HEAD TRAUMA
CHapter 6 oUtLine
objectives iNtRoductioN ANAtomy Review
• Scalp
• Skull
• Meninges
• Brain
• Ventricular System
• Intracranial Compartments physiology Review
• Intracranial Pressure
• Monro–Kellie Doctrine
• Cerebral Blood Flow
clAssificAtioNs of heAd iNjuRies
• Severity of Injury
• Morphology
evideNce-bAsed tReAtmeNt guideliNes
• Management of Mild Brain Injury (GCS Score 13–15)
• Management of Moderate Brain Injury (GCS Score 9–12)
• Management of Severe Brain Injury (GCS Score 3–8) pRimARy suRvey ANd ResuscitAtioN
• Airway and Breathing
• Circulation
• Neurological Examination
• Anesthetic, Analgesics, and Sedatives
secoNdARy suRvey diAgNostic pRoceduRes
medicAl theRApies foR bRAiN iNjuRy
• Intravenous Fluids
• Correction of Anticoagulation
• Hyperventilation
• Mannitol
• Hypertonic Saline
• Barbiturates
• Anticonvulsants suRgicAl mANAgemeNt
• Scalp Wounds
• Depressed Skull Fractures
• Intracranial Mass Lesions
• Penetrating Brain Injuries pRogNosis
bRAiN deAth teAmwoRk
chApteR summARy bibliogRAphy
After reading this chapter and comprehending the knowledge components of the ATLS provider course, you will be able to:
1. Describe basic intracranial anatomy and the physiological principles of intracranial pressure, the Monro–Kellie Doctrine, and cerebral blood flow.
2. Describe the primary survey and resuscitation of patients with head and brain injuries.
3. Describe the components of a focused neurological examination.
4. Explain the role of adequate resuscitation in limiting secondary brain injury.
5. Identify the considerations for patient transfer, admission, consultation, and discharge of patients with head injuries.
OBJECTIVES
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104 CHAPTER 6 n Head Trauma
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H
ead injuries are among the most common types of trauma encountered in emergency departments (EDs). Many patients with severe brain injuries die before reaching a hospital; in fact, nearly 90% of prehospital trauma-related deaths involve brain injury. Approximately 75% of patients with brain injuries who receive medical attention can be categorized as having mild injuries, 15% as moderate, and 10% as severe. Most recent United States data estimate 1,700,000 traumatic brain injuries (TBIs) occur annually, including 275,000 hospitalizations and 52,000 deaths.TBI survivors are often left with neuropsychological impairments that result in disabilities affecting work and social activity. Every year, an estimated 80,000 to 90,000 people in the United States experience long-term disability from brain injury. In one average European country (Denmark), approximately 300 individuals per million inhabitants suffer moderate to severe head injuries annually, and more than one-third of these individuals require brain injury rehabilitation. Given these statistics, it is clear that even a small reduction in the mortality and morbidity resulting from brain injury can have a major impact on public health.
The primary goal of treatment for patients with suspected TBI is to prevent secondary brain injury. The most important ways to limit secondary brain damage and thereby improve a patient’s outcome are to ensure adequate oxygenation and maintain blood pressure at a level that is sufficient to perfuse the brain. After managing the ABCDEs, patients who are determined by clinical examination to have head trauma and require care at a trauma center should be transferred without delay. If neurosurgical capabilities exist, it is critical to identify any mass lesion that requires surgical evacuation, and this objective is best achieved by rapidly obtaining a computed tomographic (CT) scan of the head. CT scanning should not delay patient transfer to a trauma center that is capable of immediate and definitive neurosurgical intervention.
Triage for a patient with brain injury depends on how severe the injury is and what facilities are available
within a particular community. For facilities without neurosurgical coverage, ensure that pre-arranged transfer agreements with higher-level care facilities are in place. Consult with a neurosurgeon early in the course of treatment. nBOX 6-1 lists key information to communicate when consulting a neurosurgeon about a patient with TBI.
A review of cranial anatomy includes the scalp, skull, meninges, brain, ventricular system, and intracranial compartments (n FIGURE 6-1).
sCaLp
Because of the scalp’s generous blood supply, scalp lacerations can result in major blood loss, hemor-rhagic shock, and even death. Patients who are subject to long transport times are at particular risk for these complications.
skULL
The base of the skull is irregular, and its surface can contribute to injury as the brain moves within the skull during the acceleration and deceleration that occurs during the traumatic event. The anterior fossa houses the frontal lobes, the middle fossa houses the temporal lobes, and the posterior fossa contains the lower brainstem and cerebellum.
