Handbook of Neurosurgery 7th Ed

30. SAH and aneurysms

30.1. Introduction to SAH

Etiologies

Etiologies of subarachnoid hemorrhage (SAH) include¹:

• trauma: the most common cause of SAH^{2, 3}

• “spontaneous SAH”

A. ruptured intracranial aneurysms: 75-80% of spontaneous SAHs (see page 1055)

B. cerebral arteriovenous malformation (AVM): 4-5% of cases (AVMs more commonly cause ICH & IVH than SAH - see page 1099)

C. certain vasculitides that involve the CNS (see Vasculitis and vasculopathy, page 74)

D. rarely due to tumor (many case reports^4-15)

E. cerebral artery dissection (may also be post-traumatic)

• carotid artery: see page 1162

• vertebral artery: may cause intraventricular blood (especially 4th and third ventricle), see page 1163

F. rupture of a small superficial artery

G. rupture of an infundibulum (see page 1039)

H. coagulation disorders:

• iatrogenic or bleeding dyscrasias

• thrombocytopenia

I. dural sinus thrombosis

J. spinal AVM: usually cervical or upper thoracic (see page 507)

K. pretruncal nonaneurysmal SAH: see page 1085

L. rarely reported with some drugs: e.g. cocaine (see page 276)

M. sickle cell anemia

N. pituitary apoplexy: see page 635

O. no cause can be determined in 14-22% (see SAH of unknown etiology, page 1083)

Incidence

Estimated annual rate of aneurysmal SAH in most western populations: 6-8 per 100,000 population^{16, 17}.

Outcome of aneurysmal SAH

• 10-15% of patients die before reaching medical care

• mortality is 10% within first few days

• 30-day mortality rate was 46% in one series¹⁶, and in others over half the patients died within 2 weeks of their SAH¹⁸

• overall mortality is ≈ 45% (range: 32-67%)¹⁹

• causes of mortality

25% die as a result of medical complications of SAH²⁰

• neurogenic pulmonary edema: see page 28

• neurogenic stunned myocardium: see page 1054

about 8% die from progressive deterioration from the initial hemorrhage^{21 (p 27)}

• among patients surviving the initial hemorrhage treated without surgery, rebleeding is the major cause of morbidity and mortality (see page 1043), the risk is ≈ 15-20% within 2 weeks. The goal of early surgery (see Timing of aneurysm surgery, page 1060) is to reduce this risk

• of those reaching neurosurgical care, vasospasm (see page 1045) kills 7%, and causes severe deficit in another 7%²²

• about ≈ 30% of survivors have moderate to severe disability¹⁹

• ≈ 66% of those who have successful aneurysm clipping never return to the same quality of life as before the SAH^{19, 23}

• patients ≥ 70 yrs age fare worse for each neurologic grade²⁴

Miscellaneous facts about SAH

• peak age for aneurysmal SAH is 55-60 years, ≈ 20% of cases occur between ages 15-45 yrs²⁵

• 30% of aneurysmal SAHs occurs during sleep

• 50% of patients with aneurysms have warning symptoms, usually 6-20 days before SAH²⁶ (see Presentation other than major rupture, page 1056)

• headache is lateralized in 30%, most to the side of the aneurysm

• SAH is complicated by intracerebral hemorrhage in 20-40%, by intraventricular hemorrhage in 13-28% (see page 1056), and by subdural blood in 2-5% (usually due to p-comm aneurysm when over convexity, or distal anterior intracerebral artery (DACA) aneurysm with interhemispheric subdural (see page 1068))

• soft evidence suggests that rupture incidence is higher in spring and autumn

• patients ≥ 70 yrs age have a higher proportion with a severe neurologic grade²⁴

Risk factors for SAH¹

• hypertension

• oral contraceptives

• substance abuse

cigarette smoking²⁷

following cocaine abuse: see page 276

alcohol consumption²⁸: controversial²⁹

• diurnal variations in blood pressure³⁰

• pregnancy and parturition (see Pregnancy & intracranial hemorrhage, page 1086)

• slight increased risk during lumbar puncture and/or cerebral angiography in patient with cerebral aneurysm

• slight increased risk with advancing age¹⁶

• conditions with an increased incidence of cerebral aneurysms (see page 1057)

CLINICAL FEATURES

SYMPTOMS OF SAH

Sudden onset of severe H/A (see below), usually with vomiting, syncope (apoplexy), neck pain (meningismus), and photophobia. If there is LOC, patient may subsequently recover consciousness³¹. Focal cranial nerve deficits may occur (e.g. third nerve palsy from aneurysmal compression, causing diplopia and/or ptosis). Low back pain may develop due to irritation of lumbar nerve roots by dependent blood.

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. They 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 due to minor hemorrhages will have blood on CT or LP. However, warning headaches may also occur without SAH and may be due to aneurysmal enlargement or to hemorrhage confined within the aneurysmal wall³². Warning H/A are usually sudden in onset, severe, and clear within 1 day.

Differential diagnosis of severe, acute, paroxysmal headache (25% will have SAH³³):

1. subarachnoid hemorrhage, AKA “warning headache” or sentinel H/A (see above)

2. benign “thunderclap headaches” (BTH) or crash migraine³⁴. Severe 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 symptoms. There are no clinical criteria that can reliably differentiate these from SAH³⁵. There is no subarachnoid blood on CT and LP, which should probably be performed on at least the first presentation to R/O SAH. Earlier recommendations to angiogram these individuals³⁶ have since been tempered by experience^{37, 38}

3. reversible cerebral vasoconstrictive syndrome (RCVS)³⁹ (AKA benign cerebral angiopathy or vasculitis⁴⁰): 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. > 50% report prior use of vasoconstrictive substances (cocaine, marijuana, nasal decongestants, ergot derivatives, SSRIs, interferon, nicotine patches) sometimes combined with binge drinking. May also occur post-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, CVA)

4. 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 sexual arousal⁴¹). In a series of 21 patients⁴² neurologic 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 for 2-7 yrs. Recommendations for evaluation are similar to that for thunderclap headaches above

SIGNS

Meningismus (see below), hypertension, focal neurologic deficit (e.g. oculomotor palsy, hemiparesis), obtundation or coma (see below), ocular hemorrhage (see below).

Meningismus

Nuchal rigidity (especially to flexion) often ensues in 6 to 24 hrs. Patients may have a positive Kernig sign (flex thigh to 90° with knee bent, then straighten knee, positive sign if this causes pain in hamstrings) or Brudzinski sign (flex patient’s neck, involuntary hip flexion is a positive sign).

Coma following SAH

Coma may follow SAH because of any one or a combination of the following⁴³:

1. increased ICP

2. damage to brain tissue from intraparenchymal hemorrhage (may also contribute to increased ICP)

3. hydrocephalus

4. diffuse ischemia (may be secondary to increased ICP)

5. seizure

6. low blood flow (reduced CBF) due to reduced cardiac output (see page 1054)

Ocular hemorrhage

Three types of ocular hemorrhage (OH) may be associated with SAH. They occur alone or in various combinations in 20-40% of patients with SAH⁴⁴.

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 higher mortality rate⁴⁵

2. (intra)retinal hemorrhage: may surround the fovea

3. hemorrhage within the vitreous humor (Terson syndrome). Occurs in 4-27% of cases of aneurysmal SAH^46-48, usually bilateral. May occur with other causes of increased ICP including ruptured AVMs. Funduscopy reveals vitreous opacity. Often missed on initial examination. When sought, usually present on initial exam, however it may develop as late as 12 days post SAH, and may be associated with rebleeding⁴⁷. The mortality rate may be higher in SAH patients with vitreous hemorrhage than in those without. Patients should be followed for complications of OH (elevated intraocular pressure, retinal membrane formation → retinal detachment, retinal folds⁴⁹). Most cases clear spontaneously in 6-12 mos. Vitrectomy should be considered in patients whose vision fails to improve⁴⁸ or if more rapid improvement is desired⁵⁰. The long-term prognosis for vision is good in ≈ 80% of cases with or without vitrectomy⁵⁰

The pathomechanics of OH may be due to compression of the central retinal vein and the retinochoroidal anastomoses by elevated CSF pressure⁴⁸ causing venous hypertension and disruption of retinal veins.

WORK-UP OF SUSPECTED SAH

1. tests to diagnose SAH

A. non-contrast high-resolution CT scan: see below

B. if CT is negative: LP in suspicious cases (for findings, see below)

2. test to identify source of SAH. Options: CTA, MRA, or digital subtraction angiography (DSA). The choice needs to take into account the patient’s age, renal function, and even best guess of where an aneurysm might be located

A. MRA: no radiation, and 2D-TOF MRA (see page 132) does not use contrast. Poor sensitivity for aneurysm detection early after SAH (see below)

B. CTA vs. angiogram: one needs to balance the risk of the procedure and ease of obtaining it against the information expected to be obtained

1. total iodine load in a healthy adult should be < 90 gm in 24 hours. In older patients and/or possible 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 cases you do not have to wait 24 hours

2. if there is concern about renal function (e.g. serum creatinine > 100 μmol/L) hydrate the patient and optionally give Mucomyst® (see page 124)

3. 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 endovascular treatment in most cases⁵¹, DSA is still necessary in some

3. if CTA/angiogram is negative: see SAH of unknown etiology, page 1083

LABORATORY/RADIOGRAPHIC FINDINGS

CT SCAN

A good quality (e.g. no motion artifact) non-contrast high-resolution CT will detect SAH in ≥ 95% of cases if scanned within 48 hrs of SAH. Blood appears as high density (white) within subarachnoid spaces. For subtle SAH, look in the occipital horns of the lateral ventricles and the dependent portions of the sylvian fissures. CT also assesses:

1. ventricular size: hydrocephalus occurs acutely in 21% of aneurysmal ruptures⁵² (also see Hydrocephalus after SAH, page 1044)

2. hematoma: intracerebral hemorrhage or large amount of subdural blood with mass effect may need emergent evacuation

3. infarct: not sensitive in first 24 hours after infarct (see page 1012)

4. amount of blood in cisterns and fissures: important prognosticator for vasospasm (see page 1046) and can identify pretruncal hemorrhage (see page 1085)

5. CT can predict aneurysm location based on the pattern of blood in ≈ 78% of cases (but mostly for MCA and A-comm aneurysms)⁵³

A. blood predominantly in anterior interhemispheric fissure (± blood in lateral ventricles) or within the gyrus rectus suggests a-comm aneurysm

B. blood predominantly in 1 sylvian fissure is compatible with p-comm or MCA aneurysm on that side

C. blood predominantly in the prepontine or peduncular cistern suggests a basilar apex or SCA aneurysm

D. blood predominantly within ventricles: (also see page 1056)

1. blood primarily in 4th and third ventricle: suggests lower posterior fossa source, such as PICA aneurysm or VA dissection

2. blood primarily in the 3rd ventricle suggests a basilar apex aneurysm

6. with multiple aneurysms, CT may help identify which one bled by the location of blood (see above). For other “clues”, see page 1080)

Differential diagnosis of SAH on CT

Things that can mimic the appearance of SAH on CT include:

1. pus

2. following contrast administration: sometimes IV, and especially intrathecal

3. occasionally the pachymeningeal thickening seen in spontaneous intracranial hypotension (see page 305)

LUMBAR PUNCTURE

The most sensitive test for SAH. However, false positives may occur, e.g. with traumatic taps (see Differentiating SAH from traumatic tap, page 298).

