CONTENTS

HISTORY .........................................................................................................................................................................1 PHYSICAL EXAM .............................................................................................................................................................3 SALIENT FEATURES ........................................................................................................................................................8 INITIAL IMPRESSION ......................................................................................................................................................8 DIFFERENTIAL DIAGNOSIS .............................................................................................................................................9 Skull fracture (excl. base of skull) ..............................................................................................................................9 Base of skull fracture .................................................................................................................................................9 Cerebral contusion ....................................................................................................................................................9 Intracerebral haemorrhage (ICH) ............................................................................................................................10 Subdural haematoma (SDH) ....................................................................................................................................10 Epidural haematoma (EDH) .....................................................................................................................................10 Intraventricular haemorrhage (IVH) ........................................................................................................................11 Traumatic subarachnoid haemorrhage (SAH) .........................................................................................................11 Diffuse axonal injury (DAI).......................................................................................................................................11 Mild traumatic brain injury (mTBI) ..........................................................................................................................11 FINAL DIAGNOSIS:........................................................................................................................................................12 DEFINITION ..................................................................................................................................................................12 ETIOLOGY .....................................................................................................................................................................12 EPIDEMIOLOGY ............................................................................................................................................................13 PATHOPHYSIOLOGY .....................................................................................................................................................14 STEP-BY-STEP DIAGNOSTIC APPROACH .......................................................................................................................15 Initial clinical evaluation ..........................................................................................................................................15 Neurologic assessment ...........................................................................................................................................15 Pupillary examination..............................................................................................................................................16 Ocular movement examination...............................................................................................................................16 Oculocephalic testing ..............................................................................................................................................17 Oculovestibular testing ...........................................................................................................................................17 Motor examination .................................................................................................................................................18 Sensory examination ...............................................................................................................................................18 Peripheral reflex examination .................................................................................................................................18 Laboratory Studies ..................................................................................................................................................19 Imaging Studies .......................................................................................................................................................19

CT scan ................................................................................................................................................................19 Criteria for immediate request for CT scan of the head (adults) ........................................................................19 Criteria for CT scan to be performed within 1 hour of receipt of request by radiology department .................20 Criteria for CT scan to be performed within 8 hours of injury ............................................................................20 Criteria for immediate request for CT imaging of the cervical spine (adults) .....................................................20 Skull radiographs .....................................................................................................................................................22 MRI ..........................................................................................................................................................................22 Angiography ............................................................................................................................................................22 PROGNOSIS ..................................................................................................................................................................23 PLAN OF MANAGEMENT .............................................................................................................................................24 Criteria for admission ..............................................................................................................................................24 Transfer from secondary settings to a neuroscience unit .......................................................................................24 Medical ....................................................................................................................................................................24 Surgical ....................................................................................................................................................................25 Diet ..........................................................................................................................................................................25 Activity.....................................................................................................................................................................25 Observation of admitted patients ...........................................................................................................................25 Discharge .................................................................................................................................................................26 Outpatient appointments .......................................................................................................................................26 COMPLICATIONS ..........................................................................................................................................................26 Posttraumatic seizures ............................................................................................................................................26 Hydrocephalus ........................................................................................................................................................27 Deep vein thrombosis .............................................................................................................................................27 Heterotopic ossification ..........................................................................................................................................27 Spasticity .................................................................................................................................................................27 GI and GU complications .........................................................................................................................................28 Gait abnormalities ...................................................................................................................................................28 CONSEQUENCES OF TRAUMATIC BRAIN INJURY .........................................................................................................29 Neurological impairment (motor, sensory and autonomic) ...................................................................................29 Cognitive impairment ..............................................................................................................................................29 Personality and behavioural changes......................................................................................................................29 Common lifestyle consequences .............................................................................................................................29 REFERENCES:................................................................................................................................................................30

NAYAN MAHARJAN MDIII 1 February 5, 2013

HISTORY
Identifying data: E.S., 38 y.o is a Filipino married male, roman catholic from san Jose Florida Blanca, Source and reliability: wife (90%) CC: Motor Vehicle Accident History of present illness: On January 20, 2013 at 5:00 in the afternoon (3 hours Pta). Pt, on his way home from a christening party, claimed to be under the influence of alcohol by the source, was on board his single type motorcycle taxiing at a speed of approximately 40 kph, hit an electric post on a local road in Benedicto, Florida Blanca. The source, implied a direct hit on the patient's head (left forntal aspect) and the concrete post as he is not wearing a protective helmet. She also mentioned that upon impact patient lost his consciousness.She (source) could not recall the actual position of the patient after the collision. 7:00 pm (1 hour PTa). He was rushed by the locals to a district hospital in Florida Blanca in which he was attended. He was inserted with a bag assisted ventilation and was advised to be transferred to JBLMRH for a more comprehensive care. 8:00 pm. Patient arrived at JBLMRH-Emergency department. Pt regained consciousness. He was attempted to be inserted with a nasogastric tube but as the attending staff inserts the tube, patient vomited. It was described that the vomitus is approximately 1 cup in quantity, and was characterized to be blood tinged and contains food particles. Due to the vomiting and possibly through the intentional act of the patient the ventilator was displaced as per the source it was no longer reapplied and the NGT was no longer reapplied as well. Source mentioned that at times, the patient is disoriented and usually would not respond to some questions due to his condition. Aside for the vomiting there were no more observations made by the source, there were no complaints of body/ extremity pains nor any other accompanying manifestations. Source furthered that during the dates January 20, 2013 up to January 29, 2013, the parient's condition improved gradually as he's swelling on his left eye subsided and he could be able to walk to the CR with support.

NAYAN MAHARJAN MDIII 2 February 5, 2013

Past medical history Allergy to shrimp Unrecalled immunization. Childhood illness: chickenpox, mumps. Age unrecalled. No history of previous hospitalizations & surgery. Family history: Father: 75 year old, history of tuberculosis Mother: 65 year old, history of urinary stone surgery Sibling 1) male: 48 year old, apparently well 2) female: 41 year old, apparently well 3) male: (patient) 4) male: 38 year old, apparently well 5) female: 37 year old, died at motorvehicular accident 6)female: apparently well 7)female: apparently well 8)female: apparently well Wife: 40 year old, obese Children 1). 16 year old boy, apparently well 2). 13year old girl, apparently well 3). 11 year old girl, apparently well 4). 7 year old boy, apparently well Personal and social the family does not know how many sticks of cigarette per day and for how long, as for the type of alcohoic beverage the patient is drinking it is usually brandy (emperador) and beer (red horse) Diet and Environment Patient eats 3 times a day. His usual breakfast consist of soft food like bread, milk noodles, porage and rice with soup. For lunch and dinner, he eats half cup rice with fish or pork. He has no food restrictions. They buy food from the market and his wife cooks for the family. Their source of water is Jetmatiz. The patient lives in mixed type house with 7 people residing in it. There are 2 bedrooms and 2

NAYAN MAHARJAN MDIII 3 February 5, 2013

bathroom which is septic tank type with flush. The house is well ventilated and well lighted. The garbage is collected is burn regularly.

