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Neuro Critical Care > 330 Neuro CritCare, HIE, SAH > Flashcards

330 Neuro CritCare, HIE, SAH Flashcards

1
Q

2 Principal types of edema or swelling of brain tissue

A
  1. Vasogenic edema

2. Cytotoxic edema

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2
Q

Influx of fluid and solutes into the brain through an incompetent blood brain barrier

A

Vasogenic edema

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3
Q

Results from cellular swelling, membrane breakdown and ultimately cell death

A

Cytotoxic edema

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4
Q

Pathway of irreversible cell death due to inadequate delivery of substrates (oxygen, glucose) to sustain cellular function

A

Ischemic cascade

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5
Q

The Ischemic Cascade process as seen in ischemic stroke, global cerebral ischemia, traumatic brain injury

A
  1. Release of excitatory amino acids (glutamate)
  2. Influx of calcium and sodium ions disrupting cellular homeostasis
  3. Activate proteases and lipases
  4. Lipid peroxidation and free radical-mediated cell membrane injury
  5. Cytotoxic edema
  6. Necrotic cell death and tissue infarction
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6
Q

Areas of ischemic brain tissue that have not yet undergone irreversible infarction and are potentially salvageable if ischemia can be reversed

A

Penumbra

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7
Q

Factors that exacerbate ischemic brain injury causing events known as secondary brain insults

A
  1. Hypotension and hypoxia = further reduce substrate delivery to vulnerable brain tissue
  2. Fever, seizures, hyperglycemia = increase cellular metabolism, outstripping compensatory process
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8
Q

Cell death that occurs without cerebral edema and therefore often not seen on brain imaging

A

Apoptotic cell death

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9
Q

Provides the driving force for circulation across the capillary beds of the brain

A

Cerebral perfusion pressure (CPP)

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10
Q

Defined as MAP minus ICP

A

Cerebral perfusion pressure (CPP)

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11
Q

Physiologic response whereby cerebral blood flow (CBF) is regulated via alterations in cerebrovascular resistance in order to maintain perfusion over physiologic changes such as neuronal activation or changes in hemodynamic function

A

Autoregulation

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12
Q

Factors that strongly influences CBF

A
  1. pH (acidosis)
  2. PaCO2 (hypercapnia)

Acidosis and hypercapnia increases CBF while the opposite causes decrease.

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13
Q

T or F: Hyperventilation can lower ICP?

A

True.

Mediated thru decrease in both CBF and intracranial blood volume

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14
Q

CSF pathway

A
  1. Produced (principally) in choroid plexus of each lateral ventricle
  2. Exits the brain via foramens of Luschka and Magendie
  3. Flows over the cortex to be absorbed into the venous system along the superior sagittal sinus
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15
Q

Approximate amount of CSF

A

150 mL

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16
Q

Cerebral blood volume

A

150 mL

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17
Q

Vicious cycle seen in traumatic brain injury, massive intracerebral hemorrhage, large hemispheric infarcts with significant tissue shifts

A
  1. Obstruction of CSF outflow, edema of cerebral tissue, or increase in volume of tumor or hematoma INCREASES ICP
  2. DIMINISHED cerebral perfusion
  3. Tissue ischemia
  4. Vasodilation via autoregulatory mechanisms to restore cerebral perfusion
  5. INCREASE cerebral blood volume INCREASES ICP, LOWERS CPP, provokes further ischemia
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18
Q

EEG findings in metabolic encephalopathy

A

Generalized slowing

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19
Q

Screening that should be performed in patients with encephalopathy of unknown cause

A

Serum or urine toxicology screens

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20
Q

When is it preferable to perform neuroimaging study prior to lumbar puncture?

