A ) DESCRIBE IN DETAIL ABOUT TRAUMATIC BRAIN INJURY ?
B ) DISCUSS ITS ETIOPATHOGENESIS AND MANAGEMENT ?
A 2 INTRODUCTION
1 Traumatic brain injury (TBI) is a nondegenerative, noncongenital insult to the brain from an external mechanical force, leading to permanent or temporary impairment of cognitive, physical, and psychosocial functions, with an associated diminished or altered state of consciousness.
2 Group of the American Congress of Rehabilitation Medicine defines mild head injury as "a traumatically induced physiologic disruption of brain function, as manifested by one of the following:
A ) Any period of loss of consciousness (LOC),
B ) Any loss of memory for events immediately before or after the accident,
C ) Any alteration in mental state at the time of the accident,
D ) Focal neurologic deficits, which may or may not be transient.
3 The other criteria for defining mild TBI include the following:
A ) GCS score greater than 12
B ) No abnormalities on computed tomography (CT) scan
C ) No operative lesions
D ) Length of hospital stay less than 48 hours
4 The following criteria define moderate TBI:
A ) Length of stay at least 48 hours
B ) GCS score of 9-12 or higher
C ) Operative intracranial lesion
D ) Abnormal CT scan findings
5 The National Institutes of Health Traumatic Coma Data Bank
The National Institutes of Health (NIH) sponsored the Traumatic Coma Data Bank (TCDB)revealed that severe TBI is indicated when the GCS score is below 9 within 48 hours of the injury.
1 TBI accounts for approximately 40% of all deaths from acute injuries
2 The mortality rate for deaths outside of the hospital is approximately 17 per 100,000 people; it is approximately 6 per 100,000 people for patients who are hospitalized.
3 The initial GCS score and, therefore, the severity of the TBI help to predict the likelihood of death from the injury.
4 The mortality rate is high in severe TBI and is low in moderate TBI.
5 Rates are higher among children aged 0-4 years.
6 Death and hospitalization rates are highest among black children aged 0-9 years, compared with whites, in TBIs related to motor vehicle accidents (MVAs)
7 High-risk populations
A ) Some particular segments of the populace are at increased risk of sustaining a TBI, including the following:
A.1 Young people
A.2 Low-income individuals
A.3 Unmarried individuals
A.4 Members of ethnic minority groups
A.5 Residents of inner cities
A.7 Individuals with a history of substance abuse
A.8 Individuals who have suffered a previous TBI
8 Men are approximately twice as likely as women to sustain a TBI.
8.1 This ratio approaches parity as age increases because of the increased likelihood of TBI caused by falls, for which males and females have similar risks in later life.
8.2 The male-to-female mortality rate for TBI is 3.4:1.
8.3 However, the cause-specific ratio for firearm-related injuries is 6:1, while that for injuries related to MVAs is 2.4:1.
Mechanism of injury
1 MVAs are the leading cause of TBI in the general population
2 Falls are the second leading cause of TBI.
3 Falls account for 20-30% of all TBIs.
4 In individuals aged 75 years or older, falls are the most common cause of TBI.
5 Very young persons also commonly sustain TBI due to falls.
6 Firearms are the third leading cause of TBI (12% of all TBIs) and are a leading cause of TBI among individuals aged 25-34 years.
7 Gunshot-related, fatal TBIs are higher among men than among women
8 Alcohol is a major factor in many TBIs and often is associated with the leading causes of TBI.
1 Traumatic brain injury (TBI) is the result of an external mechanical force applied to the cranium and the intracranial contents, leading to temporary or permanent impairments, functional disability, or psychosocial maladjustment
2 TBI can manifest clinically from concussion to coma and death.
3 Injuries are divided into 2 subcategories: (1) primary injury, which occurs at the moment of trauma, and (2) secondary injury, which occurs immediately after trauma and produces effects that may continue for a long time.
4 The physical mechanisms of brain injury are classified using the following categories:
Impact loading - Collision of the head with a solid object at a tangible speed
Impulsive loading - Sudden motion without significant physical contact
Static or quasistatic loading - Loading in which the effect of speed of occurrence may not be significant
4.1 Impact loading causes TBI through a combination of contact forces and inertial forces.
4.2 Inertial force ensues when the head is set in motion with or without any contact force, leading to acceleration of the head.
