Managing Head Injury at the District Hospital

Pre-test This patient probably has: Bilateral maxillary fractures Nasal fracture Basal skull fracture Frontal skull fracture

Pre-test A 70 year old man was a hit by a car. His family bring him to the district hospital. He is unconscious. He does not open his eyes, does not make any sounds, and has no motor response to stimulation. Both pupils are fixed and dilated. What statements are true? He has a very poor prognosis and will probably die from his head injury. You should intubate and transfer him immediately to the provincial hospital. His GCS is 7. You should check his corneal and gag reflex. He should receive dilantin to prevent a seizure.

Pre-test A 16 year old boy was in a motor bike accident. He was not wearing a helmet. He is unconscious, airway open and breathing 4 times per minute. His blood pressure is 180/100, pulse 64. His pupils are reactive and not dilated. Which statements are true? He probably has increased intracranial pressure. He should be intubated and hyperventilated at about 20 breaths/ minute. He should receive IV fluid. He should receive IV antihypertensive medicine. You should talk to family about sending him to the provincial hospital.

Pre-test Which statements about subdural hematomas are true? Subdural hematomas: Result from arterial bleeding in the brain Result from torn veins on surface of brain Are often associated with diffuse axonal injury Are most common in children Have better prognosis than epidural hematomas

Pre-test A young man was admitted to the district hospital yesterday after suffering a head injury. His initial GCS was 11. Today his GCS is 9 and his right pupil is now dilated and not reactive. Which of the following statements are true? He has developed a delayed intracranial hematoma He has developed diffuse cerebral edema You should talk to his family about transfer to the provincial hospital He should receive mannitol He should receive D5W IV fluid

Introduction Severe head injury Age is a predictor of outcome Most frequent cause of trauma death Traffic accident most common cause Poor prognosis / High mortality and morbidity rates Difficult decisions to make Difficult diagnosis with no CT scan High cost for patient to get transport and have family come and stay at provincial hospital High cost of CT scan Patient may have poor outcome Age is a predictor of outcome Young patients may do well / Old patients often do poorly

Introduction to Head Injuries TIME can be CRITICAL Intracranial Hemorrhage Progressing Edema Brain injury from bleed or edema Increased ICP Cerebral Hypoxia Permanent Damage Severity can be difficult to know

Mechanisms of Head Injury Mechanism of Injury Blunt Injury Motor vehicle collision / Pedestrian collision Assault Fall Penetrating Injury Gunshot wound Stab wound UXO

Pathophysiology Blood supply to brain autoregulated as body tries to make sure brain has enough oxygen 3 types of autoregulation

Pathophysiology Pressure Autoregulation Viscousity Autoregulation If BP , cerebral arteries dilate to keep constant blood supply to brain Viscousity Autoregulation If viscousity , cerebral arteries vasodilate Metabolic Autoregulation If pO2, cerebral artery vasodilation If pCO2, cerebral artery vasodilation

Brain Anatomy Intracranial volume Brain CSF Blood vessel volume Dilatation with high pCO2 Constriction with low pCO2 Head Trauma - 12 12

Intracranial Perfusion Cranial volume fixed 80% = Cerebrum, cerebellum & brainstem 12% = Blood vessels & blood 8% = CSF Increase in size of one component diminishes size of another Inability to adjust = increased ICP

Intracranial Perfusion Compensating Cranial Perfusion for ICP Compress venous blood vessels Arterial vasoconstriction in brain Reduction in free CSF Push brain into spinal cord De-compensating Cranial Perfusions for ICP: Increase in ICP Rise in systemic BP to perfuse brain Further increase ICP ICP BP

Factors Affecting ICP Cerebral Edema / Cerebral hematoma Systemic Systolic BP Low BP = Poor Cerebral Perfusion High BP = Increased ICP Carbon Dioxide & Oxygen levels The Balance: Brain needs sufficient perfusion (O2 delivery), but does not tolerate high ICP

Intracranial Pressure Role of Systemic Hypotension Hypotension or under resuscitation will cause higher ICP Systemic hypotension Brain autoregulation Cerebral vasodilation Increase ICP If systemic systolic BP < 90 mmHg even 1 occasion, mortality is 1.5 - 2 X higher AVOID HYPOTENSION IN PATIENTS WITH HEAD INJURY

