saburhcoind homerrahge

1. SUBARACHNOID
HEMORRHAGE
Dr Mohit Rohra
Reliance Hospital, Navi Mumbai

2. Acute Hemorrhagic Stroke
• Extravasation of blood in the cranial vault that in turn impairs
perfusion of normal brain tissue
• Four times more likely than ischemic stroke to cause death
• Cannot be reliably distinguished from ischemic stroke based on
clinical criteria
• Noncontrast CT evaluation is needed to detect the presence of
bleeding.
• The estimated volume of extravasated blood and the level of
consciousness are the two best predictors of outcome.

3. Subtypes of Hemorrhagic Stroke
• Defined based on the location of blood
• Blood located within the brain proper is called an intraparenchymal
hemorrhage.
• Epidural space - epidural hematoma
• Subdural space - subdural hematoma
• Subarachnoid space - subarachnoid hemorrhage
• Blood located in the ventricular system is an intraventricular
hemorrhage.

4. Subarachnoid Hemorrhage (SAH) - Causes
• Rupture of an intracranial aneurysm – Most common
• Hypertension
• Smoking, Cocaine abuse
• Heavy alcohol use
• Female sex
• History of prior SAH
• Family history of cerebral aneurysms and SAH.
• Autosomal dominant polycystic kidney disease
• Fibromuscular dysplasia

5. Clinical presentation
• Sudden onset of “the worst headache of my life”
• Associated with nausea/vomiting, stiff neck, brief or persistent loss of
consciousness, and focal neurological deficits.
• SAH can present with sudden onset of loss of consciousness, coma,
collapse, or seizure-like symptoms.

6. Diagnosis
• Non-contrast CT scan - Sensitivity is highest in the first 12 hours (98%–
100%) but decays over time: 93% at 24 hours and only 57% to 85% at six
days post-SAH.
• Lumbar Puncture – Performed when CT scan is negative but clinical
suspicion of SAH is high.
• Cerebral spinal fluid (CSF) analysis will reveal a presense of RBC’s, WBC’s,
xanthochromia and bilirubin.
• Advances in brain magnetic resonance imaging (MRI) sequences such as
gradient echo, proton density, diffusion-weighted imaging, and fluid-
attenuated inversion recovery have improved the sensitivity of MRI to
detect SAH in the setting of negative CT and high clinical suspicion.

7. Detection of potential cerebral aneurysm
• CT angiogram (CTA) – most common. Sensitivity:77-100%,
Specificity:79-100%
• Conventional cerebral angiography – Gold Standard
• Magnetic resonance angiogram - sensitivity and specificity is inferior
to CTA
• Negative CTA with high suspicion of aneurysm – Cerebral angiography

8. Prognostication and Grading of severity

9. Radiographic scale- Modified Fischer Scale

10. Management

11. Initial Stabilization
• Reversing or stabilizing acute life threatening sequelae- ABC
• Protection of Airway
• Cardiovascular Support
• Seizure control
• Avoid Hypertension and hypotension
• Antifibrinolytics – conflicting evidence (2a,B) (10)

12. Aneurysm Treatment
• Definitive treatment with complete obliteration of the bleeding aneurysm should be performed
as early as possible.
• Typical treatments include open surgical clipping and endovascular coil embolization of the
aneurysm.
• Optimal modality of aneurysm treatment depends on aneurysm factors such as size, morphology,
location, as well as patient factors such as periprocedural risk and comorbidities. One large
prospective randomized trial (ISAT) compared aneurysm clipping to coil embolization in patients
clinically amendable to either modality and showed no significant difference in mortality rate at
one year (8.1%–10.1%) but greater disability with open surgical approach (21.6% vs. 15.6%). In
contrast, the coil embolization group had higher rebleeding rate (2.9% vs. 0.9%) and a higher
incidence of needing additional aneurysm treatments. (1)
• Results of ISAT combined with pt preference are leading to increase in endovascular treatment.
• Surgical treatment preferred in : Hematoma, aneurysm difficult to visualise angiographically,
requirement of bypass for distal perfusion,

14. Treatment of Complications of SAH & Aneurysm
treatment
• Vasospasm – Occurs in 70% of pts, starts 3-4 days after aneurysm rupture, peaks at 7-10
days and resolves by 14-21 days.(2)
• Delayed cerebral ischemia : clinical syndrome of focal neurologic deficit that develops in
one third of patients, typically 4 to 14 days after aneurysm rupture, and is a major cause
of death and disability after subarachnoid hemorrhage has occurred.
• DCI – Multifactorial pathogenesis, not related to vasospasm alone.(3,4,5)
• Worsened with hypovolemia, hypotension and anaemia.
• Target euvolemia(1,B), induced hypertension (1,B). Optimal Hb – unclear.(10)
• Prophylactic hypervolemia (3,B) – widely practiced - worse outcome (6,7,10)
• Nimodipine – 60mg 4 hrly orally for 21 days – All patients (1,A)(8,10)
• Balloon angioplasty/ intra-arterial vasodilator therapy(2a,B) - reasonable in patients with
symptomatic cerebral vasospasm, particularly those who are not rapidly responding to
hypertensive therapy(10)
• Daily transcranial Doppler – employed in some centers, value unclear.(2a,B)(10)

