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Neurosurgery > Subarachnoid hemorrhage > Flashcards

Subarachnoid hemorrhage Flashcards

1
Q

What is the Subarachnoid space?

A

The space between Dura and

Pia mater

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2
Q

What does the Subarachnoid space contain?

A

Cerebrospinal fluid (CSF), Conductive arteries & Cerebral veins

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3
Q

What is a Subarachnoid hemorrhage?

A

Bleeding into the subarachnoid space

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4
Q

What 2 types of subarachnoid hemorrhages are there?

A

Those caused by TBI and the spontaneous ones

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5
Q

What’s the most common type of SAH?

A

Traumatic Brain Injury, but within the spontaneous type it’s ruptured Aneurysms (80%)

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6
Q

Characteristics of Traumatic Subarachnoid

Hemorrhage

A

Bleeding is on the surface of the cortex - cause by moderate to severe TBI

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7
Q

Which philosopher predicted the outcome of an Aneurysmal subarachnoid hemorrhage?

A

Hippocrates

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8
Q

Incidence and mortality of Aneurysmal SAH

A

Incidence: 6-9 /100 000 per year
Overall mortality 40
In hospital mortality 25%

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9
Q

Incidence of delayed vasospasm

A

50 90% (peak on day 5 10 after aneurysm rupture)

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10
Q

Vasospasm

A

A vasospasm is the narrowing of the arteries caused by a persistent contraction of the blood vessels, which is known as vasoconstriction. This narrowing can reduce blood flow

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11
Q

Incidence of secondary infarction

A

30 35%

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12
Q

Infarction

A

death of tissue resulting from a failure of blood supply

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13
Q

Risk factors for SAH

A

– Hypertension
– Cigarette smoking
– Female gender female : male = 1.5:1)

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14
Q

Characteristics of Aneurysmal SAH

A

Bleeding occurs at the base of the brain where we have the circle of Willis

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15
Q

Percent of strokes cause by an SAH

A

5%

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16
Q

% of aSAH patients die before they start medical treatment

A

15%

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17
Q

Of the ~60% that survives the SAH, what are the outcomes?

A

1/3 severe neurological deficits
1/3 mild neurological deficits
1/3 good Outcome

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18
Q

Time devision of the acute and late stage of an SAH

A

Acute: 6-12 hrs (some say 24 hrs)

Later stage: up to 14 days after

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19
Q

What are the immediate symptoms of an SAH

A 
– Headache (all patients )
– Neck pain
– Fainting , unconsciousness may regain consciousness
– Epileptic seizures
– Hypertension, bradycardia (Cushing mechanism due to increased ICP)
– Dilated pupils
– Aspiration
– Apnea
– Sudden Death ( est. 15 %!)

Almost all of these can be traced back to an increase in Inter-cranial pressure

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20
Q

What type of imaging do we often do to diagnose SAH?

A

CT & an angiogram

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21
Q

Intubation

A

Intubation is a procedure that’s used when you can’t breathe on your own. Your doctor puts a tube down your throat and into your windpipe to make it easier to get air into and out of your lungs. A machine called a ventilator pumps in air with extra oxygen.

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22
Q

When do we intubate patients?

A

When they have a Glasgow Coma Score of below 9 –> lead to long term mechanical ventilation in many poor grade SAH patients

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23
Q

Why do we perform an external ventricular drainage

A
  1. to decrease inter-cranial pressure
  2. to clear blood from the CSF
  3. to reduce risk of Hydrocephalus
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24
Q

What things to we have to deal with in the acute phase?

A

Hydrocephalus (occlusive)
Excessive Hypertension
Brain edema
Intracerebral Hemorrhage

25
Q

How do we fix intracerebral hemorrhage?

A

Emergency surgery to occlude it

26
Q

How do we fix brain edema?

A

Osmotherapy, Craniectomy (cut open skull to let the brain swell)

27
Q

How do we fix Excessive Hypertension?

A

Antihypertensive medication

28
Q

Where are aneurysms usually placed?

A

At bifurcation (where the vessel split into two) usually at the large vessels of the circle of Willis (rarely on the surface of the brain)

29
Q

What is an aneurysm on the surface of the brain called?

A

an infectious/mycotic aneurysm

30
Q

What are the 2 methods for occluding an aneurysm?

A

Surgical clipping & endovascular coiling

31
Q

Which vital parameters do we monitor in the ICU?

