Head Injury 2

Traumatic Brain Injury (Ⅱ ) Department of Neurosurgery,The First Affiliated Hospital of Zhengzhou University Xu Bin

Classification The

primary brain injury (1) Concussion (2) Contusion and laceration  The secondary brain injury (1) Brain edema (2) Intracranial hematoma

BRAIN INJURY Primary injury results at the time of impact;secondary injury is progressive brain damage arising as a consequence of hematoma,edema formation,ischemia or hypoxia damage leading to later and progressive neurological deficits.

A.Concussion:concussion is a clinical diagnosis and is manifested by temporary dysfunction that is most severe immediately after injury and clears within 24 hours.It may be accompanied by a variety of autonomic abnormalities,including bradycardia,hypotension and sweating.

A concussion may result when the head strikes against an object or is struck by an object.Concussions may produce unconsciousness or bleeding in or around the brain.

Clinical findings 1.A transient disturbance of consciousness following head injury.It less than 30 minutes. 2.A post-traumatic amnesia. 3.Giddiness,headache, dizziness. 4.CT scan is normal.

Loss of consciousness often but not invariably accompanies concussion.Amnesia for the event is common and variable degrees of temporary lethargy,irritability and memory dysfunction are hallmarks of cerebral concussion.

Because concussion is not a fatal injury,data from pathologic examination (necropsy) are sparse;there is either no demonstrable damage or only minor inflammation of the white matter.

B.Cerebral Contusion:Cerebral contusion can be demonstrated by CT scan as small areas of hemorrhage in the cerebral parenchyma.Contusions usually produce neurological deficits that persist for longer than 24 hours.Extravasation of red cells into gray and white matter can be demonstrated in fatal cases.

Craniocerebral trauma is the most common cause of subarachnoid hemorrhage and blood is present in the cerebrospinal fluid in many patients(although lumbar puncture should not be done after a head injury).

Focal neurological deficits may include weakness,speech disorders,memory or affect abnormalities or rarely visual dysfunction. Cerebral contusion may resolve with the disappearance of neurological deficits or focal or global deficits may persist.Blood-brain barrier defects and cerebral edema are common with cerebral contusion.

Frontal contusions on head CT scan image (arrow)

A head injury of sufficient force to bruise the brain. The bruising of the brain will often involve the surface of the brain and cause an extravasation of blood without rupture of the pia-arachnoid. Often associated with a concussion.

Brain contusion

C.Laceration: Even without skull fracture,if sufficient force is delivered to the skull,the brain may be lacerated as a result of rapid movement and shearing of brain tissue.The pia and arachnoid overlying the surface of the brain may be torn and accompanying laceration of blood vessels results in intracerebral hemorrhage.

Focal neurological deficits are the rule and a neurological deficit will often be permanent,although considerable improvement can occur with time.

D.Diffuse Axonal Injury Diffuse white matter injury is associated with anatomic disruption of axons throughout both cerebral hemispheres.This primary shearing injury is associated with high mortality and substantial neurological morbidity.It results from rotational forces that are perpendicular to the axis of the white matter,causing axonal transection.

Diffuse Axonal Injury

The brain is a complex network of interconnections. Critical nerve tracts can be sheared and stressed during an accelerationtype of injury.

Diffuse axonal injury is a very serious injury, as it directly impacts the major pathways of the brain.

Despite severe shearing injury,the brain may appear grossly normal,but numerous axonal transections are seen microscopically in white matter within two weeks of injury.Classically,small hemorrhages are present in the corpus callosum and cerebral peduncles on CT scan.Fiber tract demyelinization subsequently develops,extending throughout the cerebral hemispheres and into the brainstem.

Diagnosis Triage of head-injury patients must be accurate and rapid.Injuries can range from minor impact without loss of consciousness to severe coma-producing fatal head injury.Successful management demands careful data gathering so that a rational course can be planned.

It must include a rapid categorization of hemispheric and brain stem function so that changes in subsequent examinations will indicate improvement or deterioration of the patient and help direct further management.

ASSESSMENT  Special

Tests – Pupillary response – PEARL – Visual acuity – Eye chart – Ophthalmoscope – Back of eye (retina, blood vessels)

This is particularly valuable in that it can be repeated by various observers at different times and reliably indicate change in the patient’s status.The sum of eye opening,motor response and verbal response scores is known as the Glasgow Coma Score,a system widely used to evaluated head-injured patients.

Glasgow Coma Scale

Differential diagnosis In the absence of an adequate history,unconsciousness may result from a wide variety of structural or metabolic lesions.Most head injury is attended by some abnormality of the scalp such as abrasions or subgaleal hematomas.However,in a few patients there is no external evidence of injury and a variety of causes must be considered.

Coma,hemiplegia and eye deviation pius evidence of chronic hypertension(funduscopic changes,cardiomegaly) suggest a hypertensive intracerebral hematoma.Obtundation,fever and a stiff neck suggest meningitis,either bacterial or perhaps chemical,from spontaneous subarachnoid hemorrhage.

