SAH

Question 1

🧠 Subarachnoid Hemorrhage (SAH)
Epidemiology
Risk Factors

Oh’s and college lectures

Answer 1

🧬 Epidemiology
* Responsible for 10% of all strokes
* F:M ≈ 1.25:1
* Age: Younger patients; peak incidence in 6th decade

🧪 Modifiable Risk Factors
* Smoking
* Heavy alcohol intake
* Hypertension
* Possibly: Use of sympathomimetics (e.g. cocaine)
* Genetic susceptibility

=> ASSOCIATIONS:
Coarctation of aorta
Ehlerdanlos syndrome
Marfan’s
PCKD

Question 2

⚠️ Etiology

Answer 2

• Most common cause: Rupture of berry aneurysm

=>Other causes:
* Non-aneurysmal perimesencephalic hemorrhage
* Arteriovenous malformations (AVMs)
* Cerebral amyloid angiopathy
* Mycotic aneurysms
* Pituitary apoplexy

M/C site of rupture of Berry aneurysms:
Anterior circulation- ICA- PCA junction>ACA>MCA
Vertebrobasilar art- account for 4% cases

perimesencephalic haemorrhage- bleeding around brain stem- primarily involving perimesencephalic cisterns- usually benign

Question 3

🩺 Clinical Features

Answer 3

1* Thunderclap headache (severe, sudden onset) foll by period of reduced GCS
2* H/O similar previous headaches- ?
sentinel headache
3* Meningism signs in awake patients:
* Neck stiffness
* Photophobia
* Vomiting
4* Focal deficits depending upon site of rupture
5* Seizures

Question 4

Role of CT

Answer 4

=> Protect airway before CT if concerns regarding potential loss of airway
=>CTB (Non-contrast CT Brain)
* Sensitivity highest in first 6 hrs

=>If CT negative and high index of suspicion:
* Perform LP after 12 hours → Look for xanthochromia

=>CTA to localize aneurysm

Question 5

Grading systems

Answer 5

• WFNS
• Fischer
• Hess and hunt
• PAASH
• Claasson

Question 6

WFNS

Answer 6

📊 WFNS Grading
* Regarded as standardised clinical score
* Most common method for assessing clinical severity.

-> Based on:
* GCS
* Focal neurology

**=>Motor part of score most imp.** =>	Gives indication about clinical prognosis .

standard but reliant on accurate GCS

Question 7

Hunt and Hess

Answer 7

Clinical grading used to classify severity of SAH

good grade- 1-3 ; poor grades- 4,5
*Thick is defined as filling one or more cisterns or fissures, out of a total of 10 cisterns/fissure

=>Developed as an index of surgical risk
->subjective parameters- eg- mild headache, stupor etc that cannot be quantified

Question 8

🧮 PAASH Score

Answer 8

• Stands for :
  Prognosis on Admission of Aneurysmal Subarachnoid Haemorrhage
• Validated for SAH prognosis
• Some benefit over WFNS
• ❗Not widely used

=>Claasson-
* Takes into account additive risk of SAH and Intraventricular Haemorrhage
* Goes from I to V-> I-> no blood–>blood filling one or more cisterns or fissures–> b/l IVH

Question 9

Fishcher Grading

Answer 9

CT based grading- gives an indication of probability of developing DCI

Predicts likelyhood of vasospasm

Question 10

⚠️ Other Poor Prognostic Signs (apart from high WFNS)

Answer 10

• High Grade
• Amount of blood
• Multiple comorbidities-esp- systemic HTN, liver disease, prev. SAH, IHD, Smoking
• Advanced age
• DIC
• Anaemia
• Hypoglycaemia
• Electrolyte derangements
  =>Medical complications:
• Pneumonia/sepsis
• Renal/metabolic issues

✅ Better prognosis seen in high-volume centres (>260 SAH/year)

Treatable causes of poor grade- hydrocephalus, seizures, hypoglycemia, Anemia

Question 11

Complications
⚕️ Medical Complications in SAH

Answer 11

• Aspiration pneumonia
• ARDS
• Neurogenic stress CMP-
• Arrhythmias
• Takotsubo cardiomyopathy
• SIADH
• Liver and renal dysfunction

Neurogenic stress CMP- clinical syndrome of Chest pain, dyspnoea, hypoxia, pulmonary oedema, Cardiogenic shock
Myocardial injury occurs due to sympathetic stimulation, catecholamine surge–> ⬆️trops, arrhythmias, WMA, takotsubo CMP
-> will need supportive care, balance cardiac and neuro needs, consider COP monitoring

Question 12

🧠 Causes of Neurological deterioration in SAH

Answer 12

=>Think Broad.

