Aneurysms - Introduction, Grading, Special Conditions

| 14.02.23 - 13:48 XVII Part XVII Subarachnoid Hemorrhage and Aneurysms 85 Aneurysms –Introduction, Grading, Special Conditions 1416 86 Critical Care of Aneurysm Patients 1432 87 SAH from Cerebral Aneurysm Rupture 1453 88 Aneurysm Type by Location 1473 89 Special Aneurysms and Non- Aneu...

| 14.02.23 - 13:48 XVII Part XVII Subarachnoid Hemorrhage and Aneurysms 85 Aneurysms –Introduction, Grading, Special Conditions 1416 86 Critical Care of Aneurysm Patients 1432 87 SAH from Cerebral Aneurysm Rupture 1453 88 Aneurysm Type by Location 1473 89 Special Aneurysms and Non- Aneurysmal SAH 1486 https://ebooksmedicine.net/neurosurgery-book | 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 | 14.02.23 - 13:48 85.6 Work-up of suspected SAH 85.6.1 Overview 1. tests to diagnose SAHa) non-contrast high-resolution CTscan: very sensitive and specific (see below) b) if CTis negative: LP in suspicious cases. Very sensitive, but only 65 –80% specific (see below) c) with CT, the concern is a false negative test (missing a SAH), and with LP the concern is a false positive (a bloody tap mimicking a SAH). However, the combination of a negative CTand a negative LP is extremely strong in ruling out SAH 70 2. tests to identify source of SAH. Options: CTA, MRA, or catheter angiography. The choice needs to take into account the patient ’s age, renal function, and even best guess of where an aneurysm might be locateda) MRA (p. 243). Pros: no radiation, and 2D-TOF MRA does not use contrast. Cons: poor sensitiv-ity for aneurysm detection early after SAH (see below)b)CTA vs. digital subtraction catheter angiogram (DSA): one needs to balance the risk of the pro - cedure and ease of obtaining it against the information expected to be obtained!total iodine load in a healthy adult should be < 90 gm in 24 hours. In older patients and/orpossible compromised renal function, this volume should be less. CTA typically uses 65 –75 cc of contrast with !300 mg iodine/ml, or !21 gm iodine. The amount of contrast with a cerebral arteriogram varies. However, if an angiogram is needed after a CTA, in most casesyou do not have to wait 24 hours !if there is concern about renal function (e.g., serum creatinine > 100 mcmol/L) hydrate thepatient and optionally give Mucomyst® (p. 232)!catheter angiography (DSA) may be necessary after a positive CTA to better delineate the anatomy, or to determine dominant filling and cross flow, or in highly suspicious cases with a negative CTA (see below). While CTA permits reliable assessment of feasibility of endovas- cular treatment in most cases, 71DSA is still necessary in some 3. if CTA/angiogram is negative: see SAH of unknown etiology (p. 1494) 85.6.2 Laboratory/radiographic findings CT scan "Sensitivity and specificity. High-quality non-contrast CT(no motion artifact, 3rd generation or newer high-resolution CTscanner) is very sensitive to intracranial SAH. Sensitivity decreases with time as the blood dissipates.!within 6 hrs of SAH: sensitivity is 98 –100%, specificity 100%, negative predictive value 99.4%, pos- itive predictive value 100% (in240 adults with new acute H/A peaking in #1 hr 72) !sensitivity of CT< 12 hrs after SAH: !98% !after 12 hrs, the sensitivity is too low to rely on noncontrast CTalone to exclude the potentially lethal diagnosis of ruptured aneurysm. But it can be helpful if positive#sensitivity of CT< 24 hrs of SAH: !93% #CT< 72 hrs of SAH: !80% #CT1 week after SAH: !50% "Findings. Blood appears as high density (white) within subarachnoid spaces ("Fig. 85.1). Subtle hints for SAH: look for blood in the occipital horns of the lateral ventricles and the dependent por-tions of the Sylvian fissures.CTalso assesses: 1. ventricular size: acute hydrocephalus after aneurysmal rupture (p. 1426) occurs in 21% 73 2. hematoma: intracerebral hemorrhage or large amount of subdural blood with mass e!ect may need emergent evacuation (most common with MCA aneurysms)3. amount of blood in cisterns and fissures: important prognosticator for vasospasm (p. 1441) andcan identify pretruncal nonaneurysmal hemorrhage (p. 1496)4.CTcan predict aneurysm location based on the pattern of blood in !78% of cases (but mostly for MCA and AComA aneurysms) 74 a) blood predominantly in anterior interhemispheric fissure (± blood in lateral ventricles)("Fig. 88.1) or within the gyrus rectus suggests AComA aneurysm b) blood predominantly in 1 Sylvian fissure is compatible with PComA or MCA aneurysm on thatside ("Fig. 85.1) c) blood predominantly in the prepontine or peduncular cistern suggests a basilar apex or SCAaneurysm Subarachnoid Hemorrhage and Aneurysms 1420 85 https://ebooksmedicine.net/neurosurgery-book | 14.02.23 - 13:48 d)blood predominantly within ventricles (p. 1454)!blood primarily in 4th and 3rd ventricle ("Fig. 88.2): suggests lower posterior fossa source, such as PICA aneurysm (p. 1480) or VAdissection !blood primarily in the 3rd ventricle suggests a basilar apex aneurysm 5. with multiple aneurysms, CTmay help identify which one bled by the location of blood (see above). See also other “clues ”(p. 1490) 6.!CTis not sensitive for infarct in the first 24 hours after infarct (see CTscan with acute ischemic infarct (p. 1559))"Di!erential diagnosis of SAH on CT. Things that can mimic the appearance of SAH on CTinclude: 1. pus: as in meningitis2. following contrast administration: sometimes IV, and especially intrathecal3. occasionally the pachymeningeal thickening seen in spontaneous intracranial hypotension(p. 421) CT angiography (CTA) CTA (p. 238), a 64-slice CTA is 98% sensitive and 100% specific for detecting aneurysms > 3 mm diam- eter, 75and in a prospective study detected 97% of aneurysms, and was deemed as safe and e!ective when used as the initial and sole imaging study for ruptured and unruptured cerebral aneurysms. 76 CTA shows a 3-dimensional image (as can modern catheter angiography), which can help di !erenti- ate adherent vessels from those arising from the aneurysm. CTA also demonstrates the relation to nearby bony structures which can be important in surgical planning. CTA may also be used for eval- uation of vasospasm. 77 Lumbar puncture The most sensitive test forSAH, approaching 100%, with a negative predictive value of 100% for SAH. However, false positives —e.g., with traumatic taps (Di !erentiating SAH from traumatic tap (p. 1814)) —occur with enough frequency that the specificity may be in the range of 80% 78and possibly as low as 65%. 75Skipping the LP and going right to CTA is controversial with arguments both for79and against. 80The LP is more helpful to rule-out SAH if CSF has no blood. sf ssc V4 th th iph ipc ac ihf B A Fig. 85.1 SAH on CT. Image: axial CTscan in patient with SAH (and intraparenchymal hematoma) from a ruptured right middle cerebral artery aneurysm.Image: A: CTslice through the suprasellar cistern (ssc) showing a classic SAH pattern, with blood in the ssc, interhe- mispheric fissure (ihf) & Sylvian fissures (sf).B:CTslice slightly above the ssc showing SAH in the interpeduncular cistern (ipc), the ambient cisterns (ac) as well as intraparenchymal hematoma (iph) from the aneurysmal rupture.Note the dilated temporal horns (th) suggesting early hydrocephalus and blood in the 4th ventricle (V4). Aneurysms –Introduction, Grading, Special Conditions 1421 85 https://ebooksmedicine.net/neurosurgery-book | 14.02.23 - 13:48 !Caution: lowering the CSF pressure with an LP may possibly precipitate rebleeding by increas- ing the transmural pressure (p. 1427) (the pressure across the aneurysm wall). Therefore removeonly a small amount of CSF (several ml) and use a small (#20 Ga) spinal needle. Findings (also, see "Table 23.4): 1. opening pressure: usually elevated with SAH2. appearance:a) non-clotting bloody f luid that does not clear with sequential collection tubesb) xanthochromia (XTC): yellow coloration ("Fig. 85.2) of CSF supernatant due to the lysis of RBCs which releases heme pigments that break down to bilirubin. XTC is the most reliable means