PHYSICAL EXAM
General: Patient was seen in bed with IV line on his right hand and urinary catheter attached. He is confused and incoherent. He is brown-skinned, medium built male. Vital signs: BP: 140/90mmHg RR: 17cpm HR: 76bpm Temperature: 35.8 C

Skin: Warm, smooth, brown, with good turgor. No rash, petechiae, ecchymoses, jaundice, cyanosis. Dark hair with normal quantity, distribution and texture. Nails without clubbing or cyanosis. Head: with normally distributed black hair; face is symmetrical with no deviations in the jaw; No masses, nodules depressions noted. Stitches seen on the left temporal lobe. Eyes: Racoons eyes with hyphema on the left side. Both the eyes are bruised. Positive ROR on both eyes. On pupillary light reflex, left pupil remained dilated while right pupil showed positive pupillary light reflex. EOMs were intact however, the patient could not see the objects on left upper and left lower field of vision. Ear: auricles are firm, not tender, no discharges, and tympanic membrane intact. Nose: septum midline, No polyps, no nasal discharge. Throat and mouth: Lips were dark but not cyanotic; teeth, oral mucosa, uvula, tongue, and tonsils were normal. Neck: Neck is supple with no scars, masses, swelling, and deformities. Trachea is located at midline and there is no apparent thyroid enlargement. There is also no tenderness and pain. Thorax (chest and lungs): Symmetrical chest expansion, without chest retractions. There is no lagging on both lun fields. There are crackles on the both lower lung field during inspiration and expiration. Cardiovascular: Adynamic precordium. Rhythm is regular. No thrills and heaves, apex beat located in the 5th ICS left mid clavicular line. There is no peripheral edema, cyanosis or pallor. Extremities are warm and well perfused. Capillary refill is less than 2 seconds. No carotid bruits. Breast: Symmetric. No masses; nipples without discharge. Abdomen: Abdomen is flat, umbilicus midline. no dilated veins, or rashes. No tenderness or guarding. There are no masses or hepatosplenomegaly. The liver span was approximately 5-6 cm in the right

NAYAN MAHARJAN MDIII 4 February 5, 2013 midclavicular line. Spleen and kidneys are also not palpable. Normoactive bowel sounds. No bruits. Musculoskeletal/extremities: No joint deformities. Good range of motion in hands, wrists, elbows, shoulders, spine, hips, knees, ankles. 5/5 muscle strength on all extremities. Peripheral Vascular: Absence of varicosities on both lower extremities. No edema on both lower extremities. Pulse at different sites (radial, femoral, popliteal, dorsalisredis, posterior tibia) =2. Neurological Examination: Glasgow coma scale Eye-opening Response: Spontaneous eye opening 4 Verbal Response: Inappropriate words 3 Motor Response: Obeys commands 6 GCS: 13 MENTAL STATUS EXAMINATION: Appearance casual dress, normal grooming and hygiene Attitude calm Behavior some unusual behavior like repeating the same answer whenever asked a question Speech Incoherent Affect normal Mood neutral Thought Processes Incoherent Thought Content incoherent Perception cannot be assessed/ determined Orientation not oriented to time, place, and person Memory/ Concentration Weak Insight/Judgement cannot be assessed/ determined

Mini mental status examination:

NAYAN MAHARJAN MDIII 5 February 5, 2013 Date orientation: patient cannot state the date/ incoherent Place orientation: patient cannot state the place where he is/ incoherent Register three objects: patient cannot follow instructions Serial sevens: patient cannot follow instructions Naming: can name 3 objects. Repeating a phrase: cannot repeat any phrase, incoherent Verbal commands: can follow verbal commands intermittently Written commands: cannot follow written commands Writing: cannot write anything Drawing: cannot draw any shapes or figure Score: 4/30 Cranial Nerves: CN I olfaction intact, can smell ..what? CN II right intact, left pupil dilated, anisocoric CN III, IV, VI intact EOM, full and equal conjugate eye movements, no ptosis CN V- Intact V1-V3, can clench jaw CN VII intact able to raise eyebrows, and smile CN VIII intact, gross intact hearing, no nystagmus CN IX, X intact, uvula midline CN XI intact, able to raise shoulder CN XII intact, tongue in midline in phonation and protrusion Sensory Examination: Touch: can perceive light touch from a fine brush

NAYAN MAHARJAN MDIII 6 February 5, 2013 Sharp/Dull: can/not differentiate sharp and dull objects with eyes closed Proprioception: can/not perceive whether his finger or toe moved up or down with his eyes closed Stereognosis: can/not identify ballpen with eyes closed Graphesthesia: can/not identify numbers, letters, and objects drawn on the palm of his hand while his eyes were closed MMT: graded 5/5 on upper and 5/5 lower extremities with good range of motion Deep Tendon Reflexes: Biceps Right 2+ Left 2+ Triceps 2+ 2+ Brachioradialis Patella Achilles Plantar 2+ 2+ 2+ 2+ 2+ 2+ 2+ 2+

2+: Average/Normal 1+: Slightly diminished

Primitive Reflexes: Absent Babinskis Sign, Chaddocks sign Coordination Test: (-) Finger to nose (-) Heel to shin (-) Rapid alternating movements (-) Fine motor Rombergs Test not done Gait: Not assessed Aphasia: (+) Wernickes aphasia

NAYAN MAHARJAN MDIII 7 February 5, 2013 ASSESSMENT OF HIGHER CORTICAL FUNCTION No obvious gaze preference or hemiparesis Sensory inattention (-) visual inattention (-) tactile inattention

(+) left side lesion (+) aphasia o Fluency not impaired (spontaneous speech) o Repetition not impaired (can repeat hello) o Comprehension impaired (cannot follow raise your right arm) o Naming not impaired (can name ballpen, watch) o Reading impaired (cannot read raise your right arm) o Writing impaired (doesnt know what to do when given paper and pen)

(-) right side lesion (-) apraxia Agnosia cannot be assessed since patient is suffering from loss of sensation and language ability is impaired

Parietal lobe function o Frontal lobe (+) grasp reflex and palmomental reflex, glabella tap (-) optic atrophy (+) expressive dysphasia (-) labile emotion, personality changes intact

Temporal lobe (+) receptive dysphasia Short and long term memory not tested since patient cannot comprehend

Occipital lobe (-) cortical blindness

NAYAN MAHARJAN MDIII 8 February 5, 2013

SALIENT FEATURES
Subjective findings 38 year old, male Driving under influence of alcohol without helmet Over speeding(~40km/hr) High impact motor vehicular accident Direct hit on the patient's head (left forntal aspect) Loss of consciousness Blood tinged vomitus containing food particles Disoriented, unresponsive

Objective findings Confused and incoherent Left temporal lobeand frontal lobe injury Racoons eyes with hyphema on the left side Negative pupillary light reflex on left eye Left homonymous hemianopsia GCS of 13 indicate mild traumatic injury,(but it was taken during the time of interview) Speech Incoherent Incoherent thought Processes Not oriented to person, place and time Memory/ Concentration Weak Cannot follow instruction Mini-mental examination score of 4/30 indicate dementia Impaired Proprioception, Stereognosis and Graphesthesia Negative Coordination Test: Finger to nose, Heel to shin, Rapid alternating movements and Fine motor Wernickes aphasia Impaired comprehension, reading and writing

INITIAL IMPRESSION
On the basis of history and PE our initial impression is TRAUMATIC BRAIN INJURY AND MULTIPLE SKULL FRACTURE.

