Head injury out line of management

Professor Panna Lal Saha

Professor of Surgery & Head Department of Surgery

BGC Trust Medical College Chittagong

Introduction
500,000 cases of head injury occur in the USA each year 10 % of these die prior reaching a hospital Of These 80% mild 10% moderate 10% severe > 20% of the head injury patients suffer varying degrees of disability

Anatomy

Anatomy
The head can be divided into the following layers: 1) Scalp. 2) Skull. 3) Meninges. 4) Brain. 5) Cerebrospinal fluid. 6) Tentorium.

Scalp
1. 2. 3. 4. 5. S : skin C : connective tissue A: aponeurosis (galea) L: loose areolar tissue P: pericranium

Bleeding from scalp laceration can result in major blood loss especially in children

Skull
It is composed of Cranial vault and base. The floor of the cranial cavity is divided into 3 parts: - Anterior fossa frontal lobe - Middle fossa temporal lobe - posterior fossa brain stem and cerebellum

Meninges
1. Dura 2. Arachnoid 3. pia
Subdural space is a potetial space exist in which hemorrhage can occur Cerebrospinal fluid circulate between the arachnoid and pia matter in the subarachnoid space

Brain
parietal

frontal

Consist of: 1) Cerebrum:

Frontal Parietal Temporal occipital

2) Cerebellum. 3) Brain stem:

Midbrain Pons medulla

occipital

temporal

Cerebrospinal Fluid
It is produced at a rate of 30 ml / hour.

Tentorium
Divide the head into: Supratentorial: Anterior fossa Middle fossa Infratentorial: Posterior fossa

Physiology

Cerebral blood flow

Normal CBF is approximately 50ml/100 g of brain/min If CBF < 20 ml/min the EEG activity will gradually disappear, and at CBF of 5ml/min cell death In normal person the Autoregulation maintain a constant CBF between MAP of 50 and 160 (mm Hg). In head injured patient its severely disturbed.
MAP < 50 mm Hg CBF declines steeply MAP > 160 mm Hg passive dilation of the cerebral vessels increase in CBF

Intracranial pressure
Several pathological processes that affect the brain can cause elevation of the intracranial pressure. ICP can have consequences that adversely affect brain function and hence the patient outcome. So elevated ICP not only indicate the presence of a problem but can often contribute to the problem
10 mm Hg - normal ICP 20 mm Hg abnormal 40 mm Hg sever elevation

Cerebral Perfusion Pressure

It can be calculated by: CPP = MAP ICP
Perfusion pressure of less than 70 mm Hg is generally associated with poor outcome following a head injury. This indicate the priority of maintaining the cerebral perfusion in the management of severe head injury patient.

Classification of head injuries

 Head injuries are classified according to:

1) Mechanism of injury. 2) severity of the injury. 3) Morphology of the injury.

1) Mechanism
This can be : 1) Blunt injury which is divided into: - High velocity(automobile). - Low velocity (fall, assult).

1) Mechanism
Penetrating injury e.g gunshot wounds or other penetrating wounds.

2) Severity
This classified according to Glasgow coma Scale into: 1) Mild (GCS score 14-15). 2) Moderate (GCS score 9-13). 3) Severe (GCS score 3-8).

Type
Eyes Open

Stimulus

Type of Response
Spontaneously To verbal command To pain No response Obeys Localized pain Flexion-withdrawal Flexion-abnormal Extension No response Oriented and converses Disoriented and converses Inappropriate words Incomprehensible sounds No response

Points
4 3 2 1 6 5 4 3 2 1 5 4 3 2 1

Best Motor Response

To verbal command To painful stimulus

Best Verbal Response

Lowest score = 3, Highest score = 15

3) Morphology
Skull Fracture

Vault

Linear vs stellate Depressed / nondepresed Open / closed With/without CSF leakage With/without nerve palsy Epidural Subdural Intracerebral Mild concussion Classic concussion Diffuse axonal injury