✖ Caution: lowering the CSF pressure may possibly precipitate rebleeding by increasing the transmural pressure (see page 1044). Therefore remove only a small amount of CSF (several ml) and use a small (≤ 20 Ga) spinal needle.

Findings (also, see Table 14-5, page 299):

1. opening pressure: elevated

2. appearance:

A. non-clotting bloody fluid that does not clear with sequential tubes

B. xanthochromia: yellow coloration of CSF supernatant (specimen must be centrifuged in the lab) due to heme pigments released by the breakdown of RBCs. The most reliable means of differentiating traumatic tap from SAH. Usually not apparent until 2-4 hours after the SAH. 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. Spectrophotometry is more sensitive than visual inspection, but may lack sufficient specificity to warrant widespread use⁵⁴. False positives: xanthochromia may occur with jaundice or high protein levels in the CSF

3. cell count: RBC count usually > 100,000 RBCs/mm³. Compare RBC count in first to last tube (should not drop significantly)

4. protein: elevated due to blood breakdown products

5. glucose: normal, or reduced (RBCs may metabolize some glucose with time)

MRI

Not sensitive for SAH acutely within the first 24-48 hrs⁵⁵ (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 helpful in determining which of multiple aneurysms bled⁵⁶ (see page 1080).

MAGNETIC RESONANCE ANGIOGRAPHY (MRA)

Based on a systematic review, sensitivity is 87% and specificity is 92% for detecting intracranial aneurysms (IAs) (compared to catheter DSA) with significantly poorer sensitivity for aneurysms < 3 mm diameter^57-59.

MRA’s ability to detect IAs depends on aneurysm size, rate and direction of blood flow in the aneurysm relative to the magnetic field, and aneurysmal thrombosis and calcification. MRA may be most useful as a screening test in high-risk patients including patient’s with two first degree relatives with IAs, especially those who are also smokers or hypertensive themselves⁶⁰.

CT ANGIOGRAPHY (CTA)

See page 128. Many centers have shown good results with CTA, with a prospective study detecting 97% of aneurysms and demonstrating CTA as safe and effective when used as the initial and sole imaging study for ruptured and unruptured cerebral aneurysms⁶¹. CTA shows a 3-dimensional image (as can modern catheter angiography) which can help differentiate 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 use is increasing for evaluation of vasospasm⁶².

CEREBRAL ANGIOGRAM

The gold standard for evaluation of cerebral aneurysms. Current state of the art uses digital subtraction angiography (DSA). Sometimes referred to as “catheter angiogram” to distinguish from other techniques. Demonstrates source (usually aneurysm) in ≈ 80-85% (remainder are so-called “SAH of unknown etiology”, see page 1083). Shows if radiographic vasospasm is present (clinical vasospasm almost never occurs < 3 days following SAH, see Vasospasm, page 1045) and assesses primary feeding arteries, collateral flow in case of a need for arterial sacrifice.

General principles:

1. study the vessel of highest suspicion first (in case patient’s condition should change, necessitating discontinuation of procedure)

2. continue to do complete 4 vessel angiogram (even if aneurysm(s) have been demonstrated) to rule out additional aneurysms and assess collateral circulation

3. if there is an aneurysm or suspicion of one, obtain additional views to help delineate the neck and orientation of the aneurysm (see index for specific 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 VA injection if there is enough flow to reflux down the contralateral VA. Occasionally it is necessary to see more of the contralateral VA than what refluxes to PICA

B. flow contrast through the ACoA: if both ACAs fill from one side, this is usually satisfactory. It may be necessary to perform a cross compression AP study with carotid injection (first, rule-out plaque in the carotid to be compressed), or use a higher injection rate to facilitate flow through the ACoA

C. if an infundibulum (see below) colocalizes to the SAH, it may be unwise to label the case as angiogram-negative⁶³ and exploration is recommended

Infundibulum

A funnel shaped initial segment of an artery, to be distinguished from an aneurysm. Found in 7-13% of otherwise normal arteriograms^{65, 66}, with a higher incidence in cases of multiple or familial aneurysms. Bilateral in 25%⁶⁶. Most commonly found at the origin of the p-comms, but they rarely occur at other sites. Criteria (somewhat arbitrary) for differentiating infindibula from aneurysms are shown in Table 30-1. Infundibula may represent incomplete remnants of previous fetal vessels^{67 (p 272)}

Although they may bleed^{63, 68-70}, there is less risk of rupture than with a saccular aneurysm (no infundibulum < 3 mm in size bled⁷¹ in the cooperative study). However, infundibula have been documented to progress to an aneurysm which may bleed (13 case reports in 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 the artery if it can be done safely (infundibula lack a true neck).

Table 30-1 Criteria of an infundibulum

1. triangular in shape

2. mouth (widest portion) < 3 mm64

3. vessel at apex

Angiographic findings

1. general features to take note of when analyzing an aneurysm on angiogram (special considerations for specific aneurysms are covered in designated sections)

A. size of aneurysm dome:

1. MRI or CT helps with this since the aneurysm may be partially thrombosed and the filling part may be much smaller than the overall size

2. large aneurysms (≥ 15 mm dia.) are associated with lower rates of complete occlusion by endovascular coiling^{72, 73}

B. neck size

1. narrow necks < 5 mm are ideal for coiling⁷⁴

2. broad necks ≥ 5 mm are associated with increased risk of incomplete occlusion and recanalization with coiling⁷³

3. stent or balloon-assisted coiling may be needed for wide necked aneurysms. Stents should be avoided if possible see page 1060

C. dome:neck ratio ≥ 2 is associated with higher rate of coil occlusion⁷⁴

2. basilar bifurcation aneurysms: see page 1074

30.2. Grading SAH

Two widely quoted grading scales are presented here.

HUNT AND HESS GRADE

See Table 30-2 and Table 30-3 for grading 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 of grade).

Analysis of data from the International Cooperative Aneurysm Study revealed that with normal consciousness, Hunt and Hess (H&H) grades 1 and 2 had identical outcome, and that hemiparesis and/or aphasia had no effect 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.

A. also appears in the literature as World Federation of Neurological Surgeons

WORLD FEDERATION OF NEUROSURGICAL SOCIETIES^A (WFNS) GRADING OF SAH

The WFNS Committee on a Universal SAH Grading Scale^{77, 78} grading system is shown in Table 30-4. It uses the Glasgow Coma Scale (GCS) (see Table 12-1, page 279) to evaluate level of consciousness, and uses the presence or absence of major focal neurologic deficit to distinguish grade 2 from grade 3.

Table 30-2 Hunt and Hess classification* of SAH⁷⁵

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 athero-sclerosis, COPD) or severe vasospasm on arteriography.

* original paper did not consider patient’s age, site of aneurysm, or time since bleed; patients were graded on admission and pre-op

Table 30-3 Modified classification⁷⁶ adds the following

Grade	Description
0	unruptured aneurysm
1 a	no acute meningeal/brain reaction, but with fixed neuro deficit

Table 30-4 WFNS SAH grade⁷⁷

WFNS grade	GCS score*	Major focal deficit†
0‡
1	15	–
2	13-14	–
3	13-14	+
4	7-12	+ or –
5	3-6	+ or –

* GCS = Glasgow Coma Scale, see Table 12-1, page 279

^† aphasia, hemiparesis or hemiplegia (+ = present, – = absent)

^‡ intact aneurysm

30.3. Initial management of SAH

Initial management concerns

1. rebleeding: the major concern during the initial stabilization

2. hydrocephalus: precipitous development acute hydrocephalus may be obstructive (due to blockage of CSF flow by blood clot), but presence of ventriculomegaly early after SAH as well as at later stages is often due to communicating hydrocephalus (due toxic effect of blood breakdown products on arachnoid granulations) (see Hydrocephalus after SAH, page 1044)

3. delayed ischemic neurologic deficit (DIND), usually attributed to vasospasm. Begins to be of concern several days following the SAH

4. hyponatremia with hypovolemia: see page 1043

5. DVT and pulmonary embolism: see page 42

6. seizures: see page 1041

7. determining source of bleeding: should be investigated early with CTA or catheter angiography. The timing and choice of study takes into consideration the patient’s condition (unstable or pre-morbid patients are not candidates), the feasibility of early treatment (ideal), and the likelihood of endovascular therapy (based on patient’s age and predicted aneurysm location as well as availability)

Goals of medical management related to neurologic injury

In addition to prevention of hyponatremia, hypovolemia, seizures, etc. (see above), the goals of initial medical management include:

1. augmenting CBF: the main device for accomplishing this is hyperdynamic therapy (see page 1052). Goals are:

A. increasing cerebral perfusion pressure (CPP)

B. improving blood rheology: RBC aggregability increases after SAH⁷⁹

C. maintaining euvolemia: the majority of patients become hypovolemic in the first 24 hrs after SAH. Also, avoid prophylactic hyper volemia

D. maintaining normal ICP

2. neuroprotection: there are currently no medications shown to be effective or approved for use as neuroprotective agents for this or any other type of brain injury. Animal studies have shown time and again that the concept may someday be translated into clinical practice⁸⁰

30.3.1. Monitors/tubes

Also see Admitting orders below.

1. arterial-line: for patients who are hemodynamically unstable, stuporous or comatose, those with difficult to control hypertension, or those requiring frequent labs (e.g. ventilator patients)

2. intubate patients who are comatose or unable to protect airway (e.g. stridorous)

3. pulmonary-artery catheter (PA-catheter, AKA Swann-Ganz catheter): the safety and efficacy of this device has been debated in the critical care literature for over a decade now, with some calling for a moratorium on PA catheter use⁸¹. It is possible that newer technologies may supplant the need for this invasive procedure while allowing close hemodynamic monitoring⁸². Nevertheless, a PA catheter can be considered for:

A. Hunt and Hess (H&H) grade ≥ 3 (except good grade 3 patients)

B. patients with possible CSW or SIADH

C. hemodynamically unstable patients

4. cardiac rhythm monitor: arrhythmias may occur following SAH (see page 1054)

5. intraventricular catheter (IVC) AKA ventriculostomy. Possible indications:

A. patients developing acute hydrocephalus following SAH or in those with significant intraventricular blood (allows measurement of ICP as well as drainage of blood laden CSF). IVC causes symptomatic improvement in almost two-thirds⁵². May increase the risk of rebleeding (see page 1044), however, the risk of untreated hydrocephalus is probably higher⁸³

B. H&H grade ≥ 3 (except good grade 3 patients). If a high grade patient improves with an IVC, the prognosis may be more favorable. If ICP is elevated, management includes the use of mannitol (see Treatment measures for elevated ICP, page 876)

30.3.2. Admitting orders

1. admit to ICU (monitored bed)

2. VS with neuro checks q 1 hr

3. activity: BR with HOB at 30°. SAH precautions (i.e. low level of external stimulation, restricted visitation, no loud noises)

4. nursing

A. strict I’s & O’s

B. daily weights

C. knee high TED hose and pneumatic compression boots (PCB)

D. indwelling Foley catheter if patient lethargic, incontinent, or unable to void in urinal or bedpan. Consider temperature sensing catheter for strict fever control

5. diet: NPO (in preparation for surgery or endovascular intervention)

6. IV fluids: early aggressive fluid therapy to head off cerebral salt wasting

A. NS + 20 mEq KCl/L at ≈ 2 ml/kg/hr (typically 140-150 ml/hr) (see Blood pressure and volume management below)

B. if Hct < 40%⁸⁴, give 500 ml of 5% albumin over 4 hrs upon admission

7. medications (avoid IM medications to reduce pain)

A. prophylactic anticonvulsants

1. seizure incidence: excluding seizures at the time of hemorrhage, ≈ 3% of patients with SAH have seizures during the acute illness⁸⁵. 5% have a seizure in the immediate post-op period with or without SAH⁸⁶. 10.5% incidence in 5 years follow-up (20% for MCA, 9% for PCA, and 2.5% for ACA aneurysms)⁸⁷

2. use of prophylactic anticonvulsants is controversial⁸⁸, however, a generalized seizure may be devastating in the presence of a tenuous aneurysm, and thus AEDs are given by many authorities⁸⁹ at least for 1 week post-op⁸⁶

3. Keppra® (levetiracetam): start with 500 mg PO or IV q 12 hours

4. if levetiracetam not available: phenytoin may be used. Avoid IV if possible because of pain and phlebosclerosis (circumvented with fosphenytoin). Load with 17 mg/kg, maintenance of 100 mg TID

5. some prophylaxis is provided by barbiturates (e.g. phenobarbital) when given for sedation (see below) or burst suppression in the O.R.

