sah: what are the causes of sah?
TRANSCRIPT
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
Non-neurological complications
Subacute (day 3-30)Vasospasm
Chronic (day >30)Chronic hydrocephalus
Rebleeding:Most serious complication
Occurs in first 3 days
Emergency treatment crucial
Poor prognosis
Fisher grade 3 4
SAH: ComplicationsAcute (day 0-3)
Rebleeding
Acute hydrocephalus
Cerebral edema
Non-neurological complications
Subacute (day 3-30)Vasospasm
Chronic (day >30)Chronic hydrocephalus
SAH: ComplicationsAcute (day 0-3)
Rebleeding
Acute hydrocephalus
Cerebral edema
Non-neurological complications
Subacute (day 3-30)Vasospasm
Chronic (day >30)Chronic hydrocephalus
Cerebral edema:
SAH
Decompressive craniectomy
Rebleeding
SAH: ComplicationsAcute (day 0-3)
Rebleeding
Acute hydrocephalus
Cerebral edema
Non-neurological complications
Subacute (day 3-30)Vasospasm
Chronic (day >30)Chronic hydrocephalus
SAH: Non-neurological complications
ECG abnormalities
Myocardial distress
Acute respiratory syndromes (Edema, ARDS)
Na & K abnormalities
Due to sympathetic nervous system activation
SAH: ComplicationsAcute (day 0-3)
Rebleeding
Acute hydrocephalus
Cerebral edema
Non-neurological complications
Subacute (day 3-30)Vasospasm
Chronic (day >30)Chronic hydrocephalus
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