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What is Head Injury
• Literally refers to trauma to the head. This may or may not include injury to the brain. However, the terms traumatic brain injury and head injury are often used interchangeably in the medical literature. • Brain injuries are common cause for morbidity and mortality in trauma patients. • Patient can came presenting with from minimal cognitive dysfunction to a vegetative state. • Primary injury occurs at time of trauma • Secondary injury occurs due to hypoperfusion (hypotension, increased ICP), hypoxia, hyperglycemia, or anemia. • Common causes: traffic accidents, home and occupational accidents, falls, and assaults.
Type of Head Injuries
Scalp injury Scalp hematomas Scalp laceration Scalp avulsion Skull fracture Craniocerebral injury Linear fracture Depressed fracture Cerebral concussion Diffuse axonal injury (DIA) Contusion and laceration of the brain Intracranial hematomas
APPROACH PATIENT WITH HEAD INJURY
• The initial approach to the patient is the rapid assessment of airway, breathing and circulation, and appropriate intervention if indicated. • Simultaneously, all patients with blunt trauma require cervical spine immobilization until injury is excluded. This is typically accomplished by applying a hard collar or placing sandbags on both sides of the head with the patient's forehead taped
– Tension pneumothorax , open pneumothorax , flail chest with underlying pulmonary contusion
– Hemorrhagic shock Massive hemothorax Massive hemoperitoneum, Mechanically unstable pelvis fracture, Extremity losses, Cardiogenic shock, Cardiac tamponade, Neurogenic shock, Cervical spine
• Danger and disability • Environment
Assessment of injury
• Primary survey
– The first step in patient management is performing the primary survey, the goal of which is to identify and treat conditions that constitute an immediate threat to life. The ATLS (Advanced Trauma Life Support) course refers to the primary survey as assessment of the "ABCs" (Airway with cervical spine protection, Breathing, and Circulation)
1.Airway and cervical spine • Always assume that patient has cervical spine injury • Place in hard collar and keep on until cervical spine has been 'cleared' • If patient can talk then he is able to maintain own airway • If airway compromised initially attempt a chin lift and clear airway of foreign bodies • If gag reflex present insert nasopharyngeal airway • If no gag reflex patient will need endotracheal intubation • In the comatose patient, the tongue may fall backward and obstruct the hypopharynx; this may be relieved by either a chin lift or jaw thrust. • If unable to intubate will require a
2. Breathing and ventilation
• Check position of trachea, respiratory rate and air entry, adequate oxygenation and ventilation must be assured • Tension pneumothorax, open pneumothorax, and flail chest with underlying pulmonary contusion diagnoses should be made during the initial physical examination • Tension pneumothorax is implied by respiratory distress and hypotension in combination with any of
– tracheal deviation away from the affected side, lack of or decreased breath sounds on the affected side, and subcutaneous emphysema on the affected side. – Patients may have distended neck veins due to impedance of the superior vena cava,
• open pneumothorax or "sucking chest wound" occurs with full-thickness loss of the chest wall, permitting free communication between the pleural space and the atmosphere.
– This compromises ventilation due to equilibration of atmospheric and pleural pressures, which prevents lung inflation and alveolar ventilation, and results in hypoxia and hypercarbia. – Complete occlusion of the chest wall defect without a tube thoracostomy may convert an open pneumothorax to a tension pneumothorax
• Flail chest three or more contiguous ribs are fractured in at least two locations. Paradoxical movement of this free-floating segment of chest wall may be evident in patients with spontaneous ventilation, due to the negative intrapleural pressure of inspiration.