B. sedation (not oversedation): e.g. with propofol

C. analgesics: fentanyl (unlike morphine, does not cause histamine release. Lowers ICP) 25-100 mcg (0.5-2 ml) IVP, q 1-2 hrs PRN (avoid Demerol® because it may lower seizure threshold)

D. dexamethasone (Decadron®): may help with H/A and neck pain. Effect on edema controversial. Usually given pre-op prior to craniotomy

E. stool softener in patients able to take PO (docussate 100 mg PO BID)

F. anti-emetics: avoid phenothiazines which may lower seizure threshold. Use e.g. Zofran® (ondansetron) 4 mg IV over 2-5 minutes, may repeat in 4 & 8 hours, and then q 8 hours for 1-2 days

G. calcium channel blockers (see Calcium channel blockers, page 1053): nimodipine (Nimotop®) 60 mg PO/NG q 4 hrs initiated within 96 hrs of SAH (some use 30 mg q 2 hrs to avoid periodic dips in BP). IV administration is equally as effective⁹⁰ where available

H. H₂ blockers (e.g. ranitidine) or proton pump inhibitors (e.g. Prevacid® (lansoprazole) 30 mg p.o. or IV q d): to reduce risk of stress ulceration

I. ✖ these agents impair coagulation and are used with caution: ASA, dextran⁹¹, heparin, and repeated administration of hetastarch (Hespan®)^{92, 93} over a period of days

8. oxygenation

A. in non-intubated patient: O₂ 2 L per NC PRN (based on ABG) if tolerated

B. in ventilated patient: strive for normocarbia and pO₂ > 100 mm Hg

9. HTN: SBP 120-150 mm Hg by cuff is a guideline with unclipped aneurysm (see Blood pressure and volume management below)

10. labs

A. ABG, electrolytes, CBC, PT/PTT on admission

B. ABG, electrolytes, CBC q day (ABG q 6 hrs if patient unstable, electrolytes q 12 hrs if hyponatremia develops, see Hyponatremia following SAH below)

C. serum and urine osmolality if urine output high or low (see Syndrome of inappropriate antidiuretic hormone secretion (SIADH), page 10)

D. follow Hct and (optional) serum fibrinogen (to assess viscosity, important for blood flow in vasospasm)

E. CXR daily until stable: patients undergoing triple-H therapy can develop dangerous pulmonary edema as they “fall off” the Starling curve with volume expansion. Patients with SAH are also rarely at risk for neurogenic pulmonary edema⁹⁴, see page 28

F. if available, transcranial doppler to monitor MCA, ACA, ICA, VA and BA velocities and Lindegaard ratio (see page 1048) q Mon, Weds & Fri

30.3.3. Blood pressure and volume management

With an unsecured (unclipped or uncoiled) aneurysm, gentle volume expansion with slight hemodilution and mild elevation of blood pressure may help prevent or minimize the effects of vasospasm⁹⁵ and cerebral salt wasting. However, extreme hypertension must be avoided (to reduce risk of rebleeding). Hypervolemia is to avoided since it does not mitigate vasospasm and increases complications⁹⁶.

With a secured aneurysm, aggressive volume expansion with hyperdynamic therapy is commonly used (see page 1052).

Initial blood pressure

Ideal blood pressure is controversial, and must take patient’s baseline into consideration, SBP ≈ 120-150 by cuff is a guideline.

If blood pressure is labile, labetalol or nicardipine should be used in conjunction with an arterial-line. Avoid hypotension as it may exacerbate ischemia.

Long acting drugs (e.g. ACE inhibitors such as Vasotec (see page 20 for IV, or page 21 for PO)) should be started in patients requiring continued therapy. In patients who were normotensive prior to SAH with easily controlled hypertension, Vasotec may be used PRN in conjunction with a beta blocker (e.g. labetalol, see page 21).

30.3.4. Hyponatremia following SAH

Background

Hypovolemia and hyponatremia frequently follow SAH as a result of natriuresis and diuresis. Although hyponatremia had been attributed to a rise in ADH⁹⁷ (thought to produce SIADH with hyper volemia), the ADH increment is usually transient, lasting only ≈ 4 days and hypervolemia did not occur. Another theory is based on the fact that there is often a delayed peak in atrial natriuretic factor (ANF) (a 28-amino acid polypeptide) after an initial smaller rise⁹⁸ that was frequently followed by urinary loss of sodium (cerebral salt wasting (CSW), see page 13) that mimics SIADH, and volume depletion. Although CSW has clearly been shown to be the cause of hyponatremia in the majority of these patients⁹⁹, there are still doubts that ANF is the operative natriuretic factor in SAH¹⁰⁰. A rise in ANP and brain natriuretic peptide (BNP) after SAH is associated with the development of a negative fluid balance¹⁰¹.

Routine labs are identical in SIADH and CSW¹⁰², but the extracellular fluid volume (which is more difficult to measure) is low in CSW and is normal or elevated in SIADH (see Table 2-5, page 14 for a comparison of the two conditions). The neurologic effects of hyponatremia (see page 9) may mimic delayed ischemic neurologic deficit from vasospasm, and hyponatremic patients have about 3 times the incidence of delayed cerebral infarction after SAH than normonatremic patients¹⁰³.

Factors that may increase the risk of hyponatremia after SAH include: history of diabetes, CHF, cirrhosis, adrenal insufficiency, or the use of any of the following drugs: NSAIDs, acetaminophen, narcotics, thiazide diuretics¹⁰⁴.

Treatment

✖ Caution! Restricting fluids which is the treatment for SIADH may be hazardous in the case of CSW (which is more likely to occur after SAH than is SIADH) since dehydration increases blood viscosity which exacerbates ischemia from vasospasm¹⁰³.

• treat hypovolemia with infusions of crystalloid (e.g. NS), PRBCs, or colloids (avoid repeated administration of hetastarch, see above)

• treat the hyponatremia of CSW as outlined on see page 14. NB: too rapid correction or over-correction carries the risk of osmotic myelinolysis, see page 11

30.3.5. Rebleeding

Approximately 3000 North Americans die each year from rebleeding of ruptured cerebral aneurysms¹¹⁵. For untreated ruptured aneurysms, the maximal frequency of rebleeding is in the 1st day (4% on day 1), then 1.5% daily for 13 d. 15-20% rebleed within 14 d, 50% will rebleed within 6 months, thereafter the risk is ≈ 3%/yr^A with a mortality rate of 2%/yr¹¹⁶. 50% of deaths occur in the 1st month. In a study of 33 patients who rebled, the highest risk of rebleeding occurred in the first 6 hours following SAH¹¹⁷.

A. to understand the calculation of cumulative risk for aneurysmal rupture, see page 1100 (that discussion is related to AVMs but the same concepts pertain to aneurysms)

The rebleeding risk increases in patients with higher Hunt and Hess grades¹¹⁷.

Pre-operative ventriculostomy (e.g. for acute post-SAH hydrocephalus) (see page 1044) and possibly lumbar spinal drainage (see page 1062) increase the risk of rebleeding.

The risk of rebleeding in SAH of unknown etiology and with AVMs, as well as the risk of bleeding with incidental multiple unruptured aneurysms, are all similar at ≈ 1%/yr (may actually be less in SAH of unknown etiology, see page 1083)¹¹⁸.

Prevention of rebleeding

The optimal method of preventing rebleeding is early coiling or surgical clipping. Bed rest and hyperdynamic therapy do not prevent rebleeding⁸⁹.

Antifibrinolytic therapy: The role of clot lysis in early rebleeding is uncertain.

tranexamic acid (Cyklokapron®)DRUG INFO

Reduces the risk of early rebleeding¹¹⁹.

Rx: 1 gm IV as soon as diagnosis of SAH is verified (if patient is to be transported to another facility for definitive care, the dose is given before transport), followed by 1 gm q 6 hours until the aneurysm is occluded; this treatment did not exceed 72 hours.

✖ epsilon-aminocaproic acid (Amicar®)DRUG INFO

(EACA) an antifibrinolytic agent, competitively inhibits activation of plasminogen to plasmin. Existing plasmin is neutralized by endogenous antiplasmins. EACA does reduce the risk of rebleeding. However, the incidence of hydrocephalus and delayed ischemic deficits (vasospasm) are increased¹²⁰ with prolonged use. There may also be a lag of 24-48 hrs before effectiveness occurs¹²¹. Because of the increased rate of cerebral infarction, EACA was found not to reduce early mortality, and its use was discouraged.

Reevaluation in a non-randomized study¹²² excluding grade IV and V patients, suggests that the problems with EACA may be minimized by use of an IV loading dose (to eliminate the lag-period to effectiveness) and by limiting the length of time of use to that time until the patient can undergo early surgery. Further study is needed.

Rx high-dose¹²²: EACA 10 gm IV loading dose, followed by 48 gm/day continuous maintenance infusion. Maintenance dose is adjusted to serum EACA levels.

30.3.6. Hydrocephalus after SAH

For hydrocephalus after traumatic SAH, see page 906.

ACUTE HYDROCEPHALUS

The frequency of hydrocephalus (HCP) on the initial CT after SAH depends on the defining criteria used, with a reported range of 9-67%¹²³. A realistic range is ≈15-20% of SAH patients, with 30-60% of these showing no impairment of consciousness^{123, 124}. 3% of those without HCP on initial CT develop HCP within 1 week¹²³.

Factors felt to contribute to acute HCP include: blood interfering with CSF flow through the Sylvian aqueduct, fourth ventricle outlet, or subarachnoid space, and/or with reabsorption at the arachnoid granulations.

