Gastrointestinal manifestations of diabetic ketoacidosis

The evaluation of gastrointestinal symptoms in patients with diabetic acidosis frequently challenges the physician's clinical acumen. Faced with a seriously ill patient, he must judge whether the abdominal pain, nausea, or vomiting are a consequence of the metabolic decompensation, and hence likely to resolve with correction of the ketoacidosis, or if these symptoms signal a serious underlying intra-abdominal process (e.g., cholecystitis, appendicitis, etc.) which may have precipitated the development of ketoacidosis. The pathogenesis of the reversible gastrointestinal symptoms which frequently accompany diabetic acidosis has not been rigorously defined and may be multifactorial, involving metabolic, humoral, and neural processes. Careful attention to the medical history and abdominal examination greatly facilitates distinguishing patients with intra-abdominal pathology from those with reversible symptoms secondary to ketoacidosis. Similarly, the judicious use of laboratory tests (electrocardiography, blood counts, urinalysis, serum enzyme profile, and abdominal roentgenograms) materially aids in differential diagnosis. Finally, clinical suspicion of an acute abdominal process should prompt early surgical consultation and, if required, surgical intervention as the acidosis is being brought under control.     

Selected developments in the understanding of diabetic ketoacidosis.

Advances in the understanding of diabetic ketoacidosis have contributed to the recent decrease in the morbidity and mortality associated with this condition. The role of counterregulatory hormones in its pathogenesis is considerable, but insulin deficiency is necessary for diabetic ketoacidosis to develop. Therapy begins with identification and treatment of the factors precipitating ketosis. Isotonic saline is the fluid of choice for initial intravenous therapy; subsequently 0.45% saline is appropriate. Sodium bicarbonate is necessary only if the arterial pH is less than 7.1, and phosphate should be given only when the serum phosphate level is below 0.5 mg/dl (0.16 mmol/l). Factors other than pH are important in causing the hyperkalemia so commonly seen at the time of presentation, but whether or not hyperkalemia is present potassium supplementation is almost always necessary and should be given as long as the urinary output is adequate. Intravenous doses of insulin as low as 5 to 15 U/h are sufficient in most cases, but the occasional patient will require larger amounts. Close clinical and biochemical monitoring is necessary for successful management.     

Treatment of diabetic ketoacidosis with a computer-controlled bedside monitoring and infusion system.

A metabolic monitoring system is described that allows the simultaneous and automatic in vivo analysis of the metabolic parameters glucose, pH, and pCO2 as well as the computer-controlled automation of the possible necessary infusion therapy. This bedside system has proved to be useful in treating acidotically and non-acidotically decompensated diabetes mellitus. Our experience with this system is as follows: 1. quick correction of the acidosis without danger of alkalosis, 2. shorter period of treatment, 3. considerably reduced insulin requirement, 4. no danger of hypoglycemia, and 5. minimum net blood withdrawal (1.2 ml/h). The efficiency of this system is demonstrated by examples.     

Renal tubular acidosis during therapy for diabetic ketoacidosis.

A young woman presented with typical diabetic ketoacidosis. Five hours after insulin had been given hyperchloremic metabolic acidosis developed. This could not be attributed to gastrointestinal loss of bacarbonate, ingestion of HCI or carbonic anhydrase inhibitor, or the administered fluids and electrolytes. The combination of hyperchloremic metabolic acidosis and a urine pH of 5.6 during acidemia prompted specific studies that established the presence of disorders of renal acidification. A transient defect of hydrogen ion secretion in the distal nephron was suggested by the decrease in urine-blood Pco-2 gradient after administration of sodium bicarbonate. Proximal renal tubular acidosis was indicated by the reduced bicarbonate threshold that persisted for approximately 7 weeks.     

Recurrent diabetic ketoacidosis: causes, prevention and management

Longitudinal studies indicate that 20% of paediatric patients account for 80% of all admissions for diabetic ketoacidosis (DKA). The frequency of DKA peaks during adolescence and, although individuals generally go into remission, they may continue to have bouts of recurrent DKA in adulthood. The evidence for insulin omission being the behavioural precursor to recurrent DKA is reviewed and discussed. Thereafter the range of possible psychosocial causes is explored and the evidence for each discussed. Approaches to assessing the individual and their family to identify aetiology and therefore appropriate intervention are considered and treatment options reviewed. Finally, the paper examines potential risk factors for recurrent DKA, possible strategies for identifying these early and how to use these assessments to prevent subsequent recurrent DKA.