JC27 (Surgery) - Raised ICP and hydrocephalus Flashcards

1
Q

Normal range of ICP for adults, children and infants

Pathological range for intracranial hypertension

A

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

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2
Q

Symptoms of raised ICP

A

• 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

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3
Q

Ddx of raised ICP **

A

 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

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4
Q

Signs of raised ICP

A
  • 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
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5
Q

Explain the Monro-Kellie-Burrows Doctrine on raised ICP

A

• 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

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6
Q

Compensatory mechanisms for increased brain parenchyma volume

A

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

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7
Q

Formula for cerebral perfusion pressure

A

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

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8
Q

Formula for cerebral blood flow

A

CBF = CPP/ CVR = (MAP – ICP)/ CVR
o CBF = Cerebral blood flow
o CPP = Cerebral perfusion pressure
o CVR = Cerebrovascular resistance

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9
Q

Describe changes in cerebral blood flow over cerebral perfusion pressure

A

Changes in CPP regulated by autoregulation of cerebrovascular resistance > maintain relatively constant level of cerebral blood flow

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10
Q

Describe effect of hypertension on cerebral blood flow

A

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

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11
Q

Pathophysiology of brain cell excitotoxicity from ischemia

A

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
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12
Q

Levels of decreasing cerebral blood flow and associated cellular changes

Define CBF threshold for ischemia and infarction

A

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

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13
Q

Define vasogenic and cytotoxic edema in brain parenchyma

A

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

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14
Q

List 5 types of brain herniation

A

Uncal transtentorial herniation

Cerebellar tonsillar (coning) herniation

Subfalcine (Cingulate) herniation

Central herniation

Transcalvarial/ fungus/ External herniation

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15
Q

Define uncal transtentorial herniation and associated s/s

A

 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)

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16
Q

Define cerebellar tonsillar herniation (coning) and asso. s/s

A

 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

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17
Q

Define subfalcine/ cingulate herniation and asso. S/S

A

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
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18
Q

Define central herniation and asso. s/s

A

 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

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19
Q

Define transcalvarial/external herniation

A

Brain squeezes through a fracture or surgical site in skull

20
Q

Components of Glasgow Coma Score

Use and indication

A

Initial GCS for prognosis
Trend for monitoring deterioration or improvement

Components:
Eye opening E1-4
Motor response M1-6
Verbal response V1-5

21
Q

Classification of brain injury severity with GCS

Cut-off for intubation

A

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

22
Q

ICP monitoring methods

Contraindications of ICP monitoring

A

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

23
Q

Limitations of GCS

A

Eye - swollen, trauma
Muscle - Spinal cord injury, limb injury, muscle relaxant
Verbal - Language barrier, intubation
Drugs - relaxants, sedatives

24
Q

Lumbar puncture can be used to monitor ICP. True or False?

A

False - Absolute contraindicated against raised ICP

LP can decompress ICP quickly and creating pressure gradient, causing coning of brainstem

25
Acute management of raised ICP
1. Resuscitation: - Airway intubation - Breathing: oxygenation, avoid hyperventilation - Circulation: BP control for CPP > 60 mmHg 2. Fluid: euvolemic and normo-osmolar 3. Sedation: decrease metabolic demand, ventilation asynchrony, venous congestion, sympathetic responses 4. Posture: - head elevation at 30o – 45o for carotid arterial flow and venous drainage - Avoid neck collar, excessive flexion or rotation of neck
26
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
27
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)
28
Explain rationale behind tight glucose control in raised ICP
Hypoglycaemia > seizure and brain injury Hyperglycaemia > lactic acidosis Seizure increase brain swelling and metabolic demand
29
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
30
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
31
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
32
Rational behind barbiturate coma for raised ICP Side effects
e.g. Pentobarbital Reduce cerebral metabolism >> ↓ demand for cerebral blood flow (CBF) >> ↓ ICP S/E: Hypotension ,Myocardial depression
33
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)
34
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
35
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 ```
36
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
37
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
38
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
39
List 4 congenital causes of hydrocephalus
Aqueductal stenosis Neural tube defect Congenital infection Congenital mass lesions
40
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
41
Clinical manifestation of raised ICP in adults
``` Broad spectrum of compressive symptoms: ICP symptoms Motor deficit Cognitive dysfunction LOC Incontinence ...etc ```
42
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
43
Sole indication of lumbar puncture in raised ICP?
Communicating hydrocephalus No blockage of CSF flow between ventricles and subarachnoid space
44
Treatment of hydrocephalus
1. ABC 2. LP (communicating hydrocephalus) or EVD (unstable) 3. CSF- shunting, endoscopic third ventriculostomy, treat underlying disease
45
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)
46
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