The Event Physician Head Injuries

Emergency Sports Medicine Scalp lacerations and bleeding

• Scalp wounds may bleed profusely- must be stopped. • Suturing is usually adequate • Difficult on field of play • Venous -digital compression • Bleeding that does not stop ~arterial in origin ~ fracture? • digital compression should not be excessive ~ risk of pressing fractured bone further into the cranium. • cover wound- use turban bandage. Occasionally, i.v. fluid may be needed if blood loss is significant Cranial/Cerebral injuries

• common in sports • Some serious, most are not • 6 issues we must be concerned about • Scalp wounds • Cranial Fractures • Cerebral Contusions • Cerebral Hematomas • Cerebral Oedema • Concussion • Concomitant neck injuries Anatomy:

• Scalp • Cranium and face - 22 bones • Mandible – only movable • Cerebrum + meninges • Sinuses – absorb force Brain

• Well protected by meninges and skull • Sinuses • CSF • Brain no energy stores ~constant supply of blood and O2 • Therefore – sensitive to reduced blood flow/O2 Fracture types

• external cranium is exposed to compression forces at point of contact, whereas internal bone is exposed to tensile forces • If point of contact is thick and strong, then the energy may be conducted around the cranium and cause a fracture at a weaker point. • Intracranial lesions accompany roughly two-thirds of skull fractures • Open fractures ~infection, air entry, meningitis or pneumocephalus CSF leakage • Linear fractures – commonest • Splinter fractures – after blow • Compression / impression fractues – extremely dangerous • Penetrating fractures Localisation:

• Frontal – often depressed and if so, associated with brain contusions • Parietal • Temporal – associated with epidural hematomas - linear, can spread to basis • Occipital • Basilar ~CSF leakage from the ear or nose, blood behind the tympanum (hemotympanum), Battle’s Sign and Raccoon Eyes. Inspection:

• Local Inspection for cuts and bruises • ? depressed fracture l – so look for but don’t press on indentations • Large hematoma over a fracture • Pain and tenderness • Penetrating wounds skade f.eks. spiker etc • CSF leakage ears, mouth, nose. Sweet taste sugar CSF. Inspection:

• bleeding nose may indicate basal fracture, a bleeding ear almost always does. • examine ear canals and drums- no bleeding, but blood behind an intact drum, may indicate a basal fracture. • Thickening of the temporalis muscle – facial, cranial fracture? • Blood may also come from the mouth • Battle's sign • Binocular Hematomas – note the white corneas – no bleeding - Basilar fractures Battle’s Sign

Battle’s Sign – mastoid ecchymosis, indicates posterior basilar fracture, but absence does not exclude a fracture. Binocular Hematoma

Note clear white cornea Subconjunctival Hematoma

• Can be present with a basilar fracture Clinical findings – cranial fracture

• As with TBI • Neurological findings and altered states of consciousness • Hypotension (severe head injury – impending shock or death/ bleeding other source) • Hypertension (in mild or moderate TBI, body compensate blood loss via by vasoconstriction, resulting in elevated blood pressure). May also occur in acute spinal injuries. Clinical findings 2 – cranial fracture • Increased respiratory Rate – the body tries to compensate for trauma induced cerebral hypoxia by breathing faster. • Decreased Respiratory rate – may be sign of a major TBI and impending death. • Raised Temperature – mild increase found with TBI; beware Meningitis, encephalitis or other systemic infections as cause of collapse - not TBI/combo. Treatment cranial fractures:

• treat any life-threatening complications first • stabilise cranial (and cervical) fractures • constant re-appraisal of Vital signs, Level of consciousness, Neurological deterioration • ABC/ Oksygen • Stop bleeding NB Cranium • Cover wounds • Do not remove foreign bodies or bone fragments Always

• Maintain patent airways • max Oxygen supply, 12 – 15 L, 100% • Apply semi-rigid cervical collar • Maintain Ventilation • Stop scalp, non-intracranial hemorrhage • Establish i.v. lines and give adequate fluid – not too much – normo-tension is the goal. • Cover cranial and other wounds • Spine board or vacuum mattress • Elevate the head • Don’t lie on wound • Cont. Neuro evaluation • Use checklist Never

• Never Remove penetrating intracranial foreign bodies – bleeding will worsen • Never Compress arterial bleeding from a cranial fracture site; digital pressure will probably not stop the bleeding and may worsen the bleeding by pressing bone fragments further into the brain Transport and contact

• patient supine position with the Head elevated • patient should not lie on wound or fracture site • Continuous neurological evaluation – use check list • Continuous respiratory and circulatory evaluation • Ensure correct cervical and spinal immobilisation • Ensure careful lifting and movement of the patient.