3. Circulation and haemorrhage control
– Carotid pulse: systolic blood pressure at least 60mmHg – Femoral pulse: systolic blood pressure at least 70mmHg – Radial pulse: systolic blood pressure at least 80mmHg
• Assess pulse, capillary return and state of neck veins
• • • • • • • • •
At this point in the patient's evaluation, any episode of hypotension (defined as a SBP <90 mmHg) is assumed to be caused by hemorrhage until proven otherwise. Identify exsanguinating haemorrhage and apply direct pressure Place two large calibre intravenous cannulas for IV fluids Take venous blood for FBC, U+Es (urea and electrolites), and Cross match Take sample for arterial blood gasses Give intravenous fluids Crystalloid or colloid in adequate volume Attach patient to ECG monitor Insert urinary catheter External control of hemorrhage should be achieved promptly while circulating volume is restored. Manual compression of
4. DISABILITY • Glasgow Coma Scale (GCS) score should be determined for all injured patients. Assess level of consciousness using AVPU method
– A = alert – V = responding to voice – P = responding to pain – U = unresponsive
• Assess pupil size, equality and responsiveness
5. EXPOSURE • Fully undress patients • Avoid hypothermia
6. FLUID RESUSCITATION • Classic signs and symptoms of shock are tachycardia, hypotension, tachypnea, mental status changes, diaphoresis, and pallor • The goal of fluid resuscitation is to re-establish tissue perfusion. Fluid resuscitation begins with a 2 L (adult) or 20 mL/kg (child) IV bolus of isotonic crystalloid, typically Ringer's lactate. • Hypovolumic shock
– – – –
Up to 15% blood volume loss (750ml) 15-30% blood volume loss (750 - 1500ml) 30-40% blood volume loss (1500 - 2000ml) Loss greater than 40% (>2000ml)
– With trauma and head injury, the most immediate plain radiograph is
• Skull • Cervical spine – to exclude cervical injury • Chest – to identify lung contusion or mediastinal injury, bony injury, simple pneumthorax or heamatorax, diaphragmatic injury and correct placement of chest drain and CVP line • Pelvis – diagnose of pelvic fracture
• Secondary Survey
– Once the immediate threats to life have been addressed, a thorough history is obtained and the patient is examined in a systematic fashion. – The patient and surrogates should be queried to obtain an AMPLE history (Allergies, Medications, Past illnesses or Pregnancy, Last meal, and Events related to the injury).
• Face, head and neck
– Digital examination of the cranium, facial skeleton, cervical vertebrae and associated soft tissue to exclude fracture
• Central nervous system
– Check the pupil, GCS score.
– Detail chest examination with thoracic spine
• Abdomen and pelvis
– Exclude any abdominal injury and pelvic fracture – Do “spring test” for ribs n pelvis
– Presence of pain, pallor, pulselessnes, coldness and poor capillary refill
GCS IN ADULT AND PEDIATRIC PATIENT
Glasgow coma scale
⇒A scale for measuring level of consciousness, especially after a head injury, in which scoring is determined by three factors: amount of eye opening, verbal responsiveness, and motor responsiveness
GCS in Adult
Minimal head injury - ( GCS 15 , no loss of consciousness or amnesia ) Mild head injury - ( GCS 13 - 15 , amnesia or short loss of consciousness or impaired alertness / memory ) Moderate head injury - ( GCS 9 - 12 , loss of consciousness longer than 5 minutes or focal neurological deficit ) Severe head injury - ( GCS 5 - 8 , coma ) Critical head injury - ( GCS 3 - 4 , deep coma ).
GCS in paediatrics
CLOSE HEAD INJURY AND PENETRATING INJURY
• Classification type of head injury are
– Close head injury / blunt trauma
• The dura still intact • Associated with multiple wide distribution injuries
– Penetrating head injury
• Dura is breached • Damage is localize to the path of bullet or knife
Brain injury Secondary brain
Primary brain injury
injury • delayed pathophysiologica l consequences of TBI • Includes
– Cerebral oedema – Increased intracranial pressure (ICP) – Haemorrhage – Seizures – Ischaemia due to vasospasm, vascular/brain compression – Infection.
