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INTRODUCTION: - Any injury that results in trauma to the scalp, skull, or brain can be classified as a head injury. The terms traumatic brain injury and head injury are often used interchangeably in medical literature. Unlike a broken bone where trauma to the body is obvious, head trauma can sometimes be obvious or discrete. In the case of an open head injury, the skull is cracked and broken by an object that makes contact with the brain, this leads to bleeding. Other obvious symptoms can be neurological in nature. The person may become sleepy, behave abnormally, lose consciousness, vomit, develop a severe headache, have mismatched pupil sizes, and/or be unable to move certain parts of the body. While these symptoms happen right after head injury occurs, many problems can develop later in life. Alzheimer’s disease, for example, is much more likely to develop in a person who has experienced a head injury. ANATOMY & PHYSIOLOGY:- :BRAIN: Brain in divided into 3 main components: cerebrum, brainstem & cerebellum. CEREBRUM Cerebrum is composed of left & right hemispheres. Both the hemispheres can be further divided into 4 major lobes: frontal, temporal, parietal & occipital. Lobes of cerebral hemispheres Functions Frontal Controls higher cognitive functions, memory retention, voluntary eye movements, voluntary motor movements, expressive speech in broca’s area. Temporal lobe Contains wernicke’s area , which is responsible

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INTRODUCTION: -

Any injury that results in trauma to the scalp, skull, or brain can be classified as a head injury. The terms traumatic brain injury and head injury are often used interchangeably in medical literature. Unlike a broken bone where trauma to the body is obvious, head trauma can sometimes be obvious or discrete. In the case of an open head injury, the skull is cracked and broken by an object that makes contact with the brain, this leads to bleeding. Other obvious symptoms can be neurological in nature. The person may become sleepy, behave abnormally, lose consciousness, vomit, develop a severe headache, have mismatched pupil sizes, and/or be unable to move certain parts of the body. While these symptoms happen right after head injury occurs, many problems can develop later in life. Alzheimer’s disease, for example, is much more likely to develop in a person who has experienced a head injury.

ANATOMY & PHYSIOLOGY:-

:BRAIN:

Brain in divided into 3 main components: cerebrum, brainstem & cerebellum.

CEREBRUM

Cerebrum is composed of left & right hemispheres. Both the hemispheres can be further divided into 4 major lobes: frontal, temporal, parietal & occipital.

Lobes of cerebral hemispheres

Functions

Frontal Controls higher cognitive functions, memory retention, voluntary eye movements, voluntary motor movements, expressive speech in broca’s area.

Temporal lobe Contains wernicke’s area , which is responsible for receptive speech & for integration of somatic, visual & auditory data.

Parietal lobe Controlling & interpreting spatial informationOccipital lobe Processing of sight

These divisions are useful to delineate the portions of neocortex (gray matter), which makes up the outer layer of cerebral hemispheres. Neurons in specific parts of the neocortex are essential for various highly

complex & sophisticated aspects of mental functioning such as language, memory & appreciation of visual spatial relationships.

Basal ganglia are a group of paired structures located centrally in the cerebrum & midbrain, near lateral ventricles of both cerebral hemispheres. It controls & facilitates learned & automatic movements.

Thalamus (part of diencephalon) is lying above the brain stem & below the basal ganglia. It is the major relay center for sensory & other afferent (i.e., cerebellar) inputs to the cerebral cortex.

Hypothalamus is located just below the thalamus & slightly in front of the midbrain. It regulates the ANS & endocrine system.

Limbic system located lateral to hypothalamus, near the inner surfaces of the cerebral hemispheres. It is concerned with emotion, aggression, feeding behaviour & sexual response.

BRAINSTEM

It includes midbrain, pons & medulla.

Ascending & descending fibers pass through the brainstem going to & from the cerebrum & cerebellum. The cell bodies , or nuclei ,of cranial nerves iii to xii are in the brainstem.

Reticular formation a diffusely arranged group of neurons & their axons that extends from the medulla to the thalamus & hypothalamus, is also located here. Its functions include relaying sensory information, influencing excitatory & inhibitory control of spinal motor neurons, & controlling vasomotor & respiratory activity.

RAS , a part of the reticular formation , is the regulatory system for arousal.

Medulla acts as respiratory, vasomotor & cardiac function regulatory center.

Brainstem also contains centers for sneezing, coughing, hiccupping, vomiting, sucking & swallowing.

CEREBELLUM

Cerebellum located in the posterior part of the cranial fossa, along with the brainstem under the occipital lobe of cerebrum.

Its function is maintain coordinate voluntary movement & to maintain trunk stability & equilibrium.

:PROTECTIVE STUCTURES:

MENINGES

It consists of 3 protective layers: dura, arachnoid & pia mater.

The flax cerebri is a fold of the dura mater , that separates both hemispheres & preventing expansion of brain tissue.

SKULL

The three bone layers of the skull.

The human skull is anatomically divided into two parts: the neurocranium, formed by eight cranial bones that houses and protect the brain—and the facial skeleton (viscerocranium) composed of fourteen bones, not including the three ossicles of the inner ear.

The term skull fracture typically means fractures to the neurocranium, while fractures of the facial portion of the skull are facial fractures, or if the jaw is fractured, a mandibular fracture.

NEUROCRANIUM:

The eight cranial bones are separated by sutures : one frontal bone, two parietal bones, two temporal bones, one occipital bone, one sphenoid bone, and one ethmoid bone.

The bones of the skull are in three layers: the hard compact layer of the external table (lamina externa), the dipole (a spongy layer of red bone

marrow in the middle, and the compact layer of the inner table (Lamina interna).

SCALP

The scalp is the anatomical area bordered by the face anteriorly and the neck to the sides and posteriorly.

Structure:

The scalp is usually described as having five layers, which can conveniently be remembered as a mnemonic.

