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1 Management of the acute Head Injury Judith Fewings Consultant Therapist Neurosurgery
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OVERVIEW Traumatic brain injury (TBI) is a nondegenerative, noncongenital insult to the brain from an external mechanical force, with an associated diminished or altered state of consciousness. Traumatic Brain Injury has a dramatic impact on the health of the nation It accounts for 15-20% of deaths in people aged 5-35 yrs old in the UK (1) 3
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4 EPIDEMIOLOGY ACCOUNTS FOR 1% OF ALL ADULT DEATHS (1) 50% OF ALL RTA DEATHS 1.4 MILLION HEAD INJURIES/YEAR ATTEND THE E/D (2) 150,000 ADMITTED PER YEAR (3) OF THESE 3,500 ARE ADMITTED TO A NEUROSURGICAL UNIT (3)
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J.Fewings 17th Nov 2011 5 EPIDEMIOLOGY (CONT) 5,000 DIE IN BRITAIN EACH YEAR DUE TO HEAD INJURY SOME OF THESE DEATHS ARE INEVITABLE BUT OTHERS ARE POTENTIALLY PREVENTABLE IN ADDITION TO THE HIGH MORTALITY, APPROX 60% OF SURVIVORS HAVE SIGNIFICANT ONGOING DEFICITS ie PHYSICAL/COGNITIVE (4)
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INCIDENCE HIGH RISK POPULATIONS YOUNG PEOPLE LOW INCOME INDIVIDUALS UNMARRIED INDIVIDUALS ETHNIC MINORITY GROUPS INNER CITY RESIDENTS MEN INDIVIDUALS WITH HISTORY OF SUBSTANCE ABUSE INDIVIDUALS WITH A HISTORY OF PREVIOUS TBI (5,6,7) J.Fewings 17th Nov 2011 6
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BRAIN ANATOMY The meninges are protective coverings of the brain specifically. The meninges consist of three layers DURA MATER means “tough mother” , it’s the tough, leathery outer layer on the brain. It looks kind of silvery in person. ARACHNOID MATER looks spidery as the name would suggest due to the large number of blood vessels running through it. PIA MATER or “little mother” and is very thin and delicate adheres closely to the brains crevices called SULCI J.Fewings 17th Nov 2011 7
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BRAIN ANATOMY Meninges = protective triple layer cover Dura mater = outer layer Arachnoid = middle layer Pia mater = inner layer J.Fewings 17th Nov 2011 8
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CEREBROSPINAL FLUID OR CSF A CLEAR FLUID FILLING THE ENTIRE SUBARACHNOID SPACE LIQUID CUSHION AROUND THE BRAIN AND SPINAL CORD VALUABLE DIAGNOSTIC AID DEEP IN THE BRAIN IS AN INTERCONNECTING SERIES OF CHAMBERS CALLED THE VENTRICULAR SYSTEM CSF CONTINUOUSLY SECRETED AT 500ML PER DAY BY THE CHOROID PLEXUS AT THE HEART OF THE CHAMBERS J.Fewings 17th Nov 2011 9
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CSF FLOW J.Fewings 17th Nov 2011 10
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FUNCTIONS OF THE CSF To keep the brain tissue buoyant, acting as a cushion or "shock absorber“ To act as the vehicle for delivering nutrients to the brain and removing waste To flow between the cranium and spine and compensate for changes in intracranial blood volume J.Fewings 17th Nov 2011 11
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CLASSIFICATION OF HEAD INJURY THREE MAIN METHODS USED TO CLASSIFY HEAD INJURY. TYPE OF BRAIN INJURY THAT HAS OCCURED ( WHAT) MECHANISM OF THE INJURY (HOW) SEVERITY OF THE INJURY (OBJECTIVE MEASURE USING GLASGOW COMA SCALE (GCS) J.Fewings 17th Nov 2011 12
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J.Fewings 17th Nov 2011 13 CLASSIFICATION OF HEAD INJURY TYPE = FOCAL EDH/ASDH/ICH ; MECHANISM = DIRECT BLOW TO THE HEAD OR FALL TENDS TO BE LOCAL DAMAGE & SKULL FRACTURE E.g FALL, BASEBALL BAT TO HEAD TYPE= DIFFUSE DAI ; MECHANISM = ACCELERATION/DECELERATION FORCES SHEARING & CONTUSIONS E.g RTA’S TYPE= PENETRATING ; MECHANISM = LOW /HIGH VELOCITY LOCAL DAMAGE & ALONG TRACT E.g DART/GUN SHOT
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J.Fewings 17th Nov 2011 14
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CT SCAN (NORMAL) J.Fewings 17th Nov 2011 15 Normal CT
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CONTUSION /HAEMATOMA J.Fewings 17th Nov 2011 16 Normal CT Large frontal contusion with shift
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SCAN INTERPRETATION NORMAL SCAN Reasonable grey/white matter differentiation Preserved Ventricular spaces Good Sulci and Gyri pattern (seen on top slices of CT) FRONTAL CONTUSION OR BRAIN BRUISE Predominately Left sided Significant swelling Mass effect causing brain shift Blood = White Air = Black Frontal air sinus Right posterior contusion = contra-coup injury Skin swelling posteriorly Probably initial posterior injury J.Fewings 17th Nov 2011 17
