HEAD INJURY

INTRODUCTION

Head injury refers to trauma to the head. This may or may not include injury to the brain. However, the terms traumatic brain injury and head injury are often used interchangeably in the medical literature.Head trauma has a poor potential for good outcome.Deaths from head trauma occurs at three time points after the injury.,immediately after the injury,2 hours after the injury,and approximately 3 weeks after the injury.

 

INCIDENCE

The incidence (number of new cases) of head injury is 300 per 100,000 per year (0.3% of the population), with a mortality of 25 per 100,000 in North America and 9 per 100,000 in Britain. Head trauma is a common cause of childhood hospitalization.

CAUSES
Common causes of head injury are motor vehicle traffic collisions, home and occupational accidents, falls, and assaults. Bicycle accidents are also a common cause of head injury-related death and disability, especially among children.

Types of head injury

• Scalp lacerations
• Skull fractures
• Minor head trauma
• Major head trauma

Scalp lacerations
Scalp lacerations are the most minor type of head trauma. Because the scalp contains many blood vessels with poor constrictive abilities,most scalp injuries are associated with profuse bleedingThe major complication associated with scalp laceration is infection.

Skull fracture
Skull fractures arefrquently with head traumaThere are several types of skull fractures

• Linear
• Depressed
• Simple,communited,or compound fracture
• Basillar skull fracture

CLINICAL MANIFESTAIONS OF DIFFERENT TYPES OF SKULL FRACTURE

• Frontal fracture-CSF rhinorrhea ,pneumocranium
• Orbital Fracture-Periorbiatal ecchymosis,(racoon eyes)
• Temporal Fracture-Oval shape bruise behind the ear in the mastoid region(Battle s sign)CSF Otorrhea
• Parietal Fracture-Deafness ,CSF or brain otorrhea,bulging of the tympanic membrane caused by blood or CSF,facial paralysis,loss of taste,Battle s sign
• Basillar skull fractures-CSF or brain otorrhea,bulging of the tympanic membrane caused by blood or CSF,Battles sign,tinnitus or hearing difficulty,facial paralysis,vertigo.

Common Symptoms of skull fracture can include:

• leaking cerebrospinal fluid (a clear fluid drainage from nose, mouth or ear) may be and is strongly indicative of basilar skull fracture and the tearing of sheaths surrounding the brain, which can lead to secondary brain infection.
• visible deformity or depression in the head or face; for example a sunken eye can indicate a maxillar fracture
• an eye that cannot move or is deviated to one side can indicate that a broken facial bone is pinching a nerve that innervates eye muscles
• wounds or bruises on the scalp or face.
• Basilar skull fractures, those that occur at the base of the skull, are associated with Battle's sign, a subcutaneous bleed over the mastoid, hemotympanum, and cerebrospinal fluid rhinorrhea and otorrhea.

MINOR HEAD TRAUMA

• Brain injuries are classified as major and minor.Concussion is a minor head injury.It is a sudden transient mechanical head injury with distruption of the neural activity and loss of consciousness.The patient maynot loss full consciousness with the head injury
• Signs of concussion includes a brief distruption of LOC,amnesia regarding the event and headacheThe manifestations are short term duration.If the patient has not loss consciousness or if the loss of consciousness lasts for more than 5minutes,the patient is discharged from the with notification to return back if the symptoms persists.
• Post concussion syndrome is usually seen from 2weeks to 2 months after the concussion.Symptoms includes persistent headache,lethargy,personality and behavioural changes,short attention span,decreased short term memory,and changes in intellectual ability.This affects the patients ability for activities of daily living

MAJOR HEAD TRAUMA
Major head trauma includes cerebral contusions and lacerations.Both injuries represent severe trauma to the brain..Contusions and intercerebral lacerations are generally associated with closed injuries
A contusion is the bruising of the brain tissue within a focal area that maintains the integrity of the piamater and arachnoid layers.A contusion develops areas of hemorrhage,infarction,necrosis and edema.With contusion the phenomenon of counter coup injury is often noted.Damage from coup counter coup injury occurs occurs due to the mass movement of brain inside the skull.Contusions or lacerations occurs at the site of direct impact on the skull(coup)and a secondary area on the opposite side away from the injury(countercoup)leading to multiple contused areas.Bleeding around the contusion site is usually minimal,and the blood is reabsorbed slowly.Neurological findings demonstrates generalized disturbance in LOC.Seizures are a common complication of brain contusion.