=>Metabolic causes:
⬇️O2, ⬆️Co2, ⬇️glycemia, ⬇️Na
Drugs
Hyperthermia
=>Neurological Causes:
* DCI (Delayed Cerebral Ischemia)
* Rebleed
* Parenchymal hematoma
* Hydrocephalus
* Seizures

Question 13

🚨 Complications

Rebleed

**Q. Risk Factors for rebleed

Q. Role of TXA in rebleed**

Answer 13

=>Rebleed- Most dreaded complication

• ⚠️ Most likely in first few hours post-admission.
• May be heralded by clinical deterioration:
• May require urgent intubation/resuscitation.
• Degree of initial bleed correlates with risk.

=> Risk factors:
* Aneurysm >7mm (especially posterior circulation).
* Degree of initial bleed
* Poor grade SAH.
* High SBP.
* Age and sex of pt
* Also related to the degree of aneurysm occlusion after Tt

=>ISAT suggested ⬆️ed risk with coiling, but other studies have not confirmed this finding.
=>Role of TXA:
* Small studies show benefit in reducing early rebleed in selected patients with aneurysms awaiting intervention.
* Risk of thrombosis must be balanced.

• ⚠️ Rebleed- not always unsurvivable- treatment should be attempted
• ISAT- found higher incidence of rebleed with coiling compared to clipping, however, other studies have not confirmed this.

Question 14

🧠 Acute Hydrocephalus
Assessment and management

Answer 14

• Can occur within first 24 hrs post ictus.
• Clinical triad:
  
  • ↓ GCS (altered consciousness)
  • Sluggish pupillary responses
  • Sunset eyes (bilateral downward eye deviation)

=>Cause- Active distension of ventricular system due to altered CSF dynamics:
* Acute hydrocephalus caused by obstruction of flow by blood products or adhesions
* ⬇️ ed CSF absorption caused by reduced reabsorption by arachnoid granulations-> occurs after 2wks or later–> more likely to be shunt dependent.[Routine fenestration of Lamina terminalis not useful for preventing shunt dependence]

=>Risk high if:
* Intraventricular extension
* Low initial GCS
* Hyponatremia
* HTN
* Older age
* Use of antifibrinolytic agents
* NOT related to coiling vs clipping

• Urgent repeat CT is warranted.
• If confirmed → EVD (external ventricular drain).
• Although EVD is req., ⬆️ed ventriculitis risk after 3days-> monitor

Question 15

🧠 DCI (Delayed Cerebral Ischemia)
Incidence and Definition

Answer 15

=> Caused by vasospasm — very common post-SAH:
* Seen in ~70% on angiography.
* not all are symptomatic.

=>DCI =
* i).new focal neurological deficit that persists for >1hr
OR
ii). drop in GCS by ≥2 points persisting for >1hr
&/OR
iii). Cerebral infarction that typically occurs 4–12 days post-SAH which is not directly related to aneurysm Tt or other causes of neuro deficit are ruled out.

• Oral nimodipine 60 mg q4h for 21 days:
  
  • Reduces risk of ischemic stroke by ~34%, improves neurological outcomes
• IV nimodipine if oral route not tolerated.
• Must be titrated against BP (risk of hypotension).

Delayed Cerebral Deterioration is a clinically detectable neurological deterioration post initial stabilisation that is NOT due to Rebleed. It is an umbrella that covers deteriorations due to Cerebral oedema; Hydrocephalus; DCI; Seizures; Fever; electrolyte abnormalities.

Question 16

Early vasospasm

Answer 16

• Radiological narrowing seen in patients at the time of presentation or shortly after admission to hospital
• Not associated with conventional vasospasm
• Indepent Poor Marker of prognosis

Question 17

Risk Factors for DCI

Answer 17

=>Two major key factors - Amount of blood and Location of blood in the brain
* Poor clinical grade
* Longer duration of unconciousness
* Age<50yrs
* Hyperglycemia
* HTN/ Smoking/ Cocaine

=>Thick basal cistern blood and blood in Lateral ventricles- high likelyhood of vasospasm.