S: The skin on the head from which head hair grows. It contains numerous sebaeceous glands and hair follicles.

C: Connective tissue. A dense subcutaneous layer of fat and fibrous tissue that lies beneath the skin, containing the nerves and vessels of the scalp.

A: The aponeurosis called epicranial aponeurosis (or galea aponeurotica) is the next layer. It is a tough layer of dense fibrous tissue which runs from the frontalis muscle anteriorly to the occipitalis posteriorly.

L: The loose areolar connective tissue layer provides an easy plane of separation between the upper three layers and the pericranium. This layer is sometimes referred to as the "danger zone" because of the ease by which infectious agents can spread through it to emissary veins which then drain into the cranium. The loose areolar tissue in this layer is made up of random collagen I bundles, collagen III. It will also be rich in glycosaminoglycans (GAGs) and will be constituted of more matrix than fibers.

P: The pericranium is the periosteum of the skull bones and provides nutrition to the bone and the capacity for repair. It may be lifted from the bone to allow removal of bone windows (craniotomy).

BLOOD SUPPLY OF BRAIN

CEREBRAL CIRCULATION

Cerebral circulation or blood supply of the brain arises from the internal carotid arteries(anterior circulation) and the vertebral arteries(posterior circulation). Each internal carotid artery supplies the ipsilateral hemisphere, whereas the basilar artery form by the junction of the two vertebral arteries, supplies structures within the posterior fossa (cerebellum and brain stem).The circle of Wills arise from the basilar

artery and the two internal carotid arteries. This vascular circle may act as a safety valve when differential pressures are present in these arteries. It also may function as an anstomotic pathway when occlusion of a major artery on one side of the brain occurs. In general, the two anterior cerebral arteries supply the medial and anterior portion of the frontal lobes. The two middle cerebral arteries supply the outer portions of the frontal, partial, and superior temporal lobes. The two posterior cerebral arteries supply the medial portions of the occipital and inferior temporal lobes. Venous blood drain from the brain through the dural sinuses, which form channels that drain into the two jugular veins.

SCALP CIRCULATION

The blood supply of the scalp is via five pairs of arteries, three from the external carotid (superficial temporal artery, occipital artery &  posterior auricular artery) and two from the internal carotid( supratrochlear artery & supraorbital artery ). 

Note: The walls of the blood vessels are firmly attached to the fibrous tissue of the superficial fascial layer, hence cut ends of vessels here do not readily retract; Even a small scalp wound may bleed profusely.

INNERVATION OF SCALP

The innervation of scalp can be remembered using the mnemonic, "Z-GLASS" for, Zygomaticotemporal nerve, Greater occipital nerve,Lesser occipital nerve, Auriculotemporal nerve, Supratrochlear nerve and Supraorbital nerve.

LYMPHATIC

Occipital and posterior auricular nodes, parotid nodes, submandibular and deep cervical nodes .

EPIDEMIOLOGY IN INDIA:-

Traumatic brain injuries (TBIs) are a leading cause of morbidity, mortality, disability and socioeconomic losses in India and other developing countries. It is estimated that nearly 1.5 to 2 million persons are injured and 1 million succumb to death every year in India. Road traffic injuries are the leading cause (60%) of TBIs followed by falls (20%-25%) and violence (10%). Alcohol involvement is known to be present among 15%-20% of TBIs at the time of injury. The rehabilitation needs of brain injured persons are significantly high and increasing from year to year. India and

other developing countries face the major challenges of prevention, pre-hospital care and rehabilitation in their rapidly changing environments to reduce the burden of TBIs.

CAUSES:-

Motor vehicle traffic collisions ,Home and occupational accidents, falls, Assaults.

CLASSIFICATION :-

There are many ways that head injuries can be classified. The three most useful descriptions are:

Severity Morphology Mechanism of injury Time of showing impact or consequences

Classification as per Severity

1. Severity based on Glassgow Coma Scale

Best Eye Response. (4)

No eye opening. Eye opening to pain. Eye opening to verbal command. Eyes open spontaneously.

Best Verbal Response. (5)

No verbal response Incomprehensible sounds. Inappropriate words. Confused Orientated

Best Motor Response. (6)

No motor response. Extension to pain. Flexion to pain. Withdrawal from pain. Localising pain. Obeys Commands.

Mild head inury (GCS 14 - 15) Moderate head injury (GCS 9 - 13) Severe head injury (GCS 3 - 8)

2. SEVERITY OF TBI BASED ON THE DURATION OF LOC

Severity of TBI Finding

Mild Mental status change or LOC < 30 min

Moderate Mental status change or LOC 30 min to 6 h

Severe Mental status change or LOC > 6 h

Morphological classification

Head injuries may also be classified by injury type. There are two broad categories:

1. Focal injuries2. Diffuse injuries

Focal injuries have an identifiable area of involvement. Examples include:

1. Cerebral contusion2. Extradural haemorrhage:3. Scalp lacerations4. Skull fractures5. Subarachnoid haemorrhage6. Subdural haemorrhage

Diffuse injuries involve the entire brain. Examples include:

1. Concussion2. Diffuse axonal injury

Classification as per time of showing impact:

PRIMARY INJURY :

Induced by mechanical force and occurs at the moment of injury; the 2 main mechanisms that cause primary injury are contact (eg, an object

striking the head or the brain striking the inside of the skull) and acceleration-deceleration.

SECONDARY INJURY :

Not mechanically induced; it may be delayed from the moment of impact, and it may superimpose injury on a brain already affected by a mechanical injury

Head injury as per Mechanism of injury:

Head injuries may also be classified by the mechanism of injury. The two broad categories used are:

BLUNT HEAD INJURY:

Blunt force trauma is defined as trauma to tissue or organs without penetration through the skin. It also can be called closed (non-missile) head injury is where the dura mater remains intact. The skull can be fractured, but not necessarily.

