lecture Head Trauma

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Head Trauma : 

Head Trauma By Dr/waleed fawzy Specialist Of General Surgery

Edwin Smith Papyrus : 

Edwin Smith Papyrus

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The Edwin Smith Papyrus is the world's earliest known medical document, written in hieratic around the 17th century BCE. It is the ancient textbook on trauma surgery, and describes anatomical observations and the examination, diagnosis, treatment, and prognosis of numerous injuries in exquisite detail. The papyrus contains the first descriptions of the cranial sutures, the meninges, the external surface of the brain, the cerebrospinal fluid, and the intracranial pulsations.

Introduction : 

Introduction 50,000 cases of head injury/year in U.S 10 % die prior to reach hospital. 100000 RTA /year in saudi Arabia. 4000 death/year. RTA costs about 2 billion dollar/year in Saudi Arabia

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One million patients attend A&E each year in UK with head injury 80% are minor (GCS 13-15( 10% are moderate (GCS 9-12) 10% are severe (GCS <8( Severe head injuries account for 50% of trauma related deaths

Pathophysiology of brain injury : 

Pathophysiology of brain injury

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Intracranial pressure Normal ICP 10 mm Hg (136 mm water) Pressure > 20 mm Hg considered abnormal. Pressure > 40 mmHg is sever elevation

Monro-Kellie Doctrine : 

Monro-Kellie Doctrine The total volume of intracranial content must remain constant as the cranium is non-expansile box

Cerebral perfusion pressure : 

Cerebral perfusion pressure Perfusion pressure< 70 mm Hg. Is associated with poor outcome Maintaining CPP is a very important priority in management of head injury patients CPP = MAP-ICP

Cerebral Blood Flow : 

Cerebral Blood Flow Normal CBF 50 ml/100 gm of brain/min. (10-15% of cardiac output). 20-25 ml/100gm brain/min.? EEG disappears. 5 ml/100gm/min ? there is cell death.

Primary brain injury : 

Primary brain injury Damage caused at time of impact Can be focal or diffuse Diffuse axonal injury is due to deceleration and shearing forces Dependent on extent of initial injury Difficult to treat

Secondary brain injury : 

Secondary brain injury Insult imposed after initial injury due to: Hypoxemia Hypercapnia Systemic hypotension Intracranial hematoma Intracranial hypertension Early treatment is aimed at the prevention of secondary injury Autoregulation of cerebral blood flow is lost after head injury

Anatomy Of The Head : 

Anatomy Of The Head A-Scalp 1-skin 2-connective tissue 3-aponeurosis (galea) 4-loose areolar tissue 5-pericranium Common injury: Subgaleal hematoma

Skull Vault : 

Skull Vault

B-Skull : 

B-Skull Cranial vault (Calvarium): Thin in the temporal region The base: irrigular The floor: Ant.fossa frontal lobes middle fossa temporal lobes Post.fossa lower brain stem & cerebellum

Meninges : 

Meninges The Dura Mater tough & fibrous Not attached to the arachnoid forming a potential space (the Subdural space) The veins that travel from the brain surface to the SSS Called the bridging veins These veins may tear and leads to SDH.

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At specific sites the dura splits to enclose large venous sinuses. The midline superior sagital sinus drains into the transverse & sigmoid sinuses. The sigmoid sinuses are more dominant on the rt. side,if torn can lead to massive Hge.

Meningeal Arteries : 

Meningeal Arteries Lie between the dura & the internal surface of the skull (The epidural Space) It grooves the inner surface of the skull, laceration of these arteries cause epidural Hematoma (EDH)

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2. Arachnoid mater Bleeding in this area cause subarachnoid Hge. (usually caused by ruptured aneurysm and Head injury). CSF circulates between Pia and Arachnoid 3. pia mater: is firmly attached to the brain

The Brain : 

The Brain Consists of: The Cerebrum The Cerebellum The brainstem

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Brain stem 3rd Ventricle Cerebellum

Function of Different brain areas : 

Function of Different brain areas The Frontal lobe: emotions& motor function The parietal lobe: sensory function & spatial orientation The temporal lobe: regulates certain memory function The lt temporal lobe: speech in all rt handed and most of lt handed persons.

