Fanconi et al.

(1988)

Switzerland

RCT

PEDro=6

N=25

Population: TBI; Dexamethasone Group (n=13): Mean Age=7.5yr; Mean Time Post Injury=2 hr; Mean GCS=5.5. Control Group (n=12): Mean Age=7.4yr; Mean GCS=4.5.

Intervention: Patients were randomized to receive either dexamethasone or a placebo over a period of 3 d before a 3 d washout phase. Patients receiving dexamethasone were administered 1 mg/kg dose once a day. Respiratory data was recorded every hour for 3 d and outcomes were assessed at 6 mo follow-up.

Outcome Measure: Glasgow Outcome Scale (GOS), Cortisol Levels, Respiratory Complication Rates.

1.        There was no significant difference between the two groups in GOS scores at 6mo follow-up (p>0.050).

2.        Endogenous cortisol production was almost completely suppressed within 24 hr of administering dexamethasone and was still lower than controls during the washout phase.

3.        Patients receiving dexamethasone experienced a greater frequency of bacterial pneumonia but there were no differences between groups regarding duration of mechanical ventilation, ICP, blood pressure, or peak inspiratory pressure.

Kloti et al.

(1987)

Switzerland

RCT

PEDro=6

N=24

Population: TBI; Dexamethasone Group(n=12): Mean Age=7.8yr; Mean GCS=5.5. Control Group (n=12): Mean Age=7.6yr; Mean GCS=4.5.

Intervention: Patients were randomized to receive either dexamethasone or a placebo over a period of 3 d before a 3 d washout phase. Patients receiving dexamethasone were administered 1 mg/kg dose a day. Respiratory data was recorded every hour and outcomes were assessed at 6mo follow-up.

Outcome Measure: Cortisol levels.

1.        Endogenous cortisol production was almost completely suppressed within 24 hr of administering dexamethasone and was still significantly lower than in controls from day 2 to day 6 (all p<0.050).

2.        Cortisol levels were up to 20 times higher in the control group compared with those who were treated with dexamethasone.