A 
MABP: mean artery blood pressure
HR: Heart rate
Cardiac Output
ICP: inter-cranial pressure
StiO2: saturation of oxygen in the brain tissue
Electrolytes
32
Q

What are some complications og aSAH?

A

increase ICP, infections, electrolyte imbalances (diabetes insipidus)

33
Q

How do we monitor for delayed cerebral vasospasms?

A

neurological surveillance (if the patient is awake), Transcranial Doppler sonography (2-3 times a day), Functional imaging (CT)

34
Q

Treatment of delayed cerebral vasospasms?

A

Calcium antagonists, Hyperdynamic therapy, balloon angioplasty & pharmacological vasospasmolysis

35
Q

Long term Complications of an aSAH

A 
Hydrocephalus (posthemorrhagic)
Cranioplasty
Moderate to severe handicaps
Long rehabilitation
Reduced Quality of life
36
Q

Early and late stage pathophysiology

A

Early: bleeding, direct damage caused by the bleeding into the brain
Late: strokes

37
Q

How long does Global Ischemia last in SAH patients?

A

30 min

38
Q

What causes Global Ischemia?

A

Increase cranial pressure

39
Q

What’s the formula for cerebral perfusion pressure?

A

CPP = MABP - ICP

40
Q

Can we treat the Global Ischemia in SAH patients?

A

No. Since it only lasts 30 min, the patients are not yet in the hospital

41
Q

How long does the Acute Vasoconstriction last?

A

Onset is right at SAH and local cerebral blood-flow is “back up” to 80% after 2.5 hours, but is still present there

42
Q

Can we treat Acute Vasoconstriction?

A

Yes, we do causal treatment

43
Q

When do delayed Cerebral Vasospasm occur?

A

day 3-14

44
Q

How many percent gets Vasospasms?

A

70% - for 1/3 it’s delayed

45
Q

Riskfactors for Delayed Cerebral Ischemia (DCI)

A 
Delayed Vasospasm - but also:
Cortical Depolarizations
Hypermetabolism
Elevated body and brain temperature
Hb- toxicity
Lack of NO (nitric oxide)
Imbalance of vasoconstrictants and vasorelaxants

–> Mismatch between demand and supply of oxygen and nutrients

46
Q

What controls the size of the Infarction?

A

severity and duration of ischemia

47
Q

Does reducing vasospasms lead to less death and lower infarctions?

A

No - this is why we now look at the acute phase

48
Q

What is the the strongest predictor of outcome after aneurysmal SAH?

A

Neurological state on hospital admission

49
Q

Filament Model of SAH

A

you create a hole in the vessel between the anterior and middle cerebral artery

50
Q

Increasing levels of nitric oxide in a mouse model of SAH lead to?

A

Decreased cerebral perfusion pressure and increase in cerebral blood flow in both hemispheres. It increased activity and decreased hippocampal damage

51
Q

What may be a decisive factor for the pathogenesis of early perfusion deficit?

A

NO depletion

52
Q

Findings regarding the mousemodel of SAH on Oxidative Metabolism

A

we have more oxygen, but it might not be utilized.

We see ischemia increasing, which supports the idea that the brain is not using the oxygen

53
Q

PDH

A

key enzyme from the aerobic to anaerobic pathway

54
Q

Function of CO2 in SAH

A

you can influence vessel diamater –> more CO2 = more dilated vessel

55
Q

Increased inter-cranial pressure can experimentally be controlled how?

A

ICP controlled by continuous CSF drainage

56
Q

Increasing CO2 levels in SAH patients led to?

A

Increase in cerebral blood flow and higher oxygen saturation of the brain tissue. The effects extended long after the stop in CO2 happened (sustained effect)

57
Q

Optimal time to increase CO2 levels in SAH patients?

A

45 min

58
Q

Summary points

A

Majority of spontaneous SAH originates from intracranial aneurysms
SAH results in sequence of 3 kinds of ischemia
–Acute global ischemia
–Acute multifocal “ vasoconstriction
–Delayed cerebral ischemia
In the past decades , research has mainly focussed on delayed cerebral ischemia with limited success
Wide field of research
Severe disease with high mortality and morbidity neurological deficits
High economic burden

59
Q

(perhaps) future therapies

A

Intrathecal therapy with vasodilators
Targeting hemoglobin toxicity and inflammation
Using PaCO2 modulation

Neurosurgery (10 decks)

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