Intracranial Pressure Role of Hypoxemia Brain more sensitive to ischemia after trauma Hypoxemia Cerebral vasodilation Increase ICP Higher mortality in patients with hypoxemia and head injury AVOID HYPOXEMIA IN PATIENTS WITH HEAD INJURY

Intracranial Pressure Role of Carbon Dioxide Increase of CO2 Cerebral Vasodilation Encourage blood flow Reduce hypercarbia Reduce hypoxia Contributes to  ICP Hyperventilation decreases CO2 in Brain Cerebral vasoconstriction Results in cerebral anoxia AVOID HYPERCARBIA IN PATIENTS WITH HEAD INJURY

Pressure Can Cause Structural Displacement Increased pressure Compresses brain tissue Brain starts to herniate through foramen magnum into brainstem Compromises blood supply Signs & Symptoms of pressure on brainstem Altered mental status Pupil dilation Irregular breathing Bradycardia Hypertension

Scalp Injuries Scalp wound Highly vascular, can bleed a lot Management Can cause shock in a child In adult, shock usually indicates another cause Management No unstable fracture: Direct pressure & suture Unstable fracture: Dressings, avoid direct pressure Head Trauma - 21 21

Skull Fractures Skull fracture Suspect fracture Management Linear nondisplaced Depressed Compound Suspect fracture Large contusion or darkened swelling Management Dressing, avoid excess pressure Head Trauma - 22 22

Skull Fracture Excess force needed to fracture skull Types Linear Depressed Open Impaled Object

Skull Fracture Depressed skull fracture Should be referred to provincial hospital for bone elevation if: Depth of depression more than width of surrounding bone Open fracture Neurologic deficit from increased ICP

Basal Skull Unprotected Spaces weaken structure Relatively easier to fracture

Skull Fracture Basal Skull Fracture Signs Battle’s Signs Raccoon Eyes Retroauricular Ecchymosis Associated with fracture of auditory canal and lower areas of skull Raccoon Eyes Bilateral Periorbital Ecchymosis Associated with orbital fractures

Basal Skull Fracture Battle’s sign Raccoon eyes Basilar skull fracture indicated by any of following: Bleeding from ear or nose Clear or serosanguineous fluid running from nose or ear Swelling and/or discoloration behind ear (Battle’s sign) Swelling and discoloration around both eyes (raccoon eyes) Battle’s sign can occur from immediately following injury to within 1–2 hours postinjury. Raccoon eyes are a sign of anterior basilar skull fracture. Through thin cribriform plate in upper nasal cavity and allow spinal fluid and/or blood to leak out. Raccoon eyes with or without drainage from nose are an absolute contraindication to inserting a nasogastric tube or nasotracheal intubation. Head Trauma - 27 27

Basal Skull Fracture Other signs: Hemotympanum (blood behind tympanic membrane) Rhinorrhea or Otorrhea (Check fluid for ‘halo’ sign) NO NG tube because it is possible that tube could pass through fracture and go intracranial

Skull Fracture Basal Skull Fracture May tear dura Permit CSF to drain through nose or ear Evaluate fluid for “Halo” sign Blood CSF

Forces that cause skull fracture can also cause brain injury. Head Trauma - 30 30

Classification Primary Occur at time of injury Secondary Secondary injury caused by factors resulting from the primary injury (ie. cerebral edema)

Brain Injury Primary brain injury Immediate damage due to force Coup and contracoup Occur at time of injury Head Trauma - 32 32

Primary Brain Injury Types Coup Injury at site of impact Contrecoup Injury on opposite side from impact

Secondary Brain Injury Response to injury Swelling of brain Increased ICP Decreased blood flow to brain Perfusion decreases Cerebral ischemia (hypoxia) Head Trauma - 34 34

Secondary Brain Injury Results from hypoxia or decreased perfusion Response to primary injury Develops over hours Management Good prehospital care can help to reduce secondary injury Head Trauma - 35 35

Signs & Symptoms of Brain Injury Altered Mental Status Unconscious Confusion Alteration in personality Amnesia Retrograde Antegrade Cushing’s Reflex Increased BP Bradycardia Erratic respirations Other Vomiting Body temperature changes Changes in pupil reactivity Decorticate posturing

