A 20-year-old adolescent female is brought to the emergency room by her mother because the daughter seems confused and is behaving strangely. The mother reports the patient has always been healthy and has no significant medical history, but she has lost 20 lb recently without trying and has been complaining of fatigue for 2 or 3 weeks. The patient had attributed the fatigue to sleep disturbance, as recently she has been getting up several times at night to urinate. This morning, the mother found the patient in her room, complaining of abdominal pain, and she had vomited. She appeared confused and did not know that today was a school day.
On examination, the patient is slender, lying on a stretcher with eyes closed, but she is responsive to questions. She is afebrile, and has a heart rate 118 bpm, blood pressure 125/84 mm Hg, with deep and rapid respirations at the rate of 24 breaths per minute. Upon standing, her heart rate rises to 145 bpm, and her blood pressure falls to 110/80 mm Hg. Her funduscopic examination is normal, her oral mucosa is dry, and her neck veins are flat. Her chest is clear to auscultation, and her heart is tachycardic with a regular rhythm and no murmur. Her abdomen is soft with active bowel sounds and mild diffuse tenderness, but no guarding or rebound. Her neurologic examination reveals no focal deficits.
Laboratory studies include serum Na 131 mEq/L, K 5.3 mEq/L, Cl 95 mEq/L, CO2 9 mEq/L, blood urea nitrogen (BUN) 35 mg/dL, creatinine 1.3 mg/dL, and glucose 475 mg/dL. Arterial blood gas reveals pH 7.12 with PCO2 24 mm Hg and PO2 95 mm Hg.
Urine drug screen and urine pregnancy test are negative, and urinalysis shows no hematuria or pyuria, but 3+ glucose and 3+ ketones.
Chest radiograph is read as normal, and plain film of the abdomen has nonspecific gas pattern but no signs of obstruction.
Most likely diagnosis: Diabetic ketoacidosis (DKA).
DISCUSSION
DKA occurs as a result of severe insulin deficiency and may be the initial presentation of diabetes mellitus, as in this patient. In all patients with DKA, one must be alert for precipitating factors, such as infection, pregnancy, or severe physiologic stressors, such as myocardial infarction. Careful management and close monitoring will be required to correct fluid and electrolyte deficits and to prevent complications such as hypokalemia and cerebral edema.
CLINICAL APPROACH to DIABETIC KETOACIDOSIS
Diabetic ketoacidosis is a clinical syndrome that results when the triad of anion gap metabolic acidosis, hyperglycemia, and ketosis is present and is caused by a significant insulin deficiency. It is a medical emergency, with an overall mortality rate less than 5% if patients receive prompt and appropriate medical treatment. The majority of episodes are preventable, and many of the deaths also are preventable with proper attention to detail during management
CLINICAL PRESENTATION OF DIABETIC KETOACIDOSIS
Patients with diabetes have an underlying impairment in glucose metabolism and, when challenged by a stress, an increase in insulin requirements. If they are unable to meet these insulin requirements, DKA may result. The most common precipitating events are infections such as pneumonia or urinary tract infection, vascular disorders such as myocardial infarction, or other stressors such as trauma. Diabetic ketoacidosis may be the presentation of newonset diabetes, or it can occur in patients with established diabetes because of failure to use insulin for whatever reason or because of use of other medications (eg, glucocorticoids) that interfere with insulin action. An episode of DKA evolves over a short period of time, typically less than 24 hours. The patient with DKA has the signs and symptoms of hyperglycemia, acidosis, and dehydration. Polyuria, polydipsia, weight loss, visual blurring, and decreased mental status are related to hyperglycemia and osmotic diuresis. Nausea, vomiting, abdominal pain, fatigue, malaise, and shortness of breath may be related to the acidosis. Typical signs include reduced skin elasticity, dry mucus membranes, hypotension, and tachycardia related to volume depletion. Kussmaul respirations, deep and rapid breathing, represent hyperventilation in an attempt to generate a respiratory alkalosis to compensate for the metabolic acidosis. One may also note the fruity breath odor typical of ketosis.
Management of DIABETIC KETOACIDOSIS
The goal of treatment is restoration of metabolic homeostasis with correction of precipitating events and biochemical deficits, which consists of the following:
1. Replacement of fluid losses with improvement of circulatory volume
2. Correction of hyperglycemia and, in turn, plasma osmolality
3. Replacement of electrolyte losses
4. Clearance of serum ketones
5. Identification and treatment of precipitating cause and complications
Close monitoring of the patient is important.
A flow sheet recording vital signs, input and output, insulin dosage, and metabolic progress is important. Serum glucose concentration should be measured every 1 hour, and levels of serum electrolytes and phosphate must be assessed every 3 to 5 hours. Urinalysis, urine and blood cultures, ECG, and chest X-ray should be obtained to identify precipitating factors and complications.
