JC27 (Surgery) - Raised ICP and hydrocephalus Flashcards
Normal range of ICP for adults, children and infants
Pathological range for intracranial hypertension
Normal range of ICP
• Adults = 10 – 15 mmHg (≤ 15 mmHg)
• Young children: 3 – 7 mmHg
• Infants: 1.5 – 6 mmHg
Intracranial hypertension: ≥ 20 mmHg
Measured via ventricular or lumbar puncture
Symptoms of raised ICP
• Vomiting
• Headache
o Usually early morning headache
o Mediated via the pain fibers of CN V in the dural and blood vessels
• Blurring of vision
o often unilateral and brief (seconds) that clear completely
o spontaneously with postural changes
o Chronic papilledema can lead to progressive visual field loss in the form of peripheral field contraction and even blindness
• ↓ Consciousness
o Mass effect, compression on midbrain reticular formation
Ddx of raised ICP **
Intracranial mass lesions - Brain tumour, hematoma, abscess
Cerebral edema
• Cerebral infarction
• Acute hypoxic ischemic encephalopathy
• Traumatic brain injury
Hydrocephalus
Obstruction of venous outflow
• Venous sinus thrombosis
• Jugular vein compression
• Neck surgery
Seizure
Idiopathic intracranial hypertension
Signs of raised ICP
- Cushing’s triad = Hypertension + Bradycardia + Irregular respiration (late feature)
- Cushing ulcer ( gastro-duodenal ulcer produced by elevated intracranial pressure, causing excess vagal stimulation and gastric acid secretion)
- Papilloedema (late feature)
o Compression of optic nerve and central retinal vein - CN III, IV, VI palsy
o Binocular horizontal diplopia resulting from unilateral or bilateral lateral rectus palsy - Spontaneous periorbital bruising
Explain the Monro-Kellie-Burrows Doctrine on raised ICP
• Brain parenchyma = 80% + CSF = 10% + Blood = 10%
o ICP = function of the volume and compliance of each component
o Pressure-volume relationship that keeps the dynamic equilibrium inside rigid skull
o Decrease in one component should be compensated by increase in the other
Compensatory mechanisms for increased brain parenchyma volume
Compensatory mechanisms allow volume to increase with minimal elevation in ICP
o Displacement of CSF into thecal sac
o ↓ Volume of cerebral venous blood by venoconstriction and extracranial drainage
Formula for cerebral perfusion pressure
CPP = MAP – ICP (if ICP > JVP)
(OR) CPP = MAP – JVP (if JVP > ICP)
o CPP = Cerebral perfusion pressure
o MAP = Mean arterial pressure (MAP)
o ICP = Intracranial pressure
o JVP = Jugular venous pressure
As the ICP increases, the CPP drops. CPP is the force that pushes blood through the cerebral vasculature. Intracranial pathology that increases the ICP reduces blood flow to the brain tissue, and thus, a sympathetically driven compensatory rise in MAP is initiated to increase the CPP
Formula for cerebral blood flow
CBF = CPP/ CVR = (MAP – ICP)/ CVR
o CBF = Cerebral blood flow
o CPP = Cerebral perfusion pressure
o CVR = Cerebrovascular resistance
Describe changes in cerebral blood flow over cerebral perfusion pressure
Changes in CPP regulated by autoregulation of cerebrovascular resistance > maintain relatively constant level of cerebral blood flow
Describe effect of hypertension on cerebral blood flow
Chronic hypertension > high BP > arterial vasoconstriction in brain to prevent damage to distal brain vessels > maintain perfusion
Acute reduction of BP > chronic arterial vasoconstriction fail to react > ischemic symptoms
Pathophysiology of brain cell excitotoxicity from ischemia
Brain cells:
- Obligative aerobic respiration, glucose-dependent
- Decreased cerebral blood flow cause anaerobic respiration and lactic acidosis
- Lactate cannot be recycled
- Decrease ATP formation > Failure of Na-K-ATPase pump > loss ionic gradient
- Deregulated depolarization of presynaptic neurons from Ca influx
- Excessive release of glutamate > excitotoxicity
Levels of decreasing cerebral blood flow and associated cellular changes
Define CBF threshold for ischemia and infarction
CBF:
35-50: decrease protein synthesis
25-35: Anaerobic metabolism, glutamate release
18-25: Lactic acidosis
12-18* Ischemic threshold: Electrolyte deregulation, intracellular edema
<10-12** Infarction threshold: Calcium accumulation, anoxic depolarization, cell death