of di !erentiating traumatic tap from SAH in patients with a negative head CT. The minimum amount of time required forbilirubin to become detectable in the CSF, as well as the minimum amount of blood that needs to enter the CSF to produce XTC remains unknown. XTC is usually not apparent until 2–4 hours after the SAH. It is present in almost 100% by 12 hours after the bleed, and remains in 70% at 3 weeks, and is still detectable in 40% at 4 weeks.False positives: XTC may occur with jaundice or high protein levels in the CSF. Very bloody specimens may need to be centrifuged in the lab to be able to look for XTC. Spec- trophotometry is more sensitive than visual inspection, but may not be specific enough towarrant widespread use 81,82 3. cell count: RBC count is usually > 100,000 RBCs/mm 3in SAH 4. compare RBC count in first to last tube: a reduction of RBC count from the first tube to the last tube of 70% with < 500 RBC/mm 3in the final tube has been suggested to be diagnostic of a trau- matic tap 83(controversial (p. 1814)) 5. protein: elevated due to blood breakdown products6. glucose: normal or reduced (RBCs may metabolize some glucose with time) MRI Not sensitive for SAH acutely within the first 24 –48 hrs 84(too little met-Hb), especially with thin layers of blood. Better after !4–7 days (excellent for subacute to remote SAH, > 10 –20 days). FLAIR MRI is the most sensitive imaging study for detecting blood in the subarachnoid space. May be help - fulin determining which of multiple aneurysms bled (p. 1490). 85 Magnetic resonance angiography (MRA) Compared to catheter DSA, sensitivity is 87% and specificity is 92% for detecting intracranial aneur- ysms (IAs). Sensitivity is significantly worse for aneurysms < 3 mm diameter. 86,87,88 MRA ’s ability to detect IAs depends on aneurysm size, rate and direction of blood f low in the aneurysm relative to the magnetic field, and aneurysmal thrombosis and calcification. MRA may bemost useful as a screening test in high-risk patients, including patients with two first-degree rela- tives with IAs, especially those who are also smokers or hypertensive themselves. 89 A B Fig. 85.2 Xanthochromic CSF inA,compared to normal CSF in B. Subarachnoid Hemorrhage and Aneurysms 1422 85 https://ebooksmedicine.net/neurosurgery-book | 14.02.23 - 13:48 Catheter angiogram General informationInjection of radio-opaque (iodinated) contrast (“dye ”) into selective vessels using a catheter typically inserted into the femoral artery at the upper thigh, while taking serial X-rays to obtain a “video-like ” representation of the vasculature.The gold standard for evaluation of cerebral aneurysms. Current state of the art uses digital sub - traction angiography (DSA). Demonstrates source (usually aneurysm) in !80–85%; remainder are so-called “SAH of unknown etiology ”(p. 1494). Shows if radiographic vasospasm is present —clinical vasospasm (p. 1439) almost never occurs < 3 days following SAH —and assesses primary feeding arteries, collateral f low in case of a need for arterial sacrifice. General principles:1. study the vessel of highest suspicion first (incase patient ’s condition should change, necessitating discontinuation of procedure)2. continue to do complete 4-vessel angiogram (even if aneurysm(s) have been demonstrated) torule out additional aneurysms and assess collateral circulation3. if there is an aneurysm or suspicion of one, obtain additional views to help delineate the neckand orientation of the aneurysm (see index forspecific aneurysm) 4. !if no aneurysm is seen, before an arteriogram can be considered negative, must:a) visualize both PICA origins :1–2% of aneurysms occur at PICA origin. Both PICAs can usually be visualized with one VAinjection if there is enough flow to ref lux down the contralateral VA . Occasionally it is necessary to see more of the contralateral VAthan what ref luxes to PICA and selective catheterization may be requiredb)flow contrast through the ACoA :ifboth ACAs fillfrom one side, this isusually satisfactory. Itmay be necessary toperform across compression AP study with carotid injection (first, rule out plaque in the carotid to becompressed), oruse ahigher injection rate tofacilitate flow through the ACoA c) if an infundibulum (see below) co-localizes to the SAH, it may be unwise to label the case asangiogram-negative, and exploration is recommended by some 90 InfundibulumA funnel-shaped initial segment of an artery, to be distinguished from an aneurysm. Found in 7–13% of otherwise normal arteriograms, 91,92 with a higher incidence in cases of multiple or familial aneur- ysms. Bilateral in 25%. 