PENETRATING HEAD INJURY:

Penetrating trauma can be defined as injuries caused by foreign objects penetrating the skin and disrupting underlying tissue and organs. The penetrating object transfers it's kinetic energy to the body. This energy is then dissipated into the surrounding tissue, often focussed in a small area.

DIFFERENT TYPES OF HEAD INJURY IN DETAILS:

SCALP LACERATIONS

WHAT IS SCALP LACERATION: The blunt force due to the direct effect of scalp laceration (scalp laceration) for sharpening cutting or larger.

SYMPTOMS OF SCALP LACERATION: Scalp blood vessels is extremely rich, dense and scalability small subcutaneous tissue, so once the scalp fracture. Not easy to shrink blood vessels and bleeding are many and difficult to stop on their own. Scalp laceration is large, and often in the short-term internal massive blood loss caused by hemorrhagic shock.

CAUSES: For sharpening cutting or larger due to the direct effect of the blunt force.

DIAGNOSIS: Sharp cuts wound neatly serrated edge cracked blunt injury to the scalp and scalp contusions and abrasions.

TREATMENTS : Scalp laceration main emergency treatment to stop bleeding. The most common method is bandaged, and then wound debridement in areas where conditions permit.

SKULL FRACTURES

A head injury may cause skull fracture, which may or may not be associated with injury to the brain.

CLASSIFICATION OF SKULL FRACTURES:

TYPE DESCRIPTION

Linear

Linear skull fractures are breaks in the bone that transverse the full thickness of the skull from the outer to inner table. They are usually fairly straight with no bone displacement. The common cause of injury is blunt force trauma where the impact energy transferred over a wide area of the skull.Linear skull fractures are usually of little clinical significance unless they parallel in close proximity or transverse a suture, or they involve a venous sinus groove or vascular channel. The resulting complications may include suture diastasis, venous sinus thrombosis, and epidural hematoma. In young children, although rare, the possibility exists of developing a growing skull fracture especially if the fracture occurs in the parietal bone.

Depressed

A depressed skull fracture is a type of fracture usually resulting from blunt force trauma, such as getting struck with a hammer, rock or getting kicked in the head. These types of fractures—which occur in 11% of severe head injuries—are comminuted fractures in which broken bones displace inward. Depressed skull fractures present a high risk of increased pressure on the brain, or a hemorrhage to the brain that crushes the delicate tissue.Compound depressed skull fractures occur when there is a laceration over the fracture, putting the internal cranial cavity in contact with the outside environment, increasing the risk of contamination and infection. In complex depressed fractures, the dura mater is torn. Depressed skull fractures may require surgery to lift the bones off the brain if they are pressing on it.

Simple

Fracture without fragmentation or communicating lacerations.

Comminuted

Multiple liner fracture with fragmentation of bone into many pieces.

Compound

A fracture in conjunction with an overlying laceration that tears the epidermis and the meninges—or runs through the paranasal sinuses and the middle ear structures, putting the outside environment in contact with the cranial cavity—is a compound fracture.Compound fractures may either be clean or contaminated. Intracranial air (pneumocephalus) may occur in compound skull

fractures. The most serious complication of compound skull fractures is infection. Increased risk factors for infection include visible contamination, meningeal tear, loose bone fragments and presenting for treatment more than eight hours after initial injury.

Compound elevate

A compound elevated skull fracture is a rare type of skull fracture where the fractured bone is elevated above the intact outer table of the skull. This type of skull fracture is always compound in nature. It can be caused during an assault with a weapon where the initial blow penetrates the skull and the underlying meninges and, on withdrawal, the weapon lifts the fractured portion of the skull outward. It can also be caused the skull rotating while being struck in a case of blunt force trauma, the skull rotating while striking an inanimate object as in a fall, or it may occur during transfer of a patient after an initial compound head injury.

Growing skull fracture

A growing skull fracture (GSF) also known as a craniocerebral erosion or leptomeningeal cyst due to the usual development of a cystic mass filled with cerebrospinal fluid is a rare complication of head injury usually associated with linear skull fractures of the parietal bone in children under 3. It is characterized by a diastatic enlargement of the fracture.The primary causative factor is a tear in the dura mater.

Cranial burst skull fracture

A cranial burst skull fracture usually occurring with severe injuries in infants less than 1 year of age is a closed, diastatic skull fracture with cerebral extrusion beyond the outer table of the skull under the intact scalp.Acute scalp swelling is associated with this type of fracture. In equivocal cases without immediate scalp swelling the diagnosis may be made via the use of magnetic resonance imaging thus insuring more prompt treatment and avoiding the development of a "growing skull fracture".

Diastatic fracture

Diastatic fractures occur when the fracture line transverses one or more sutures of the skull causing a widening of the suture. While this type of fracture is usually seen in infants and young children as the sutures are not yet fused it can also occur in adults. When a diastatic fracture occurs in adults it usually affects the lambdoidal suture as this suture does not fully fuse in adults until about the age of 60.

CLINICAL MANIFESTATIONS OF SKULL FRACTURES DEPENDING ON INVOLVED AREA

LOCATION SYNDROME / SEQUELEFrontal fracture Exposure of brain to the contaminants through frontal air

sinus, possible association Orbital fracture raccon eye

Temporal fracture

battle’s sign

Parietal fracture deafness, otorreoaPosterior fossa fracture

occipital bruising, cortical blindness

Basilar skull fracture

Basilar skull fractures are linear fractures that occur in the floor of the cranial vault (skull base), which require more force to cause than other areas of the neurocranium. Thus they are rare, occurring as the only fracture in only 4% of severe head injury patients.Basilar fractures have characteristic signs: blood in the sinuses; a clear fluid called cerebrospinal fluid (CSF) leaking from the nose (rhinorrhea) or ears (otorrhea); periorbital ecchymosis often called 'raccoon eyes' (bruising of the orbits of the eyes that result from blood collecting there as it leaks from the fracture site); and retroauricular ecchymosis known as "Battle's sign" (bruising over the mastoid process).