Define vasogenic and cytotoxic edema in brain parenchyma
Vasogenic: Injury to cerebral blood vessels > extravasation of fluid and serum proteins by BBB disruption
Cytotoxic: injury to astrocytes cause intracellular swelling by disruption of intracellular ionic balance
List 5 types of brain herniation
Uncal transtentorial herniation
Cerebellar tonsillar (coning) herniation
Subfalcine (Cingulate) herniation
Central herniation
Transcalvarial/ fungus/ External herniation
Define uncal transtentorial herniation and associated s/s
Medial part of temporal lobe (uncus) is squeezed to move towards the tentorium cerebelli
Vertical displacement of diencephalon and midbrain
* Ipsilateral pupillary dilatation (CNIII compressed against skull base)**
* Unconsciousness (Midbrain reticular formation compressed)**
* Contralateral hemiplegia (Corticospinal tracts in ipsilateral hemisphere disrupted) or ipsilateral hemiplegia (if contralateral cerebral peduncle is compressed)
* Hemianopia or Cortical Blindness (one or both side posterior cerebral arteries compressed against tentorium)
Define cerebellar tonsillar herniation (coning) and asso. s/s
Space-occupying lesion in cerebellum
Cerebellar tonsils move downwards through foramen magnum
Brainstem and upper cervical spinal cord compression
* Impaired consciousness
* Cardiorespiratory arrest
* Nystagmus
* Midbrain compression = midsized and unreactive pupils; pontine hemorrhage gives pinpoint and unreactive pupils; supratentorial lesion with tentorial herniation occurred first = unequal pupils
Define subfalcine/ cingulate herniation and asso. S/S
Most common herniation, causes midline shift
Innermost part of frontal lobe** is squeezed under part of the falx cerebri**
Displace and insert pressure on the cingulate gyrus
Affects the corpus callosum beneath the falx cerebelli
S/S:
- compress the ipsilateral anterior cerebral artery»infarction of the paramedian cortex»contralateral lower limb weakness
- dominant hemisphere and contralateral arcuate fasciculus involved»conductive aphasia, receptive/sensory aphasia, or expressive/motor aphasia
- Papilloedema
Define central herniation and asso. s/s
Diencephalon and parts of temporal lobes of both cerebral hemispheres squeezed through a notch in tentorium cerebelli
Compression on diencephalon, midbrain, pons and medulla oblongata
S/S:
- Bilateral damage to midbrain: Mid-sized fixed pupils, Decerebrate posture
- Brainstem damage: Loss of all brainstem reflexes, Cheyne- Stokes respiration to apnea, disappearing decrebrate posture, brain dead
Define transcalvarial/external herniation
Brain squeezes through a fracture or surgical site in skull
Components of Glasgow Coma Score
Use and indication
Initial GCS for prognosis
Trend for monitoring deterioration or improvement
Components:
Eye opening E1-4
Motor response M1-6
Verbal response V1-5
Classification of brain injury severity with GCS
Cut-off for intubation
Mild: LOC <30 mins
GCS 13-15
Moderate: LOC >30 min, <24 hours
GCS 9-12
Severe: LOC >24hours
GCS <8
GCS=<8 require intubation
ICP monitoring methods
Contraindications of ICP monitoring
External ventricular drain (EVD) gold standard for ICP
(catheter inserted into lateral ventricles through skull)
Continuous BP monitoring
C/O: Awake, conscious patient, Bleeding tendency
Limitations of GCS
Eye - swollen, trauma
Muscle - Spinal cord injury, limb injury, muscle relaxant
Verbal - Language barrier, intubation
Drugs - relaxants, sedatives
Lumbar puncture can be used to monitor ICP. True or False?
False - Absolute contraindicated against raised ICP
LP can decompress ICP quickly and creating pressure gradient, causing coning of brainstem
Acute management of raised ICP
- Resuscitation:
- Airway intubation
- Breathing: oxygenation, avoid hyperventilation
- Circulation: BP control for CPP > 60 mmHg - Fluid: euvolemic and normo-osmolar
- Sedation: decrease metabolic demand, ventilation asynchrony, venous congestion, sympathetic responses
- Posture:
- head elevation at 30o – 45o for carotid arterial flow and venous drainage
- Avoid neck collar, excessive flexion or rotation of neck
Target blood pressure control for raised ICP?
