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Head Trauma Workup

  • Author: Craig R Ainsworth, MD; Chief Editor: John Geibel, MD, DSc, MSc, MA  more...
 
Updated: Jan 09, 2015
 

Laboratory Studies

After the patient has been stabilized and an appropriate neurologic examination has been conducted, the diagnostic evaluation may begin. Patients with TBI do not require any additional blood tests beyond the standard panel of tests obtained in all trauma patients. A urine toxicology screen and an assessment of the blood alcohol level are important for any patient who has an altered level of consciousness because any central nervous system depressant can impair consciousness.

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Imaging Studies

Skull radiographs

Once an important part of the head injury evaluation, skull radiographs have been replaced by CT scans and are rarely used in patients with closed head injury.

Skull radiographs are occasionally used in the evaluation of penetrating head trauma, and they can help provide a rapid assessment of the degree of foreign body penetration in nonmissile penetrating head injuries (eg, stab wounds).

Skull radiographs are sometimes used in patients with gunshot wounds to the head to screen for retained intracranial bullet fragments.

CT scan

A CT scan is the diagnostic study of choice in the evaluation of TBI because it has a rapid acquisition time, is universally available, is easy to interpret, and is reliable.

When first introduced more than 25 years ago, CT scans of the brain required almost 30 minutes to complete. This acquisition time has decreased steadily; the current generation of ultrafast CT scanners can perform a head CT scan in less than 1 minute, faster than the time required to enter patient's demographic data into the scanner.

The standard CT scan for the evaluation of acute head injury is a noncontrast scan that spans from the base of the occiput to the top of the vertex in 5-mm increments.

Three data sets are obtained from the primary scan, as follows: (1) bone windows, (2) tissue windows, and (3) subdural windows. These different types of exposure are necessary because of the significant difference in exposure necessary to visualize various intracranial structures. The bone windows allow for a detailed survey of the bony anatomy of the skull, and the tissue windows allow for a detailed survey of the brain and its contents. The subdural windows provide better visualization of intracranial hemorrhage, especially those hemorrhages adjacent to the brain (eg, subdural hematomas).

Each intracranial structure has a characteristic density, which is expressed in Hounsfield units. These units are defined according to a scale that ranges from (-) 1000 units to (+) 1000 units. Air is assigned a density of (-) 1000 units, water is assigned a density of 0 units, and bone has a density of (+) 1000 units. On this scale, CSF has a density of (+) 4 to (+) 10 units, white matter has a density of (+) 22 to (+) 36 units, and gray matter has a density of (+) 32 to (+) 46 units. Extravascular blood has a density of (+) 50 to (+) 90 units, and calcified tissue and bone have a density of (+) 800 to (+) 1000 units.

When reviewing a CT scan, using a systematic approach and following this same protocol each time are important. Consistency is much more important than the specific order used.

  • First, examine the bone windows for fractures, beginning with the cranial vault and then examining the skull base and the facial bones.
  • Next, examine the tissue windows for the presence of (1) extra-axial hematomas (eg, epidural hematomas, subdural hematomas), (2) intraparenchymal hematomas, or (3) contusions.
  • Next, survey the brain for any evidence of pneumocephalus, hydrocephalus, cerebral edema, midline shift, or compression of the subarachnoid cisterns at the base of the brain.
  • Finally, examine the subdural windows for any hemorrhage that may not be visualized easily on the tissue windows.

Skull fractures may be classified as either linear or comminuted fractures. Linear skull fractures are sometimes difficult to visualize on the individual axial images of a CT scan. The scout film of the CT scan, which is the equivalent of a lateral skull x-ray film, often demonstrates linear fractures. The intracranial sutures are easily mistaken for small linear fractures. However, the sutures have characteristic locations in the skull and have a symmetric suture line on the opposite side. Small diploic veins, which traverse the skull, may also be interpreted as fractures. Comminuted fractures are complex fractures with multiple components. Comminuted fractures may be displaced inwardly; this is defined as a depressed skull fracture.

Extra-axial hematomas include epidural and subdural hematomas. Epidural hematomas are located between the inner table of the skull and the dura. They are typically biconvex in shape because their outer border follows the inner table of the skull and their inner border is limited by locations at which the dura is firmly adherent to the skull. Epidural hematomas are usually caused by injury to an artery, although 10% of epidural hematomas may be venous in origin. The most common cause of an epidural hematoma is a linear skull fracture that passes through an arterial channel in the bone. The classic example of this is the temporal epidural hematoma caused by a fracture through the course of the middle meningeal artery. Epidural hematomas, especially those of arterial origin, tend to enlarge rapidly.

