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Neurosurgery > Intracranial bleeding pt.2 > Flashcards

Intracranial bleeding pt.2 Flashcards

1
Q

How would a CSF test tube vial with xanthochromia or possible xanthochromia look like?

A

Pink or yellow tint

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2
Q

What is xanthochromia in the CSF a result of?

A

Represents hemoglobin degradation products (bilirubin)

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3
Q

DSA advantage

A

DSA is believed to have the highest resolution to detect intracranial aneurysms and define their anatomic features and remains the gold standard test for this indication

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4
Q

What aneurysm size can CTA and MRA detect?

A
  • Both can identify aneurysms ≥3 mm with a high degree of sensitivity, but they do not achieve the resolution of conventional angiography (ie, DSA)
  • Small aneurysms (especially ≤2 mm) may not be reliably identified
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5
Q

Rates of rupture of small aneurysms vs bigger aneurysms

A

Although small aneurysms rupture less frequently than large aneurysms , they are more common, and rupture of small aneurysms (approximately 5 mm or less) accounts for nearly one-half of SAH cases

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6
Q

What are the chances of detecting SAH on first angiogram? Should it be done again?

A
  • No angiographic cause of SAH is evident in up to 25 percent of cases
  • It is critical to repeat the angiogram in 4 to 14 days if the initial angiogram is negative
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7
Q

Which test is recommended in patients performing repeat angiograms who have suffered from SAH?

A

The recommended follow-up test in this setting is usually DSA.

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8
Q

Chance of finding an aneurysm on repeat angiography of a patient who has suffered from SAH?

A
  • Up to 24 percent of all SAH patients with initial negative angiography have an aneurysm found on repeat angiography
  • This may increase to as much as 49 percent in patients with initial evidence of SAH in CT and without perimesencephalic SAH
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9
Q

What are possible complications of SAH?

A

A variety of early complications can occur with SAH, including rebleeding, hydrocephalus, cerebral edema, vasospasm and delayed cerebral ischemia, seizures, hyponatremia, cardiopulmonary abnormalities, and neuroendocrine dysfunction

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10
Q

What is the Fisher scale?

A
  • Index of vasospasm risk
  • Tells us the amount of blood present in hemorrhage and the thickness of the blood layer based upon a computed tomography (CT)-defined hemorrhage pattern
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11
Q

What is the Fisher scale?

A
  • Index of vasospasm risk (but not clinical outcome) based upon a computed tomography (CT)-defined hemorrhage pattern
  • Tells us the amount of blood present in hemorrhage and the thickness of the blood layer
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12
Q

What is the modified Fisher scale?

A

Similar index to the Fischer scale that provides risk of delayed cerebral ischemia due to vasospasm

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13
Q

Modified Fisher scale grading

A

Grade:
0 No SAH or IVH (intraventricular hemorrhage)
1 Minimal SAH and no IVH
2 Minimal SAH with bilateral IVH
3 Thick SAH (completely filling one or more cistern or fissure) without bilateral IVH
4 Thick SAH (completely filling one or more cistern or fissure) with bilateral IVH

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14
Q

What were the best predictors of delayed cerebral ischemia due to vasospasm?

A

Thick SAH completely filling any cistern or fissure and bilateral IVH

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15
Q

What is the risk of delayed cerebral ischemia according to Fisher scale and modified fisher scale?

A
  • Both are similar when it comes to percentage for each grade
  • Grade:
    1: 21% (24 for modified)
    2: 25% (33)
    3:31% (33)
    4:37% (40)
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16
Q

Choice of SAH grading scale

A
  • Based on individual or institutional preference
  • No scale is optimal to help direct management, detect clinical changes over time, and guide prognosis
  • In addition, there are few validation studies of these scales and no prospective controlled comparison studies
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17
Q

Fisher scale grading

A

Grade:

1: No blood detected

2: Diffuse deposition or thin layer with all vertical layers of blood (in interhemispheric fissure, insular cistern, or ambient cistern) less than 1 mm thick

3: Localized clots and/or vertical layers of blood 1 mm or more in thickness

4: Group 4: Intracerebral or intraventricular clots with diffuse or no subarachnoid blood

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18
Q

What is the Hunt-Hess scale?

A

index of surgical risk with initial clinical grade correlating with the severity of hemorrhage

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19
Q

Hunting and Hess grading

A
  • The grade is advanced one level for the presence of serious systemic disease (eg, hypertension, diabetes, severe arteriosclerosis, chronic pulmonary disease) or vasospasm on angiography
  • Grade:
    0: for unruptured aneurysms and a grade 1a for a fixed neurologic deficit without other signs of SAH
    1: Asymptomatic or mild headache and slight nuchal rigidity
    2: Moderate to severe headache, stiff neck, no neurologic deficit except cranial nerve palsy
    3: Drowsy or confused, mild focal neurologic deficit
    4: Stupor, moderate or severe hemiparesis
    5: Deep coma, decerebrate posturing (abnormal body posture that involves the arms and legs being held straight out, the toes being pointed downward, and the head and neck being arched backward. The muscles are tightened and held rigidly)
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20
Q

Survival rate based on Hunt-Hess Scale for SAH

A

1: 70%
2: 60%
3:50%
4:20%
5:10%

IMPORTANT NOTE: Interobserver variability is moderate, some of the data also suggests grouping of grades (0-2)(3)(4-5) in terms of significant difference in risk of poor outcome or death between

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21
Q

Most common confirmed (to the best one can be) primary causes of death in SAH?

