Upper gastrointestinal (GI) dysmotility, an entity commonly found in the intensive care unit setting, can lead to insufficient nutrient intake while increasing the risk of infection and mortality. Further, overcoming the altered motility with early enteral feeding is associated with a reduced incidence of infectious complications in intensive care unit patients. Upper GI dysmotility in critical care patients is a common occurrence, and there are many causes for this problem, which affects a very heterogenous population with a multitude of underlying medical abnormalities. Therefore, it is of utmost importance to identify this widespread problem and subsequently institute a proper therapy as rapidly as possible. Prokinetic pharmacotherapies are currently the mainstay for the management of disordered upper GI motility. Future therapies, aimed at the underlying pathophysiology of this complex problem, are under investigation. These aim is to reduce the side effects of the currently available options, while improving on nutrition delivery in the critically ill. This review discusses the pathophysiology, clinical manifestations, diagnosis, and treatment of upper GI motility disturbances in the critically ill.
BACKGROUND
Human papillomaviruses (HPVs) commonly cause proliferative lesions of squamous epithelia, and infection with certain HPV types carries a high risk of malignant transformation, especially in the uterine cervix but also at other sites, including the esophagus. We used molecular techniques to detect and type HPV in an in situ squamous cell carcinoma in the esophagus of a 39‐year‐old woman.
METHODS
DNA was extracted from paraffin sections of the esophageal lesion and of the uterine cervix (which was removed several years earlier), and analyzed for HPV by polymerase chain reaction (PCR). Primers complementary to highly conserved regions of the open reading frame of most genital HPVs were used to amplify a ∼450 base pair product that contained both conserved and divergent regions. The PCR products were hybridized with probes specific for HPV‐6, HPV‐11, HPV‐16, and HPV‐18, and with a consensus probe. A conspicuous band in the esophageal sample failed to hybridize with any of the probes. The amplimer was subcloned and sequenced. The sequence was compared with other known HPVs.
RESULTS
The intraepithelial neoplasia in the patient's cervical cone biopsy contained HPV‐16. The esophageal lesion contained HPV that did not hybridize with probes for types 6, 11, 16, or 18, but exhibited 98.3% homology with HPV‐73.
CONCLUSIONS
Squamous cell carcinoma in situ of the esophagus may be associated with infection by HPV‐73. Cancer 1996;77:2440‐4.
We report a case of combined small and large intestinal infarction caused by rheumatoid vasculitis in a 60-yr-old man who had a long history of rheumatoid arthritis and presented with abdominal pain and constipation. Eventually, he developed signs of peritonitis and underwent exploratory laparotomy and was found to have sigmoid and ileal infarction secondary to rheumatoid vasculitis.
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