NAYAN MAHARJAN MDIII 9 February 5, 2013

DIFFERENTIAL DIAGNOSIS
History History of a high-velocity, direct impact to skull, a fall from height, or motor vehiclerelated injury Exam Evidence of scalp haematoma, crepitance, laceration or bony deformity; GCS and focal deficits vary depending on underlying intracranial injury 1 tests Head CT (non-contrast): will detect most skull fractures using the bone windows, and most underlying injury using the brain windows; compared to a suture, a fracture tends to be wider at the centre and more narrowed at the ends, more than 3 mm in width, and runs in straight lines with angulated turns; a fracture can be linear or comminuted, and may be depressed through the inner table Head CT (non-contrast): will detect most skull fractures using the bone windows, and most underlying injury using the brain windows
st

Other tests Skull x-ray: skull fracture

Skull fracture (excl. base of skull)

Base of skull fracture

History of high-velocity impact to the back of the head; may report clear fluid or blood draining from nose or ears; may report facial numbness, vertigo, or hearing deficits Post-auricular or periorbital ecchymosis, CSF otorrhoea or rhinorrhoea, haemotympanum, cranial nerve VII and VIII deficits Test for CSF leak on bloody discharge, tautransferrin measurement: tautransferrin positive Test for CSF leak on bloody discharge, glucose measurement: glucose positive Test for CSF leak, application of bloody discharge to tissue paper: positive halo/double ring sign (a drop of the bloody discharge is applied to tissue paper; a clear halo that extends beyond the central spot of blood suggests a CSF leak) Head MRI: haemorrhagic contusions are hyperdense on T1weighted imaging and hypodense on T2-

Cerebral contusion
History of direct impact or acceleration/deceleration typically due to fall or motor vehicle-related injury; may have history of loss of consciousness Scalp trauma may be present; depending on severity; GCS may be normal or decreased; if severe may have focal deficits, seizures, or signs Head CT (non-contrast): single or multiple parenchymal lesions, contusions commonly found on the frontal and temporal poles;

NAYAN MAHARJAN MDIII 10 February 5, 2013

of increased ICP approximately half are haemorrhagic: a focus of hyperdensity, surrounded by a hypodense area representative of oedema; nonhaemorrhagic lesions may be difficult to see on initial CT Head CT (non-contrast): hyperdense area of hemorrhage, surrounded by a hypodense area of oedema weighted imaging; nonhaemorrhagic lesions are hypodense on T1weighted imaging and hyperdense on T2 imaging

Intracerebral haemorrhage (ICH)

History of direct impact or rapid acceleration/deceleration typically due to fall or motor vehicle-related injury; witnesses may report lucid period, followed by progressive altered mental status Evidence of scalp trauma is common; seizures or focal neurological deficits related to area of haemorrhage may be present; evidence of raised ICP and herniation: altered mental status, pupillary irregularity, extension to pain, respiratory irregularity, papilloedema, fundal haemorrhage Head MRI: acute haemorrhage is hyperdense on T1weighted imaging and hypodense on T2weighted imaging

Subdural haematoma (SDH)

History of direct impact or rapid acceleration/deceleration due to fall or motor vehiclerelated injury; increased risk in patients with bleeding diathesis, anticoagulant medications, alcohol abuse; history of a fall is more common in patients with significant cerebral atrophy Scalp trauma may be present; focal neurological deficits may develop, altered mental status depending on size of lesion; may have signs of increased ICP as haematoma size increases Head CT (non-contrast): characteristically crescent-shaped; blood does not cross the midline; in the setting of acute bleeding areas of hypodense and hyperdense haematoma produce a swirling appearance Head MRI: T1-weighted MRI will appear as hypointense or isointense acutely; T2weighted imaging will display SDH as hyperintense within the first few hours, progressing to a hypointensity over the ensuing week MRI head: can aid in the visualisation of small EDH; signal intensity as similar to that seen with SDH

Epidural haematoma (EDH)

History of direct impact, patient may have had a lucid interval and then progressive deterioration of GCS Commonly scalp trauma over the temporal bone; focal neurological deficits and progressive altered mental status Head CT (non-contrast): a hyperdense extra-axial lesion with smooth margins on CT; a lentiform appearance, forming a biconvex shape as blood pushes on the brain surface; blood does not cross suture lines; swirling areas of varying density indicates active bleeding

NAYAN MAHARJAN MDIII 11 February 5, 2013 Intraventricular haemorrhage (IVH)

History of direct impact or rapid acceleration/deceleration due to fall or motor vehiclerelated injury; depending on degree of hydrocephaly, the patient may present with headache, vomiting, and ataxia or have progressed to an altered mental status Signs are due to secondary obstructive hydrocephalus and raised ICP: papilloedema, fundal haemorrhage, decreased consciousness; signs of herniation include pupillary dilation, bilateral ptosis, impaired upgaze, extension to pain, and respiratory irregularity Head CT (non-contrast): blood in the ventricles will appear as hyperdense, commonly seen in the lateral ventricles; often other associated pathology; hydrocephalus may be seen

Traumatic subarachnoid haemorrhage (SAH)

History of direct impact or rapid acceleration/deceleration, can occur due to a fall, but must rule out aneurysmal SAH; aneurysmal SAH more likely if history of sudden onset of severe headache, meningeal symptoms, nausea; an be mild with minimal symptoms, or severe with symptoms of increased ICP: altered mental status, decreased consciousness Can be mild with minimal signs, or severe with signs of increased ICP: papilloedema, fundal haemorrhage, altered mental status, decreased consciousness; signs of herniation: pupillary dilation, bilateral ptosis, impaired upgaze, extension to pain, respiratory irregularity Head CT (non-contrast): SAH on CT can be subtle; the basilar cisterns (suprasellar and quadrigeminal cisterns) should be inspected carefully for the presence of SAH, which appears hyperdense compared to CSF CT angiography (CTA): may be performed if aetiology of SAH as traumatic is uncertain; visualises potential vascular abnormalities or active bleeding sites Head MRI: SAH present ECG: non-specific; ischaemic ECG changes in SAH include ST elevation or depression, abnormal T-wave morphology, prolonged QTc interval and Uwaves. Head CT (non-contrast): initially normal in more than half of patients with DAI; should look for oedema and petechial haemorrhage, at the grey/white junction, within the corpus callosum, and the brainstem Head CT (non-contrast): usually normal MRI: indicated when CT does not explain patients symptoms; more sensitive for micro-haemorrhage and oedema

Diffuse axonal injury (DAI)

History of direct impact or rapid acceleration/deceleration of head; depending on severity, may complain of headache or vomiting, or have had a rapid progressive deterioration of GCS and coma Patients with severe DAI present with altered mental status or coma; classically have physical exam finding out of proportion to CT findings

Mild traumatic brain injury (mTBI)

Hx of blunt trauma or acceleration/deceleration forces; can result in confusion, disorientation, or impaired consciousness, dysfunction of GCS score of 13 to 15 after 30 minutes post injury or later upon presentation for health care; other transient Head MRI: usually normal

NAYAN MAHARJAN MDIII 12 February 5, 2013

memory around the time of the injury, loss of consciousness (LOC) lasting 30 minutes or less, post-traumatic amnesia for less than 24 hours; can cause observed signs of neurological or neuropsychological dysfunction such as seizures acutely following injury; symptoms include headache, dizziness, fatigue, irritability, and poor concentration (typically referred to as 'postconcussion symptoms'); when identified soon after injury, can be used to support the diagnosis of mild TBI, but cannot be used to make the diagnosis in the absence of LOC or altered consciousness neurological abnormalities such as focal signs, seizure, and intracranial lesion not requiring surgery may be present

FINAL DIAGNOSIS:
Traumatic Brain Injury, to consider subarachnoid hemorrhage, epidural hematoma, tripod fracture and semi Le Fort II fracture.

