SAH: What are the causes of SAH?

Subarachnoid Hemorrhage

EDiNR, EDiPNR, EDER

Chief of Neuroradiology Section,Ege University Medical Faculty, Dept of Radiology

Izmir, TURKEYMacdonald RL. Delayed neurological deterioration after subarachnoid haemorrhage. Nat Rev Neurol. 2013;10:44–58

What is SAH?

• Bleeding in subarachnoid

space(Between arachnoid & pia mater which

is normally filled with CSF)

• A neurologic emergency

SAH:

Traumatic SAH occurs 35-40% of TBIs

The incidence of Aneurysmal SAH 7-10/100.000

Mortality and morbidity very high

1/3 recovery, 1/3 with complications, 1/3 fatal

What are the causes of SAH?1. Trauma

Most common cause

2. SpontaneousRuptured Aneurysm (80-85%)Unknown (7%)AVMArterial dissectionVasculitis, Amyloid angiopathyCerebral venous thrombosisTm, PRESDrug abuseetc….

Risk factors for SAH:

Peak between 50-60 years of age

Female > Male

Hypertension

Smoking, excessive alchohol intake

Family history

Drug abuse

Sickle cell disease

etc

SAH: Clinical featuresHeadache

* thunderclap or worst* reaching maximal intensity in 1 min.* Sudden onset more important than severity of HA

Nausea & vomiting

Seizure

Loss of consciousness

Neck stiffness / meningismus

Neurological deficits

CNIII, CNVI palsies

SAH: Diagnosis

Non-contrast CT

The primary choice.

Sensitivity depends on the interval betweensymptom onset and image acquisition.

100% in first 6 hours97% between 6-72 hours50% after 5 days

Because the blood density decreases by timeAcute stage 4 days later

Acute stage 8 days later

SAH: Diagnosis

SAH may be associated with:

Cerebral hematoma

Intraventricular hemorrhage

Subdural hematoma

SAH: Diagnosis

Lumbar Puncture (LP)

Recommended only if NCCT negative

Should be performed after 12 hours of symptomsto detect Xanthochromia (after red blood cell lysis)

Can be false negative / false positive (traumatic LP)

(!! Only 1% true positive with negative NCCT)

SAH: DiagnosisCTA

When NCCT positive

In the same session

Precise relationship with anatomic structures

Thrombus, calcification

Sensitivity 95-97%

DSA

Gold standard

Doubt on CTA

Better for small aneurysms

Treatment planning

Diagnosis of AVM, AVF

Should be repeated if initial DSA negative

54 y, M. Acute severe HA

SAH: DiagnosisMRI

SE, FSE, GRE, FLAIR, SWI, MRA

Sensitivity increases in the subacute phase.

<4 days: sensitivity 95%. 4-14 days: sensitivity 100%

FLAIR, SWI should be the choice

MRA 3T higher sensitivity

Rule out other causes

(Venous thrombosis, PRES, Tm, Amyloid angiopathy….)Aneurysm, SAH; MRI, MRA

Pseudo-SAH appearance on:1. FLAIRMeningitisLeptomeningeal carcinomatosisSupplemental 100% oxygenCSF pulsationMotion artifactGd leakage into CSF

2. CTMeningitisVenous sinus thrombosisLarge subdural hematomaBrain edema

SWI

53y F. Acute onset headache

SWI

Reversible cerebral vasoconstriction syndrome (RCVS)

SAH: LocationDiffuse

Perimesencephalic

Convexal

SAH: Location

Ant choroidal aneursymPartially thrombosed

DSA

Acute HA;

SAH, hematoma

MCA aneurysm

Acom aneurysmIntraventricular hemorrhage

SAH: Perimesencephalic-

Better prognosis. CTA / DSA should be performed

5% Aneurysm, AVF, Tm

SAH: ComplicationsSAH is not a monophasic disease !!

(biphasic / triphasic…. disease)

Knowledge of physiopathology is important

To understand the complications

SAH: what happens after bleeding?

Leakage of the blood to SA space leads to:

ICP CBF Activates injury cascade

Acute global ischemia, early brain injury, Anaerobic glycolysis

BBB breakdown, impaired autoregulation, cerebral edema…

Is blood a poison when out of the vessels?

Macdonald, R. L. (2013) Delayed neurological deterioration after subarachnoid haemorrhageNat. Rev. Neurol. doi:10.1038/nrneurol.2013.246

SAH: what happens after bleeding? SAH: ComplicationsAcute (day 0-3)

Rebleeding

Acute hydrocephalus

Cerebral edema

Non-neurological complications

Subacute (day 3-30)Vasospasm

Chronic (day >30)Chronic hydrocephalus

SAH: Complications

Possible complications predict the outcome.

Prediction of the complications can be done by CT.

Fisher Scale / Modified Fisher Scale

Grade CT findings

0 No SAH, No IVH

1 Focal/diffuse thin SAH, No IVH

2 Focal/diffuse thin SAH, IVH present

3 Focal/diffuse thick* SAH, No IVH

4 Focal/diffuse thick* SAH, IVH present

*Thick: completely filling at least one cistern or fissure

Complication rate increases by grade

SAH: ComplicationsAcute (day 0-3)

Rebleeding

Acute hydrocephalus

Cerebral edema




Rebleeding:Most serious complication

Occurs in first 3 days

Emergency treatment crucial

Poor prognosis

Fisher grade 3 4


Rebleeding

Acute hydrocephalus

Cerebral edema





Rebleeding

Acute hydrocephalus

Cerebral edema




Cerebral edema:

SAH

Decompressive craniectomy

Rebleeding


Rebleeding

Acute hydrocephalus

Cerebral edema




SAH: Non-neurological complications

ECG abnormalities

Myocardial distress

Acute respiratory syndromes (Edema, ARDS)

Na & K abnormalities

Due to sympathetic nervous system activation


Rebleeding

Acute hydrocephalus

Cerebral edema




SAH: Vasospasm !Most common (and dangerous)

Occurs between day 3-15

The risk depends on Fisher Grade !!

Degradation of blood products in CSF lead to

release of vasoactive mediators

Vasoconstruction

Leading to decreased CBF

27 y, M. Acute HA; 27 y, M. Acute HA; 3 days later

Vasospasm

Pcom aneurysm

ICA + Basilar artery

27 y, M. Acute HA; 8 days later

27 y, M. Acute HA; 13 days later 27 y, M. Acute HA; 15 days later

27 y, M. Acute HA; 1 7 days later SAH:

SAH:

SAH is di-tri phasic disease

Imaging findings are important for management

Follow-up imaging has a crucial role

Each change in clinical condition should be verified by imaging modalities

We must be aware of imaging findings to choose optimal imaging modality !!

THANKS FOR YOUR ATTENTION

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SAH: What are the causes of SAH?

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