• results from the immediate mechanical forces that cause brain damage • Result of
– Direct contact, such as a blow to the head – Direct contact due to the brain striking against the internal surface of the skull – Inertial forces originating from rapid acceleration/deceleratio n such as that experienced in a motor vehicle collision. Notably, contact forces can also induce acceleration of the brain commonly leading to a combination of focal
CLINICAL SIGN AND SYMPTOMS OF HIGH ICP
Signs and Symptoms of Increase ICP Symptoms Signs
Headache. Pupillary Dilatation, Abducens Back Pain. (Crn VI) Palsies, Papilledema. Cushing's Triad (Increased Ringing In The Ears or Hearing Loss Nausea And Vomiting Systolic Blood Pressure, A Vision Problems, Such As Blurry Vision Or Widened Pulse Pressure, Double Vision Painful Eye Movements Bradycardia, And An Abnormal Neck Pain Respiratory Pattern) Feeling Tired And Wanting To Sleep In Children, A Slow Heart Rate Unsteadiness While Standing Or Walking, Is Especially Suggestive Of High Known As Ataxia Altered Level Of Consciousness, ICP. Weakness, local or generalized.
Irregular Respirations (Interference Of The Respiratory Drive) Hyperventilation (Brain Stem Or Tegmentum Is Damaged)
Neurological examination Taking
Symptoms of neurological disorders; 1. Headache, back, neck or facial pain (when asking about pain, include SOCRATES; site, onset, character, radiation, assoc symptoms, time (progression), exacerbating and relieving factors, and severity) 2. Fits and faints 3. Dizziness or vertigo 4. Disturbances of vision, hearing or smell 5. Disturbances of gait 10.Loss of disturbed sensation, or weakness in limb(s) 11.Disturbances of sphincter control (bladder, bowels) 12.Involuntary movements or tremor
Past Medical History
Ask about head or spinal injuries History of epilepsy or convulsions Any previous operations Treatment (anti-convulsants, contraceptive pills, antihypertensive agents, steroids, anticoagulants, antiplatelet agents - Risk factors that may predispose development of cerebrovascular disease (Hypertension, DM, Hyperlipidemia, smoking, MI) - Previous dx of peripheral vascular disease or of coronary artery disease (↑ risk of 29/9/2009 30 CV disease)
- Smoking history - Occupation and exposure to toxins (e.g. heavy metals) - Alcoholism
o Blackouts o Nutrition related conditions; e.g. peripheral neuropathy due to thiamine deficiency o Withdrawal syndrome; e.g. tremor, hallucination o Cerebellar dysgeneration o Alcoholic dementia o Alcoholic myopathy o Autonomic neuropathy
Fa m i y H i ry sto -l
A n y h i ry o f n e u ro l g i lo r m e n ta l sto o ca d i a se sh o u l b e d o cu m e n te d se d
Head • Scalp- inspect & palpate for laceration, swelling, bony depression and distortion • Orbits- palpate the margins of the orbits for depression/irregularities • Eyes- size, reflex, movement & visual acuity - Panda eyes subconjuctival hemorrhage - Diplopia fracture of floor of orbit
Signs of intracranial hemorrhage • Face – palpate cheek bone for a ‘step’ & asymmetry, loss of
sensation facture of cheek bone due to damage of infra-orbital nerve Jaw & temperomandibular joint – malocclusion & open bite deformityfractured jaw & numbness of lower lip Mouth, teeth & gums - record no of missing/damaged teeth xray exclude possibility inhaled & lodged to the lung Nose – palpate and detect any bloody/fluid dischargeanterior cranial fossa fracture Ear – blood/fluid discharge bruising behind ears (Battle’s sign)post cranial fossa fracture Neck – palpate for bruising, deformity & any subcutaneous surgical emphysema
• Chest – inspect for flail chest multiple contiguous rib fractures resulting in free-floating ribs with paradoxical motion on respiration) - Rib fracturesinjuries to great vessles, lung, spleen & liver - Sternal fracturecardiac injuries - Increase width of mediastinum aortic dissection - Check for hemothorax, pnuemothorax and cardiac temponade • Abdomen - intra-abdominal hemorrhage - Increase abdominal distension, tenderness & guarding are significant signs -Skin bruising, penetrating wounds & assoc. rib fracture possibility organ damag - Blood from urethra/frank hematuria kidney, bladder/urethral damage