Findings associated with acute HCP include¹²⁴:

• increasing age

• admission CT findings: intraventricular blood, diffuse subarachnoid blood, and thick focal accumulation of subarachnoid blood (intraparenchymal blood did not correlate with chronic HCP, and patients with a normal CT had a low incidence)

• hypertension: on admission, prior to admission (by history), or post-op

• by location:

posterior circulation aneurysms have a higher incidence of HCP

MCA aneurysms correlate with low incidence of HCP

• miscellaneous: hyponatremia, patients who were not alert on admission, use of preoperative antifibrinolytic agents, and low Glasgow outcome score

Treatment

About half the patients with acute HCP and impaired consciousness improved spontaneously¹²³. Patients in poor grade (H&H IV-V) with large ventricles may be symptomatic from the HCP and consideration should be given to ventriculostomy which caused improvement in ≈ 80% of patients in whom it was used¹²³. There is probably an increased risk of aneurysmal rebleeding in patients undergoing ventriculostomy shortly after SAH^{123, 125, 126} especially if performed early and if ICP is lowered precipitously. The mechanism is controversial, but may be due to an increase in the transmural pressure (the pressure across the aneurysm wall which equals the difference between arterial pressure and ICP).

When a ventriculostomy is used, it is recommended to keep ICP in the range of 15-25 mm Hg¹²⁷ and to avoid rapid pressure reduction (unless absolutely necessary) to decrease the risk of IVC induced aneurysmal rebleeding.

CHRONIC HCP

Chronic HCP is due to piaarachnoid adhesions or permanent impairment of the arachnoid granulations. Acute HCP does not inevitably lead to chronic HCP. 8-45% (reported range in literature¹²⁸) of all ruptured aneurysm patients, and ≈ 50% of those with acute HCP following SAH need permanent CSF diversion. The presence of intraventricular blood increases this risk¹²⁸. There is controversy as to whether the use of ventriculostomy for acute HCP increases¹²⁹ or possibly even decreases¹²⁸ the incidence of shunt dependency.

30.4. Vasospasm

Key concepts:

• delayed cerebral ischemic symptoms and/or cerebral arterial narrowing on angiography that follows some cases of SAH (usually), trauma, or other insults

• time course: almost never before day 3 post SAH, peak incidence 6-8 days post SAH, rarely starts after day 17. Main time of risk: 3-14 days post SAH

• risk factors: higher SAH grade, more blood on CT

• results in pathologic changes within the vessel walls (not just vasoconstriction)

• diagnosis: may be clinical, angiographic, or with transcranial Doppler

• treatment: none are curative. Mainstays: “triple H” therapy (hypertension, hypervolemia, hemodilution), direct vasodilatation (angioplasty or intraarterial verapamil), and possibly routine use of statins following SAH

Cerebral vasospasm is a condition that is most commonly seen following aneurysmal subarachnoid hemorrhage (SAH), but may also follow other intracranial hemorrhages (e.g. intraventricular hemorrhage from AVM¹³⁰, and SAH of unknown etiology), head trauma (with or without SAH)¹³¹, brain surgery, lumbar puncture, hypothalamic injury, infection, and may be associated with preeclampsia (see page 73). Vasospasm has two not-necessarily reconcilable definitions (see Definitions below):

1. clinical vasospasm: see below

2. radiographic vasospasm: see below

30.4.1. Definitions

CLINICAL VASOSPASM

AKA delayed ischemic neurologic deficit (DIND), AKA symptomatic vasospasm. A delayed ischemic neurologic deficit following SAH. Clinically characterized by confusion or decreased level of consciousness sometimes with focal neurologic deficit (speech or motor). The diagnosis is one of exclusion, and sometimes cannot be made with certainty.

For clinical findings, see page 1045.

RADIOGRAPHIC VASOSPASM (AKA ANGIOGRAPHIC VASOSPASM)

Arterial narrowing demonstrated on cerebral angiography, often with slowing of contrast filling. The diagnosis is solidified by previous or subsequent angiograms showing the same vessel(s) with normal caliber. Since only larger arteries may be visualized angiographically, the diagnosis is limited to narrowing of these vessels. In some cases a DIND corresponds to a region of vasospasm seen angiographically.

30.4.2. Characteristics of cerebral vasospasm

Clinical findings

Findings usually develop gradually, and may progress or fluctuate. May include:

1. non-localizing findings

A. new or increasing H/A

B. alterations in level of consciousness (lethargy…)

C. disorientation

D. meningismus

2. focal neurological signs may occur including cranial nerve palsies and focal motor deficits. Also, symptoms may cluster into one of the following “syndromes” (vasospasm incidence is higher in the distribution of the ACA than in that of the MCA)

A. anterior cerebral artery (ACA) syndrome: frontal lobe findings pre-dominate (abulia, grasp/suck reflex, urinary incontinence, drowsiness, slowness, delayed responses, confusion, whispering). Bilateral anterior cerebral artery distribution infarcts are usually due to vasospasm following an ACoA aneurysm rupture

B. middle cerebral artery (MCA) syndrome: hemiparesis, monoparesis, aphasia (or apractagnosia of non-dominant hemisphere - inability to use objects or perform skilled motor activities, due to lesions in the lower occipital or parietal lobes; subtypes: ideomotor apraxia and sensory apraxia)

Incidence

• radiographic cerebral vasospasm (CVS) is identified in 30-70% of arteriograms performed around the 7th day following SAH, whereas DIND associated with radiographic CVS occurs in only 20-30% of patients with SAH²²

• radiographic CVS may occur in the absence of clinical deficit, and vice-versa

Severity

• CVS is the most significant cause of morbidity and mortality in patients surviving SAH long enough to reach medical care, even exceeding direct effects of aneurysmal rupture as well as rebleeding

• CVS ranges in severity from mild reversible dysfunction, to severe permanent deficits secondary to ischemic infarction in 7% of SAH patients, extensive enough to be fatal in 7% of SAHs²²

• earlier onset of CVS is associated with greater deficit

Time course of vasospasm

• onset: almost never before day 3 post-SAH¹³²

• maximal frequency of onset during days 6-8 post-SAH (however, rarely can occur as late as day 17). Typical atrisk period is quoted as days 3-14

• clinical CVS is almost always resolved by day 12 post-SAH. Once radiographic CVS is demonstrated, it usually resolves slowly over 3-4 weeks

• onset is usually insidious, but ≈ 10% have an abrupt and severe deterioration

Correlated findings

• blood clots are especially spasmogenic when in direct contact with the proximal 9 cm of the ACA and the MCA

• not all patients with SAH develop CVS, and CVS can follow other insults besides SAH (e.g head trauma without SAH)

• the Hunt and Hess grade on admission correlates with the risk of CVS (see Table 30-5)

• the amount of blood on CT correlates with the severity of CVS^{133, 134} (see Table 30-6) (also holds true for traumatic SAH³)

• higher incidence with increasing age of patient

• a history of active cigarette smoking is an independent risk factor¹³⁵

• history of preexisting hypertension

• there is good but not perfect correlation between the site of major blood clots on CT, the focality of delayed ischemic neurological deficits, and the visualization of angiographic CVS in corresponding arteries

• pial enhancement on CT ≈ 3 days after SAH (with IV contrast administration) may correlate with higher risk of CVS (indicates increased permeability of BBB)¹³⁶, but this is controversial¹³⁷

• for patients undergoing early surgery, if there is little SAH left on a CT done 24 hours post-op, there is little risk of vasospasm

• antifibrinolytic therapy reduces rebleeding, but increases the risk of hydrocephalus and vasospasm¹²⁰ (see page 1043)

• angiographic dye can exacerbate CVS

• hypovolemia

Table 30-5 Correlation of DIND with Hunt and Hess grade

Hunt and Hess grade	% DIND (clinical vasospasm)
1	22%
2	33%
3	52%
4	53%
5	74%

30.4.3. Pathogenesis

Poorly understood. Risk of developing vasospasm is higher in cases where arterial blood at high pressure contacts the vessels at the base of the brain. Rarely occurs in the setting of intraparenchymal or intraventricular hemorrhage (e.g. from AVM) or in SAH with distribution limited to the cerebral convexity.

Pathological changes observed within the vessel wall are outlined in Table 30-7.

Table 30-7 Pathological changes in vasospasm

Time	Vessel layer	Pathologic change
day 1-8	adventitia	↑ inflammatory cells (lymphocytes, plasma cells, mast cells) and connective tissue
	media	muscle necrosis and corrugation of elastica
	intima	thickening with endothelial swelling and vacuolization, opening of interendothelial tight junctions138, 139
day 9-60	intima	proliferation of smooth muscle cells → progressive intimal thickening

In humans, CVS is a chronic condition with definite long-term changes in the morphology of the involved vessels. Endothelin 1 (ET1) appears to be a critical mediator and has been shown to cause potent and prolonged vasospasm¹⁴⁰.

30.4.4. Diagnosis of cerebral vasospasm

Diagnosis requires appropriate clinical criteria, and ruling-out other conditions that can produce delayed neurologic deterioration, as shown in Table 30-8.

Table 30-8 Diagnosis of clinical vasospasm¹⁴¹

• delayed onset or persisting neuro deficit • onset 4-20 days post-SAH • deficit appropriate to involved arteries • rule-out other causes of deterioration • rebleeding • hydrocephalus • cerebral edema • seizure • metabolic disturbances: hyponatremia… • hypoxia • sepsis • ancillary tests (see text) • transcranial Doppler • CBF studies • SPECT • cerebral angiography

ANCILLARY TESTS FOR VASOSPASM

In addition to angiographically demonstrating vasospasm:

• transcranial doppler (TCD): see below

• alterations in intracranial pulse wave¹⁴²

• CTA: can demonstrate vasospasm¹⁴³

• MRA: may be useful for management of vasospasm (not a practical alternative to conventional angiography)¹⁴⁴

• continuous quantitatively analyzed EEG monitoring in the ICU:

a decline of the percent of alpha activity (defined here as 6-14 Hz) called “relative alpha” (RA) from a mean of 0.45 to 0.17 predicted the onset of vasospasm earlier than TCD or angiographic changes¹⁴⁵

a decline of total EEG power (amplitude) was 91% sensitive for predicting vasospasm¹⁴⁶

• alterations in cerebral blood flow (CBF):

MRI: DWI and PWI may detect early ischemia (see page 132)

CT perfusion study (see page 128)

xenon CT: may detect large global changes in CBF, but too insensitive to detect focal blood flow changes^{147, 148}

positron emission tomography (PET)¹⁴⁹ or SPECT scans (nonquantitative, and takes longer than xenon studies)

Transcranial doppler (TCD)

Noninvasive method of semiquantitatively measuring velocity of blood flow in a specific artery through the skull (in regions of thinner bone - insonation windows) utilizing ultrasound phase shift.

Narrowing of the arterial lumen as occurs in vasospasm elevates the blood flow velocity which may be detected with TCD^150-152. Detectable changes may precede clinical symptoms by up to 24-48 hrs. Findings are often more helpful when baseline studies performed before vasospasm is likely to have begun are available.

Typical values are shown for the MCA in Table 30-9. Also, daily increases of > 50 cm/sec may suggest vasospasm. There is less correlation between velocities and vasospasm in the anterior cerebral arteries (ACA). Distinguishing vasospasm from hyperemia (which increases blood flow velocities in both the MCA and the ICA) is facilitated by using the ratio of these velocities (the so-called Lindegaard ratio) also shown in Table 30-9.

Once values become elevated, it often takes several weeks to go back down.