92Most commonly found at the origin of the PComAs, but they rarely occur at other sites. Criteria fordi!erentiating infundibula from aneurysms are shown in "Table 85.1. Infun- dibula may represent incomplete remnants of previous fetal vessels. 93(p272) Although they may bleed, 90,95,96,97 there is less risk of rupture than with a saccular aneurysm (no infundibulum < 3 mm in size bled 98in the cooperative study). However, infundibula have been docu- mented to progress to an aneurysm (i.e., they are preaneurysmal) which may bleed (13 case reportsin the literature as of 2009). Recommended treatment: at the time of surgery for another reason,consider treating an infundibulum with wrapping, or placing in an encircling clip, or sacrificing theartery if it can be done safely (infundibula lack a true neck). Angiographic findings1. general features to take note of when analyzing an aneurysm on angiogram (special considera-tions for specific aneurysms are covered in designated sections)a) size of aneurysm dome:!MRI or CThelps with this since the aneurysm may be partially thrombosed and the portion that is patent and fills with contrast and is therefore visualized on angiogram may be muchsmaller than the actual size!large aneurysms ("15 mm dia.) are associated with lower rates of complete occlusion by endovascular coiling 99,100 b) neck size!narrow necks < 5 mm are ideal forcoiling 101 Table 85.1 Criteria of an infundibulum 1. triangular in shape2. mouth (widest portion) < 3 mm a 94 3. vessel at apexaa widely accepted but probably arbitrary dimension Aneurysms –Introduction, Grading, Special Conditions 1423 85 https://ebooksmedicine.net/neurosurgery-book | 14.02.23 - 13:48 !broad necks "5 mm are associated with increased risk of incomplete occlusion and recanal- ization with coiling 100 !stent or balloon-assisted coiling may be needed for wide-necked aneurysms. Stents shouldbe avoided if possible (p. 1923) c) dome:neck ratio "2 is associated with higher rate of successful coil occlusion 101 2.forbasilar bifurcation aneurysms (p. 1482) 85.7 Grading SAH 85.7.1 General information Four grading scales are in common use. The two most widely quoted grading scales, the Hunt-and- Hess and the WFNS, are presented below. 85.7.2 Hunt and Hess grade See "Table 85.2 and "Table 85.3 forgrading system. Grades 1 and 2 were operated upon as soon as an aneurysm was diagnosed. Grade "3 managed until the condition improved to Grade 2 or 1. Exception: life-threatening hematoma or multiple bleeds (which were operated on regardless ofgrade).Analysis of data from the International Cooperative Aneurysm Study revealed that with normalconsciousness, Hunt and Hess (H&H) grades 1 and 2 had identical outcome, and that hemiparesisand/or aphasia had no e!ect on mortality. Mortality:Admission Hunt and Hess Grade 1 or 2: 20%.Patients taken to O.R. (for any procedure) at H&H Grade 1 or 2: 14%. Major cause of death in Grade 1 or 2 is rebleed.Signs of meningeal irritation increases surgical risk. 85.7.3 World Federation of Neurosurgical Societies / World Federation of Neurological Surgeons (WFNS) grading of SAH Due to lack of data on the significance of features such as headache, nuchal rigidity, and major focalneurologic deficit, the WFNS Committee on a Universal SAH Grading Scale 104,105 developed the grad- ing system shown in "Table 85.4. It employs the Glasgow Coma Scale ("Table 18.1) (GCS) to grade the level of