• Laceration involves actual tearing of barin tissue and often occurs in association with depressed and compound fractures and penetrating injuries.Tissue damage is severe but surgical repair cannot be done because of the texture of the brain tissue.If bleeding is deep into the brain parenchyma then focal neurological symptoms are suspected.
• When the head injury is major hemorrhage is suspected.This hemorrhage manifests as a space occupying lesion which is accompanied by unconsciousness,hemiplegia on the contralateral side,and a dilated pupil.
• As hematoma expands,symptoms of increased ICP becomes more severe,prognosis becomes more severe because of intercerbral hemorrhage.

PATHOPHYSIOLOGY
1. Diffuse axonal injury is a widespread axonal damageoccuring after a mild,moderate or severe injury
2. Due to the etiological factors(immediate tearing of the axon from the traumatic injury)
3. The damage occurs primarily around the axons in the subcortical white matter of the cerebral hemispheres,basal ganglia,thalamus and the brain stem
4. The axons will get sheared Axonal disconnection and axonal swelling occurs

COMPLICATIONS

• Epidural hematoma
• Subdural hematoma
• Intracerebral hematoma
• Subarachnoid hemorrhage

CLINICAL FEATUERES

• Presentation varies according to the injury. Some patients with head trauma stabilize and other patients deteriorate. A patient may present with or without neurologic deficit.
• Patients with concussion may have a history of seconds to minutes unconsciousness, then normal arousal. Disturbance of vision and equilibrium may also occur.
• Common symptoms of head injury include coma, confusion, drowsiness, personality change, seizures, nausea and vomiting, headache and a lucid interval, during which a patient appears conscious only to deteriorate later.^[5]

Because brain injuries can be life threatening, even people with apparently slight injuries, with no noticeable signs or complaints, require close observation. The caretakers of those patients with mild trauma who are released from the hospital are frequently advised to rouse the patient several times during the next 12 to 24 hours to assess for worsening symptoms.
The Glasgow Coma Scale is a tool for measuring degree of unconsciousness and is thus a useful tool for determining severity of injury. The Pediatric Glasgow Coma Scale is used in young children.

Diagnosis and prognosis

• Head injury may be associated with a neck injury. Bruises on the back or neck, neck pain, or pain radiating to the arms are signs of cervical spine injury and merit spinal immobilization by application of a cervical collar and possibly a long board
• If the neurological examination is normal this is reassuring, however a serious intra-cranial injury may still be present. If the patient developing a worsening headache, has a seizure, develops one sided weakness, or has persistent vomiting than the patient should be advised CTimmediately

Imaging

• The need for imaging in patients who have suffered a minor head injury is debated. A non-contrast CT of the head should be performed immediately in all those who have suffered a moderate or severe head injury.

MANAGEMENT OF HEAD-INJURED PATIENTS

• The management of head-injured patients depends on the GCS following resuscitation.
• Patients with a mild head injury (GCS 14-15) should be admitted to a ward where thorough and frequent neurological observations can be ensured.
• CT scan of the patient’s head should be performed promptly, and the local neuro-surgical unit contacted.
• Patients with a mild head injury should be observed until they make a complete neurological recovery and are only discharged if a responsible adult can supervise them at home for a further few days.
• All patients with a GCS of 13 or less should receive a CT scan of their head although many authorities would advocate a CT scan on all whose GCS is not normal.
• Those with an acute lesion on CT scan or evidence of diffuse cerebral oedema should be urgently discussed with the local neurosurgical unit, with the CT images transferred immediately, either by computer image-link or courier.
• All CT scans should be accompanied by a provisional radiology report from the referring hospital.
• Other indications for neurosurgical referral include compound depressed skull fracture, severely depressed fracture, deteriorating GCS score even with a normal scan and cerebrospinal fluid otorrhoea and rhinorrhoea.
• The following details are necessary when making a neurosurgical referral: name, age, sex, date, time and mechanism of injury, initial GCS on scene (documented by paramedics) and GCS following resuscitation (before administration of anaesthetic agents should they be required), evidence of deteriorating GCS, pupil reaction, vital observations, previous medical and drug history, previous functional ability and mobility in the case of elderly patients, other injuries and management of the patient since injury.