Dementia pugilistica , or "punch-drunk syndrome", caused by repetitive head injuries, for example in boxing or other contact sports

A severe injury may lead to a coma or death Shaken baby syndrome — a form of child abuse

Concussion

Concussion derives from the Latin term concutere ("to shake violently") or concussus ("action of striking together"), is the most common type of traumatic brain injury. The terms mild brain injury, mild traumaticbrain injury (MTBI), mild head injury (MHI), minor head trauma, and concussion may be use interchangeably.

Concussion defined as a head injury with a temporary loss of brain function, concussion causes a variety of physical, cognitive, and emotional symptoms, which may not be recognized if subtle.

Three grading systems have been most widely followed: by Robert Cantu, the Colorado Medical Society, and the American Academy of Neurology. Each employs three grades, as summarized in the following table:

Comparison of historic concussion grading scales – not currently recommended for use by medical professionalsGuidelines  Grade I Grade II Grade IIICantu Post-traumatic

amnesia <30 minutes, no loss of consciousness

Loss of consciousness <5 minutes or amnesia lasting 30 minutes–24 hours

Loss of consciousness >5 minutes or amnesia >24 hours

Colorado Medical Society

Confusion, no loss of consciousness

Confusion, post-traumatic amnesia, no loss of consciousness

Any loss of consciousness

American Academy of Neurology

Confusion, symptoms last <15 minutes, no loss of consciousness

Symptoms last >15 minutes, no loss of consciousness

Loss of consciousness (IIIa, coma lasts seconds, IIIb for minutes)

SIGNS AND SYMPTOMS

Physical

1. Headache is the most common MTBI symptom.2. Dizziness 3. Vomiting4. Nausea 5. Lack of motor coordination 6. Difficulty balancing 7. Problems with movement or sensation8. Visual symptoms include light sensitivity,seeing bright light, blurred

vision, and double vision.9. Tinnitus, or a ringing in the ears, is also commonly reported.10. Concussive convulsions are thought to result from temporary

loss or inhibition of motor function, and are not associated either with epilepsy or with more serious structural damage.

Cognitive and emotional

1. Confusion 2. disorientation 3. difficulty focusing attention4. Loss of consciousness

5. Post-traumatic amnesia, in which events following the injury cannot be recalled is a hallmark of concussion A person may repeat the same questions, be slow to respond to questions or directions, have a vacant stare, or have slurred or incoherent speech.

6. Changes in sleeping pattern 7. difficulty with reasoning, concentrating, and performing everyday

activities.8. Concussion can result in changes in mood including crankiness, loss

of interest in favorite activities or items, tearfulness, and displays of emotion that are inappropriate to the situation. Common symptoms in concussed children include restlessness, lethargy, and irritability.

PATHOPH YSIOLOGY

The pathology of a concussion seems to start with the disruption of the cell membrane of nerve cells.

This results in a migration of potassium from within the cell into the extracellular space with subsequent release of glutamate which potentiates further potassium shift, in turn resulting in depolarization and suppression of nerve activity.

In an effort to restore ion balance, the sodium-potassium ion pumps increase activity, which results in excessive ATP (adenosine triphosphate) consumption and glucose utilization.

Lactate accumulates but, paradoxically, cerebral blood flow decreases, which leads to a proposed "energy crisis."

After this increase in glucose metabolism, there is a subsequent lower metabolic state which may persist for up to 4 weeks after injury.

A completely separate pathway involves a large amount of calcium accumulating in cells, which may impair oxidative metabolism and begin further biochemical pathways that result in cell death.

Again, both of these main pathways have been established from animal studies and the extent to which they apply to humans is still somewhat unclear.

Red flag criteria : warning features

1. Seizure

2. Worsening headache

3. Difficulty waking-up

4. Seeing double

5. Problem recognizing people or places

6. Repeated vomiting7. Focal neurological problems8. Not usual self

COMPLICATIONS OF CONCUSSION:

1. Post-concussion syndrome

In post-concussion syndrome, symptoms do not resolve for weeks, months, or years after a concussion, and may occasionally be permanent. Symptoms may include headaches, dizziness, fatigue, anxiety, memory and attention problems, sleep problems, and irritability. Symptoms usually go away on their own within months.

2. Dementia pugilistica

Chronic encephalopathy is an example of the cumulative damage that can occur as the result of multiple concussions or less severe blows to the head. The condition called dementia pugilistica, or "punch drunk" syndrome, which is associated with boxers, can result in cognitive and physical deficits such as parkinsonism, speech and memory problems, slowed mental processing, tremor, and inappropriate behavior. It shares features with Alzheimer's disease.

3. Second-impact syndrome

Second-impact syndrome, in which the brain swells dangerously after a minor blow, may occur in very rare cases. The condition may develop in people who receive a second blow days or weeks after an initial concussion, before its symptoms have gone away

Intracranial hemorrhage

An intracranial hemorrhage (ICH) is a hemorrhage, or bleeding, within the skull.

CAUSES

Blood vessel within the skull is ruptured or leaks. It can result from physical trauma (as occurs in head injury) or nontraumatic causes (as occurs in hemorrhagic stroke) such as a ruptured aneurysm.

Anticoagulant therapy, as well as disorders with blood clotting can heighten the risk that an intracranial hemorrhage will occur.

DIAGNOSIS

CT scan (computed tomography) is the definitive tool for accurate diagnosis of an intracranial hemorrhage.

CLASSIFICATION

1. Intra-axial hemorrhage:

Intra-axial hemorrhage is bleeding within the brain itself, or cerebral hemorrhage. This category includes –

1.a. intraparenchymal hemorrhage, or bleeding within the brain tissue

1.b. intraventricular hemorrhage, bleeding within the brain's ventricles (particularly of premature infants).

