Head Trauma


Anatomy

  1. Scalp
    • composed of 5 layers (mnemonic SCALP):
      • Skin
      • Connective tissue
      • Aponeurosis (galea)
      • Loose connective tissue
      • Pericranium
    • because the scalp has such a generous blood supply, scalp lacerations can result in major blood loss, especially in infants and children
    • initial management of a bleeding scalp laceration is to apply a pressure dressing
    • large hematomas can collect below the galea
    • the galea should be repaired when closing scalp lacerations

  2. Skull
    • composed of the cranial vault (calvaria) and the base

    1. Calvaria
      • formed anteriorly by the frontal bone and posteriorly by the parietal and occipital bones

      Calvaria - Side View Calvaria - Top View


    2. Base
      • formed by the frontal, ethmoid, sphenoid, temporal, and occipital bones
      • floor of the skull base is divided into anterior, middle, and posterior fossa
      • cranial nerves exit the skull via foramina located in the skull base

      Bones of the Base of the Skull
  3. Meninges
    1. Dura Mater
      • tough fibrous membrane that adheres firmly to the internal surface of the skull
      • meningeal arteries lie between the dura and the skull (epidural space)
      • because the dura is not attached to the underlying arachnoid, a potential space (subdural space) exists into which hemorrhage can occur
      • dura encloses the large venous sinuses that provide the venous drainage for the brain (superior sagittal, transverse, sigmoid sinuses)

    2. Arachnoid
      • thin, transparent layer
      • cerebrospinal fluid (CSF) circulates between the arachnoid and pia mater
      • head trauma may cause accumulation of blood in this space (subarachnoid hemorrhage)

    3. Pia Mater
      • firmly attached to the surface of the brain

      Meninges
  4. Brain
    1. Cerebrum
      • composed of right and left hemispheres separated by the falx cerebri, a dural reflection from the inferior aspect of the superior sagittal sinus
      • hemisphere that contains the language centers is referred to as the dominant hemisphere (left hemisphere in virtually all right-handed people and 85% of left-handed people)
      • cerebrum is composed of 4 lobes:
        • frontal lobe: concerned with emotions, motor function, speech
        • parietal lobe: concerned with sensory function and spatial orientation
        • temporal lobe: concerned with speech, memory
        • occipital lobe: concerned with vision

    2. Cerebellum
      • responsible mainly for coordination and balance
      • located in the posterior fossa

      Cerebrum
    3. Brainstem
      • composed of the midbrain, pons, and medulla
      • midbrain connects the cerebral hemispheres to the pons and medulla
      • midbrain and upper pons contain the reticular activating system, which is responsible for the state of alertness
      • medulla contains vital cardiorespiratory centers

      Brainstem
  5. Cerebrospinal Fluid
    • produced by the choroid plexus, which is located in the lateral ventricles
    • CSF travels from the lateral ventricles, through the foramen of Monro, into the 3rd ventricle, and then, via the aqueduct of Sylvius, into the 4th ventricle
    • CSF exits from the ventricular system into the subarachnoid space, where it is eventually reabsorbed into the venous circulation through the arachnoid granulations that project into the superior sagittal sinus
    • presence of blood in the CSF can plug the arachnoid granulations and impair CSF reabsorption, leading to increased intracranial pressure (communicating hydrocephalus)

    Cerebral Ventricles
  6. Tentorium
    • tentorium cerebelli divides the head into the supratentorial compartment (anterior + middle fossae) and infratentorial compartment (posterior fossa)
    • midbrain passes through a large opening in the tentorium known as the tentorial notch
    • oculomotor nerve runs along the edge of the tentorium

    Tentorium
    1. Brain Herniation
      • a supratentorial mass or edema may cause downward brain herniation through the tentorial notch
      • medial part of the temporal lobe (uncus) is the part of the brain that usually herniates
      • as the brain herniates downward, the oculomotor nerve becomes compressed against the tentorium
      • parasympathetic fibers (pupillary constrictors) lie on the surface of the oculomotor nerve
      • compression of these parasympathetic fibers leads to pupillary dilatation as a result of unopposed sympathetic activity
      • with further compression of the oculomotor nerve, full oculomotor paralysis occurs, causing the eye to deviate inferiorly and laterally (‘down and out’)
      • uncal herniation also causes compression of the corticospinal tract in the midbrain
      • this motor tract crosses to the opposite side at the foramen magnum; therefore, compression of the corticospinal tract results in weakness of the opposite side of the body (contralateral hemiplegia)
      • ipsilateral pupillary dilatation with contralateral hemiplegia is the classic syndrome of tentorial herniation