Table 30-9 Interpretation of transcranial doppler for vasospasm

Mean MCA velocity (cm/sec)	MCA:ICA (Lindegaard) ratio	Interpretation
< 120	< 3	normal
120-200*	3-6	mild vasospasm*
> 200	> 6	severe vasospasm

* velocities in this range are specific for vasospasm but are only ≈ 60% sensitive

30.4.5. Treatment for vasospasm

See page 1050 for management protocol.

Numerous treatments for cerebral arterial vasospasm have been evaluated. See the survey articles by Wilkins^{153, 154} for an extensive list of agents and techniques studied. Vasospasm in humans does not respond to the large variety of drugs that reverse experimental vasospasm in animal models.

PREVENTION OF VASOSPASM

Vasospasm can often be mitigated by preventing post-SAH hypovolemia and anemia by employing hydration and blood transfusion. Although early aneurysm treatment (clipping or coiling) does not prevent CVS (in fact, manipulation of vessels may increase the risk), it facilitates treatment of CVS by eliminating the risk of rebleeding (permitting safe use of hyperdynamic therapy) and removal of clot (see below) may reduce the incidence of CVS (see Timing of aneurysm surgery, page 1060 for discussion of early surgery). Routine use of statins shows promise for reducing effects of vasospasm (see below). ✖Prophylactic (i.e. before vasospasm has been diagnosed) hyperdynamic therapy (triple H therapy - see page 1052) is not indicated (it may cause complications and does not provide any benefit)⁹⁶.

VASOSPASM TREATMENT OPTIONS

Treatment options fall into the following categories:

1. direct pharmacological arterial dilatation

A. smooth muscle relaxants:

1. calcium channel blockers*: did not succeed in counteracting vasospasm, but they may provide a neuroprotectant effect (see page 1053)

2. endothelin receptor antagonists^†: ET_A antagonists (clazosentan) and ET_A/B antagonists^{155, 156}

B. sympatholytics

C. intraarterial papaverine^§157,158: short-lived (see below)

D. αICAM-1 inhibition^† (antibody to intracellular adhesion molecule)

2. direct mechanical arterial dilatation: balloon angioplasty^§ (see below)

3. indirect arterial dilatation: utilizing hyperdynamic therapy* (see below)

4. surgical treatment to dilate arteries: cervical sympathectomy^‡159

5. removal of potential vasospasmogenic agents

A. removal of blood clot: does not completely prevent vasospasm

1. mechanical removal at the time of aneurysm surgery^{160, 161}

2. subarachnoid irrigation with thrombolytic agents^† at the time of surgery or post-op through cisternal catheters^162-165 (must be initiated within ≈ 48 hrs of clipping) or intrathecally¹⁶⁶. Hazardous with incompletely clipped aneurysm¹⁶⁵

B. CSF drainage: via serial lumbar punctures, continuous ventricular drainage, or postoperative cisternal drainage¹⁶⁷

6. protection of the CNS from ischemic injury:

A. calcium channel blockers* (see page 1053)

B. NMDA (N-methyl-D-aspartate) receptor antagonists^†

1. Selfotel®: a selective competitive NMDA receptor antagonist (like PCP & ketamine), and like these agents, may cause hallucinations, paranoia, delerium… at all but the lowest doses¹⁶⁸. Recently abandoned in studies for use in acute stroke due to an increase in brain-related deaths¹⁶⁹. No benefit demonstrated in severe closed head injury¹⁷⁰

2. eliprodil

3. cerestat

C. free radical scavengers^†

1. tirilazad mesylate (Freedox®): a 21-aminosteroid. Improved outcome was observed in males given 6 mg/kg/d¹⁷¹ (females metabolize the drug at 3-4 x the rate as males, and a study with 15 μg/kg/d in females is planned). Overall the drug does not look as promising as it did initially

2. nicaraven¹⁷²

7. improvement of the rheologic properties of intravascular blood to enhance perfusion of ischemic zones (also an endpoint of hyperdynamic therapy)* (see page 1052)

• includes: plasma, albumin, low molecular weight dextran^‡, perfluorocarbons^†, mannitol (see page 1063)

• the optimal hematocrit is controversial, but ≈ 30-35% is a good compromise between lowered viscosity without overly reducing O₂ carrying capacity (hemodilution is used to lower Hct; phlebotomy is not used)

8. other pharmacologic agents: statins

9. extracranial-intracranial bypass around zone of vasospasm^‡173,174

* technique that is generally accepted for standard usage

^§ technique that is accepted for use but not necessarily standard or available at all centers

^† experimental or research technique with potential for future application

^‡ technique not generally used or no longer accepted

Promising agents in trials

• nicardipine prolonged release implants (NPRIs): placed intra-op in the cisterns (where thick clots were located) decreased the incidence of vasospasm in patients with thick blood clots (Fisher Group 3, see Table 30-6, page 1046)¹⁷⁵

• clazosentan (AXV-034343): a selective endothelin IA receptor antagonist¹⁷⁶: reduces frequency and severity of vasospasm

• statins: meta-analysis¹⁷⁷ of 3 small studies showed a reduction in radiographic vasospasm, DIND, and mortality with the use of statins. This suggests that routine use of statins after SAH by be warranted. Agents reported:

A. simvastatin 80 mg/d^{178, 179}

B. pravastatin 40 mg/d¹⁸⁰

Vasodilatation by angioplasty

Catheter directed balloon angioplasty of vessels demonstrated to be in vasospasm^{181, 182}: available only in centers with interventional neuroradiologists. Risks of the procedure: arterial occlusion, arterial rupture, displacement of aneurysm clip^{183, 184}, arterial dissection. Only feasible in large cerebral vessels (distal arteries not accessible). Clinical improvement occurs in ≈ 60-80%.

Criteria for transluminal balloon angioplasty (TBA):

1. failure of hyperdynamic therapy

2. ruptured aneurysm is repaired

3. optimal results when performed within 12 hours of onset of symptoms

4. may be done immediately post-clipping for vasospasm that was observed pre-op

5. controversial: asymptomatic vasospasm seen on the contralateral side during angioplasty for ipsilateral vasospasm. Some would balloon the asymptomatic side, but others cite the complication rate and would observe

6. ✖ cerebral infarction (CVA): a contraindication to TBA

Vasodilatation by intraarterial drug injection

Vasodilatation by intraarterial drug (IAD) injection may be considered the “poor-man’s” angioplasty since it could be performed by angiographers who are not interventional neuroradiologists. However, the effects are shorter-lived and less profound at their peak than with angioplasty. While IAD can be repeated, this requires multiple arterial catheterizations. IAD is still of value to help open up vessels to allow placement of the angioplasty balloon, and for vessels inaccessible to angioplasty balloons.

Agents used for vasodilatation:

1. papaverine: usually 200-300 mg infused over 30 mins. May exacerbate vasospasm in some cases¹⁸⁵, may produce thrombocytopenia¹⁸⁶, and unless carefully titrated, it can elevate ICP¹⁸⁷. Largely abandoned because of limited success

2. verapamil: angiography of ICA is performed. If vasospasm is seen, 8 mg of vera-pamil is injected over 2 minutes (Rx: mix 2 vials of Verapamil (each vial is 5 mg in 2 cc) with 6 cc of NS to get 10 mg in 10 cc, inject 8 cc to give 8 mg). Then the other ICA is checked, and similarly injected if indicated. Can also be done in vertebral arteries. Takes 30 minutes for full effect. First ICA that was injected is then rechecked for improvement. Watch BP for hypotension

3. nicardipine: a dihydropiridine calcium channel blocker which acts preferentially on vascular smooth muscle more than cardiac smooth muscle. Restores vessels to at least 60% of normal diameter. 70% of those treated had no stroke on CT. May cause a drop in SBP, but not > 30%¹⁸⁸. Rx intraarterial therapy: 10-40 mg per procedure

30.4.6. Vasospasm management “protocol”

Table 30-10 shows a quick reference guide for vasospasm treatment.

ROUTINE MONITORING FOR ALL SAH PATIENTS

1. serial neuro exams

2. daily CBC with differential

3. transcranial doppler monitoring (where available): usually Mon-Weds-Fri

SPECIFIC TREATMENTS

Patients with clinical suspicion of vasospasm (DIND), or with transcranial doppler (TCD) increases of > 50 cm/sec or with absolute velocities > 200:

1. move patient to the ICU and placed on triple-H therapy for 6 hours if this is not already instituted

2. option: perfusion CT or MRI (if available)

3. if no response to 6 hrs of triple-H therapy, or if perfusion CT suggests vasospasm, patient is taken to angiography to confirm presence of vasospasm and for interventional neuroradiologic treatment (intraarterial verapamil, angioplasty…)

When a patient develops signs suggestive of vasospasm:

1. diagnostic measures (primarily to rule-out other causes of deficit)

A. STAT non-contrast CT to rule-out hydrocephalus, edema, infarct or rebleed

B. STAT bloodwork

1. electrolytes to rule-out hyponatremia⁹⁷

2. CBC to assess rheology and rule-out sepsis or anemia

3. ABG to rule out hypoxemia

C. repeat TCD if available to detect changes indicative of vasospasm

2. treatment measures

A. insert ICP monitor if ICP felt to be problematic, treat elevated ICP with mannitol or CSF drainage before institution hyperdynamic therapy (HDT) (caution: the diuresis from mannitol works against hypervolemia; also, exercise caution in lowering ICP with unsecured aneurysm, see page 1044)

B. administer O₂ to keep pO₂ > 70 mm Hg

C. activity: bed rest, HOB elevated to ≈ 30°

D. TED hose and/or sequential compression boots

E. A-line to monitor BP

F. PA catheter to monitor PCWP and cardiac output when possible (central line to monitor CVP when PA catheter cannot be placed)

G. monitoring labs:

1. ABG and H/H daily

2. serum and urine electrolytes and osmolalities q 12 hr (creatinine elevations may indicate peripheral ischemia from vasopressors)

3. CXR daily

4. frequent EKG

H. strict I & O measurements

I. continue calcium channel blockers (see below)

J. initiate hyperdynamic (triple-H) therapy (see below)

Table 30-10 QUICK REFERENCE GUIDE: Post-clipping management pertinent to vasospasm*