Meninges
The meninges cover the brain and consist of three layers: the dura mater, arachnoid mater, and pia mater (n FIGURE 6-2). The dura mater is a tough,
ANAtomy Review
box 6-1 neurosurgical consultation for patients with tbi
When consulting a neurosurgeon about a patient with TBI, communicate the following information:
• Patient age
• Mechanism and time of injury
• Patient’s respiratory and cardiovascular status (particularly blood pressure and oxygen saturation)
• Results of the neurological examination, including the GCS score (particularly the motor response), pupil size, and reaction to light
• Presence of any focal neurological deficits
• Presence of suspected abnormal neuromuscular status
• Presence and type of associated injuries
• Results of diagnostic studies, particularly CT scan (if available)
• Treatment of hypotension or hypoxia
• Use of anticoagulants
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n FIGURE 6-2 The three layers of the meninges are the dura mater, arachnoid mater, and pia mater.
n FIGURE 6-1 Overview of cranial anatomy. The arrows represent the production, circulation, and resorption of cerebrospinal fluid.Advanced Trauma Life Support for Doctors Student Course Manual, 9e
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Third ventricle
Arachnoid villus
Choroid
plexus Superior sagittal sinus
Straight sinus Subarachnoid
space
Subarachnoid space
Central canal of cord Spinal cord
Midbrain Cerebral aqueduct Fourth ventricle Choroid plexus
Cerebellum
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fibrous membrane that adheres firmly to the internal surface of the skull. At specific sites, the dura splits into two “leaves” that enclose the large venous sinuses, which provide the major venous drainage from the brain. The midline superior sagittal sinus drains into the bilateral transverse and sigmoid sinuses, which are usually larger on the right side.
Laceration of these venous sinuses can result in massive hemorrhage.
Meningeal arteries lie between the dura and the internal surface of the skull in the epidural space.
Overlying skull fractures can lacerate these arteries and cause an epidural hematoma. The most commonly injured meningeal vessel is the middle meningeal artery, which is located over the temporal fossa. An expanding hematoma from arterial injury in this location can lead to rapid deterioration and death.
Epidural hematomas can also result from injury to the dural sinuses and from skull fractures, which tend to expand slowly and put less pressure on the underlying brain. However, most epidural hematomas constitute life-threatening emergencies that must be evaluated by a neurosurgeon as soon as possible.
Beneath the dura is a second meningeal layer:
the thin, transparent arachnoid mater. Because the dura is not attached to the underlying arachnoid membrane, a potential space between these layers exists (the subdural space), into which hemorrhage can occur. In brain injury, bridging veins that travel from the surface of the brain to the venous sinuses within the dura may tear, leading to the formation of a subdural hematoma.
The third layer, the pia mater, is firmly attached to the surface of the brain. Cerebrospinal fluid (CSF) fills the space between the watertight arachnoid mater and the pia mater (the subarachnoid space), cushioning the brain and spinal cord. Hemorrhage into this fluid-filled space (subarachnoid hemor-rhage) frequently accompanies brain contusion and injuries to major blood vessels at the base of the brain.
brain
The brain consists of the cerebrum, brainstem, and cerebellum. The cerebrum is composed of the right and left hemispheres, which are separated by the falx cerebri. The left hemisphere contains the language centers in virtually all right-handed people and in more than 85% of left-handed people. The frontal lobe controls executive function, emotions, motor function, and, on the dominant side, expression of speech (motor speech areas). The parietal lobe directs sensory function
and spatial orientation, the temporal lobe regulates certain memory functions, and the occipital lobe is responsible for vision.
The brainstem is composed of the midbrain, pons, and medulla. The midbrain and upper pons contain the reticular activating system, which is responsible for the state of alertness. Vital cardiorespiratory centers reside in the medulla, which extends down-ward to connect with the spinal cord. Even small lesions in the brainstem can be associated with severe neurological deficits.
The cerebellum, responsible mainly for coordination and balance, projects posteriorly in the posterior fossa and connects to the spinal cord, brainstem, and cerebral hemispheres.
VentriCULar systeM
The ventricles are a system of CSF-filled spaces and aqueducts within the brain. CSF is constantly produced within the ventricles and absorbed over the surface of the brain. The presence of blood in the CSF can impair its reabsorption, resulting in increased intracranial pressure. Edema and mass lesions (e.g., hematomas) can cause effacement or shifting of the normally symmetric ventricles, which can readily be identified on brain CT scans.
intraCraniaL CoMpartMents
Tough meningeal partitions separate the brain into regions. The tentorium cerebelli divides the intracranial cavity into the supratentorial and infratentorial compartments. The midbrain passes through an opening called the tentorial hiatus or notch. The oculomotor nerve (cranial nerve III) runs along the edge of the tentorium and may become compressed against it during temporal lobe herniation. Parasympathetic fibers that constrict the pupils lie on the surface of the third cranial nerve;
compression of these superficial fibers during herniation causes pupillary dilation due to un- opposed sympathetic activity, often referred to as a
“blown” pupil (nFIGURE 6-3).
