Proton pump inhibitors intravenous

Intravenous proton pump inhibitors increasingly are being used in critically ill patients to reduce the incidence of stress-related mucosal bleeding despite a lack of any controlled trials demonstrating their efficacy. In the absence of trials that establish efficacy and optimal dosing for proton pump inhibitors, intravenous H2 antagonists remain the preferred drugs for this indication. 

Intravenous H2-receptor antagonist (preferred) or intravenous proton pump inhibitor (PPI)... 

Less common causes of peptic ulceration include Zollinger-Ellison syndrome (ZES), cancer chemotherapy, radiation, and vascular insufficiency. ZES is caused by a gastrin-producing tumor called a gastrinoma and results in gastric acid hypersecretion. High-dose oral proton pump inhibitor (PPI) therapy is the initial treatment of choice for ZES intermittent intravenous PPI therapy may be required for any patient in whom oral therapy is contraindicated.1... 

Disruption of host defenses owing to intravenous catheters, indwelling Foley catheters, burns, trauma, surgery, and increased gastric pH (secondary to antacids, H2 blockers, and proton pump inhibitors) may place patients at higher risk for infection. Breaks in and entry into the skin provide a route for infection because the natural barrier of the skin is disrupted. Increased gastric pH can allow for bacterial overgrowth and has been associated with an increased risk of pneumonia.18... 

H2 antagonists are extremely safe drugs. Adverse effects occur in less than 3% of patients and include diarrhea, headache, fatigue, myalgias, and constipation. Some studies suggest that intravenous H2 antagonists (or proton pump inhibitors) may increase the risk of nosocomial pneumonia in critically ill patients. 

Five proton pump inhibitors are available for clinical use omeprazole, lansoprazole, rabeprazole, pantoprazole, and esomeprazole. All are substituted benzimidazoles that resemble H 2 antagonists in structure (Figure 62-3) but have a completely different mechanism of action. Omeprazole is a racemic mixture of R- and S-isomers. Esomeprazole is the S-isomer of omeprazole. All are available in oral formulations. Esomeprazole and pantoprazole are also available in intravenous formulations (Table 62-2). 

For patients without a nasoenteric tube or with significant ileus, intravenous H2 antagonists are preferred to intravenous proton pump inhibitors because of their proven efficacy and lower cost. Although proton pump inhibitors are increasingly used, there are no controlled trials demonstrating efficacy or optimal dosing. 

Reversible peripheral edema has been reported in five women taking the proton pump inhibitors omeprazole, lansoprazole, or pantoprazole for 7-15 days for peptic disorders in recommended standard doses (29). Edema disappeared within 2-3 days of withdrawal and reappeared in all five patients after re-exposure. High-dose intravenous infusions of omeprazole and pantoprazole (8 mg/hour) caused peripheral edema in three of six young female volunteers and two of six female volunteers respectively. The edema disappeared within 24 hours of stopping the infusion. Similar high doses of omeprazole did not produce edema in male volunteers. Subsequent studies performed on 10 female volunteers to elucidate the cause of the edema did not show any changes in concentrations of serum hormones or Cl esterase inhibitor. 

Stress ulcers are ulcers of the stomach or duodenum that occur in the context of a profound illness or trauma requiring intensive care. The etiology of stress-related ulcers differs somewhat from that of other peptic ulcers, involving acid and mucosal ischemia. Because of limitations on the oral administration of drugs in many patients with stress-related ulcers, intravenous H2 receptor antagonists have been used extensively to reduce the incidence of GI hemorrhage due to stress ulcers. Now that intravenous preparations of proton pump inhibitors are available, it is likely that they will prove to be equally beneficial. 

Prepare to administer intravenous Protonix, a proton-pump inhibitor. 

Pantoprazole is a substituted benzimidazole sulfoxide proton pump inhibitor (Fig. 11). Like other proton pump inhibitors such as lansoprazole, all chiral benzimidazoles are administered as racemic mixtures. Pantoprazole is metabolized to pantoprazole sulphone as a major metabolite, and pantoprazole sulfide as a minor metabolite (Fig. 11). The reoxidation of pantoprazole sulfide to pantoprazole occurs in vivo, resulting in chiral inversion of pantoprazole enantiomers. Significant chiral inversion occurred after intravenous and oral administration of (-F)-pantoprazole [139]. The mechanism of this inversion has not yet been identified. 

Enns RA, Gagnon YM, Rioux KP, et al. (2003) Cost-effectiveness in Canada of intravenous proton pump inhibitors for all patients presenting with acute upper gastrointestinal bleeding. Aliment Pharmacol Ther 17 225-233... 

Metz DC, Forsmark C, Lew EA, et al. Replacement of oral proton pump inhibitors with intravenous pantoprazole to effectively control gastric acid hypersecretion in patients with Zollinger-Ellison syndrome. Am J Gastroenterol 2000 96(12) 3274-3280. 

On admission to the hospital he was started on intravenous fluids. Liver enzymes were thought to be elevated due to massive creatinine kinase elevation, which improved with fluids. Renal function did not improve and the patient continued to be oliguric with dark brown coloured urine. Acute tubular necrosis was confirmed and haemodialysis was initiated. The patient was started on proton pump inhibitors for heartburn. His recovery was slow, but he became more alert and oriented and he was able to stand up with significant ataxia. 

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