Subdural hematomas are located between the dura and the brain. Their outer edge is convex, while their inner border is usually irregularly concave. Subdural hematomas are not limited by the intracranial suture lines; this is an important feature that aids in their differentiation from epidural hematomas. Subdural hematomas are usually venous in origin, although some subdural hematomas are caused by arterial injuries. The classic cause of a posttraumatic subdural hematoma is an injury to one of the bridging veins that travel from the cerebral cortex to the dura. As the brain atrophies over time, the bridging veins become more exposed and, as a result, are more easily injured. Occasionally, the distinction between a subdural and an epidural hematoma can be difficult. The size of an extra-axial hematoma is a more important factor than whether the blood is epidural or subdural in location. In addition, a mixed hematoma with both a subdural and an epidural component is not uncommon.

Intra-axial hematomas are defined as hemorrhages within the brain parenchyma. These hematomas include intraparenchymal hematomas, intraventricular hemorrhages, and subarachnoid hemorrhages. Subarachnoid hemorrhages that occur because of trauma are typically located over gyri on the convexity of the brain. The subarachnoid hemorrhages that result from a ruptured cerebral aneurysm are usually located in the subarachnoid cisterns at the base of the brain. Cerebral contusions are posttraumatic lesions in the brain that appear as irregular regions, in which high-density changes (ie, blood) and low-density changes (ie, edema) are present. Frequently, 1 of these 2 types of changes predominates within a particular contusion. Contusions are most often caused by the brain gliding over rough surfaces, such as the rough portions of the skull that are present under the frontal and temporal lobes.

CT scans may be used for classification and for diagnostic purposes. Marshall et al published a classification scheme that classifies head injuries according to the changes demonstrated on CT scan images.[3] This system defines 4 categories of injury, from diffuse injury I to diffuse injury IV.

  • In diffuse injury I, evidence of any significant brain injury is lacking.
  • In diffuse injury II, either no midline shift or a shift of less than 5 mm is present and the CSF cisterns at the base of the brain are widely patent. In addition, no high-density or mixed-density lesions (contusions) of greater than 25 mL in volume are present.
  • In diffuse injury III, a midline shift of less than 5 mm is present, with partial compression or absence of the basal cisterns. No high- or mixed-density lesions with a volume greater than 25 mL are present.
  • Diffuse injury IV is defined as midline shift greater than 5 mm with compression or absence of the basal cisterns and no lesions of high or mixed density greater than 25 mL

MRI

MRI has a limited role in the evaluation of acute head injury. Although MRI provides extraordinary anatomic detail, it is not commonly used to evaluate acute head injuries because of its long acquisition times and the difficulty in obtaining MRIs in persons who are critically ill. However, MRI is used in the subacute setting to evaluate patients with unexplained neurologic deficits.

MRI is superior to CT scan for helping identify diffuse axonal injury (DAI) and small intraparenchymal contusions. DAI is defined as neuronal injury in the subcortical gray matter or the brainstem as a result of severe rotation or deceleration. DAI is often the reason for a severely depressed level of consciousness in patients who lack evidence of significant injury on CT scan images and have an ICP that is within the reference range.

Magnetic resonance angiography may be used in some patients with TBI to assess for arterial injury or venous sinus occlusion.

Angiography

Once a common diagnostic study in persons with acute head injury, angiography is rarely used in the evaluation of acute head injury today. However, conventional angiography has been the screening and diagnostic modality of choice for identifying blunt cerebrovascular injuries (BCVI) in trauma patients.[4]

Before the development of the CT scan, cerebral angiography provided a reliable means for demonstrating the presence of an intracranial mass lesion.

Angiography in used in acute head injury only when a vascular injury may be present. This includes patients with unexplained neurologic deficits, especially in the setting of temporal bone fractures, and patients with clinical evidence of a potential carotid injury (eg, hemiparesis, Horner syndrome).

Goodwin et al found that conventional angiography is more accurate than 16- or 64-slice CT angiography as a screening tool for BCVI in trauma patients.[4] In a prospective study, 158 patients underwent CT angiography (16-slice or 64-slice) at the time of injury assessment, followed 24-48 hours later with conventional angiography of the cerebral vasculature. CT angiography detected only 13 true cerebrovascular injuries (40.6%) in 12 patients, whereas conventional angiography identified 32 injuries in 27 patients.[4] For detection of cerebrovascular injury, CT angiography had a sensitivity of 0.97 (95% confidence interval [CI], 0.92-0.99) and a specificity of 0.41 (95% CI, 0.22-0.61).