DEFINITION
Traumatic brain injury (TBI) affects up to 2% of the population per year, and constitutes the major cause of death and severe disability among young people. By far, the most important complication of TBI is the development of an intracranial hematoma, which complicates 25 to 45% of severe TBI cases, 3 to 12% of moderate TBI cases, and approximately 1 in 500 patients with mild TBI (20). Without effective surgical management, an intracranial hematoma may transform an otherwise benign clinical course with the expectation of recovery to a situation in which death or permanent vegetative survival will occur. Moreover, prolonged delay in the diagnosis or evacuation of an intracranial hematoma may produce a similar result.

ETIOLOGY
Mechanism of injury Common causes of fatal injuries vary according to gender, age, race, and geographical location. Such causes are as follows:

NAYAN MAHARJAN MDIII 13 February 5, 2013

MVAs are the leading cause of TBI in the general population, especially among whites in the United States. MVAs account for approximately 50% of all TBIs. In the United Kingdom, MVAs are the third most common cause of TBI, after falls and assaults. Falls are the second leading cause of TBI. Falls account for 20-30% of all TBIs. In individuals aged 75 years or older, falls are the most common cause of TBI. Very young persons also commonly sustain TBI due to falls. 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. Gunshot-related, fatal TBIs are higher among men than among women and are more prevalent among African Americans than they are among whites. Work-related TBIs constitute an estimated 45-50% of all TBIs. Incidence varies from 37 cases per 100,000 people for military employees (57% are related to transportation) to 15 cases per 100,000 people for civilians (50% are because of falls). While the incidence of TBIs from major causes decreased significantly following the introduction of safety measures (eg, seatbelts, helmets), the rate of TBI from gunshots has increased. Alcohol is a major factor in many TBIs and often is associated with the leading causes of TBI.

EPIDEMIOLOGY
Traumatic brain injury (TBI), also known as acquired brain injury, head injury, or brain injury, causes substantial disability and mortality. It occurs when a sudden trauma damages the brain and disrupts normal brain function. TBI may have profound physical, psychological, cognitive, emotional, and social effects. The diagnosis of mild TBI appears to be vastly underdiagnosed in the setting of systemic trauma, even in trauma centers. According to the Center for Disease Control and Prevention's National Center for Injury Prevention and Control, the following annual statistics apply in the United States: At least 1.4 million people sustain a TBI. Approximately 50,000 people die from a TBI. Approximately 475,000 TBIs occur among infants, children, and adolescents aged 0-14 years. About 80,000-90,000 people experience the onset of a long-term disability due to a TBI. The following groups are at particular risk for TBI: Males are about twice as likely as females to sustain a TBI. Infants and children aged 0-4 and adolescents aged 15-19 years are the 2 age groups at highest risk for a TBI. Adults aged 75 years or older have the highest rates of TBI-related hospitalization and death. A TBI is caused by an excessive force, blow, or penetrating injury to the head. The leading causes of TBI are as follows: Falls (28%)

NAYAN MAHARJAN MDIII 14 February 5, 2013

Motor vehicle crashes (20%) Being struck by or against objects (19%) Assaults (11%)

Mortality rates after brain injury are highest in people with a severe TBI. In the first year after a TBI, people who survive are more likely to die from seizures, septicemia, pneumonia, digestive conditions, and all external causes of injury than are other people of similar age, sex, and race. However, the mortality rate after severe TBI has decreased since the late 20th century. In one study, researchers estimated that the economic burden of TBI in the United States was approximately $37.8 billion in 1985. This estimate included $4.5 billion in direct expenditures for hospital care, extended care, and other medical care and services; $20.6 billion in work-related losses and disability; and $12.7 billion in lost income from premature death.

PATHOPHYSIOLOGY
External mechanical force applied to the cranium and the intracranial contents, leading to temporary or permanent impairments, functional disability, or psychosocial maladjustment, is the usual cause of TBI/ Injuries are divided into 2 subcategories: 1. Primary injury, which occurs at the moment of trauma, such is the case of our patient 2. Secondary injury, which occurs immediately after trauma and produces effects that may continue for a long time. The following information is focused on primary injury since this is much more related to our patients case. The physical mechanisms of brain injury are classified using the following categories: 1. Impact loading - Collision of the head with a solid object at a tangible speed; such as the case of our patient. Impact loading causes TBI through a combination of contact forces and inertial forces. 2. Impulsive loading - Sudden motion without significant physical contact; Inertial force ensues when the head is set in motion with or without any contact force, leading to acceleration of the head. Contact force occurs when impact injury is delivered to the head at rest. 3. Static or quasistatic loading - Loading in which the effect of speed of occurrence may not be significant; 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. Contact or inertial forces may strain the brain tissue beyond its structural tolerance, leading to injury. Strain is the amount of tissue deformation caused by an applied mechanical force. The 3 basic types of tissue deformation are as follows: 1. Compressive - Tissue compression 2. Tensile - Tissue stretching 3. Shear - Tissue distortion produced when tissue slides over other tissue

NAYAN MAHARJAN MDIII 15 February 5, 2013

STEP-BY-STEP DIAGNOSTIC APPROACH

Initial clinical evaluation The initial evaluation of patients with TBI involves a thorough systemic trauma evaluation according to the advanced trauma life support (ATLS) guidelines. Once this has been completed and the patient is stable from a cardiopulmonary standpoint, attention may be directed to a focused head injury evaluation. The evaluation of the spine for potential injury is critically important in patients with TBI because approximately 10% of those with severe head injuries have a concomitant spine injury. Many of these injuries are cervical spine injuries. Attempt to obtain a thorough history of the mechanism of the trauma and the events immediately preceding the trauma. Specific information, such as the occurrence of syncope or the onset of a seizure prior to a fall or a motor vehicle accident, prompts a more extended evaluation of the etiology of such an event. Because many patients with TBI have altered levels of consciousness, the history is often provided by family members, police officers, paramedics, or witnesses. Neurologic assessment After sufficient information has been obtained regarding patient history, appropriate physical and neurologic examinations are performed. The neurologic assessment begins with ascertaining the GCS score. This is a screening examination and does not substitute for a thorough neurologic examination. In addition to determining the GCS score, the neurologic assessment of patients with TBI should include the following:

Brainstem examination Pupillary examination, ocular movement examination, corneal reflex, gag reflex Motor examination Sensory examination Reflex examination

Many patients with TBI have significant alterations of consciousness and/or pharmaceuticals present that limit the scope of the neurologic examination. When such factors limit the neurologic examination, noting their presence is important.

