Head Injury


brain, complications, hypotension, injury, trauma


Case Synopsis

A 22-year-old previously healthy man sustained a head injury, as well as an unstable pelvic and femur fracture, following a motorcycle accident. He was initially combative but quickly became obtunded with a Glasgow Coma Scale (GCS) score of 9 (E3V3M3; see Table 58.1 ). His blood pressure was 95/40 mm Hg, and his heart rate was 100 beats per minute. He had a dilated, unreactive right pupil. Tracheal intubation was performed at the scene, and he was transported to the trauma center. A computed tomography scan revealed a large right epidural hematoma with a midline shift. Initial hematocrit was 32% after the administration of 2 L of crystalloid. His blood pressure was 130/80 mm Hg and his heart rate was 120 beats per minute. He was scheduled for emergent evacuation of the epidural hematoma, followed by open reduction and internal fixation of the femur and pelvis.

TABLE 58.1

Glasgow Coma Scale Score

Eye Opening Verbal Response Motor Response
Spontaneous 4 Oriented 5 Obeys commands 6
To speech 3 Confused 4 Localizes to pain 5
To pain 2 Inappropriate 3 Withdraws to pain 4
None 1 Incomprehensible 2 Flexes to pain 3
None 1 Extends to pain 2
None 1

Problem Analysis


Traumatic brain injury (TBI) is an acquired insult to the brain tissue due to an external blunt or penetrating mechanical force that may evolve into transient or long-term impairment of cognitive, physical, and psychosocial functions. In addition, TBI is often accompanied by other extracranial injuries.


The incidence of head injury is rising. The Centers for Disease Control and Prevention (CDC) estimated that TBI accounted for approximately 2.5 million emergency department (ED) visits. From these presentations, approximately 87% (2,213,826) patients were treated in and released from EDs, another 11% (283,630) were hospitalized and discharged, and approximately 2% (52,844) died.

Falls are the leading causes of nonfatal TBI (35%), followed by motor-vehicle–related injuries (17%) and strikes or blows to the head from or against an object (including sports related) (17%). Overall, motor-vehicle traffic incidents constitute the most common cause of TBI-related deaths, followed by self-inflicted/suicide and falls.

TBI is the commonest cause of death and disability among people under age 40. Improved understanding of the disease process and technologic advancements have reduced the TBI mortality rate by 8.2% in the last decade.

Initial damage to neural tissue directly due to trauma is considered the primary injury and includes cerebral contusion, diffuse axonal injury, hemorrhage into the epidural or subdural space, and intraparenchymal hemorrhage. Secondary injury is defined as any insult to the brain occurring after the initial injury that results in further neuronal damage. Although cerebral ischemia or hypoxia is the ultimate cause of secondary brain injury after TBI, systemic or local insults such as elevated intracranial pressure (ICP), systemic hypotension, and hypoxemia often contribute to secondary injury.

Neuronal death is likely mediated by complex biochemical processes involving the release of excitatory amino acids (e.g., glutamate) and the cellular influx of calcium. Actual cell death may be necrotic or apoptotic in nature. Preventing or reducing secondary brain injury is the focus of most medical management strategies, both in the operating room and subsequently in the intensive care unit (ICU).

TBI is often associated with other injuries (as illustrated in the case synopsis). Thus anesthesiologists may care for a patient during initial resuscitation, surgical intervention for TBI (e.g., evacuation of subdural hematoma, decompressive craniectomy), and/or during laparotomy or fixation of incidental orthopedic injuries, as well as subsequently in the ICU.


Primary Traumatic Brain Injury

TBI is suspected when head trauma is associated with any of the clinical signs affecting the consciousness, memory, mental status, and/or neurologic function. Severity of TBI is commonly assessed by the GCS, which assigns a score to the patient’s best motor, verbal, and eye-opening abilities ( Table 58.1 ). A total score of 8 or less indicates severe TBI. Use of the GCS to evaluate patients with TBI reduces interobserver variability and allows for the comparison of serial examinations to evaluate disease resolution or progression. However, it is evident from the prior description that severe TBI is a heterogeneous disease, and patients with different pathophysiologic mechanisms can manifest with the same GCS score. In addition, use of the GCS as a prognostic indicator is controversial, and assignment of a GCS score is appropriate only after adequate cardiopulmonary resuscitation, especially when it is accompanied by severe hypotension or hypoxia.

