Aneurysms - Introduction, Grading, Special Conditions

| 14.02.23 - 13:48 85 Aneurysms –Introduction, Grading, Special Conditions 85.1 Introduction and overview 85.1.1 Definitions Subarachnoid hemorrhage : blood in the subarachnoid space (i.e., between the arachnoid membrane and the pia mater).Aneurysm : (from the Greek aneurusma “dilatation ”). An ou...

| 14.02.23 - 13:48 85 Aneurysms –Introduction, Grading, Special Conditions 85.1 Introduction and overview 85.1.1 Definitions Subarachnoid hemorrhage : blood in the subarachnoid space (i.e., between the arachnoid membrane and the pia mater).Aneurysm : (from the Greek aneurusma “dilatation ”). An outpouching in the wall of an artery. May be focal (as in saccular AKA berry aneurysm) or fusiform. May be congenital or developmental.Etiologies:1. congenital2. developmentala) f low-related: generally at branch points of arteries, usually due to shear forces at these loca-tions. Obsolete theory that this is due to underlying weakness of the media layer of the arte-rial wall at that location. Risk is increased in high f low states (e.g., chronic hypertension, drug-related e.g., cocaine, feeding vessels of AVMs …) b) mycotic (p. 1492): due to infectionc) posttraumatic (p. 1491)d)conditions with abnormalities of blood vessels, including: autosomal dominant polycystickidney disease (ADPKD) (p. 1455), vasculopathy (e.g., fibromuscular dysplasia (p. 209)), con-nective tissue disorders (Marfan syndrome (p. 1576), Ehlers-Danlos …) Dissecting aneurysm (p. 1576): results from a tear in the arterial lining which allows blood to enterthe arterial wall. Usually traumatically induced.Pseudoaneurysm (p. 1576) (false aneurysm): a blood clot adjacent to a rent in the arterial wall. 85.1.2 Miscellaneous facts about SAH 1. may be posttraumatic or spontaneous. Trauma is the most common cause2. most cases of spontaneous SAH are due to aneurysmal rupture3. peak age foraneurysmal SAH (aSAH) is 55 –60 yrs, !20% of cases occur between ages 15 –45 yrs 1 4. 30% of aSAHs occur during sleep5. sentinel headaches that precede the aSAH-associated ictus have been reported by 10 –50% of patients and most commonly occur within 2–8 weeks before overt SAH. 2,3,4 6. headache is lateralized in 30%, most to the side of the aneurysm7. SAH is complicated by: a) intracerebral hemorrhage in 20 –40% b) intraventricular hemorrhage (p. 1454) in 13 –28% c) subdural blood in 2–5%. When the subdural blood is over the convexity, it is usually due to PComA aneurysm. With an interhemispheric subdural hematoma, it is usually due to a distal anterior intracere-bral artery (DACA) aneurysm (p. 1475) 8. soft evidence suggests that rupture incidence is higher in spring and autumn9. patients "70 yrs of age have a higher proportion with a severe neurologic grade 5 10. seizures may occur in up to 20% of patients after SAH, most commonly in the first 24 hours, and are associated with ICH, HTN, and aneurysm location (MCA & acomm) 6,7 85.1.3 Outcome of aneurysmal SAH 1. 10 –15% of patients die before reaching medical care 2. mortality is 10% within first few days3. 30-day mortality rate was 46% in one series, 8and in others over half the patients died within 2 weeks of their SAH 9 4. median mortality rate in epidemiological studies from U.S. has been 32% vs. 44% in Europe and 27% in Japan (may be an underestimate based on underreported prehospital death) 10 5. causes of mortality a) 25% die as a result of medical complications of SAH 11 Subarachnoid Hemorrhage and Aneurysms 1416 85 https://ebooksmedicine.net/neurosurgery-book | 14.02.23 - 13:48 !neurogenic pulmonary edema (p. 1439)!neurogenic stress cardiomyopathy (p. 1438) (AKA neurogenic stunned myocardium) b) about 8% die from progressive deterioration from the initial hemorrhage 12 (p 27) 6. among patients surviving the initial hemorrhage treated without surgery, rebleeding (p. 1437) is the major cause of morbidity and mortality. The risk is!15–20% within 2 weeks. The goal of early surgery (p. 1462) is to reduce this risk 7. of those reaching neurosurgical care, vasospasm (p. 1439) kills 7%, and causes severe deficit in another 7% 13 8. about !30% of survivors have moderate to severe disability, 14with rates of persistent depend- ence estimated between 8–20% in population-based studies 10 9. !66% of those who have successful aneurysm clipping never return to the same quality of life asbefore the SAH 14,15 10. patients "70 yrs of age fare worse foreach neurologic grade. 5A multivariate analysis revealed age and WFNS grade to be most predictive of long-term outcome, regardless of treatmentmodality 16 11. the severity of clinical presentation is the strongest prognostic indicator 85.2 Etiologies of SAH Etiologies of subarachnoid hemorrhage (SAH) include 17: 1. trauma: the most common cause of SAH. 18,19 In all of the following discussion, only non- traumatic (i.e., “spontaneous ”) SAH will be considered 2.