Diabetes insipidus: Clinical sciences

Diabetes insipidus, or DI for short, is a type of polyuria-polydipsia syndrome, meaning increased fluid intake and urination, specifically resulting in more than 3 liters per day of dilute urine. The most common cause of polyuria-polydipsia syndrome is diabetes mellitus; but three other causes include diabetes insipidus, which can be central or nephrogenic; and primary polydipsia. In central DI, the pituitary doesn’t make enough vasopressin, also called antidiuretic hormone or ADH for short, which normally increases water reabsorption in the kidneys; while with nephrogenic DI, the kidneys don’t respond to vasopressin.

Finally, in primary polydipsia, there’s increased fluid intake, which naturally suppresses vasopressin secretion.

Now, if your patient presents with a chief concern suggesting diabetes insipidus, first, perform an ABCDE assessment to determine if they’re unstable or stable.

If unstable, stabilize their airway, breathing, and circulation. Next, obtain IV access and put your patient on continuous vital sign monitoring, including blood pressure, heart rate, and pulse oximetry. Finally, if needed, provide supplemental oxygen.

Now, here’s a clinical pearl! In most cases, patients with diabetes insipidus can compensate for the fluid loss through increased fluid intake. However, individuals who aren’t able to drink fluids, like those with impaired regulatory thirst mechanisms or impaired consciousness, can develop severe dehydration and hyperosmolality! Severe dehydration can cause hypotension, renal hypoperfusion, subsequent tubular necrosis, and even shock.

On the flip side, hyperosmolality leads to an osmotic shift of intracellular fluid toward the extracellular space, causing neurons in the brain to become dehydrated. Eventually, this causes various neurologic manifestations, including irritability, seizures, and even coma. Now, let’s go back to the ABCDE assessment and take a look at stable patients.

In this case, obtain a focused history and physical examination. Most patients will compensate for the fluid loss through increased fluid intake, so the typical presentation will include a patient who reports symptoms associated with polyuria, such as urinary frequency, nocturia, and enuresis. Additionally, they’ll report excessive thirst and increased fluid intake!

In some individuals, history might reveal recent neurosurgery, head trauma, lithium use, or a family history of diabetes insipidus.

On the other hand, there are no signs of dehydration on the physical exam since patients compensate by increased fluid intake! In other words, most of your patients will have normal skin turgor and moist mucous membranes! With these findings, you should suspect polyuria-polydipsia syndrome.

Your next step is to obtain a fingerstick glucose level to rule out diabetes mellitus. If that’s ruled out, obtain the patient’s 24-hour urine output on unrestricted fluid intake, and order labs, including urine and plasma osmolality, as well as serum sodium.

First, assess the 24-hour urine output. If it’s less than 50 milliliters per kilogram of body weight, you can rule out polyuria and consider alternative diagnoses.

On the other hand, if urine output is greater than 50 milliliters per kilogram, you are dealing with polyuria.

Next, you should assess urine osmolality (Uosm), meaning how concentrated the urine is. If urine osmolality is higher than 800 milliosmoles per kilogram, that suggests concentrated urine, so consider alternative diagnoses.

However, if urine osmolality is less than 800 milliosmoles per kilogram, that suggests dilute urine, so polyuria-polydipsia syndrome!

Next, assess serum sodium levels and plasma osmolality.

If serum sodium is 135 millimoles per liter or less, and plasma osmolality is 280 milliosmoles per kilogram or less, you can diagnose primary polydipsia!
Management involves restricting fluid intake and addressing the underlying cause. For example, if it’s associated with psychiatric conditions, you should consult your psychiatry team and consider appropriate therapies.

But, in most individuals, serum sodium and plasma osmolality are normal, so be sure to order the water deprivation test to determine the exact cause of polyuria-polydipsia syndrome!

To perform this test, first, restrict the patient’s fluid intake over a prolonged period of time, typically up to 17 hours, and check the urine osmolality every 1 to 2 hours. Normally, fluid restriction stimulates vasopressin secretion, increasing water reabsorption in the kidneys, which concentrate the urine and increase osmolality!

So, if upon water deprivation, urine osmolality increases over 800 milliosmoles per kilogram, the patient’s ability to concentrate urine is normal, so you can diagnose primary polydipsia.

Even though this case is mild, management also relies on restricting free water intake and addressing the underlying cause of excessive fluid intake.

Finally, if the urine osmolality remains below 300 milliosmoles per kilogram, your patient’s ability to concentrate the urine is impaired, so diagnose diabetes insipidus.