepsin for their formation. Ulcers differ from gastritis and erosions in that they extend deeper into the muscularis mucosa. The three common forms of peptic ulcers include Helicobacter pylori (HP)-associated ulcers, nonsteroidal antiinflammatory drug (NSAID)-induced ulcers, and stress-related mucosal damage (also called stress ulcers). 

Either low-dose unfractionated heparin or low-molecular weight heparin are effective A in preventing deep vein thrombosis Stress ulcer prophylaxis... 

Z0337 Yamazaki, M., and H. Shirota. Application of experimental stress ulcer test in mice for the survey of neurotropic naturally occurring drug materials. Shoyakugaku Zasshi 1981 35 96—102. 

Pare, WJ., Redei, E. Depressive behavior and stress ulcer in Wistar Kyoto rats. J. Physiol 87, 229-238, 1993. 

Prophylaxis of stress ulceration in intensive care units is the major interest to the anaesthetist. Here, it is given in a dose of 1 g every 6 hours via nasogastric tube. Several studies have shown sucralfate to be comparable in efficacy to H2 blockers. It has been claimed, but not proved, to result in a reduction in morbidity and mortality from nosocomial pneumonias in comparison to H2 antagonists. The latter, by raising gastric pH, eliminate the acid barrier to colonisation of the gut by pathogens, which sucralfate does not do. 

There are numerous accounts in the literature of increased bioavailability in animals when changing the solid state. Kato and Kohetsu (1981) showed that form II amobarbital is more rapidly absorbedn vivo than form I. Dissolution rate experiments in water at(3"Showed a 1.6 times faster dissolution ratei vitro for form II compared to form I. Yokoyama et al. (1981) found that form III of 6-mercaptopurine was 1.5 times as bioavailable in rabbits as form I. It was six to seven times as soluble as the form I polymorph in studies by Kuroda et al. (1982). Kokubu et al. (1987) examined the therapeutic effect of different polymorphs of cimetidine in inhibition of ulcers in the rat. Pharmacokinetic studies found that form C was 1.4-1.5 times as bioavailable as forms A and B. This translated into a greater protection against stress ulceration, as shown in Table 19.4. The effec of form C was signiLcant compared to forms A, B, and D, which were all equivalent. 

Kokubu, H, Morimoto, K, Ishida, T, Inoue, M, and Morisaka, K. (1987). Bioavailability and inhibitory effect for stress ulcer of cimetidine polymorphs in rdtst,. J. Pharm, 35 181-183. 

Stollman N, Metz DC. Pathophysiology and prophylaxis of stress ulcer in intensive care unit patients. J CritCare. 2005 20 35-45. 

Yang YX, Lewis JD. Prevention and treatment of stress ulcers in critically ill patients. Semin Gastrointest Dis. 2003 14 11-19. 

Review all oral medications to assess their potential toxicity given the patient s current state. Suggest stopping the indometacin, ramipril and gli-clazide, with a view to restarting the latter two when the patient is more stable. Continue the ranitidine, as the patient is at risk of developing stress ulceration. 

Stress ulcer prophylaxis 40 mg p.o. q.d. initially, then 20-40 mg daily... 

In another study of stress ulcer prophylaxis, 53 critically ill patients were randomized to receive sucralfate 1 g 6-hourly, cimetidine 300 mg 8-hourly, or cimetidine 900 mg/day by continuous intravenous infusion (14). Although bacterial colonization was increasingly likely in patients with a persistent alkaline gastric environment, gastric luminal pH and the degree of bacterial colonization of the stomach were similar in the three groups. 

Hanisch EW, Encke A, Naujoks F, Windoh J. A randomized, double-blind trial for stress ulcer prophylaxis shows no evidence of increased pneumonia. Am J Surg... 

Ortiz JE, Sotthe FD, Sigel P, Nasraway SA. Gastric colonization as a consequence of stress ulcer prophylaxis a prospective, randomized trial. Pharmacotherapy 1998 18(3) 486-91. 

Ginsengoside Rbi (60) is a representative of the saponins derived from 20(5)-protopanaxadiol. It exhibits central nervous system-depressant and antipsychotic activity, protection against stress ulcer, increase of gastrointestinal motility and weak anti-inflammatory action. Rgi (61) -the major saponin of 20(5)-protopanaxatriol - shows weak CNS-stimulant action, antrfatigue activity and blood pressure activity [108,109] (O Scheme 25). 

American Society of Health-System Pharmacists Therapeutic Guidelines on Stress Ulcer Prophylaxis. Am J Health Syst Pharm 1999 56 347-379. 

MacLaren R, Jarvis CL, Eish DN. Use of enteral nutrition for stress ulcer prophylaxis. Ann Pharmacother 2001 35 1614-1623. 

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