Raised Intracranial Pressure

Report
RAISED INTRACRANIAL
PRESSURE
03/05/12
Jeremy Kam
Intern
Royal Melbourne Hospital
OVERVIEW AND OBJECTIVES
 Basic Principles
 Review Basic Anatomy of Skull and Spinal Cord
 Review Basic Physiology of CSF production and flow
 Monro Kellie Doctrine and concepts of CBF and CPP
 Conceptualising ICP
 Spectrum of Intracranial Pressure
 Causes of Raised ICP
 Assessment of Raised ICP
 Symptoms
 Signs and basic examination techniques
 Investigating ICP
 Management
 Monitoring
 Treatment
CONTENTS OF THE SKULL AND
THE MONRO KELLIE DOCTRINE
1 . Skull is a rigid box: The volume inside the cranium is a fixed
volume (nearly).
2. The cranial contents incompressible (nearly)
3. The cranium and its constituents (blood, CSF, and brain tissue)
create a state of volume equilibrium, such that any increase in
volume of one of the cranial constituents must be compensated by
a decrease in volume of another
FIXED BOX: SKULL/SPACE
1. BRAIN
2. CSF
3. BLOOD
INTRACRANIAL VOLUME
INTRACRANIAL PRESSURE
“Intracranial pressure (ICP) is the pressure
inside the skull and thus in the brain tissue and
cerebrospinal fluid (CSF).”
Constantly changing: exercise, coughing, straining,
respiratory cycle
ICP normal values
Age Group
Normal Range
(mmHg)
Adults and older
children
< 10-15
Young Children
3-7
Term Infants
1.5-6
Standing
0
INTRACRANIAL PRESSURE VS
INTRACRANIAL VOLUME
INTRACRANIAL PRESSURE VS
INTRACRANIAL VOLUME
CEREBRAL PERFUSION PRESSURE
CPP = MAP – ICP
CEREBRAL PERFUSION PRESSURE = MEAN ARTERIAL PRESSURE –
INTRACRANIAL PRESSURE
Why do we care?
1. Brain survival depends on cerebral blood flow meeting cerebral
metabolic requirements
2. Cerebral blood flow depends on Cerebral Perfusion Pressure
3. CPP depends upon ICP
Normal CPP > 50 mmHg
CEREBRAL BLOOD FLOW
INTRACRANIAL HYPERTENSION (FINALLY)
 What happens if ICP is too high?
CPP = MAP – ICP
 As ICP increases. Where MAP is constant. CPP will decrease.
 Ideally CPP > 70-80mmHg
 This is bad.
 IC-HTN = ICP >20mmHg for >10 minutes
 Increased ICP  Decreased CPP  Decreased CBF
 MAP will compensate for awhile.
CBF = CPP/CVR
INTRACRANIAL HYPERTENSION
 Why do we care?
 Raised ICP may CAUSE problems itself e.g herniation,
decrease in cerebral perfusion  ischemia  edema
 Raised ICP may be a SIGN of problems being caused e.g mass
ef fect; tumour, haemorrhage
CAUSES OF RAISED ICP
SPECTRUM OF RAISED ICP




ACUTE VS CHRONIC
SEVERE VS MILD
SYMPTOMS AND SIGNS from raised ICP
SYMPTOMS AND SIGNS from CAUSE of raised ICP
 E.g:
Acute Traumatic Intracranial Haemhorrhage  Mass Ef fect
Vs
Neoplasm causing Mass ef fect
CAUSES OF RAISED ICP
INTRACRANIAL HAEMHORRAGES
 Subdural
Hematoma
 Epidural
Hematoma
 Intracerebral
Haemorrhage
 Subarachnoid
Haemorrhage
 Cerebral
Contusion
SPACE OCCUPYING LESION
Brain Abscess:
 Develop as a result of a localized
bacterial cerebritis followed by
necrosis and encapsulation
 Mechanisms:
 – Haematogenous
 – Extension from neighbouring
structures
 – Penetrating injuries
 Symptoms of infection may be
absent in 50% of cases
 Treatment: Excision drainage
HYDROCEPHALUS
1 O b s t r uc t iv e hy d ro c eph a lus – o b s t r uc t io n
f r o m l e s i o n a l o n g v e n t r i c l e s y s te m . E . g t u m o r,
c o l l o id c y s t , p r i m a r y s te n o s i s .
2 C o m m un i c a t in g hy d ro c e p h a l us - ( a )
o b s t r uct i o n to f l o w o f C S F t h r o ug h t h e b a s a l
c i s te r n s o r ( b ) f a i l ur e o f a b s o r p t i o n o f C S F
t h r o ug h t h e a r a c h n o i d g r a n u l a t i o n s o v e r t h e
c e r e b r al h e m i s p h e r e s . T h e m o s t c o m m o n
c a u s e s o f c o m m un i ca t i n g hy d r o ce p h a l us a r e
i n f e c t i o n ( e s p e c i a l l y b a c te r ia l a n d
t u b e rc ul o us ) a n d s u b a r a c h n o id h a e m o r rh a g e
( e i t h e r s p o n t a n e o us , t r a um a t i c o r
p o s to p e r a t i v e ).
Tr e a t m e n t : Ve n t r i c ul o p e r ito n e a l S h u n t ,
3 r d Ve n t r i c ul o s to my
TRAUMATIC BRAIN INJURY
CEREBRAL OEDEMA
 Middle cerebral artery
occlusion causing
extensive infarction with
mass effect. The
appearances after
decompressive
craniotomy are shown in
the third panel.
SYMPTOMS AND SIGNS
1 . Decreased LEVEL OF CONSCIOUSNESS - DROWSINESS
 MOST IMPORTANT
 never put down to simple sleepiness – measure Glasgow Coma Scale
 Requires serial assessment  Progressive decrease in GCS = worsening ICP state
2. Altered MENTAL STATUS
 Confusion, restlessness, lethargy, difficulty thinking,
3. HEADACHE
 Frontal, worse after lying down, Relieved by vomiting, Severe, Worse with coughing
and straining
4. NAUSEA and VOMITING
 Persistent
5. VISUAL CHANGES




