Neurosurgery Case 1

Case 1 : Diagnosis and Management of Head Trauma III – Section D Group 3 November 29, 2006

Sindiong, Robertito Paolo Sio, Cherry Ann Sison. Lincoln So, Imee T Solis, Ma. Rachelle So- Reyes, Jamil Laurence Sto. Domingo, Braulio II Suller, Armida

GT, a 22 year old male, while walking along Gov. Forbes St., was side swept by a speeding 10wheeler truck. He was seen by bystanders and was immediately brought to STUH. At the emergency room, vital signs were as follows: BP 110/70, PR 95/min, RR 20/min. A 5 cm laceration was noted over the left temporal area, and multiple abrasions and lacerations over the face and extremities. He was noted to be confused, with spontaneous eye opening, and localizes upon painful stimuli. Pupils were 2mm, equally reactive to light.

The surgical intern on duty immediately inserted an IV line. A plain skull x- ray was then requested, which revealed a linear fracture over the left temporal area. On the way back, he was noted to be less responsive. The left extremity withdraws to pain, while the right was noted to be in extended position. There was eye opening on painful stimuli and no verbal output. Pupils: 3mm RTL, 5mm nonreactive left.

1. Discuss the classification of head injury

Mild head injury - GCS 13 - 15 Moderate head injury – GCS 9 – 12 Severe head injury – GCS 3 – 8

Classification of head injury Penetrating head injury – the dura is pierced Compressive head injuries – the skull is compressed between two forces - massive injury that usually results in instantaneous death

Classification of head injury Closed or Blunt head injuries - Major problem in civilian life - Head is suddenly accelerated or decelerated as a result of a non-penetrating blow - Dura remains intact

Concussion • Temporary neuronal dysfunction after nonpenetrating trauma • CT scan normal • Memory difficulties common • Brain in hypermetabolic state • Second impact syndrome – Brain more susceptible to trauma in 1st 1-2 weeks

Concussion Colorado medical society system • Grade 1 – head trauma patients with confusion • Grade 2 – patients with amnesia • Grade 3 – patients who lose consciousness

Contusion • • • •

Bruise of the brain Breakdown of small vessels Bright on CT scan Small amounts of blood in injured parenchyma • Edema may develop causing mass effect

Contusion • Enlarge or develop into true hematoma • Contre coup injury – Contusions in brain tissue opposite site of impact – Decelerations of brain against skull

Diffuse axonal injury • Damage to axons due to rotational acceleration and then deceleration • Axons may completely be disrupted and retract forming axon balls • MRI – hemorrhage, usually in corpus callosum and dorsolateral midbrain

Penetrating injury Subtypes • Missile (bullets and fragmentation devices) • Nonmissile (knives and ice picks) • X-ray and CT scan • Cerebral angiography considered if object passes near a major artery or dural venous sinus

Penetrating injury • Operative exploration necessary to remove objects sticking out of the cranium • Debridement, irrigation, hemostasis, and closure • Small object w/in brain parenchyma often left alone

Penetrating injury • High-velocity weapons create shockwave that destroys surrounding tissue • Patient treated w/ antibiotics

1. Differentiate primary brain injury from secondary brain injury.

Primary Brain Injury • also Impact damage • the initial injury to the brain as a direct result of the trauma • sudden and profound injury to the brain that is considered to be more or less complete at the time of impact • occurs at the time of the car accident, gunshot wound, or fall • instantaneous onset

Primary Brain Injury • from blow, acceleration, deceleration, or rotation of the brain when it is slammed back and forth on bony prominences inside the skull

Primary Brain Injury • Clinical effects: – immediate – maximal – irreversible – e.g. concussion, contusion, acute subdural hematoma, diffuse axonal injury

Secondary Brain Injury • refers to the changes that evolve over a period of time (from hours to days) after the primary brain injury • any subsequent injury to the brain after the initial insult • can result from systemic hypotension, hypoxia, elevated ICP, or as the biochemical result of a series of physiologic changes initiated by the original trauma

Secondary Brain Injury • includes an entire cascade of cellular, chemical, tissue, or blood vessel changes • contribute to further destruction of brain tissue • Complication of primary injury

Secondary Brain Injury • Clinical effects: – – – –

delayed progressive preventable e.g. dec cerebral perfusion, inc ICP, cerebral edema, hypoxemia, circulatory shock – hypoxia, ischemia, brain swelling, infection, hematoma

Brain edema

3. Explain and assign the Glasgow Coma Scale

Glasgow Coma Scale Glasgow coma scale  Conscious level assessment  Used to determine deterioration or improvement in patient’s condition  Developed in 1974 by Teasdale and Jennett in Glasgow, England