A

Patients with coma or profound encephalopathy

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21
Q

Conditions where ICP monitoring should be considered

A
  1. Primary neurologic disorders (Stroke, traumatic brain injury)
  2. Severe traumatic brain injury (GCS = 8)
  3. Large tissue shifts from supratentorial ischemic or hemorrhagic stroke
  4. Hydrocephalus from SAH, intraventricular hemorrhage or posterior fossa stroke
  5. Fulminant hepatic failure
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22
Q

What levels should ICP and CPP be maintained?

A

ICP : <20mmHg
CPP : >/= 60mmHg

See Table 330-2 for the stepwise approach to treatment of elevated ICP.
p. 1780

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23
Q

Condition occurs from lack of delivery of oxygen to the brain because of extreme hypotension (hypoxia-ischemia) or hypoxia due to respiratory failure

A

Hypoxic-Ischemic Encephalopathy (HIE)

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24
Q

Causes of HIE

A
  1. Myocardial infarction
  2. Cardiac arrest
  3. Shock
  4. Asphyxiation
  5. Paralysis of respiration
  6. Carbon monoxide or Cyanide poisoning
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25
Q

Another term for HIE caused by carbon monoxide/cyanide poisoning

A

Histotoxic hypoxia

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26
Q

In hypoxia-ischemia, consciousness is lost within seconds.

Time when circulation is restored affects recovery.
How long will it be for full recovery to occur?

A

Ideally:
WITHIN 3-5 mins = full recovery may occur

BEYOND 3-5 mins = some degree of permanent cerebral damage usually results

In extreme cases:
8-10 mins of global cerebral ischemia may still make relatively full recovery

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27
Q

Factor that gives better prognosis for HIE patients

A

Better prognosis = patients with INTACT BRAINSTEM FUNCTION

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28
Q

Part of the brain frequently affected in HIE that explains why selective persistent memory deficits may occur after brief cardiac arrest

A

Hippocampus

Hippocampal CA1 neurons are vulnerable to even brief episodes of hypoxia-ischemia

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29
Q

A specific form of HIE that occurs at the distal territories between the major cerebral arteries and can cause cognitive deficits, including visual agnosia, and weakness that is greater in proximal than in distal muscle groups

A

Watershed infarcts

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30
Q

Basis for diagnosis of HIE

A

Based on history

Usually necessary:
BP <70mmHg systolic
PaO2 <40mmHg

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31
Q

Cause of HIE confirmed by measuring carboxyhemoglobin and suggested by cherry red color of venous blood and skin

A

Carbon monoxide intoxication

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32
Q

Treatment goal for HIE

A

Restoration of normal cardiorespiratory function

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33
Q

Based on International Liason Committee on Resuscitation: “Unconscious adult patients with spontaneous circulation after out-of-hospital cardiac arrest should be cooled to 32-24 deg C for 12-24 h when initial rhythm was Vfib.”

Advantage and disadvantage of hypothermia as part of treatment for HIE.

A

Advantage:
Targets neuronal cell injury cascade and has neuroprotective properties in experimental models

Disadvantage:
Coagulopathy
Increased risk of infection

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34
Q

Treatment for severe carbon monoxide intoxication

A
  1. Hyperbaric oxygen

2. Anticonvulsants (not given prophylactically)

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35
Q

Anticonvulsants for treatment of posthypoxic myoclonus

A
  1. Oral Clonazepam 1.5-10mg daily

2. Valproate 300-1200mg daily in divided doses

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36
Q

T or F:
Myoclonic status epilepticus within 24h after primary circulatory arrest indicates very poor prognosis even if seizures are controlled?

A

True

37
Q

Part of the brain that may be affected in carbon monoxide and cyanide intoxication responsible for a parkinsonian syndrome of akinesia and rigidity without tremor

A

Basal ganglia

38
Q

A confusional state characterized by disordered perception, frequent hallucinations, delusions, and sleep disturbance

A

Delirium

39
Q

T or F:

Presence of delirium is associated with worsened outcome in critically ill patients?