Pupillary Dysfunction
Changes in Vision
VI nerve Palsy – false localising sign
Papilloedema - requires more than 24 hours
GLASGOW COMA SCALE
ABDUCENS PALSY
PAPILLOEDEMA






Ve n o u s e n g o r g em e n t ( u s u a l l y t h e f i r s t s i g n s )
loss of venous pulsation
h e m o r rh a g e s o v e r a n d / o r a d j a c e n t to t h e o p t i c d i s c
b l u r r in g o f o p t i c m a r g i n s
e l ev a t i o n o f o p t i c d i s c
P a to n ' s l i n e s = r a d i a l r et i n a l l i n e s c a s c a d i n g f r o m t h e o p t i c d i s c
PROGRESSION OF SIGNS
Continuous
to a r o u s e
DECREASE in GCS
 s t u p o r o u s c o m a to s e  d i f f i c u l t y
VISUAL CHANGES
 P u p i l s b e c o m e u n i l a t e r a l l y e n l a r g e d p r o g r e s s i n g to fi x e d a n d d i l a te d – e v e n t u a l l y
b i l a te r a l l y fi x e d a n d d i l a te d
 Papilloedema
NEUROLOGICAL F UNCTION
 D e c o r t i c a t e o r D e c e r e b r a t e Po s t u r i n g
 L o s s o f c o r n e a l a n d g a g r e fl e x e s
 Hemiplegia –that progresses
VITAL SIGNS






B r a d yc a r d i a
I n c r e a s i n g H y p e r te n s i o n – w i t h w i d e n i n g p u l s e p r e s s u r e
I r r e g u l a r Re s p i r a t i o n – n e u r o g e n i c H y p e r v e n t i l a t i o n
Re s p i r a t o r y a r r e s t
C u s h i n g ' s Tr i a d
Hyperthermia
S I G N S O F B R A I N H E R N IAT I ON
CUSHING’S TRIAD
seen in 33% of IC-HTN
1. HYPERTENSION (Widening Pulse Pressure)
2. BRADYCARDIA
3. RESPIRATORY IRREGULARITY
INDICATES IMPENDING HERNIATION
BRAIN HERNIATION SYNDROMES
 Transtentorial:
 Foramen Magnum
 Subfalcine
SEVERIT Y AND INDICATIONS
Indications for Treatment:
ICP ≥ 20- 25 mmHg as the upper limit. Initiate Treatment for ICP > 20 mmHg –
in combination with clinical exam and brain CT findings.
Herniation can still occur at ICP < 20
Higher mortality and worse outcomes among patients with ICP persistently >20
compared to < 20.
CPP Targets:
Avoid CPP < 50mmHg
Initiate treatment when CPP falls below 60mmHg
INVESTIGATIONS
LUMBAR PUNCTURE IS
CONTRAINDICATED