“spontaneous SAH ” a) ruptured intracranial aneurysms (p. 1454): 75–80% of spontaneous SAHs b) cerebral arteriovenous malformation (AVM): 4–5% of cases. AVMs more commonly cause ICH &IVH than SAH (p. 1505) c) certain vasculitides that involve the CNS, see Vasculitis and vasculopathy (p. 203)d)rarely due to tumor (many case reports 20,21,22,23,24,25,26,27,28,29,30,31 ) e) cerebral artery dissection (may also be posttraumatic)!carotid artery (p. 1578)!vertebral artery (p. 1579): may cause intraventricular blood (especially 4th and 3rdventricle) f)rupture of a small superficial arteryg)rupture of an infundibulum (p. 1423)h) coagulation disorders:!iatrogenic or bleeding dyscrasias!thrombocytopenia i)dural sinus thrombosisj)spinal AVM (p. 1395): usually cervical or upper thoracic k) cortical subarachnoid hemorrhagel) pretruncal nonaneurysmal SAH (p. 1496) (perimesencephalic hemorrhage)m) rarely reported with some drugs: e.g., cocaine (p. 215)n) sickle cell diseaseo) pituitary apoplexy (p. 865)p) no cause can be determined in 14 –22% (p. 1494) 85.3 Incidence of aneurysmal SAH (aSAH) Estimated annual rate of aSAH in the United States: 9.7 –14.5 per 100,000 population. 32,33 Reported rates are lower in South and Central America, 34and higher in Japan and Finland. 35Incidence of SAH increases with age (avg. age of onset > 50 33,36,37,38 ); tends to be higher in women (1.24 times higher than men), 34and appears to be higher in African Americans and Hispanics (compared to Cauca- sians). 32,39,40 85.4 Risk factors for aSAH See references. 17,41 1. behavioral!hypertension!cigarette smoking 42 !alcohol abuse Aneurysms –Introduction, Grading, Special Conditions 1417 85 https://ebooksmedicine.net/neurosurgery-book | 14.02.23 - 13:48 !sympathomimetic drugs such as cocaine (p. 215), amphetamines (including “crystal meth ”) !exercise/sports: weight training, 43especially when performed with valsalva maneuver, carries a low risk of precipitating bleeding from a pre-existing aneurysm 2. gender and race (see above)3. history of cerebral aneurysm!ruptured aneurysm!unruptured aneurysm (esp. those that are symptomatic, larger in size, and located in posteriorcirculation)!morphology: bottleneck shape 44and increased ratio of size of aneurysm to parent vessel have been associated with increased risk of rupture 45,46 4. family history of aneurysms (at least 1 first-degree family member and especially if "2 are a!ected) 5. genetic syndromes!autosomal dominant polycystic kidney disease (p. 1455)!type IVEhlers-Danlos syndrome 6. pregnancy: controversial. Studies have found evidence forincreased risk while others have not (p. 1425) 85.5 Clinical features 85.5.1 Symptoms of SAH Sudden onset of severe H/A (see below), usually with vomiting, syncope (apoplexy), neck pain (men-ingismus), and photophobia. If there is LOC, patient may subsequently recover consciousness. 47Focal cranial nerve deficits may occur (e.g., third nerve palsy from aneurysmal compression of the thirdcranial nerve, causing diplopia and/or ptosis). Low back pain may develop due to irritation of lumbar nerve roots by dependent blood. 85.5.2 Headache The most common symptom, present in up to 97% of cases. Usually severe (classic description: “the worst headache of my life”) and sudden in onset (paroxysmal). The H/A may clear and the patient may not seek medical attention (referred to as a sentinel hemorrhage or headache, or warning headache; they occur in 30 –60% of patients presenting with SAH). If severe or accompanied by reduced level of consciousness, most patients present for medical evaluation. Patients with H/A dueto minor hemorrhages will have blood on CTor LP. However, warning headaches may also occur without SAH and may be due to aneurysmal enlargement or to hemorrhage confined within theaneurysmal wall. 48Warning H/A are usually sudden in onset, milder than that associated with a major rupture, and may last a few days. Di!erential diagnosis of severe, acute, paroxysmal headache (25% will have SAH 49): 1. subarachnoid hemorrhage: including “warning headache ”or sentinel H/A (see above) 2. benign “thunderclap headaches ”(BTH) or crash migraine. 50Severe global headaches of abrupt onset that reach maximal intensity in < 1 minute, accompanied by vomiting in !50%. They may recur, and are presumably a form of vascular headache. Some may have transient focal symp- toms. There are no clinical criteria that can reliably di !erentiate these from SAH 51(although seiz - ures and diplopia, when they occurred, were always associated with SAH). There is nosubarachnoid blood on CTor LP (CT and/or CTA should probably be performed on at least the first presentation to R/O SAH). Earlier recommendations to angiogram these individuals 52have since been tempered by experience 53,54 3. reversible cerebral vasoconstrictive syndrome (RCVS) 55(AKA benign cerebral angiopathy or vas- culitis 56): severe H/A with paroxysmal onset, ± neurologic deficit, and string-of-beads appearance on angiography of cerebral vessels that usually clears in 1–3 months. More than 50% report prior use of vasoconstrictive substances (cocaine, marijuana, nasal decongestants, ergot derivatives,SSRIs, interferon, nicotine patches) sometimes combined with binge drinking. May also occurpost-partum. Complications occurred in 24% including:a) usually during the 1st week: SAH, ICH, seizures, RPLS b) usually during the 2nd week: ischemic events (TIA, stroke)4. airplane headache: usually sudden, often (but not exclusively) with onset during take-o !