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J.Fewings 17th Nov 2011 18 DIFFUSE BRAIN INJURY Mild concussion  Severe, ischemic insult ©ACS Normal CT
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SCAN INTERPRETATION NORMAL SCAN Reasonable grey/white matter differentiation Preserved Ventricular spaces Good Sulci and Gyri pattern (seen on top slices of CT) DIFFUSE AXONAL INJURY No fissures present No Ventricular CSF Looks swollen or TIGHT J.Fewings 17th Nov 2011 19
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ACUTE SUBDURAL HAEMATOMA J.Fewings 17th Nov 2011 20 Normal CT
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SCAN INTERPRETATION NORMAL SCAN Reasonable grey/white matter differentiation Preserved Ventricular spaces Good Sulci and Gyri pattern (seen on top slices of CT) Left Acute Sub Dural Haematoma Blood under the first dural layer (white) Falx Cerebri =Central dural fold this maintains two hemisperes Blood in this layer looks more widespread due to small gap between layers with serous fluid to prevent friction J.Fewings 17th Nov 2011 21
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J.Fewings 17th Nov 2011 22 Extradural Haematoma
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J.Fewings 17th Nov 2011 23
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Discussion on EDH 16 year old with cricket ball NATASHA RICHARDSON J.Fewings 17th Nov 2011 24
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J.Fewings 17th Nov 2011 25 CLASSIFICATION OF HEAD INJURY SEVERITY Based on Glasgow Coma Scale (GCS) - MILD ( 13 -15) MODERATE ( 9-12) SEVERE ( 3-8)
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J.Fewings 17th Nov 2011 26 CLASSIFICATION (CONT) HEAD INJURIES ARE ASSESSED USING THE GLASGOW COMA SCALE (GCS) GCS IS OUT OF 15 ( MINIMUM SCORE IS 3) SEVERE HEAD INJURY IS CLASSED AS A GCS OF LESS THAN 8
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Glasgow Coma Scale (GCS) J.Fewings 17th Nov 2011 27 Eye opening Spontaneous = 4 To speech = 3 To painful stimulation = 2 No response = 1 Motor response Follows commands = 6 Makes localizing movements to pain = 5 Makes withdrawal movements to pain = 4 Flexor (decorticate) posturing to pain = 3 Extensor (decerebrate) posturing to pain = 2 No response = 1 Verbal response Oriented to person, place, and date = 5 Converses but is disoriented = 4 Says inappropriate words = 3 Says incomprehensible sounds = 2 No response = 1
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J.Fewings 17th Nov 2011 28
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J.Fewings 17th Nov 2011 29 INTRA CRANIAL PRESSURE (ICP) SKULL IS A FIXED BOX CONTAINING; BLOOD = 5- 10 % BRAIN = 80-85 % C.S.F = 10-15 % H.I = ANOTHER VOLUME ; OEDEMA, BLOOD Normal ICP = 0-15 mmHg Sustained increases cause problems
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J.Fewings 17th Nov 2011 30 Monro-Kellie Doctrine Mechanism of ICP ©ACS
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J.Fewings 17th Nov 2011 31 Increased Volume – Pressure The consequences ICP can squeeze the soft brain tissue Preventing blood circulating to the brain tissue Damage can then occur to brain cells Excessive ICP can cause permanent damage ICP is monitored via a thin probe inserted into a lateral ventricle of the brain Normal ICP is usually less than 15mmHg
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ICP Monitoring J.Fewings 17th Nov 2011 32
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J.Fewings 17th Nov 2011 33 Volume – Pressure Curve ©ACS Volume of Mass 60- 55- 50- 45- 40- 35- 30- 25- 20- 15- 10- 5- ICP (mm Hg)
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J.Fewings 17th Nov 2011 34 Brain Shifts / Herniation If the pressure continues to build the brain gets SHIFTED Ultimately to herniate( be pushed down through) the foramen magnum (junction between the skull and the spinal cord at the base of the skull) Brain stem then is squashed and death occurs
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J.Fewings 17th Nov 2011 35 Brain Shifts / Herniation
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J.Fewings 17th Nov 2011 36 CEREBRAL HAEMODYNAMICS NORMALLY, CEREBRAL BLOOD FLOW IS KEPT CONSTANT ( MAP 50 -150) ACHIEVED BY ALTERING ARTERIAL VASCULAR RESISTANCE (size of the vessel diameter) THIS IS KNOWN AS AUTOREGULATION Following H.I AUTOREG’N IS LOST CEREBRAL BLOOD FLOW DEPENDS ON ARTERIAL BLOOD PRESSURE.