The part of the brain that usually herniates through the tentorial notch is the medial part of the temporal lobe, known as the uncus (nFIGURE 6-4). Uncal herni-ation also causes compression of the corticospinal (pyramidal) tract in the midbrain. The motor tract crosses to the opposite side at the foramen magnum, so compression at the level of the midbrain results in weakness of the opposite side of the body (con-tralateral hemiparesis). Ipsilateral pupillary dilat-
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ion associated with contralateral hemiparesis is the classic sign of uncal herniation. Rarely, the mass le-sion pushes the opposite side of the midbrain against the tentorial edge, resulting in hemiparesis and a dilated pupil on the same side as the hematoma.
Physiological concepts that relate to head trauma include intracranial pressure, the Monro–Kellie Doctrine, and cerebral blood flow.
intraCraniaL pressUre
Elevation of intracranial pressure (ICP) can reduce cerebral perfusion and cause or exacerbate ischemia. The normal ICP for patients in the resting state is approximately 10 mm Hg. Pressures greater than 22 mm Hg, particularly if sustained and refractory to treatment, are associated with poor outcomes.
Monro–keLLie doCtrine
The Monro–Kellie Doctrine is a simple, yet vital concept that explains ICP dynamics. The doctrine states that the total volume of the intracranial contents must remain constant, because the cranium is a rigid container incapable of expanding. When the normal intracranial volume is exceeded, ICP rises. Venous blood and CSF can be compressed out of the container, providing a degree of pressure buffering (nFIGURE 6-5
and nFIGURE 6-6). Thus, very early after injury, a mass such as a blood clot can enlarge while the ICP remains normal. However, once the limit of displacement of CSF and intravascular blood has been reached, ICP rapidly increases.
CerebraL bLood FLow
TBI that is severe enough to cause coma can markedly reduce cerebral blood flow (CBF) during the first few hours after injury. CBF usually increases over the next 2 to 3 days, but for patients who remain comatose, it PHYSIOLOGY REVIEW 107
n FIGURE 6-3 Unequal pupils: the left is greater than the right.
n FIGURE 6-5 Volume–Pressure Curve. The intracranial contents initially can compensate for a new intracranial mass, such as a subdural or epidural hematoma. Once the volume of this mass reaches a critical threshold, a rapid increase in ICP often occurs, which can lead to reduction or cessation of cerebral blood flow.
n FIGURE 6-4 Lateral (Uncal) Herniation. A lesion of the middle meningeal artery secondary to a fracture of the temporal bone may cause temporal epidural hematoma. The uncus compresses the upper brain stem, involving the reticular system (decreasing GCS), the oculomotor nerve (pupillary changes), and the corticospinal tract in the midbrain (contralateral hemiparesis).
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physiology Review
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remains below normal for days or weeks after injury.
There is increasing evidence that low levels of CBF do not meet the metabolic demands of the brain early after injury. Regional, even global, cerebral ischemia is common after severe head injury for both known and undetermined reasons.
The precapillary cerebral vasculature typically can reflexively constrict or dilate in response to changes in mean arterial blood pressure (MAP). For clinical purposes, cerebral perfusion pressure (CPP) is defined as mean arterial blood pressure minus intracranial pressure (CPP = MAP – ICP). A MAP of 50 to 150 mm Hg is “autoregulated” to maintain a constant CBF (pressure autoregulation). Severe TBI can disrupt pressure autoregulation to the point that the brain cannot adequately compensate for
changes in CPP. In this situation, if the MAP is too low, ischemia and infarction result. If the MAP is too high, marked brain swelling occurs with elevated ICP.
Cerebral blood vessels also constrict or dilate in response to changes in the partial pressure of oxygen (PaO2) and the partial pressure of carbon dioxide (PaCO2) in the blood (chemical regulation). Therefore, secondary injury can occur from hypotension, hypoxia, hypercapnia, and iatrogenic hypocapnia.