Basilar
Focal

Intracranial lesions

Diffuse

Skull fractures

1) Skull fractures

The significance of skull fracture should not be underestimated since it takes considerable force to fracture the skull. linear vault fracture increase the risk of an intracranial heamatoma by about 400 times in a conscious patient and by 20 in comatose patient. Fragment depressed more than the thickness of the skull require surgical elevation Open or compound skull fracture require early surgical repair

Cont
Basal skull fractures usually require CT scan with bone window The presence of clinical signs of basal skull fracture should increase the index of suspicion and help in its identification: Periorbital ecchymosis ( Raccoon eye) Retroauicular ecchymosis ( Battles sign) CSF leakage 7th nerve palsy times in comatose one.

Management

Scalp wounds
They are usually tolerated well and cause few complications. Shave the hair around the wound and clean the wound before suturing. Bleeding from a deep scalp wound usually can be controlled by applying direct pressure cauterizing or ligating large vesseles.

Depressed skull fractures

Need to be elevated if the degree of depression is greater than the thickness of the adjacent skull.
Less significant depressed fracture can safely be managed with closure of the overlying scalp laceration.

Intracranial lesions

2) Intracranial lesions
These lesions may be classified as focal or diffuse, although the two forms frequently coexist. Diffuse brain injury is the most common type of head injury. It represent a continuum of brain damage produced by increasing amounts of acceleration-deceleration forces In general they have a normal CT scan but demonstrate altered sensorium or even deep coma.

2) Intracranial lesions
Based on the depth and duration of coma , diffuse injuries may be classified as mild concussion ,classic concussion and diffuse axonal damage.

 Consciousness is preserved but there is a noticeable degree of temporary neurological dysfunction . These injuries are common and, because of their mild degree, often go unnoticed . The mildest form of concussion results in confusion and disorientation without amnesia (loss of memory) .

Mild concussion

Classic Cerebral Concussion

There is a loss of consciousness which is transient and reversible. This condition always is accompanied by some degree of severity of posttraumatic amnesia. The length of amnesia is a good measure of the severity of the injury. Many patients with classic cerebral concussion have no sequale other than amnesia for the events relating to the injury, but some patients may have more long-lasting neurological deficits e.g. memory difficulties and depression.

 Term used to define prolonged post traumatic coma that is not due to mass lesion or ischemic insult These patients are rendered deeply comatose and remain so for prolonged periods They often demonstrate evidence of decortications or decerbration and often remain severely disabled , if they survive These patients often exhibit autonomic dysfunction such as Hypertension, Hyperhydrosis, and Hyperpyrexia.

Diffuse axonal injury

Focal intracranial lesions

Intracranial bleeding Venous bleeding Slow, insidious onset Arterial bleeding Signs and symptoms will be apparent within a few hours

Epidural hematoma

Epidural hematoma
Occurs in the potential space between the dura and the cranium. Also referred to as extradual. Caused by a blow to the head causes an interruption to the dura vesseles including branches of the middle meningeal arteries, veins, dura venous sinuses and skull vesseles.

Epidural hematoma
Non traumatic causes of EDH includes infectious disease of the skull Vascular malformation of the dura matter, Metastasis to the skull, Spontaneous EDH in patient with couaglopathy.

10-20% of patient with head trauma and 17% of previously conscious patient following head trauma have EDH.

Epidural hematoma
In traumatic EDH Hematoma forms extremely fast Within 10 20 minutes after injury. patient may present with external evidence of head injury such as scalp laceration, cephal hematoma, or contusions. Systemic injuries may also be present. Most often the head injury is in the temporal or temporoparietal region. Patient with epidural hematoma may present with the classical lucid interval (20-50% of cases) or talk and die.

