Page 539 - ACCCN's Critical Care Nursing

516 P R I N C I P L E S A N D P R A C T I C E O F C R I T I C A L C A R E

the time-intensive nature of administering antacids every gastric epithelium, stimulates mucus and bicarbonate
1–2 hours. Furthermore, antacids can contribute to secretion, stimulates epithelial renewal, improves mucosal
further complications (e.g. aluminium toxicity, hypo- blood flow and enhances prostaglandin release. 196 Given
phosphataemia, diarrhoea or hypermagnesaemia). These orally or via a nasogastric tube, sucralfate is well tolerated
factors have led to their infrequent use within the critical but appears to be less effective than H 2 RAs in decreasing
care setting. 200,218,219 clinically significant bleeding. 228 Earlier reports compar-
ing sucralfate with ranitidine showed a decrease in the
Histamine-2-Receptor Antagonists development of pneumonia in those patients receiving
sucralfate; however, these findings were not supported in
Histamine-2-receptor antagonists (H 2 RAs) are commonly 228
used in the critically ill to inhibit the production of gastric a subsequent Level I randomised controlled trial.
acid, which is achieved by the drug binding to the
histamine-2 receptor on the basement membrane of the Enteral Nutrition
parietal cell. 196 However, gastric acid secretion may also It is thought that the presence of enteral feeding solution
occur through stimulation of the acetylcholine or gastrin results in an increase in intragastric pH, thereby minimis-
220
receptors present in parietal cells; therefore complete ing acid injury. Several studies have demonstrated a lower
blocking of gastric acid production does not occur when incidence of stress-related bleeding in mechanically-
230
H 2 RAs are used. A further limitation of H 2 RA is the devel- ventilated 229 and burn patients, while others were
opment of tolerance that may occur within 72 hours unable to show a significant effect on increasing gastric
221
231
of administration. Nevertheless, this pharmacological pH. A lack of well-designed prospective studies examin-
strategy to prevent stress-related mucosal disease remains ing the role of enteral nutrition in stress-ulcer prophylax-
commonplace in critical care. 222 sis prevents the use of this therapy as a sole therapeutic
The decrease in gastric acidity as a result of H 2 RA use may agent for this purpose. 201
be beneficial from the perspective of preventing stress-
related mucosal disease, but changes in gastric pH could LIVER DYSFUNCTION
lead to bacterial overgrowth in the stomach, microaspira-
tion, and consequently an increase in the incidence of The liver performs the vital functions of controlling meta-
nosocomial pneumonia, 223 although there is some bolic pathways, participating in digestion, immunologi-
research that does not support this notion. 209 cal protection, detoxifying chemicals and clearing toxins
and drugs. Therefore, liver dysfunction can have broad-
Proton Pump Inhibitors ranging consequences, for example alterations in meta-
bolic processes (such as glucose homeostasis), failure to
Proton pump inhibitors (PPIs) have a greater ability to produce clotting factors (with resultant severe haemor-
maintain an increased intragastric pH than H 2 RAs. 224 rhage) and ‘other organ’ effects such as brain, lung and
These drugs work by irreversibly binding to the proton kidney dysfunction and injury. Accordingly, liver dysfunc-
pump, effectively blocking all three receptors responsible tion can impact substantially on the nursing care needs
for gastric acid secretion by the parietal cell. 196,201 PPIs of the critically ill patient.
are also able to limit vagally-mediated gastric acid
secretion. 200
RELATED ANATOMY AND PHYSIOLOGY
Clinical evaluation of the efficacy of PPIs is somewhat The liver is the largest internal organ, weighing approxi-
limited; few studies have specifically studied the prophy- mately 1200–1600 g in the adult. It receives approxi-
lactic use of PPIs for stress-related mucosal diseases 12,225-227 mately 25% of total cardiac output through a dual
and many are limited by small sample sizes. Although vascular supply consisting of the hepatic artery and portal
PPIs are similar to H 2 RA in the ability to raise the gastric vein. 232 About 75% of the hepatic blood flow arises from
pH above 4, a level considered adequate to prevent stress the portal vein with the remaining 25% from the hepatic
ulceration, PPIs are more likely to maintain the pH at artery. Anatomically, the liver consists of 4 lobes: the
greater than 6, which may be necessary to maintain major left and right lobes, and the minor caudate and
clotting in those patients at risk of rebleeding from peptic quadrate lobes. The right lobe is considerably larger than
ulcer. 201
the left lobe. Functionally, the liver is divided into eight
PPIs that may be administered intravenously include segments each with their own inflow and outflow blood
omeprazole, esomeprazole and pantoprazole. Omepra- supply and biliary drainage. Hepatic lobules, or liver
zole has the highest potential for drug interation and acini, are small units consisting of a single or double layer
interferes with the metabolism of some drugs commonly of hepatocytes arranged in plates interspersed with capil-
used in intensive care, including cyclosporine, diazepam, laries (sinusoids) that receive inflowing blood from the
phenytoin and warfarin. Pantoprazole has the lowest portal vein and hepatic artery. To safeguard the body from
203
potential for drug interactions. 200 the entrance of toxins absorbed from the intestines, the
sinusoids are lined by macrophages known as Kupffer
Sucralfate cells. The hepatic vein then drains effluent blood from
1
Sucralfate provides protection against stress-related the liver into the general circulation.
mucosal disease through a number of mechanisms. The liver has a drainage system for bile (used in the
Sucralfate provides a protective barrier on the surface breakdown and absorption of lipids from the intestine),