A
  • 55% = neurological devastation due to direct effects of primary hemorrhage
  • 17% = aneurysm rebleeding
  • 15% = medical complications
22
Q

WHat is interobserver variability?

A

The difference in the measurements between observers

23
Q

What is the Glasgow coma scale?

A
  • Method for evaluating the level of consciousness in a number of neurologic conditions
  • Grades coma severity
24
Q

GCS grading

A

The GCS assigns points based on three parameters of neurologic function/ responsiveness:
●Eye opening (spontaneous = 4, response to verbal command = 3, response to pain = 2, no eye opening = 1)
●Best verbal response (oriented = 5, confused = 4, inappropriate words = 3, incomprehensible sounds = 2, no verbal response = 1)
●Best motor response (obeys commands = 6, localizing response to pain = 5, withdrawal response to pain = 4, flexion to pain = 3, extension to pain = 2, no motor response = 1)

25
Q

GCS grade interpretation

A
  • Scored between 3 and 15, 3 being the worst and 15 the best
  • The components of the GCS should be recorded individually; for example, E2V3M4 results in a GCS score of 9
  • A score of 13 or higher correlates with mild brain injury, a score of 9 to 12 correlates with moderate injury, and a score of 8 or less represents severe brain injury
26
Q

Possible complications of SAH include (in order of time)

A

1 Rebleeding
2 Hydrocephalus
3 Delayed cerebral ischemia (due to cerebral vasospasm)

27
Q

What determines if an SAH patient will make it to the hospital to get treated?

A

If a clot forms in place of the ruptured aneurysm

28
Q

Risk of rebleeding

A
  • The patient is at substantial risk of early rebleeding (4 to 14 percent in the first 24 hours, with maximal risk in the first 2 to 12 hours) associated with high mortality
  • In first month, risk is 35%
  • Within six months, risk is 50%
  • ## After first year, risk is 3% per year
29
Q

Mortality from aneurysmal rebleed?

A
  • The mortality associated with rebleeding is reported to be as high as 70 percent
  • In first month, 50% mortality
  • Within six months, 70% mortality
  • After first year, 67% mortality
30
Q

Risk factors associated with rebleeding include:

A

Factors identified as predictors of rebleeding include:
●Longer time to aneurysm treatment (To avoid rebleeding, treat aneurysm very soon (within 6-12 hours at least)
●Worse neurologic status on admission
●Larger aneurysm size (> 10mm in size)
●High systolic blood pressure
●Presence of intracerebral or intraventricular blood
●Acute hydrocephalus
- Aneurysms in posterior circulation
- Poor Hunt-Hess grade (3-4)

31
Q

Should LP be performed in SAH aneurysmal rebleeds

A

Lumbar puncture is harder to evaluate because xanthochromia from the initial bleeding can persist for two weeks or more.

32
Q

How can one prevent a rebleed from an intracranial aneurysm?

A

Aneurysm treatment is the only effective treatment for the prevention of rebleeding

33
Q

Reasons why ICP increases in SAH

A

May develop due to a number of factors including hemorrhage volume, acute hydrocephalus , reactive hyperemia after hemorrhage and/or ischemia, and distal cerebral arteriolar vasodilation

34
Q

Occurence of increased ICP in SAH

A

54 percent, including 49 percent of those considered to have a good clinical grade (Hunt and Hess grades I to III)

35
Q

Occurrence of hydrocephalus in SAH patients

A

Hydrocephalus affects 20 to 30 percent of patients with SAH

36
Q

When is does hydrocephalus occur in SAH?