Condition	Management
No vasospasm • clinically intact • normal TCD	1. hemodynamics: A. normotension (SBP > 120 mm Hg) or 30% above baseline B. normal SVR (800-1200) 2. IVF: NS 200 ml/hr
Subclinical vasospasm • high TCDs (> 200 cm/sec) and/or radiographic evidence of vasospasm • clinically intact	1. monitors: PA-catheter, A-line 2. elderly and patients with CAD: EKG, cardiac echo & cardiac enzymes to assess left ventricle function 3. monitor for signs/symptoms of adverse effects of triple-H therapy (chest pain, pulmonary rhonchi, EKG changes…) 4. hemodynamics A. maintain SBP 160-220 mm Hg. If pressors necessary: 1. dopamine + levophed§ 2. add Neosynephrine§ if tachycardia > 140-150 BPM 3. if SBP still low: consider dobutamine§ if SVR > 800 and PCWP within desired parameters B. keep SVR WNL C. maintain PCWP 12-14 mm Hg 5. fluids: monitor I’s & O’s and serum sodium A. IVF: NS + Plasmanate 200-250 ml/hr (Δ to 1/2 NS if Na > 150) B. begin DDAVP§ if UO > 200 ml/hr x 4 hrs 6. hematocrit: keep Hct ≤ 33%
Clinical vasospasm • DIND • high TCDs and/or radiographic vasospasm	1. increase SBP to try and reverse DIND 2. increase PCWP to 18-21 mm Hg (monitor CXR for pulmonary edema) 3. refractory cases: consider cerebral angiography ± angioplasty (see page 1049) or ± intraarterial verapamil (see page 1050)
§ TRIPLE-H THERAPY QUICK REFERENCE (Hypertension, Hypervolemia, Hemodilution) 1. hypertension A. dopamine (see page 22) 1. start at 2.5 μg/kg/min (renal dose) 2. titrate up to 15-20 μg/kg/min B. levophed 1. start at 1-2 μg/min 2. titrate every 2-5 minutes: double the rate up to 64 μg/min, then increase by 10μg/min C. Neosynephrine (phenylephrine): does not exacerbate tachycardia 1. start at 5 μg/min 2. titrate every 2-5 minutes: double the rate up to 64 μg/min, then increase by 10μg/min up to a max of 10 μg/kg D. dobutamine: positive inotrope 1. start at 5 μg/kg/min 2. increase dose by 2.5 μg/kg/min up to a maximum of 20 μg/kg/min 2. hypervolemia A. fluids: normal saline ± plasmanate: 200-250 ml/hr B. DDAVP: antidiuretic (counteracts urinary loss of circulating fluid volume) 1. 2-4 μg SQ q d in divided doses 2. reduce or hold for volume overload or excessive hemodilution 3. hemodilution A. target hematocrit (Hct): ≤ 33% B. transfuse for Hct < 25%

* see text for details

HYPERDYNAMIC THERAPY (HDT) - “TRIPLE-H THERAPY”

AKA “triple-H” therapy (for: hypervolemia, hypertension and hemodilution)¹⁸⁹ or induced arterial hypertension. Elevating systemic blood pressure by expanding circulating blood volume has demonstrated benefit^{190, 191}, but may not reduce overall morbidity and mortality¹⁹². Inducing HTN may be risky with an unclipped ruptured aneurysm. In the case of multiple aneurysms, the risk of hemorrhage from a previously unruptured aneurysm appears low enough to justify volume expansion once the ruptured aneurysm has been clipped¹⁹³. Initiating therapy before CVS is apparent may minimize morbidity from CVS^{95, 194} (patients with SAH often develop hypovolemia early in their course^{103, 195, 196}, and once CVS is evident, changes have already occurred, some possibly irreversible).

PROTOCOL FOR HYPERDYNAMIC THERAPY (modified¹⁹⁰)

Monitors

• indwelling urinary catheter (Foley)

• A-line: essential

• PA catheter: highly recommended. Consider employing one with a pacing port in case this is needed to counteract reflex bradycardia. A catheter with continuous cardiac output (cCO) measuring capability is ideal, which avoids the need to inflate balloon periodically

• some centers monitor transcranial doppler (TCD)

• perfusion CT

Endpoints

✖ to avoid severe cerebral edema or hemorrhagic infarction, do not institute in patient who demonstrates massive edema or a large ischemic infarct coincident with the onset of DIND, especially within the first 6 days post-SAH¹⁹⁷

• use fluids, pressors… (see below) to increase SBP in 15% increments until neurologically improved or the following endpoints all reached

elevate CVP to 8-12 cm H₂O, or PCWP to 18-20 mm Hg^A (for unclipped aneurysms: CVP 6-10 cm H₂O, PCWP 6-10 mm Hg)

maximum BP in clipped aneurysms: SBP < 240 mm Hg, mean BP < 150 (for unclipped aneurysm: SBP < 160)

reduction of elevated TCD readings back towards baseline

• then allow BP to fall to level required to sustain acceptable neurologic function

• if triple-H therapy fails, use endovascular techniques if available (see page 1049)

A. these CVPs and PCWPs are given as a guideline. It is best to determine what CVP or PCWP optimizes the individual patient’s cardiac output, and then maintain that level

Methods of inducing hyperdynamic therapy

Proceed to each step only if needed to meet above endpoints or reverse neurologic deficit.

1. volume expansion: goal is euvolemia or very slight hypervolemia

A. primary IV fluid is crystalloid, usually isotonic (e.g. NS)

B. blood (whole or PRBC) when Hct drops < 40%

C. colloid: plasma fraction or 5% albumin (at 100 ml/hr) to maintain 40% Hct (if Hct is > 40%, use crystalloids⁸⁴)

D. mannitol 20% at 0.25 gm/kg/hr as a drip may improve rheologic properties of blood in the microcirculation (avoid hypovolemia from resultant diuresis)

E. ✖ avoid hetastarch (Hespan®) and dextran which impair coagulation (see page 1042)

F. replace urinary output (U.O.) with crystalloid (if Hct < 40%, then use 5% albumin, usually @ ≈ 20-25 ml/hr)

2. pressors: also see Cardiovascular agents for shock, page 22. A SBP of 100-220 may be required to reverse ischemic symptoms, and is generally safe with a clipped aneurysm in the absence of underlying ischemic heart disease

A. dobutamine: a pure ß agonist. May improve blood flow in cerebral microcirculation at stable MAP. Rx: start at 5 μg/kg/min and titrate to maximize cardiac output (usually 5-18 μg/kg/min)

B. dopamine may alternatively be used (see page 22)

C. if symptoms not reversed after 30-60 mins, add phenylephrine, an alpha agonist. Rx: start at 2 μg/kg/min and titrate to maximize MAP (usually 2-15 μg/kg/min)

3. bradycardia (reflex vagal response) is treated with atropine 1 mg IM q 3-4 hrs to keep pulse 80-120 (or pace through PA catheter pacing port)

4. compensatory diuresis: replace U.O. with albumin (see above). Diuresis may be counteracted with vasopressin (Pitressin®). Caution needs to be exercised due to possible exacerbation of hyponatremia. Use either:

• aqueous vasopressin 5 U SQ titrate to urine output < 200 ml/hr

OR

• vasopressin IV drip, start at 0.1 U/min and titrate up to 0.5 U/min to keep urine output < 200 ml/hr

5. fludrocortisone (Florinef®) 2 mg/d (NB: this dose is ≈ 10 times higher than the homeostatic dose for adrenal replacement therapy, see page 34) or desoxycortisone 20 mg/d in divided doses

6. digitalis if vascular congestion seen on CXR accompanied by decreased cardiac output or ABG deterioration

Complications of hyperdynamic therapy:

1. intracranial complications¹⁹⁷

A. may exacerbate cerebral edema and increase ICP

B. may produce hemorrhagic infarction in an area of previous ischemia

2. extracranial complications

A. pulmonary edema in 17%

B. 3 rebleeds (1 fatal)

C. dilutional hyponatremia in 3%

D. MI in 2%

E. complications of PA catheter¹⁹⁸:

1. catheter related sepsis: 13%

2. subclavian vein thrombosis: 1.3%

3. pneumothorax: 1%

4. hemothorax: may be promoted by coagulopathy from dextran¹⁹⁷

NEUROLOGICAL OUTCOME

The above protocol was used in 58 patients with vasospasm (22 unsecured aneurysm, 2 SAH of unknown etiology) with the following results: neurological improvement occurred in 81%; temporary in 7%. No change was seen in 16%. 10% deteriorated.

CALCIUM CHANNEL BLOCKERS

Trials with calcium channel blockers

Calcium channel blockers (CCB) (AKA calcium antagonist) block the “slow-channel” of calcium influx which reduces the contraction of smooth and cardiac muscle, but does not affect skeletal muscle. It is thus theorized that the abnormal contraction of vascular smooth muscle that may contribute to vasospasm may be mitigated by the administration of CCBs.

CCBs may be more beneficial in neuroprotection than in preventing vasospasm. Their beneficial impact may derive from a number of possible effects:

1. increased red blood cell deformability (which improves blood rheology)

2. prevention of calcium entry into ischemic cells which may mediate the injury from cerebral infarction¹⁹⁹

3. anti-platelet aggregating effect²⁰⁰

4. dilatation of collateral leptomeningeal arteries²⁰¹

Agents presently available

1. nimodipine (Nimotop® - brand discontinued in U.S.): a CCB with preferential CNS action. Blocks dihydropyridine-sensitive (L-type) calcium channels. Does not alter radiographic vasospasm²⁰², and there is no statistically significant difference in mortality. However, outcome is improved²⁰³.

Rx: 60 mg PO or per NG q 4 hrs (monitor BP)^{202, 204, 205} initiated within 96 hrs of SAH. Dosage is halved for liver failure. IV form is similarly effective⁹⁰ where available. Administer either for 21 days or until the patient is discharged home in good neurological condition, whichever occurs first¹⁴¹

2. nicardipine (Cardene®)²⁰⁶: initial trials with indicated a lower incidence of vasospasm in the highest dose group²⁰⁷, however it has subsequently been shown to be no better than placebo in overall outcome (however, it may reduce the need for HDT). Given as an IV drip at 148 μg/kg/hr (high dose²⁰⁷: 0.15 mg/kg/hr)

3. miscellaneous: nifedipine (20 mg PO start TID and increase to QID), diltiazem, and others. Systemic effects usually limit dosage. Less widely used in the U.S. since nimodipine was approved by the FDA in 1989

Side effects of CCBs

Possible side effects include:

1. systemic hypotension: may be mitigated by IV volume expansion

2. renal failure

3. pulmonary edema

30.4.7. Neurogenic stunned myocardium (NSM)

Key concepts:

• impaired cardiac function (reduced ejection fraction) not attributable to underlying coronary artery disease or myocardial abnormalities. May be reversible

• cardiac enzymes (troponin) tend to be lower than expected for the degree of myocardial impairment, distinguishes NSM from acute MI

• putative mechanism: catecholamine surge (possibly in myocardial sympathetic nerves) as a result of hypothalamic stimulation or injury from the SAH

• possible sequalae: hypotension, CHF, arrhythmias… all of which may further exacerbate cerebral ischemia

• peak incidence: 2 days to 2 weeks post SAH

• risk factors: higher Hunt and Hess grade

• treatment: may include dobutamine (for SBP < 90 and low SVR) and/or milrinone (for SBP > 90 and increased SVR)

Previously AKA reversible postischemic myocardial dysfunction¹⁰⁵. Classically seen in patients following cardiac surgery, and attributed to a defect in troponin-I (TnI)¹⁰⁶. Some patients may develop myocardial hypokinesis following SAH¹⁰⁷. May appear compatible with an MI on echocardiography, yet, troponin levels are typically lower (often < 2.8 ng/ml) than would be predicted given the level of myocardial impairment¹⁰⁸. Peak incidence: 2 days to 2 weeks post SAH. The condition reverses completely in most cases within about 5 days. However, ≈ 10% of patients may progress on to an actual MI.

Stroke volume and cardiac output are reduced. Hypotension does not always occur since the reduced cardiac output (CO) may be offset by an increase in SVR. However, the reduced CO may impair the ability to tolerate barbiturates administered for cerebral protection during early surgery due to their myocardial suppressant effect. Intraoperative TEE monitoring may be a useful guide for titrating pressors. The reduced CO may also impede the use of hyperdynamic therapy for vasospasm.

Arrhythmias & EKG changes

EKG changes in over 50% of cases of SAH and include: broad or inverted T-waves, Q-T prolongation, S-T segment elevation or depression, U-waves, premature atrial or ventricular contraction, SVT, V-flutter or V-fib¹⁰⁹, bradycardia. In some cases EKG abnormalities may be indistinguishable from an acute MI^{110, 111}.

