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Table 15.4 Hyperventilation for the Acute Management of Intracranial Pressure Post ABI

Author Year

Country

Research Design

PEDro

Sample Size

Methods Outcomes

Muizelaar et al. (1991)

USA

RCT

PEDro=7

N=113

 

Population: TBI; Treatment Group 1 (TG1, n=36): Mean Age=28 yr; Gender: Male=27, Female=9; Mean GCS=5.6. Treatment Group 2 (TG2, n=36): Mean Age=34 yr; Gender: Male=22, Female=14; Mean GCS=5.6. Control Group (CG; n=41): Mean Age=32 yr; Gender: Male=29, Female=12; Mean GCS=5.7.

Intervention: Participants were randomized to receive normal ventilation (PaCO2>35 mmHg, CG), hyperventilation (PaCO2=25 mmHg, TG1) or hyperventilation plus intravenous tromethamine (0.3 M, TG2) for 5 days. Outcomes were assessed before and after treatment.

Outcome Measure: Glasgow Outcome Score (GOS).

1.        At 3 mo and 6 mo, the number of patients with favorable outcome (GOS=4-5) was significantly lower in TG1 group than in CG and TG2.

2.        The interaction between group and GOS was found to be significant (p<0.02), indicating that the detrimental effect of hyperventilation was limited to patients with better prognosis on admission (GCS=4-5).

3.        At 12 mo, this difference in outcome between groups was no longer significant (p=0.13).

4.        There were no significant differences in GOS outcome at any of the 3 time points between TG2 and CG.

Mohammed et al. (2013)

Trinidad

Case Series

N=197

Population: ABI; Median Age=39 yr; Gender: Male=164, Female=33; Median GCS=5.

Intervention: Participants who received therapeutic hyperventilation were retrospectively analyzed.

Outcome Measures: Clinical Outcome, Mortality.

1.        Overall mortality was 38.6%.

2.        Mortality was higher after intensive treatment (PaCO2 <30 mmHg, 46.8%) than moderate treatment (PaCO2>30 mmHg, 33.6%), but this difference was not significant (p=0.06).

3.        GCS at discharge was a significant predictor of outcome (OR=0.17, p<0.001), but GCS at admission was not (OR=0.87, p=0.95).

Coles et al. (2002)

UK

Case Series

N=33

Population: TBI; Mean Age=32 yr, Gender: Male=26, Female=7; Time Post Injury<7 days; GCS Range<13.

Intervention: Participants who received therapeutic hyperventilation (PaCO2<30 mmHg) were retrospectively analyzed.

Outcome Measures: Intracranial Pressure (ICP), Cerebral Perfusion Pressure (CPP), Cerebral Blood Flow (CBF).

1.        Hyperventilation significantly decreased ICP (p<0.001), increased CPP (p<0.0001), and worsened CBF (p<0.0001).

Oertel et al. (2002)

USA

Pre-Post

N=33

Population: TBI; Mean Age=33 yr; Gender: Male=28, Female=5; Median GCS=7.

Intervention: Participants received hyperventilation (PaCO2<30 mmHg) over 13 days.

Outcome Measures: Intracranial Pressure (ICP), Mean Arterial Pressure (MAP).

1.        Hyperventilation significantly decreased ICP (p<0.001) but not MAP (p=0.11) after treatment.

Diringer et al.

(2000)

US

Case Series

N=9

Population: TBI; Mean Age=27 yr; Gender: Male=8, Female=1; Mean Time Post Injury=11.2 hr; Mean GCS=5.6.

Intervention: Participants who received therapeutic hyperventilation (PaCO2<30 mmHg) were retrospectively analyzed.

Outcome Measures: Cerebral Blood Flow (CBF), Cerebral Blood Volume (CBV), Cerebral Venous Oxygen Content (CvO2), Cerebral Metabolic Rate of Oxygen (CMRO2).

1.        Hyperventilation significantly decreased CBF (p<0.001), CBV (p<0.001), and CvO2 (p<0.02), but not CMRO2.

Thiagarajan et al. (1998)

India

Case Series

N=18

Population: TBI; Mean Age=28 yr; Gender: Male=12, Female=6; Median GCS=7.

Intervention: Participants who received therapeutic hyperventilation (PaCO2=25 mmHg) and hyperoxia (PaO2=200-250 mmHg) were retrospectively analyzed.

Outcome Measures: Jugular Venous Bulb Oxygen Saturation (SJvO2), Arteriovenous Oxygen Content Difference (AVDO2).

1.        Hyperventilation significantly decreased SJvO2 and AVDO2 (p<0.0001), but values returned to baseline when hyperoxia was induced (or PaCO2=30 mmHg).