4.3 Contact force occurs when impact injury is delivered to the head at rest.
4.4 Static or quasistatic loading is rare and occurs when a slowly moving object traps the head against a fixed rigid structure and gradually squeezes the skull, causing many comminuted fractures that may be enough to deform the brain and lead to fatal injury.
4.5 Contact or inertial forces may strain the brain tissue beyond its structural tolerance, leading to injury.
4.6 Strain is the amount of tissue deformation caused by an applied mechanical force.
4.7 The 3 basic types of tissue deformation are as follows:
Compressive - Tissue compression
Tensile - Tissue stretching
Shear - Tissue distortion produced when tissue slides over other tissue
4.8 Types of Primary Injuries
4.8.1 Primary injuries can manifest as focal injuries (eg, skull fractures, intracranial hematomas, lacerations, contusions, penetrating wounds), or they can be diffuse (as in diffuse axonal injury).
4.8.1 .A Intracranial hemorrhages
A ) Epidural hematoma occurs from impact loading to the skull with associated laceration of the dural arteries or veins, often by fractured bones and sometimes by diploic veins in the skull’s marrow.
B ) More often, a tear in the middle meningeal artery causes this type of hematoma.
C ) When hematoma occurs from laceration of an artery, blood collection can cause rapid neurologic deterioration.
22.214.171.124 Subdural hematoma tends to occur in patients with injuries to the cortical veins or pial artery in severe TBI. The associated mortality rate is high, approximately 60-80%.
2 ) SECONDARY INJURY
2.1 Secondary injuries may develop over a period of hours or days following the initial traumatic assault.
2.2 Secondary brain injury is mediated through the following neurochemical mediators :
1 Excitatory amino acids
A ) Excitatory amino acids (EAAs), including glutamate and aspartate, are significantly elevated after a TBI.
B ) EAAs can cause cell swelling, vacuolization, and neuronal death.
C ) EAAs can cause an influx of chloride and sodium, leading to acute neuronal swelling.
D ) EAAs can also cause an influx of calcium, which is linked to delayed damage.
E ) Along with N-methyl-D-aspartate receptor agonists, which also contribute to increased calcium influx, EAAs may decrease high-energy phosphate stores (adenosine 5’-triphosphate, or ATP) or increase free radical production.
F ) EAAs can cause astrocytic swellings via volume-activated anion channels (VRACs).
2 Endogenous opioid peptides
2.1 These may contribute to the exacerbation of neurologic damage by modulating the presynaptic release of EAA neurotransmitters.
2.2 Activation of the muscarinic cholinergic systems in the rostral pons mediates behavioral suppression, which often is observed in TBI, as well as LOC.
2.3 Heightened metabolism in the injured brain is stimulated by an increase in the circulating levels of catecholamines from TBI-induced stimulation of the sympathoadrenomedullary axis and serotonergic system (with associated depression in glucose utilization contributing to further brain injury.
3 Other biochemical processes leading to a greater severity of injury include an increase in extracellular potassium, leading to edema; an increase in cytokines, contributing to inflammation; and a decrease in intracellular magnesium, contributing to calcium influx.
4 Based on the effect on astrocytes, which are the cells that exhibit hypertrophic and hyperplastic responses to central nervous system (CNS) injury, increased production of protein kinase B/Akt with activation of P2 purinergic receptors has been implicated in neuronal survival in TBIs.
5 Increased intracranial pressure (ICP)
The severity of a TBI tends to increase due to heightened ICP, especially if the pressure exceeds 40 mm Hg.
Increased pressure also can lead to cerebral hypoxia, cerebral ischemia, cerebral edema, hydrocephalus, and brain herniation.
6 Cerebral edema
Edema may be caused by the effects of the above-mentioned neurochemical transmitters and by increased ICP.
Disruption of the blood-brain barrier, with impairment of vasomotor autoregulation leading to dilatation of cerebral blood vessels, also contributes.
1 Certain facilities are equipped to handle TBI better than others; initial measures include transporting patients to an appropriate treatment center.
2 Both during transport and in hospital the primary concerns are ensuring proper oxygen supply, maintaining adequate blood flow to the brain, and controlling raised intracranial pressure (ICP),
3 since high ICP deprives the brain of badly needed blood flow and can cause deadly brain herniation.
4 Treatment of raised ICP is as simple as tilting the patient’s bed and straightening the head to promote blood flow through the veins of the neck.
5 Sedatives, analgesics and paralytic agents are often used.
6 Hypertonic saline can improve ICP by reducing the amount of cerebral water (swelling), though it is used with caution to avoid electrolyte imbalances or heart failure.