      Uncal Herniation Blown Pupil


Physiology

  1. Intracranial Pressure (ICP)
    • normal ICP = 10 mm Hg
    • ICP > 20 mm Hg is abnormal and ICP > 40 mm Hg is severely abnormal
    • the higher the ICP following head injury, the worse the outcome

    1. Monro-Kellie Doctrine
      • the cranial vault is a nonexpansile box
      • within this box is the brain, CSF, venous blood, and arterial blood
      • the total volume of the box must remain constant
      • the addition of a mass or swelling will raise ICP unless an equal volume of CSF and venous blood is squeezed out
      • once this compensatory mechanism is exhausted, even a small increase in the size of the mass will lead to an exponential increase in ICP:

      Intracranial Pressure vs Volume Curve
  2. Cerebral Perfusion Pressure (CPP)
    • CPP = MAP – ICP
    • if ICP is elevated, then blood pressure must be maintained at normal or supranormal levels to maintain CPP
    • maintaining cerebral perfusion is of primary importance in the management of head injury patients

  3. Cerebral Blood Flow (CBF)
    • autoregulation maintains a constant CBF between mean arterial pressures of 50 and 160 mm Hg
    • below a MAP of 50 mm Hg, CBF declines significantly; above a MAP of 160 mm Hg, CBF increases significantly
    • autoregulation is often severely disturbed in head-injured patients

Classification of Injuries

  1. Glasgow Coma Scale

    2. Glasgow Coma Scale
  2. Severity of Injury
    • GCS score is used to quantify neurological findings and allows uniformity in description of patients with head injury
    • coma is defined as the inability to obey commands, utter words, and open the eyes
    • severe head injury (coma) is defined as a GCS score between 3 and 8
    • moderate head injury is a GCS score between 9 and 13
    • mild head injury is a GCS score of 14 and 15

  3. Types of Injury
    1. Skull Fractures
      • may be seen in the calvaria or skull base, may be open or closed, linear or stellate, depressed or non-depressed
      • basal skull fractures require CT scanning with bone windows for identification
      • clinical signs of a basal skull fracture include periorbital ecchymosis (raccoon eyes), retroauricular ecchymosis (Battle’s sign), CSF leaks (rhinorrhea, otorrhea), and VIIth nerve palsy
        • Basilar Skull Fracture
      • a linear skull fracture increases the risk of intracranial hematoma by 400 times in a conscious patient and by 20 times in an unconscious patient
      • depressed skull fractures require surgical elevation when the fragments are depressed more than the thickness of the skull
      • open skull fractures also require surgical repair since the dura is often torn, resulting in a direct communication between the skin and cerebral surface

      Depressed Skull Fracture
    2. Focal Intracranial Lesions
      1. Epidural Hematoma
        • relatively uncommon (0.5% of all head-injured patients, 9% of comatose patients)
        • most often located in the temporal or temporoparietal region
        • most commonly results from a torn middle meningeal artery as a result of a skull fracture
        • 1/3 result from venous bleeding (torn venous sinuses)
        • have a lenticular shape on CT scan
        • patients may present with the classic lucent interval followed by rapid deterioration (‘talk and die’)
        • if recognized and treated early, prognosis is usually excellent because direct damage to the underlying brain is often limited

        Epidural Hematoma
      2. Subdural Hematoma
        • much more common than epidural hematomas (30% of severe head injuries)
        • typically occurs as a result of tearing of the bridging veins between the cerebral cortex and draining venous sinuses
        • usually covers the entire surface of the cerebral hemisphere
        • prognosis is much worse than for epidural hematomas because the underlying brain injury is usually more severe