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J.Fewings 17th Nov 2011 37 CEREBRAL HAEMODYNAMICS (CONT) FLOW IS MAINTAINED BY ENSURING THAT THE CEREBRAL PERFUSION PRESSURE (CPP) >70mmHg. CPP(70) = MAP(90) – ICP(20) INADEQUATE FLOW LEADS TO- REGIONAL HYPOXIC AREAS BLOOD/BRAIN BARRIER BREAKDOWN TOXIN PRODUCTION /FURTHER OEDEMA INCREASE IN I.C.P
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J.Fewings 17th Nov 2011 38 OXYGEN AND CARBON DIOXIDE BRAIN ONLY METABOLISES AEROBICALLY USES 1/6 OF OUR CARDIAC OUTPUT 20% OF OUR OXYGEN CONSUMPTION CARBON DIOXIDE HAS MOST POTENT EFFECT ON CEREBRAL VESSELS An increase of CO2 CAUSES VASODILATION 1KPA CO2 RISE = 20% INCREASE IN CBF (Cerebral Blood Flow ) INCREASE IN C.B.F = INCREASE IN I.C.P
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J.Fewings 17th Nov 2011 39 SEVERE HEAD INJURY – INITIAL MANAGEMENT ‘AIMED AT PREVENTING SECONDARY BRAIN INJURY’ Oxygen needs to get to the brain cells AVOID- HYPOXIA , (Lack of oxygen) HYPERCARBIA, (Too much carbon dioxide) HYPOTENSION, (Low blood pressure) ANAEMIA, (Not enough red blood cells, for O2 to adhere to) HYPONATRAEMIA, (Low sodium/salt ) PYREXIA, (Temperatures) SEIZURES, (Fits)
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WHY DO HEAD INJURED PATIENTS DEVELOP CHEST PROBLEMS DECREASE IN CONSCIOUS LEVEL POOR AIRWAY PROTECTION MECHANICAL OBSTRUCTION TONGUE, VOMIT, TEETH FACIAL FRACTURES BRAINSTEM DAMAGE ALTERED RESPIRATORY PATTERN COUGH /SWALLOW SUPPRESSION ASSOCIATED TRAUMA C-SPINE INSTABILITY / CORD INJURY FRACTURES / RIBS, LONG BONES DROWSINESS REDUCED TIDAL(TOTAL LUNG) VOLUME / ATELECTASIS (SMALL AIRWAY COLLAPSE) NON -COMPLIANCE POSITIONING 30% HEAD UP (AIDS VENOUS RETURN (OF CIRCULATION FROM HEAD, so helps with keeping intracranial pressure down) J.Fewings 17th Nov 2011 40
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J.Fewings 17th Nov 2011 41 WHY DO HEAD INJURED PATIIENTS DEVELOP CHEST PROBLEMS ALTERED MOOD AGGRESSIVE / NONCOMPLIANT HYPERTONICITY STIFF CHEST WALL & ABDOMINALS HYPOVENTILATION NEUROGENIC PULMONARY OEDEMA LUNG ALVEOLAR OEDEMA – POOR GASEOUS DIFFUSION / OXYGEN EXCHANGE. ?HYPOTHALAMIC MEDIATED CHANGES TO PULMONARY VASCULAR RESISTANCE. RAPID ONSET - DECREASE IN SAO2 NOT ALLEVIATED WITH FIO2
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J.Fewings 17th Nov 2011 42 MEDICAL MANAGEMENT AIMED AT MINIMISING SECONDARY DAMAGE; CEREBRAL HYPOXIA (lack of oxygen to brain), CEREBRAL OEDEMA (swelling), RAISED ICP (Intracranial Pressure ), INFECTION MAINTAIN AIRWAY VENTILATE HYPERVENTILATE - PACO2 = 4.0 - 4.5 MONITOR I.C.P MONITOR, CAPNOGRAPH ( ETCO2), BP ( MAP ), CPP.