Motor Response 6 – follows commands 5 – localizes 4 – withdraws 3 – decorticate 2 – decerebrate 1 – no response

Glasgow Coma Scale Eye Opening 4 – spontaneous 3 – to voice 2 – to pain 1 – no eye opening

Verbal Response 5 – oriented 4 – confused 3 – inappropriate 2 – incomprehensible 1 – no sound

In our patient’s case… AT THE E.R. Motor: localizes pain on painful stimuli (5) Eye opening: spontaneous eye opening (4) Verbal: confused (4) Total: 13 (Moderate)

ON THE WAY BACK… Motor: L withdraws to pain, R extended (4) Eye opening: eye opening on painful stimuli (2) Verbal: no verbal output (1) Total: 7 (Severe)

Total = M+V+E = 3-15 • Severity – Mild – Moderate – Severe

GCS 14-15 9-13 3-8

Death/Vegetative 5% 27%-54% 54%-80%

***Should always have a high index of suspicion for cervical spine injury and other multiple injured organs

4. Discuss the presentation of brain herniation syndromes in the setting of trauma.

Monro - Kellie doctrine • Total intracranial volume is fixed because of the inelastic nature of the skull Vi/c = V (brain) + V (CSF) + V (blood) • ~ 1500 ml – 85- 90% brain – 10% intravascular cerebral blood volume – <3% CSF

Compliance • Based on the pressure volume index within the intracranial vault Compliance = change in volume change in pressure

Intracranial compliance Head injury Cerebral edema Increase relative volume of the brain Pressure within the skull rises Herniation

Intracranial compartment • Divided into 3 compartments by 2 major dural structures: 1. Tentorium cerebelli – supra (cerebral hemispheres) and infratentorial (brainstem and cerebellum) compartments

2. Falx cerebri – divides the supratentorial compartment into left and right hemispheres

Herniation • Displacement of a portion of the brain from its normal compartment into another one • Terminal event: ischemia  infarction • Types of herniation syndromes: 1. Uncal or transtentorial 2. Cingulated or subfalcine 3. Central transtentorial herniation 4. Tonsillar herniation

Uncal / Transtentorial Herniation • Most dramatic and most common herniation syndrome • Herniation of the inferomedial part of the temporal lobe (uncus) into the tentorial notch • Progressively impaired consciousness, anisocoria (ipsilateral), hemiplegia & hemiparesis (contralateral) • Compress third cranial nerve

Cingulated / Subfalcine Herniation • Cingulate gyrus on the medial aspect of the frontal lobe is displaced across the midline under the free edge of the falx • may compromise blood flow through the anterior cerebral artery complexes • Headache, weakness of the lower extremities (contralateral), NO anisocoria • Can occur in conjunction with transtentorial herniations

Central Herniation • Downward displacement of the diencephalons and midbrain centrally thru the tentorial incisura • May cause significant upper brainstem compression • bilaterally small reactive pupils, CheyneStokes respirations, loss of vertical gaze, bilateral arm dysesthesia, obtundation

Tonsillar herniation • Results from acute expansion of posterior fossa lesions • cerebellar tonsils herniate thru the foramen magnum into the upper spinal canal, compressing the medulla and upper cervical spinal cord • cardiorespiratory arrest, hypertension, CheyneStokes respiration, neurogenic hyperventilation, impaired consciousness, pposturing problems • worst prognosis

Patient • GCS of 7 (severe head injury) • Linear fracture on L temporal area • L = withdraws to pain, R = extended (decerebrate) • No verbal output • Pupils  R = 3mm RTL, L = nonreactive (anisocoric)

Uncal or Transtentorial Herniation

Anisocoria Uncal herniation Ipsilateral compression of the oculomotor nerve Dysfunction of the parasympathetic fibers Unopposed sympathetic response LIGHT Ipsilateral dilated pupil

Contralateral hemiparesis / hemiplegia Uncal herniation Compression of the ipsilateral cerebral peduncle Signals traveling through the cortical & spinal tracts unable to decussate Contralateral hemiparesis / hemiplegia

5. Differentiate cerebral concussion, contussion, and diffuse axonal injury

Concussion • A concussion occurs when the head hits or is hit by an object, or when the brain is jarred against the skull, with sufficient force to cause temporary loss of function in the higher centers of the brain • Diffuse type of brain injury

Concussion

Concussion • Symptoms of concussion include: – – – – – – – – – – –

headache disorientation as to time, date, or place confusion dizziness vacant stare or confused expression incoherent or incomprehensible speech incoordination or weakness amnesia for the events immediately preceding the blow nausea or vomiting double vision ringing in the ears