Brain Areas : 

Brain Areas

Cerebrospinal fluid : 

Cerebrospinal fluid Produced by the choroid plexus 30ml/hr It is located in the lateral ventricle CSF comes through foramen of Monro to the 3rd ventricle and pass through Aqueduct of Sylvius to the 4th ventricle It then exit into the subarachnoid space. It is reabsorbed into the venous circ.through the arachnoid granulation that project into SSS.

Tentorium : 

Tentorium Tentorium cerebelli divides the head into: 1-supratentorial compartment comprising the anterior and middle cr.fossa 2-Infratentorial compartment containing the post.fossa. The midbrain connects the cerebral hemisheres to the rest of the brain stem,and it passes through a large aperture in the tentorium called the tentorial incisura

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Facial n.

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Falx cerebri Tentorium Sagital section thrx the Head

Tentorium : 


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The Oculomotor IIIrd nerve runs along the edge of the tentorium and may become compressed against it during downward brain herniation. Parasympathetic fibers that are pupillary constrictors lie on the surface of the IIIrd nerve causes pupillary dilatation due to unopposed sympathetic activity,with further compression of the IIIrd nerve , full Oculomotor paralysis occur causing the eye to deviate “down and out”

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The part of the brain that usually herniates thr tentorial notch is the medial part of the temporal lobe, known as the uncus. Uncal Herniation causes compression of the pyramidal tract in the midbrain. The motor tract crosses the opposite side at the foramen magnum and compression causes contralateral hemiplegia.

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The ipsilateral pupillary dilatation + contralateral Hemiplegia is called : classic tentorial Herniation. The Ipsilateral pupillary dilatation + Ipsilateral Hemiplegia can occur: Kernohan’”s Notch Syndrome

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Dilated Pupil

Classification : 

Classification A-Mechanism of injury: Blunt injury: falls, automobile collisions and blunt assault. Penetrating injury: gunshot and stab wounds

Penetrating injury from low velocity bullet : 

Penetrating injury from low velocity bullet

B.Severity Of Injury : 

B.Severity Of Injury Mild GCS Score 14-15 Moderate GCS Score 9-13 Sever GCS Score 3-8

C.Morphology Of Injury : 

C.Morphology Of Injury Skull Fractures. Vault Linear vs. Stellate Depressed/Nondepressed Open/Closed Basilar with/without csf leak with/without VII nerve palsy

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2. Intracranial lesions Focal Epidural Subdural Intracerebral Diffuse Mild Concussion Classic Concussion Diffuse Axonal Injury

Basal Skull Fracture : 

Basal Skull Fracture Signs: Periorbital Ecchymosis (Raccoon Eyes) Retroauricular Ecchymosis (Battle’s Sign) CSF Leak : 1-Rhinorrhea or 2- otorrhea V11 Nerve Palsy

Epidural hematoma : 

Epidural hematoma 0.5% of all head injuries &9% of comatosed Presents with lucid interval (talk & die) Biconvex in shape Most often temporal or tempoparietal Result from tearing of middle meningeal a. May be venous in 30% from torn venous sinuses especially in parietoccipital or post.fossa.

Epidural Hematoma : 

Epidural Hematoma

Subdural Hematoma : 

Subdural Hematoma More Common occur due to tear of the bridging veins between the cerebral cortex and draining venous sinus. It covers the entire surface of hemisphere prognosis much worse than epidural one. Needs very rapid surgical intervention.

Subdural Hematoma : 

Subdural Hematoma The site of hematoma

Contusions & Intracerebral Hematoma : 

Contusions & Intracerebral Hematoma Pure cerebral contusions are common. Always seen with subdural hematoma. Contusions can coalesce or evolve to form an intracerebral hematoma. Can occur in any part of the brain including cerebellum and brainstem.

