Page 539 - Clinical Application of Mechanical Ventilation

Critical Care Issues in Mechanical Ventilation 505

Treatments for HIE depend on the underlying cause, as well as the severity of the
damage to the brain. Treatment options typically focus on ventilation, perfusion, and
seizure control. Hypothermia using cooling blankets has been used to reduce oxygen
consumption and to minimize the effects of cerebral hypoxia. Hyperbaric oxygen
therapy increases the oxygen-carrying capacities of the plasma and is most useful
in conditions with increased dysfunctional hemoglobins such as carbon monoxide
poisoning.

TRAumA BRAIn InjuRy

The major causes of traumatic brain injury (TBI) include motor vehicle crashes,
falls, assaults, sports-related injuries, penetrating trauma, and explosive blasts and
combat injuries. The male-to-female ratio for TBI is about 2-to-1, and most patients
with TBI are younger than 35 years old. While motor vehicle crashes cause most
deaths and injuries to young people, falls are the leading cause of death and dis-
ability from TBI in people older than 65 years (Ghajar, 2000).
The normal ICP is 8 to 12
mm Hg (the clinical normal is Almost 100% of patients with severe head injury and two-thirds of those with
up to 20 mm Hg). moderate head injury become permanently disabled in performing some daily func-
tions. In the U.S., there are about 600,000 new TBI cases per year. The direct
cost of caring for these patients after discharge from the hospital is estimated to be
$25 billion annually (Crippen, 2011).
ICP . 20 mm Hg reduces The brain is contained within the skull, a rigid and nonelastic structure which
CPP and increases the likeli-
hood of cerebral hypoxia or has a capacity of about 1,500 mL. Under normal conditions, the brain occupies 85
ischemia and death.
to 90% of this intracranial compartment. The intravascular cerebral blood volume
and cerebrospinal fluid account for about 10% and 3% of this volume, respectively.
The brain has a very low compliance and cannot tolerate significant rapid volume
expansion (e.g., cerebral edema, hematoma). Significant volume expansion within
a rigid skull will cause the intracranial pressure (ICP) to rise. The normal range for
The clinical normal range
for CCP is 70–80 mm Hg. A ICP is 8–12 mm Hg (the clinical normal is up to 20 mm Hg). An increase of ICP
suboptimal CPP (,70 mm higher than 20 mm Hg will lower the CPP (TCPP 5 MAP 2 cICP). The clinical
Hg) can cause cerebral hy-
poxia or ischemia and death. normal range for CCP is 70–80 mm Hg. A suboptimal CPP (,70 mm Hg) can
cause cerebral hypoxia or ischemia and death.

Delayed Brain Injury

Neurological damage does not always occur at the moment of impact (primary
injury). The events that happen afterwards (secondary injury) may lead to brain
swelling, increase in intracranial pressure (ICP), and decrease in CPP and cere-
bral blood flow (Irwin et al., 2003). Ischemia of the brain tissues is the end result
when CPP cannot provide adequate perfusion to the brain. Secondary neuro-
logical injury to the brain is the leading cause of in-hospital deaths following
primary TBI (Marshall et al., 1991). Another risk factor for secondary injury is
systemic hypotension. Systemic hypotension lowers the MAP and CPP (TCPP 5
TMAP 2 ICP).

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