Signs & Symptoms of Brain Injury Origin of Symptoms Frontal Lobe Injury Alterations in personality Occipital Lobe Injury Visual disturbances Cortical Disruption Reduce mental status or Amnesia Retrograde Unable to recall events before injury Antegrade Unable to recall events after trauma “Repetitive Questioning” Focal Deficits Hemiplegia, Weakness, or Seizures

Primary Brain Injury Categories Focal Occur at a specific location in brain Types Cerebral Contusion Intracranial Hemorrhage Epidural hematoma Subdural hematoma Intracerebral Hemorrhage Diffuse Concussion Moderate Diffuse Axonal Injury Severe Diffuse Axonal Injury

Focal Brain Injury Cerebral Contusion Occurs when brain hits bone prominences of skull in blunt trauma Results from coup-contrecoup injury Caused by capillary bleeding into brain tissue 50% of moderate to severe closed head injuries Symptoms Prolonged unconsciousness Severe confusion / amnesia Possible neurological deficit Personality changes Vision changes Speech changes

Focal Brain Injury Intracranial Hemorrhage Epidural Hematoma 5% of severe head injuries More common in younger patients Often from skull fracture that tears middle meningeal artery Bleeding between dura mater and skull Rapid bleeding with rapid deterioration

Focal Brain Injury Intracranial Hemorrhage Epidural hematoma Level of consciousness Initial loss of consciousness “Lucid interval” follows Consciousness declines within 6 hours Associated symptoms Ipsilateral dilated fixed pupil Signs of increasing ICP Unconsciousness Contralateral paralysis If identified early enough, those who get surgery can do well Suspect in young patients with possible temporal skull fracture . Head Trauma - 41 41

Focal Brain Injury Intracranial Hemorrhage Subdural Hematoma Bleeding within meninges Inside dura mater & within subarachnoid space More often associated with diffuse axonal injury than epidural hematoma Usually higher force injury Slow bleeding from veins between brain and venous sinuses Cerebral atrophy (ie. in elderly or alcoholic patients) puts pts at higher risk

Focal Brain Injury Intracranial Hemorrhage Subdural Hematoma Signs progress over several days Slow deterioration of mentation Worse prognosis than epidural hematoma patients 50 - 90% mortality

Focal Brain Injury Intracranial Hemorrhage Subdural hematoma Signs & symptoms Headache Fluctuations in level of consciousness Focal neurological signs (ie. weakness of one side or limb, slurred speech) Head Trauma - 44 44

Focal Brain Injury Intracerebral hemorrhage Arterial or venous Surgery is often not helpful Level of consciousness Alterations common Associated symptoms Varies with region and degree Pattern similar to stroke Headache and vomiting Head Trauma - 45 45

Diffuse Brain Injury Due to stretching forces placed on individual nerve cells Injury distributed throughout brain Types Concussion Moderate Diffuse Axonal Injury Severe Diffuse Axonal Injury

Diffuse Brain Injury Diffuse axonal injury Generalized edema No structural lesion Most common injury from severe blunt head trauma Head Trauma - 47 47

Diffuse Brain Injury Concussion Mild form of Diffuse Axonal Injury (DAI) Nerve dysfunction without anatomic damage CT scan usually normal Short episode of: Loss of consciousness Confusion Event amnesia Headache, dizziness, nausea GCS usually 14 or 15 Usually good recovery

Diffuse Brain Injury Moderate Diffuse Axonal Injury Same mechanism as concussion, but more severe bruising of brain tissue Signs & Symptoms Prolonged unconsciousness Persistent confusion Loss of concentration Retrograde & antegrade amnesia Mood or personality changes

Diffuse Brain Injury Severe Diffuse Axonal Injury Significant mechanical disruption of nerve cells Cerebral hemispheres AND brainstem High mortality rate Signs & Symptoms Prolonged unconsciousness Cushing’s reflex Decorticate or Decerebrate posturing Dilated fixed pupils

Extremity Posturing Decorticate Decerebrate Arms flexed and legs extended Decerebrate Arms extended and legs extended Head Trauma - 51 51