A

True

40
Q

A centrally acting alpha 2 agonist that reduce delirium and shorten duration of mechanical ventilation compared to benzodiazepines

A

Dexmedetomidine

41
Q

Triad of Wernicke’s Disease

A
  1. Global confusion
  2. Impairment of eye movements (ophthalmoplegia)
  3. Gait ataxia

Only 1/3 of patients presents with these

42
Q

Type of encephalopathy wherein systemic response to infectious agents leads to release of circulating inflammatory mediators that contribute to encephalopathy

A

Sepsis-Associated Encephalopathy

Cytokines: TNF, IL-1, IL-2, IL-6

43
Q

Diagnosis of Sepsis-associated encephalopathy

A

Clinical but requires exclusion of structural, metabolic, toxic and infectious causes.

44
Q

Reflexes associated with sepsis-associated encephalopathy

A
  1. Hyperreflexia

2. Frontal release signs (Grasp or snout reflex)

45
Q

Prognosis after treatment of sepsis-associated encephalopathy

A

Treatment of underlying critical illness almost always results in substantial improvement but long term dysfunction similar to dementia can be present

Severe disability or minimally conscious states are uncommon

46
Q

Disorder that presents as quadriplegia and pseudobulbar palsy

A

Central Pontine Myelinosis

47
Q

Predisposing factors for Central Pontine Myelinosis

A
  1. Severe underlying medical illness or nutritional deficiency
  2. Rapid correction of hyponatremia or with hyperosmolar states
48
Q

Pathology of Central Pontine Myelinosis

A

Demyelination without inflammation in the base of pons, with relative sparing of axons and nerve cells

49
Q

Modality useful in diagnosis of Central Pontine Myelinosis

A

MRI

Shows symmetric area of abnormal high signal intensity within the basis pontis

50
Q

Therapeutic guidelines for restoration of severe hyponatremia

A

= 10mmol/L (10meq/L) within 24 hours

AND

20mmol/L (20meq/L) within 48 hours

51
Q

Common and preventable disorder due to deficiency of thiamine occuring mostly in alcoholics

A

Wernicke’s disease

52
Q

Which in the symptoms of Wernicke’s disease improves FIRST after thiamine administration?

A

Ocular palsy (within hours)

53
Q

An amnestic state with impairment in recent memory and learning frequently persistent as symptoms of Wenicke’s disease recede

A

Korsakoff’s psychosis

54
Q

T or F:

Wernicke’s disease is a medical emergency

A

True

55
Q

Treatment of Wernicke’s Disease

A

Thiamine 100mg IV or IM stat then DAILY until patient resumes normal diet to be given PRIOR to IV glucose solution

56
Q

When is intubation considered in patients with peripheral nervous system (PNS) involvement?

A

Maximal inspiratory force falls to

57
Q

General principles of respiratory evaluation in patients with PNS involvement

A
  1. Assessment of pulmonary mechanics [Maximal Inspiratory Force(MIF) and vital capacity (VC)
  2. Evaluation of strength of bulbar muscles
58
Q

Most common PNS complication related to critical illness

A

Critical illness polyneuropathy

59
Q

Electrophysiology of critical illness polyneuropathy

A

Diffuse, symmetric, distal axonal sensorimotor neuropathy; axonal degeneration

60
Q

Decreases the risk of critical illness polyneuropathy

A

Aggressive glycemic control with insulin infusion

61
Q

Treatment of critical illness polyneuropathy

A

Supportive.

Treat the underlying illness.

62
Q

Recovery period in critical illness polyneuropathy

A

Weeks to months

Needs long-term ventilatory support and care even after underlying critical illness has resolved

63
Q

Early signs of foodborne botulism

A

Diplopia

Dysphagia

64
Q

Treatment for botulism

A

Supportive.

Antitoxin early in course may limit duration of neuromuscular blockade

65
Q

Overall term describing several different discrete muscle disorders (muscle weakness and wasting) that may occur in critically ill patients

A

Critical illness myopathy

66
Q

An asthmatic patient required high-dose glucocorticoids and nondepolarizing neuromuscular blocking agents (pancuronium, veruconium, rocuronium, cisatracurium) to facilitate mechanical ventilation. What type of myopathy can occur?