These constitute the only indication for lumbar puncture;if focal findings are present,the lumbar puncture should be preceded by a CT scan.If cerebral infection is clinically likely,antibiotics can be stared before diagnostic studies.Diabetic,renal or hepatic causes of coma can be diagnosed with appropriate blood test.

Diagnosis ＆ Management of Depressed States of Consciousness Definitions The clinical definition of consciousness ranges from alert wakefulness to deep coma.An alert,wakeful patient responds immediately and appropriately to all stimuli.A stuporous patient responds only when aroused by vigorous stimulation.

Coma implies failure to respond to stimulation.Most cases of depressed states of consciousness lie between these extremes and are best categorized by accurate descriptions of their responses to specific stimuli-eg,auditory,visual and tactile(touch or pain).

Diagnostic Possibilities Depressed states of consciousness may be due to many causes.Trauma is usually obvious,both on the history and on examination of the patient.Metabolic disorders(eg,diabetes mellitus,uremia,poisoning,electrolyte imbalance,hypoxia) may similarly alter the state of consciousness.

In addition to an accurate history and physical examination,laboratory investigations are required to establish a diagnosis of metabolic coma. Patients with intracranial neoplasms may be alert,comatose or at any level of consciousness in between.A progressive,unrelenting history is a valuable criterion of this initial diagnosis.

Central nervous system infections (eg,encephalitis,meningitis) are usually accompanied by systemic signs of infection and a progressively worsening course.Cerebral abscess,on the other hand,behaves more like an expanding neoplasm than a fulminating infection.

Vascular occlusions(emboli,thrombosis) usually cause abrupt neurological deficits without grossly impaired consciousnesss,whereas cerebral hemorrhage typically causes abrupt coma with profound neurological deficits.

Conversely,subarachnoid hemorrhage may occur without any alteration of wakefulness.Degenerative,dementing illness that dull consciousness but characteristically do not produce coma.

Diagnostic Tools Laboratory and radiographic tests help to establish the clinical diagnosis.Routine examination should introduce a complete blood count,urinalysis,plasma glucose,blood urea nitrogen and serum electrolytes.Cerebrospinal fluid analysis is an essential step toward diagnosis of meningitis or subarachnoid hemorrhage.

Lumbar puncture is rarely helpful in the assessment of head trauma and probably is contraindicated during the initial workup after injury. Most patients with depressed consciousness should undergo CT scanning or MRI to establish the presence or absence of an intracranial mass lesion.Appropriate therapy depends on the early recognition of the specific intracranial problem.

Complications Primary cerebral injuries cause cell death or dysfunction on impact.Because many of these injuries are the result of traffic accidents.Secondary injuries arise as a result of brain and body changes after the impact.

A.Hemorrhage: Head injury can cause bleeding into the epidural,subdural or subarachnoid spaces or intracerebrally into brain tissues.Epidural and subdural hematomas are discussed below.

Impact between brain and adjacent bone can result in vascular disruption and focal hemorrhage into the cortex or subcortical white matter.This may cause local brain cell death and often results in marked local cerebral edema.Even without a definite intracerebral hematoma,areas of contusion can create a mass effect and even herniation in severe cases.

Subarachnoid hemorrhage is common and occasionally impedes cerebrospinal fluid drainage,requiring shunting procedures in a few patients. Subdural hygromas are accumulations of cerebrospinal fluid or cerebrospinal fluid mixed with a small amount of blood.

They arise when fluid escapes through a tear in the arachnoid into the subdural space.They can create a focal mass effect and may have to be evacuated through bur holes.

B.Traumatic Vascular Malformations: A carotid cavernous fistula may arise if the cavernous portion of carotid artery is lacerated by a fracture of the sphenoid bone,causing a major arteriovenous communication.

Symptoms may be delayed for a month or more following injury and are often heralded by progressive retro-orbital pain followed by chemosis and proptosis of one or both eyes.Papilledema and engorgement of the retinal veins are usually present.These lesions generally can be cured.

C.Cerebrospinal Fluid Leak: Basal skull fractures involving paranasal sinuses may result in cerebrospinal fluid rhinorrhea or otorrhea,which is indicated by a mixture of clear fluid and blood coming from the nose or ear.

Cerebrospinal fluid leak may not be readily apparent soon after the injury.Measurements of the glucose content of the fluid are inaccurate because both nasal secretions and blood contain sufficient amounts of glucose to give a positive test.

When a drop of fluid is placed on filter paper,a double ring (“halo test”) will appear if cerebrospinal fluid is mixed with blood;blood alone usually gives a single red circle.

Because cerebrospinal fluid otorrhea or rhinorrhea may be accompanied by meningitis or brain abscess formation,leakage of the fluid must be stopped.If meningitis occurs,the most likely causative organisms are Haemophilus influenzae,Streptococcus pneumoniate or other streptococci,all of which are common inhabitants of the paranasal sinuses.