Along with the GCS, the pupils should be examined for pupil size, symmetry, and reactivity to light. With acute unilateral mass lesions, an ipsilateral dilated and unreactive pupil suggests uncal herniation. In contrast, bilateral fixed and dilated pupils suggest severe intracranial hypertension that may result in brain herniation.

Vital signs may reflect the patient’s overall clinical status aside from any TBI. For example, hypotension and tachycardia may be due to concealed hemorrhage with a large bone fracture, and hypertension may be due to pain. Vital signs also provide significant insight into the nature of TBI. Severe hypertension may be a compensatory phenomenon (i.e., to preserve cerebral perfusion pressure [CPP] with elevated ICP; CPP is mean arterial pressure [MAP] minus ICP). Severe systemic hypertension with bradycardia is an ominous sign (Cushing reflex). It signifies impending brain herniation and requires immediate therapeutic intervention.

Computed Tomography Findings

Cranial computed tomography (CT) is highly sensitive for detecting intracranial hemorrhage and acute mass lesions. CT findings that support a significantly elevated ICP include the following:

  • Mass lesion greater than 25 mL

  • Midline shift of 5 mm or more

  • Compression of the basal cisterns or lateral ventricles

  • Medial displacement of the uncus

Secondary Brain Injury

Secondary brain injury can be caused by either systemic or cerebral factors ( Table 58.2 ). Among these, hypoxia and hypotension are most likely to have an adverse effect on TBI outcome. However, the neurologic and systemic manifestations of primary TBI may obscure the signs of secondary injury due to cerebral hypoxia or ischemia. Although the calculation of CPP (which requires an arterial line and ICP monitor) is useful with abnormal head CT findings, even a normal CPP does not preclude the development of secondary ischemia or cerebral hypoxia.

TABLE 58.2

Risk Factors for Secondary Brain Injury

Cerebral Factors Systemic Factors
Increased intracranial pressure Hypotension

  • Expanding mass lesions


  • Hypercapnia


  • Hypoxemia


  • Venous obstruction (cervical collar, poor positioning)


  • Systemic hypotension (compensatory cerebral vasodilation)

Excessive hyperventilation Hypo-osmolar state
Posttraumatic vasospasm (traumatic subarachnoid hemorrhage) Coagulopathy
Seizures Fever

Technologic advances have allowed the clinician to gain better insights about the injured brain and its functions.

Cerebral Perfusion and Oxygenation Monitors

Intracranial Pressure Monitor

Either a fiberoptic intraparenchymal probe or an intraventricular catheter can be used to monitor ICP. With continuous intraarterial pressure monitoring, CPP (CPP = MAP − ICP) can be continuously displayed in specialty monitors and allow optimal management of brain perfusion pressure. Although recent literature suggests that vigilant clinical management based on imaging can achieve similar patient outcome as ICP-based management, for now ICP monitoring remains the cornerstone of management of TBI patients and can still be considered the gold standard, allowing judicious clinical decisions based on instant feedback.

Jugular Venous Oximetry

A jugular venous bulb oximetric catheter (JBC) continuously measures brain venous oxygen saturation (SjvO 2 ). Inadequate brain perfusion increases oxygen extraction, causing a decrease in SjvO 2 , whereas nonfunctioning brain tissue extracts little oxygen, resulting in high SjvO 2 values (luxury perfusion). Thus SjvO 2 less than 55% or greater than 75% is associated with a poor prognosis. SjvO 2 catheters are especially useful to monitor cerebral metabolic rate (CMR) when global intervention such as deliberate hyperventilation is used to reduce global cerebral blood flow (CBF) and consequently ICP. JBC lactate concentrations may also reveal increased anaerobic brain metabolism if they are higher than simultaneously drawn arterial lactate concentrations. A limitation of JBC is that it monitors only global CBF-CMR balance. SjvO 2 values can be normal despite small regional areas of ischemia or infarction. Despite initial enthusiasm, this has been largely superseded by brain tissue oxygen tension sensors.