Bilateral contusion & intracerebral hematoma : 

Bilateral contusion & intracerebral hematoma

Diffuse Injuries : 

Diffuse Injuries Mild Concussion Classic Cerebral Concussion Diffuse Axonal Injury

A. Mild Concussion : 

A. Mild Concussion Consciousness is preserved inspite of temporary neurological dysfunction like confusion , disorientation but no loss of memory

B. Classic Cerebral Concussion : 

B. Classic Cerebral Concussion An injury that results in a L.O.C. Ass’ post traumatic Amnesia Length of amnesia is a good measure of the severity of injury. Amnesia is transient & reversible. and returns to full consciousness by 6 hours. Other symptoms: dizziness, nausea, anosmia and depression. this referred as a post-concussion syndrome

C. Diffuse Axonal Injury : 

C. Diffuse Axonal Injury Definition: Prolonged post-traumatic coma that is not due to mass lesion or ischemic insults. These patients are deeply comatosed, and remain so for prolonged periods. Often show sign of decerebration or decortication, they can exhibit autonomic dysfunction , such as HTN, Hyperhydrosis and hyperpyrexia. Distinguishing between DAI and Hypoxic Brain Injury is difficult and indeed they may coexist.

Management : 


Management Of Mild Head Injury : 

Management Of Mild Head Injury Def.: Patient is awake & may be oriented History: Name, age sex ,occupation Mech. of Injury ,Time of Injury L.O.C Immediate post-injury Subsequent level of consciousness Amnesia Headache Seizures

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General exam to exclude systemic injuries Limited neurological exam. Cervical spine x-ray Bl.Alcohol level, urine toxicology screen C.T Scan head except completely asymptomatic & neurologically normal

Criteria for admission : 

Criteria for admission No CT Scan Available Abnormal CT Penetrating head injury H/O LOC Deteriorating level of Consciousness. Moderate to sever headache. Significant Alcohol intake

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Skull fracture CSF Leak Significant associated injury. No reliable companion Amnesia.

Criteria for discharge from ER : 

Criteria for discharge from ER Does not meet any of the criteria. Discuss with the patient to return if any problem or symptom occur. F/U within one week.

Management of Moderate Head Injury GCS 9-13 : 

Management of Moderate Head Injury GCS 9-13 Initial Exam Same as for mild head injury plus baseline Blood workup. CT Scan for head Admission for Observation.

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After Admission Frequent neurological Checks. F/U Ct sacn , if condition deteriorates, or preferably before discharge. If the patient improves ,discharge with f/u in the clinic. If the patient stops following simple commands, repeat CT scan,and manage as sever head injury

Management of Sever Head InjuryGCS 3-8 : 

Management of Sever Head InjuryGCS 3-8 Assessment & Management: ABCs. 1ry Survey & Resuscitation. With critical trauma you may never get beyond the primary survey 2ry Survey & AMPLE History. A = Allergies M = Medications P = Past medical history L = Last oral intake E = Events leading up to incident Neurological re-evaluation: Eye opening Pupillary light Reaction Motor response Occulocephalic Doll’s Eye Occulo-vestibular Caloric test

Initial Assessment (Primary Survey) : 

Initial Assessment (Primary Survey) Airway with C-Spine Control Return head to neutral position Stabilize without traction Noisy breathing is obstructed breathing But all obstructed breathing is not noisy

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Airway with C-Spine Control Anticipate airway problems with Decreased level of consciousness Head trauma Facial trauma Neck trauma Upper thorax trauma Severe Burns to any of these areas Open, Clear, Maintain.

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Breathing Ask yourself the next questions: Is oxygen getting to the blood? Is air moving? Is it moving adequately? Is it moving at an adequate rate?

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Breathing Look Listen Feel

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Breathing Oxygenate immediately if: Decreased level of consciousness Shock Severe hemorrhage Chest pain Chest trauma Dyspnea Respiratory distress Multi-system trauma

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Breathing If you think about giving oxygen, GIVE IT!!

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Breathing Consider assisted ventilations if: Respirations < 12 Respirations > 24 Tidal volume ? Respiratory effort ? If you can’t tell if ventilations are adequate, they aren’t!!

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Indications for intubation and ventilation GCS less than or equal to 8 Loss of protective laryngeal reflexes Ventilatory insufficiency as judged by blood gases PaO2 less than 9kPa )67 mm hg) PaCO2 greater than 6kPa (45 mm hg) Spontaneous hyperventilation Respiratory arrhythmia Bilateral fractured mandible Copious bleeding into mouth Seizures

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Circulation Is the heart beating? Is there serious external bleeding? Is the patient perfusing? How do we know?

