Downloaded 54 times
Uploaded byShambhavi Sharma
sub arachnoid hemorrhage
Subarachnoid haemorrhage (SAH) is a neurological emergency caused by bleeding into the subarachnoid space surrounding the brain. The most common cause is a ruptured saccular aneurysm. Patients typically experience a sudden severe headache and may experience loss of consciousness or focal neurological deficits. Diagnosis is confirmed through CT scan or lumbar puncture. Treatment focuses on securing the aneurysm through surgical clipping or endovascular coiling, managing vasospasm, and preventing rebleeding. Outcomes depend on the severity of the initial bleed and development of complications.
More Related Content
Similar to sub arachnoid hemorrhage
More from Shambhavi Sharma
sub arachnoid hemorrhage
- 1. SUBARACHNOID HAEMORRHAGE 1 Presented by : ShambhaviSharma Intern Surgery Department KISTMCTH
- 2.
- 3. SUBARRACHNOID HAEMORRHAGE • Hemorrhagein the subarachnoid space • SAH is a neurological emergency • Less common but an important cause of stroke 3
- 4. Epidemiology 9.7-14.5 per 100,000population • peak age for aneurismal SAH is 55–60 years, ≈ 20% of cases occur between ages 15–45 yrs • higher in women (1.24 times higher than men) • higher in African Americans(2.1 times higher than whites) 4
- 5.
- 6. SAH- etiology • CLASSIFIEDAS: TRAUMATIC NON TRAUMATIC • Excluding head trauma, the most common cause of SAH is rupture of a SACCULAR ANEURYSM. • Other causes : bleeding from a vascular malformation (AV malformation or dural AV fistula ) Extension into the subarachnoid space from a primary intracerebral haemorrhage. Mycotic aneurysms Associated with genetic disorders 6
- 7. Mechanism of formationof aneurysms developmental defect in the media & elastica focal destruction of internal elastic membrane caused by hemodynamic forces acting at bifurcations & branching of arteries local weakness in vessel wall, intima bulges out covered only by adventitia The sac gradually enlarges and subsequently rupture 7
- 8.
- 9. SACCULAR ("BERRY") ANEURYSM •Autopsy and angiography studies have found that about 2% of adults harbor intracranial aneurysms, • Size- 2 mm. to 2-3 cm 9
- 12.
- 13. PATHOPHYSIOLOGY • Saccular aneurysmsoccur at the bifurcations of the large to medium-sized intracranial arteries. Rupture is into the subarachnoid space, basal cisterns the parenchyma of the adjacent brain. • Approximately 85% of aneurysms occur in the anterior circulation, mostly on the circle of Willis. • About 20% of patients have multiple aneurysms, - - many at mirror sites bilaterally. 13
- 14.
- 15.
- 16. • Aneurysms canundergo small ruptures and blood leaks into the subarachnoid space, so-called SENTINEL BLEED. SYMPTOMS are usually due to rupture of aneurysm and resultant SAH • some present with mass effect on cranial nerves or brain parenchyma. • Aneurysmal rupture usually occurs while the pt is active • may occur while straining on stool, sexual intercourse, lifting a heavy weight or some other sustained exertion • 30% of aneurysmal SAHs occurs during sleep 16
- 17. Four patterns ofpresentations: Pt. is stricken with severe headache & vomiting , and falls unconscious immediately Severe generalized headache occurs suddenly but pt remains lucid with varying degrees of neck stiffness Rarely pt suddenly becomes unconscious without any preceding complaint. patient may die within min to hours 17
- 18. • In patientswho survive initial rupture the most feared complication is rerupture which may occur at any time from minutes to 2-3 wks 18
- 19. HEADACHE In ~45% ofcases,sudden onset severe headache associated with exertion is the presenting complaint. "the worst headache of life"; usually generalized, often with neck stiffness, vomiting is common 19
