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 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.