        Subdural Hematoma
      3. Cerebral Contusions and Hematomas
        • often associated with subdural hematomas
        • most occur in the frontal and temporal lobes
        • occur as a result of the brain hitting the undersurface of the skull
        • small contusions may coalesce into larger hematomas
        • large hematomas may require surgical evacuation because of mass effect

        Cerebral Contusion
    3. Diffuse Brain Injuries
      • represent a continuum of brain damage produced by increasing amounts of acceleration-deceleration forces
      • most common type of head injury

      1. Mild Concussion
        • consciousness is preserved, but there is temporary neurological dysfunction (confusion, disorientation without amnesia)
        • syndrome is completely reversible

      2. Classic Concussion
        • results in a loss of consciousness
        • patients return to full consciousness within 6 hours
        • accompanied by posttraumatic amnesia
        • most patients have no sequelae other than amnesia for the event
        • some patients develop post-concussion syndrome and have long-lasting neurologic deficits (memory difficulties, dizziness, nausea, anosmia, depression)

      3. Diffuse Axonal Injury
        • prolonged posttraumatic coma that is not due to a mass lesion or ischemic insult
        • caused by a shearing injury to the axons
        • head CT scan may appear normal
        • recovery is difficult to predict and patients often remain severely disabled, if they survive

Management of Head Trauma

  • CT scan should be obtained on all head injury patients who report any loss of consciousness, amnesia to the event, confusion, or severe headache

  1. Mild Head Injury (GCS 13 – 15)
    • 80% of patients with head injury fall into this category
    • patients are awake, but may report brief loss of consciousness or disorientation, amnesia to the event, or severe headache
    • GCS 13: 25% have CT evidence of trauma, and 1.3% will require neurosurgical intervention
    • GCS 15: 10% have CT evidence of trauma, and 0.5% will require neurosurgical intervention
    • patients who are awake/alert, asymptomatic, with no neurologic deficits may be discharged, ideally to a companion who can observe them for another 24 hours
    • patients who are symptomatic, or who have CT abnormalities, should be admitted and have a neurosurgery consult

  2. Moderate Head Injury (GCS 9 – 12)
    • patients are able to follow simple commands but usually are confused or somnolent
    • may have focal deficits such as hemiparesis
    • ~ 10% to 20% of patients deteriorate and lapse into coma
    • 40% of patients will have an abnormal CT scan and 8% will require surgery
    • patients should be admitted to the ICU and have frequent neuro status checks
    • follow up CT in 24 hours, or any time that there is a change in neuro status
    • avoid hypotension, hypoxia, hypoventilation

  3. Severe Head Injury (GCS 3 – 8)
    1. ABCDE
      1. Airway and Breathing
        • brain injury is worsened by secondary insults (hypoxia, hypotension)
        • securing a definitive airway is mandatory
        • patient should be ventilated with 100% FiO2
        • hyperventilation should be used cautiously and only when neurologic deterioration has occurred
        • aim for a PCO2 of 35 mm Hg initially

      2. Circulation
        • hypotension should be corrected with aggressive use of isotonic fluids and blood products
        • aim for an SBP ≥ 100 mm Hg
        • hypotension is assumed to be the result of severe blood loss, not the head injury
        • every patient should undergo FAST exam to eliminate an abdominal source of bleeding
        • if the patient remains hypotensive, then correction of the hypotension (laparotomy, thoracotomy) takes precedence over the neurological evaluation
        • if the patient becomes hemodynamically stable after resuscitation, then the first priority is a head CT scan

      3. Neurological Exam
        • rapid minineurologic exam (GCS score, pupillary light response, focal deficit) is performed once the patient’s cardiopulmonary status has been stabilized
        • alcohol, drugs can confound the neurologic assessment
        • exam should be done prior to sedating or paralyzing the patient, if possible
        • long-acting paralytic agents should be avoided
        • motor responses can be elicited by nail bed or nipple pressure
        • multiple serial exams should be performed in order to detect deterioration as early as possible

    2. Diagnostic Procedures
      • emergency CT scan of the head must be obtained as soon as possible
      • the important CT findings are the presence of an intracranial hematoma, contusions, midline shift (mass effect), obliteration of the basal cisterns
      • a shift of 5 mm or greater usually indicates that surgery is needed

