Diabetes Insipidus

Case Presentation:

My patient is a 30 year old man presented for the chief complaint of frequent urination after being admitted to the hospital 3 days ago following an auto accident. He has suffered from some fractures and head injury. The patient has been in a coma, but responds to pain stimuli. Also noted was warm and dry skin. In addition, neurological signs suggest traces of twitching. In the past 24 hours the patients urine output has increased, approximately eliminating 12L/day (normal range of 1-2 L/day). In addition, his serum sodium levels have increased to 149mEq/dL. His computerized tomography (CT) scan revealed a contusion over the left parietal area of the cerebrum. Prior to being admitted patient had been in good health.

Differential Diagnoses:

According to the chief complaint of frequent urination several conditions could be the cause. The signs and symptoms that the patient has can be the result of diabetes mellitus, a condition that results from the lack or impaired response to insulin leading to increased blood sugar. Central diabetes insipidus, is a deficiency of the anti-diuretic hormone, and can also be a diagnosis of the complications given. Nephrogenic diabetes insipidus (NDI) is another possible diagnosis due to a defect in the tubules of the kidney. This form of DI has very similar symptoms; however, NDI can is caused by other factors. NDI can be caused by certain drugs (such as lithium), increased calcium levels in the body (hypercalcemia) or even kidney disease (ncbi.nlm.nih.gov). Another diagnosis could be dipsogenic diabetes insipidus, caused by a defect or damage to the thirst mechanism located in the hypothalamus (kidney.niddk.nih.gov). All of these are differential diagnoses for the chief complaint and signs/symptoms noted; therefore, laboratory testing must be done to confirm or exclude possible conditions. In order to make a final diagnosis the following tests were requested, water deprivation and urinalysis.

Laboratory Test:

Urinalysis is the collection of 1-2 ounces of urine. It screens for metabolic and kidney disorders in the urine. This exam consists of the physical, chemical and microscopic exam of the urine. The visual, examines urines appearance. The chemical test uses a dipstick (thin, plastic stick with strips of chemicals) which is placed in the urine to detect abnormalities. This test checks for the following: pH, concentration, protein, sugar, blood, infection, ketones, and bilirubin. The microscopic test is the examination of white blood cells, red blood cells, epithelial cells, casts (proteins), bacteria, and crystals in the urine under a microscope (labtestsonline.org).

Lab results:

Physical: light yellow, clear-indicates dilute urine, lots of water in urine.

Chemical: specific gravity-1.005 (usually 1.010-1.025; possible range 1.005-1,030)(Copestead, 687), is the concentration of solid particles in urine. Patient with diabetes insipidus will have fewer particles. Because patient is receiving intravenous fluid can be why the patient has a low specific gravity number. Specific gravity of 1.005 or less is a sign of dilute urine. Sodium level of 150meq (normal 135-145), increased sodium levels is called hypernatremia (discussed later). Increased pH 7.8 is associated with acid/base imbalance. Urine osmolality, 186 mosm/kg, is a measure of solute concentration (labtestsonline.org). When the osmolality is low, urine will become dilute (<300 mosm/kg) (emedicine.medscape.com).

Microscopic: All components normal

The water deprivation is the primary test that helps determine the cause of diabetes insipidus. This test determines if diabetes insipidus (DI) is caused by excessive intake of fluid, a defect in ADH (anti-diuretic hormone) production or defect in the kidney's response to ADH. A fluid deprivation test is done by restricting the individuals' water intake. The test measures changes in body weight, urine output and composition ((kidney.niddk.nih.gov). When a steady level of urine osmolality is reached vasopressin is injected. In a patient with Central diabetes insipidus the osmolality increases after injection. In those with nephrogenic DI, there is little or no response to vasopressin (Copstead, 939).

Lab results:

Initial urine osmolality was 190 mosm/kg. After 6 hours of fluid deprivation and two evaluations of the urine osmolality, the urine osmolality remained in range of 180-190 mosm/kg. Once this plateau was reached and the urine was not being concentrated, patient was administered an intramuscular dose of ADH. After the injection, the patient's urine osmolality was increased to 450 mosm/kg. Due to this increase level of osmolality patient is diagnosed with diabetes insipidus.

Final