INITIAL MANAGEMENT

• The fundamental goals of resuscitation of the head-injured patient are the restoration of circulating volume, blood pressure, oxygenation, and ventilation.
• The physician should initiate maneuvers that serve to lower ICP and do not interfere with these aims as early as possible during resuscitation of any patient with a head injury.
• Treatment modalities such as hyperventilation and mannitol administration that have the potential of exacerbating intracranial ischemia or interfering with resuscitation should be reserved for patients who show signs of intracranial hypertension such as evidence of herniation or neurological deterioration.

USE OF MANNITOL:
Mannitol is effective for control of raised ICP after severe TBI. Effective doses range from 0.25 to 1 g/kg/body weight.

USE OF BARBITURATES IN THE CONTROL OF INTRACRANIAL HYPERTENSION

• High-dose barbiturate therapy is efficacious in lowering ICP and decreasing mortality in the setting of uncontrollable ICP refractory to all other conventional medical and surgical ICP-lowering treatments, in salvageable TBI patients. Utilization of barbiturates for the prophylactic treatment of ICP is not indicated. The potential complications attendant on this form of therapy mandate that its use be limited to critical care providers and that appropriate systemic monitoring be undertaken to avoid or treat any hemodynamic instability. When barbiturate coma is utilized, consideration should also be given to monitoring arteriovenous oxygen saturation as some patients treated in this fashion may develop oligemic cerebral hypoxia.

NUTRITION

•   Replace 140% of resting metabolism expenditure in nonparalyzed patients and 100% in paralyzed patients using enteral or parenteral formulas containing at least 15% of calories as protein by day 7 after injury.