Brain Tissue Oxygen Tension

Brain tissue oxygen tension (PbrO 2 ) sensors provide a continuous measurement of brain parenchymal oxygen tension. This reflects the balance between local brain supply and demand for oxygen. The normal PbrO 2 is in the range of 23 to 35 mm Hg. A PbrO 2 value of less than 20 mm Hg represents compromised brain tissue oxygenation and is the threshold at which an intervention should be considered. The BOOST II trial has shown that the addition of PbrO 2 monitoring to existing ICP/CPP-guided management results in a statistically significant decrease in duration and severity of brain hypoxia, along with a 10% reduction in mortality and a trend toward reduced mortality and improved neurologic outcome at 6 months. This is an invasive monitor, and for it to be optimally effective it should be placed in the brain tissue most at risk, that is, the ischemic penumbra—a feat that is seldom accomplished. Instead it is often placed in the frontal lobe, in combination with the ICP monitor.

Near-Infrared Spectroscopy

Near-infrared spectroscopy is based on reflectance spectroscopy; it measures the light reflected from chromophobes in the brain (hemoglobin) to derive the regional oxygen saturation. It provides information on the balance between flow and metabolism. It is generally accepted that normal range varies between 60% and 75%, with a coefficient of variation of almost 10%. Extracranial contamination of light reflection is a potential source of artifact.

Transcranial Doppler Ultrasonography

Transcranial Doppler ultrasonography (TCD) allows estimation of cerebrovascular resistance, displaying increased pulsatility with elevated ICP, and can be a confirmatory test for intracranial circulatory arrest. Recent studies suggest that continuous monitoring of flow velocity with TCD may allow optimal blood pressure (BP) management by determining the BP range where cerebral autoregulation is most robust.


Microdialysis catheters are placed in brain parenchyma, where they continuously perfuse the brain with a perfusate and sample small volumes of fluid (the dialysate), which is tested for lactate and pyruvate, glutamate, glucose, and glycerol concentration. Lactate-to-pyruvate ratios greater than 40 suggest insufficient cerebral oxygen delivery, inadequate glucose supply, or underlying neuronal mitochondrial dysfunction. However, a time lapse of at least an hour is needed to collect and analyze samples, and this time lag hinders real-time clinical decision making. It remains essentially a research tool at the present time.

Risk Assessment and Implications

Hypoxemia and Hypercapnia

TBI patients are at increased risk for airway obstruction and hypoventilation. These lead to hypoxemia and hypercapnia, which cause cerebral vasodilation. The latter may aggravate any elevated ICP.

Elevated Intracranial Pressure

An acute mass lesion increases ICP and reduces CPP. Increased ICP can lead to brain herniation, with catastrophic consequences.

Systemic Hypotension and Hypovolemia

Adults usually do not become hypovolemic and hypotensive as a result of blood loss from TBI alone. In contrast, small children can lose enough blood with TBI to become hypotensive. Other injuries (e.g., splenic rupture, large bone fractures) can make TBI patients hypotensive and further compromise CPP in those with increased ICP. Compensatory hypertension and bradycardia (Cushing reflex) with elevated ICP may further complicate the clinical picture. Thus in patients with TBI, normotension and tachycardia can still be compatible with severe hypovolemia, with the latter “concealed” by increased systemic vascular resistance (Cushing reflex). Thus an “adequate” blood pressure may give clinicians a false sense of security regarding the progress of resuscitation. Should the elevated ICP be relieved by decompressive craniectomy or evacuation of an intracranial hematoma, sudden profound hypotension or cardiac arrest may occur.

Of all the factors associated with secondary brain injury, systemic hypotension is likely the most significant. With impaired cerebral autoregulation, it invariably leads to reduced CPP. Patients with intact autoregulation but reduced intracranial compliance are also at risk for impaired CPP with hypotension. A reduced MAP indirectly dilates cerebral vasculature to maintain cerebral blood flow, resulting in increased cerebral blood volume and ICP. This increase in ICP further compromises CPP, leading to further compensatory cerebral vasodilation. This vicious circle is referred to as the vasodilator cascade ( Fig. 58.1 ).

Feb 18, 2019 | Posted by in ANESTHESIA | Comments Off on Head Injury
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