Possible mechanism

Hypothalamic ischemia may lead to increased sympathetic tone and the resultant catecholamine surge may produce subendocardial ischemia¹¹² or coronary artery vasospasm¹⁰⁷. The catecholamine surge appears to be more focal (i.e. in the heart) than systemic.

Treatment

Interventions that have been studied for increasing cardiac output in NSM^{113, 114}:

• milrinone: used when SBP > 90 mmHg and normal SVR, or when the patient is on chronic beta blockers

• dobutamine: more effective with hypotension (SBP < 90 mmHg) and low SVR

• other options: stellate ganglion block, magnesium

30.5. Cerebral aneurysms

EPIDEMIOLOGY

Incidence difficult to estimate. Range of autopsy prevalence of aneurysms: 0.2-7.9% (variability depends on use of dissecting microscope, hospital referral and autopsy pattern, overall interest). Recent studies²⁰⁸ indicate prevalence of 5%. Ratio of ruptured:un-ruptured (incidental) aneurysm is 5:3 to 5:6 (rough estimate is 1:1, i.e. 50% of these aneurysms rupture)²⁰⁹. Only 2% of aneurysms present during childhood²¹⁰.

ETIOLOGY

The exact pathophysiology of the development of aneurysms is still controversial. In contrast to extracranial blood vessels, there is less elastic in the tunica media and adventitia of cerebral blood vessels, the media has less muscle, the adventitia is thinner, and the internal elastic lamina is more prominent^{211, 212}. This, together with the fact that large cerebral blood vessels lie within the subarachnoid space with little supporting connective tissue^{213 (p 1644)}may predispose to the development of aneurysms. Aneurysms tend to arise in areas where there is a curve in the parent artery, in the angle between it and a significant branching artery, and point in the direction that the parent artery would have continued had the curve not been present²¹⁴.

The etiology of aneurysms may be:

• congenital predisposition (e.g. defect in the muscular layer of the arterial wall, referred to as a medial gap)

• “atherosclerotic” or hypertensive: presumed etiology of most saccular aneurysms, probably interacts with congenital predisposition described above

• embolic: as in atrial myxoma

• infectious (so called “mycotic aneurysms”, see page 1082)

• traumatic (see Traumatic aneurysms, page 1081)

• associated with other conditions (see below)

LOCATION

Saccular aneurysms, AKA berry aneurysms are usually located on major named cerebral arteries at the apex of branch points which is the site of maximum hemodynamic stress in a vessel²¹⁵. More peripheral aneurysms do occur, but tend to be associated with infection (mycotic aneurysms) or trauma. Fusiform aneurysms are more common in the vertebrobasilar system. Dissecting aneurysms should be categorized with arterial dissection (see page 1160).

Saccular aneurysms location:

• 85-95% in carotid system, with the following 3 most common locations:

ACoA (single most common): 30% (ACoA & ACA more common in males)

p-comm: 25%

middle cerebral artery (MCA): 20%

• 5-15% in posterior circulation (vertebro-basilar)

≈ 10% on basilar artery: basilar bifurcation, AKA basilar tip, is the most common, followed by BA-SCA, BA-VA junction, AICA

≈ 5% on vertebral artery: VA-PICA junction is the most common

• 20-30% of aneurysm patients have multiple aneurysms²¹⁶ (see page 1080)

PRESENTATION OF ANEURYSMS

MAJOR RUPTURE

The most frequent presentation

1. most commonly produces SAH (see page 1034), which may be accompanied by:

2. intracerebral hemorrhage: occurs in 20-40% (more common with aneurysms distal to the Circle of Willis, e.g. MCA aneurysms)

3. intraventricular hemorrhage: occurs in 13-28%²¹⁷ (see below)

4. subdural blood in 2-5%

Intraventricular hemorrhage

See page 1228 for other etiologies of intraventricular hemorrhage (IVH).

IVH occurs in 13-28% of ruptured aneurysms in clinical series (higher in autopsy series)²¹⁷ and appears to carry a worse prognosis (64% mortality)²¹⁷. The size of the ventricles on admission was the most important prognosticator (large vents being worse). Patterns that may occur:

1. distal PICA aneurysms: may rupture directly into 4th ventricle through the foramen of Luschka²¹⁸

2. a-comm aneurysm: it has been asserted that IVH occurs from rupture through the lamina terminalis into the anterior 3rd or lateral ventricles, however, this is not always borne out at the time of surgery

3. distal basilar artery or carotid terminus aneurysms: may rupture through the floor of the 3rd ventricle (rare)

PRESENTATION OTHER THAN MAJOR RUPTURE

May be thought of as possible “warning signs”.

1. mass effect

A. giant aneurysms: including brain stem compression producing hemiparesis and cranial neuropathies

B. cranial neuropathy (average latency from symptom to SAH was 110 days^B) including:

1. oculomotor (3rd nerve) palsy (ONP): occurs in ≈ 9% of p-comm aneurysms^219A, less common with basilar apex aneurysm. Symptoms of ONP may include:

a. extraocular muscle palsy (eye deviates “down and out” → diplopia)

b. ptosis

c. dilated unreactive pupil ( non-pupil-sparing third nerve palsy is the classic finding of 3rd nerve compression - see page 835)

The development of a third nerve palsy in a patient with an unruptured aneurysm is a medical emergency as it probably results from aneurysmal expansion and may portend impending rupture.

2. visual loss due to²²⁰

a. compressive optic neuropathy with ophthalmic artery aneurysms: characteristically produces nasal quadrantanopsia

b. chiasmal syndromes due to ophthalmic, a-comm, or basilar apex aneurysms

3. facial pain syndromes in the ophthalmic or maxillary nerve distribution that may mimic trigeminal neuralgia can occur with intracavernous or supraclinoid aneurysms^{220, 221}

C. intra- or suprasellar aneurysm producing endocrine disturbance²²² due to pituitary gland or stalk compression

2. minor hemorrhage: warning or sentinel hemorrhage (see Headache, page 1035). This group had the shortest latency (10 days) between symptom and SAH^B

3. small infarcts or transient ischemia due to distal embolization (including amaurosis fugax, homonymous hemianopsia…)²²⁰: average latency from symptom to SAH was 21 days^B

4. seizures: at surgery, an adjacent area of encephalomalacia may be found²²⁰. The seizures may arise as a result of localized gliosis and do not necessarily represent aneurysmal expansion as there is no data to indicate an increased risk of hemorrhage in this group

5. headache²²⁰ without hemorrhage: abates after treatment in most cases

A. acute: may be severe and “thunderclap” in nature³⁶, some describe as “worst headache of my life”. Has been attributed to aneurysmal expansion, thrombosis, or intramural bleeding³², all without rupture

B. present for ≥ 2 weeks: unilateral in about half (often retro-orbital or periorbital), possibly due to irritation of overlying dura. Diffuse or bilateral in the other half, possibly due to mass effect → increased ICP

6. incidentally discovered (i.e. asymptomatic, e.g. those found on angiography, CT or MRI obtained for other reasons)

A. ruptured and unruptured p-comm aneurysms

B. the average latency quoted for some of these symptoms comes from a retrospective study of patients presenting with SAH who were identified as having a warning symptom²⁶

30.5.1. Conditions associated with aneurysms

• autosomal dominant polycystic kidney disease: (see below)

• fibromuscular dysplasia (FMD): prevalence of aneurysms in renal FMD is 7%, in aortocranial FMD 21%

• arteriovenous malformations (AVM) including moyamoya disease (see AVMs and aneurysms, page 1100)

• connective tissue disorders²²³:

A. Ehlers-Danlos, especially type IV (deficient collagen type III) which also has a high rate of arterial dissection including with angiography or coiling

B. Marfan syndrome (see page 1161)

C. pseudoxanthoma elasticum

• multiple other family members with intracranial aneurysms. Familial intracranial aneurysm syndrome (FIA): 2 or more relatives, third degree or closer, harbor radiographically proven aneurysms (also, see Familial aneurysms, page 1080)

• coarctation of the aorta²²⁴

• Osler-Weber-Rendu syndrome

• atherosclerosis²⁹

• bacterial endocarditis

AUTOSOMAL DOMINANT POLYCYSTIC KIDNEY DISEASE

Adult polycystic kidney disease is seen in 1 of every 500 autopsies, and approximately 500,000 people in the U.S. carry the mutant gene for autosomal dominant polycystic kidney disease (ADPKD). Renal function is usually normal during the first few decades of life, with progressive chronic renal failure ensuing. HTN is a common sequelae. Transmission is autosomal dominant, with 100% penetrance by 80 yrs of age²²⁵. Cystic disease of other organs may occur (viz.: liver in ≈ 33%, and occasionally lung, pancreas)²²⁶.

Reported prevalence of aneurysms with ADPKD: 10-30%²²⁷, with 15% being a reasonable estimate²²⁸. Most were located on the MCA, with multiple aneurysms present in 31%²²⁹. In addition to the increased incidence of aneurysms, there appears to be an increased risk of rupture²³⁰, with 64% occurring before age 50. As a result, patients with ADPKD carry a 10-20 fold increased risk of SAH compared to the general population²³¹. Aneurysms are rarely detectable before age 20 years. The average rate of rupture of incidental aneurysms is ≈ 2%/yr (see Unruptured aneurysms, page 1077).

Recommendations

Using the above statistics, together with the life expectancy of patients with ADPKD, and other estimations (of operative morbidity and mortality, etc.), results of decision analysis is that arteriography not be routinely employed in patients older than 25 yrs²²⁷. However, patients with symptoms possibly due to unruptured aneurysms, and those with SAH, should undergo angiography and subsequent surgical repair of any aneurysms discovered (especially those > 1 cm diameter). A decision analysis study²²⁸ determined that screening with MRA was beneficial compared to treating patients once they became symptomatic. In a young patient with ADPKD with either a history of aneurysms or a kindred of ADPKD with aneurysms, repeat screening may be effectively repeated every ≈ 2-3 years (in a kindred of ADPKD without aneurysms, every 5-20 yrs was recommended)²²⁸.

30.6. Treatment options for aneurysms

The optimal treatment for an aneurysm depends on the condition of the patient, the anatomy of the aneurysm, the ability of the surgeon, and must be weighed against the natural history of the condition. Also, treatment of the aneurysm facilitates treatment of vasospasm, should it occur.

Natural history:

1. risk of bleeding into subarachnoid space

A. for ruptured aneurysms: this is the risk of rebleeding: see page 1043

B. for unruptured aneurysms: see page 1077

C. for cavernous carotid artery aneurysms: this risk is low (see page 1079)

2. spontaneous thrombosis of an aneurysm is a rare occurrence^232-234 (estimates in autopsy series is 9-13%²³⁴). However they may reappear^{235, 236}, and delayed rupture may occur sometimes even years later

Although still controversial, endovascular treatment should be initially considered in treating amenable ruptured aneurysms. For unruptured aneurysms, see page 1077.

Therapies that do not directly address the aneurysm

The hope here is that the aneurysm will not bleed and that it will thrombose (see above).