NURSING PROCESS

ASSESSMENT

• The health history may include the following questions:
• The time of the injury,The etiologies of injury,The direction of the force of the blow,any history of
• loss of consciousness,duration of the loss of consciousness etc....
  NURSING DIAGNOSIS   Ineffective airway clearance and ventilation related to hypoxia
• Assess the patency of airway.
• Keep the unconscious patient in a position that facilitates drainage of the secretions with the head of the bed elevated to about 30 degrees to decrease intracranial venous pressure.
• Establish effective suctioning procedures to facilitate drainage of the secretions.
• Encourage deep breathing and coughing exercises.
• Guard against aspiration and respiratory insufficiency.
• Monitor arterial blood gas values to determine adequate cerebral blood flow.
• Monitor the patient who is receiving mechanical ventilation
  Fluid volume deficit related to disturbance of consciousness and hormonal dysfunction
• Assess the level of fluid volume deficit to obtain a baseline data.
• Serum electrolytes should be monitored especially in patients with osmotic diuretics,those with inappropriate antidiuretic hormone secretion and those with post traumatic diabetes insipidus
• Serial studies of blood and urine electrolyes and osmolality is carried out because headinjuries are accompanied by disorders of sodium regulation.
• Endocrine function is evaluated by monitoring the serum electrolytes,blood glucose values,and intake and output.
• A daily record of daily weight is maintained to see whether there is diabetes insipidus.
  Altered nutrition less than body requirement related to metabolic changes,fluid restriction and inadequate intake.
• Head injury patients will present with metabolic changes that increases calorie requirement and nitrogen excretion
• If the patient cannot tolerate oral feedings endotracheal feedings is encouraged.the enteral tube has to be aspirated for residual feeding to prevent distension,regurgitation,and aspiration
• A continuous drip infusion to regulate the feeding.
• The feeding tube should be kept in mind until the swallowing reflex is initiated
  Risk for injury(self directed or directed towards others)related to disorientation,restlessness and brain damage
• Assess the risk of injury to the patient.
• Assess the patient to ensure that airway is adequate and bladder is not distended.
• To protect the patient from injury and dislodging of the body ,use padded side rails or wrap the patients hands in mitts.
• Avoid restraints because it may cause increase in the ICP
• Avoid opiods as a means of controlling restlessness as it may cause respiratory depression,constrict the pupils and alter the patients responsiveness.
• Minimize the environmental stimuli,keep the room quiet,limit visitors,speak calmly and frequent orientation has to be given
  Risk for altered body temperature related to damage to temperature regulating mechanism
• Assess the level of temperature of the patient.
• Monitor the temperature of the patient every 4 hours
• If the temperature rises efforts are undertaken to control the temperature by providing acetaminophen and cooling blankets are provided.
• If infection is suspected culture is done to identify the organism and antibiotics has to be initiated.
  Potential for impaired skin integrity related to bed rest,hemiparesis,hemiplegia,and immobility
• Assess all the body surfaces and record every 8 th hourly.
• Turn the patient every 2 to 4 hours
• Provide skin care every 4 hours
• Assist the patient to get out of the bed and chair three times a day.
  Altered thought process(deficits in intellectual function,communication ,memory,information processing)related to brain injury
• Assess the patient for memory deficits,decrease in ability to sustain the focus and attention to a task(easily getting distracted),reduced ability to focus information and reduced thinking etc....
• Psychiatric or emotional problems should be estimated
• Cognitive rehabilitation therapies are initiated to improve the cognive functioning of the patient
• The patient should be provided emotional and psychological support.
  Potential for sleep pattern disturbance related to headinjury and frequent neurological checks
• Assess the level of sleep pattern of the patient.Allow the patient for long hours of uninterrupted rest and sleep.
• Enviornmental noise is reduced and the lights should be dimmed to promote sleep
• Enhance all measures to prevent sleep disturbances
• Back rubs and other strategies can improve the sleep pattern of the patient

Advanced Management Measures

A.   Maintaining or Decreasing ICP

o  Maintaining ICP at Less than 20 mm Hg Improves Outcomes

Uncontrolled intracranial hypertension leads to an absence of cerebral perfusion and results in brain death.

o  Draining Cerebrospinal Fluid (CSF) Decreases ICP

The cranial compartment is a rigid box containing three components: the brain, blood, and CSF. The Monro-Kellie hypothesis states that a normal ICP can be maintained as one component increases as long as there is a corresponding decrease of another component. Therefore, decreasing one of the three components decreases ICP.

o  Do Not Induce Hyperventilation to Decrease ICP

Hyperventilation induced vasoconstriction and decreased the blood component within the cranial vault, resulted in decreased cerebral blood flow and precipitated further cerebral ischemia

o  Administering Sedation Prevents ICP Increases

Both agitation and coughing in patients with severe TBI increase the cerebral metabolic rate for oxygen consumption, which could negatively affect secondary cellular brain injury. Endotracheal suctioning is a necessary intervention in severe TBI, but it may cause deleterious increases in ICP.

o  Administering Mannitol Is Effective in Decreasing ICP

Infusions of mannitol immediately increase vascular volume and produce an osmotic effect within 15–30 minutes. The diuretic effect of mannitol can cause increased sodium and serum osmolarity levels, and should be monitored at regular intervals. Mannitol is infused via intravenous bolus through a filter. Mannitol 20% contains 20 g of mannitol in 100 cc. Eighty percent of a 100 g dose appears in the urine within 3 hours of infusion.

o  Elevate the Head of the Bed (HOB) 30 Degrees to Maintain or Decrease ICP

Elevating the HOB is thought to promote intracranial venous return and increase CSF drainage from the head, resulting in decreased ICP

o  Removing or Loosening Rigid Cervical Collars May Decrease ICP

Rigid cervical collars are used in severe TBI until spinal stability is confirmed. These collars may impede venous outflow and cause pain and discomfort, elevating ICP

o  Administering Intensive Insulin Therapy May Reduce ICP

Hyperglycemia is common in severe TBI and has a negative effect on outcome.

o  Maintaining Normothermia May Prevent ICP Increases

Hyperthermia is prevalent in the TBI population, with reported rates as high as 68% within 72 hours of injury.