• Contact with hospital: • Inform the hospital of the patients status and expected time of arrival, deterioration - recontact Ding dong Traumatic Brain Injury TBI

• Concussion • Contusion - oedema • Cerebral Hematoma Shearing, Bleeding and hematoma Shearing or torsional forces – white matter vessels damaged/ bleeding –tissue ischemia/ dural vessel damage - hematoma/ raised ICP/ reduced blood to brain tissue. Cerebral tissue ischemia and swelling/oedema leads to a lower PO2 and a higher PCO2. Raised PCO2 stimulates a vasodilation of arterial vessels, which results in further raised ICP. Pressure further compresses dilated arteries and further interferes with cerebral blood flow to already ischemic blood cells and thus worsens the ischemia. Injury site

• Area of contact (coup) • Bouncing (contrecoup) • Occasionally sutures – dura is ripped off Anatomy of a man’s brain Predisposing conditions:

• coagulopathy and anticoagulant therapy • depressed skull fracture or basilar fracture, • focal neurologic deficits, • multiple injuries, • shunt-treated hydrocephalus • AND LAST BUT NOT LEAST a recent history of head injury Concussion

• after a blow • No CT signs of brain injury • Diagnosis • Loss of consciousness - LOC • Headache, nausea, vomiting • Amnesia (minutes-hours) - retrograde amnesia • Impaired intellectual function One of the issues that was speculated upon at the Vienna conference was whether concussion represents a unitary phenomenon with a linear spectrum of injury severity or whether Types of concussion

• different concussion sub-types exist and may present with different clinical manifestations (confusion, memory problems, loss of consciousness) • may be dependent on anatomic localization (cerebral, brain stem) • biomechanical impact (rotational or linear force) • genetic phenotype (ApoE4 positive or negative) • neuropathological change (structural injury, no structural injury) or an as yet undefined difference. • factors may be independent or combined • Must be several types as clinical outcome with the same impact force cause different clinical findings LOC - significance

• Traditional evaluation groundstone • Still relevant if prolonged • Used to be primary measure of severity • limitations in sporting concussive injury. • Studies imply that short term LOC is not associated severity • LOC not necessarily ~complex concussion • LOC is a very important finding if non-concussive head injury present – i.e. hematoma, contusion Amnesia – Significance!

• Maybe more important • new interest • role of post-traumatic amnesia as a measure of injury severity? • Publications seem to imply that the sum of symptoms, severity and duration of the clinical post-concussive symptoms may be more important than the presence or duration of amnesia alone. • Further it must be noted that retrograde amnesia varies with the time of measurement post-injury and hence is poorly reflective of injury severity. Cerebral contusion:

• brain exposed to external forces - bruising • direct, indirect contrecoup ichemia and necrosis • smaller arteries, petechial hemorrhage, swelling of the brain tissue due to edema and even tissue destruction • ischemic damage~arterial injury • findings vary with location and size of the brain contusion • frontal and temporal regions (often basal aspects of) most common Cerebral Contusion:

• CT scan • R. extensive bruising - large, diffuse grey area • White patches within grey - bleeding. • grey represents oedema • cortical contusion – purple • Cm scale to measure level of oedema • "Cortical contusion > 1cm in diameter. Frontal Lobe

• Frontal Lobes • most vulnerable, commonest injury site mild - moderate TBI • may result in • difficulty in speaking • formulating response • disturbance or loss of fine movements and strength of the arms, hands and fingers • reduced facial expressions. Temporal Lobe

• Temporal Lobes • Disturbed hearing • difficulty in recognizing faces • difficulty in understanding spoken words • Short-term memory loss • right lobe damage can cause persistent talking, increased aggressive behaviour. Parietal Lobe

• Parietal Lobes – Damage may cause several unusual symptoms • Inability to name an object (Anomia) • difficulty reading (Alexia) • difficulty with drawing object • difficulty in distinguishing left from right • Apraxia • difficulties with eye and hand coordination. Occipital Lobe

• Occipital Lobes – • Visual Field defects, difficulty with identifying colors (Color Agnosia), Visual illusions - inaccurately seeing objects, Word blindness, difficulty in recognizing drawn objects. Difficulties with reading and writing. Dysautoregulation Syndrome

• Diffuse cerebral oedema - Second impact syndrome • Primary head injury – remaining brain oedema and increased vulnerability to injury • Premature RTP • Young athletes and teenagers • second blow - further oedema - loss of the brain’s ability to control cerebral blood inflow (autoregulation) - rapidly increase in flow, intracranial pressure rises uncontrollably, cardio-respiratory failure and maybe death. Diffuse Axonal Injury:

