Background
Neuroendocrine dysfunction may occur after a traumatic brain
injury (TBI), specifically Diabetes Insipidius (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.
Resources
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 (2nd ed.). Philadelphia, PA: Wolters Kluwer.
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 qdaily 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
Published 9/20/19 (Kara Willett, A Bernard)