Epidural hematoma
Initially, the concussive force that caused the head injury results in an alteration of consciousness. After recovering consciousness, the EDH continues to expand until the mass effect of the hemorrhage itself results in increased intracranial pressure, a decreased level of consciousness, and a possible herniation of the brain. With severe intracranial hypertension, the cerebral perfusion is compromised resulting in a Cushing response.

Epidural hematoma
The classic Cushing triad involves systemic hypertension, bradycardia, and respiratory depression. This response will be elevated by the evacuation of the mass

Investigations

Lab studies
Hematocrit level, chemistries, and coagulation profile are essential in the assessment of a patient with intracranial bleeding. Severe head injury can cause release of tissue thromboplastins, which can result in DIC. In adults, EDH rarely causes a significant drop in the hematocrit level within the rigid skull cavity. In infants, whose blood volume is already limited, EDH within an expansile cranium with open sutures can result in significant blood loss.

 Skull X-Ray may reveal a fracture crossing the vascular shadow of the middle meningeal artery branches.An occipital, frontal, or vertex fracture also might be observed. > 90% of EDH cases are associated with skull fractures. In children, this rate is less because of greater skull deformability.

Imaging

 CT scanning is the most accurate and sensitive method of diagnosing. Itll appear Biconvex or lenticular in shape as its limited by the adherence of the dura to the inner table of the skull, especially at the suture lines.

CT scanning

CT scanning
The signal density of the hematoma compared with the brain parenchyma changes over time after the injury. The acute phase is hyperdense (bright signal on CT scan).The hematoma then becomes isodense at 2-4 weeks, and then it becomes hypodense (dark signal) thereafter. Hyper acute blood may be observed as isodense or low-density areas, possibly indicating ongoing hemorrhage or a low serum hemoglobin level.

CT scanning
Hydrocephalus may be present in patients with a large posterior fossa EDH exerting a mass effect and obstructing the fourth ventricle. Approximately 10-50% of EDH cases are associated with other intracranial lesions. These lesions include subdural hematomas, cerebral contusions, and intracerebral hematomas

MRI
Acute blood on MRI is isointense, making this modality less suited to detection of hemorrhage in acute trauma. However, mass effect can be observed when its extant.

Therapy

1.Conservative Therapy
Not all cases of acute EDH require immediate surgical evacuation. However, If treated early , the prognosis is usually excellent because the direct damage to the underlying brain is usually limited Outcome is directly related to the neurological status of the patient before surgery. If a lesion is small and the patient is in good neurological condition, observing the patient with frequent neurological examinations is reasonable.

Conservative therapy
Early follow-up scanning can be used to assess for further increase in hematoma size prior to deterioration If a rapid size increase is noted, then surgery is indicated When treating patients with spontaneous EDH, the underlying primary disease process must be addressed in addition to the fundamental principles discussed above

2.Surgical management
Criteria for immediate surgical intervention is an EDH with: 1) Volume greater than 30 ml. 2) Thickness of 15 mm. 3) A midline shift beyond 5 mm. as most patients with such an EDH experience a worsening of the conscious state and/or exhibit lateralizing signs.

Surgical management
Location is also an important factor in the surgical decision.
Temporal hematomas, if they are large or expanding, may lead to uncal herniation and more rapid deterioration. While, EDH in the posterior fossa, which is often related to interruption of the lateral venous sinus, often requires prompt evacuation because of the limited space available compared with the supratentorial compartment.

Surgical management
In the preCT scan era, drilling exploratory burr holes was common especially when the patient demonstrated lateralizing signs or rapid deterioration. Now with fast-scan techniques, this type of exploration is rarely required. Its only reserved for patients with definitive localizing signs and clinical evidence of intracranial hypertension who are unable to tolerate a CT scan because of severe hemodynamic instability and/or for patients who require immediate surgical intervention for systemic injuries.