2. Extra-axial hemorrhage

Extra-axial hemorrhage, bleeding that occurs within the skull but outside of the brain tissue, falls into three subtypes:

2.a. Epidural hemorrhage (extradural hemorrhage) :

It occur between the dura mater and the skull, is caused by trauma.

Cause- It may result from laceration of an artery, most commonly the middle meningeal artery. This is a very dangerous type of injury because the bleed is from a high-pressure system and deadly increases in intracranial pressure can result rapidly.

Clinical presentations:

Patients have a loss of consciousness (LOC), then a lucid interval, then sudden deterioration (vomiting, restlessness, LOC)

Head CT shows lenticular (convex) deformity.

Epidural hematoma:

Epidural hematoma (EDH) is a rapidly accumulating hematoma between the dura mater and the cranium.

Clinical presentation:-

These patients have a history of head trauma with loss of consciousness, then a lucid period, followed by loss of consciousness

Clinical onset occurs over minutes to hours. Many of these injuries are associated with lacerations of the middle meningeal artery.

Diagnostic criteria: A "lenticular", or convex, lens-shaped extracerebral hemorrhage that does not cross suture lines will likely be visible on a CT scan of the head. Although death is a potential complication, the prognosis is good when this injury is recognized and treated.

2.b. Subdural hemorrhage:

It results from tearing of the bridging veins in the subdural space between the dura and arachnoid mater.

Head CT shows crescent-shaped deformity.

Subdural hematoma:

Subdural hematoma occurs when there is tearing of the bridging vein between the cerebral cortex and a draining venous sinus.

Causes - 1. arterial lacerations on the brain surface 2. cerebral cortex injury .

Clinical features-depend on the site of injury and severity of injury.

1. loss of consciousness 2. Clinical onset occurs over hours.

Diagnostic study: A crescent shaped hemorrhage compressing the brain that does cross suture lines will be noted on CT of the head.

Treatment -Craniotomy and surgical evacuation is required if there is significant pressure effect on the brain.

Complications-

focal neurologic deficits depending on the site of hematoma and brain injury

increased intra cranial pressure leading to herniation of brain ischemia due to reduced blood supply and seizures.

Subarachnoid hemorrhage: It occur between the arachnoid and pia meningeal layers, like intraparenchymal hemorrhage.

Causes -Trauma or from ruptures of aneurysms or arteriovenous malformations.

Classic presentation: sudden onset of a severe headache (a thunderclap headache).

This can be a very dangerous entity, and requires emergent neurosurgical evaluation, and sometimes urgent intervention.

Subarachnoid hematoma:

A subarachnoid hematoma is bleeding into the subarachnoid space—the area between the arachnoid membrane and the pia mater surrounding the brain.

Causes- 1. head injury 2. ruptured cerebral aneurysm.

Symptoms:

a severe headache with a rapid onset ("thunderclap headache"), vomiting confusion or a lowered level of consciousness sometimes seizures

Diagnosis - CT scan of the head, occasionally by lumbar puncture.

Treatment is by prompt neurosurgery or radiologically guided interventions with medications and other treatments to help prevent recurrence of the bleeding and complications. Since the 1990s, many aneurysms are treated by a minimal invasive procedure called "coiling", which is carried out by instrumentation through large blood vessels. However, this procedure has higher recurrence rates than the more invasive craniotomy with clipping.

Hematoma type

Epidural Subdural      

Location Between the skull and the outer endosteal layer of the dura mater

Between the dura and the arachnoid

Involved vessel

Temperoparietal locus (most likely) - Middle meningeal artery

Bridging veins

Frontal locus - anterior ethmoidal arteryOccipital locus - transverse or sigmoid sinusesVertex locus - superior sagittal sinus

Symptoms(depend on severity)

Lucid interval followed by unconsciousness

Gradually increasing headache and confusion

CT appearance Biconvex lens Crescent-shaped

CEREBRAL CONTUSION

Cerebral contusion, Latin contusio cerebri, a form of traumatic brain injury, is a bruise of the brain tissue. Like bruises in other tissues, cerebral contusion can be associated with multiple microhemorrhages, small blood vessel leaks into brain tissue.

Signs and symptoms : headache; confusion; sleepiness; dizziness; loss of consciousness; nausea and vomiting; seizures; and difficulty with coordination and movement, difficulty with memory, vision, speech, hearing, managing emotions, and thinking. Signs depend on the contusion's location in the brain.

Causes:

Often caused by a blow to the head, contusions commonly occur in coup or contre-coup injuries. In coup injuries, the brain is injured directly under the area of impact, while in contrecoup injuries it is injured on the side opposite the impact.

Contusions occur primarily in the cortical tissue, especially under the site of impact or in areas of the brain located near sharp ridges on the inside of the skull. The brain may be contused when it collides with bony protuberances on the inside surface of the skull. The protuberances are located on the inside of the skull under the frontal and temporal lobes and on the roof of the ocular orbit. Thus, the tips of the frontal and temporal lobes located near the bony ridges in the skull are areas where contusions frequently occur and are most severe. For this reason, attention, emotional and memory problems, which are associated with damage to frontal and temporal lobes, are much more common in head trauma survivors than are syndromes associated with damage to other areas of the brain.

Treatment:

Since cerebral swelling presents a danger to the patient, treatment of cerebral contusion aims to prevent swelling. Measures to avoid swelling include prevention of hypotension (low blood pressure), hyponatremia (insufficient sodium), and hypercapnia (increased carbon dioxide in the blood).

Due to the danger of increased intracranial pressure, surgery may be necessary to reduce it.

Diffuse axonal injury

Diffuse axonal injury (DAI) is a brain injury in which damage in the form of extensive lesions in white matter tracts occurs over a widespread area. DAI is one of the most common and devastating types of traumatic brain injury, and is a major cause of unconsciousness and persistent vegetative state after head trauma.It occurs in about half of all cases of severe head trauma.