- 20. Pain at othersites • Occipital and posterior cervical pain may signal a posterior /anterior inferior cerebellar artery (PICA/AICA) aneurysm. • Pain in or behind the eye and in the low temple can occur with an expanding MCA aneurysm 20
- 21. Loss of consciousness •sudden transient loss of consciousness in nearly half of patients • 6-16% patients develop seizures • In 10% of cases, aneurysmal bleeding is severe enough to cause loss of consciousness for several days. 21
- 22. Ocular hemorrhage • Dueto compression of central retinal vein and retrochoroidal anastomoses by elevated CSF pressure causing venous hypertension and disruption of retinal veins • Occurs in 20-40% of patients • Types: subhyaloid/preretinal hemorrhage intraretinal hemorrhage Viterous hemorrhage(Terson syndrome) 22
- 23. FOCAL NEUROLOGICAL DEFICITS •ACA or MCA bifurcation aneurysms may rupture into the adjacent brain or subdural space and form a hematoma large enough to produce mass effect. hemiparesis, aphasia, progressive drowsiness or slow mentation 23
- 24. • Third nervepalsy : aneurysm at the junction of post. Communicating & post. Cerebral arteries • A sixth nerve palsy: an aneurysm in the cavernous sinus uni or bilateral palsy could be because of raised ICP • Unilateral blindness : aneurysm lying anteromedially in the circle of willis usually at the origin of opthalmic artery 24
- 25. Transient paresis ofone or both lower limbs : ant comunicating A. aneurysm that has interfered with circulation in ant. Cerebral arteries. Hemiperesis or aphasia suggests aneurysm at the first bifurcation of middle cerebral artery 25
- 26. D/D severe headache Migraine headache ingestion of sympathomimetic drugs ingestion of tyramine containg foods in a pt. who is taking MAO inhibitors phaeochromocytoma Cerebral venous thrombosis, Diffuse vasospasm (call-flemming syndrome), Hypertensive encephalopathy, Intracranial or extracranial arterial dissection 26
- 27. DELAYED NEUROLOGIC DEFICITS 1.RERUPTURE/REBLEED, 2.HYDROCEPHALUS 3.VASOSPASM 4.HYPONATREMIA. 27
- 28.
- 29. 29 Body system involvedcomplications Volume status,electrolyte and metabolic disturbance Hypovolemia,hyponatremia,hyperglycemi a,hypokalemia Cardiac complications ECG Changes,myocardial ischaemia,elevated troponin,systemic and pulmonary hypertension,arrythmias,neurogenic stunned myocardial syndrome Pulmonary complications Neurogenic pulmonary edema,aspiration,pneumonia
- 30. Investigations 1.diagnose SAH: noncontrast CT Scan 2.identify source of SAH: CT angiography,MR angiography, catheter angiography 30
- 31. NON CONTRAST CTSCAN. • CT Scan is Initial investigative procedure More than 95% of cases have enough blood to be visualized on a high-quality NONCONTRAST CT SCAN obtained within 48 h. locate the underlying aneurysm, identify the cause of any neurologic deficit, and predict delayed vasospasm 31
- 32.
- 33.
- 34.
- 35.
- 36. lumbar puncture • UsuallyCSF becomes grossly bloody within 30 minutes of bleed with RBC counts upto 1 million/c mm or more • Lysis of the red blood cells and subsequent conversion of hemoglobin to bilirubin stains the spinal fluid yellow( xanthochromia) within 2-4 h max by 12 hrs • lasts for 1–4 weeks, depending on the amount of subarachnoid blood • Protein: high due to blood breakdown products • Glucose: normal or reduced 36
- 37. Angiography CT angiography • forlocating the aneurysm and its relation with nearby bony structures • Evaluation of vasospasm MR angiography 87% sensitive 92% specific Catheter angiogram GOLD STANDARD Demonstrates source in 80-85% cases 37
- 38.
- 39.
- 40.
- 41.