Signs & Symptoms of Brain Injury Upper Brainstem Compression Increasing blood pressure Reflex bradycardia Vagus nerve stimulation Irregular respirations Decorticate posturing

Signs & Symptoms of Brain Injury Physiological Changes Lower Brainstem Injury Pupils dilated and unreactive Irregular respirations Irregular pulse rate Hypotension Decerebrate posturing Loss of response to painful stimuli

Signs & Symptoms of Brain Injury Eye Signs Physiological Issues Indicate pressure on CN-III (Oculomotor Nerve) Pressure on nerve from increased ICP causes eyes to be sluggish, then dilated, and finally fixed Pupil Size & Reactivity Reduced Pupil Responsiveness Depressant drugs or Cerebral Hypoxia Fixed & Dilated Extreme Hypoxia

Pupils Both dilated Anisocoria Unilaterally dilated Eyelid closure Nonreactive: brainstem Reactive: often reversible Unilaterally dilated Reactive: ICP increasing Nonreactive (altered LOC): increased ICP Nonreactive (normal LOC): not from head injury Eyelid closure CN III: can be affected by increased ICP and cause ptosis and downward deviation Rapid Fluttering: often hysteria Head Trauma - 55 55

Glasgow Coma Scale Suspect severe brain injury GCS <9 *Decorticate posturing to pain **Decerebrate posturing to pain Head Trauma - 56 56

Cerebral Herniation Syndrome Brain forced downward CSF flow obstructed, pressure on brainstem Level of consciousness Decreasing, rapid progression to coma Associated symptoms Ipsilateral pupil dilatation, out-downward deviation Contralateral paralysis or decerebrate posturing Decorticate posturing Respiratory arrest / Death Head Trauma - 57 57

Decreased level of consciousness is an early indicator of brain injury or rising ICP. Head Trauma - 58 58

Early efforts to maintain brain perfusion can be life-saving. Head Trauma - 59 59

Initial Assessment Assess and Record Pupils (size and reaction to light) GCS Head Trauma - 60 60

Initial Assessment Pupils Bilateral fixed and dilated Very poor prognosis Patient may not benefit from transfer Can assess brainstem function Corneal reflex Gag reflex Single fixed and dilated pupil Suggests ipsilateral uncal herniation May be able to save patient Needs aggressive treatment to decrease ICP Head Trauma - 61 61

Initial Assessment GCS GCS 14 - 15: Suggests mild head injury GCS 9 - 13: Suggests moderate head injury GCS < 9: Suggests severe head injury GCS decreases by 2: Suggests increasing ICP Head Trauma - 62 62

Full Clinical Assessment Examine head in detail Scalp lacerations Skull fractures Signs of basal skull fracture Check cranial nerves, if possible Make sure patient can move all limbs You must also do a thorough assessment looking for other injuries Protect C-spine Head Trauma - 63 63

Initial Treatment If GCS < 9 & pupils not fixed/dilated & no decorticate signs Intubate Prevent brain hypoxia Oxygen to prevent hypoxemia (O2 sat > 95%) If intubated, ventilate 8 - 10 / minute with high flow oxygen Both hypoventilation & hyperventilation can cause cerebral ischemia and increased mortality Hyperventilation is ONLY used if acute deterioration and need to decrease ICP quickly Head Trauma - 64 64

Is ICP severe enough to outweigh cerebral ischemia? International Trauma Life Support, 6e Cerebral Herniation Is ICP severe enough to outweigh cerebral ischemia? Head Trauma - 65 65

Hyperventilation Cerebral herniation syndrome Herniation danger outweighs hypoxia Indications for hyperventilation GCS <9 with decerebrate posturing GCS <9 with dilated or nonreactive pupils Initial GCS <9, then drops >2 points If signs resolve, stop hyperventilation. Head Trauma - 66 66

Hyperventilation Rates Age Group No Hyperventilation Adult 8–10 per minute 20 per minute Children 15 per minute 25 per minute Infants 30 per minute Normal Ventilation Hyperventilation Head Trauma - 67 67

Initial Treatment Prevent Brain Hypoxia Prevent Hypotension Single instance increases mortality Adult (systolic <90 mmHg): increases mortality > 150% Child (systolic < age appropriate): increases mortality even more than adults Fluid administration for traumatic brain injury Titrate to 110–120 mmHg systolic to maintain cerebral perfusion Head Trauma - 68 68