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To Determine the cause of Hypotension D.P.L F.A.S.T C.T.SCAN

Common sites Of Blood Loss : 

Common sites Of Blood Loss

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If there is hypotension, this usually not due to the brain injury itself, except in the terminal stage when medullary failure occur. Hypotension is a marker of sever blood loss also spinal cord injury, cardiac contusion or tamponade and tension pneumothorax.

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Circulation No carotid pulse? CPR PASG Survival rate from cardiac arrest secondary to trauma is very low

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Disability (CNS Function) Level of consciousness = Best brain perfusion sign Use GCS initially Check pupils The eyes are the window of the CNS

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Disability Decreased Level Of Consciousness = Brain injury Hypoxia Hypoglycemia Shock NEVER think drugs, alcohol, or personality first

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Expose and Examine You can’t treat what you don’t find! If you don’t look , you won’t see! Remove ALL clothing from critical patients ASAP Avoid delaying resuscitation while disrobing patient Cover patient with blanket when finished

Primary Resuscitation : 

Primary Resuscitation Immobilize C-spine (manual & rigid collar) Keep airway open Oxygenate Rapidly extricate to long board . Begin assisted ventilation . Expose & Protect from exposure Apply and consider inflation of PASG Consider intubation Establish IVs

2 ry SurveyTo detect any major systemic injuryRequiring care by other specialties : 

2 ry SurveyTo detect any major systemic injuryRequiring care by other specialties

Neurological Examination : 

Neurological Examination GCS Pupillary light response Doll’s Eye Movement (occulocephalic). Calorics (occulovestibular) Corneal Response.

Important Consideration : 

Important Consideration 1-Neurological exam. should be done prior to sedation or paralyzing the patient. 2-It is not allowed to use long acting paralytic agents. 3-Succinylcholine,vecuronium or very small dose pancuronium are recommended.

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4-Small repeated doses of i.v morphine (4-6 mg) are used in providing analgesia & sedation that is reversible. 5-serial exam. Should be performed because of variability of response over time. 6-Early sign of temporal lobe herniation is mild dilatation of pupil and sluggish pupillary response. 7-With worsening of herniation there is further dilatation of pupil followed by ptosis & paresis of medial rectus.? Down& out position of the eye that is diagnostic of IIIrd Nerve palsy.

Pupillary Light ResponseValadka AB, Narayan 1996 : 

Pupillary Light ResponseValadka AB, Narayan 1996

Diagnostic procedures : 

Diagnostic procedures 1-C.T Scan: within 30 min after injury should be repeated whenever there is change in the patient clinical status. The scalp may demonstrate subgaleal hematoma. Skull may be seen better on bone window. The presence of intracranial hematoma, shift of the midline, the septum pellucidum which lies between the two lateral ventricles,should be in the midline. An actual shift of 5 mm or more is considered significant and usually indicates surgery.

Indications for CT : 

Indications for CT GCS less than 13 at any point since the injury GCS equal to 13 or 14 at 2 hours after the injury Suspected open or depressed skull fracture Any sign of basal skull fracture Post-traumatic seizure Focal neurological deficit More than one episode of vomiting Amnesia for greater than 30 minutes of events before impact If LOC in patients older then 65 years, coagulopathy or dangerous mechanism of injury

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2-Angiography: May be done in the absence of C.T in Acute Head Injury. Supratentorial mass lesion usually can be detected by lateral shift of the ant.cerebral artery and vein.

