Background

Neuroendocrine dysfunction may occur after a traumatic brain injury (TBI), specifically Diabetes Insipidus (DI).

DI is classified as either central or nephrogenic.

- Central DI (CDI) results from impairment in the synthesis, transport, or release of antidiuretic hormone (ADH).

- Nephrogenic DI (NDI) results from receptor, or downstream, unresponsiveness to circulating ADH. Both CDI and NDI result in loss of ADH effect resulting in polyuria, dehydration, dilute urine, hypernatremia and a hyperosmolar state.

DI post TBI is central, and the lack of production versus secretion of ADH can stem from direct disruption of the hypothalamus or pituitary, interruption of the blood supply to these parts of the brain and/or increased ICP or edema causing herniation of the brain and subsequent compression of the pituitary stalk or gland due to trauma. Post traumatic DI is usually diagnosed in the first days after head trauma. Most cases are transient, however, in rare occasions DI becomes permanent and requires long-term treatment.

Diagnosis of DI can be elusive in poly-traumatized patients due to large volume blood loss, large volume replacements and administration of hyperosmotic fluids. Management of DI consists of close monitoring of fluid and electrolyte balance along with hormonal replacement.

As soon as polyuria is recognized, it is important to rule out other causes. This includes administration of hyperosmolar fluids (mannitol or hypertonic saline), hyperglycemia, diuretics, massive volume resuscitation, or cerebral salt wasting.

The hallmark of DI is dilute urine in the face of hypertonic plasma.

See below for guideline for diagnosis/management of DI post TBI.

PROTOCOL - Triggered by UOP > 350 ml/hr for > 2 hours and Specific Gravity of < 1.010

Monitoring/Evaluation

· Water pitcher at bedside with RN encouragement to drink

o If unable to take po, then NS at 75cc/hr at least

· Q2hr I/O recording at least; foley if indicated

· Q4hr Specific Gravity

· Q6hr serum Na evaluation

Treatment

· Urine output >350/hr for >2hrs and Specific Gravity < 1.010 – give DDAVP

o For expected single administration in first 24hrs postop – 1microgram IV

o For continued administration or planned dosing – use po (100microgram daily or 50 micrograms bid orally)

o Schedule goals: prefer nightly dosing for q-daily dosing

· Na 150-155; give 1L ½NS IV

· Na 155 and above; give 2L ½NS IV

EXCEPTIONS:

· If ICP elevated, coordinate with NSGY prior to administration of therapies (may adjust Na goals)

· If significant renal dysfunction requiring dialysis, consult nephrology/endocrinology

References

1. Capatina, C., Paluzzi, A., Mitchell, R., & Karavitaki, N. (2015). Diabetes Insipidus after Traumatic Brain Injury. Journal of Clinical Medicine, 4(7), 1448–1462.

2. Kalra, S., Zargar, A. H., Jain, S. M., Sethi, B., Chowdhury, S., Singh, A. K., Malve, H. (2016). Diabetes insipidus: The other diabetes. Indian Journal of Endocrinology and Metabolism, 20(1), 9–21.

3. Marino, P. L. (2017) The Little ICU Book (2^nd ed.). Philadelphia, PA: Wolters Kluwer.