70 research outputs found
Acute effects of intracranial hypertension and ARDS on pulmonary and neuronal damage: a randomized experimental study in pigs
Abstract
PURPOSE:
To determine reciprocal and synergistic effects of acute intracranial hypertension and ARDS on neuronal and pulmonary damage and to define possible mechanisms.
METHODS:
Twenty-eight mechanically ventilated pigs were randomized to four groups of seven each: control; acute intracranial hypertension (AICH); acute respiratory distress syndrome (ARDS); acute respiratory distress syndrome in combination with acute intracranial hypertension (ARDS + AICH). AICH was induced with an intracranial balloon catheter and the inflation volume was adjusted to keep intracranial pressure (ICP) at 30-40 cmH2O. ARDS was induced by oleic acid infusion. Respiratory function, hemodynamics, extravascular lung water index (ELWI), lung and brain computed tomography (CT) scans, as well as inflammatory mediators, S100B, and neuronal serum enolase (NSE) were measured over a 4-h period. Lung and brain tissue were collected and examined at the end of the experiment.
RESULTS:
In both healthy and injured lungs, AICH caused increases in NSE and TNF-alpha plasma concentrations, extravascular lung water, and lung density in CT, the extent of poorly aerated (dystelectatic) and atelectatic lung regions, and an increase in the brain tissue water content. ARDS and AICH in combination induced damage in the hippocampus and decreased density in brain CT.
CONCLUSIONS:
AICH induces lung injury and also exacerbates pre-existing damage. Increased extravascular lung water is an early marker. ARDS has a detrimental effect on the brain and acts synergistically with intracranial hypertension to cause histological hippocampal damage
Pre-injury Comorbidities Are Associated With Functional Impairment and Post-concussive Symptoms at 3-and 6-Months After Mild Traumatic Brain Injury: A TRACK-TBI Study
Introduction: Over 70% of traumatic brain injuries (TBI) are classified as mild (mTBI),
which present heterogeneously. Associations between pre-injury comorbidities and
outcomes are not well-understood, and understanding their status as risk factors may
improve mTBI management and prognostication.
Methods: mTBI subjects (GCS 13–15) from TRACK-TBI Pilot completing 3- and
6-month functional [Glasgow Outcome Scale-Extended (GOSE)] and post-concussive
outcomes [Acute Concussion Evaluation (ACE) physical/cognitive/sleep/emotional
subdomains] were extracted. Pre-injury comorbidities >10% incidence were included
in regressions for functional disability (GOSE ≤ 6) and post-concussive symptoms by
subdomain. Odds ratios (OR) and mean differences (B) were reported. Significance was
assessed at p < 0.0083 (Bonferroni correction).
Results: In 260 subjects sustaining blunt mTBI, mean age was 44.0-years and 70.4%
were male. Baseline comorbidities >10% incidence included psychiatric-30.0%, cardiac
(hypertension)-23.8%, cardiac (structural/valvular/ischemic)-20.4%, gastrointestinal15.8%, pulmonary-15.0%, and headache/migraine-11.5%. At 3- and 6-months
separately, 30.8% had GOSE ≤ 6. At 3-months, psychiatric (GOSE ≤ 6: OR = 2.75,
95% CI [1.44–5.27]; ACE-physical: B = 1.06 [0.38–1.73]; ACE-cognitive: B = 0.72
[0.26–1.17]; ACE-sleep: B = 0.46 [0.17–0.75]; ACE-emotional: B = 0.64 [0.25–1.03]), headache/migraine (GOSE ≤ 6: OR = 4.10 [1.67–10.07]; ACE-sleep: B = 0.57
[0.15–1.00]; ACE-emotional: B = 0.92 [0.35–1.49]), and gastrointestinal history
(ACE-physical: B = 1.25 [0.41–2.10]) were multivariable predictors of worse outcomes.
At 6-months, psychiatric (GOSE ≤ 6: OR = 2.57 [1.38–4.77]; ACE-physical: B = 1.38
[0.68–2.09]; ACE-cognitive: B = 0.74 [0.28–1.20]; ACE-sleep: B = 0.51 [0.20–0.83];
ACE-emotional: B = 0.93 [0.53–1.33]), and headache/migraine history (ACE-physical:
B = 1.81 [0.79–2.84]) predicted worse outcomes.
Conclusions: Pre-injury psychiat
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