15. Hyponatremia(9)
• Common – 30% patients
• SIADH ( MC) , Cerebral Salt wasting, acute cortisol insufficiency,
excessive fluid therapy, diuretic therapy.
• Increase in natriuretic peptide secretion, inhibition of the renin-
aldosterone system and excessive adrenergic activity, may contribute
to hyponatremia
• Can increase cerebral edema and ICT further increasing risk of
neurological injury

16. Management of hyponatremia in SAH(9,10)
• Daily check of electrolytes ( More frequently when hypertonic saline is
used)
• Hyponatremia treated with fluid restriction is associated with poor SAH
outcome. Avoid hypovolemia. Avoid hypotonic fluids and diuretics.
• Maintain on sodium chloride-based fluids (i.e., 0.9% saline)
• SIADH – Fluid restriction not feasible in SAH.
• 3% NS – Can be used (2a,B). Watch for pontine demyelinosis, pulmonary
edema
• Fludrocortisone – Limited ability, associated with fluid overload (2a,B)
• Vasopressin receptor antagonists (e.g., conivaptan). Not recommended.
(Diuresis, hypovolemia, worse outcome)

18. Neurogenic cardiac and pulmonary injuries
• Cardiac dysfunction (Stress cardiomyopathy) – common – cathecholamine
surge – not related to coronary ischaemia
• Elevated troponin levels (35%), RWMA ( 25%), Arrythmias (35%)
• Wide clinical spectrum – dyspnoea, hypoxemia, pulmonary edema,
cardiogenic shock , death
• Supportive treatment – Maintain adequate blood pressure, cerebral
perfusion and oxygen delivery
• Pulmonary dysfunction – edema, ALI, ARDS (20%) – neurogenic pulmonary
edema when present in absence of cardiac dysfunction – unclear
pathophysiology
• Treatment – Supportive – Maintain adequate oxygen delivery to brain ,
avoid hypovolemia

19. Fever and SIRS
• Fever - Highly prevalent (72%)
• Risk factors - poor-grade SAH, more blood in the subarachnoid space,
and intraventricular blood.
• Oral antipyretics – not very effective and surface cooling devices may
be required.
• SIRS – Prevelant – Mostly of non infectious etiology
• Associated with poor outcome, vasospasm and increased mortality.

20. Rebleeding
Vasospasm

21. References
1. Molyneux AJ, Kerr RS, Yu LM, et al. International Subarachnoid Aneurysm Trial (ISAT) of neurosurgical clipping versus endovascular coiling in 2143 patients with
ruptured intracranial aneurysms: a randomised comparison of effects on survival, 53 Chapter 5 Subarachnoid Hemorrhage dependency, seizures, rebleeding,
subgroups, and aneurysm occlusion. Lancet, 2005;366(9488):809–817.
2. Dorsch NW, King MT. A review of cerebral vasospasm in aneurysmal subarachnoid haemorrhage. I. Incidence and effects. J Clin Neurosci 1994;1:19-26.
3. 25. Rowland MJ, Hadjipavlou G, Kelly M, Westbrook J, Pattinson KT. Delayed cerebral ischaemia after subarachnoid haemorrhage: looking beyond vasospasm. Br J
Anaesth 2012;109:315-29.
4. 26. Macdonald RL, Pluta RM, Zhang JH. Cerebral vasospasm after subarachnoid hemorrhage: the emerging revolution. Nat Clin Pract Neurol 2007;3:256-63.
5. 48. Lucke-Wold BP, Logsdon AF, Manoranjan B, et al. Aneurysmal subarachnoid hemorrhage and neuroinflammation: a comprehensive review. Int J Mol Sci 2016;17:
497.
6. 51. Lennihan L, Mayer SA, Fink ME, et al. Effect of hypervolemic therapy on cerebral blood flow after subarachnoid hemorrhage: a randomized controlled trial.
Stroke 2000;31:383-91.
7. Zwienenberg-Lee M, Hartman J, Rudisill N, et al. Effect of prophylactic transluminal balloon angioplasty on cerebral vasospasm and outcome in patients with Fisher
grade III subarachnoid hemorrhage: results of a phase II multicenter, randomized, clinical trial. Stroke 2008;
39:1759-65
8.Dorhout Mees SM, Rinkel GJ, Feigin VL, et al. Calcium antagonists for aneurysmal subarachnoid haemorrhage. Cochrane Database Syst Rev 2007;3:CD000277.
9.Neena I. Marupudi and Sandeep Mittal. Diagnosis and Management of Hyponatremia in Patients with Aneurysmal Subarachnoid Hemorrhage. J. Clin. Med. 2015, 4,
756-767
10. E. Sander ConnollyJr , Alejandro A. Rabinstein Guidelines for the Management of Aneurysmal Subarachnoid Hemorrhage A Guideline for Healthcare
Professionals From the American Heart Association/American Stroke Association Stroke. 2012;43:1711–1737