Question 18

Pathophys of DCI

Answer 18

OxyHb- when comes in contact with abluminal side of the vessel- induces vasospasm via
* Ca dependent and independent pathways
* Freeradical induced injury
* Imbalance between VC and VD substances.

Question 19

DCI cont..
What monitoring would you use?

Answer 19

=>Repeated clinical exam - imp but limited sensitivity esp in pts with poor grade SAH
📈 Monitoring
=>TCD (Transcranial Doppler):
* MCA blood flow velocity >120 cm/sec.

• Not all patients with high Doppler velocities or angiographic vasospasm have symptoms.
• If ↓ consciousness with ↑ Doppler velocity and no other cause (e.g. hydrocephalus, metabolic), assume DCI → initiate treatment.
• Sensitivity of TCD for monitoring is questionable-> better for large vessel involvement.

=>Multimodal monitoring with
- cont EEG
- -Brain tissue O2 monitoring
- -Cerebral microdialysis if available

=>Emerging evidence in favour of perfusion scan with regions of reduced perfusion

=>Diagnosis-

• CTA followed by DSA + intra-arterial verapamil or papaverine can be used.
• CTA/DSA: Confirms angiographic vasospasm.
• MRA- useful but time factor limits uuse

Question 20

💊 Treatment of DCI

Answer 20

I) Euvolemia is essential → improves CBF and outcomes.

II) Hypertension:
* Induced in a stepwise fashion if vasospasm suspected.
* Requires frequent neuro checks (GCS, exam) at each step.

III) Cerebral angioplasty or direct vasodilators.

IV) Always re-evaluate for other causes of ↓ consciousness (e.g. rebleed, hydrocephalus, metabolic derangement).

v) Surgical Tt- Cisternal infusion of urokinase after clipping to ⬇️ clot size or intratheral urokinase post coiling are more experimental modalities.

->In high-grade SAH (low GCS/sedated):
multimodal monitoring to detect early deterioration.

=>Cerebral angioplasty along with intra arterial VD used in recurrent or refractory vasospasm-> bigger vessels more suitable for ballooning, smaller vessels more suitable for intra arterial VD

Question 21

🧠 Parenchymal Hematoma

Answer 21

• Worse prognosis than SAH alone.
• Causes mass effect → may require evacuation.
• Can be addressed with simultaneous clipping of aneurysm.
  * Early removal may improve outcomes.

Question 22

⚡ Seizures

Q. risk factors for seizures
Q. when would you consider AEDs in SAH
Q. Role of AEDs in SAH

Answer 22

-> Prophylactic AEDs not routinely recommended.

->Consider AEDs if high risk (e.g. MIHIR mnemonic):
* MCA aneurysm
* Infarction
* H: High-grade SAH
* I: Intracerebral hematoma
* R: Rebleed
* Seizure at presentation
* GCS < 8

• AED of choice: Levetiracetam.

=> If not improving neurologically:
* Suspect NCSE.
* Consider EEG monitoring.

=>Phenytoin prophylaxis- esp >7days asso with worse outcomes; 3 days Tt not different to 7day with less SE

=>⬆️ risk of NCSE with Clipping as Tt

=>NCSE- prediction for bad outcome, clinical seizures- no clear evidence for bad outcome.

Question 23

🧪 Imaging – Workup for Stroke / SAH

Answer 23

=> CTB = initial test to diagnose SAH.
* Localizes arterial bleeding.

=> CTA: Better for aneurysm identification (especially anterior circulation).

=> MRI: Helps localize blood later(>48hrs when blood has denatured)

=> DSA = gold standard via arterial catheter.

=> LP:
* If CT negative but high suspicion persists.
* Perform ≥12 hrs post ictus to detect xanthochromia.

Question 24

🧠 Monitoring

Answer 24

• ICP: Especially in cases with hydrocephalus or parenchymal hematoma.

