TRAUMATIC BRAIN INJURY
Any trauma patient with altered level of con-sciousness must be considered to have a traumatic brain injury (TBI) until proven otherwise . The presence or suspicion of a TBI mandates attention to maintaining cerebral perfu-sion and arterial oxygenation during all aspects of care. The most reliable clinical assessment tool in determining the significance of TBI in a nonse-dated, nonparalyzed patient is the Glasgow coma scale (GCS, Table 27–2). A declining motor score is suggestive of progressing neurological deteriora-tion, prompting urgent neurosurgical evaluation and possible surgical intervention. Although trauma patients frequently have head injuries, few head inju-ries require emergent neurosurgical intervention.
TBIs are categorized as either primary or sec-ondary. Primary brain injuries are usually focal inju-ries directly related to trauma, disrupting normal anatomy or physiology, or both. Four categories of primary brain injury are seen: (1) subdural hematoma; (2) epidural hematoma; (3) intraparen-chymal hemorrhage; and (4) nonfocal, diffuse neu-ronal injury disrupting axons of the central nervous system. These injuries potentially compromise cere-bral blood flow and elevate intracranial
pressure (ICP). Death occurring soon after significant head trauma is usually a result of the primary brain injury.
Acute subdural hematoma is the most com-mon condition warranting emergency neurosurgery and is associated with the highest mortality. Small bridging veins between the skull and brain are disrupted in deceleration or blunt force inju-ries, resulting in blood accumulation and compres-sion of brain tissue. The accumulation of blood raises ICP and compromises cerebral blood flow. Morbidity and mortality are related to the size of the hematoma and magnitude of the midline shift of intracranial contents. Midline shifts of intracra-nial contents may exceed the size of the hematoma, suggesting a significant contribution of cerebral edema. Acute subdural hematomas should be sur-gically evacuated, particularly in patients with ele-vated ICP.
Epidural hematoma occurs when the middlecerebral artery or other cranial vessels are disrupted, most often in association with a skull fracture. This injury accounts for less than 10% of neurosurgi-cal emergencies and has a much better prognosis than acute subdural hematoma. The patient with an epidural hematoma may initially be conscious-ness, followed by progressive unresponsiveness and coma. Emergent surgical decompression is indi-cated when supratentorial lesions occupy more than 30 mL volume and infratentorial lesions occupy more than 10 mL volume (brainstem compression may occur at much lower hematoma volumes). A small epidural hematoma may not require imme-diate evacuation if the patient is neurologically intact, if close observation and repeated neurologi-cal examinations are possible, and if neurosurgical resources are available should emergent decompres-sion become necessary.
Intraparenchymal injuries are caused by rapiddeceleration of the brain within the skull, usu-ally involving the tips of the frontal or temporal lobes. They represent nearly 20% of neurosurgical emergencies following trauma. These injuries tend to be associated with signif icant edema, necrosis, and infarcts in the tissue surrounding the dam-aged tissue. Intraparenchymal injury may coexist with a subdural hematoma. There is no consensus regarding the surgical interventions that should be performed for intraparenchymal hemorrhage, but surgical decompression may be necessary to reduce dangerously sustained increased ICP.
Diffuse neuronal injury results from events resulting in rapid deceleration or movement of the brain tissue of sufficient force to disrupt neurons and axons. This form of brain injury is more common in children than in adults. The extent of the injury may not be obvious in the period soon after injury but will become apparent with serial clinical and radiographic (magnetic resonance imaging) exami-nations. The greater the extent of diffuse neuronal injury following trauma, the higher will be the mor-tality and severe disability. Surgical interventions are not indicated for these injuries unless a decompres-sive craniectomy is required for relief of refractory elevated ICP .
Secondary brain injuries are considered poten-tially preventable injuries. Systemic hypotension (systolic blood pressures <90 mm Hg), hypoxemia (Pao2<60 mm Hg), hypercapnia (Paco2>50 mm Hg), and hyperthermia (temperature >38.0°C) have a negative impact on morbidity and mortality following head injuries, likely because of their contributions to increasing cerebral edema and ICP. Hypotension and hypoxia are recognized as major contributors to poor neurological recov-ery from severe TBI. Hypoxia is the single most important parameter correlating to poor neuro-logical outcomes following head trauma and should be corrected at the earliest possible opportunity. Hypotension (mean arterial blood pressure <60 mm Hg) should also be treated aggressively, using fluid or vasopressors, or both, to assure cere-bral perfusion.
In the absence of a clot requiring evacuation, medi-cal interventions are the primary means of treating elevated ICP following head trauma. Normal cerebral perfusion pressure (CPP), the difference between mean arterial pressure and ICP (ie, MAP − ICP CPP), is approximately 10 mm Hg. ICP monitoring is not required for conscious and alert patients; in addi-tion, patients who are intentionally anticoagulated or who have bleeding diathesis in response to trauma should not have ICP monitoring. However, an ICP monitor should be placed when serial neurological examinations and additional clinical assessments reveal impairment, or when there is an increased risk for elevated ICP (Table 39–1). Interventions to reduce ICP are indicated when readings are higherthan 20–25 mm Hg. Although multiple studies have evaluated interventions aimed at improving CPP and managing ICP without finding obvious outcomes benefit for any treatment scheme, current Brain Trauma Foundation guidelines recommend maintaining CPP between 50 and 70 mm Hg and ICP at less than 20 mm Hg for patients with severe head injury.
Cerebral blood flow is related to arterial car-bon dioxide concentration in a dose-dependent relationship. As arterial carbon dioxide levels decrease, cerebral vasoconstriction occurs, reduc-ing ICP. Conversely, as arterial carbon dioxide levels rise, cerebral vasodilation occurs, increasing ICP. Changes in arterial carbon dioxide levels exert a prompt cerebral blood flow and ICP response, mak-ing hyperventilation an effective intervention when brain herniation is suspected or proven. However, this intervention must be appreciated in the context of TBI: hyperventilation in the presence of systemic hypotension increases the risk of neurological isch-emia and should be avoided in the early stages of resuscitation for patients with TBI.
Osmotic diuretic therapy is another com-monly used and widely accepted method for reduc-ing elevated ICP. Intravenous mannitol doses of 0.25–1.0 g/kg body weight are effective in draw-ing intravascular fluid into the vascular system. As extravascular fluid is drawn into the vascular sys-tem, brain edema and ICP will decrease. Because this intervention is very effective for inducing brisk diuresis, serum osmolarity and electrolytes (particu-larly potassium) must be monitored.
Barbiturate coma is an intervention thatattempts to decrease cerebral metabolic rate, cerebral blood flow, and cerebral oxygen demand in order to reduce elevated ICP and suppress the metabolic rate of ischemic cells until cerebral perfusion improves. Hypotension is commonly associated with this ther-apy, which should limit its use in the hemodynami-cally unstable patient. Vasopressors may be used in order to maintain CPP between 50 and 70 mm Hg. The pentobarbital dose administered is based upon electroencephalographic evidence of burst suppres-sion in order to maximally reduce the cerebral meta-bolic rate of oxygen.
The presence of a severe head injury in the pres-ence of other major traumatic injuries and ongo-ing hemorrhage creates a situation in which patient management goals may conflict. As noted above, in the head-injured patient requiring emergent decompression, mean blood pressures must be maintained between 50 and 70 mmHg to assure adequate CPP and prevention of secondary isch-emic neurological injuries. In patients without brain injury, hemorrhage is usually treated with a more hypotensive goal until bleeding is controlled. Deference is paid to the most life-threatening condition as the priority intervention with the expectation that CPP be maintained throughout, even if this approach results in greater transfusion requirements.
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