Position of emergency burr holes

Surgical management
Surgical treatment of epidural hematomas involve: 1. opening the skull over the site of hemorrhage.The EDH is readily apparent after elevating the bone flap, and it is removed. 2. Coagulation of bleeding dural vessels is usually performed. 3. Epidural tack-up sutures are placed from the dura to the craniotomy bone edge and to the center of the craniotomy flap to tamponade epidural bleeding from areas beyond the craniotomy edges and to prevent recurrence

Surgical management
If the patient presents with a dilated pupil or clinical signs of intracranial hypertension, a small incision is first made in an area considered to be over the hematoma. Then a rapid burr hole is made, and the epidural is partially evacuated. This maneuver often allows for some initial pressure relief until the entire epidural blood clot can be evacuated. Follow-up CT scans are performed to determine the extent of clot evacuation. These scans can also help evaluate for delayed hematomas.

Subdural hematoma

Subdural Hematoma
Much more common than epidural Occur most frequently from tearing of a bridging vein between the cerebral cortex and a draining venous sinus Also can be associated with arterial laceration on the brain surface

Sudural hematoma
Normally cover the entire surface of the hemisphere Prognosis is much worse than epidural Hematoma forms slowly signs and symptoms may not be appear until hours after injury.

Subdural hematoma
A subdural hematoma (SDH) is classified by the amount of the time that has elapsed from the time of the inciting event, if known, to the diagnosis. When the inciting event is unknown, the appearance of the hematoma on CT or MRI can help date the hematoma. Its classified to: 1) Acute SDH: <72hrs and appear hyperdense on CT compared to the brain.

Subdural hematoma
2) Subacute SDH: 3- 20 days and is isodense or hypodense compared to the bain.
3) Chronic SDH: older than 20 days and are hypodense compared to the brain.

Acute subdural hematoma

Pathophysiology
- The usual mechanism to produce an acute SDH is high-speed impact to the skull. This causes brain tissue to accelerate relative to a fixed dural structure, which, in turn, tears blood vessels. - This mechanism also leads to associated contusions, brain edema, and diffuse axonal injury - The ruptured blood vessel often is a vein connecting the cortical surface to the dural sinuses

Pathophysiology
Alternatively, a cortical vessel can be damaged by direct laceration. An acute SDH due to a ruptured cortical artery may be associated with only minor head injury, and no cerebral contusions may be associated

Clinically
- Acute SDHs are most likely to occur after head injury from a fall, motor vehicle accident, or an assault. - SDH occurs in men more frequently than in women, with a ratio in the range of 3:1. - Patients found to have an acute SDH are on average older than other trauma patients. - In one study, the average age of a trauma patient without an acute SDH was 26 years, while the average age of patients with an acute SDH was 41 years.

Clinically
- Therefore, older patients appear to be at greater

risk for developing an acute SDH after head injury. This is believed to be due to older patients having more atrophy, which allows more sheer force against bridging veins immediately after impact. - The clinical presentation of an acute SDH depends on the size of the hematoma and the degree of any associated parenchymal brain injury. Common neurological findings include :

Clinically
1) Altered level of consciousness

2) A dilated pupil ipsilateral to the hematoma 3) Failure of the ipsilateral pupil to react to light. 4) Hemiparesis contralateral to the hematoma. The patient should be examined for related injuries (using guidelines established by ATLS Committee on Trauma) such as spinal cord injury or long bone fractures

Investigations
1) lab Studies:

coagulation profile and platelet count should be done to determine whether defective coagulation was involved in the formation of the acute SDH. 2) imaging: CT scan needs to be performed on an emergent basis when an acute SDH is suspected and should be obtained immediately after stabilizing the patient using standard advanced trauma life support (ATLS) guidelines

Acute SDH
Acute SDH appears on CT scan as a crescentshaped hyperdense area between the inner table of the skull and the surface of the cerebral hemisphere.

Management
Conservative: - Small acute SDHs less than 5 mm thick on axial
CT images, without sufficient mass effect to cause midline shift or neurological signs, can be followed clinically - The patient with an acute SDH should be transfused with fresh frozen plasma (FFP) and platelets to maintain the PT within the normal range and the platelet count above 100,000.