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MEDICAL MANAGEMENT ASSESS HOURLY NEURO OBS (so GCS , pupils, etc) CONTROL FITTING ANTI-EPILEPTICS MAINTAIN Cerebral Perfusion Pressure ABOVE 70MMHG DECREASE METABOLIC DEMANDS CONTROL PYREXIA (temperature) 1 DEGREE RISE IN TEMP INCREASES O2 DEMAND BY 5% PROMOTE VENOUS DRAINAGE HEAD UP 30 MIDLINE HEAD POSITION C.S.F DRAINAGE EXTERNAL VENTRICULAR DRAIN (EVD),(ALLOWS DRAINAGE OF BRAIN FLUID TEMPORARILY) DECOMPRESS FOCAL CLOTS BONE FLAP REMOVAL( FROM SKULL TO PROVIDE SPACE FOR BRAIN TO SWELL, WILL BE REPLACED EVENTUALLY WHEN MEDICALLY STABLE) J.Fewings 17th Nov 2011 43
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EMERGENCY EVACUATION OF ACUTE SUBDURAL J.Fewings 17th Nov 2011 44
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J.Fewings 17th Nov 2011 45
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J.Fewings 17th Nov 2011 47
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Bi-Frontal Bone Flap Deficit J.Fewings 17th Nov 2011 49
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J.Fewings 17th Nov 2011 50 MEDICAL MANAGEMENT DRUGS To allow patient to be intubated and ventilated, SEDATIVES - Midazolam, Propofol, Alfentanyl. PARALYTICS – Atracurium To aid reduction in brain swelling, DIURETICS – Mannitol, Frusemide
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J.Fewings 17th Nov 2011 51 PHYSIOTHERAPY ASSESSMENT ESTABLISH BASELINE PARAMETERS VENTILATION HYPERVENTILATED? (TO DECREASE C02, AND SO CEREBRAL VESSEL SIZE, THEREFORE INCREASING SPACE IN SKULL) HUMIDIFICATION To aid secretion removal from lungs Blood Pressure BP DIRECTLY AFFECTS Cerebral Perfusion Pressure , MONITOR VIA ARTERIAL LINE (MEAN ARTERIAL PRESSURE or MAP)
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J.Fewings 17th Nov 2011 52 PHYSIOTHERAPY ASSESSMENT G.C.S / NEUROMOTOR STATUS IF PT PARALYSED/SEDATED, PUPIL SIZE/REACTION IS ONLY INDICATOR OF NEURO STATUS WEANING (from sedation ) – OBSERVE RANGE AND QUALITY OF MOVEMENTS. ASSESS FOR TONAL PROBS CXR ASPIRATION ,COMMON DUE TO LOSS OF AIRWAY PROTECTION (LOW GCS) AT TIME OF INJURY. RIB FRACTURES / LUNG CONTUSIONS PULMONARY OEDEMA MAY BE NEUROGENIC IN ORIGIN
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J.Fewings 17th Nov 2011 53 PHYSIOTHERAPY ASSESSMENT ABG’S (Blood Gases more accurate reflection of Oxygen in body than external finger probe) PACO2 (carbon dioxide) 4.0 - 4.5 KPA PAO2 (oxygen)12 -14 KPA INFUSIONS SEDATION -IS IT ADEQUATE? DOES PT NEED A BOLUS FOR TREATMENT POSITIONING BP / ICP LABILITY, VENOUS OBSTRUCTION (NECK POSITION), C-SPINE STABILITY, BONE-FLAP DEFICITS TONE ISSUES (CONSIDER SPLINTING TO MAINTAIN MUSCLE LENGTH AND RANGE OF MOVEMENT)
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J.Fewings 17th Nov 2011 54 PHYSIOTHERAPY TREATMENT USUALLY INDICATED MAINTAIN GOOD OXYGENATION TO BRAIN TO AID PREVENTION OF INFECTION / DECREASE METABOLIC DEMAND TO ENSURE GOOD POSITIOING IN ACUTE PHASE ULTIMATELY AFFECTS FUNCTIONAL ABILITIES IN REHAB SHORT, FREQUENT RX INITIALLY
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J.Fewings 17th Nov 2011 55 PHYSIOTHERAPY TREATMENT ADAPT TREATMENT TECHNIQUES FOR CHEST CARE AS REQUIRED, PERCUSSION SLOW , ONE HANDED SHAKING/ VIBRATIONS CARE TAKEN TO ALLOW INTRA THORACIC PRESSURE TO NORMALISE DURING RX INCREASE IN INTRATHORACIC PRESSURE PREVENTS VENOUS RETURN INCREASE IN I.C.P