NAYAN MAHARJAN MDIII 16 February 5, 2013 Pupillary examination A careful pupillary examination is a critical part of the evaluation of patients with TBI, especially in patients with severe injuries. When muscle relaxants have been administered to a patient, the only aspect of the neurologic examination that may be evaluated is the pupillary examination. A normal pupillary examination result consists of bilaterally reactive pupils that react to both direct and consensual stimuli. Bilateral small pupils can be caused by narcotics, pontine injury (due to disruption of sympathetic centers in the pons), or early central herniation (mass effect on the pons). Bilateral fixed and dilated pupils are secondary to inadequate cerebral perfusion. This can result from diffuse cerebral hypoxia or severe elevations of ICP preventing adequate blood flow into the brain. Pupils that are fixed and dilated usually indicate an irreversible injury. If due to systemic hypoxia, the pupils sometimes recover reactivity when adequate oxygenation is restored. A unilateral fixed (unresponsive) and dilated pupil has many potential causes. A pupil that does not constrict when light is directed at the pupil but constricts when light is directed into the contralateral pupil (intact consensual response) is indicative of a traumatic optic nerve injury. A unilateral dilated pupil that does not respond to either direct or consensual stimulation usually indicates transtentorial herniation. Unilateral constriction of a pupil is usually secondary to Horner syndrome, in which the sympathetic input to the eye is disrupted and the pupil constricts due to more parasympathetic than sympathetic stimulation. In patients with TBI, Horner syndrome may be caused by an injury to the sympathetic chain at the apex of the lung or a carotid artery injury. A unilateral constricted pupil can be caused by a unilateral brainstem injury, but this is quite rare. A core optic pupil is a pupil that appears irregular in shape. This is caused by a lack of coordination of contraction of the muscle fibers of the iris and is associated with midbrain injuries. Ocular movement examination When the patient's level of consciousness is altered significantly, a loss of voluntary eye movements often occurs and abnormalities in ocular movements are frequently present. These abnormalities can provide specific clues to the extent and location of injury. Ocular movements involve the coordination of multiple centers in the brain, including the frontal eye fields, the paramedian pontine reticular formation (PPRF), the medial longitudinal fasciculus (MLF), and the nuclei of the third and sixth cranial nerves. In patients in whom voluntary eye movements cannot be assessed, oculocephalic and oculovestibular testing may be performed.

NAYAN MAHARJAN MDIII 17 February 5, 2013 Oculocephalic testing Oculocephalic testing (doll's eyes) involves observation of eye movements when the head is turned from side to side. This maneuver helps assess the integrity of the horizontal gaze centers. Before performing oculocephalic testing, the status of the cervical spine must be established. If a cervical spine injury has not been excluded reliably, oculocephalic testing should not be performed. When assessing oculocephalic movements, the head is elevated to 30 from horizontal and is rotated briskly from side to side. A normal response is for the eyes to turn away from the direction of the movement as if they are fixating on a target that is straight ahead. This is similar to the way a doll's eyes move when the head is turned; this is the origin of the term doll's eyes. If the eyes remain fixed in position and do not rotate with the head, this is indicative of dysfunction in the lateral gaze centers and is referred to as negative doll's eyes. Some patients may have negative doll's eyes and normal oculovestibular reflexes. Oculovestibular testing Oculovestibular testing, also known as cold calorics, is another method for assessment of the integrity of the gaze centers. Oculovestibular testing is performed with the head elevated to 30 from horizontal to bring the horizontal semicircular canal into the vertical position. Oculovestibular testing requires the presence of an intact tympanic membrane; this must be assessed before beginning the test. In oculovestibular testing, 20 mL of ice-cold water is instilled slowly into the auditory canal. If is no response occurs within 60 seconds, the test is repeated with 40 mL of cold water. When cold water is irrigated into the external auditory canal, the temperature of the endolymph falls and the fluid begins to settle. This causes an imbalance in the vestibular signals and initiates a compensatory response. Cold-water irrigation in the ear of an alert patient results in a fast nystagmus away from the irrigated ear and a slow compensatory nystagmus toward the irrigated side. If warm water is used, the opposite will occur; the fast component of nystagmus will be toward the irrigated side, and the slow component will be away from the irrigated side. This is the basis for the acronym COWS, which stands for cold opposite, warm same. This refers to the direction of the fast component of nystagmus. As the level of consciousness declines, the fast component of nystagmus fades gradually. Thus, in unconscious patients, only the slow phase of nystagmus may be evaluated.

NAYAN MAHARJAN MDIII 18 February 5, 2013 A normal oculocephalic response to cold-water calorics (ie, eye deviation toward the side of irrigation) indicates that the injury spares the PPRF, the MLF, and third and sixth cranial nerve nuclei. This means that the level of injury must be rostral to the reticular activating system in the upper brainstem. If a unilateral frontal lobe injury is present, the eyes are deviated toward the side of injury prior to caloric testing. Cold-water irrigation of the opposite ear results in a normal response to caloric testing (ie, eye deviation toward the irrigated side) because the injury is in the frontal region and spares the pontine gaze centers. When a pontine injury is present, the eyes often deviate away from the side of injury. In this situation, cold-water irrigation of the contralateral ear does not cause the gaze to deviate toward the irrigated ear because an injury has occurred at the level of the pons and the pontine gaze centers are compromised. A dysconjugate response to caloric testing suggests an injury to either the third or sixth cranial nerves or an injury to the MLF, resulting in an internuclear ophthalmoplegia. If caloric testing causes a skew deviation, in which the eyes are dysconjugate in the vertical direction, this indicates a lesion in the brainstem. The exact location of injury that results in skew deviation is not known. Motor examination After completing the brainstem examination, a motor examination should be performed. A thorough motor or sensory examination is difficult to perform in any patient with an altered level of consciousness. When a patient is not alert enough to cooperate with strength testing, the motor examination is limited to an assessment of asymmetry in the motor examination findings. This may be demonstrated by an asymmetric response to central pain stimulation or a difference in muscle tone between the left and right sides. A finding of significant asymmetry during the motor examination may be indicative of a hemispheric injury and raises the possibility of a mass lesion. Sensory examination Performing a useful sensory examination in patients with TBI is often difficult. Patients with altered levels of consciousness are unable to cooperate with sensory testing, and findings from a sensory examination are not reliable in patients who are intoxicated or comatose. Peripheral reflex examination A peripheral reflex examination can be useful to help identify gross asymmetry in the neurologic examination.

NAYAN MAHARJAN MDIII 19 February 5, 2013 This may indicate the presence of a hemispheric mass lesion. Laboratory Studies After the patient has been stabilized and an appropriate neurologic examination has been conducted, the diagnostic evaluation may begin. Patients with TBI do not require any additional blood tests beyond the standard panel of tests obtained in all trauma patients. A urine toxicology screen and an assessment of the blood alcohol level are important for any patient who has an altered level of consciousness because any central nervous system depressant can impair consciousness. Imaging Studies CT scan For our case CT scan is the best modality for in the evaluation of TBI because it has a rapid acquisition time, is universally available, is easy to interpret, and is reliable. The standard CT scan for the evaluation of acute head injury is a noncontrast scan that spans from the base of the occiput to the top of the vertex in 5-mm increments. Three data sets are obtained from the primary scan, as follows: (1) bone windows, (2) tissue windows, and (3) subdural windows. These different types of exposure are necessary because of the significant difference in exposure necessary to visualize various intracranial structures. The bone windows allow for a detailed survey of the bony anatomy of the skull, and the tissue windows allow for a detailed survey of the brain and its contents. The subdural windows provide better visualization of intracranial hemorrhage, especially those hemorrhages adjacent to the brain (eg, subdural hematomas). According to NICE (National Institute for Health and Clinical Excellence) guidelines, following are the criteria to request for CT Scan of the head: Criteria for immediate request for CT scan of the head (adults) GCS less than 13 on initial assessment in the emergency department. GCS less than 15 at 2 hours after the injury on assessment in the emergency department. Suspected open or depressed skull fracture. Any sign of basal skull fracture (haemotympanum, panda eyes, cerebrospinal fluid leakage from the ear or nose, Battles sign). Post-traumatic seizure. Focal neurological deficit. More than one episode of vomiting. Amnesia for events more than 30 minutes before impact.