A study by Emmett et al confirmed that angiography is the criterion standard for BCVI diagnosis, but that CT angiography should be added as a screening criterion in order to capture BCVI that goes unrecognized in asymptomatic trauma patients.[5]

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Other Tests

Initial clinical evaluation

The initial evaluation of patients with TBI involves a thorough systemic trauma evaluation according to the advanced trauma life support (ATLS) guidelines. Once this has been completed and the patient is stable from a cardiopulmonary standpoint, attention may be directed to a focused head injury evaluation.

The evaluation of the spine for potential injury is critically important in patients with TBI because approximately 10% of those with severe head injuries have a concomitant spine injury. Many of these injuries are cervical spine injuries.

Attempt to obtain a thorough history of the mechanism of the trauma and the events immediately preceding the trauma. Specific information, such as the occurrence of syncope or the onset of a seizure prior to a fall or a motor vehicle accident, prompts a more extended evaluation of the etiology of such an event. Because many patients with TBI have altered levels of consciousness, the history is often provided by family members, police officers, paramedics, or witnesses.

Neurologic assessment

After sufficient information has been obtained regarding patient history, appropriate physical and neurologic examinations are performed.

The neurologic assessment begins with ascertaining the GCS score. This is a screening examination and does not substitute for a thorough neurologic examination.

In addition to determining the GCS score, the neurologic assessment of patients with TBI should include the following:

  • Brainstem examination – Pupillary examination, ocular movement examination, corneal reflex, gag reflex
  • Motor examination
  • Sensory examination
  • Reflex examination

Many patients with TBI have significant alterations of consciousness and/or pharmaceuticals present that limit the scope of the neurologic examination. When such factors limit the neurologic examination, noting their presence is important.

Pupillary examination

A careful pupillary examination is a critical part of the evaluation of patients with TBI, especially in patients with severe injuries. When muscle relaxants have been administered to a patient, the only aspect of the neurologic examination that may be evaluated is the pupillary examination.

Several factors can alter the pupillary examination results. Narcotics cause pupillary constriction (meiosis), and medications or drugs that have sympathomimetic properties cause pupillary dilation (mydriasis). These effects are often strong enough to blunt or practically eliminate pupillary responses. Prior eye surgery, such as cataract surgery, can also alter or eliminate pupillary reactivity.

Proper assessment of the pupillary response requires the use of a strong light source to override any of the potential factors that may affect pupillary reaction. Each pupil must be assessed individually, with at least 10 seconds between assessment of each eye to allow consensual responses to fade prior to stimulating the opposite eye.

A normal pupillary examination result consists of bilaterally reactive pupils that react to both direct and consensual stimuli. Bilateral small pupils can be caused by narcotics, pontine injury (due to disruption of sympathetic centers in the pons), or early central herniation (mass effect on the pons).

Bilateral fixed and dilated pupils are secondary to inadequate cerebral perfusion. This can result from diffuse cerebral hypoxia or severe elevations of ICP preventing adequate blood flow into the brain.

Pupils that are fixed and dilated usually indicate an irreversible injury. If due to systemic hypoxia, the pupils sometimes recover reactivity when adequate oxygenation is restored.

A unilateral fixed (unresponsive) and dilated pupil has many potential causes. A pupil that does not constrict when light is directed at the pupil but constricts when light is directed into the contralateral pupil (intact consensual response) is indicative of a traumatic optic nerve injury.

A unilateral dilated pupil that does not respond to either direct or consensual stimulation usually indicates transtentorial herniation.

Unilateral constriction of a pupil is usually secondary to Horner syndrome, in which the sympathetic input to the eye is disrupted and the pupil constricts due to more parasympathetic than sympathetic stimulation. In patients with TBI, Horner syndrome may be caused by an injury to the sympathetic chain at the apex of the lung or a carotid artery injury. A unilateral constricted pupil can be caused by a unilateral brainstem injury, but this is quite rare.

A core optic pupil is a pupil that appears irregular in shape. This is caused by a lack of coordination of contraction of the muscle fibers of the iris and is associated with midbrain injuries.