consciousness, and uses the presence or absence of major focal neurologic deficit to dis-tinguish grade 2 from grade 3. Table 85.2 Hunt and Hess classification aof SAH 102 Grade Description 1 asymptomatic, or mild H/A and slight nuchal rigidity 2 Cr. N. palsy (e.g., III, VI), moderate to severe H/A, nuchal rigidity 3 mild focal deficit, lethargy, or confusion 4 stupor, moderate to severe hemiparesis, early decerebrate rigidity 5 deep coma, decerebrate rigidity, moribund appearance Add one grade for serious systemic disease (e.g., HTN, DM, severe atherosclerosis, COPD) or severe vasospasmon arteriography.aoriginal paper did not consider patient ’s age, site of aneurysm, or time since bleed; patients were graded on admission and pre-op Table 85.3 Modified classification 103adds the following Grade Description 0 unruptured aneurysm 1a no acute meningeal/brain reaction, but with fixed neuro deficit Subarachnoid Hemorrhage and Aneurysms 1424 85 https://ebooksmedicine.net/neurosurgery-book | 14.02.23 - 13:48 85.8 Pregnancy and intracranial hemorrhage 85.8.1 General information Intracranial hemorrhage (subarachnoid or intraparenchymal) is a rare occurrence during pregnancy(estimated range of incidence: 0.01 –0.05% of all pregnancies 106) and yet is responsible for 5–12% of maternal deaths during pregnancy.Intracranial hemorrhage of pregnancy (ICHOP) commonly occurs in the setting of eclampsia, andis more commonly intraparenchymal 107and may be associated with loss of cerebrovascular autore- gulation PRES (p. 202). 108 HELLP syndrome (hemolysis, elevated liver enzymes, and low platelet count) is a severe variant of pre-eclampsia. 109Symptoms of eclampsia with or without ICHOP include H/A, mental status changes, and seizures.It has been asserted that risk of aneurysmal SAH does not appear to be increased in pregnancy,delivery, and puerperium. 110,111 A literature review of 154 reported cases of ICHOP-related SAH revealed that 77% were aneurysmal and 23% were from ruptured AVM (other series show the per- centage of AVMs range from 21 –48%). Mortality is !35% for aneurysmal and !28% for AVM hemor- rhage (the latter being higher than in non-gravid patients). There is an increasing tendency for bleeding with advancing gestational age for both aneurysms and AVMs (earlier it had been assertedthat this held true foraneurysms only 112). Patients with ICHOP having AVMs tend to be younger than those with aneurysm, paralleling theoccurrence in the general population. One major oft-quoted study showed an increased risk of hem-orrhage from AVMs during pregnancy 113(citing an 87% hemorrhage rate); however, another investi - gation disputes this assertion, 114and found the risk of hemorrhage to be 3.5% during the pregnancy in patients with no history of hemorrhage, or 5.8% in those with previous hemorrhage. Anotherstudy evaluated risk of aneurysm rupture during pregnancy and delivery from the Nationwide Inpa- tient data and calculated the rupture risk during pregnancy and delivery to be 1.4% and 0.05%, respectively. 115 Literature review 106 found that the risk of recurrent hemorrhage following ICHOP from aneurysm or AVM during the remainder of the pregnancy was 33–50%. 85.8.2 Management modifications for pregnant patients Modifications of evaluation and treatment techniques may be necessary forthe pregnant patient. 1. neuroradiologic studiesa)CAT scan: with shielding of the fetus, CAT scanning of the brain produces minimal radiation exposure to the childb) MRI:!generally felt to have low potential forcomplications; however, many centers will not do MRI during first trimester.!gadolinium-based contrast agents (GBCAs) are teratogenic in animals in high repeateddoses. It has not been studied in human pregnancy. A cohort of 26 women who receivedGBCAs during the first trimester showed no evidence of teratogenicity or mutagenicity. 