• Upper & lower limbs– palpate all major bones to detect any bony deformity & swelling • Circulation – palpate radial & pedal pulses asymmetrical pulses indicate vascular injury - Persisting pallor in one limb severe ischemia - Compartment syndrome(pain, tenderness & swelling over ant. shin/calf muscle) ischemia, obliterate the pulses, muscle and nerve death • Nerves – examine both upper and lower limbs of peripheral nerves -Test power, tone, strength, coordination, sensation, and reflexes • Back (thoraco-lumbar spine) – paralysis/muscle weakness spinal cord injury
• Break in the bone in the skull, caused by head injury • Fragments
– Lacerate or bruise brain – Damage blood vessels – Intracranial hematomas – Epidural hematomas
• Dissection of cerebral arteries
• Simple linear fracture is by far the most common type of fracture, especially in children younger than 5 years. • Temporal bone fractures represent 15-48% of all skull fractures. • Basilar skull fractures represent 19-21% of all skull fractures. • Depressed fractures are frontoparietal (75%), temporal (10%), occipital (5%), and other (10%). • Most of the depressed fractures are open fractures (75-90%).
• Most common – 69% • Low-energy blunt trauma, widely distributed force • Little significance unless runs thru vascular channel, venous sinus groove or a suture:
– Vascular channel Epidural hematoma – Venous sinus groove Venous sinus thrombosis – Suture Sutural diastasis
• Growing fracture brain swelling • Most patients are asymptomatic and present without LOC. Swelling occurs at the site of impact, and the skin may or may not be breached. •
Fracture Width >3mm
Widest at centre and narrows Same width throughout at end On X-ray Appear darker Lighter Site Pattern Turns Usually over temporoparietal Specific anatomical sites area Usually straight line Not in straight line Angular Curvaceous
• • • • Linear fracture at the base of the skull Associated with dural tear Require > force, thus rare – 4% Characteristic
– – – – – – – – Blood in sinuses CSF leak – nose/ear CSF rhinorrhea Raccoon eyes Battle’s sign – clotting behind ear Cranial nerve palsy Hemotympanum Ocular nerve entrapment: 1-10%
• Likely to get meningitis • HANS device usage in high risks
• Temporal bone fracture. • 75% of all skull base fractures. • 3 subtypes of temporal fractures are longitudinal, transverse, and mixed.
Tra n sve rse
Lo n g i d i a l tu n
• Longitudinal fracture
– Occurs in the temporoparietal region and involves the squamous portion of the temporal bone, the superior wall of the external auditory canal, and the tegmen tympani. – These fractures may run either anterior or posterior to the cochlea and labyrinthine capsule, ending in the middle cranial fossa near the foramen spinosum or in the mastoid air cells, respectively. – Longitudinal fracture is the most common of the 3 subtypes (70-90%).
• Transverse fractures
– Begin at the foramen magnum and extend through the cochlea and labyrinth, ending in the middle cranial fossa (5-30%).
• Mixed fractures
– Have elements of both longitudinal and transverse fractures.
• Petrous temporal bone fracture
– Battle sign.
• CSF otorrhea and bruising over the mastoids
• Anterior cranial fossa fractures
– Raccoon eyes
• CSF rhinorrhea and bruising around the eyes
• Longitudinal temporal bone fractures
– Conductive deafness
• Ossicular chain disruption and of • Greater than 30 dB that lasts longer than 6-7 weeks.
– Temporary deafness
• Resolves in less than 3 weeks is due to • Hemotympanum and mucosal edema in the middle ear fossa. • Facial palsy, nystagmus, and facial numbness are secondary to involvement of the VII, VI, and V cranial nerves, respectively.
• Transverse temporal bone fractures
– Involve the VIII cranial nerve and the labyrinth, resulting in nystagmus, ataxia, and permanent neural hearing loss. –
Occipital condylar fracture
• High-energy blunt trauma with axial compression, lateral bending, or rotational injury to the alar ligament. • 3 types based on the morphology and mechanism of injury with alternative classification into displaced and stable, ie, with and without ligamentous injury.