Ocular movement examination

When the patient's level of consciousness is altered significantly, a loss of voluntary eye movements often occurs and abnormalities in ocular movements are frequently present. These abnormalities can provide specific clues to the extent and location of injury.

Ocular movements involve the coordination of multiple centers in the brain, including the frontal eye fields, the paramedian pontine reticular formation (PPRF), the medial longitudinal fasciculus (MLF), and the nuclei of the third and sixth cranial nerves. In patients in whom voluntary eye movements cannot be assessed, oculocephalic and oculovestibular testing may be performed.

Oculocephalic testing

Oculocephalic testing (doll's eyes) involves observation of eye movements when the head is turned from side to side. This maneuver helps assess the integrity of the horizontal gaze centers.

Before performing oculocephalic testing, the status of the cervical spine must be established. If a cervical spine injury has not been excluded reliably, oculocephalic testing should not be performed.

When assessing oculocephalic movements, the head is elevated to 30° from horizontal and is rotated briskly from side to side.

A normal response is for the eyes to turn away from the direction of the movement as if they are fixating on a target that is straight ahead. This is similar to the way a doll's eyes move when the head is turned; this is the origin of the term doll's eyes.

If the eyes remain fixed in position and do not rotate with the head, this is indicative of dysfunction in the lateral gaze centers and is referred to as negative doll's eyes. Some patients may have negative doll's eyes and normal oculovestibular reflexes.

Oculovestibular testing

Oculovestibular testing, also known as cold calorics, is another method for assessment of the integrity of the gaze centers. Oculovestibular testing is performed with the head elevated to 30° from horizontal to bring the horizontal semicircular canal into the vertical position.

Oculovestibular testing requires the presence of an intact tympanic membrane; this must be assessed before beginning the test.

In oculovestibular testing, 20 mL of ice-cold water is instilled slowly into the auditory canal. If is no response occurs within 60 seconds, the test is repeated with 40 mL of cold water.

When cold water is irrigated into the external auditory canal, the temperature of the endolymph falls and the fluid begins to settle. This causes an imbalance in the vestibular signals and initiates a compensatory response.

Cold-water irrigation in the ear of an alert patient results in a fast nystagmus away from the irrigated ear and a slow compensatory nystagmus toward the irrigated side. If warm water is used, the opposite will occur; the fast component of nystagmus will be toward the irrigated side, and the slow component will be away from the irrigated side. This is the basis for the acronym COWS, which stands for cold opposite, warm same. This refers to the direction of the fast component of nystagmus.

As the level of consciousness declines, the fast component of nystagmus fades gradually. Thus, in unconscious patients, only the slow phase of nystagmus may be evaluated.

A normal oculocephalic response to cold-water calorics (ie, eye deviation toward the side of irrigation) indicates that the injury spares the PPRF, the MLF, and third and sixth cranial nerve nuclei. This means that the level of injury must be rostral to the reticular activating system in the upper brainstem.

If a unilateral frontal lobe injury is present, the eyes are deviated toward the side of injury prior to caloric testing. Cold-water irrigation of the opposite ear results in a normal response to caloric testing (ie, eye deviation toward the irrigated side) because the injury is in the frontal region and spares the pontine gaze centers.

When a pontine injury is present, the eyes often deviate away from the side of injury. In this situation, cold-water irrigation of the contralateral ear does not cause the gaze to deviate toward the irrigated ear because an injury has occurred at the level of the pons and the pontine gaze centers are compromised.

A dysconjugate response to caloric testing suggests an injury to either the third or sixth cranial nerves or an injury to the MLF, resulting in an internuclear ophthalmoplegia.

If caloric testing causes a skew deviation, in which the eyes are dysconjugate in the vertical direction, this indicates a lesion in the brainstem. The exact location of injury that results in skew deviation is not known.

Motor examination

After completing the brainstem examination, a motor examination should be performed. A thorough motor or sensory examination is difficult to perform in any patient with an altered level of consciousness.

When a patient is not alert enough to cooperate with strength testing, the motor examination is limited to an assessment of asymmetry in the motor examination findings. This may be demonstrated by an asymmetric response to central pain stimulation or a difference in muscle tone between the left and right sides. A finding of significant asymmetry during the motor examination may be indicative of a hemispheric injury and raises the possibility of a mass lesion.

Sensory examination

Performing a useful sensory examination in patients with TBI is often difficult.

Patients with altered levels of consciousness are unable to cooperate with sensory testing, and findings from a sensory examination are not reliable in patients who are intoxicated or comatose.