NAYAN MAHARJAN MDIII 20 February 5, 2013 Criteria for CT scan to be performed within 1 hour of receipt of request by radiology department GCS less than 13 on initial assessment in the emergency department. GCS less than 15 at 2 hours after the injury. Suspected open or depressed skull fracture. Any sign of basal skull fracture (haemotympanum, panda eyes, cerebrospinal fluid leakage from the ear or nose, Battles sign). More than one episode of vomiting in adults; three or more episodes of vomiting in children. Post-traumatic seizure. Coagulopathy (history of bleeding, clotting disorder, current treatment with warfarin) providing that some loss of consciousness or amnesia has been experienced; patients receiving antiplatelet therapy may be at increased risk of intracranial bleeding, though this is currently unquantified clinical judgement should be used to assess the need for an urgent scan in these patients. Focal neurological deficit.

Criteria for CT scan to be performed within 8 hours of injury Amnesia for events more than 30 minutes before impact (the assessment of amnesia will not be possible in pre-verbal children and is unlikely to be possible in any child aged under 5 years). Age 65 years or older providing that some loss of consciousness or amnesia has been experienced. Dangerous mechanism of injury (a pedestrian struck by a motor vehicle, an occupant ejected from a motor vehicle or a fall from a height of greater than 1 m or five stairs) providing that some loss of consciousness or amnesia has been experienced.

Criteria for immediate request for CT imaging of the cervical spine (adults) GCS below 13 on initial assessment. Has been intubated. Plain film series is technically inadequate (for example, desired view unavailable), suspicious or definitely abnormal. Continued clinical suspicion of injury despite a normal X-ray. The patient is being scanned for multi-region trauma.

Skull fractures may be classified as either linear or comminuted fractures. Linear skull fractures are sometimes difficult to visualize on the individual axial images of a CT scan. The scout film of the CT scan,

NAYAN MAHARJAN MDIII 21 February 5, 2013 which is the equivalent of a lateral skull x-ray film, often demonstrates linear fractures. The intracranial sutures are easily mistaken for small linear fractures. However, the sutures have characteristic locations in the skull and have a symmetric suture line on the opposite side. Small diploic veins, which traverse the skull, may also be interpreted as fractures. Comminuted fractures are complex fractures with multiple components. Comminuted fractures may be displaced inwardly; this is defined as a depressed skull fracture. Extra-axial hematomas include epidural and subdural hematomas. Epidural hematomas are located between the inner table of the skull and the dura. They are typically biconvex in shape because their outer border follows the inner table of the skull and their inner border is limited by locations at which the dura is firmly adherent to the skull. Epidural hematomas are usually caused by injury to an artery, although 10% of epidural hematomas may be venous in origin. The most common cause of an epidural hematoma is a linear skull fracture that passes through an arterial channel in the bone. The classic example of this is the temporal epidural hematoma caused by a fracture through the course of the middle meningeal artery. Epidural hematomas, especially those of arterial origin, tend to enlarge rapidly. Subdural hematomas are located between the dura and the brain. Their outer edge is convex, while their inner border is usually irregularly concave. Subdural hematomas are not limited by the intracranial suture lines; this is an important feature that aids in their differentiation from epidural hematomas. Subdural hematomas are usually venous in origin, although some subdural hematomas are caused by arterial injuries. The classic cause of a posttraumatic subdural hematoma is an injury to one of the bridging veins that travel from the cerebral cortex to the dura. As the brain atrophies over time, the bridging veins become more exposed and, as a result, are more easily injured. Occasionally, the distinction between a subdural and an epidural hematoma can be difficult. The size of an extra-axial hematoma is a more important factor than whether the blood is epidural or subdural in location. In addition, a mixed hematoma with both a subdural and an epidural component is not uncommon. Intra-axial hematomas are defined as hemorrhages within the brain parenchyma. These hematomas include intraparenchymal hematomas, intraventricular hemorrhages, and subarachnoid hemorrhages. Subarachnoid hemorrhages that occur because of trauma are typically located over gyri on the convexity of the brain. The subarachnoid hemorrhages that result from a ruptured cerebral aneurysm are usually located in the subarachnoid cisterns at the base of the brain. Cerebral contusions are posttraumatic lesions in the brain that appear as irregular regions, in which high-density changes (ie, blood) and lowdensity changes (ie, edema) are present. Frequently, 1 of these 2 types of changes predominates within a particular contusion. Contusions are most often caused by the brain gliding over rough surfaces, such as the rough portions of the skull that are present under the frontal and temporal lobes. CT scans may be used for classification and for diagnostic purposes. Marshall et al published a classification scheme that classifies head injuries according to the changes demonstrated on CT scan images. This system defines 4 categories of injury, from diffuse injury I to diffuse injury IV.

In diffuse injury I, evidence of any significant brain injury is lacking.

NAYAN MAHARJAN MDIII 22 February 5, 2013

In diffuse injury II, either no midline shift or a shift of less than 5 mm is present and the CSF cisterns at the base of the brain are widely patent. In addition, no high-density or mixed-density lesions (contusions) of greater than 25 mL in volume are present. In diffuse injury III, a midline shift of less than 5 mm is present, with partial compression or absence of the basal cisterns. No high- or mixed-density lesions with a volume greater than 25 mL are present. Diffuse injury IV is defined as midline shift greater than 5 mm with compression or absence of the basal cisterns and no lesions of high or mixed density greater than 25 mL

Skull radiographs

Once an important part of the head injury evaluation, skull radiographs have been replaced by CT scans and are rarely used in patients with closed head injury. Skull radiographs are occasionally used in the evaluation of penetrating head trauma, and they can help provide a rapid assessment of the degree of foreign body penetration in nonmissile penetrating head injuries (eg, stab wounds). Skull radiographs are sometimes used in patients with gunshot wounds to the head to screen for retained intracranial bullet fragments.