A

Thick-filament myopathy

Good prognosis.
Takes weeks or months for recovery.
Prevention: Avoid nd neuromuscular blocking agents

67
Q

Most common cause of SAH

A

Rupture of saccular aneurysm

Excluding head trauma

68
Q

Rate of rebleeding if patient survives the aneurysm

A

First 2 weeks : 20%
First month : 30%
Per year afterward: 3%

69
Q

Annual risk of rupture for aneurysms <10 mm and >/=10mm in size

A

<10mm : 0.1%

>/= 10mm: 0.5-1%

70
Q

3 most common locations of anuerysms

A
  1. Terminal internal carotid artery
  2. Middle cerebral artery bifurcation
  3. Top of the basilar artery
71
Q

Aneurysms from infected emboli due to bacterial endocarditis usually located distal to first bifurcation of major arteries of the circle of Willis.

A

Mycotic aneurysm

72
Q

Location of saccular aneurysms

A

Bifurcations of large to medium-sized intracranial arteries

85% of aneurysms occur in anterior circulation, mostly on circle of Willis

73
Q

Factors increasing the risk of rupture of aneurysm

A
  1. > 7mm diameter
  2. Top of basilar artery
  3. Origin of posterior communicating artery
74
Q

Hallmark of aneurysmal rupture

A

Sudden headache + absence of focal neurologic symptoms

Focal neurologic symptoms occur if hematoma produce mass effect

75
Q

Variant of migraine that stimulates SAH

A

Thunderclap headache

76
Q

Hunt-Hess scale Grade that presents with severe headache and normal mental status

A

Grade 2

77
Q

Hunt-Hess scale Grade presents with stupor, moderate to severe motor deficit, and may have intermittent reflex posturing

A

Grade 4

Grade 4 and 5 have 80% mortality rate

78
Q

4 major causes of delayed neurologic deficits

A
  1. Rerupture
  2. Hydrocephalus
  3. Vasospasm
  4. Hyponatremia
79
Q

Incidence of rerupture of UNTREATED aneurysm following SAH

A

First month : 30% peak in first 7 days

60% mortality rate, poor outcome

80
Q

T or F:

Hyponatremia in SAH should be treated with free-water restriction

A

False.

This can increase the risk of stroke.
Clears over 1-2 weeks.
Contraindicated in pt at risk for vasospasm

81
Q

Hallmark of aneurysmal rupture

A

Blood in CSF

82
Q

Xanthochromic spinal fluid is caused by conversion of hemoglobin to bilirubin that stains the spinal fluid yellow within 6-12 hours and lasts for how long?

A

1 - 4 weeks

83
Q

When is lumbar puncture indicated in patients suspected with SAH?

A

Only if CT scan is not available

84
Q

Imaging for suspected SAH

A

Noncontrast CT scan within 72h

Once SAH is confirmed:
Four-vessel conventional xray angiography

Alternative: CT angiography

85
Q

Structural myocardial lesions produced by catecholamines and excessive discharge of sympathetic neurons occur after SAH. Reversible cardiomyopathy causes shock or CHF.

ECG findings in SAH:

A
  1. ST segment and T wave changes similar to ischemia
  2. prolonged QRS complex
  3. increased QT interval
  4. prominent “peaked” or deeply inverted symmetric T waves

*Asymptomatic troponin elevation is common

86
Q

Leading cause of morbidity and mortality following aneurysmal SAH

A

Vasospasm

Treatment: Nimodipine 60mg PO every 4h

87
Q

T or F:

All patients should have pneumatic compression stockings applied to prevent pulmonary embolism

A

True

88
Q

T or F:
Unfractionated heparin can be administered SC for DVT prophylaxis following endovascular treatment (craniotomy + surgical clipping) of SAH

A

True

Neuro Critical Care (2 decks)

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