Keep relatively hypertensive***
o Large shift in BP should be avoided especially hypotension
o Hypotension with hypoxemia induce reactive vasodilation and elevation in ICP *****
o Hypertension should only be treated when CPP > 120 mmHg or ICP > 20 mmHg
Explain rationale behind tight ventilation rate control in raised ICP
Hyperventilation > decrease pCO2 > increase vasoconstriction > massive increase in cerebral vascular resistance > decrease cerebral blood flow > hypoperfusion, ishaemia
o ↑ Vasoconstriction = ↓ ICP = ↑ CPP = ↑ CBF (desirable)
o ↑↑ Vasoconstriction (excessive) = ↑ CVR = ↓ CBF (undesirable)
Explain rationale behind tight glucose control in raised ICP
Hypoglycaemia > seizure and brain injury
Hyperglycaemia > lactic acidosis
Seizure increase brain swelling and metabolic demand
List 7 treatments for raised ICP
Osmotherapy: mannitol, frusemide
Corticosteroid: only for raised ICP from CNS infection or tumors
Barbituates
Anti-epileptic drugs: seizure control
Mechanical ventilation
Hypothermia therapy
Decompressive craniectomy, craniotomy, EVD
Rationale behind osmotherapy for raised ICP
Contraindications (4)
Osmotic diuretics reduce brain volume by drawing free water out of the tissue into the circulation to be excreted in kidneys
C/O:
- renal failure > acute tubular necrosis
- Shock:hypovolemia, CHF
- hypernatremia, osmolarity > 320 mmol/L
- Hemorrhagic trauma
Rationale behind corticosteroid use for raised ICP
Indication and contraindications
Anti-inflammatory
Indication: Vasogenic edema e.g. peri-tumor edema, CNS infections
C/O: Traumatic brain injury, cerebral infarction or hemorrhage, stroke
Rational behind barbiturate coma for raised ICP
Side effects
e.g. Pentobarbital
Reduce cerebral metabolism»_space; ↓ demand for cerebral blood flow (CBF)»_space; ↓ ICP
S/E: Hypotension ,Myocardial depression
Rational behind Anti-epileptic drugs for raised ICP
Indication and Contraindication
Seizure can both complicate and increase metabolic demand, ICP
Indication: Suspected seizures and prophylaxis for supra-tentorial lesions
C/O: infratentorial lesions (cerebellum)
Rational behind therapeutic hypothermia for raised ICP
Indication and Contraindication and side effects
Cool to 32-34 degrees
Neuroprotection by decrease metabolic rate
Indication: Post-cardiac-arrest brain injury
C/O: stroke, trauma
S/E: High risk of infection (e.g. pneumonia), coagulopathy
Rational behind craniectomy for raised ICP
Indications, complications
- Removes rigid bony skull to increase potential volume of intracranial contents
- Improves brain tissue oxygenation
Indication: Massive infarction, post-traumatic brain injury brain swelling
Complications o Herniation through skull defect o Spinal fluid leakage o Wound infection o Epidural and subdural hematoma
Define and classify 2 types of hydrocephalus
excessive amount of CSF accumulates within cerebral ventricles or subarachnoid spaces which are dilated
Obstructive (non-communicating) hydrocephalus
• Obstruction in CSF circulation leading to accumulation of CSF in cerebral ventricles
Communicating hydrocephalus
• Impaired absorption of CSF leading to accumulation of CSF in cerebral ventricles
Route of CSF drainage through brainstem
Choroid plexus in lateral ventricles
> Foramen of Monro to Third ventricle
> Aqueduct of Sylvius to Fourth ventricle
> 2 lateral foramen of Luschka and 1 central Foramen of Magendie to subarachnoid space
> arachnoidal vili reabsorption
> Superior sagittal sinus
Mechanisms of hydrocephalus (3)
- ↑ CSF production - Choroid plexus papilloma
- ↓ CSF absorption - Bacterial meningitis (leads to arachnoid granulation adhesions)
- Obstruction of CSF flow - Aqueductal stenosis, Tumour
List 4 congenital causes of hydrocephalus
Aqueductal stenosis
Neural tube defect
Congenital infection
Congenital mass lesions
Clinical manifestation of raised ICP in infants
Head deformity (infants)
• Macrocephaly
o Widely split sutures
o Full or distended anterior fontanelle
- Frontal bossing
- Dilated and prominent scalp veins
Clinical manifestation of raised ICP in adults
Broad spectrum of compressive symptoms: ICP symptoms Motor deficit Cognitive dysfunction LOC Incontinence ...etc
Normal pressure hydrocephalus:
- classic clinical triad
- Diagnosis
NPH = ICP normal despite large ventricles
Normal pressure hydrocephalus can occur in people of any age, but it is most common in the elderly. It may result from:
- subarachnoid hemorrhage
- Head trauma
- Infection
- Tumor
- Complications of surgery
Typical clinical presentation:
- Gait disturbance, Cognitive decline, Urinary incontinence
Imaging studies: CT brain, MRI CSF studies
Sole indication of lumbar puncture in raised ICP?
Communicating hydrocephalus
No blockage of CSF flow between ventricles and subarachnoid space
Treatment of hydrocephalus
- ABC
- LP (communicating hydrocephalus) or EVD (unstable)
- CSF- shunting, endoscopic third ventriculostomy, treat underlying disease
Types of CSF shunts and complications
Types of shunting
o Ventriculo-peritoneal (VP) shunt
o Ventriculo-atrial (VA) shunt
Complications:
o Ventriculitis due to shunt infection
o Mechanical failure due to obstruction/ dislodgement of ventricular catheter
o Overdrainage, herniation
o Nephritis (VA), Bowel perforation and peritonitis (VP)
Rationale behind third ventriculostomy for hydrocephalus
Indication
- Perforation is made to connect 3rd ventricle to subarachnoid space, bypass obstruction e.g. Pineal tumor
- Indicated in obstructive hydrocephalus but NOT communicating hydrocephalus
