Comparison of Arterial and Venous Blood Gas Values in the Initial Emergency Department Evaluation of Patients With Diabetic Ketoacidosis,☆☆,

Presented in part at the Society for Academic Emergency Medicine Annual Meeting, Denver, CO, May 1996.
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Abstract

Study objective: To determine whether venous blood gas values can replace arterial gas values in the initial emergency department evaluation of patients with suspected diabetic ketoacidosis. Methods: This prospective comparison was performed in an adult university teaching hospital ED. Samples for arterial and venous blood gas analysis were obtained during initial ED evaluations. The venous gas samples were collected with samples for other blood tests at the time of intravenous line insertion. Both arterial and venous samples were obtained before the initiation of treatment. Result: Data from 44 episodes of diabetic ketoacidosis in 38 patients were analyzed. Laboratory findings of those patients with diabetic ketoacidosis were as follows (mean±SD): arterial pH, 7.20±.14; venous pH, 7.17±.13; serum glucose, 33.8±16 mmol/L (609±288 mg/dL); arterial HCO 3, 11.0±6.0 mmol; venous HCO 3, 12.8±5.5 mmol/L; serum CO 2, 11.8±5.0 mmol/L; and anion gap, 26.7±7.6 mmol/L. The mean difference between arterial and venous pH values was 0.03 (range 0.0 to 0.11). Arterial and venous pH results (r=.9689) and arterial and venous HCO 3 results (r=.9543) were highly correlated and showed a high measure of agreement. Conclusion: Venous blood gas measurements accurately demonstrate the degree of acidosis of adult ED patients presenting with diabetic ketoacidosis. [Brandenburg MA, Dire DH: Comparison of arterial and venous blood gas values in the initial emergency department evaluation of patients with diabetic ketoacidosis. Ann Emerg Med April 1998; 31:459-465.]

Section snippets

INTRODUCTION

Diabetic ketoacidosis (DKA) is a metabolic derangement consisting of high blood glucose concentration, measurable ketone bodies, and metabolic acidosis, and is an endocrinologic emergency responsible for approximately 110,000 hospital admissions in the United States annually.1 DKA is the most common serious and life-threatening acute complication of diabetes. The mortality rate is currently estimated at 2% to 10% for patients hospitalized with DKA.1, 2, 3

Determination of arterial blood gas

METHODS

Patients presenting to the ED at University Hospital in Oklahoma City, the adult teaching hospital for the University of Oklahoma, College of Medicine, were eligible for this study if they had a fingerstick bedside blood glucose measurement in excess of 13.9 mmol/L (>250 mg/dL), urine dipstick result positive for ketones, and the emergency physician clinically suspected DKA before the results of further laboratory tests were known. This protocol was reviewed by the Office of Research

RESULTS

A convenience sample of 61 patients with 68 suspected episodes of DKA was enrolled into this study during a 14-month period (no patient was enrolled more than twice). Data on 23 patients with 24 episodes were omitted from anal-ysis for the following reasons: patient did not have acidosis, 14; serum ketone results were negative, 5; no venous blood gas analysis was done, 2; no arterial blood gas analysis was done, 1; no serum ketone analyses were done, 1; and patient was not hyperglycemic, 1.

DISCUSSION

At present, there is no consensus definition in the medical literature regarding the diagnostic criteria for DKA.2 Our study criteria are most similar to the diagnostic guidelines used by Fleckman.17, 18

In DKA, mortality is related to the age and state of consciousness of the patient, and the degree of acidosis, hyperglycemia, and azotemia.19 Determination of acid-base status, therefore, has prognostic as well as diagnostic value. To clearly characterize the acidosis, a measurement of the

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    From the Section of Emergency Medicine & Trauma, University of Oklahoma Health Sciences Center, Oklahoma City, OK.

    ☆☆

    Address for reprints: Daniel J Dire, MD, Section of Emergency Medicine & Trauma, PO Box 26307, Room EB319, Oklahoma City, OK 73126-0307, 405-271-5135

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