- 42. OTHER INVESTIGATIONS Close monitoring(daily or twice daily) of electrolytes : hyponatremia occur precipitously during the first 2 weeks following SAH An asymptomatic troponin elevation is common. ECG ECHO 42
- 43. TREATMENT The medical managementof SAH focuses on • Managing blood pressure and maintaining euvolemia • Maintaining ICP • Preventing rebleeding prior to treatment, • Managing vasospasm, delayed neurological deficits • managing seizures • Treating hydrocephalus, • Treating hyponatremia, 43
- 44. • bed restin a quiet room • stool softeners to prevent straining. • If Headache or neck pain is severe, mild sedation and analgesia • Extreme sedation is avoided because it can obscure changes in neurologic status. • Adequate hydration 44
- 45. Prevention of vasospasm •Calcium channel blockers: oral nimodipine should be administered in all patients with aSAH • Maintainance of euvolemia and normal circulating volume • Induction of hypertension is recommended for patients with DCI unless BP is elevated at baseline 45
- 46. POST SAH SEIZURES 46 •Prophylactic anticonvulsant may be considered in immediate post hemorrhagic state • Routine long term use of anticonvulsant is not recommended • long term use of anticonvulsant may be considered in patients with risk factors for deayed seizure disorder (prior seizure, intracerebral hematoma, intractable hypertension,infarction,or MCA aneurysm)
- 47. Antifibrinolytic therapy • Forpatients with aneurismal SAH where: 1. unavoidable delay in t/t of aneurysm 2.pt with significant risk of re bleeding 3. no compelling medical contraindications Upto 72 hrs of therapy with tranexemic acid or aminocaproic acid is reasonable 47
- 48. Acute hydrocephalus • CSFdiversion or lumbar drain Chronic hydrocephalus Permanent CSF diversion for symptomatic patients 48
- 49. INTERVENTIONAL MANAGEMENT • Earlyaneurysm repair prevents rerupture/rebleeding and allows the safe application of techniques to improve blood flow (e.g., induced hypertension and hypervolemia) should symptomatic vasospasm develop. • An aneurysm can be "clipped" or "coiled” 49
- 50. Angiographic findings: generalfeatures to take note when analysing anuerysm 1.size of aneurysm dome 2.neck size 3.dome neck ratio Large aneurysms > 15 mm diameter are a/w lower rates of complete occlusion by endovascular coiling Narrow neck <5 mm are ideal for coiling Broad neck > 5mm a/w increased risk of incomplete occlusion and recanalization by coiling Stent or balloon assisted coiling may be needed for wide necked aneurysm Dome neck ratio : > or equal to 2 are a/w higher rate of successful coil occlusion 6 50
- 51. 51 SURGICAL REPAIR •Involves placinga metal clip across the aneurysm neck, thereby immediately eliminating the risk of rebleeding. •This approach requires craniotomy and brain retraction, which is associated with neurologic morbidity.
- 52.
- 53.
- 54.
- 55.
- 56. 56 Add another gradefor serious illnesses,or evidence of vasospasm in CT angiography
- 57.
- 58. Management based onHH scale Grades 1 & 2 • Current approach is to go for intervention within 24 hrs This will prevent rebleed and will allow measures to be taken to improve cerebral circulation • Grade 3 patients- if their condition allows , they too would be benefitted by the procedure • Grade4/5- the outcome is generally poor but by putting a ventricular drain and improving the grade, pt are sometimes taken for intervention 58
- 66. 66 Endovascular techniques involve placingplatinum coils, or other embolic material, within the aneurysm via a catheter that is passed from the femoral artery.
- 67. NEWER DRUGS • Magnesium •Statins • Endothelin receptor antagonist • Tirilizad • Erythropoietin 67
- 68. References • Bailey andlove’s Short Practice of Surgery,26th edition • AHA/ASA guideline for management of aneurysmal suarachnoid hemorrhage, june 2012 • Giovanni Grasso, et al authors, Management of aneurysmal SAH : state of the art and future perspectives, surgical neurology international ,2017 68
- 69.
- 70.