•petechial haemorrhages usually an indication of very severe primary brain injury. •Petechial haemorrhages tend to occur the interface of grey - white matter • also in dorsolateral quadrant of the midbrain - orange arrow and elsewhere •on this scan, lateral and third ventricle visible - no midline shift- characteristic of diffuse axonal injury - numerous petechial haemorrhages - no evidence of brain swelling, or midline shift. Raised Intracranial pressure

• Unconscious, decreasing consciousness • Increasing BP • Pulse strong, quick, slow (< 60 /min) • Irregular breathing or arrest • Dilated pupil that do not respond to light • Papilloedema on ophthalmoscopy • Paresis/hemiparesis • Headache, nausea, vomiting Contusions

• easily visible on CT and MRI scans • Often small subarachnoid bleedings – provoking a mild inflammatory reaction due to the presence of blood in the CSF. Cerebral Hematoma

• Bleed between Extradural hematoma cranium and brain • Closed box – no Epidural hematoma room Subdural hematoma • Pressure increase – raised ICP Intra-cerebral bleed • Potentially fatal may Intra-ventricular need surgery hematoma • Diagnostic hallenge

Extradural Hematoma 1

• Blow to head • Bleeding between cranium - dura • Often linear temporal fract. • Middle meningeal artery • Hematoma grows • Pressure rises – r ICP • Less space for brain • Ischemia – bruising • Clinic – not unlike epidural hematoma Epidural Hematoma

• Some are venous – often less serious • Increased mortality 0 – 5, > 55 år gammel (unusual due to stiff dura • Mortality: • Not comatøse - 0%! • Light coma - 9% • Deep coma - 20% • (UCLA) Epidural Hematoma 2

• CT Scan • haematoma has a concave shape as is bone and the dura and not lying on the brain itself. • Limited by dural attachments A + P • Midline shift • Note frontal horns ~relation to the falx cerebri Epidural Hematoma 2

• Findings • Less response to stimuli • Heavy in head • Pupil dilates on injured • Strong headache side • Appears intox • Loose light reflex • Nausea, Vomiting, • Increasing strength loss, Seizures paresis of opposite side • Often LOC, then regain, of body then new LOC • Rising BP, falling pulse • More and more and RR somnolent • Sudden resp arrest Subdural Hematoma

• Usually venous • Increase in ICP • 2 types: • Massive Acute – severe trauma, often fatal • Lesser –children, elderly • Gradual rise in ICP • Clinical findings – more gradual onset – less severe but may increase in severity Acute Subdural Haematoma 1

• R.acute haematoma • associated cortical contusion > 1 cm • midline shift > 5 mms - yellow dots • lateral ventricles pushed to the left • third ventricle not visible • Obvious need for surgical evacuation Acute Subdural Hematoma 2

• L. acute haematoma • Through higher part of brain • L. ventricle compressed • Midline deviation to R. • R. lateral ventricle larger than normal due to r ICP blocking CSF escape • This dilatation of contralateral ventricle is serious sign • Obvious need for rapid surgical evacuation Penetrating injuries

• Violence • Falls traffic injuries • Knives, shotgun

Examination of patient with TBI

• Vital signs • Serious findings: • Eyes • Abnormal function • Level of • LOC consciousness • Changes in cosciousness • Aggressivity, irritated • confused Vital signs

• Check BP – rising, falling? • Strong, more rapid pulse? • (Shock is not typical with head injuries) • RR – quality and frequency: - Rapid and shallow -Cheyne-Stokes resp. • Abdomen – extremities – signs of bleeding? • Rigid abdomen? • Rising temperature Respiratory pattern:

• rate and depth of respiration • Hyperventilation • Hypoventilation • respiratory centre -brainstem medulla • Cheyne-Stoke respiration upper brainstem • Ataxic respiration • lower brainstem may cause central neurogenic respiration with shallow and rapid respiration – a most serious form of dysfunction. Cheyne-Stokes respiration

• Pathological respiratory pattern due to respiratory centre damage • Rhythmic regular variations in respiratory depth, frequency and apnoeic intervals • After the interval breaths are initially superficial then deeper Average respiratory rates-age:

• Newborn: Average 44 breaths per minute • Infants: 20–40 breaths per minute • Preschool children: 20–30 breaths per minute • Older children: 16–25 breaths per minute • Adults: 12–20 breaths per minute • Adults during strenuous exercise 35–45 breaths per minute • Athletes' peak 60–70 breaths per minute Neurological examination;

