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ICU > Neurology in ICU > Flashcards

Neurology in ICU Flashcards

1
Q

How to assess the GCS of a patient?

A

check, observe, stimulate, rate

eye opening E1-4

  • spontaneous
  • to sound (introduce and ask)
  • to pressure (peripheral stimulus and applied for 10sec with increasing intensity)
  • none

verbal V1-5

  • ask their name/mth/place (orientated)
  • confused
  • words
  • sounds
  • none
motor response M1 -6 
grasp and release fingers or stick out tongue 
- obeys commands 
- central stimulus at trapezius pinch first for 10sec or supraorbital notch
- localising
- normal flexion 
- abnormal flexion 
- extension 
- none 
better side response
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2
Q

What are some causes of SAH? What are some statistics about causation?

A 
Aneurysmal 
Types: 
- saccular (berry) 
- fusiform 
- lateral
Non aneurysmal e.g. traumatic

1:50 have aneurysms 3:2 female to male

15% die before hospital
3-5% of all stroke

most common is ACA 40% then MCA 34% and PCA 20%

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3
Q

What are the grades of SAH?

A

Grade 1 - GCS 15 motor deficit absent
Grade 2 13-14absent motor deficit
Grade 3 13-14 present motor deficit
Grade 4 GCS 7-12 with present or absent motor deficit
Grade 5 GCS 3-6 with present or absent motor deficit

Can also scale based on CT findings
1- no blood
2 - thin layer of subarachnoid blood (<1mm)
3 - localised clot or thick layer of Subarachnoid blood
4 - intracerebral or intraventicular blood with diffuse or no subarachnoid blood

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4
Q

What is the initial Prevention strategies post SAH?

A

Prevent secondary injury

  • unprotected airway - hypoxemia and hypercapnoea (worsening cerebral oedema)
  • inadequate cerebral perfusion (increase ICP due to obstruction hydrocephalus or hypotension (meds)
  • seizure (increased cerebral demand)
Airway protection 
Ventilation 
Cerebral perfusion (CPP = MAP-ICP) 
Seek/treat obstructive hydrocephalus (EVD) 
Terminate seizure early 
Prevent hypoglycemia 
Prevent hyperthermia
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5
Q

How do we prevent Re-bleeds?

A
  • securing aneurysm - coiling and clipping (DSA if proximal and small, neurosurg if distal or large)
  • preventing HTN (aim SBP <140) with analgesia, sedation, anti-hypertensive
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6
Q

What is the pathophysiology to delayed cerebral ischaemia?

A

4-14 days - early vasospasm independent poor prognostic sign

  • oxygenated Hb contacts intraluminal wall of vessel causing breakdown
  • calcium dependent/independent pathways
  • imbalance in vasoactive agents (endothelin, arachadonic acid)
  • neuronal mechanisms leading to increased vascular tone
  • free radicals
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7
Q

What is therapy for vasospasm prevention?

A

Enteral nimodipine

  • reduces risk of delayed ischaemia
  • 60mg q4hrly

Triple H therapy

  • HTN - MAP >150 but under 200
  • CVP 8-12mmHg - maintenance fluids
  • Haemodilation - decrease viscosity

Intravascular vasodilator DSA for 3-5days

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8
Q

What is an EVD? How does it work to measure ICP?

A

external ventricular drain - small catheter placed into the anterior horn of ventricles of the brain
- 25mls/hr by choroid plexus in lateral ventricles

ECD measures pressures via a transducer that is like invasive arterial or CVP monitor
CSF draining helps reduce ICP

  • EVD height set by neurosurgeons.
  • TBH 5+, SAH 10-15cm. ICP must exceed 15mmHG for any drainage of CSF.

Usually raised to a certain height (15cm above the tragus) when ICP is above the pressure CSF will drain

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9
Q

What is part of routine EVD screening?

A

CSF sampling 3x a week to check for ventriculitis

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10
Q

What are some complictions of an EVD?

A

mechanical

  • misplacement
  • rebleeding
  • occlusion

Infection (up to 28%)

  • ventriculitis
  • meningitis
  • cerebritis
  • abscess
  • subdural empyema

Human

  • overdrainage
  • inadvertant clamping
  • incorrect height
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11
Q

Discuss some brain physiology and how it related to pressures.

A

Skull is rigid - Monroe Kellie doctrine. 130mls CSF, 150mls blood, 1400mls brain tissue. Increase in any compartment will increase pressure.

  • increased oedema
  • increased CSF (obstruction)
  • increased blood volume (vasodilation secondary to hypercapnoea)
  • extrinsic mass or lesion (SDH, EDH, ICH, tumour)

to maintain ICP there is a reduction in volume in other compartments - reduced compliance
CPP = MAP - ICP

normal ICP = 3-15

CPP <50 may cause ischaemia, CPP >150 leads to hyperaemia.

Factors that affect flow:

  • carbon dioxide - pCO2 rises vasodilation occurs
  • nervous system - autonomic controls MAP
  • metabolic - energy metabolites cause vasodilation locally
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12
Q

The EVD has stopped draining at the bedside, describe how you would manage the patient?

A

1) go to the bedside
2) exclude equipment error looking for kink/damage/leak/dislodgement
3) ensure reference level at the tragus and the height hasn’t changed
4) lower the level briefly to observe for drainage
5) contact neurosurg

A blocked EVD may lead to increased ICP. Inform the neurosurg reg and never attempt to flush.

Common blockage reasons:

  • clots or debris
  • accidental clamp
  • dislodgement
  • CSF leak or rising pressure
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13
Q

A patient with seizures has raised ICP post SAH with an EVD drain in, what is your initial management?

A

1) check equipment (right height at tragus/no kinks)

2) improve cerebral venous drainage by
(head at 30 degrees, midline and using an ETT fastener that doesn’t go around the neck)

3) Reduce cerebral demands (treat seizure, treat hyperthermia, ensure adequate analgesia, consider muscle relaxant)
4) Ensure adequate supply by (avoid hypocapnoea, avoid hypoglycemia, cerebral perfusion pressure >60, treat anaemia, avoid hypoxaemia)
5) Reduce ICP (treat surgical cause (haematoma), drain CSF, maintain normocapnoea as hypercapnoea will cause cerebral vasodilation, increase osmolality (hypertonic saline aiming for Na+ of 150-155)

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14
Q

What are some interventions for raised ICP?

A

1) Sedation/analgesia
- reduce aggitation/metabolic demand
- propofol
- thipentone for refractory ICP

2) Hypertonic saline - increasingly used over mannitol - better co-efficient across the BBB - hyponatremia worsens brain oedema.
Mannitol works 1-5mins after IV admin with peak at 40mins. Will cause plasma expansion however its permeable and may worsen vasogenic oedema

3) Mass removal
4) CSF drainage
5) Decompressive craniectomy

Minimal evidence
Hypothermia - not supported
Steroids - if there is a brain tumour (IV dexamethasone)

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15
Q

A patient 7 days post neurosurg spikes a temperature and is more drowsy than usual - what is your ddx? how would you assess her?

A

Initial management
1) Treat if WCC high, high protein and combined high cell index (ratio of CSF leuk/erythrocyte to blood leuk/erythrocyte >5)

2) Full septic screen
3) Check CSF appearance
4) Inform neurosurg reg ?removal of EVD

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ICU (7 decks)

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