Subarachnoid hemorrhage

Question 1

What is the Subarachnoid space?

Answer 1

The space between Dura and

Pia mater

Question 2

What does the Subarachnoid space contain?

Answer 2

Cerebrospinal fluid (CSF), Conductive arteries & Cerebral veins

Question 3

What is a Subarachnoid hemorrhage?

Answer 3

Bleeding into the subarachnoid space

Question 4

What 2 types of subarachnoid hemorrhages are there?

Answer 4

Those caused by TBI and the spontaneous ones

Question 5

What’s the most common type of SAH?

Answer 5

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

Question 6

Characteristics of Traumatic Subarachnoid

Hemorrhage

Answer 6

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

Question 7

Which philosopher predicted the outcome of an Aneurysmal subarachnoid hemorrhage?

Answer 7

Hippocrates

Question 8

Incidence and mortality of Aneurysmal SAH

Answer 8

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

Question 9

Incidence of delayed vasospasm

Answer 9

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

Question 10

Vasospasm

Answer 10

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

Question 11

Incidence of secondary infarction

Answer 11

30 35%

Question 12

Infarction

Answer 12

death of tissue resulting from a failure of blood supply

Question 13

Risk factors for SAH

Answer 13

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

Question 14

Characteristics of Aneurysmal SAH

Answer 14

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

Question 15

Percent of strokes cause by an SAH

Answer 15

5%

Question 16

% of aSAH patients die before they start medical treatment

Answer 16

15%

Question 17

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

Answer 17

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

Question 18

Time devision of the acute and late stage of an SAH

Answer 18

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

Later stage: up to 14 days after

Question 19

What are the immediate symptoms of an SAH

Answer 19

– 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

Question 20

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

Answer 20

CT & an angiogram

Question 21

Intubation

Answer 21

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.

Question 22

When do we intubate patients?

Answer 22

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

Question 23

Why do we perform an external ventricular drainage

Answer 23

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

Question 24

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

Answer 24

Hydrocephalus (occlusive)
Excessive Hypertension
Brain edema
Intracerebral Hemorrhage

Question 25

How do we fix intracerebral hemorrhage?

Answer 25

Emergency surgery to occlude it

Question 26

How do we fix brain edema?

Answer 26

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

Question 27

How do we fix Excessive Hypertension?

Answer 27

Antihypertensive medication

Question 28

Where are aneurysms usually placed?

Answer 28

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)

Question 29

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

Answer 29

an infectious/mycotic aneurysm

Question 30

What are the 2 methods for occluding an aneurysm?

Answer 30

Surgical clipping & endovascular coiling

Question 31

Which vital parameters do we monitor in the ICU?

Answer 31

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

Question 32

What are some complications og aSAH?

Answer 32

increase ICP, infections, electrolyte imbalances (diabetes insipidus)

Question 33

How do we monitor for delayed cerebral vasospasms?

Answer 33

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

Question 34

Treatment of delayed cerebral vasospasms?

Answer 34

Calcium antagonists, Hyperdynamic therapy, balloon angioplasty & pharmacological vasospasmolysis

Question 35

Long term Complications of an aSAH

Answer 35

``` Hydrocephalus (posthemorrhagic) Cranioplasty Moderate to severe handicaps Long rehabilitation Reduced Quality of life ```

Question 36

Early and late stage pathophysiology

Answer 36

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

Question 37

How long does Global Ischemia last in SAH patients?

Answer 37

30 min

Question 38

What causes Global Ischemia?

Answer 38

Increase cranial pressure

Question 39

What's the formula for cerebral perfusion pressure?

Answer 39

CPP = MABP - ICP

Question 40

Can we treat the Global Ischemia in SAH patients?

Answer 40

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

Question 41

How long does the Acute Vasoconstriction last?

Answer 41

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

Question 42

Can we treat Acute Vasoconstriction?

Answer 42

Yes, we do causal treatment

Question 43

When do delayed Cerebral Vasospasm occur?

Answer 43

day 3-14

Question 44

How many percent gets Vasospasms?

Answer 44

70% - for 1/3 it's delayed

Question 45

Riskfactors for Delayed Cerebral Ischemia (DCI)

Answer 45

``` 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

Question 46

What controls the size of the Infarction?

Answer 46

severity and duration of ischemia

Question 47

Does reducing vasospasms lead to less death and lower infarctions?

Answer 47

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

Question 48

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

Answer 48

Neurological state on hospital admission

Question 49

Filament Model of SAH

Answer 49

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

Question 50

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

Answer 50

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

Question 51

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

Answer 51

NO depletion

Question 52

Findings regarding the mousemodel of SAH on Oxidative Metabolism

Answer 52

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

Question 53

PDH

Answer 53

key enzyme from the aerobic to anaerobic pathway

Question 54

Function of CO2 in SAH

Answer 54

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

Question 55

Increased inter-cranial pressure can experimentally be controlled how?

Answer 55

ICP controlled by continuous CSF drainage

Question 56

Increasing CO2 levels in SAH patients led to?

Answer 56

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)

Question 57

Optimal time to increase CO2 levels in SAH patients?

Answer 57

45 min

Question 58

Summary points

Answer 58

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

Question 59

(perhaps) future therapies

Answer 59

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