Raised ICP and hydrocephalus Flashcards

1
Q

Brain contents are ____-_____ml

Tissue ___-___ml

Intracellular fluid ___-_____ml

Extracellular fluid ___-___ml

A

Brain contents are 1300-1750ml

Tissue 300-400ml

Intracellular fluid 900-1000ml

Extracellular fluid 100-150ml

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2
Q

Inside the cranium the brain makes up 1300-1750ml (__-__%)

Blood makes up 100-150ml (_-_%)

CSF makes up ___-___ml (8-12%)

A

Inside the cranium the brain makes up 1300-1750ml (80-85%)

Blood makes up 100-150ml (5-8%)

CSF makes up 100-150ml (8-12%)

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3
Q

What is intracranial pressure when at rest?

A

7-15mmHg

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4
Q

What are the immediate compensatory mechanism for expanding masses in the cranium?

A
  • Decrease in CSF volume by moving it out of FM
  • Decrease in blood volume by squeezing sinuses
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5
Q

What are the delayed compensatory mechanisms for expanding masses in the cranium?

A

Decrease in extracellular fluid

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6
Q

CSF is secreted from the ____ _____ -> ________ _____ -> __________ ______ (______ and ____) -> _____ _____ (________ _________)

A

CSF is secreted from the choroid plexus -> ventricular system -> subarachnoid space (magendie and luschka) -> venous system (arachnoid granulations)

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7
Q

About ____ml of CSF is secreted in 24hr

Any obstruction to this flow will cause?

A

About 500ml of CSF is secreted in 24hr

Any obstruction to this flow will cause increased intracranial pressure and hydrocephalus

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8
Q

MAP- ___= CPP

What is CPP?

A

MAP- ___= CPP

CPP is cerebral blood flow NOT ICP- intracranial pressure

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9
Q

Cerebral blood flow = cerebral ———- ——–

​cerebral ——- ———-

A

Cerebral blood flow = cerebral perfusion pressure

​cerebral vascular resistance

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10
Q

Over a wide range of BP (__-_____mmHg) CBF remains constant

A

Over a wide range of BP (50-150mmHg) CBF remains constant

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11
Q

What is pressure autoregulation?

A

Regulation of CBF by dilation or constriction of arterioles in response to changes in BP or ICP

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12
Q

What is metabolic autoregulation?

A

Regulation of CBF whereby arterioles dilate in response to chemicals e.g. lactic acid and CO2

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13
Q

How does autoregulation occur?

A

Unknown

  • myogenic theory- reaction of smooth muscle to stretch
  • humoral theory- metabolic by-products
  • neurogenic theory- perivascular nerves
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14
Q

What are the three classes of causes of increased ICP?

A

Mechanism

  1. Mass effect (tumour, infarct, contusions, haematoma, abscess -> distort surrounding brain
  2. Brain swelling (ischaemia/anoxia, acute liver failure, encephalopathy, IIH, hypercarbia) -> increase CPP but minimal tissue shift.
  3. Increase in central venous pressure (venous sinus thrombosis, heart failure, obstruction of jugular veins)
  4. Problems with CSF flow
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15
Q

What are the causes of problems with CSF flow?

A

Obstruction- obstructive hydrocephalus

masses, chiari syndrome

Increased production

choroid plexus papilloma

Decreased absorption

  • SAH
    • meningitis*
    • malignant meningeal disease*
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16
Q

What is normal ICP in;

Adults

Newborn

Young Children

Older children

A

What is normal ICP in;

Adults: 7-15mmHg

Newborn: 1.5-5 mmHg (often <0)

Young Children: 3-6 mmHg

Older children: 10-15mmHg

17
Q

What are the early signs of raised ICP

A
  • ↓ level of consciousness
  • headache
  • Pupillary dysfunction +/- papilloedema
  • changes in vision
  • Nausea and vomiting
18
Q

What are the late signs of raised ICP

A
  • Coma
  • Fixed, dilated pupils
  • Hemiplegia
  • Bradycardia→ Cushing’s triad
  • Hyperthermia
  • ↑ urinary output
19
Q

What are the goals of therapy for patients with raised ICP?

A

Maintain CPP

Prevent ischaemia and brain compression

20
Q

What does management for raised ICP include?

A
  • Maintain head in midline to facilitate blood flow
  • Loosen tube ties, collars etc
  • HoB 30-45 degrees elevation
  • Avoid gagging, coughing etc
  • Decrease environmental stimuli
  • Treat hyperthermia
  • Maintain fluid balance and normal electrolytes
  • Maintain normocarbia
21
Q

What is the medical management of raised ICP?

A
  • Use diuretics (mannitol, hypertonic saline, furosemide, urea)
  • barbiturate coma
  • antiepileptics
  • surgical decompressoin
  • other surgical treatment
    • remove mass lesions
    • CSF diversion
22
Q

What are the different classifications of hydrocephalus?

A

Communicating vs non-communicating

Congenital vs acquired

23
Q

Describe communicating hydrocephalus

A

Enlargement of 3rd and 4th ventricels

  • sulcal effacement, temporal horns, rounded 3rd and enlarged 4th
24
Q

Describe obstructive hydrocephalus

A

Aqueductal stenosis

Enlarged frontal horns, temporal tip dilatation, rounded 3rd but small or normal 4th

25
Q

What is hakim’s triad?

A

Abnormal gait, urinary incontinence, dementia

26
Q

What is the aetiology of normal pressure hydrocephalus?

A

Possibly decreasing brain elastance

27
Q

What are the investigations for normal pressure hydrocephalus?

A

LP

lumbar drain test

lumbar infusion studies

28
Q

What is the treatment for low pressure hydrocephalus

A

VP shunt

Medium or low pressure valve

29
Q

What are the signs and symptoms of hydrocephalus in women of reproductive age?

A
  • Headache
  • Double vision
  • Visual blurring
  • tinnitus
  • radicular pain
  • Papilloedema→ 25% severe/permanent visual loss
30
Q

What is the aetiology of hydrocephalus in women of child-bearing age?

A

CSF imbalance

hormonal- oestrogen

Venous pressure- transverse/sigmoid sinus stenosis

31
Q

What investigations should be carried out in hydrocephalus of childbearing age

A

–LP

–CT/MR head

–CTV

–Fundoscopy+/- ophthalmology review

32
Q

What is the treatment for hydrocephalus in women of childbearing age?

A
  • Weight loss, possibly bariatric surgery
  • Carboanhydrase inhibitors (Acetazolamide, Topiramate)
  • Diuretics
  • CSF diversion
    • LP- or VP-shunt
  • Interventional radiology
    • Intracranial venous sinus plasty
    • Intracranial venous sinus stenting
  • ONSF : optic nerve sheath fenestration