7 Mannitol, an osmotic diuretic appears to be equally effective at reducing ICP
8 Diuretics, drugs that increase urine output to reduce excessive fluid in the system, may be used to treat high intracranial pressures, but may cause hypovolemia (insufficient blood volume).
9 Hyperventilation (larger and/or faster breaths) reduces carbon dioxide levels and causes blood vessels to constrict; this decreases blood flow to the brain and reduces ICP, but it potentially causes ischemia and is, therefore, used only in the short term.
10 Administration of corticosteroids is associated with an increased risk of death, and so it is recommended that they not be given routinely
11 Hypotension (low blood pressure), which has a devastating outcome in TBI, can be prevented by giving intravenous fluids to maintain a normal blood pressure
12 Body temperature is carefully regulated because increased temperature raises the brain’s metabolic needs, potentially depriving it of nutrients.
13 Seizures are common. While they can be treated with benzodiazepines, these drugs are used carefully because they can depress breathing and lower blood pressure.
14 TBI patients are more susceptible to side effects and may react adversely or be inordinately sensitive to some pharmacological agents.
15 During treatment monitoring continues for signs of deterioration such as a decreasing level of consciousness.
16 Surgery can be performed on mass lesions or to eliminate objects that have penetrated the brain.
17 Mass lesions such as contusions or hematomas causing a significant mass effect (shift of intracranial structures) are considered emergencies and are removed surgically.
18 For intracranial hematomas, the collected blood may be removed using suction or forceps or it may be floated off with water.
19 In penetrating brain injury, damaged tissue is surgically debrided, and craniotomy may be needed.
20 Craniotomy, in which part of the skull is removed, may be needed to remove pieces of fractured skull or objects embedded in the brain.
21 Decompressive craniectomy (DC) is performed routinely in the very short period following TBI during operations to treat hematomas; part of the skull is removed temporarily (primary DC).
22 DC performed hours or days after TBI in order to control high intracranial pressures (secondary DC) has not been shown to improve outcome in some trials and may be associated with severe side-effects
REHABILITATION OR STAGE AFTER RECOVERY OF ACUTE STATE
1 TO CLEAR THE CHEST AND TO ENHANCE BREATHING
A ) POSTURAL DRAINAGE
B ) VIBRATION / PERCUSSION
C ) MECHANICAL SUCTION
2 TO PREVENT JOINT STIFFNESS AND DEFORMITY FROM MUSCULAR CONTRACTION BY PASSIVE MOVEMENT OR ROM EXERCISES
3 TO ENHANCE FUNCTIONAL ACTIVITIES CONFINED TO BED
4 TO PREVENT PRESSURE SORES
5 BLADDER CARE
6 PROPER POSITIONING
PRINCIPLES OF PHYSIOTHERAPY FOR THE CONSCIOUS PATIENT
A ) ENCOURAGE ACTIVE COUGHING AND HUFFING
B ) ASSISTED ACTIVE EXERCISES TO FACILITATE VOLUNTARY MOVEMENT
C ) ESTABLISH COMMUNICATION BOTH VERBALLY AND NON VERBALLY
D ) INCREASE IN SENSORY AWARENESS BY USE OF TOUCH AND PRESSURE
E ) REEDUCATION OF RIGHTING AND EQUILIBRIUM REACTIONS
F ) REEDUCATE FUNCTIONAL ACTIVITIES BY CHOOSING THE RIGHT ACTIVITIES AND ADAPTIVE AIDS
ROLE OF PHYSIOTHERAPY
1 SUPPORTED SEATING AND STANDING = IT PROMOTES NORMAL PROPRIOCEPTION , POSTURAL TONE AND JOINT ALIGNMENT
2 APPROPRIATE WHEELCHAIR AND SUPPORTING SYSTEMS TO MAINTAIN HEAD AND TRUNK IN GOOD POSITION
3 USE OF AIDS AND ORTHOSIS
4 REHAB OF MOTOR CONTROL - USE OF SUSPENDED HARNESS AND WALKING WITH SUPPORT IN A TREADMILL
5 USE OF STRENGTH TRAINING AND AEROBIC EXERCISES
6 TEACHING THE INTERMITTENT SELF CATHETERISATION
7 MEDICINE FOR NEUROPATHIC PAIN
8 MANAGEMENT OF AGITATION