– Type I - secondary to axial compression resulting in comminution of the occipital condyle. This is a stable injury. – Type II – results from a direct blow, and, despite being a more extensive basioccipital fracture, type II fracture is classified as stable because of the preserved alar ligament and tectorial membrane. – Type III – an avulsion injury as a result of forced rotation and lateral bending. This is potentially an unstable fracture.
• Very rare and serious injury. • Most of the patients with occipital condylar fracture, especially with type III, are in a coma and have other associated cervical spinal injuries. • These patients may also present with other lower cranial nerve injuries and hemiplegia or quadriplegia
• High-energy impact sustained in motor vehicle accidents. • Longitudinal, transverse, and oblique types have been described in the literature. • A longitudinal fracture carries the worst prognosis, especially when it involves the vertebrobasilar system. • Cranial nerves VI and VII deficits are usually coined with this fracture type.
Nerve involvement of basilar fracture
• Vernet syndrome or jugular foramen syndrome
– Involvement of the IX, X, and XI cranial nerves with the fracture. – Difficulty in phonation and aspiration and ipsilateral motor paralysis of the vocal cord, soft palate (curtain sign), superior pharyngeal constrictor, sternocleidomastoid, and trapezius.
• Collet-Sicard syndrome
– glossolaryngoscapulopharyngeal hemiplegia – occipital condylar fracture with IX, X, XI, and XII cranial nerve involvement.
Depressed skull fracture
• High-energy direct blow small surface area with a blunt object such as a baseball bat • Comminution of fragments starts from the point of maximum impact and spreads centrifugally • Most are over the frontoparietal region because the bone is thin and the specific location is prone to an assailant's attack.
• Very serious - 11% of severe head injury • Comminuted fractures, bone displaced inward • High risk of increasing ICP • Crush delicate tissue • Complex – torn dura matter • May require surgery to lift the bone
• Approximately 25% of patients with depressed skull fracture do not report LOC, and another 25% lose consciousness for less than an hour. The presentation may vary depending on other associated intracranial injuries, such as epidural hematoma, dural tears, and seizures.
INDICATION FOR CT SCAN
CT vs MRI
CT M RI S u ffi e n t to d e te ct cl n i ci i ca l y S e n si ve to l ti S u p e ri r i o b d e d a nn b l to su b tl l si n i p o rta n tn l e te ctidgasku l m e e l e e o M a y D e m o n stra te fi d i g s o f frai e re .a n a g e m e n t.n n g u ctu m d Able(toi D A I d ffu se bone, soft n j ry )and u image a xo n a litissue su ch a s m i all h the o rrh a g e blood vesselscro ata e msame time. s.
More on CT
D e te cti g Pa th o l g y T h a t n o D i rts T h e N o rm a lA n a to m y sto Advantages O f T h e B ra i n D i ffe re n ti ti g a n i a e m i a n sch c H a e m o rrh a g e s , i fa rct fro m a ce re b ra lb l e d . n e N e o p l sm s , a I e n ti d fyi g sp a ce o ccu p yi g n n A b sce sse s . l si n s ( su ch a s tu m o u rs a n d e o a b sce sse s) D e te cti g h yd ro ce p h a l s . n u
B ra i I fa rcti n , n n o A rte ri ve n o u s M a l o fo rm a ti n s, o Disadvantages A n e u rysm s , S m a l e si n s (< 1 cm ) o r ll o Le ss S e n si ve S ti lFo r ti l b ra i ste m l si n s m a y b e n e o D e te cti g W h i M a tte r D i a se n te se m i d sse A n d Le p to m e n i g e a lD i a se . n se E a rl y i fa rcti n (< 6 -8 h o u rs) n o m a y n o t b e se e n .
Indications for CT.
– Construct a Focused history. – Witnesses of the trauma or individuals who know the patient may be helpful in ascertaining the details of the traumatic event and other valuable patient information. – Past medical and surgical history, drug/alcohol use and allergies are important.