• Level of consciousness • Level of intellectual • Important for diagnosis, function – concentration, level of care, baseline. memory, orientation, • Glasgow Coma Scale • Respiratory pattern • If the patient regains • Pupillary size and pattern consciousness try to • Eyes and eye movements evaluate the extent of • Motor function pre– incident and post– • Coordination incident amnesia, as well as : Pupillary size and reaction:

• Pupils equal and react to light – PEARL • Ipsilateral and consensual • may find a normal sized but unreactive pupil • or a fixed dilated pupil • Bilateral dilatation - often severe brain damage. • Examine early and often, as signs may diappear • False security before calamity • NB - photophobia with normal reflexes, may indicate a cerebral lesion. Eye inspection and movements:

• Binocular hematomas - facial/cranial fracture. • Papilloedema - not often looked for • Eye movements difficult to evaluate in an unconscious patient. • Sunken eye - orbital fracture? • Exophthalmos – fracture? • Doll's eyes movement – brainstem dysfunction - should not be tested for due to the possibility of concommitant spinal injury. • Nystagmus, diplopia Level of consciousness:

• Note • Conscious or not, confused, aggressive, somnolent, awaken with shouting/shaking/light pain stimuli (pin prick) /strong pain stimuli • Speech – slurred, cant make a sentence • Consciousness changes ~deterioration • Warn hospital of evt changes • Beware this pasient: LOC, regain, LOC ~ hematoma Level of intellectual function:

• conscious but still have serious cerebral lesions. • Amnesia • Concentration ability • (count from 79 down to 70: what is your telephone number – repeat backwards i.e. last number first), • Memory (quiz about recent events you would expect the athlete to know about – give him/her a word and request this word after 4 – 5 minutes) • Orientation (where are you, how did you get here, what time is it), Motor function:

• Apply peripheral noxious • Decerebrate rigidity indicates stimuli brain-stem damage • pinching of limbs, pin prick • bilateral poor prognosis tests to elicit • Complete flaccidity with no • (a) an Appropriate response – response to stimuli brushing away the source of • severe CNS depression stimulus • intoxification - drug overdose? • (b) an Inappropriate response – indicating decerebrate or • Cranial nerve injury decorticate rigidity. • changes in smell, hearing, taste, speech, smiling, eye movement, shoulder • Motor response useful in shrugging) localising the level of a spinal • raised intracranial pressure i.e. injury. papilloedema. • No response - A paralysed limb Coordination:

• Absence of injury and the patient is able to stand • has normal vital signs • Normal mental status • Then elementary coordination and balance tests • finger –nose test (with eyes closed and open), • Romberg test etc. Glasgow Coma Scale Motor response M - score

• Moves extremities on command• 6 • Adequate movement to pain stim 5 • Withdraws extrem on stimulus 4 • Decortical body position 3 • Decerebrate body position 2 • No response 1 Eye responseE - score

• Spontaneous, normal movements 4 • Opens eyes on command 3 • Opens eyes on painful stim away from face 2 • Does not open eyes 1 Verbal response V - score

• Awake, orientated 5 • Confused but answers questions 4 • Understandable words, inappropriate speech 3 • Incomprehensible words, mumbling 2 • No Sounds 1 Glasgow Coma Scale Conclusion

• 14 - 15 Grade 1 Mild – may have headache, nausea, vomiting

• 9 - 13 Grade 2 Moderate - Redusert bevissthet, kan utføre ting på kommando, kan være våkne med fokale utfall

• 4 - 8 Grade 3 Severe - Betydelig nedsatt bevissthet, ikke i stand til å følge kommando

• 3 poeng Grade 4 Clinical brain death, with no neurological response Våkne,delvis orienterte Glasgow Coma Scale

Eye opening (E) Eye opening (E) Spontaneous 4 Spontaneous 4 To loud voice 3 To loud voice 3 To pain 2 To pain 2 Nil 1 Nil 1 Best Motor Response (M) Best Motor Response (M) Obeys 6 Obeys 6 Localizes 5 Localizes 5 Withdraws(flexion) 4 Withdraws(flexion) 4 Abnormal flexion posturing 3 Abnormal flexion posturing 3 Extension posturing 2 Extension posturing 2 Nil 1 Nil 1 Verbal response (V) Verbal response (V) Oriented 5 Oriented 5 Confused, disoriented 4 Words 4 Inappropriate words 3 Vocal sounds 3 Incomprehensible sounds 2 Cries 2 Nil 1 Nil 1 Hodeskader Headache and stiff neck

• Subarachnoid hemorrhage?