    3. Nonsurgical Management of Severe Head Injury
      1. IV fluids
        • goal is to maintain normovolemia
        • both dehydration and volume overload are harmful to the head-injured patient
        • hypotonic fluids should be avoided
        • must monitor serum sodium concentration (avoid hyponatremia, which can worsen brain edema)
        • avoid glucose-containing fluids, since hyperglycemia is harmful to the injured brain
        • normal saline or lactated Ringer’s should be used for resuscitation

      2. Correction of Anticoagulation
        • reversal of aspirin and Plavix will require platelets and/or DDAVP
        • Coumadin reversal will require vitamin K and/or prothrombin complex concentrate (PCC, Kcentra)
        • heparin and Lovenox may be reversed with protamine
        • direct thrombin inhibitors (dabigatran, Pradaxa) can be reversed with idarucizumab (Praxbind)
        • factor Xa inhibitors (Xarelto) may be partially reversed with PCC

      3. Hyperventilation
        • should be used cautiously
        • ↓ PCO2 → ↑ cerebral vasoconstriction → ↓ intracranial volume → ↓ ICP
        • however, too aggressive or prolonged hyperventilation can cause cerebral ischemia by causing severe cerebral vasoconstriction
        • PCO2 should be kept at 35 mm Hg
        • brief periods of hyperventilation (PCO2 between 25 to 30 mm Hg) can be used for acute neurological deterioration until other treatments are initiated (surgery, e.g.)
        • PCO2 > 45 should also be avoided, since it leads to cerebral vasodilation and increased ICP

      4. Mannitol
        • used to reduce ICP by causing an osmotic diuresis
        • should not be given to a hypotensive patient since it can worsen hypovolemia and cerebral ischemia
        • given as a 1 g/kg IV bolus
        • lasix is often used in conjunction with mannitol

      5. Hypertonic Saline
        • concentrations of 3% to 23.4% are used
        • may be preferable in hypotensive patients, since it does not act as a diuretic
        • no evidence that it is superior to mannitol in lowering ICP

      6. Barbiturates
        • effective in reducing ICP refractory to other methods
        • since they can cause hypotension and cardiovascular depression, they should not be used during resuscitation or in any hypotensive patient

      7. Anticonvulsants
        • 15% of patients with severe head injury develop posttraumatic epilepsy
        • prophylactic anticonvulsants reduce the incidence of seizures in the first week of injury but not thereafter
        • acute seizures must be controlled with anticonvulsants as soon as possible, since prolonged seizures may cause secondary brain injury

      8. Steroids
        • no beneficial effect in reducing ICP or improving outcome from severe head injury

    4. Emergency Surgical Management
      1. Depressed Skull Fractures
        • will require elevation when the depth of depression is greater than the thickness of the skull
        • open skull fractures will require irrigation, debridement, dural closure, and prophylactic antibiotics
        • for less severe skull fractures, closure of the overlying scalp laceration is indicated

      2. Intracranial Mass Lesions
        • if a neurosurgeon is not available, the patient should be transferred as soon as possible to a hospital with a neurosurgeon
        • A CT scan is not required before transfer to definitive care
        • if an intracranial hematoma is imminently life-threatening and there is no time for transfer, emergency craniotomy or burr holes may be considered if someone adequately trained in the procedure is available
        • emergency procedures should only be done with the advice and consent of a neurosurgeon
        • bone flap craniotomy is the definitive lifesaving procedure
        • the burr hole should be placed on the side of the larger pupil

      3. Penetrating Brain Injuries
        • CT scanning is strongly recommended
        • when the trajectory is near the skull base or a major dural venous sinus, or if there is substantial subarachnoid hemorrhage, then vascular imaging should be considered
        • prophylactic antibiotics are appropriate

    5. Brain Death
      1. Clinical criteria
        • GCS = 3
        • nonreactive pupils
        • absent brainstem reflexes (corneal, gag)
        • no spontaneous ventilation during formal apnea testing
        • absence of hypothermia or drug intoxication

      2. Ancillary Tests
        • no EEG activity
        • no cerebral blood flow (Doppler studies, angiography)







References

  1. ATLS Student Manual, 10th ed., pgs 102 - 126
  2. Cameron, 11th ed., pgs 1001 - 1005