DAI can occur in every degree of severity from very mild or moderate to very severe. Concussion may be a milder type of diffuse axonal injury.

Mechanism

Unlike brain trauma that occurs due to direct impact and deformation of the brain, DAI is the result of traumatic shearing forces that occur when the head is rapidly accelerated or decelerated, as may occur in auto accidents, falls, and assaults. It usually results from rotational forces or severe deceleration. Vehicle accidents are the most frequent cause of DAI; it can also occur as the result of child abuse such as in shaken baby syndrome.

The major cause of damage in DAI is the disruption of axons, the neural processes that allow one neuron to communicate with another. Tracts of axons, which appear white due to myelination, are referred to as white matter. Acceleration causes shearing injury, which refers to damage inflicted as tissue slides over other tissue. When the brain is accelerated, parts of differing densities and distances from the axis of rotation slide over one another, stretching axons that traverse junctions between areas of different density, especially at junctions between white and grey matter.

Diagnosis:

1. Diffuse injury has more microscopic injury than macroscopic injury and is difficult to detect with CT and MRI, but its presence can be inferred when small bleeds are visible in the corpus callosum or the cerebral cortex.

2. Newer studies such as Diffusion Tensor Imaging are able to demonstrate the degree of white matter fiber tract injury even when the standard MRI is negative.

Since axonal damage in DAI is largely a result of secondary biochemical cascades, it has a delayed onset, so a person with DAI who initially appears well may deteriorate later. Thus injury is frequently more severe than is realized, and medical professionals should suspect DAI in any patients whose CT scans appear normal but who have symptoms like unconsciousness.

DAI IS CLASSIFIED INTO GRADES BASED ON SEVERITY OF THE INJURY:-

Grade I- widespread axonal damage is present but no focal abnormalities are seen.

Grade II- damage found in Grade I is present in addition to focal abnormalities, especially in the corpus callosum.

Grade III-damage encompasses both Grades I and II plus rostral (Rostral (Latin: rostrum; beak or nose): situated toward the oral or nasal region)brain stem injury and often tears in the tissue.

TREATMENT:

DAI currently lacks a specific treatment beyond what is done for any type of head injury, including stabilizing the patient and trying to limit increases in intracranial pressure (ICP).

Potential treatments

Polyethylene glycol acts as a membrane sealant, and may serve to prevent the aforementioned devastating calcium influx. Rats treated with polyethylene glycol immediately following DAI induction showed no cytotoxic edema on diffusion weighted MRI 7 days later unlike controls.

Common Diagnostic studies

CT identifies and localizes lesions, cerebral edema, and bleeding. Skull and cervical spine X-ray identify fracture and displacement.

Complete blood count, coagulation profile, electrolyte levels, serum osmolarity, arterial blood gases, and other laboratory tests monitor for complications.

Neuropsychological test during rehabilitation phase determine cognitive deficits.

TREATMENT:-

The Brain Injury Association of America endorses the Brain Trauma Foundation's Guidelines for the Management of Severe Brain Injury and the Colorado Traumatic Brain Injury   Medical Treatment Guidelines . 

EMERGENCY MANAGEMENT:

Assessment Findings

1. Surface findings:- Scalp lacerations Fracture or depressions Bruises or contusions on face, battle’s sign (bruising around

eyes) Raccon eyes

2. Respiratory – Central neurogenic hyperventilation Chyne- stokes respirations Decresed oxygen saturation Pulmonary edema

3. Central nervous system- Unequal / dilated pupils Asymmetric facial movements Garbled speech, abusive speech Confusion Decreased level of consciousness Combativeness Involuntary movements Seizures Bowel & bladder incontinence Flaccidity Depressed or hyperactive reflexes Decerebrate or decorticate posturing GCS<12 CSF leaking from ears or nose

Interventions:1. Initial—

Ensure patent airway Stabilize cervical spine Administer oxygen via non – rebreather mask. Establish IV access with two large-bore catheters to infuse

normal saline or lacted ringer’s solution Control external bleeding with sterile pressure dressing

2. Ongoing Monitoring- Maintain patient warmth using blankets , warm IV fluids,

overhead warming lights, warm humidified oxygen Monitor vital signs, level of consciousness, oxygen saturation,

cardiac rhythm, GCS score, pupil size & reactivity. Anticipate need for intubation if gag reflex is impaired or

absent Administer fluids cautiously to prevent fluid overload &

increasing ICP Assume neck injury with head injury.

Medications 

Anti-Anxiety Agents may lesson feelings of uncertainty, nervousness, and fear.

Anti-Coagulants may be used to prevent blood clots. Anti-Convulsants may be used to prevent seizures Phenytoin

(Dilantin) Anti-Depressants may be used to treat symptoms of depression.

Anti-Psychotics may be used to target psychotic symptoms of combativeness, hostility, hallucinations, and sleep disorders.

Muscle Relaxants may be used to reduce muscle spasms or spasticity.

Sedative-Hypnotic Agents may be used to induce sleep or depress the central nervous system in areas of mental and physical response, awareness, sleep, and pain.

Stimulants may be used to increase levels of alertness and attention.

Analgesic; codein phosphate

Anesthetic; Lidocin (Xylocaine) Anticonvulsant; Barbiturate; pentobarbital (Nembutal), if unable to

control ICP with diuresis Diuretic; mannitol (Osmitrol), furosemide (Lasic) to combat cerebral

edema Dopamine (Intropin) to maintain cerebral perfusion pressure above

50 mmHg (if blood pressure is low and ICP is elevated) Glucocorticoid; dexamethasone (Decadron) to reduce cerebral

edema Histamin-2 (H2) receptor antagonist such as cimetidine (tagamet),

ranitidine (Zantag), famotidine (Pepcid), nizatidine (Axid) Mucosal barriel fortifier; sucralfate (Carafate) Posterior pituitary : vasopressin (Pitressin) if client develops

diabetes insipidus.