(less common) or landing of aircraft. Short-lasting (by definition: #30 minutes after completion of ascent or descent 57; however, in one series 76% of H/A otherwise typical forairplane H/A lasted > 30 minutes 58), usually unilateral, primarily orbitofrontal (occasionally with spread to parietal Subarachnoid Hemorrhage and Aneurysms 1418 85 https://ebooksmedicine.net/neurosurgery-book | 14.02.23 - 13:48 region). Typically jabbing or stabbing in quality. Ipsilateral nasal congestion, a stu !y feeling of the face, or tearing may occur in < 5%. 57Pathogenesis may be related to obstructed drainage of sinuses (“aerosinusitis ”or barosinusitis); however, a vascular mechanism may be possible. H/A may respond to triptans (19%) or acetaminophen (5%). 58 5.benign orgasmic cephalgia : a severe, throbbing, sometimes “explosive ”H/A with onset just before or at the time of orgasm (distinct from pre-orgasmic headaches which intensify with sex-ual arousal 59). In a series of 21 patients 60neurologic exam was normal in all, and angiography done in 9 was normal. 9 had a history of migraine in the patient or a family member. No other symptoms developed in 18 patients followed for2–7 yrs. Recommendations for evaluation are similar to that forthunderclap headaches above 85.5.3 Signs Meningismus (see below), hypertension, focal neurologic deficit (e.g., oculomotor palsy, hemipare-sis), obtundation or coma (see below), ocular hemorrhage (see below). Meningismus Nuchal rigidity (especially to f lexion) often ensues in 6 to 24 hrs. Patients may have a positive Kernigsign (f lex thigh to 90° with knee bent, then straighten knee, positive sign if this causes pain in ham-strings) or Brudzinski sign (f lex the supine patient ’s neck, involuntary hip f lexion is a positive sign). Coma following SAH Coma may follow SAH because of any one or a combination of the following 61: 1. increased ICP2. damage to brain tissue from intraparenchymal hemorrhage (may also contribute to increasedICP)3. hydrocephalus4. di !use ischemia (may be secondary to increased ICP) 5. seizure6. reduced CBF (p. 1438) low blood f low (e.g., due to reduced cardiac output) Ocular hemorrhage Three types of ocular hemorrhage (OH) may be associated with SAH. They occur alone or in variouscombinations in 20 –40% of patients with SAH. 62 1. subhyaloid (preretinal) hemorrhage: seen funduscopically in 11 –33% of cases as bright red blood near the optic disc that obscures the underlying retinal vessels. May be associated with a highermortality rate 63 2. (intra)retinal hemorrhage: may surround the fovea3. hemorrhage within the vitreous humor (Terson syndrome). First described by the French oph-thalmologist Albert Terson. Occurs in 4–27% of cases of aneurysmal SAH, 64,65,66 usually bilateral. May occur with other causes of increased ICP including ruptured AVMs. Funduscopy reveals vit-reous opacity. The location of the origin of the vitreous hemorrhage di !ers in various reports (subhyaloid, epiretinal, subinternal limiting membrane). 67May be more common with anterior circulation aneurysms (especially ACoA), although 1 study found no correlation with location. 65 Also rarely reported with SDH and traumatic SAH. Often missed on initial examination. Whensought, usually present on initial exam; however, it may develop as late as 12 days post SAH, andmay be associated with rebleeding. 65The mortality rate may be higher in SAH patients with vit- reous hemorrhage than in those without. Patients should be followed forcomplications of OH (elevated intraocular pressure, retinal membrane formation !retinal detachment, retinal folds 68). Most cases clear spontaneously in 6–12 mos. Vitrectomy should be considered in patients whose vision fails to improve 66or if more rapid improvement is desired. 69The long-term prognosis for vision is good in !80% of cases with or without vitrectomy 69 The pathomechanics of OH are controversial. OH was originally attributed to extension of the blood from the subarachnoid space into the vitreous, but no communication exists between these two spaces. In actuality may be due to compression of the central retinal vein and the retinochoroidalanastomoses by elevated CSF pressure, 66causing venous hypertension and disruption of retinal veins. Aneurysms –Introduction, Grading, Special Conditions 1419 85 https://ebooksmedicine.net/neurosurgery-book