Peripheral reflex examination

A peripheral reflex examination can be useful to help identify gross asymmetry in the neurologic examination.

This may indicate the presence of a hemispheric mass lesion.

Other factors

Notably, Ley et al have suggested that diabetic patients with moderate-to-severe TBI are increased risk of mortality, with the likely contributing factor being insulin deficiency.[6]

Intracranial hypertension (ICH) and cerebral hypoperfusion (CH) are secondary insults in patients with TBI that are hard to predict. Stein et al conducted a study to determine whether cytokine levels are indicative of impending ICH or CH in patients with severe TBI. They found that interleukin 8 (IL-8) shows the most promise as a potential biomarker of impending ICH and CH. Results showed higher serum IL-8 levels in patients with poor neurologic outcome and a moderate correlation between serum IL-8 levels with ICH and CH and between cerebrospinal fluid (CSF) levels of IL-8 and cerebral perfusion pressure (CPP).[7]

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Contributor Information and Disclosures
Author

Craig R Ainsworth, MD Medical Director, Intensive Care Unit, Associate Program Director, Internal Medicine Residency Program, Critical Care Medicine Physician, William Beaumont Army Medical Center

Craig R Ainsworth, MD is a member of the following medical societies: American College of Chest Physicians, American College of Physicians, Society of Critical Care Medicine

Disclosure: Nothing to disclose.

Coauthor(s)

Gregory S Brown, Jr, MD Staff Physician, Department of Pulmonary and Critical Care, William Beaumont Army Medical Center

Gregory S Brown, Jr, MD is a member of the following medical societies: Alpha Omega Alpha, American College of Chest Physicians, American College of Physicians, American Thoracic Society

Disclosure: Nothing to disclose.

Specialty Editor Board

Francisco Talavera, PharmD, PhD Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Received salary from Medscape for employment. for: Medscape.

Chief Editor

John Geibel, MD, DSc, MSc, MA Vice Chair and Professor, Department of Surgery, Section of Gastrointestinal Medicine, and Department of Cellular and Molecular Physiology, Yale University School of Medicine; Director, Surgical Research, Department of Surgery, Yale-New Haven Hospital; American Gastroenterological Association Fellow

John Geibel, MD, DSc, MSc, MA is a member of the following medical societies: American Gastroenterological Association, American Physiological Society, American Society of Nephrology, Association for Academic Surgery, International Society of Nephrology, New York Academy of Sciences, Society for Surgery of the Alimentary Tract

Disclosure: Received royalty from AMGEN for consulting; Received ownership interest from Ardelyx for consulting.

Acknowledgements

David W Crippen, MD, FCCM Associate Professor, Department of Critical Care Medicine, University of Pittsburgh Medical Center; Medical Director, Neurovascular Critical Care, Presbyterian-University Hospital

David W Crippen, MD, FCCM is a member of the following medical societies: American College of Critical Care Medicine, European Society of Intensive Care Medicine, and Society of Critical Care Medicine

Disclosure: Nothing to disclose.

Michael A Grosso, MD Consulting Staff, Department of Cardiothoracic Surgery, St Francis Hospital

Michael A Grosso, MD is a member of the following medical societies: American College of Surgeons, Society of Thoracic Surgeons, and Society of University Surgeons

Disclosure: Nothing to disclose.

Scott Shepard, MD Assistant Professor, Department of Surgery, Section of Neurosurgery, UMDNJ-Robert Wood Johnson School of Medicine

Disclosure: Nothing to disclose.

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Table 1. Glasgow Coma Scale
Eye Opening
Score 1 Year or Older 0-1 Year
4 Spontaneously Spontaneously
3 To verbal command To shout
2 To pain To pain
1 No response No response
Best Motor Response
Score 1 Year or Older 0-1 Year
6 Obeys command  
5 Localizes pain Localizes pain
4 Flexion withdrawal Flexion withdrawal
3 Flexion abnormal (decorticate) Flexion abnormal (decorticate)
2 Extension (decerebrate) Extension (decerebrate)
1 No response No response
Best Verbal Response
Score >5 Years 2-5 Years 0-2 Years
5 Oriented and converses Appropriate words Cries appropriately
4 Disoriented and converses Inappropriate words Cries
3 Inappropriate words; cries Screams Inappropriate crying/screaming
2 Incomprehensible sounds Grunts Grunts
1 No response No response No response
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