Case 8

A 25-Year-Old Female With Polyuria and Polydipsia

Gina Rossetti, Eric Hsieh

A 25-year-old Caucasian female with a history of type 1 diabetes presents to the emergency department with 3 days of polyuria, polydipsia, and dysuria. The morning of presentation she also developed a fever, nausea, and abdominal pain. She has no shortness of breath, cough, chest pain, or diarrhea. Because of her nausea, she has not been eating and has stopped taking her insulin to avoid hypoglycemia. She comes to your medical intensive care unit (ICU) for further management.

How does the history help narrow your differential diagnosis?

This is a 25-year-old female with a history of diabetes now presenting with urinary symptoms suggestive of a urinary tract infection (UTI). Diabetic ketoacidosis must be considered in diabetic patients who have infections, abdominal catastrophes, medication noncompliance, and myocardial infarctions.

On physical exam, the patient’s temperature is 39.1 °C (102.3 °F). Her pulse rate is 136/min, her blood pressure is 106/58 mm Hg, and her respiration rate is 26/min. She is alert and oriented but is breathing rapidly and has a fruity odor on her breath. Her pupils are equal, round and reactive to light, and extraocular eye movements are intact. Her tympanic membranes are clear and she has no tenderness on palpation of her sinuses. Her neck is supple with no lymphadenopathy or jugular venous pulsation. Her breath sounds are clear to auscultation. Her cardiovascular exam is significant for tachycardia; however, she has a regular rate and rhythm with no murmurs, rubs, or gallops. Her abdominal exam is significant for tenderness to palpation in all four quadrants as well as right costovertebral angle tenderness. Her extremities are warm with no cyanosis, clubbing, or edema. Her neurologic exam is intact. Her serum glucose is 440 mg/dL. The basic metabolic panel (BMP) is significant for a sodium of 126 mEq/L, a potassium of 4.8 mEq/L, a chloride of 86 mEq/L, a bicarbonate of 12 mEq/L, a blood urea nitrogen of 32 mg/dL, and a creatinine of 1.4 mg/dL. The phosphorus is 6.0 mg/dL. The complete blood count (CBC) is significant for a leukocytosis of 18,000 µ/L. The arterial blood gas shows a pH of 7.2, a partial pressure of carbon dioxide (pCO₂) of 32 mm Hg and a bicarbonate (HCO₃) of 14 mEq/L.

What is your differential diagnosis?

Considering the patient’s elevated glucose, anion gap of 28, acidosis, and precipitating UTI, she likely has diabetic ketoacidosis (DKA).

Urinalysis reveals 4+ glucose, 30 white blood cells (WBCs), large bacteria, and positive nitrites.

Diagnosis: Diabetic ketoacidosis precipitated by a urinary tract infection

What is the definition of diabetic ketoacidosis?

Although there is no consensus on the definition of DKA, the diagnosis requires the presence of an anion gap, metabolic acidosis, and ketonemia. Although they are usually hyperglycemic, 1 to 7% of patients may have a glucose level less than 200 mg/dL. In other words, you have to have the D (diabetes), the K (ketonemia), and the A (acidosis) to call it DKA.

What are the most common precipitating factors of DKA?

The most common precipitating factor is infection. A UTI and pneumonia are the two most common sources, although it is important to consider a less obvious source such as bacteremia, cellulitis, occult sinusitis, tooth abscess, or perirectal abscess. Other common precipitating factors include a new diagnosis of diabetes and lack of insulin compliance. Patients can also present with an abdominal catastrophe such as cholecystitis, pancreatitis, appendicitis, diverticulitis, perforated viscus, or acute ischemic bowel. Less common causes include myocardial infarction, pregnancy, drugs (glucocorticoid, β-agonists, cocaine, pentamidine), and stroke. Many times, however, no precipitating factor is identified.

Step 2/3

Clinical Pearl

Rhinocerebral mucormycosis is associated with DKA. It is important to consider this diagnosis in the presence of facial pain, facial numbness, orbital swelling, proptosis, visual changes, or bloody nasal discharge.

Step 1

Basic Science Pearl

Physical stress and infection in the setting of decreased insulin leads to the release of hormones such as cortisol, catecholamines, and glucagon. These hormones act upon the liver to increase gluconeogenesis, glycogenolysis, and conversion of free fatty acids to ketone bodies. In addition, decreased insulin and increased glucagon act to stimulate the muscle cells to release amino acids and the fat cells to release glycerol and free fatty acids. These act as additional substrates for the liver to produce ketones and glucose, which are then released into the blood stream.