– GCS and Pupillary reflexes, – Full neurological examination. – Evidence of basilar skull fracture: blood in the middle ear cavity (haemotympanum), raccoon eyes (periorbital ecchymosis), post-auricular ecchymosis, CSF leakage (rhinorrhoea or otorrhoea). – Associated spinal injury: spinal tenderness, paraesthesias, incontinence, extremity weakness, priapism. – Carotid dissection: carotid bruits – Abnormal eye findings: papilledoema, retinal haemorrhage.
– Arterial blood gas. – FBC including platelets. – Serum electrolytes and urea. – Serum glucose. – Coagulation status: PT, INR, activated PTT. – Blood alcohol level and toxicity screening if indicated. – Urine analysis: specific gravity, osmolality (to detect endocrine complications such as diabetes insipidus or Syndrome of Inappropriate Antidiuretic Hormone).
Rules of Standard Guidance.
The Canadian CT Head Rule. The New Orleans Criteria.
* Both guidelines contain 7 criteria to guide the use of CT in patients with mild injury and have been validated. * Patients under 16 years of age were not included in the initial Canadian CT rule derivation or validation.
The Canadian CT Head Rule.
• CT is required for patients with minor head injuries (minor head injury is
defined as witnessed LOC, definite amnesia or witnessed disorientation in patients with a GCS score of 13 to 15)
with any one of the following. •
High Risk (for neurologicaol intervention)
Medium Risk (for brain injury for CT scan)
Amnesia more than 30 GCS less than 15 at 2 hours after injury minutes before impact Suspected open or depressed (retrograde amnesia) skull fracture Any sign of basal skull fracture Dangerous mechanism (pedestrian struck by (haemotympanum , raccoon eyes [periorbital ecchymosis ], CSF motor vehicle, occupant otorrhoea/rhinorrhoea, Battle ejected from motor sign [ecchymosis of the vehicle, fall from mastoids]) 2 or more episodes of vomiting height more than 3 feet Aged 65 years or above or 5 stairs).
New Orleans Criteria.
• CT is required for patients with minor head trauma (minor head injury was
defined as LOC in patients with normal findings on a brief neurological examination and a GCS score of 15, as determined by a physician upon arrival at the emergency department) with
any one of the following:
High Risk (for neurolsurgical intervention) Headache
Vomiting Aged more than 60 years Drug or alcohol intoxication Persistent anterograde amnesia (deficits in short-term memory) Evidence of traumatic soft-tissue or bone injury above clavicles Seizure (suspected or witnessed)
The derivation set for the criteria also contained a history of coagulopathy as a clinical parameter, although this was not included in the final validation. Where possible this history should be obtained and considered with respect to CT scanning.
Interpretation of CT.
• Basic Interptetation
– Most of the picture are non-specific. – CT picture are depending on the density of the structure.
– Pre-Contrast Study.
– Comparison with CSF and Brain Tissue » Higher than CSH and lower than Brain Tissue (Protein, Blood , Debris) » Tumor, Abcess,Resolving Hematoma, Evolution Infarct. – Lower that CSF » Fat or cholesterol ; Congenital Tumor ; dermoir , epidermoid, lipoma. » Air ; Head injury,
– Comparison with Cranium Bone – Iso or higher than bone » Ossification, calcification, metallic iatrogenic, blood pooling. – Less than bonebut higher that brain tissues » Haemorrhage, compected cellurity.
– As brain Parenchyma. » Iso-density to CSF (Water like congtent) » Chronic haematoma, chronic infarct, porencephaly, congenital cycts ,
• Post Contrast CT.
– Gyral, ribbon, cortical. – Solid. – Rim or Ring. – Mural Nodular. – Linear and Dot. – Heterogeneous. – No Enhancement. –
Changes in adjacent tissue
Edema pattern in CT
– Vasogenic Edema
Tumors, infection, late infarct aling white matters, fingerlike.
