Critically ill patients have an increased metabolic demand requiring nutritional support. Early enteral feeding following a major insult has been advantageous. The gut seems to be involved in the evolution of multiple organ failure, and early feeding may help to prevent this by preventing gut mucosal atrophy, increasing hepatosplanchnic blood flow, maintaining immunocompetence, reducing bacterial translocation, preserving gut flora, and preventing stress ulceration. Special formulas may enhance immunocompetence and protect the mucosa if given early.
If enteral feeding is not tolerated, other measures to protect the gastric mucosa will be required. H 2 antagonists will reduce acid secretion but may allow overgrowth of bacteria in the stomach, increasing the risk of nosocomial pneumonia. Sucralfate, which is a mucosal barrier agent, will not cause bacterial overgrowth. The role of gastric tonometry in assessing gastric and splanchnic perfusion is still being evaluated.
Nosocomial respiratory infection is common in ventilated patients. Therapeutic strategies which reduce the incidence of infection include selective decontamination of the gut (Selective De.coD.ta.min.a.tioD.lll of the Digestivell llT.ra.Ct.lllT.ria!.i.St.S„' C.ollaboEalivellGioy&lQQS ). Allowing rest periods during enteral feeding may allow acidity to return to the stomach and kill bacteria, thereby reducing the likelihood of nosocomial infection ( Lee et al 1990).
The prevention of acute renal failure when shock occurs revolves around the restoration of adequate oxygen delivery to the kidneys and avoidance of further nephrotoxic insults. Fluid resuscitation alone may not be sufficient to maximize renal blood flow. Historically, dopamine has been used in low-dose infusion (2-4 Mg/kg/min) to increase urine output, possibly by increasing cardiac output rather than by a specific dopaminergic vasodilator effect. Maximum fluid loading with concomitant diuretic infusion to prevent the onset of renal failure is also used. This is achieved with colloids, nitrates, norepinephrine and furosemide (frusemide). The diuretics mannitol and furosemide have both been used to increase urine output; however, adequate intravascular volume should be assured.
There is no evidence at present that any specific regimen will prevent acute renal failure. However, avoidance of nephrotoxic insults, such as unmonitored use of aminoglycosides, non-steroidal anti-inflammatory drugs, angiotensin-converting enzyme inhibitors, and contrast agents, is paramount in the patient with perilous renal function.
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