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


CT Brain
MRI Brain
Biopsy
Angiography
Transcranial Doppler Flow Velocity
MANAGEMENT - MONITORING
Indications for ICP Monitoring:
 CT CRITERIA:
 For salvageable patients with severe traumatic brain injury – GCS ≤ 8 after
cardiopulmonary resuscitation
 Abnormal admitting brain CT (60% risk of IC -HTN)
or
 Normal brain CT but with ≥2 risk factors (=60% risk of IC –HTN vs 13% r.f -ve):
• Age >40 years
• SBP < 90 mmHg
• Decerebrate or decorticate posturing on motor exam – unilateral or bilateral
 Neurological criteria – where GCS ≥ 9 – low risk for IC -HTN – serial
neurological exam
 M ultiple system injur y – where ICP likely to be ef fected by inter ventions
e.g large volume IV fluids, PEEP
 Traumatic IC M ass – EDH, SDH, depressed skull fracture
 Post Op – may elect
 Non -traumatic
 Contraindications to ICP monitoring: “awake” patient, coagulopathy
INVASIVE ICP MONITORING
 Intraventricular Catheter – IVC
 Most accurate, allows therapeutic CSF drainage
 May be difficult to insert into compressed or displaced ventricles, may
obstruct
 Intraparenchymal monitor
 Subarachnoid Screw (bolt)
MANAGEMENT
1 . MAINTAIN CEREBRAL PERFUSION PRESSURE by LOWERING ICP
 Re duc e s i z e o f bra i n VOLUM E by de c re a sing c e re bra l vo lume , CSF fl ui d vo l ume,
o r bl o o d vo lume w h i l e m a in t aining c e re bra l pe r fus i on
 M a ke m o re S PACE – e . g s urg i c al de c o m pression
 G OAL ICP < 2 0 m m H g a n d CP P > 5 0 m m H g
2.DECREASE METABOLIC DEMANDS
3. PREVENT COMPLICATIONS
 GI risk of developing C ushing stress ulcers and GI bleeding. Give PPIs and H2 antag.
 F l u i d a n d e l e c t r o l y t e s – d i a b e t e s i n s p i d u s - d e s m o p r e s s i n . C l o s e m o n i to r i n g o f
electrolytes.
 H e m a to l o g i c a l – D I C c a n o c c u r a f te r s e v e r e h e a d i n j u r y. C o a g u l o p a t h i e s a g g r e s s i v e l y
t r e a te d F F P a n d V i t K 10 m g a d a i l y.
 Nutrition
4. IDENTIFY CAUSE – TREAT
 e . g re m ove s pa c e o c c upy i n g l e sions, i n ser t V P s h un t
BLOOD VOLUME
↓ ICP via ↑ Venous Outflow
Elevation of Head of Bed 30-45 degrees
 optimised trade of f between promoting Venous Outflow vs
Reducing MAP
Keep Neck Straight Midline ,
tape
av o i d t i g h t t r a c h
Maintain CPP with Normotension
Av o i d H y p ote n s i o n ( S B P < 9 0 m m H g ) A c h i eve d v i a
n o r m al i s i n g i n t r ava s c ula r v o l ume . U s e o f p r e s s o r s i f
needed.
C o n t r o l hy p e r te n s i o n i f p r e s e n t , N i t ro p r us s i d e i f n i l t a c hy
v s b et a b l o c ke r i f t a c hy
Hyper ventilation
M ay b e n e c e s s a r y f o r b r i e f p e r i o d s w h e n a c u te n e u r o l o g ic
d ete r i o r a t i o n . D o n o t u s e p r o p hy l ac t i c al l y. S h o r t te r m .
 Ve ntilate to N O R M O c a r bi a PaCO 2 = 3 5 -4 0 mmHg)
 Avoid H y p ox i a (PaO 2 < 6 0 mmHg or sat 9 0 %) – maintain air way and
oxyge nation ↓ O 2 = bad
BRAIN VOLUME
OSMOTIC AGENTS
 Mannitol - Ef fects occur within 20 minutes; does not cross intact blood brain barrier; obser ve for rebound ICP; 0.25-1 gm/k g IV over 24h
 Frusemide 10-20mg IV q6 hour s. PRN ICP > 20.
 Hyper tonic Saline - When refractor y to mannitol – 3% saline infusion or
bolus – if serum osmolarity greater than 320 – hold no more benefit
EUVOLEMIA
CORTICOSTEROIDS
 Decreases cerebral edema in brain tumor s
 Reduce CSF producti on, stabilize blood -brain barrier and cell membranes > overall improvement of neuronal function
 Dexamethasone
CSF VOLUME
Drain CSF
 Ventriculostomy – Pliable catheter inser ted into lateral ventricle on
nondominant side
 Can remove CSF intermittently or continuously
 Removal of even small amount will dramatically decrease ICP
 Shunts
DECREASING METABOLIC DEMAND
TEMPERATURE CONTROL
 Antipyretic medications, cooling blanket
SEIZURE CONTROL
 Phenytoin: 15-18 mg/kg; not to exceed 50 mg/min
 Diazepam: 5-10 mg bolus at 2 mg/min
 Barbiturates (Pentobarbital & thiopental) when not responsive to
conventional therapy
SEDATION
 Paralyzing agents; CV monitoring; endotracheal intubation; mechanical
ventilation; ICP monitoring; arterial pressure monitoring
 Reduce sympathetic tone
ENVIRONMENT
 dark room – free from noise minimise stimulus.
SURGICAL MANAGEMENT
Decompressive Craniectomy
 Considered for IC-HTN refractory to medical treatment.
Surgical Mx of subdural, epidural or intraparenchymal
hematoma.

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