Diagnosis and Management of Combined Central Diabetes Insipidus and Cerebral Salt Wasting Syndrome After Traumatic Brain Injury.
BACKGROUND
Combined central diabetes insipidus and cerebral salt wasting syndrome after traumatic brain injury (TBI) is rare, is characterized by massive polyuria leading to severe water and electrolyte disturbances, and usually is associated with very high mortality mainly as a result of delayed diagnosis and improper management.


METHODS
We retrospectively reviewed the clinical presentation, management, and outcomes of 11 patients who developed combined central diabetes insipidus and cerebral salt wasting syndrome after traumatic brain injury to define distinctive features for timely diagnosis and proper management.


RESULTS
The most typical clinical presentation was massive polyuria (10,000 mL/24 hours or >1000 mL/hour) refractory to vasopressin alone but responsive to vasopressin plus cortisone acetate. Other characteristic presentations included low central venous pressure, high brain natriuretic peptide precursor level without cardiac dysfunction, high 24-hour urine sodium excretion and hypovolemia, and much higher urine than serum osmolarity; normal serum sodium level and urine specific gravity can also be present. Timely and adequate infusion of sodium chloride was key in treatment. Of 11 patients, 5 had a good prognosis 3 months later (Extended Glasgow Outcome Scale score ≥6), 1 had an Extended Glasgow Outcome Scale score of 4, 2 died in the hospital of brain hernia, and 3 developed a vegetative state.


CONCLUSIONS
For combined diabetes insipidus and cerebral salt wasting syndrome after traumatic brain injury, massive polyuria is a major typical presentation, and intensive monitoring of fluid and sodium status is key for timely diagnosis. To achieve a favorable outcome, proper sodium chloride supplementation and cortisone acetate and vasopressin coadministration are key.
Department of Neurosurgery, Huashan Hospital, Fudan University, Shanghai, China.
Xuehai
X
Wu
Worldwide Medical Center, Huashan Hospital, Fudan University, Shanghai, China.
Xiaolan
X
Zhou
Department of Neurosurgery, Huashan Hospital, Fudan University, Shanghai, China.
Liang
L
Gao
Department of Neurosurgery, Huashan Hospital, Fudan University, Shanghai, China.
Xing
X
Wu
Department of Neurosurgery, Jinshan Hospital, Fudan University, Shanghai, China.
Li
L
Fei
Department of Neurosurgery, Huashan Hospital, Fudan University, Shanghai, China.
Ying
Y
Mao
Department of Neurosurgery, Huashan Hospital, Fudan University, Shanghai, China. Electronic address: hujin_dana@126.com.
Jin
J
Hu
Department of Neurosurgery, Huashan Hospital, Fudan University, Shanghai, China.
Liangfu
L
Zhou
D000293:Adolescent; D000328:Adult; D001930:Brain Injuries / Q000150:complications* / Q000175:diagnosis / Q000628:therapy; D002648:Child; D020790:Diabetes Insipidus, Neurogenic / Q000175:diagnosis* / Q000209:etiology / Q000628:therapy*; D005260:Female; D006801:Humans; D007010:Hyponatremia; D007177:Inappropriate ADH Syndrome / Q000175:diagnosis* / Q000209:etiology / Q000628:therapy*; D008297:Male; D008875:Middle Aged; D011141:Polyuria / Q000175:diagnosis / Q000209:etiology / Q000628:therapy; D012189:Retrospective Studies; D016896:Treatment Outcome; D055815:Young Adult
Central diabetes insipidus; Cerebral salt wasting syndrome; Cortisone acetate; Polyuria; Traumatic brain injury; Vasopressin