Make every effort to enhance cerebral perfusion and blood flow by reducing elevated ICP, maintaining normal intravascular volume and MAP, and restoring normal oxygenation and ventilation. Hematomas and other lesions that increase intracranial volume should be evacuated early. Maintaining n FIGURE 6-6 The Monro–Kellie Doctrine Regarding Intracranial Compensation for Expanding Mass. The total volume of the intracranial contents remains constant. If the addition of a mass such as a hematoma compresses an equal volume of CSF and venous blood, ICP remains normal. However, when this compensatory mechanism is exhausted, ICP increases exponentially for even a small additional increase in hematoma volume. (Adapted with permission from Narayan RK: Head Injury. In: Grossman RG, Hamilton WJ eds., Principles of Neurosurgery.
New York, NY: Raven Press, 1991.)
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a normal CPP may help improve CBF; however, CPP does not equate with or ensure adequate CBF.
Once compensatory mechanisms are exhausted and ICP increases exponentially, brain perfusion is compromised.
Head injuries are classified in several ways. For practical purposes, the severity of injury and morphology are used as classifications in this chapter (nTABLE 6-1).
(Also see Classifications of Brain Injury on MyATLS mobile app.)
seVerity oF injUry
The Glasgow Coma Scale (GCS) score is used as an objective clinical measure of the severity of brain injury (nTABLE 6-2). (Also see Glasgow Coma Scale tool on MyATLS mobile app.) A GCS score of 8 or less has become the generally accepted definition of coma or severe brain injury. Patients with a brain injury who have a GCS score of 9 to 12 are categorized as having
“moderate injury,” and individuals with a GCS score of 13 to 15 are designated as having “mild injury.” In assessing the GCS score, when there is right/left or
upper/lower asymmetry, be sure to use the best motor response to calculate the score, because it is the most reliable predictor of outcome. However, the actual responses on both sides of the body, face, arm, and leg must still be recorded.
MorpHoLogy
Head trauma may include skull fractures and intra-cranial lesions, such as contusions, hematomas, diffuse injuries, and resultant swelling (edema/hyperemia).
Skull Fractures
Skull fractures can occur in the cranial vault or skull base.
They may be linear or stellate as well as open or closed.
Basilar skull fractures usually require CT scanning with bone-window settings for identification. Clinical signs of a basilar skull fracture include periorbital ecchymosis (raccoon eyes), retroauricular ecchymosis (Battle’s sign), CSF leakage from the nose (rhinorrhea) or ear (otorrhea), and dysfunction of cranial nerves VII and VIII (facial paralysis and hearing loss), which may occur immediately or a few days after initial injury. The presence of these signs should increase the index of suspicion and help identify basilar skull fractures. Some fractures traverse the carotid canals and can damage the carotid arteries (dissection, pseudoaneurysm, or
clAssificAtioN of heAd iNjuRies
table 6-1 classifications of traumatic brain injury
Severity • Mild
• Moderate
• Severe
• GCS Score 13–15
• GCS Score 9–12
• GCS Score 3–8
Morphology • Skull fractures • Vault • Linear vs. stellate
• Depressed/nondepressed
• Basilar • With/without CSF leak
• With/without seventh nerve palsy
• Intracranial lesions • Focal • Epidural
• Subdural
• Intracerebral
• Diffuse • Concussion
• Multiple contusions
• Hypoxic/ischemic injury
• Axonal injury
Source: Adapted with permission from Valadka AB, Narayan RK. Emergency room management of the head-injured patient. In: Narayan RK, Wilberger JE, Povlishock JT, eds. Neurotrauma. New York, NY: McGraw-Hill, 1996:120.
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thrombosis). In such cases, doctors should consider performing a cerebral arteriography (CT angiography [CT-A] or conventional angiogram).
Open or compound skull fractures provide direct communication between the scalp laceration and the cerebral surface when the dura is torn. Do not underestimate the significance of a skull fracture, because it takes considerable force to fracture the skull. A linear vault fracture in conscious patients increases the likelihood of an intracranial hematoma by approximately 400 times.
Intracranial Lesions
Intracranial lesions are classified as diffuse or focal, although these two forms frequently coexist.
Diffuse Brain Injuries
Diffuse brain injuries range from mild concussions, in which the head CT is normal, to severe hypoxic, ischemic
injuries. With a concussion, the patient has a transient, nonfocal neurological disturbance that often includes loss of consciousness. Severe diffuse injuries often result from a hypoxic, ischemic insult to the brain from prolonged shock or apnea occurring immediately after the trauma. In such cases, the CT may initially appear normal, or the brain may appear diffusely swollen, and the normal gray-white distinction is absent. Another diffuse pattern, often seen in high-velocity impact or deceleration injuries, may produce multiple punctate hemorrhages throughout the cerebral hemispheres.