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J.Fewings 17th Nov 2011 56 PHYSIOTHERAPY TREATMENT SUCTION PROFOUND EFFECT ON I.C.P MAX DURATION 10 SECS INTERRUPTS VENTILATION / NEED TO PREOXYGENATE STIMULATES COUGH - INCREASES I.C.P NEED BOLUS OF SEDN? POSITIONING CAN DECREASE I.C.P BONE FLAP DEFICIT / NO PROLONGED SIDE LIE NO HEAD DOWN MONITOR TONE AND RANGE OF MOVEMENT OUT OF BED AND COMMENCE REHABILITION AS SOON AS PRACTICABLE Tone management, passive mvts, Baclofen, Bo-tox, splints
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J.Fewings 17th Nov 2011 57 PHYSIOTHERAPY TREATMENT COMMUNICATION EXPLAIN ALL TREATMENT TO PATIENT GENTLE TOUCH AND VOICE MINIMAL DISTRACTION (RADIO, LOUD CONVERSATION ,BIN LIDS ETC) MEET AND EXPLAIN TREATMENTS / REHAB PROCESS WITH RELATIVES (TIMELY AND APPROPRIATE INFO SHARING) TEAM WORK LIASE WITH M.D.T, INVOLVE OTHER THERAPIES AS REQUIRED ( OT, SALT, NEUROPSYCHOLOGY) Notification to rehab unit as soon as practicable Botulinum toxin injections / splinting / seating
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References Jennett B, MacMillan R. Epidemiology of head injury. Br Med J 1981; 282: 101–445 Kassell NF, Hitchon PW, Gerk MK, Sokoll MD, Hill TR. Hospital Episode Statistics. Available from http//www.hesonline.nhs.uk Hyam JA, Welch CA, Harrison DA, Menon DK. Case mix, outcomes and comparison of risk prediction models for admissions to adult, general and specialist critical care units for head injury: a secondary analysis of the ICNARC Case Mix Programme Database. Crit Care 2006; 10: 1–11 Dikmen SS, Machamer JE, Powell JM, Temkin NR. Outcome 3 to 5 years after moderate to severe traumatic brain injury. Arch Physical Med Rehab 2003; 84: 1449–57 Tieves KS, Yang H, Layde PM. The epidemiology of traumatic brain injury in Wisconsin, 2001. WMJ. Feb 2005;104(2):22-5, 54. [Medline]. Kraus JF, Black MA, Hessol N, et al. The incidence of acute brain injury and serious impairment in a defined population. Am J Epidemiol. Feb 1984;119(2):186-201. [Medline]. Bazarian JJ, McClung J, Shah MN, et al. Mild traumatic brain injury in the United States, 1998--2000. Brain Inj. Feb 2005;19(2):85-91. [Medline]. Lindsay K, Bone I, Callander R “ Neurology and Neurosurgery Illustrated” Second Edition, Churchhill Livingston . Whitfield P, Thomas E, Summers F, Whyte M, Hutchinson P “ HEAD INJURY , A Multidisciplinary Approach” Cambridge University Press 2009 J.Fewings 17th Nov 2011 58
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References Additional Hodgkinson DW, Berry E, Yates DW. Mild head injury—a positive approach to management. Eur J Emerg Med 1994; 1:9–12 Helmy A, Vizcaychipi M , Gupta A K - Traumatic brain injury: intensive care management , British Journal of Anaesthesia 99 (1): 32–42 (2007) Yates P J , , Williams W H, Harris, A Round A Jenkins R An epidemiological study of head injuries in a UK population attending an emergency department, J Neurol Neurosurg Psychiatry 2006;77:699-701 J.Fewings 17th Nov 2011 59
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Questions? 60 J.Fewings 17th Nov 2011