MRI : 


Methods of monitoring neurological function : 

Methods of monitoring neurological function Methods of monitoring intracranial pressure Intraventricular catheter Fibreoptic devices Strain gauge microtransducer systems Methods of monitoring cerebral blood flow Transcranial doppler Methods of monitoring cerebral oxygenation Jugular venous oxygen saturation Near-infrared spectroscopy Brain oxygen tension Methods of monitoring function Clinical neurological assessment Glasgow coma scale Electroencephalogram (EEG( Electromyography

Medical therapy Of Head Injury : 

Medical therapy Of Head Injury I.C.U can? Mortality from 50% in 1970 to 36% 1997. The aim of I.C.U To prevent 2ry damage. Hyperventilation Mannitol Lasix I.V.F

Intravenous Fluids : 

Intravenous Fluids It is especially critical in head injury not to use hypotonic fluids. The use of glucose containing fluids can result in hyperglycemia which is harmful to the injured brain. Normal saline or Ringer’s lactate should be used for resuscitation. Na+ level should be carefully monitored in these cases. Hyponatremia is associated with brain edema.

Hyperventilation : 

Hyperventilation It causes ? Pco2 ? Cerebral vasoconstriction. This reduction in intra cranial volume helps ? I.C.P. Aggressive & prolonged hyperventilation can produce cerebral ischemia. This occur if Pco2 ?<25 mm Hg

The current concept : 

The current concept Is to use hyperventilation in moderation and for limited periods. It is preferred to keep Pco2 at 30 mm Hg. Levels of Pco2 between 25-30 mm Hg are acceptable in presence of ? I.C.P

Mannitol : 

Mannitol Mannitol 20% is used widely to ? ICP. 1 gm/kg i.v bolus over 5 minutes. It should not be given to hypotensive patient, as it aggravates hypovolemia. The clear indication for use: Comatose patient who initially has normal,reactive pupil but develops pupillary dilatation with or éout hemiparesis.The patient then transferred urgently to C.T or OR. Bil.Dilated & non reactive pupil who is not hypotensive.

Furosemide (Lasix) : 

Furosemide (Lasix) Dose: 0.3-0.5 mg/kg i.v Combined with mannitol after consulting neurosurgeon

E. Steroids : 

E. Steroids It is not recommended in management of Acute Head injury.

F. Barbiturates : 

F. Barbiturates It ? ICP. Not used in Presence of Hypotension. Dosage: Adult: loading 10-12 mg/kg 3 divided doses . Maintx :1-3 mg/kg/24h i.m or i.v. Pedia.:load 15-20 mg/kg in 2 doses then maintx 3-5 mg/kg/24h

G. Anticonvulsants : 

G. Anticonvulsants Post traumatic epilepsy occur in 5% of all patients admitted to the hospital, and in 15% of sever head injury cases. Phenytoin is used for the 1st week . Dosage: Loadx : 15-20 mg/kg (25mg/min). Maintx: 200 mg p.o or i.v bid. Pediax: loadx the same. Mainx 4-7 mg/kg/24h

Surgical Management : 

Surgical Management A-Scalp Wounds: Inspection carefully, attention should be given to trivial injuries in children by pencils as it can cause penetrating injury with bad sequel if not noticed. Adequate cleansing and debridement Blood loss can be extensive , especially in children Presence of csf means dural tear

B-Depressed skull fracture : 

B-Depressed skull fracture Needs elevation if the degree of depression is greater than the thickness of adjacent skull. CT is mandatory to r/o intracranial hematoma or depression.

Curvilinear depressed fracture : 

Curvilinear depressed fracture

Depressed fracture : 

Depressed fracture

C-Intracranial Mass Lesion : 

C-Intracranial Mass Lesion Early transfer of the patient to a hospital with a neurosurgeon. In Rural Areas: Burr holes may be considered, the purpose of it to is to preserve life by partially evacuating a life threatening intracranial hematoma.

Indications for referral to neurosurgeon : 

Indications for referral to neurosurgeon Persistent coma (GCS<8) after initial resuscitation Unexplained confusion persisting for › 4 hours Deterioration in GCS after admission A seizure without full recovery Progressive focal neurological signs Definite or suspected penetrating injury CSF leak

Emergency Burr Holes : 

Emergency Burr Holes Should be considered in the contest of the following: The majority of comatosed patients do not have hematoma

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A burr hole placed as little as 2 cm away from hematoma may not locate it. Only a small portion of epidural or subdural hematoma can be adequately evacuated, as blood is often clotted. A burr hole itself can cause brain damage or Hge.

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Thank You

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