A
  • It usually presents within the first few minutes to hours after SAH
  • It can also be a later complication
37
Q

Cause of hydrocephalus in SAH

A
  • Hydrocephalus after SAH is thought to be caused by obstruction of cerebrospinal fluid (CSF) flow by blood products or adhesions or by a reduction of CSF absorption at the arachnoid granulations
  • The former occurs as an acute complication; the latter tends to occur two weeks after or later and is more likely to be associated with shunt dependence
38
Q

Clinical presentation of hydrocephalus in SAH setting

A
  • Progressive deterioration in level of consciousness, accompanied by ventricular dilation on head CT scan
  • Ocular signs of elevated ICP (miosis, downward eye deviation, or restricted upgaze) occur in many but not all patients
39
Q

Prognosis of hydrocephalus in SAH setting

A
  • Spontaneous improvement occurs in approximately 30 percent of patients with acute hydrocephalus and impaired consciousness, usually within 24 hours
    -In the remainder, acute hydrocephalus is associated with increased morbidity and mortality secondary to rebleeding and cerebral infarction
40
Q

Factors associated with risk of developing hydrocephalus in SAH setting

A
  • Factors associated with an increased risk for hydrocephalus include older age, intraventricular hemorrhage, posterior circulation aneurysms, treatment with antifibrinolytic agents, and a low Glasgow Coma Scale score on presentation
  • The incidence had also been reported to be increased in patients with hyponatremia or a history of hypertension
41
Q

What can the onset of hydrocephalus in SAH setting be divided into? Time, symptoms, and treatment too

A

Acute (within 48 hours, can cause stupor and coma), subacute (few days or weeks, progressive drowsiness or slowed mentation (abulia) with incontinence. May clear spontaneously or require temporary ventricular drain), and chronic (more rare, weeks or months, Presets as normal pressure hydrocephalus (NPH) manifested by gait difficulty, incontinence, or impaired mentation. Subtle signs may be a lack of initiative in conversation or failure to recover independence)

42
Q

What is the leading cause of morbidity and mortality in SAH?

A

In patients who initially survive SAH it’s vasospasm

43
Q

Occurence of vasospasm in SAH

A
  • Up to 70% in angiographies
  • Clinical vasospasm occurs in up to 30%
44
Q

When does vasospasm occur in SAH?

A
  • Vasospasm typically begins no earlier than day 3 after hemorrhage, reaching a peak at days 7 to 8
  • Typically does not occur after 2 weeks since rupture)
  • However, vasospasm can occur earlier, even at the time of hospital admission
45
Q

Cause of vasospasm in SAH

A
  • Vasospasm is believed to be produced by spasmogenic substances generated during the lysis of subarachnoid blood
  • Contraction of vascular smooth muscles and thickening of vessel wall
  • Evidence that decreased NO production, increased endothelin, and oxyhemoglobin are players
46
Q

Correlation between subarachnoid blood and vasospasm

A
  • There is a correlation between amount of subarachnoid blood after aneurysmal rupture and occurrence and severity of vasospasm – because of this, extensive removal of the blood by early surgery is important.
  • Prolonged exposure of cerebral arteries to perivascular blood is necessary for development of vasospasm (hence why Fisher Scale is important, as it measures the amount of blood in space)
47
Q

Factors that affect occurrence and severity of vasospasm

A
  • Prolonged exposure of cerebral arteries to perivascular blood is necessary for development of vasospasm (hence why Fisher Scale is important, as it measures the amount of blood in space)
  • Correlation between amount of subarachnoid blood after aneurysmal rupture and occurrence and severity of vasospasm
  • Other factors that may increase the risk of vasospasm include age less than 50 years and hyperglycemia
  • Most but not all studies have found that poor clinical grade (eg, Hunt and Hess grade 4 or 5, or Glasgow Coma Scale score <14) is associated with an increased risk of vasospasm
48
Q

Prevention and treatment for vasospasm and delayed cerebral ischemia in SAH

A
  • Hemodynamic augmentation is considered first-line therapy intended to raise the mean arterial pressure and thereby increase cerebral perfusion
  • To reduce the risk of poor outcomes from delayed cerebral ischemia, all patients should receive nimodipine, and euvolemia should be maintained
  • Balloon angioplasty has become the mainstay of treatment at many centers for symptomatic focal vasospasm of the larger cerebral arteries that is refractory to hemodynamic augmentation, the goal is to forcibly dilate constricted vessels and restore perfusion to the affected (ischemic) brain regions
  • In addition to angioplasty, vasodilating agents can be infused directly (intra-arterially) to relieve spasms
49
Q

Incidence of delayed cerebral ischemia

A

Occurs in approximately 30 percent of patients with aneurysmal SAH, typically between 4 and 14 days after symptom onset

50
Q

Hemodynamic augmentation strategy in delayed cerebral ischemia

A
  • The treatment involves induced hypertension with vasopressor agents such as phenylephrine, norepinephrine, or dopamine and maintenance of euvolemia using crystalloid or colloid solution
  • The addition of inotropic support with agents such as dobutamine or milrinone has been reported to be helpful in patients who do not appear to respond to pressors alone
  • Triple H therapy (hypertension, hypervolemia, hemodilution), which is controversial and considered outdated (as well as nimodipine), studies have shown that hypervolemia was not beneficial and might be harmful (i.e. blood flow is more important than pressure)
51
Q

Vasodilating agents for delayed cerebral ischemia due to vasospasm

A

Nicardipine, papaverine, verapamil

Neurosurgery (5 decks)

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