=>Multimodal monitoring for deteriorating or deeply sedated patients with high-grade SAH:
* Continuous EEG → detect NCSE.
* Jugular venous oximetry.
* Brain tissue oximetry.
* Cerebral microdialysis.
* Increasing evidence in favour of Perfusion scan- areas of hypoperfusion.

Question 25

✅ Management Principles

Answer 25

=>Immediate resuscitation * Analgesia * Corrrect coagulopathy FFP inferior to Beriplex; * No good evidence for pooled platelets in pts on antiplatelets * TXA- ⬇️es incidence of rebleed, risk to be balanced against ⬆️ risk of DVT * BP control * Earliest possible coiling/ clipping * Consider antiepileptics * Euvolemia * Nimodipine * Hydrocephalus- EVD

Question 26

Immediate Priorities

Answer 26

1. Immediate Priorities: * Airway, breathing, circulation (ABCs) * Neuro-monitoring * Analgesia * Correct coagulopathy if present. 2. **Blood Pressure Control** ->AHA recommendation: * SBP <160 mmHg * MAP <110 mmHg * No consensus on exact targets; balance ischemia vs. rebleed risk. 3. Maintain euvolumia- critical to prevent DCI 4. BP-lowering drugs * Beta-blockers, CCBs, Hydralazine, GTN, SNP **=>⚠️ Avoid cerebral vasodilatory drugs- GTN Titrability more imp. than choice of drug** ⸻ 🧪 Pharmacologic Notes * Nimodipine: * 60 mg orally every 4 hours × 21 days. * ⚠️ Some evidence that levetiracetam is preferable in seizure risk.

Question 27

🧠 General Mx

Answer 27

=>Hyperglycemia- BGL target- 6-10mmol/L =>Treat anemia- Ideal Target controversial, Preferred- 80-100 gm/L =>SCD better than stockings

Question 28

Fever in SAH

Answer 28

=>Fever- (>38.3 degrees C)-> independently asso with ⬆️ed mortality, Neurocognitive impairment =>Noninfective m/c than infective but infective causes should always be considered- extensive cultures including CSF if EVD present, CLABSI, LRTI, VAP, ventriculitis common causes. => m/c in poor grade SAH and IVH =>Nooninfective- usually starts early during the course(1-3 days), constant high temp- absent spikes. =>Aggressive control of fever imp- PCM to ⬇️ hypothalamic set point, NSAIDS to ⬇️ Prostaglandins, surface cooling with Arctic sun, IV cooling devices. Evaporative cooling with fan & ice packs- less effective. =>Control shivering if present-> Buspirone, Tt hypomagnesemia, sedation and paralysis if nothing else works ## Footnote Decreased hypothalamic set point may be responsible Neurocognitive impairment means- Functional disability and cognitive impairment

Question 29

CLABSI & VAP

Answer 29

=>CLABSI- Prevent with : * Good Hand hygiene * Full barrier precautions while insertion * Chlorhex cleaning of site * biopatch * Ab impregnated catheters * Avoid Femoral =>VAP Prevention: * Minimise intubation period * Head up position * oral and airway care * chest physio * Early EN if possible

Question 30

Hyponatremia in SAH

Answer 30

Hyponatremia * Very common- m/c/c- Pituitary Adrenal dysfunction. * M/C occurs between D- 3-14, usually prior to vasospasm. * Imp to differentiate betn. SIADH and CSW- both Hypotonic hyponatremia with ⬆️ urinary Na =>SIADH- ⬆️secr of ADH--> water retention * Tt- Fluid restriction; Hypertonic saline * Conivaptan(Vasopressin receptor antagonist ) Best AVOIDED- can cause dangerous hypovolemia =>Cerebral Salt Wasting- unclear pathophysiology; possibly ⬆️ed ANP secr due to sympathetic hyperactivity -->⬆️ed excr of Na in urine--> ⬆️ed Tubular conc of Na--> ⬆️ed water excr. * Usually Tt- IVT with 0.9% saline to maintain euvolemia. * Typically resolves spontaneously in 2–4 weeks. * Early Tt with Fludrocortisone may help * SIADH and CSW may coexist. =>Tt: *

Question 31

Anemia and SAH

Answer 31

* Target Hb- 80-100 * Some prospective registeries have shown improved outcomes with higher values * Rationale- Loss of physiological vasodilation with anemia in injured brains.-->neuronal hypoxia

