Hyponatremia Post ABI

Author/Year/
Country/Study Design/N

Methods

Outcomes

Hannon et al. (2013)
Ireland
Observational
N=100

Population: TBI; Mean Age=33yr; Gender: Male=84, Female= 16; Mean GCS=8.59.
Intervention: Participants were recruited and assessed for hyponatremia (plasma Na+ <135mmol/L) for 10d post injury.
Outcome Measures: Incidence of Hyponatremia.

  1. Hyponatremia was found in 15% of participants, with a median onset of 3d.
  2. All patients were treated with parental glucocorticoids.

Zhang et al. (2008)
China
Pre-Post
N=68

Population: Acute Craniocerebral Injury (ACI); Mean Age=27.8yr; Gender: Male=51, Female=17; Time Post Injury ≤24hr; Injury Severity: Mild=17, Moderate=18, Severe=33.
Intervention: Patients hospitalized within 24hr of ACI were assessed for post-injury hyponatremia, which was defined as blood [Na+] <135mmol/L. Those with hyponatremia received thyrotropin-releasing hormone (TRH) stimulation with IV synthetic TRH 0.3mg. 
Outcome Measure: Incidence of hyponatremia, level of ADH.

  1. 27 (39.7%) patients with ACI demonstrated hyponatremia. The incidence of hyponatremia was significantly higher for those with severe ACI compared to those with mild or moderate ACI (25 versus 2; p<0.001).
  2. Two causes of hyponatremia were identified: SIADH (n=7) and cerebral salt-wasting syndrome (n=20).
  3. TRH stimulation was shown to mitigate symptoms of hyponatremia caused by SIADH, specifically by reducing blood ADH concentration from baseline to 60min following TRH stimulation (130.87±4.32 to 72.64±3.11pg/mL; p<0.01); TRH stimulation was not effective in resolving hyponatremia caused by Cerebral Salt-Wasting Syndrome.

     

Moro et al. (2007)
Japan
Case Series
N=298

Population: TBI; Mean Age=49.3yr; Gender: Male=126, Female=51; Injury Severity: Mild/Moderate=169, Severe=8. 
Intervention: Patients were retrospectively assessed for post-injury hyponatremia, which was defined as serum [Na+] <136mmol/L. Patients who developed hyponatremia were treated with IV Na+ supplementation therapy, and if necessary, 600mg/d hydrocortisone.
Outcome Measure: Incidence of hyponatremia, administration period (d), Glasgow Outcome Scale (GOS) at 1mo from administration, serum [Na+], Na+ excretion, and urine volume.

 

  1. 50 (16.8%) of 298 patients developed hyponatremia post TBI; these patients diagnosed with hyponatremia were found to have a significantly longer administration period (18.7 versus 11.3d; p<0.001), and worse GOS (good recovery (n): 28 versus 108, p=0.02; moderate disability (n): 13 versus 12, p<0.05) than those without.
  2. 37 of 50 patients with hyponatremia responded to Na+ supplementation; however, 7 (18.9%) of these 37 patients required additional Na+ supplementation due to hyponatremia recurrence.
  3. The 13 of 37 that did not respond to Na+ therapy received hydrocortisone; serum [Na+] reached normal levels within 2d.
  4. Hydrocortisone treatment led to improvements in Na+ excretion (563.5±95.9 to 204.8±74.7mEq/d; p=0.002) and in urine volume (3.3±0.7 to 2.2±0.4L/d; p=0.005) in most patients; there were no adverse effects.