Editor's Notes
- #6 .positive family history 7-20%.2% with ADPKD
- #17 sentinel bleeds: patient may have a unusual headach esentinel headaches that precede the SAH-associated ictus have been reported by 10-50% of patients and most commonly occur within 2-8 weeks before overt SAH
- #18 With ruptue , blood at high pressure gushes in the suarachnoid space resulting in following three patterns of presentations: In rapidly evolving cases the bleed is so massive that I/c pressure approaches systemic BP, thus severely compromising the cerebral perfusion
- #20 Sudden unexplained headache at any location should raise suspicion of SAH and must be investigated,
- #22 COMA is d/t increased ICP, damage to the brain tissue from intraparenchymal hemorrhage Hydrocephalus , diffuse ischaemia, seizures,, low blood flow d/t reduced cardiac output
- #23 4-27% common with anterior circulation aneurysms. d/t raised iop----retinal membrane formation ---.retinal detachment
- #28 tendency for the hemorrhage to recur from the same site in more than one third of patients, often catastrophically The incidence of rerupture of an untreated aneurysm in the first month following SAH is ~30%, with the peak in the first 7 days. appears to be related to naturally ocuring mechanisms of clot lysis at the initial site of rupture Rerupture is associated with a 60% mortality and poor outcome. cause stupor and coma subacute hydrocephalus may develop over a few days or weeks causes progressive drowsiness or slowed mentation (abulia) with incontinence. Chronic hydrocephalus may develop weeks to months after SAH present as normal pressure hydrocephalus (NPH) manifested by gait difficulty, incontinence, or impaired mentation. Subtle signs may be a lack of initiative in conversation or a failure to recover independence Vasospasm is believed to result from direct effects of clotted blood and its breakdown products on the arteries within the subarachnoid space. Causes symptomatic ischemia and infarction in ~30% of patients major cause of delayed morbidity and death. Signs of ischemia appear 4–14 days after the hemorrhage, most often at 7 days. The severity and distribution of vasospasm determine whether infarction will occur. Spasm of major arteries produces focal symptoms referable to the appropriate vascular territory. All of these focal symptoms may present abruptly, fluctuate, or develop over a few days. In most cases, focal spasm is preceded by a decline in mental status. Patient may develop fluctuating hemiparesis or aphasia Severe cerebral edema in patients with infarction from vasospasm may increase the ICP enough to reduce cerebral perfusion pressure. may be profound and can develop quickly in the first 2 weeks following SAH. There is both natriuresis and volume depletion with SAH, so that patients become both hyponatremic and hypovolemic. Both atrial natriuretic peptide (ANP)and brain natriuretic peptide (BNP) have a role in producing this "cerebral salt-wasting syndrome.“ There may some role of antidiuretic hormone also, causing water retention Typically it clears over the course of 1–2 weeks and, in the setting of SAH, should not be treated with free-water restriction as this may increase the risk of stroke.
- #32 A high incidence of symptomatic vasospasm in the MCA and ACA has been found when early CT scans show subarachnoid clots >5 x 3 mm in the basal cisterns or layers of blood >1 mm thick in the cerebral fissures.
- #33 Collection of blood in the anterior inter-hemispheric fissure,blood in lateral ventricles,gyrus rectus: rupture of an ant. Communicating artery Blood in sylvian fissure – middle cerebral artery or post comm a
- #34 Prepontine cistern : basilar apex /sca aneurysm blood
- #35 4th and third ventricle:lower posterior fossa source PICA or VA dissetion Third ventricle : basilar apex aneurysm
- #37 False positive in increased protein in csf or jaundice
- #38 DYE KEPT IN FEMORAL ARTERY. TAKING SERIAL X-RAYS.DEMON
- #43 ECG changes suggestive of subendicardial or myocardial ischemia Elevation of troponis/CPK (MB) levels In some patients cardiac dysfunction may be severe enough to cause fall in EF % and heart failure There is evidence that structural myocardial lesions produced by circulating catecholamines and excessive discharge of sympathetic neurons may occur after SAH, causing these ECG changes and a reversible cardiomyopathy sufficient to cause shock or congestive heart failure. Hyponatremia D. Insipidus Albuminuria, Glycosuria leukocytosis
- #45 avoid decrease in blood volume predisposing to brain ischemia
- #47 Tripple h therapy, NIMODIPINE ACTION,NICARDIPINE