OTHER TREATMENTS:-

Cervical collar (until neck injury is ruled out)

Craniotomy; surgical incision into te cranium (may be necessary to evacuate a hematoma or evacuate contents to make room for swelling to prevent herniation)

Oxygen (O2) Therapy; intubation and mechanical ventilation (to provide controlled hyperventilation to decrease elevate ICP)

Restricted oral intake for 24 to 48 hours Ventriculostomy; insertion of a drain into the ventricles (to drain CSF

in the presence of hydrocephalus, which may occur as a result of head injury; can also be used to monitor ICP).

Acute RehabilitationAs early as possible in the recovery process, individuals who sustain brain injuries will begin acute rehabilitation. The treatment is provided in a special unit of the trauma hospital, a rehabilitation hospital or another

inpatient setting. During acute rehabilitation, a team of health professionals with experience and training in brain injury work with the patient to regain as many activities of daily living as possible. Activities of daily living including dressing, eating, toileting, walking, speaking and more. 

Postacute RehabilitationWhen patients are well enough to participate in more intensive therapy, they may be transferred to a postacute rehabilitation setting, such as a residential rehabilitation facility. The goal of postacute rehabilitation is to help the patient regain the most independent level of functioning possible. Rehabilitation channels the body's natural healing abilities and the brain's relearning processes so an individual may recover as quickly and efficiently as possible. Rehabilitation also involves learning new ways to compensate for abilities that have permanently changed due to brain injury. There is much that is still unknown about the brain and about brain injury rehabilitation. Treatment methods and technologies are rapidly advancing as knowledge of the brain and its function increases.

Subacute Rehabilitation Patients who cannot tolerate intensive therapy may be transferred to a subacute rehabilitation facility. Subacute rehabilitation programs are designed for persons with brain injury who need a less intensive level of rehabilitation services over a longer period of time. Subacute programs may also be designed for persons who have made progress in the acute rehabilitation setting and are still progressing but are not making rapid functional gains. Subacute rehabilitation may be provided in a variety of settings, often a skilled nursing facility or nursing home.

Day Treatment (Day Rehab or Day Hospital) Day treatment provides rehabilitation in a structured group setting during the day and allows the person with a brain injury to return home at night.

:NURSING MANAGEMENT:

NURSING ASSEment

Related Factors:

Hydrocephalus, Increased cerebral blood flow (hypercapnea, hyperemia), Injury with cerebral edema, Intracranial mass, Systemic hypotension. Defining Characteristics

1.Decreased level of consciousness (LOC): confusion, disorientation, somnolence, lethargy, and coma; 2.Headache; 3.Vomiting; 4.Papilledema; Pupil asymmetry; 5.Decreased pupil reactivity;6.Impaired memory, 7.judgment, thought processes;8.Glasgow Coma Scale (GCS) score less than 13; 9.Unilateral or bilateral VI nerve palsy; 10.Repeated increases in ICP greater than 10 mm Hg for more than 5 minutes;11.Elevated ICP waveforms; 12.Baseline ICP>10 mm Hg; 13.Wide amplitude ICP waveform; 14.Volume pressure response test variation;15.Decreased cerebral blood flow (CBF); 16.Decreased cerebral perfusion pressure (CPP); 17.Hypertension; 18.Increased or decreased heart rate with arrhythmias; 19.Widening pulse pressure; 20.vertigo, agitation, and restlessness; 21.Cerebrospinal fluid leakage at ears and nose, which may indicate skull fracture; 22.Contusions about eyes and ears indicating skull fractures; 23.Irregular respirations; 24.Cognitive deficit; 25.Pupillary abnormality; 26.Sudden onset of neurologic deficits; 27.Otorrhea indicating posterior fossa skull fracture; 28.Rhinorrhea indicating anterior fossa skul fracture.

ONGOING ASSESSMENT

1. Assess neurologic status as follows: LOC per Glasgow Coma Scale--pupil size, symmetry, and reaction to light; extraocular movement (EOM); gaze preference; speech and thought processes; memory; motor-sensory signs and drift; increased tone; increased reflexes; Babinski reflex.

Deteriorating neurological signs indicate increased cerebral

ischemia.

2. Evaluate presence or absence of protective reflexes (e.g., swallowing, gagging, blinking, coughing, and others).

(i) Monitor vital signs.

Continually increasing ICP results in life-threatening

hemodynamic changes; early recognition is essential to survival.

(c) Monitor arterial blood gases (ABGs) and/or pulse oximetry. Recommended parameters of PaO2>80 mm Hg and PaCO2<35 mm Hg with normal ICP. If patient's lungs are being hyperventilated to decrease ICP, PaCO2 should be between 25 and 30 mm Hg.

A PaCO2<20 mm Hg may decrease CBF because of profound

vasoconstriction that produces hypoxia. PaCO2>45 mm Hg

induces vasodilation with increase in CBF, which may trigger

increase in ICP.

(i) Monitor input and output with urine-specific gravity. Report urine-specific gravity >1.025 or urine output <1.50 ml/kg/hr.

May indicate decreased renal perfusion and possible associated

decrease in CPP.

(i) Monitor ICP if measurement device is in place. Report ICP>15 mm Hg for 5 minutes.

(i) Calculate cerebral perfusion pressure (CPP). Calculate CPP by subtracting ICP from the mean systemic arterial pressure (MSAP): CPP=MSAP-ICP Determine MSAP using the following formula:

Systolic BP - Diastolic BP + Diastolic BP                3

Should be approximately 90 mm Hg to 100 mm Hg and not <50

mm Hg to ensure blood flow to brain.

