Neuro ICU

Question 1

Acute obstructive hydrocephalus

Answer 1

Interstitial edema since CSF is forced by hydrostatic pressure to move from the ventricular spaces to the interstitium of the parenchyma

Question 2

Vasogenic edema

Answer 2

extracellular accumulation of fluid that is usually associated loss of BBB, leading to leaky blood vessels usually seen around neoplasms

spared grey white, looks like fingers

Question 3

Cytotoxic edema

Answer 3

intracellular accumulation of fluid, due to failure of Na/K ATPase pumps leading intracellular edema. Most commonly seen with cytotoxic edema.

Loss of grey white differentiation vs spared in vasogenic edema

Question 4

Hypothermic protocol

Answer 4

Primarily used for initial rhythm is V fib, however can be used for PEA or aystole. Target temp of 32-34 C x 12-24 hrs

complications- coaugulopathy, arrhythmias, electrolyte abn, infections

Question 5

Uncal herniation

Answer 5

ipsilateral CN III, parasympathetic compression resulting in mydriasis leading to a fixed dilated pupil.

Contralateral hemiparesis from contralateral hemiparesis. Potential infarction of PCA in tentorial notch.

Question 6

Intraventricular catheter indications?

Answer 6

The need for ventricular CSF drainage, hemorrhage, SAH w/hydrocephalus.

It can measure ICP

Question 7

Parenchymal devices

Answer 7

inserted into the brain parenchyma and provde pressure measurements, does not allow CSF drainage and inaccurate pressure gradients with ICP readings

Question 8

Subarachnoid bolts

Answer 8

placed through a burr hole and in communication w/ the subarachanoid space. Does not allow for CSF drainage, not as accurate as intraventricular cath, but safer.

Question 9

ICP management

Answer 9

Bed elevation >30 degrees, normothermia (avoid fever), normoglycemia,normotensive

Question 10

Reducing ICP

Answer 10

Hyperventilation (lasts 10-20hrs) target reduction of pCO2 by 10mmHg or target of 30mmHg), use of osmotic agents/hypertonic solution (Na 150 goal) (constantly check serum osmolarity)

Others can be used such as corticosteroids in select cases, CSF drainage, decompression, barb coma, neuromuscular blocker, hypothermia

Question 11

Why would put someone in pentobarb coma?

Answer 11

reducing cerebral metabolic activity and blood flow. Better than propofol d/t side effects of HLD, propofol infusion syndrome.

Question 12

Stupor

Answer 12

reduced consciousness. aroused only with strong and continuous stimulation, with impaired cognitive function upon arousal.

Question 13

Coma

Answer 13

State of unresponsiveness in which cannot be aroused even with vigorous stimulation. Does not localize noxious stimuli.

Question 14

Unresponsive wakefulness “vegetative state”

Answer 14

Return of sleep-wake cycles in an unresponive patient usually previously comatose, w/lack of cognitive neurologic function; no awareness of themeslves or the environment, no purposeful or voluntary behavioral responses

Question 15

Malignant cerebral edema

Answer 15

complete MCA infractions, 50% of MCA territory on CT, younger age; plan for early hemicraniectomy <48 hours from sx onset

Question 16

Nitroprusside

Answer 16

vasodilator, avoid in ICP and renal failure. Metabolites are nitric oxide and cyanide. Infusion can lead to toxicity –> Rx w/thiosulfate

Question 17

SAH vasospasm

Answer 17

acute hydrocephelus 2/2 obstruction of cerebral aqueduct. Peak occurence 6-8 days. Sxs worsening headache, AMS/coma

Question 18

ICP waveforms

Answer 18

lundberg A waves or “plateau waves” are pathalogic and associated high risk of cerebral ischemia. Duration 5-20 mins and high amplititude

B waves are normal with duration of 1-2 mins

C waves no pathologic consequence

Question 19

GBS

Answer 19

always check NIF/VC, close cardiac and ventilatory monitoring

Question 20

Hunt and Hess scale

Answer 20

1. asymptomatic or minimal HA and slight nuchal rigid
2. moderate-severe HA, nuchal rigid, CN palsy
3. drowsiness, confusion, focal neuro deficit
4. Stupor, hemiparesis, possible decerebrate
5. Deep coma, decerebrate, moribund appearance

Question 21

Fisher grading

Answer 21

1. No SAH on CT
2. diffuse or thin vertical layer blood
3. localized clot and layer of blood
4. Intracerebral or intraventricular clots w/diffuse or no SAH

Question 22

Triple H therapy for SAH

Answer 22

hypervolemia, HTN, hemodilution

Question 23

Apneustic breathing

Answer 23

pontine lesions along with pin-point pupils and decerebrate posturing
Described as respiratory pause at full inspiration alternating with end-expiratory pause.

Question 24

Ataxic breathing

Answer 24

medullary lesions of the rhythm generator. irregular respiratory pattern (gasping pattern)

Question 25

Cheynes stokes respiration

Answer 25

forbrain lesion, severe cardiopulm disease

periodic breathing in which hyperpnea alternates with apnea and the depth of breath increases and decreases gradually.

Question 26

Non traumatic SAH follow up?

Answer 26

4 vessel angio

Question 27

Intracranial hemorrhage managment

Answer 27

endotracheal intubation
blood pressure control, SBP <140
correction of coaugs, evd, surgical decompression

Question 28

Dibigatran reversal

Answer 28

which is a direct thrombin inhibitor, reversed with idarucizumab

Question 29

Indications for intubation for GBS

Answer 29

severe oropharyngeal weakness, vital capacity less than 15-20 ml/kg or less than 1 L or reduction of 30% from baselie. Maximal expiratory pressure of less than 40 cm H20. Hypoxemia Po2 of <70 on room air

Question 30

Critical illness polyneuropathy and myopathy

Answer 30

neuromuscular disorder. Prolonged ICU stay. Reduction in CMAPs and SNAPs, with normal conduction velocities. Shows fibrillation potentials and postive sharp waves

Question 31

Brain death criteria

Answer 31

irreversible cessation of function of the brain

1. absent brainstem reflexes
2. apnea
3. absence of intoxication, neuromuscular blockage, sedation, normal body temp, SBP >90

Question 32

Decorticate rigidity

Answer 32

hemispheric dysfunction or lesion above red nuclei resulting in disinhibition of the red nuclei, with facilitation of the rubrospinal tracts (enhance flexor acvtivity)

Question 33

Decerebrate posture

Answer 33

lesions below superior colliculi/red nucleus but avoe vestibular nuclei.

below the vestibular nucleus associated with flaccid limbs