MRI MRI has a limited role in the evaluation of acute head injury. Although MRI provides extraordinary anatomic detail, it is not commonly used to evaluate acute head injuries because of its long acquisition times and the difficulty in obtaining MRIs in persons who are critically ill. However, MRI is used in the subacute setting to evaluate patients with unexplained neurologic deficits. MRI is superior to CT scan for helping identify diffuse axonal injury (DAI) and small intraparenchymal contusions. DAI is defined as neuronal injury in the subcortical gray matter or the brainstem as a result of severe rotation or deceleration. DAI is often the reason for a severely depressed level of consciousness in patients who lack evidence of significant injury on CT scan images and have an ICP that is within the reference range. Magnetic resonance angiography may be used in some patients with TBI to assess for arterial injury or venous sinus occlusion. Angiography Once a common diagnostic study in persons with acute head injury, angiography is rarely used in the evaluation of acute head injury today. However, conventional angiography has been the screening and diagnostic modality of choice for identifying blunt cerebrovascular injuries (BCVI) in trauma patients.[5]

NAYAN MAHARJAN MDIII 23 February 5, 2013 Before the development of the CT scan, cerebral angiography provided a reliable means for demonstrating the presence of an intracranial mass lesion. Angiography in used in acute head injury only when a vascular injury may be present. This includes patients with unexplained neurologic deficits, especially in the setting of temporal bone fractures, and patients with clinical evidence of a potential carotid injury (eg, hemiparesis, Horner syndrome). Goodwin et al found that conventional angiography is more accurate than 16- or 64-slice CT angiography as a screening tool for BCVI in trauma patients. In a prospective study, 158 patients underwent CT angiography (16-slice or 64-slice) at the time of injury assessment, followed 24-48 hours later with conventional angiography of the cerebral vasculature. CT angiography detected only 13 true cerebrovascular injuries (40.6%) in 12 patients, whereas conventional angiography identified 32 injuries in 27 patients. For detection of cerebrovascular injury, CT angiography had a sensitivity of 0.97 (95% confidence interval [CI], 0.92-0.99) and a specificity of 0.41 (95% CI, 0.22-0.61). A study by Emmett et al confirmed that angiography is the criterion standard for BCVI diagnosis, but that CT angiography should be added as a screening criterion in order to capture BCVI that goes unrecognized in asymptomatic trauma patients.

PROGNOSIS
Determining the patient's prognosis after TBI remains difficult and complex. The heterogeneity of patients' premorbid health status, the natures and severities of injury, the intervals from injury to initial treatment, the acute interventions, and the differences in follow-up create difficulty in developing a simple and accurate scoring system. Brown and co-authors found the following variables to be predictive of outcome:

Initial GCS score Duration of PTA Amnesia Sex Age Years of education

Cuthbert et al investigated injury severity and sociobiological and socioeconomic factors to predict discharge location (home vs not to home) in adults with moderate to severe TBI. They found GCS and acute hospital length of stay to be the most predictive in discharges to home versus not to home (ie, higher GSC and shorter LOS were more likely to be discharged to home). They also found that old age was associated with a decreased likelihood of discharge to rehabilitation and more likely to be discharged to subacute rehabilitation.

NAYAN MAHARJAN MDIII 24 February 5, 2013

PLAN OF MANAGEMENT
Criteria for admission Patients with new, clinically significant abnormalities on imaging. Patients who have not returned to GCS 15 after imaging, regardless of the imaging results. When a patient fulfils the criteria for CT scanning but this cannot be done within the appropriate period, either because CT is not available or because the patient is not sufficiently cooperative to allow scanning. Continuing worrying signs (for example, persistent vomiting, severe headaches) of concern to the clinician. Other sources of concern to the clinician (for example, drug or alcohol intoxication, other injuries, shock, suspected non-accidental injury,

Some patients may require an extended period in a recovery setting because of the use of general anaesthesia during CT imaging. Patients with multiple injuries should be admitted under the care of the team that is trained to deal with their most severe and urgent problem. Transfer from secondary settings to a neuroscience unit Local guidelines on the transfer of patients with head injuries should be drawn up between the referring hospital trusts, the neuroscience unit and the local ambulance service, and should recognise that: transfer would benefit all patients with serious head injuries (GCS 8), irrespective of the need for neurosurgery if transfer of those who do not require neurosurgery is not possible, ongoing liaison with the neuroscience unit over clinical management is essential. Medical Initial resuscitation efforts should include assessment and stabilization of airway patency, breathing and circulation. Inspection of skull for fractures and appreciation of the force and location of the impact is also mandatory. Immobilization of the spine should be followed by emergent transfer of the patient to the nearest level I trauma center supported with neurosurgical consultation. - Triage and initial management of a patient with epidural hematoma may be tailored to the degree of impairment at presentation.

NAYAN MAHARJAN MDIII 25 February 5, 2013 - Patients with a small epidural hematoma may be treated conservatively, though close observation is advised, as delayed, yet sudden, neurological deterioration may occur. - Trauma patients may require diagnostic peritoneal lavage and radiographs of the chest, pelvis and cervical spine. - Administration of IV fluids to maintain euvolemia and to provide adequate cerebral perfusion - Patients with signs of increased intra cranial pressure may be treated with osmotic diuretics and hyperventilation, with elevation of the head of the bed. - Coagulopathy or persistent bleeding may require administration of vitamin K, protamine sulfate, fresh frozen plasma, platelet transfusions, or clotting factor concentrates. Surgical Surgical evacuation of the hematoma remains to be the definitive treatment of this condition. Craniotomy or laminectomy is followed by evacuation of the hematoma, coagulation of bleeding sites, and inspection of the dura. The dura is tented to the bone and occasionally; epidural drains are employed for as long as 24 hours. Diet Enteral feedings with high caloric supplementation is required due to the hypermetabolic and catabolic phenomena associated with severe head injuries. Activity Patients being treated conservatively should undergo close observation and should avoid strenuous activity. Inpatients should remain on bed rest during the initial phase; this can be followed by a progressive increase in activity. Observation of admitted patients Observations should be performed and recorded on a half-hourly basis until GCS equal to 15 has been achieved. The minimum frequency of observations for patients with GCS equal to 15 should be as follows, starting after the initial assessment in the emergency department: half-hourly for 2 hours then 1-hourly for 4 hours then 2-hourly thereafter.

NAYAN MAHARJAN MDIII 26 February 5, 2013 Discharge No patients presenting with head injury should be discharged until they have achieved GCS equal to 15, or normal consciousness in infants and young children as assessed by the paediatric version of the Glasgow Coma Scale. All patients with any degree of head injury who are deemed safe for discharge from an emergency department or the observation ward should receive verbal advice and a written head injury advice card. The details of the card should be discussed with the patients and their carers. If necessary (for example, patients with literacy problems, visual impairment or speaking languages without a written format), other formats (for example, tapes) should be used to communicate this information. Communication in languages other than English should also be facilitated. The risk factors outlined in the card should be the same as those used in the initial community setting to advise patients on emergency department attendance. Patients and carers should also be alerted to the possibility that some patients may make a quick recovery, but go on to experience delayed complications. Instructions should be included on contacting community services in the event of delayed complications.

Outpatient appointments When a person who has undergone imaging of the head and/or been admitted to hospital experiences persisting problems, there should be an opportunity available for referral from primary care to an outpatient appointment with a professional trained in assessment and management of sequelae of brain injury (for example, clinical psychologist, neurologist, neurosurgeon, specialist in rehabilitation medicine).

