Subarachnoid Hemorrhage . neurosurgery .pptx

subarachnoid hemorrhage presentation

1. Subarachnoid Hemorrhage Samah abu saadeh 6th year medical student AL-Quds University

2. OUTLINES: Definition Etiology Clinical Features Treatment Complications

3. : Definition Its bleeding into the subarachnoid space.

4. Etiology Blunt forces Penetrating Ruptured intracranial aneurysms ( the most common) 80% Ruptured arteriovenous malformations (AVM) Nontraumatic (spontaneous) SAH Traumatic SAH : traumatic brain injury

5. Increase stress (direct and indirect effect ) Hypertension, sympathomimetic agents like amphetamine and cocaine, Smoking , Ethanol, OCP and pregnancy

6. Dysplasia of smooth muscle Infective endocarditis Connective tissue disorders Marfan Syndrome , Ehlers danlos syndrome and Polycystic kidney disease (PKD) Causes of aneurysms:

7. Site of Aneurysms 85% occur in Circle of Willis • Most commonly anterior communicating artery 30% • Posterior communicating artery 25% • Middle cerebral artery 20%

8. Anterior Communicating Artery Aneurysm Headache Visual field defects

9. Posterior Communicating Artery Aneurysm Unilateral headache, eye pain • CN III palsy • Eye: “down and out" • Ptosis • Pupil dilation – nonreactive to light

10. Types of aneurysms

11. may be triggered by an acute rise in blood pressure; physical exertion many Risk factors : Smoking Hypertension Painful stimuli

12. Thunderclap headache Sudden, severely painful headache (often described by patients as the worst headache they have ever experienced) Nuchal rigidity ,photophobia positive Meningeal signs: Clinical features

13. Nonspecific signs Impaired consciousness Signs due to mass effect Focal neurological deficits: from stroke in affected vessel. Seizures ICP symptoms : Headache, nausea, and vomiting Papilledema Abnormal gait Cushing triad (irregular breathing, widening pulse pressure, Bradycardia)

14. Its estimate the morality rate in subarachnoid hemorrhage

15. Diagnostics

16. CT head without contrast Timing: as early as possible (when performed within 6 hours of onset, sensitivity is close to 100%) Defining feature: blood in subarachnoid space ( hyperdense ) with variable extension and location ;

17. Lumbar puncture Opening pressure: normal or elevated The following may be evaluated to identify cerebrospinal fluid (CSF) features suggestive of SAH: CSF color pink to red blood-tinged discoloration xanthochromia ; yellow discoloration Cell count (normal RBC:WBC ratio) RBC count: elevated Protein: elevated

18. Neurovascular imaging CT angiography (CTA) its Can typically provide enough information to plan aneurysm repair . Its estimate the risk of vasospasm after the treatment

19. Digital subtraction angiography (DSA): gold standard for cerebral vessel imaging Indications To plan interventions A large saccular aneurysm (encircled) is seen near the bifurcation of the anterior and middle cerebral arteries

20. Prevention of re-bleeding Anticoagulant reversal Management of blood pressure and cerebral perfusion pressure Target SBP < 160 mm Hg ICP management (e.g., elevate head 30°, IV mannitol , short-term controlled hyperventilation) Initial management

21. Treatment of aneurysmal SAH All aneurysmal SAHs require definitive endovascular or microsurgical aneurysm repair as early as possible

22. Further management Prevention of vasospasm and delayed cerebral ischemia Administer oral nimodipine Treatment of hydrocephalus: may include an external ventricular drain (EVD), lumbar drainage, or permanent ventriculoperitoneal shunt

23. Vasospasm ( 2 nd cause of mortality ) Can lead to ischemic stroke Usually occurs between 3–10 days after SAH Dx : transcranial Doppler (TCD Tx:Administer oral nimodipine Recurrent bleeding Occurs in 4–14% of patients with SAH in the first 24 hours Risk of re-bleeding is highest in the first 2–12 hours after SAH Complications:

24. Hydrocephalu s Acute obstructive hydrocephalus Chronic communicating hydrocephalus Elevated ICP: hypertension, bradycardia, and irregular breathing (see Cushing triad) Seizures Focal or generalized seizures Dx : EEG Tx : antiepileptic medication like phenytoin

25. SIADH cerebral salt wasting fludrocortisone ( alderterone )

26. Pyrexia: due to irritation of hypothalamus lead to increase body temperature (this increase risk of vasospasm ) Tx : cold normal saline infusion Stress cardiomyopathy : Happened in day 1 -2 Bleeding lead to massive increase of epinephrine lead to stress on myocardium become ischemic and decrease ejection fraction and hypotension and ballooning the apex Dx : ST segment elevation and increase troponin Tx : inotropic drug like Dopamine Neurogenic pulmonary edema ncrease the permeability lead to edema Patient present with dyspnea and hypoxia

27. prognosis: Approx. 30% mortality rate in the U.S .