D.Cranial Nerve Palsy: The olfactory nerves can be torn at the cribriform plate:traumatic anosmia seldom resolves.Immediate optic nerve loss following head injury is almost always permanent;however,if progressive loss of vision develops,optic nerve decompression or administration of corticosteroids may result in partial recovery of vision.

Palsies of the third,fourth and sixth cranial nerves usually improve,although partial deficits may persist.Facial nerve palsies after temporal bone fracture may require decompression and repair of injured seventh cranial nerve.Delayed facial palsies are common and usually resolve without operation.Lower cranial nerve palsies are uncommon.

THIRD CRANIAL NERVE PALSIES Partial to complete weakness of the muscles innervated by the 3rd (oculomotor) nerve, resulting in ptosis of the lid, mydriasis, and an outwardly turned eye during primary gaze.  When the patient attempts to turn the eye inward, it moves slowly only to the midline. Upward and downward gaze is compromised in the affected eye. When downward gaze is attempted, the superior oblique muscle causes the eye to rotate inward.

E.Posttraumatic Syndrome: A variety of nonspecific complaints are common after head injury,the most prominent of which are headache,dizziness,easy fatigability and poor memory.Diminished ability to concentrate and emotional lability may also occur.While these symptoms might seem psychologic,electronystagmography and formal mental testing will often reveal some organic basis.

Psychologic testing has revealed significantly impaired mental function in many patients.Reassurance,mild sedatives or medical treatment for dizziness may improve the patient’s symptoms until they resolve,usually within weeks to months after surgery.

F.Post-traumatic Epilepsy: Patients may develop seizures shortly after injury,but these early seizures are generally of no consequence.However,an estimated 3-6% of patients who loss consciousness after head injury develop a more chronic seizure disorder.

Post-traumatic Epilepsy: Classification EARLY:within

one week of injury – Immediate = within 24 hours – Delayed early = within 1 day to 1 week LATE: after first week post injury

The presence of a subdural or epidural hematoma cause up to a 30% incidence of posttraumatic seizures and penetrating injuries of the brain with severe head injury may increase the frequency of seizure to as high as 50%.

The use of prophylactic anticonvulsants(eg,phenytoin,300mg/ d for adults)can prevent seizures while the patient is on medication but probably does not alter the frequency of seizures after anticonvulsants are discontinued.

Treatment A.Emergency Treatment: Head-injured patients require immediate emergency treatment,including maintenance of an airway and restoration of blood pressure.Unconscious patients should be intubated to prevent hypoxia,hypercapnia and aspiration.Shock must be vigorously treated with intravenous fluids while possible sources of hemorrhage in the chest or abdomen are being sought.

B.General Treatment: Patients who are comatose or who show rapid neurological deterioration demand immediate intervention.At most institutions,CT scan precedes surgery.At some centers,exploratory bur holes are made or craniotomy is undertaken without intracranial studies.

Hyperventilation(PCO2=25mmHg) can rapidly lower intracranial blood volume and intracranial pressure.Excessive hyperventilation(PCO2 ＜ 25mmHg) should be avoided because it may cause ischemia.

Hyperosmotic agents(Mannitol,0.51g/Kg body weight intravenously) will dehydrate normal brain within 15-20 minutes and will lower intracranial pressure.Until Corticosteroids have been shown to improve outcome from severe head injury,they should not be used routinely in management of craniocerebral trauma.

Antibiotic treatment should be initiated in patients with contaminated compound wounds,but there is no proof of efficacy in patients with basal skull fracture with or without cerebrospinal fluid leak.

Status epilepticus is uncommon following head injury.However,in severe head injury,anticonvulsant therapy should be initiated soon after injury with a loading dose of phenytoin sodium(15mg/Kg body weight intravenously) and continued for at least one week.Phenobarbital will increase a patient’s lethargy and make the neurological examination more difficult to interpret.

Progressive neurological deterioration is an indication for further diagnostic tests or exploratory surgery.

Primary Brain Injury 

Contusion and laceration of the brain Contusion and laceration are more severe forms of primary brain damage with gross structural changes. You can find the lesion on CT scan.

Clinical findings 1)A disturbance of consciousness following head injury large 30 min 2)A likelihood of neurological deficit following head injury 3)Changes of vital signs 4)CT scan may find brain edema and hematoma

Treatment of the primary brain injury Keeping

the air way unobstructed Pay attention to alteration of the vital signs, such as respiration, heartbeat, blood pressure and temperature and keep them normal

Treatment of the primary brain injury Drugs

often used: dehydration, diuretic, desamethasone and antibiotics, et al. When the cerebral herniation caused by brain edema or intracranial hematoma occurs, the operation should be done at once.

Post-traumatic sequelae 1. 2. 3. 4. 5.

Cerebral infarction Cerebral atrophy Hydrocephalus Infection CSF fistula