B.    Controversial Treatments for Refractory Intracranial Hypertension

It is estimated that 10%–15% of patients with severe traumatic brain injury will develop elevated ICP that is resistant to standard forms of treatment. The following modalities have demonstrated their efficacy in treating elevated ICP that is refractory to customary treatment. These interventions have some potential complication and are only advised when other conventional measures have failed.

·         Inducing Moderate Hypothermia May Decrease ICP in Refractory Intracranial Hypertension: hypothermia provides extensive neuroprotection against indirect cerebral ischemia, ICP with the induction of moderate hypothermia (33 °C–36 °C) in patients with severe TBI.

·         Administering Hypertonic Saline May Decrease ICP in Refractory Intracranial Hypertension:  Several studies support this fact even though the exact mechanism behind is unknown. When used to resuscitate trauma patients, the vascular expansion of the infusion increases mean arterial pressure. Most protocols for the infusion of hypertonic saline include a bolus followed by a continuous infusion, titrated to maintain the minimum necessary sodium level to maintain ICP at <20 addition="" and="" close="" hg.="" in="" levels="" mm="" monitoring.="" output="" require="" sodium="" span="" urine="">

·         Administering High-Dose Barbiturates May Decrease ICP in Refractory Intracranial Hypertension: High-dose barbiturates are thought to suppress cerebral metabolism, reducing cerebral metabolic demand and cerebral blood volume. Hemodynamic stability must be achieved before instituting high-dose barbiturates.

·         Hyperventilation Rapidly Decreases ICP in Emergent Intracranial Hypertension: Despite the negative effects of hyperventilation, it is an effective intervention for rapidly reducing ICP.

C.  Maintaining Adequate CPP or Increasing CPP

·         Maintaining CPP Between 50–70 mm Hg Optimizes Cerebral Perfusion: CPP is defined as the MAP minus the ICP (CPP = MAP – ICP). This pressure gradient drives cerebral blood flow, improving the likelihood of adequate oxygen and metabolite delivery.

·         Administering Norepinephrine May Maintain Adequate CPP or Increase CPP:

Vasopressors cause vasoconstriction and are routinely used to maintain or increase MAP for both systemic and cerebral perfusion in patients with severe TBI.

·         Elevating the head of the bed 0–30 Degrees May Maintain Adequate CPP or Increase CPP: While head elevation increases venous drainage from the head, it also can decrease perfusion.

·         CSF Drainage May Be an Effective Treatment for Low CPP: Decreasing the volume of CSF by drainage decreases the total intracranial volume.

D.   Monitoring Modalities

Intra Cranial            Pressure Monitoring

Carotid pulse pressure monitoring

Continues Brain tissue perfusion monitoring

Monitoring and displaying brain temperature

E.    Preventing DVT

Patients with brain injury are at potential risk for developing DVT and pharmacological treatment may be safe for DVT prophylaxis.

F.    Adequate Nutrition

·         Initiating Adequate Nutrition Within 72 Hours of Injury May Improve Outcomes. The metabolic expenditure in isolated comatose patients with TBI is at least 100%–180% higher than what would be expected in noninjured people.

·         Providing Continuous Intragastric Feeding May Improve Tolerance, Continuous feeding was better tolerated and achieved 75% of nutritional goals faster than bolus feeding

G.  Glycemic control

Glucose levels exceeding 170 mg/dl during the first 5 days post-severe TBI correlate with prolonged hospital length of stay and increased mortality

H.   Preventing seizures

·         Administering Antiepileptic Drugs Decreases the Incidence of Early Posttraumatic Seizures

·         EEG Technology May Help to Identify Patients at Risk for Seizures

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