COMPLICATIONS
Posttraumatic seizures Posttraumatic seizures (PTS) frequently occur after moderate or severe TBI. Seizures are usually general or partial, and absence seizures are uncommon. Seizures are classified according to the time elapsed after the initial injury: Immediate seizures occur in the first 24 hours. Early seizures occur in the first 2-7 days, and late seizures occur after 7 days. Temkin showed that prophylactic use of phenytoin is effective during the first week after a TBI. However, the author recommended discontinuation after 1 week if no seizures develop because of its lack of effect in preventing late PTS and because of possible cognitive adverse effects.

NAYAN MAHARJAN MDIII 27 February 5, 2013 Although phenytoin maybe effective in preventing seizures in the first week after a TBI, at least 50% of patients with TBI have late seizure activity for which phenytoin may not be effective. Hydrocephalus Hydrocephalus is characterized as communicating or noncommunicating on the basis of the causative obstruction. Noncommunicating hydrocephalus occurs secondary to an obstruction in the ventricular system before the point at which cerebrospinal fluid (CSF) exits the fourth ventricle. Communicating hydrocephalus is the most common form after TBI and occurs when the obstruction is in the subarachnoid space. Deep vein thrombosis Deep vein thrombosis (DVT) is common in persons with TBI, with an incidence as high as 54%. [21] In patients with TBI, risk factors for DVT include immobility, lower extremity fracture, paralysis, and disruption in coagulation and fibrinolysis. Complications of DVT include pulmonary embolism (PE), postthrombotic syndrome, and recurrence. Because DVT can result in PE, it can be critical. Given the rapid decline in pulmonary function when a PE has completely occluded the pulmonary capillary system, sudden death may be the first clinical sign. Other clinical signs of PE include shortness of breath, chest pain, and pulmonary crackles; these are usually present with small emboli. However, clinical signs and symptoms are often absent in the patient with DVT. Therefore, a high index of suspicion and timely medical intervention are of utmost importance. Heterotopic ossification Heterotopic ossification is described as ectopic bone formation in the soft tissue surrounding the joints. In TBI, the incidence of heterotopic ossification is 11-76%, with a 10-20% incidence of clinically significant heterotopic ossification. Heterotopic ossification generally causes joint pain and decreases range of motion (ROM). It is often associated low-grade fever, peri-articular swelling, peri-articular warmth, and peri-articular erythema. In decreasing order of frequency, heterotopic ossification occurs in the hips, knees, elbows, shoulders, hands, and spine. Risk factors associated with the development of heterotopic ossification after TBI are a posttraumatic coma lasting longer than 2 weeks, limb spasticity, and decreased mobility. The risk of heterotopic ossification is greatest during the first 3-4 months after injury. Spasticity Tone is defined as resistance to stretch or movement across a joint during relaxation. Spasticity is defined as velocity-dependent increase in tone. Rigidity is also a function of tone, but it is defined as the nonvelocity-dependent increase in tone. These 3 terms are not interchangeable.

NAYAN MAHARJAN MDIII 28 February 5, 2013 In one inpatient rehabilitation unit, spasticity was found in an estimated 25% of patients with TBI. Spasticity is most often encountered in lesions of the upper motor neurons, whereas rigidity is most common in disorders of the basal ganglia. The morbidity associated with spasticity is variable, because in some people, spasticity may assist in leg extension for walking or finger flexion for grasping. Prolonged low tone after TBI is generally predictive of poor motor recovery. Guidelines for the treatment of spasticity are generally based on (1) any resulting limitation in function, (2) pain, (3) prevention of contracture, and (4) assistance with positioning. First-line treatments for spasticity are correct positioning of the involved body segment and ROM exercises. Second-line treatments include splinting, casting, and other modalities. Treatment varies according to whether the spasticity is generalized or local. Generalized spasticity is usually treated systemically. Dantrolene sodium is preferred in patients with TBI because of its lack of cognitive and sedative adverse effects. GI and GU complications GI and GU complications remain among the most common sequelae in patients with TBI. Some of the most frequent GI complications are stress ulcers, dysphagia, bowel incontinence, and elevated levels on liver function tests. Underlying constipation and/or impaired communication and mobility are often the causes of bowel incontinence. The use of oral stool softeners, laxatives, and rectal suppositories may facilitate full bowel evacuation and improve incontinence. GU complications include urethral strictures, urinary tract infections, and urinary incontinence. An appropriate workup to evaluate GU symptoms and rule out infection is indicated. When the causes of urinary incontinence are impaired communication and mobility, a trial of a timed voiding is indicated to manage overflow incontinence. Patients are taken to the bathroom and given the opportunity to void without instrumentation every 2 hours during the day and every 4 hours overnight. If the patient is unable to void or cannot evacuate the urinary bladder to completion, intermittent straight catheterization may be necessary in the acute recovery period. Although not preferred, diapers and condom catheters may be needed if urinary incontinence does not improve. Voiding dysfunction and upper urinary tract status were studied in 57 survivors of coma resulting from TBI. Direct statistical links were found between urge incontinence, detrusor overactivity, and poor neurologic functional outcome, as well as between detrusor overactivity and right hemisphere injuries, and between impaired detrusor contractility and left hemisphere damages. Gait abnormalities Martini et al performed gait analysis on subjects with and without a remote concussion history, measuring velocity, step length, stride width, and time in single-leg versus double-leg stance. They found that subjects with a remote concussion history showed slowed walking velocity, greater time in double-

NAYAN MAHARJAN MDIII 29 February 5, 2013 leg stance, and less time in single-leg stance, speculating that the patients with concussion histories are trying to limit injury risk from falls. They suggest that patients with even remote concussion histories may have prolonged risk for fall injuries.

CONSEQUENCES OF TRAUMATIC BRAIN INJURY

Neurological impairment (motor, sensory and autonomic)

Motor function impairment coordination, balance, walking, hand function, speech Sensory loss taste, touch, hearing, vision, smell Sleep disturbance insomnia, fatigue Medical complications spasticity, post-traumatic epilepsy, hydrocephalus, heterotopic ossification Sexual dysfunction

Cognitive impairment

Memory impairment, difficulty with new learning, attention and concentration; reduced speed and flexibility of thought processing; impaired problem-solving skills Problems in planning, organising, and making decisions Language problems dysphasia, problems finding words, and impaired reading and writing skills Impaired judgement and safety awareness

Personality and behavioural changes

Impaired social and coping skills, reduced self-esteem Altered emotional control; poor frustration tolerance and anger management; denial, and selfcentredness Reduced insight, disinhibition, impulsivity Psychiatric disorders anxiety, depression, post-traumatic stress disorder, psychosis Apathy, amotivational states

Common lifestyle consequences

Unemployment and financial hardship Inadequate academic achievement Lack of transportation alternatives Inadequate recreational opportunities Difficulties in maintaining interpersonal relationships, marital breakdown Loss of pre-injury roles; loss of independence

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REFERENCES:
http://emedicine.medscape.com/article/433855-workup#showall NICE guidelines (national institute for health and clinical excellence) for head injury/ http://bestpractice.bmj.com/best-practice/monograph/515/diagnosis/step-by-step.html

Bradley, Walter G., et al., eds. (1999). Neurology in Clinical Practice. 3rd ed. Boston: Butterworth-Heinemann. UNDEFINED. (July 31, 2012). Assessment of traumatic brain injury, acute. In BestPractice. Retrieved Dec 3, 2012, from http://bestpractice.bmj.com/best-practice/monograph/679.html SCHWARTZS Principles of Surgery