• Head injury with neck injury? Treatment

• In general, management of the comatose patient depends on the cause. • essential to maintain adequate cerebral oxygenation and to establish an intravenous line for volume control and prompt medication - e.g. iv glucose/insulin; antibiotic; high dose steroid; anticonvutsants. • evaluation - treatment difficult in unconscious patient • resource consuming • hospital as quickly as possible. • > patient transport, gather more info ~ hospital Treatment 1

• recovery position or supine with head elevated • mouth, pharynx sweep, suction if necc. • Establish +maintain airway - insert oral airway. • oxygen, assist ventilation if necessary • If unconscious or severely impaired consciousness (no cough reflex), intubate, then pass an orogastric or nasogastric tube. • If intubation is impossible,crico or tracheostomy. Treatment 2

• If consciousness is not so deeply impaired, a tracheal tube may be rejected by the patient • Assess for sources of external bleeding • Consider cervical spinal precautions, if indicated • turn patient if vomiting or choking • treat cardiac arrest, - AED ready • I.v. line - infusion sets Treatment 3

• check vital signs -presence of spontaneous respirations and pulse • Thorough assessment • Cause? • Persistent syncope - more serious condition? • Manage any life threatening conditions when identified • Reassess vital signs at regular intervals (5-15 min.) or when necessary Treatment 4

• Need for glucose, diazepam? • Initiate transport to nearest appropriate treatment facility, contact them giving an update on the patients status • Monitor and treat the patient en route • if patient recovers, rest before resuming activity • retake a medical history • evaluate need for further investigation before RTP • If shock - elevate the lower limbs, unless injury Before departure – gather info:

• Time of injury • Injury mechanism • LOC! How long? • Amnesia. How long? • Seizures? • Recent head injury? • Other illnesses • Medication? • Intox Transport

• Continuous methodical observation • Check pulse, B P, RR, Level of consciousness, pupils, sensory, motor function • Note changes, warn hospital • Driv fast but caefully • Cool and airy back in the ambulance 2 tips

• Urine stick i nose or ear – if glucose present ~ CSF ? Fracture? • awaken every hour at night Concussion in Sport

• International Conference on Concussion in Sport • Vienna - 2001 • Prague - 2004 • Zurich - 2008 Summary of Zurich

• Concussion - serious neurological injury - wide spectrum symptoms signs • Previous concussion assessment protocols out - varied, subjective and inconsistent • computerized neuropsychological testing - useful but limited • Serial neurological and cognitive clinical assessments cornerstone • Certain sporting groups - specialized and conservative approach; - 15 and under, History of recurrent concussion, Co-morbidity (epilepsy, depression, ADD etc.) • Education is still the key Simple Concussion

• Historically, different grading systems • Prague - categorized as simple or complex.

• Simple Concussion • injury that progressively resolves without complication over 7–10 days • limit play while symptomatic - no further intervention required • athlete typically resumes sport without further problem • neuropsychological screening – not needed though mental status should be checked • cornerstone of management is rest until all symptoms resolve • then graded increase in exertion before RTP • Obligatory pre-RTP control Complex Concussion

• athletes suffer persistent symptoms (including persistent symptom recurrence with exertion), specific sequelae (eg, concussive convulsions, prolonged LOC, or prolonged cognitive impairment following the injury. • includes athletes who suffer multiple concussions • May be need for neuropsychological testing and other investigations should be considered in complex concussions. It is envisaged that such athletes would be managed in a multidisciplinary manner by physicians with specific expertise in the management of concussive injury such as a sport medicine doctor with experience in concussion, sports neurologist or neurosurgeon. Early complications

• Intracranial space occupying lesions: - cerebral arteries and veins - epidural, subdural or intracerebral haematomas - signs of raised ICP looked for immediately and treated

• Dysautoregulation Syndrome: Diffuse cerebral swelling - rare – mostly children, teenagers. Second impact syndrome - American Football – death after relatively minor head injury. May occur if premature RTP .

• Impact convulsions: - Convulsions (seizures) not common, occur within seconds of impact - not necessarily associated with structural brain damage - often good outcome Fieldside diagnostics Fieldside

• Orientation • Concentration • Memory • Pupils • Strength- arms + legs • Balance Coordination • Sensory-touch, pain temp • Run 50 metres, 10 push ups, twist and turn • Not ebm Orientation Concentration

• Time • Numbers backwards • Place 789 – 987, • Own data • 4567, 7654 • situation • Months of year backwards • Days of week Memory Balance/coordination

• Memory • Balance/Coordination • name teams in earlier – straight line games • stand one leg • 3 words 3 objects • finger nose immediately • Romberg • and after 5 minutes • heel knee test • recent news • match status, name team players