Contusion • Condition in which direct parenchymal injury of the brain has occurred through transmission of kinetic energy of the brain and bruising analogous to what is seen in soft tissues • Caused by the brain hitting the interior of the skull

Contusion • Coup contusion – minimal injury underlying the point of contact

• Countercoup contusion – occur at the area of the brain opposite to the blow – may show extensive damage

• Histologically indistinguishable

Contusion

contact → tissue displacement → disruption of vascular channels → hemorrhage → tissue injury and edema

Contusion • Signs and symptoms include – Severe headache – Dizziness – Vomiting – Increased size of one pupil or sudden weakness in an arm or leg – Restlessness, agitation or irritability – Memory loss or forgetfulness

Contusion CT Scan

Diffuse Axonal Injury • Results from high speed injury with stretching or shearing of brain tissues • Radiographically shows petechial hemorrhages in white matter tracts • Characterized by axonal separation • Secondary biochemical cascades are largely responsible for the damage to axons

Diffuse Axonal Injury

Diffuse Axonal Injury • The major cause of damage in DAI is the tearing of axons • Treatment is aimed at managing swelling in the brain because torn axons can not be repaired.

Diffuse Axonal Injury

Acceleration causes shearing injury, which refers to damage inflicted as tissue slides over other tissue

6. Differentiate Acute Subdural Hematoma and Acute Epidural Hematoma

Acute Epidural Hematoma  A collection of blood between the cranium and dura  Usually arterial in origin esp resulting from laceration of the middle meningeal artery associated with a fracture in the squamous portion of the temporal bone

Acute epidural hematoma

Acute Epidural Hematoma • Triphasic with a : -mild head injury leading to a transient alteration of consciousness followed by -a “lucid interval” where patient regained consciousness or is relatively symptom free, followed by -obtundation, focal deficit, ipsilateral pupillary dilatation • Consciousness is lost again when the expanding epidural hematoma compress the brain to produce focal deficit or inc ICP

Subdural hematoma • Blood collections in the potential space between the dura and the arachnoid • Usually venous in origin

Subdural hematomas • Subdural hematomas are most often caused by head injury, when rapidly changing velocities within the skull may stretch and tear small bridging veins. • subdural hemorrhages generally result from shearing injuries due to rotational or linear force

Subdural hematoma

3 Classifications of Subdural Hematoma • Acute Subdural Hematoma (1-2 days) • Subacute Subdural Hematoma (3-21 days) • Chronic subdural hematoma (>21 days)

Acute Subdural Hematoma • Usually present as an evolving intracranial mass • Collection of blood is usually small in amount but usually accompanied by severe brain contusion leading to severe brain edema

7. Discuss the management of increased intracranial pressure in head trauma.

Increased intracranial pressure in head trauma • Continuous recording of intracranial pressure must be achieved. • ICP monitors employs fiberoptic strain gauges that can be inserted directly to the cerebral cortex.

Increased intracranial pressure in head trauma • Pressure measurement through a lumbar puncture is not done because it does not reflect accurately the ICP and there is an increased risk of cerebellar or temporal lobe herniation.

Increased intracranial pressure in head trauma • The first step in lowering the high ICP is to control the factors that are know to raise the pressure such as hypoxia, hypercarbia, hyperthermia, awkward head positions, and high mean airway pressures.

If ICP exceeds 15-20 mmHg: • induce hypocarbia by controlled ventilation (pCO2 at 28 to 33 mmHg) • induce hyperosmolar dehydration (0.25 to 1.0g of 20% mannitol q 3-6hrs or 0.75 to 1 mg/kg of furosemide) to maintain serum sodium above 138 meq/L

If ICP exceeds 15-20 mmHg: • intravenous fluids with free water should be avoided so as not to intensify cerebral edema • fluids such as 5% dextrose in water, 0.5% saline, and 5% dextrose in 0.5% saline are therefore avoided • lactated Ringers solution is permissible but normal saline, with or without added dextrose is ideal

To avoid severe hypertension: use the following: • Diuretics • beta-adrenergic blocking agents • angiotensin converting enzyme inhibitors (should be used rather than agents that dilate the cerebral vasculature)

To avoid severe hypotension: • vasopressor agents such as neosynephrine is used

8. Discuss the principles of management of open skull fracture, closed skull fracture, basal skull fracture and CSF leak.