Initial Treatment Reduce Edema Edema is increased amount of water in interstitial space (ie. brain tissue) caused by Decrease plasma proteins (colloids) Increased hydrostatic pressure (high BP) Increased capillary permeability Blocked drainage

Fluid Tonicity Isotonic: concentration in fluid equal to the blood concentration (fluid stays intravascular better) 0.9% normal saline Lactated Ringers Blood Isotonic solution will help with cerebral perfusion by increasing vascular volume

Fluid Tonicity Hypotonic: concentration in fluid less than the concentration of surrounding spaces (water goes into the interstitial spaces) Fresh water 5% dextrose in water 0.45% saline 5% D/.2 saline Hypotonic solution will make cerebral edema worse

Fluid Tonicity Hypertonic: concentration in fluid greater than the concentration of surrounding spaces (pulls water from the interstitial spaces) Protein solutions Mannitol 3.3% saline Hypertonic solution can help to reduce cerebral edema

Initial Treatment Elevate head of bed 30 - 45  (if no concerns about spine) Mannitol Acts as osmotic agent (hypertonic) Reduces arterial viscousity Reduces brain swelling (draws edema out of brain) Dose: 1 gm/kg initial dose 0.25 gm/kg q 6 hour as needed Mannitol is also diuretic, so need to continue IV saline to maintain intravascular volume

Initial Treatment Do not give sedation unless needed for airway protection / ventilation But be sure it does not decrease BP because this reduces brain perfusion

Neuro Vital Signs Unilateral Fixed, Dilated Pupil or 2 point decrease in GCS Normal Pupils, but suspect intracranial injury Bilateral Fixed, Dilated Pupils Could consider Mannitol BUT Patient will probably die / Cannot change outcome Severe head injury, but might be able to save patient Treat for high ICP Transfer to Provincial Hospital for CT & treatment (May wish to be less aggressive in elderly pt) Monitor closely If GCS decreases or develops focal neuro signs, transfer to Provincial Hospital

Quality Assurance Severe head injuries can have high mortality and bad functional outcomes Discuss issues relating to improving patient or family circumstances following such an injury: Discussion about prevention Is information given to patients / families about head injury and prevention? Who has this discussion and how could this be encouraged as a health care team? Should you have policy or protocol to promote family and patient education for prevention?

Quality Assurance Discussion about patient outcome Does doctor at district hospital receive feedback on care provided from provincial hospital? Should this be done? Is this feasible? Would this help the referring doctor? Are there other quality issues you can think of?

Post-test This patient probably has: Bilateral maxillary fractures Nasal fracture Basal skull fracture Frontal skull fracture

Post-test A 70 year old man was a hit by a car. His family bring him to the district hospital. He is unconscious. He does not open his eyes, does not make any sounds, and has no motor response to stimulation. Both pupils are fixed and dilated. What statements are true? He has a very poor prognosis and will probably dies from his head injury. You should intubate and transfer him immediately to the provincial hospital. His GCS is 7. You should check his corneal and gag reflex. He should receive dilantin to prevent a seizure.

Post-test A 16 year old boy was in a motor bike accident. He was not wearing a helmet. He is unconscious, airway open and breathing 4 times per minute. His blood pressure is 180/100, pulse 64. His pupils are reactive and not dilated. Which statements are true? He probably has increased intracranial pressure. He should be intubated and hyperventilated at about 20 breaths/ minute. He should receive IV fluid. He should receive IV antihypertensive medicine. You should talk to family about sending him to the provincial hospital.

Post-test Which statements about subdural hematomas are true? Subdural hematomas: Result from arterial bleeding in the brain Result from torn veins on surface of brain Are often associated with diffuse axonal injury Are most common in children Have better prognosis than epidural hematomas

Post-test A young man was admitted to the district hospital yesterday after suffering a head injury. His initial GCS was 11. Today his GCS is 9 and his right pupil is now dilated and not reactive. Which of the following statements are true? He has developed a delayed intracranial hematoma He has developed diffuse cerebral edema You should talk to his family about transfer to the provincial hospital He should receive mannitol He should receive D5W IV fluid