Question 32

Mx of Complications

Answer 32

🩺 Systemic Medical Complications – SAH 1. Pneumonia * Management: IV fluids + antibiotic therapy 2. ARDS * Lung-protective ventilation * Recruitment maneuvers * Optimized ventilatory strategies ⸻ 🚨

Question 33

Mx of Complications

Answer 33

3. Arrhythmias * Often due to fluid shifts or sympathetic surge * Treatment: correct electrolytes, antiarrhythmics * ⚠️ DC cardioversion if unstable * Rule out seizure, embolism, or Takotsubo as differential 4. Neurogenic stress CMP- * Presentation- Dyspnoea, Hypoxia, chest pain, Arrhythmias, APO, Cardiogenic shock * Etiology: ↑ catecholamines / ↑ pulmonary capillary wedge pressure (PCWP) * ECG, Trops, Echo- WMA, stunned myocardium, COP monitoring highly recommended. Tt- CPAP,** IABP** - Avoid fluid overload

Question 34

Mx of Complications

Answer 34

5. AKI * Often from nephrotoxic drugs, contrast, or sepsis * May require RRT ⸻ 🧪 Metabolic Complications 6. Hyponatremia * Must determine cause: SIADH vs CSW * Fluid replacement: * CSW: 0.9% saline ± fludrocortisone * SIADH: fluid restriction * Maintain euvolemia * Target serum osmolality: ≥ 280 mmol/kg (correct Na slowly)

Question 35

Mx of Complications

Answer 35

Other Complications 7.** Vasopressor resistance** * Consider: hypothalamic dysfunction- Hydrocortisone 8. Fever * Look for infective source: * Antipyretics, septic screen, cooling devices 9. BGL control * Target: 6–10 mmol/L (avoid extremes) * Hyperglycemia- poor neurological outcomes; Hypoglycemia- avoid at all costs * Limited evidence for tight glycemic control 10. DVT prophylaxis * Commence after 24 hrs of definitive aneurysm repair * Chemical: enoxaparin * Mechanical: SCDs immediately 11. Transfusion triggers * Hb < 90–100 g/L (esp. in patients with vasospasm/DCI risk) 12. Stress ulcer prophylaxis * PPIs or H2 blockers, especially in ventilated or coagulopathic patients

Question 36

Clipping vs Coiling Advantages and Disadvantages

Answer 36

=>**Clipping vs Coiling is a multiidsciplinary decision**

Question 37

Advantages & Indications for Clipping

Answer 37

* Usually a single Definitive procedure * Technique with most experience behind it. * No contrast involved * Preferred in pts with: - Low Neck: Fundus ratio - Distal segment lesions - Giant aneurysms - Younger pts

Answer 38

=> Coiling is preferred for : * Elderly pts * Pts with high grade SAH =>ISAT- less death from coiling Vs Clipping if: - Good Grade - Either tt was an option - ICA/ACA aneurysm - Aneurysm <10mm.

Question 39

Prognostication

Answer 39

=>Three most imp. factors in the BAG are: * Age * Grade * Blood - amount in the brain =>None of the grading systems can predict the clinical outcome but can guide towards the prognosos bearing in mind that there are modifiable factors that make the Grade worse on persentation- NCSE, Post ictal, Drugs, Hydrocephalus. =>About 1/2 the patients with poor initial grades have good outcomes.

Question 40

Factors affecting prognosis

Answer 40

* Age * Severe comorbidities- Particularly HTN * Previous MI * Liver disease =>Aneurysmal factors- * Large aneurysm, Complex configuration * Ruptured postr circ. aneurysm * Global cerebral oedema * Intracerebral haematoma * IVH =>Modifiable: * Rebleed-> secure early, control BP * DCI-> High vigilance, euvolemia, Nimodipine * AEDs-> Stop early if no evidence of seizures * Fever-> Tt aggressively, aim normothermia * Anemia->Target 80-100 * Hyper/ Hypoglycemia-> maintain normoglycemia * Pneumonia, sepsis-> surveillance, Tt early * Tt in high volume centres-> >35 cases/yr with interventional radiology and NeuroSx available * Comprehensive Neuropsychiatric assessment if and when Pts improve foll by Multidisciplinary rehab.