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Journal of Critical Care 2002-Mar

Abdominal pain in patients with hyperglycemic crises.

Vain rekisteröityneet käyttäjät voivat kääntää artikkeleita
Kirjaudu sisään Rekisteröidy
Linkki tallennetaan leikepöydälle
Guillermo Umpierrez
Amado X Freire

Avainsanat

Abstrakti

BACKGROUND

The aim of the study was to evaluate the incidence and prognosis of abdominal pain in patients with diabetic ketoacidosis (DKA) and hyperglycemic hyperosmolar nonketotic state (HHS). Abdominal pain, sometimes mimicking an acute abdomen, is a frequent manifestation in patients with DKA. The prevalence and clinical significance of gastrointestinal symptoms including abdominal pain in HHS have not been prospectively evaluated.

METHODS

This is a prospectively collected evaluation of 200 consecutive patients with hyperglycemic crises admitted to a large inner-city teaching hospital in Atlanta, GA.We analyzed the admission clinical characteristics, laboratory studies, and hospital course of 189 consecutive episodes of DKA and 11 cases of HHS during a 13-month period starting in October 1995.

RESULTS

Abdominal pain occurred in 86 of 189 patients with DKA (46%). In 30 patients, the cause of abdominal pain was considered to be secondary to the precipitating cause of metabolic decompensation. Five of them required surgical intervention including 1 patient with Fournier's necrotizing fasciitis, 1 with cholecystitis, 1 with acute appendicitis, and 2 patients with perineal abscess. The presence of abdominal pain was not related to the severity of hyperglycemia or dehydration; however, a strong association was observed between abdominal pain and metabolic acidosis. In DKA patients with abdominal pain, the mean serum bicarbonate (9 +/- 1 mmol/L) and blood pH (7.12 +/- 0.02) were lower than in patients without pain (15 +/- 1 mmol/L and 7.24 +/- 0.09, respectively, both P <.001). Abdominal pain was present in 86% of patients with serum bicarbonate less than 5 mmol/L, in 66% of patients with levels of 5 to less than 10 mmol/L, in 36% of patients with levels 10 to less than 15 mmol/L, and in 13% of patients with bicarbonate levels 15 to 18 mmol/L. Patients with DKA and abdominal pain had a more frequent history of alcohol (51%) and cocaine abuse (13%) than those without abdominal pain (24% and 2%, respectively, both P <.001). One patient with HHS reported nausea and vomiting on admission, but abdominal pain was not reported in any patient with HHS.

CONCLUSIONS

Gastrointestinal manifestations including abdominal pain are common in patients with DKA and are associated with severe metabolic acidosis and with a history of alcohol or cocaine abuse, but not with the severity of hyperglycemia or dehydration. Our study indicates that investigation of the etiology of abdominal pain in DKA should be reserved for patients without severe metabolic acidosis or if the pain persists after the resolution of ketoacidosis.

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