These “shearing injuries,” often seen in the border between the gray matter and white matter, are referred to as diffuse axonal injury (DAI) and define a clinical syndrome of severe brain injury with variable but often poor outcome.
Focal Brain Injuries
Focal lesions include epidural hematomas, subdural hematomas, contusions, and intracerebral hema- tomas (nFIGURE 6-7).
GCS Score = (E[4] + V[5] + M[6]) = Best possible score 15; worst possible score 3.
*If an area cannot be assessed, no numerical score is given for that region, and it is considered “non-testable.” Source: www.glasgowcomascale.org
table 6-2 glasgow coma scale (gcs)
ORIGINAL SCALE REVISED SCALE SCORE
Eye Opening (E) Spontaneous To speech To pain None
Eye Opening (E) Spontaneous To sound To pressure None Non-testable
4 3 2 1 NT
Verbal Response (V) Oriented
Confused conversation Inappropriate words Incomprehensible sounds None
Verbal Response (V) Oriented Confused Words Sounds None Non-testable
5 4 3 2 1 NT
Best Motor Response (M) Obeys commands Localizes pain
Flexion withdrawal to pain Abnormal flexion (decorticate) Extension (decerebrate) None (flaccid)
Best Motor Response (M) Obeys commands Localizing Normal flexion Abnormal flexion Extension None Non-testable
6 5 4 3 2 1 NT
n BACK TO TABLE OF CONTENTS Epidural Hematomas
Epidural hematomas are relatively uncommon, occurring in about 0.5% of patients with brain injuries and 9% of patients with TBI who are comatose. These hematomas typically become biconvex or lenticular in shape as they push the adherent dura away from the inner table of the skull. They are most often located in the temporal or temporoparietal regions and often result from a tear of the middle meningeal artery due to fracture. These clots are classically arterial in origin;
however, they also may result from disruption of a major venous sinus or bleeding from a skull fracture.
The classic presentation of an epidural hematoma is with a lucid interval between the time of injury and neurological deterioration.
Subdural Hematomas
Subdural hematomas are more common than epi- dural hematomas, occurring in approximately 30%
of patients with severe brain injuries. They often de- velop from the shearing of small surface or bridg- ing blood vessels of the cerebral cortex. In contrast to the lenticular shape of an epidural hematoma on a CT scan, subdural hematomas often appear to conform to contours of the brain. Damage underlying
an acute subdural hematoma is typically much more severe than that associated with epidural hematomas due to the presence of concomitant parenchymal injury.
Contusions and Intracerebral Hematomas
Cerebral contusions are fairly common; they occur in approximately 20% to 30% of patients with severe brain injuries. Most contusions are in the frontal and temporal lobes, although they may be in any part of the brain. In a period of hours or days, contusions can evolve to form an intracerebral hematoma or a coalescent contusion with enough mass effect to re-quire immediate surgical evacuation. This condition occurs in as many as 20% of patients presenting with contusions on initial CT scan of the head. For this reason, patients with contusions generally undergo repeat CT scanning to evaluate for changes in the pattern of injury within 24 hours of the initial scan.
Evidence-based guidelines are available for the treatment of TBI. The 4th edition of the Brain Trauma Foundation Guidelines for the Management of Severe Traumatic Brain Injury were e-published in September of 2016, and the print synopsis was published in the Journal of Neurosurgery in January of 2017. The new guidelines are different in many ways from the old guidelines. New levels of evidence are labeled from highest quality to lowest: levels I, IIA, IIB, and III.
The first guidelines addressing TBI, Guidelines for the Management of Severe Traumatic Brain Injury, were published by the Brain Trauma Foundation in 1995, revised in 2000, and updated most recently in 2016.
Additional evidence-based reviews have since been published regarding the prehospital management of TBI; severe TBI in infants, children and adolescents;
early prognostic indicators in severe TBI; and combat-related head injury. The Brain Trauma Foundation TBI guidelines, which are referenced in this chapter, can be downloaded from the foundation website: http://www.
braintrauma.org. In addition, the American College of Surgeons Trauma Quality Improvement Program (TQIP) published a guideline for managing TBI in 2015.
(See ACS TQIP Best Practices in the Management of Traumatic Brain Injury.)
Even patients with apparently devastating TBI on presentation can realize significant neurological re- n FIGURE 6-7 CT Scans of Intracranial Hematomas. A. Epidural
hematoma. B. Subdural hematoma. C. Bilateral contusions with hemorrhage. D. Right intraparenchymal hemorrhage with right to left midline shift and associated biventricular hemorrhages.
A B
C D
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