– Interstitial edema,
periventricular white matter, ependymitis granularis
– Cytotoxic edema
Ischemia or infarct, gray matter
Bone Ventricles, Sulci and cistern
Classification of Cerebral Edema Type Location Site Vasogenic Extracellular White Cytotoxic Intracellular White or gray and Ischemic Intra- and White extracellular gray and HydroExtracellular White static HydroExtracellular gray White cephalic Osmotic Intra- and White and extracellular gray
BloodBrain Disrupted Barrier Intact Disrupted Disrupted Intact Intact
Probable Mechanism Increased vascular permeability Cellular failure Anoxia Increased blood pressure CSF outflow Impaired or absorption hangindent1em Relative plasma hypoosmolality
C T sca n o f a 1 6 ye a r- o l p a ti n t d e w i a typ i l th ca d i se h e a d i j ry. ffu n u T h e p a ti n t' G C S e s a t a d m i o n to ssi h o sp i lw a s 4 . ta T h e re i a sm a l s l am ount of bl od i o n th e tri o n e a n d g o cci i lh o rn o f p ta th e ri h t l te ra l g a ve n tri e ( lower cl arrow). There is a small punctate hemorrhage in the left internal capsule (upper
CT scan of a 50year-old man injured in a fall. There is a large mixed-density lesion in the left temporal lobe (lower arrow) and a similar, smaller lesion in the left orbitofrontal cortex (upper arrow). The appearance is typical of cerebral contusions.
CT scan of a large acute epidural hematoma (arrows). Epidural (or extradural) hematomas have a convex medial border, which produces the lens shape that distinguishes epidural from subdural hematomas.
CT scan of a large acute subdural hematoma (horizontal arrows). The hematoma spreads over the entire convexity of the hemisphere, so that the medial border of the hematoma is concave. Note also the large amount of midline shift. The occipital horn of the left lateral ventricle is acutely enlarged as a result of trapping of CSF by ventricular distortion and obstruction of CSF flow (vertical arrow).
CT scan of a confluent traumatic intracerebral hematoma in the left frontal lobe of a patient struck by a motor vehicle (lower arrow). There is overlying scalp swelling and contusion at the site of the blow to the head (upper arrow).
An unenhanced CT of the brain in a patient with the complications of hypertensive encephalopathy. The arrows are pointing to the end-arterial border zones with changes consistent with ischemic and hemorrhagic changes.
A schematic diagram demonstrating the concept of evolving pressure differentials with regional brain swelling from large supratentorial hemispheric infarction. Note that the clinical worsening in its early states correlates with brain tissue displacement.
1. E xtra d u ra l ( e p i u ra l d ) H e m a to m a 2. S u b d u ra lH e m a to m a 3. S u b a ra ch n o i H e m a to m a d 4. I tra ce re b ra lH e m o rrh a g e n
§ Very common in children, adolescents and young adult § Blood between skull & dura d/t rupture of meningeal artery § Usually a/w skull fracture in temporal region § Symptoms within 24 hours of trauma: - Loss of conciousness - Lucid interval with severe headache & drowsiness - Fixed & dilated pupil on the side of injury - hemiparesis on the opposite side § “Lucid interval”followed by acutely progressive evidence of increased ICP compression of brain stem coma death § Morphology: Smooth inner contour (dura), biconvex. § Need urgent diagnosis through CT scan § Mx: immediate surgery to remove clot
1. Extradural Hematoma (epidural)
# Lucid interval=> a period of consciousness after the injury before the patient became unconscious
CT scan of extradural hematoma
Extradural hematoma. Such a location for hemorrhage is virtually always the result of trauma that causes a tear in the middle meningeal artery.