Management
Surgical: - Surgery for acute SDH consists of a large
craniotomy (centered over the thickest portion of the clot) to decompress the brain, stop any active subdural bleeding, and evacuate any intraparenchymal hematomas in the immediate vicinity of the acute SDH. - The craniotomy exposure should include the sylvian fissure because this can be a likely source of a ruptured cortical vessel.

Chronic subdural hematoma

Pathophysiology
Most chronic SDHs begin as SDG. An SDG begins as a separation in the duraarachnoid interface, which then is filled by cerebrospinal fluid (CSF). Dural border cells proliferate around this CSF collection to produce a new membrane. Then, fragile new vessels grow into the membrane. These vessels can bleed and become the source of blood into the space, which results in the growth of the chronic SDH.

Pathophysiology
Chronic SDHs that form from acute SDHs have membranes between the dura and hematoma at 1 week and between the brain and hematoma at 3 weeks. The hematoma liquefies at 1-3 weeks of age and becomes hypodense on CT scan. If not resorbed, the vessels in the membranes surrounding the hematoma can hemorrhage repeatedly, resulting in the enlargement of the hematoma.

Clinically
A higher incidence of chronic SDH exists in men.The male-to-female ratio is 2:1. Most adults with chronic SDH are older than 50 years One quarter to one half of patients with chronic SDH have no identifiable history of head trauma. If a patient does have a history of head trauma, it usually is mild. The average time between head trauma and chronic SDH diagnosis is 4-5 weeks.

Clinically
Risk factors for a chronic SDH includes chronic alcoholism, epilepsy, coagulopathy, arachnoid cysts, anticoagulant therapy (including aspirin), cardiovascular disease, and thrombocytopenia, and diabetes.
Clinical presentation often is insidious, with: symptoms of decreased level of consciousness balance problems cognitive dysfunction and memory loss. Motor deficit.

Clinically
Headache, or aphasia. Acute presentation also is possible, as in the case of a patient who presents with a seizure. Neurologic examination may demonstrate hemiparesis, papilledema, hemianopsia, or third cranial nerve dysfunction. In patients aged 60 years or older, hemiparesis is a common presenting sign. In patients younger than 60 years, headache is a common presenting symptom.

Investigation
Lab studies: This includes coagulation profile, CBC and routine SU+E and LFTs test. Imaging: On a contrast-enhanced CT scan, the chronic SDH membrane will enhance to varying degrees. Typical signs of mass effect may be observed, such as midline shift and ventricular compression.

Management
Surgical: - Liquefied chronic SDHs commonly can be treated
with drainage through 1-2 burr holes. A closed drainage system sometimes is left in the subdural space for 24-72 hours postoperatively. A nonliquified chronic SDH cannot be decompressed adequately by burr holes and must be removed by craniotomy.

Contusions
Almost always seen in association with subdural hematomas. Majority occur in the frontal and temporal lobes , although it can occur in any part of the brain including the cerebellum and brainstem Contusions can in a period of hrs or days coalesce to form an intracerebral hematoma

Intracerbral hematoma

Intracerebral Hemorrhage
Hemorrhage within the substance of the brain is a relatively frequent occurrence in head injury. Usually results due to a compressive force applied to the brain. It can occur acutely with Rapid deterioration in neurological function or more commonly in delayed fashion.

 After sever head injury ICH can be found in CT in: - 20% initialy. - 35% after 24 h. - 80% after 72 h. 2 basic mechanism that produce traumatic intracerebral hematoma Coup or Countercoup injury. Other mechanism includes Injury to vessel wall due to hypoxia , CO2 accumulation and acidic PH.

ICH

ICH
Management: Surgical evacuation should be done if there is: - Deteriorating neurological status - Intracranial pressure elevations unresponsive to medical treatment - Midline shift more than 1 cm - Temporal hematoma larger than 30 cc

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