116 There have also been no reported issues related to nephrogenic systemic fibrosis (p. 243).GBCAs are FDA Class C drugs —not recommended foruse during pregnancy, but may be used if benefits outweigh potential risks. c)angiography: with shielding ofthe fetus, radiation exposure is minimal. Iodinated contrast agents pose little risk tothe fetus. The mother should bewell hydrated during and after the study 106 Table 85.4 WFNS SAH grade 104 WFNS grade GCS score a Major focal deficit b 0c 1 15 – 2 13–14 – 3 13–14 + 4 7–12 + or – 5 3–6 + or – aGCS = Glasgow Coma Scale, see !Table 18.1 baphasia, hemiparesis or hemiplegia (+ = present, –= absent) cintact (unruptured) aneurysm Aneurysms –Introduction, Grading, Special Conditions 1425 85 https://ebooksmedicine.net/neurosurgery-book | 14.02.23 - 13:48 2. antiseizure medications: see Pregnancy and antiseizure medications (p. 500)3. diuretics: the use of mannitol in pregnancy should be avoided to prevent fetal dehydration andmaternal hypovolemia with uterine hypoperfusion4. antihypertensives: nitroprusside should not be used in pregnancy5. nimodipine is potentially teratogenic in animals, the e!ect on humans is unknown. It should be used only when the potential benefit justifies the risk 85.8.3 Neurosurgical management The currently recommended treatment of a ruptured aneurysm in the pregnant patient is immediatesurgical treatment to avoid rebleeding and ischemic complications due tovasospasm. A meta-analysis has demonstrated that mother and fetus both benefit from surgical treatment —with maternal mortal - ity decreasing from 63% to11% and fetal mortality decreasing from 27% to 5%. 106,117 Successful endo- vascular treatment for aSAH has been reported, but fetal exposure to radiation is a concern. The absorbed fetal dose has been estimated to range from 0.17 to2.8 mGy, corresponding toafetal risk of a hereditary disease atbirth and a cumulative risk fora fatal cancer byage 15, which are both substan - tially lower than those which naturally occur. 118Because endovascular treatment requires heparin for systemic anticoagulation, it carries the risk of hemorrhagic implications when labor spontaneouslybegins during or around the time of embolization. 85.8.4 Obstetric management following ICHOP Several reports have indicated that the fetal and maternal outcome is no di !erent for vaginal deliv - ery vs. C-section, and is probably more dependent on whether the o!ending lesion has been treated. However, there are no formal studies to help guide the optimal treatment of pregnant women withaSAH. One strategy 117is to perform an emergent C-section, followed by aneurysm treatment, if the fetus is mature enough for survival outside the uterus. If the fetus is < 24 weeks, treat the aneurysmand maintain the pregnancy. If the fetus is between 24 –28 weeks, a strategy should be tailored according to the maternal and fetal status. C-section may be used for fetal salvage for a moribund mother in the third trimester. During vaginal delivery, the risk of rebleeding may be reduced by theuse of caudal or epidural anesthesia, shortening the second stage of labor, and low forceps delivery ifnecessary. 85.9 Hydrocephalus after SAH 85.9.1 Hydrocephalus after traumatic SAH See also posttraumatic hydrocephalus (p. 1108). 85.9.2 Acute hydrocephalus General information The frequency of hydrocephalus (HCP) on the initial CTafter SAH depends on the defining criteria used, with a reported range of 9–67%. 119A realistic range is !15–20% of SAH patients, with 30 –60% of these showing no impairment of consciousness. 119,120 3% of those without HCP on initial CT develop HCP within 1 week. 119 Factors felt to contribute to acute HCP include blood interfering with CSF f low through the Sylvian aqueduct, 4th ventricle outlet, or subarachnoid space, and/or with reabsorption at the arachnoidgranulations.Findings associated with acute HCP include 120 1. increasing age2. admission CTfindings: intraventricular blood, di !use subarachnoid blood, and thick focal accu- mulation of subarachnoid blood (intraparenchymal blood did not correlate with chronic HCP, and patients with a normal CThad a low incidence) 3. hypertension: on admission, prior to admission (by history), or post-op4. by location:a) posterior circulation aneurysms have a higher incidence of HCPb) MCA aneurysms correlate with low incidence of HCP5. miscellaneous: hyponatremia, patients who were not alert on admission, use of preoperativeantifibrinolytic agents, and low Glasgow outcome score Subarachnoid Hemorrhage and Aneurysms 1426 85 https://ebooksmedicine.net/neurosurgery-book | 14.02.23 - 13:48 Treatment About half the patients with acute HCP and impaired consciousness improved spontaneously. 