2. Subdural Hematoma
§ Blood between dura & arachnoid d/t rupture of bridging veins § More common (30%) than extradural (10%) § Underlying primary brain injury and 50% mortality § Manifest within 48 hrs. § Lateral aspect of cerebral hemispheres, 10% bilateral. § Volume of the haematoma increases ICP increase herniation (Coning=> herniation of cerebellar into foramen magnum compressing medulla cessation of respiration & death § S/S: Headache & confusion. Rarely focal signs. § Types: - Acute due to major brain injury s/s: deeply unconscious & develop neurological localizing
§ Morphology: - Clot along brain surface contour without extension into the depth of sulci. (crescent) - Hematoma surrounded by fibrous membrane (organising), attached to dura only. § Rebleeding – greatest risk in 1st few months. § Mx: Craniotomy
3. Subarachnoid haematoma
§ Most cases of traumatic SAH are a/w parenchymal haematoma § In subarachnoid space § Due to ruptured of berry aneurysm blood flows into the subarachnoid space increase in ICP + destructive and toxic effects of blood on brain parenchyma and cerebral vessels § S/S: meningeal irritation, headache, neck stiffness, Kernig’s sign +ve (inability to completely extend the leg when sitting or lying with the thigh flexed upon the abdomen)
#Berry aneurysm a small saccular aneurysm of a cerebral artery, usually at the junction of
4. Intracerebral Hematoma
• Common after a severe head injury. • Caused by a cerebral contusion fluid accumulation in the damaged brain (cerebral edema)deaths. • S/S: severe headache, nausea, seizures, and coma or death • Mx: surgery is usually avoided because it usually does not restore brain function.
– Disturbances in CSF circulation or absorption which results in the continuous increase in the ICP which leads to hydrocephalus.
– Obstructive - ; CSF circulation is blocked within the ventricular system, and there is enlargement in the ventricles proximal to the obstruction. – Communicating ; CSF absorption is blocked at the level of the arachnoid granulations. – Rarely, hydrocephalus may be due to the
Pathophysiology Increase pressure in expandable compartment
Menifestations Neonates and infants whose anterior fontanelle is still open, Symptoms includes tense or bulging fontanelle, apneic and bradycardic episodes, engorgement of the scalp veins, upward gaze palsy, gaps between the cranial sutures, rapid increases in head circumference, irritability, poor head control, and poor oral intake.
Increase pressure Children with closed fontanelle Symptoms includes lethargy or excessive in rigid compartment sleepiness, papilledema, headache, nausea, vomiting, gait disturbance, increased fussiness, or upgaze or lateral gaze palsy
• Ventriculoperitoneal shunting, – creating a shunt between the cerebral ventricles and the peritoneal cavity. • Ventriculoatrial shunt, – Right Atrium Shunt • Ventriculopleural shunt – Pleural Cavity Shunt • Endoscopic third ventriculostomy – – Children with obstructive type. – Involves fenestration of the floor of the third ventricle, thereby creating an alternative CSF pathway. • Shunt Failure OR Delayed treatment may leads to irreversible neurologic injury, including herniation, blindness, or death.
DIFFUSE AXONAL INJURY
• hx rapid acceleration/deceleration of the head, or direct impact to head; • DAI may be responsible for mild forms of cognitive impairment seen acutely with concussions; • severe DAI: generally no lucid interval, presents with immediate and persistent LOC
• Diffuse axonal injury is caused by damage to axons throughout the brain, due to rotational acceleration and then deceleration. • Axons may be completely disrupted and then retract, forming axon balls. • Small hemorrhages can be seen in more severe cases, especially on MRI. • Hemorrhage is classically seen in the corpus callosum and the dorsolateral midbrain.
• Rapid intervention with particular attention to ABCs to minimize secondary brain injury. • Treat elevated ICP only if symptomatic
– Sedate patient and elevate head of bed 300 – Brief hyperventilation may be performed acutely to cause cerebral vasoconstriction – Mannitol for osmotic diuretics and free radical scavenging – Surgical decompression of deteriorating patients via trephinaton or ventriculostomy
• Intracranial bleeds require seizure prophylaxis e.g. phenytoin and may require surgical drainage • Check coagulation studies (PT/aPTT/INR) immediately and correct any coagulopathy to minimize intracranial bleed • Depress skull fractures and penetrating trauma may require surgical repair
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