Open Skull Fracture • Have either a skin laceration over the fracture or the fracture runs through the paranasal sinuses and the middle ear structures, resulting in communication between the external environment and the cranial cavity • Involve a fracture or penetration of the bones of the skull • May be clean or contaminated/dirty

Closed Skull Fracture • Do not penetrate the bones of the skull. • Occur from a hard blow or impact that jars the brain within the skull. The rapid movement of the brain within the skull can: o Cause bruising, swelling, or tearing of the brain tissue. o Stretch, pull apart, or tear nerves or blood vessels,causing bleeding within or around the brain. • Can be more difficult to identify because there may not be visible signs of injury, such as bleeding or deformity.

Both open and closed head injuries may cause: • A concussion • A brain bruise (contusion) • Bleeding within or around the brain, a lifethreatening injury. Symptoms of this type of injury may be the same as those of a concussion. More serious symptoms usually develop within 24 hours after the injury. In rare cases, if the bleeding is slow, symptoms take longer to develop.

Imaging Studies • Skull X-ray - fracture at the vertex • CT scan - standard modality for aiding in the diagnosis of skull fractures • MRI - for suspected ligamentous and vascular injuries

Skull X-ray films - who needs them? • • • •

Impaired consciousness or neurological signs. History of loss of consciousness, amnesia, or fits. High speed injury or suspected penetrating injury. Scalp laceration to bone, large haematoma, or suspected fracture on palpation. • Persisting vomiting or headache. • Loss of cerebrospinal fluid or blood from ear or nose. • Difficulty in assessing the patient (children, drug or alcohol intoxication). The Society of British Neurological Surgeons. Guidelines for the initial management of head injuries: recommendations form the Society of British Neurological Surgeons. Br J Neurosurg 1998;12(4):349-52.

Indications for computed tomography scanning

• Persistent coma after resuscitation. • Deteriorating Glasgow coma score or progressive neurological signs. • Skull fracture if associated with (1) impaired consciousness, (2) fits, (3) neurological symptoms or signs. • Open skull fractures (including fractured base of skull).

The Society of British Neurological Surgeons. Guidelines for the initial management of head injuries: recommendations form the Society of British Neurological Surgeons. Br J Neurosurg 1998;12(4):349-52.

Treatment Open fracture  careful irrigation and debridement  broad-spectrum antibiotics + tetanus toxoid  wound exploration in the operating room under direct vision to prevent loose pieces of bone from damaging the underlying brain  repair of dural sinus tear  bony segments reassembled  if depressed: prophylaxis for posttraumatic seizures

Treatment Closed fracture  elevation depressed skull fractures if the depressed segment is more than 5 mm below the inner table of adjacent bone  repair of venous sinus tear  if depressed: prophylaxis for posttraumatic seizures

Basal Skull Fracture • a linear fracture involving the base of the skull • usually associated with a dural tear and is found at specific points on the skull base • commonly involve the roof of the orbits, the sphenoid bone, or portions of the temporal bone

Basal Skull Fracture Temporal fracture • encountered in 75% of all skull base fractures • 3 subtypes: 1. Longitudinal fracture 2. Transverse fracture 3. Mixed

Basal Skull Fracture Occipital condylar fracture • results from a high-energy blunt trauma with axial compression, lateral bending, or rotational injury to the alar ligament

Basal Skull Fracture Clinical Manifestations: • Battle's sign - ecchymosis of the mastoid process of the temporal bone (petrous temporal bone fractures) • Raccoon eyes - periorbital ecchymosis i.e. "black eyes" (anterior cranial fossa fractures) • Cerebrospinal fluid rhinorrhea and/or rhinorrhea • Cranial nerve palsy • Bleeding from the nose and ears

Basal Skull Fracture

Basal Skull Fracture • CT scan • Conservative management • No antibiotic prophylaxis needed

CSF Leak

• CSF leak is an escape of the fluid that surrounds the brain and spinal cord, from the cavities within the brain, or from the central canal in the spinal cord. • Head injury: rhinorrhea or otorrhea

Management Preoperative investigations • Coronal high definition CT scan -

fracture site

• CT cisternography -

precise location of the CSF leak

• CSF isotope infusion studies with platelet insertion into the nasal cavities

Management • Most traumatic CSF leaks resolve spontaneously; the majority resolve within the first 24 to 48 hours. • CSF rhinorrhea: Conservative management consists of a 1- to 2-week trial of bed rest with the patient in a head-up position. • CSF otorrhea secondary to recent surgery or trauma can often be treated conservatively with a compressive dressing and bed rest with head elevation. • If conservative management fails: Surgical repair

Management • If conservative management fails: surgical repair - rhinorrhea: intracranial or extracranial approach - otorrhea: subtemporal approach

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