119 Patients in poor grade (H&H IV –V) with large ventricles may be symptomatic from the HCP and con- sideration should be given to ventriculostomy which caused improvement in !80% of patients in whom it was used. 119 There may be an increased risk of aneurysmal rebleeding in patients under- going ventriculostomy shortly after SAH 119,121,122 especially if performed early and if ICP is lowered precipitously. The risk of aneurysm rebleeding with EVD has been studied in retrospective case ser-ies with mixed results. 123,124,125 The mechanism is controversial, but may be due to an increase in the transmural pressure (the pressure across the aneurysm wall which equals the di !erence between arterial pressure and ICP).When a ventriculostomy is used, it is recommended to keep ICP in the range of 15 –25 mm Hg 126 and to avoid rapid pressure reduction (unless absolutely necessary) to decrease the risk of IVC- induced aneurysmal rebleeding. One paradigm is to keep the EVD open with the drip chamber noz - zle 15 –20 cm above the tragus. Practice guideline: Acute hydrocephalus associated with aSAH Level B 41: CSF diversion (EVD or lumbar drain) for acute symptomatic hydrocephalus associated with aSAH. 85.9.3 Chronic hydrocephalus Practice guideline: Chronic hydrocephalus associated with aSAH "Level B 41: permanent CSF diversion (shunt) for symptomatic chronic hydrocephalus following aSAH."Level C 41: Weaning an EVD over > 24 hours does not appear to reduce the need for permanent CSF diversion."Level C 41: Routine fenestration of the lamina terminalis is not recommended as it does not reduce the need for permanent CSF diversion. Chronic hydrocephalus (chronic HCP) is due to pia-arachnoid adhesions or permanent impairmentof the arachnoid granulations. Acute HCP does not inevitably lead to chronic HCP. 8–45% (reported range 127) of all ruptured aneurysm patients, and !50% of those with acute HCP following SAH need permanent CSF diversion. A number of studies have attempted to identify factors predictive ofaSAH-associated shunt-dependent chronic hydrocephalus. Intraventricular blood increases thisrisk. 127There is controversy as to whether the use of ventriculostomy for acute HCP increases 128or possibly even decreases 127the incidence of shunt dependency. There may be a positive association between Fisher grade and the likelihood of requiring CSF diversion for chronic hydrocephalus. 129In addition, Hoh et al 130found age (2% increase/year), comorbidity score (presence of DM, HTN, or alco - hol abuse), admission type, insurance type (increased with Medicaid and private payer), and hospitalaneurysm volume (high > low) to be predictive of shunt placement in ruptured aneurysm patients.Treatment type (clip versus coil) has also been studied with no clear advantage for one modalityover the other (p. 1457).The method of determining which patients require shunt placement has also been studied in asingle center RCT. 131 There was no di !erence in the rate of shunt placement between those who underwent rapid weaning (< 24 hrs) versus gradual weaning (96 hrs) of the EVD (63.4% rapid versus62.5% gradual). References [1] Biller J, To!ol GJ, Kassell NF, et al. Spontaneous Subarachnoid Hemorrhage in Young Adults. Neu-rosurgery. 1987; 21:664 –667 [2] Okawara SH. Warning Signs Prior to Rupture of an Intracranial Aneurysm. Journal of Neurosurgery.1973; 38:575 –580 Aneurysms –Introduction, Grading, Special Conditions 1427 85 https://ebooksmedicine.net/neurosurgery-book