TEACHING POINTS
■ Hyperglycemia is the product of diabetes, not the cause. Although frequently appearing in association with complications of diabetes mellitus, elevations in the blood glucose level need not be present.
■ Lack of insulin leads to an excess of glucagon and other counterregulatory hormones, causing an increase in the glucagon:insulin ratio, which initiates the process of DKA. An imbalance of hormones both causes and drives DKA and hyperglycemia independently.
■ Of even more importance, a low-carbohydrate diet represents a pathway by which those without diabetes can develop ketoacidosis. In short, diets low in carbohydrates and high in fats have been shown to lower insulin levels and increase glucagon. As noted before, these are the same conditions needed to induce ketoacidosis.
■ Regardless of a patient's glucose levels, insulin is the only means by which ketoacidosis can be reversed. However, in a patient with normal or mildly elevated glucose levels, the treatment needs to be coupled with glucose administration to prevent the development
of hypoglycemia.
CASE
A 23-year-old Hispanic male with a history of type I diabetes mellitus (DM) presented to the emergency department complaining of 1 week of epigastric/left upper quadrant pain associated with nausea, vomiting, lack of appetite with decreased oral intake, and chills. The patient, who was knowledgeable about his diabetes, stated that his symptoms did not seem consistent with previous episodes of diabetic ketoacidosis (DKA) he had experienced and that he had been taking his insulin as prescribed. A review of systems was negative for recent weight loss or gain, fevers, polyuria, or polydipsia. Other pertinent medical history consisted of diabetic neuropathy, recurrent DKA, and gastroparesis. His insulin regimen consisted of insulin aspart (Novolog) 20 units and human insulin (Humulin N) 30 units every morning and evening. The patient smoked one pack of cigarettes a day. He admitted to "occasional" alcohol use but denied any recent use.
Vital signs were as follows: temperature, 98.7°F; BP, 121/91 mm Hg; pulse, 108 beats per minute; respiration rate, 16 breaths per minute; and pulse oximetry, 100% on room air. A capillary glucose level on arrival in the ED was 118 mg/dL. The patient was thin, ill-appearing, and in moderate distress from pain. His skin was warm and dry; mucous membranes were slightly moist. On auscultation, the lungs were clear and equal bilaterally. Cardiac assessment revealed mild tachycardia with no S3, S4, gallop, or murmurs. Findings on the abdominal examination were significant for tenderness over the epigastric region, as reported by the patient. Bowel sounds were present; no rebound, guarding, or masses were detected.
Given the patient's near-normal blood glucose level and his report that the symptoms were not consistent with past episodes of DKA, initial treatment consisted of IV administration of normal saline, famotidine 20 mg, metoclopramide 10 mg, and ketorolac 30 mg. However, because of his medical history, metabolic problems were still a concern and studies were ordered accordingly (Table 1).
While waiting for his laboratory results, the patient experienced relief from his nausea, vomiting, and chills, although he continued to appear ill. When his results became available, they confirmed normoglycemia, but they also demonstrated a metabolic acidosis with an anion gap. The patient was started on an insulin infusion at 5 units/hour, along with a more aggressive infusion of normal saline. To maintain serum glucose levels, 100 g dextrose 50 solution was added to the IV therapy. While in the ED, the patient's acidosis improved minimally, but his bicarbonate level continued to fall despite intervention. The patient was admitted to the ICU, and treatment with IV insulin and high-volume IV fluids was continued until his ketoacidosis resolved 3 days later. During his stay, the patient maintained that he had been compliant with his medications, although he did admit to his blood glucose levels being "all over the place." He was discharged home on his normal insulin regimen with instructions to follow up with his primary care physician.