(c) Monitor serum electrolytes, blood urea nitrogen (BUN), creatinine, glucose, osmolality, hemoglobin (HGB), and hematocrit (HCT) as indicated.

To detect treatment complications such as hypovolemia.

(c) Monitor closely when treatment of increased ICP begins to taper.

ICP may increase as treatment is tapered.

(c) Serially monitor ICP pressure and waveforms.

Sustained ICP>15 mm Hg causes transtentorial herniation and

brain stem compression/herniation with resultant compression of

the respiratory center, apnea, and cardiac arrest. Presence of A

and B waves indicates neurological deterioration; the physician

should be immediately informed.

Types of ICP waveforms:

Lundberg A waves (plateau waves) are increased ICP>50 mm Hg sustained for more than 5 minutes.

These waves indicate a neurological emergency necessitating

immediate intervention to avoid brain damage.

B waves are increased ICP, usually between 20 mm Hg to 40 mm Hg and may precede an A wave.

These can be seen with changes in respiratory pattern and must

be watched as a possible prelude to A waves.

C waves are nonpathological and often correlate with heart rate and respiratory rate.

These waves are typically <20 mm Hg and occur every 4 to 8

minutes.

Nursing Diagnosis for Brain Injury

1. Ineffective airway clearance and impaired gas exchange related to brain injury

Goal: Maintains clear airway.

Plan of Intervention: Positioning of the patient is to be done (head tilt, chin lift, extension

of the neck). Secretions that obstruct the airway should be suctioned. Blood gas analysis is to be done. Endotracheal intubation can be done. Tracheostomy can be done if there is upper airway obstruction. Lung auscultation is to be done atleast three times per day. If the patient is conscious, encourage him or her to cough out the

secretion. Hyperoxygenate the patient before and after suctioning.2. Ineffective cerebral tissue perfusion related to increased

ICP, decreased CPP, and possible seizuresGoal: Maintains cerebral perfusion with normal parameters

Plan of Intervention: Monitor determinants of tissue oxygen delivery ( e.g PaCO2, SaO2,

Hb, Cardiac output) to ensure adequate oxygenation to support brain function.

Calculate and monitor CPP to evaluate adequacy of cerebral blood perfusion.

Monitor neurologic status to determine hemodynamic status. Proper positioning ( head in neutral position or head end of the bed

is elevated 0-60 deg) Extreme rotation of the neck and flexion of the neck is avoided to

prevent compression on jugular vein. Valsalva maneuver is to be avoided. Emotional stress and frequent arousal from sleep is to be avoided. Increase blood pressure with volume expansion or inotropic or

vasoconstrictive agent as ordered to maintain hemodynamic parameters and maintain cerebral perfusion pressure (CPP)

Monitor intake output to assess effects of diuretics and corticosteroid therapy.

3. Deficient fluid volume related to decreased LOC and hormonal dysfunction

Goal: Maintains normal fluid electrolyte balance.

Plan of intervention: Assessment is to be done regarding fluid volume status including

edema, skin turgor, mucous membrane, tongue. Intake output is to be monitored strictly. Continuous hemodynamic monitoring is to be done. Electrolytes values are to be monitored regularly. Sign and symptoms of altered electrolyte level is to be identified

early. IV fluids or infusion is to be given through infusion pump in very

slow rate. Sign of increased ICP and pulmonary edema is to be monitored.4. Imbalanced nutrition, less than body requirements, related

to increased metabolic demands, fluid restriction, and inadequate intake

Goal: To maintain balanced nutritional status.Plan for intervention:

Nutritional status is to be assessed completely.

Oral intake is to be started within 3 days, if possible. Enteral(through ryles tube) or parenteral feeding is to be started if

oral feeding can not be started according to the plan of nutritionist. Strict intake output chart is to be maintained. Daily weight is to be checked if possible.5. Risk for injury (self-directed and directed at others) related

to seizures, disorientation, restlessness, or brain damage

Goal: Patient will have no injury.Plan for intervention:

Risk and possible cause of injury is to be assessed. Patient should be kept under constant observation. Protective environment is to be provided. If necessary, chemical or physical restraint is to be provided. If the patient having seizure, anti-epileptic drug, airway, suction

apparatus should be kept ready at bedside. Calm and reassuring approach is to be used always.6. Risk for infection related to presence of various invasive

lines, prolonged hospitalization.Goal: No sign and symptoms of infection.Plan for intervention:

Sign and symptom of infection is to be assessed. Strict aseptic technique is to be maintained during handling invasive

lines and performing invasive procedures. Proper hand hygiene is to be maintained. Personal hygiene of the patient is to be maintained. If CSF drainage system is present, colour, character of the CSF is to

be monitored. Broad spectrum antibiotics are to be administered.

Other nursing diagnosis--7. Risk for imbalanced body temperature related to damaged

temperature-regulating mechanisms in the brain8. Risk for impaired skin integrity related to bed rest,

hemiparesis, hemiplegia, immobility, or restlessness9. Deficient knowledge about brain injury, recovery, and the

rehabilitation process

CONCLUSION:

Head injury can be from mild to severe, depeding on that treatment also range from first aid to craniotomy with lifelong rehabilitation. So health teaching to patient & family is very necessary to make the client able to return in a normal life.

Bibliography:

1. Smeltzer SC, Bare BG, Hinkle JL, Cheever KH. Textbook of medical-Surgical Nursing. 11th ed. New Delhi:Wolters kluwer;2008. p. 2180-85.

2. Lewis LS, Heitkmper MM, Dirksen SR, Brien PG, Bucher L. Medical Surgical Nursing. 7th ed. Noida: Elsevier;2009. P. 1485-89.

3. Black JM, Hawks JH. Medical Surgical Nursing. 8th ed. Noida: Elsevier;2009. P. 1933-39

PEER GROUP PRESENTATION ON

HEAD INJURY