1. Management of the acute Head Injury
Judith Fewings
Consultant Therapist Neurosurgery
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3. 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)
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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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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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6. 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)
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7. 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
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8. BRAIN ANATOMY Meninges = protective triple layer cover Dura mater =
outer layer
Arachnoid = middle layer
Pia mater = inner layer
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9. 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
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10. CSF FLOW
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11. 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
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12. 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)
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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
Classification can be made using three methods, all used inter-changeably. These are Type ie, Focal such as EDH, SDH,ICH, Diffuse such as DAI where there is Hypoxia and Ischaemia, mostly RTAs, Penetrating with Low /High Velocity, Mechanism How it occured, ie Blow to head, acceleration/ deceleration , Stabbing, pens and darts, gunshot wounds. Severity, Measured overall objectively by the patients Glasgow Coma Scale or GCS
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15. CT SCAN (NORMAL)
Normal CT
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16. Large frontal contusion with shift
CONTUSION /HAEMATOMA
Normal CT
Large frontal contusion with shift
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17. 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
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18. DIFFUSE BRAIN INJURY Mild concussion  Severe, ischemic insult
Normal CT
Diffuse Injury
6-13 Diffuse Brain Injury
Diffuse brain injury may range from a mild concussion to a severe, ischemic insult. On the Left a Normal scan showing reasonable Grey and White matter differentiation, with preserved ventricular spaces. Good Sulcal/Gyral patterns, usually seen in the top slices of CT.
On the right , a scan which looks diffuse in nature, as we would say TIGHT brain, no ventricular CSF, no fissures seen at the sides.
The instructor might query the students about symptoms of a concussion. Typically, these include a transient loss of consciousness and retrograde or antegrade amnesia. Nausea, vomiting, and headache symptoms may worsen before lessening. Sequellae are common.
The instructor may query the students about the cause of severe diffuse brain injury. This latter type of injury usually results from a combination of trauma and hypoxia, due to airway and breathing problems at the time of injury.
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19. SCAN INTERPRETATION NORMAL SCAN No fissures present
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
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20. ACUTE SUBDURAL HAEMATOMA
Normal CT
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21. 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
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22. Extradural Haematoma
In this CT we have what is known as a Bone window and a Brain window. By doing this we can see the Focal Injury that has occurred, on the bone window a fractured Left skull, with associated soft tissue swelling, as well as the underlying EDH, which is causing shift from Left to Right. The shape of the EDH is always like a lemon /convex appearance due to the bleeding occuring Extra or above the Dura. The dura is the top most lining of the brain , it is adherent to the inner skull. As the bleeding commences it gathers under the skull, but above the dura therefore causing this contained look.
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24. Discussion on EDH 16 year old with cricket ball NATASHA RICHARDSON
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25. CLASSIFICATION OF HEAD INJURY
SEVERITY
Based on Glasgow Coma Scale (GCS) -
MILD ( )
MODERATE ( 9-12)
SEVERE ( 3-8)
The third way to classify Head Injury is by a bedside Neuromotor objective measurement known as The Glasgow Coma Scale.
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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
Eyes= Out of 4, Where 4=Spont, Speech, Pain, None.
Verbal= Orientated, Confused, Words, Sounds, None.
Motor= Obeys, Localising to P.S, Flex to P.S, Abnormal flex to P.S, Extend to P.S, None
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27. Glasgow Coma Scale (GCS)
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
Verbal response
Oriented to person, place, and date = 5
Converses but is disoriented = 4
Says inappropriate words = 3
Says incomprehensible sounds = 2
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29. INTRA CRANIAL PRESSURE (ICP)
SKULL IS A FIXED BOX CONTAINING;
BLOOD = %
BRAIN = %
C.S.F = %
H.I = ANOTHER VOLUME ; OEDEMA, BLOOD
Normal ICP = 0-15 mmHg
Sustained increases cause problems
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30. Monro-Kellie Doctrine Mechanism of ICP
Venous
Volume
Art.
Vol.
Brain
CSF
Ven.
Vol.
Art.
Brain
CSF
Mass
6-5 Monro-Kellie Doctrine
Normally in the brain any change in one volume is accompanied by a reciprocal change in the others , therefore the pressure inside remains constant , The body uses a sequence of events to allow this , such as a change in Vol of Venous blood , and then squeezing the CSF into the Spinal Subarachnoid space , but eventually all these compensations are exhausted.( This is illustrated by slow growing Tumours etc)
Normal ICP= 0-15mmHg,
Sustained increases can cause problems
Arterial
Volume
Brain
CSF
75 mL
Mass
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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
i.e An increasing ICP can squeeze the soft brain tissue , (read off slide) , We monitor this via a thin probe.
ICP, Greater than 20mmHg= Neuro Dysfunction, Greater than 40mmHg = Seizures, Greater than 60 = Death
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32. ICP Monitoring
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33. Volume – Pressure Curve
60-
55-
50-
45-
40-
35-
30-
25-
20-
15-
10- 5-
Herniation
Point of
Decompensation
ICP
(mm Hg)
Volume-Pressure Curve
The volume of the mass can increase with the pressure remaining constant, but at point of decompensation , all accomodation is lost and then a relatively small increase in the mass leads to increased pressures in the rigid skull and reduced cerebral blood flow.
The line of compensation, point of decompensation, and point of herniation.
Compensation
Volume of Mass
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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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35. Brain Shifts / Herniation
This is a cut through the head top to bottom. Front off. We can see the midline Falx, and the tent cerebelli, A= Subfalcine herniation/ midline shift, B= Uncular, C=Transtentorial(Reticular Formation,resp centre involvement) , D= Brain swelling through a bone flap, E= Cerebellar Tonsillar Herniation(loss of upward gaze, c.n 3, D.I from pit stalk compression).
E.G Left EDH lead to swollen Left hemishere, the brain tissue shifts across the midline, under the falx, to the Right . Clinically, the pt may present with a decrease in their GCS from 13 to 11 ie have some lateralsing signs such as a Right Hemiparesis/weakness
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36. CEREBRAL HAEMODYNAMICS
NORMALLY, CEREBRAL BLOOD FLOW IS KEPT CONSTANT ( MAP )
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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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
Closely monitor the B.P via arterial lines which have additional gadgetery to allow us to see the MAP and it works out the CPP automatically.
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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
Brain is v. vulnerable to hypoxia and a combination of low circ o2 and high b.p can be fatal.
Can illustrate with the carbon dioxide effect on vessels;
3.5 =o, Not enough vol, therefore ischaemia and tissue death, more oedema.
=0, volume sufficient to maintain good perfusion but a delicate balance
6=O, =increased ICP, due to increased vol , so decreased perfusion of brain
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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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40. 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)
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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
NPO, rapid onset, Altered Hydrostatic pressures, change in osmosis, therefore Pul Oedema
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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 =
MONITOR
I.C.P MONITOR, CAPNOGRAPH ( ETCO2), BP ( MAP ), CPP.
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43. 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)
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44. EMERGENCY EVACUATION OF ACUTE SUBDURAL
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49. Bi-Frontal Bone Flap Deficit
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50. To allow patient to be intubated and ventilated,
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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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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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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53. PHYSIOTHERAPY ASSESSMENT
ABG’S (Blood Gases more accurate reflection of Oxygen in body than external finger probe)
PACO2 (carbon dioxide) KPA
PAO2 (oxygen) 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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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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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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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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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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58. 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//
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, 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): [Medline].
Bazarian JJ, McClung J, Shah MN, et al. Mild traumatic brain injury in the United States, Brain Inj. Feb 2005;19(2): [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
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59. 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:
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60. Questions?
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