Management of GI Disorders
The management of patients with a chronic multisystem infection is more complex. Once a diagnosis of intestinal Whipples disease is reached, it is important to evaluate other commonly involved organ systems. After staging is completed, the choice and adequate duration of antibiotic treatment is critical for the patient’s long term outcome.
The management of the complicated abdominal wall defect can be quite complex. As more and more patients with an increasing number of co-morbidities undergo sophisticated abdominal operations, an increasing number of physicians will have the opportunity to participate in the management of these patients. Moreover, it is clear that a multidisciplinary approach affords the best possible outcome, particularly in those patients whose defect includes gastrointestinal complications such as enterocutaneous fistulas.
Sucralfate is a basic nonabsorbable aluminum salt of sucrose octasulfate. Despite weak antacid properties, the protective effect of sucralfate is not mediated by acid suppression or neutralization, but by a mucosal protective effect on the gastric mucosa. The mucosal protection afforded by sucralfate is mediated by several mechanisms, including formation of a protective barrier, stimulation of gastric mucosal blood flow, prostaglandin-mediated increase in mucus and bicarbonate secretion, and by the stimulation of a variety of growth factors that have been implicated in ulcer healing.
Dyspepsia is one of the most common problems encountered in gastroenterology practice, and it accounts for 2 to 5% of primary care visits. Prevalence estimates for dyspepsia range from 12 to 45%, with an average estimate of about 25%.
With the identification of the causative bacterium, Tropheryma whippelii, Whipples disease has grown out from its niche in textbooks and has colonized high ranked journals. Nevertheless, it is an uncommon multisystem disorder and not just an intestinal bacterial infection like many others.
Although most dyspepsia in clinical practice is functional, the diagnosis of functional dyspepsia is a diagnosis of exclusion. A search for organic etiologies should be undertaken, because therapy for many organic causes is more satisfying than therapies for functional disorders. Age, symptoms and practical concerns of the patient and physician should guide investigation of the patient’s symptoms.
As stated above, the risk of overt gastrointestinal hemorrhage and subsequent death due to stress-related erosive syndrome are closely related to the underlying disease. Therapy must therefore be directed at treating the cause of physiologic stress.
The clinical features of stress-related erosive syndrome have been well characterized since the initial endoscopic description by Lucas and colleagues in 1971. Stress-related lesions in the stomach and duodenum can be detected endoscopically within several hours of a critical illness, trauma, or surgery as multiple punctate subepithelial hemorrhages, erosions, or superficial ulcerations. Mucosal injury maybe identified in 70 to 100% of critically ill patients admitted to an intensive care unit, and the risk of developing these lesions appears to be directly correlated with the severity of the underlying illness.
Gastroesophageal variceal bleeding is an unpredictable complication of cirrhosis with an associated mortality of 15 to 30% with each bleeding episode, and about one-third of all deaths in patients with cirrhosis could be directly attributed to acute variceal bleeding. Prevention of first bleeding (primary prophylaxis) is therefore as important as treatment of acute bleeding and secondary prophylaxis. Patients with large varices or red signs, and those with an elevated hepatic venous wedge pressure gradient (> 12 mm Hg), should be treated with nonselective ?-blockers to prevent the first bleed.
Acid suppressive therapy may be of benefit in patients with functional dyspepsia and the benefit appears greatest in patients with ulcer-like symptoms. A 2 to 4 week trial of antisecretory therapy at standard doses is reasonable. Therapy should be discontinued if there is no response.
Vomiting follows stimulation of the vomiting centre in the medulla of the brain. This may be via the chemoreceptor trigger zone, which is sensitive to many drugs and to certain metabolic disturbances, or from actions on other areas such as the vestibular apparatus of the ear (in motion sickness), the cerebral cortex (in psychogenic vomiting), and multiple peripheral receptors.