1. continue medical management initiated on admission: i.e. control of HTN, continue calcium-channel blockers, stool softeners…continue bed rest for ≈ 1 week then allow bedside commode

2. treatment options generally not used

A. antifibrinolytic therapy (e.g. -aminocaproic acid (EACA)): ✖ NB: NOT USED. Reduces rebleeding, but increases the incidence of arterial vasospasm and hydrocephalus¹²⁰

B. serial LPs: an historical treatment²³⁷, may increase the risk of aneurysmal rupture

Endovascular techniques to treat the aneurysm

1. thrombosing the aneurysm:

A. “coiling” with Guglielmi electrolytically detachable coils (see below)

B. Onyx HD 500 (see page 1102) has been used for wide-necked or giant ICA aneurysms²³⁸. Out of 22 patients, there was 1 parent ICA stenosis and 2 ICA occlusions caused by Onyx migration

2. trapping: effective treatment requires distal AND proximal arterial interruption, usually by endovascular techniques²³⁹, occasionally by direct surgical means (ligation or clip occlusion), or some combination. May also incorporate vascular bypass (e.g. EC-IC bypass) to maintain flow distal to trapped segment²⁴⁰

3. proximal ligation (hunterian ligation): useful for giant aneurysms^{241, 242}. For non-giant aneurysms provides little benefit and adds the risk of thromboembolism (which may be reduced by occluding the CCA rather than the ICA²⁴²). May also elevate the risk of developing aneurysms in the contralateral circulation²⁴³

Surgical treatment options for aneurysms

1. clipping: the surgical gold standard. Surgical placement of a clip across the neck of the aneurysm to exclude the aneurysm from the circulation (see below) without occluding normal vessels

2. wrapping or coating the aneurysm: although this should never be the goal of surgery, situations may arise in which there is little else that can be done (e.g. fusiform basilar trunk aneurysms, aneurysms with significant branches arising from the dome, or part of the neck within the cavernous sinus)

A. with muscle: the first method used to surgically treat an aneurysm²⁴⁴ (the patient described died from rebleeding)

B. with cotton or muslin: popularized by Gillingham²⁴⁵. Analysis of 60 patients showed that 8.5% rebled in ≤ 6 mos, and the annual rebleeding rate was 1.5% thereafter²⁴⁶ (similar to natural history)

C. with plastic resin or other polymer: may be slightly better than muscle or gauze²⁴⁷. One study with long follow-up found no protection from rebleeding during the first month, but thereafter the risk was slightly lower than the natural history²⁴⁷. Other studies show no difference from natural course²⁴⁸

D. Teflon and fibrin glue²⁴⁹

Treatment decisions: coiling vs. clipping

Factors that favor surgical clipping:

1. younger age: lower risk of surgery, and lower lifetime risk of recurrence than with coiling

2. middle cerebral artery (MCA) bifurcation aneurysms

3. giant aneurysms: > 20 mm diameter)²⁵⁰. High recanalization rate with coiling

4. symptoms due to mass effect: clipping^{251, 252} may be better than coiling. In 13 patients with p-comm aneurysms and oculomotor nerve (3rd nerve) palsy (ONP), 6 of 7 patients clipped vs. 2 of 6 with coiling recovered completely²¹⁹. Partial ONP improved with either treatment, but complete ONP recovered in 3 of 4 patients clipped vs. 0 of 3 coiled²¹⁹

5. small aneurysm: < 1.5-2 mm diameter 250. Higher incidence of intraprocedural rupture with coiling

6. wide aneurysm neck²⁵⁰

7. patients with residual filling of the aneurysm after coiling since there is significant risk of rebleeding

Factors favorable for coiling:

1. elderly patients (> 75 yrs): there appears to be a significant reduction in morbidity with coiling compared to clipping

2. poor clinical grade

3. inaccessible ruptured aneurysms

4. aneurysm configuration⁷⁴:

A. dome-to-neck ratio (AKA fundus-to-neck ratio) ≥ 2

B. and an absolute neck diameter < 5 mm

5. posterior circulation aneurysms

6. patients on Plavix®

7. may be considered in cases where there is a failure of attempted clipping, or with aneurysms that are technically difficult to clip (a category that is very vague and varies widely with the experience of the neurosurgeon²⁵³)

Controversial areas with coiling:

1. unruptured aneurysms: unruptured M1-M2 junction MCA aneurysms are often difficult to coil because of a branch near the neck²⁵⁴

ELECTROLYTICALLY DETACHABLE COILS (EDC)

Electrolytically detachable platinum coils AKA Guglielmi detachable coils, or simply “coils”, placed either during open surgery or, more commonly, via endovascular techniques^255-257. For indications for coiling vs. clipping, see above. Goals of coiling:

1. to promote thrombosis of the aneurysmal sac to prevent (re)bleeding

2. to reduce symptoms of mass effect²⁵⁸, if any (clipping still appears to be superior to coiling for this - see above)

Available data: There has been no long-term prospective randomized trial to compare coiling to microsurgery (MS)^{253, 259}. The largest trial to date, the International Subarachnoid Hemorrhage Aneurysm Trial (ISAT)²⁶⁰ had the important shortcomings detailed in Table 30-11. Also, still unresolved: coiling vs. MS for unruptured aneurysms.

Results

Procedural morbidity rate of coiling (mostly aneurysmal rupture) ≈ 4%,; mortality = 1%²⁶¹.

Results may be reported as occlusion rates or in terms of recurrence of SAH. Depending on criteria and timing of follow-up, MS fares better than coiling with occlusion rates and prevention of recurrent SAH.

Results of ISAT study: at 1 year follow-up, there was an absolute reduction of risk of having a poor outcome by 7% with coiling (24%) than with MS (31%).

Table 30-11 Methodological short-comings of ISAT

1. only 20% of 9559 patients presenting with SAH were randomized* • selection could introduce bias • more nonrandomized patients underwent MS than EDC • guidelines not provided for which patients to consider for EDC 2. most study centers were located in Europe, Australia & Canada 3. the expertise of the surgeons and the interventionalists were not reported and were not necessarily comparable 4. the following features are not entirely representative of SAH patients at large • 80% of patients were in good clinical condition (H&H grade 1 or 2) • 93% of aneurysms were ≤ 10 mm diameter • 97% were in the anterior circulation 5. rebleeding rate: after EDC (2.4%) or MS (1.0%) was high for both groups, and the difference could be more significant beyond the 1 year follow-up provided

* most SAH patients were referred specifically for MS or EDC. The only patients that were were randomized were those for whom a panel decided it was not clear which procedure would be superior. Out-comes were not provided for non-randomized patients

Treatment failures may be due to:

1. early failure

A. intraprocedural rupture

B. vasospasm preventing endovascular treatment (< 1.5%)

C. failure to achieve initial obliteration: 39% are completely obliterated, 46% are ≥ 95% occluded, and 15% are < 95% occluded²⁶². Of aneurysms not initially occluded²⁶²:

1. 46% progressively thrombosed

2. 26% showed stable neck remnants

3. 28% showed enlargement of residual neck

2. late failure

A. failure of partially obliterated aneurysms to go on to thrombose

B. coil compaction

C. enlargement of residual neck

D. recanalization of aneurysm: 1.8% risk²⁶²

Recurrent SAH following coil placement

1. ISAT study: 0.16% at 1 year²⁶⁰

2. 5% incidence of SAH (rebleeding) within 6 months of treatment (high compared to MS) in one series of 75 patients with acutely ruptured aneurysms²⁵⁰

3. in another series of 141 coiled aneurysms²⁶² (42% incidental, 41% acutely ruptured): 1 patient rebled within 6 months (1.7% of the ruptured group)

Repeat treatment: Data on long-term efficacy is lacking. At least 20% of patients with relatively short follow-up needed retreatment in one series²⁶³. In the ISAT study, more than 4 times as many patients undergoing coiling needed additional procedures than did the MS group²⁶⁰.

Stent assisted coiling: Stent assisted coiling should rarely be used with ruptured aneurysms because of the necessity of dual antiplatelet therapy (ASA/Plavix) which increases the morbidity of subsequent ventriculostomy, shunting…

Treatment of aneurysmal rupture during coiling

1. inflate balloon if balloon assisted coiling

2. immediately reverse anticoagulation. 50 mg of protamine should be available during the procedure

3. continue to pack coils as rapidly as possible

4. insert an extraventricular drain (EVD)

30.7. Timing of aneurysm surgery

Controversy exists between so-called “early surgery” (generally, but not precisely defined as ≤ 48-96 hrs post SAH) and “late surgery” (usually ≥ 10-14 days post SAH). Also see page 1074 for timing issues related to basilar bifurcation aneurysms.

Early surgery advocated for the following reasons:

1. if successful, virtually eliminates the risk of rebleeding which occurs most frequently in the period immediately following SAH (see Rebleeding, page 1043)

2. facilitates treatment of vasospasm which peaks in incidence between days 6-8 post SAH (never seen before day 3) by allowing induction of arterial hypertension and volume expansion without danger of aneurysmal rupture

3. allows lavage to remove potentially vasospasmogenic agents from contact with vessels (including use of thrombolytic agents, see page 1048)

4. although operative mortality is higher, overall patient mortality is lower²⁶⁴

Arguments against early surgery, in favor of late surgery include:

1. inflammation and brain edema are most severe immediately following SAH

A. this necessitates more brain retraction

B. at the same time this softens the brain making retraction more difficult (retractors have more tendency to lacerate the more friable brain)

2. the presence of solid clot that has not had time to lyse impedes surgery

3. the risk of intraoperative rupture is higher with early surgery

4. possible increased incidence of vasospasm following early surgery from mechanotrauma to vessels

Factors that favor choosing early surgery include:

1. good medical condition of patient

2. good neurologic condition of patient (Hunt and Hess (H&H) grade ≤ 3)

3. large amounts of subarachnoid blood, increasing the likelihood and severity of subsequent vasospasm (see Table 30-6, page 1046). Having the aneurysm clipped permits use of hyperdynamic therapy for vasospasm (see Hyperdynamic therapy (HDT) - “Triple-H therapy”, page 1052)

4. conditions that complicate management in face of unclipped aneurysm: e.g. unstable blood pressure; frequent and/or intractable seizures

5. large clot with mass effect associated with SAH

6. early rebleeding, especially multiple rebleeds

7. indications of imminent rebleeding: (see below)

Factors that favor choosing delayed surgery (10-14 days post SAH) include:

1. poor medical condition and/or advanced age of patient (age may not be a separate factor related to outcome, when patients are stratified by H&H grade²⁶⁵)

2. poor neurologic condition of patient (H&H grade ≥ 4): controversial. Some say the risk of rebleeding and its mortality argues for early surgery even in bad grade patients²⁶⁶ since denying surgery on clinical grounds may result in withholding treatment in some patients who would do well (54% of H&H grade IV and 24% of H&H grade V patients had favorable outcome in one series²⁶⁵). Some data show no difference in surgical complications in good and bad grade patients with anterior circulation aneurysms²⁶⁷

3. aneurysms difficult to clip because of large size, or difficult location necessitating a lax brain during surgery (e.g. difficult basilar bifurcation or mid-basilar artery aneurysms, giant aneurysms)

4. significant cerebral edema seen on CT

5. the presence of active vasospasm

Conclusions

There is insufficient Class 1 data to make any firm conclusions. Therefore the following is based on trials that are non-randomized, etc.

1. there is an overall trend towards better outcome with early surgery than with later surgery, however, the advantage of early surgery (reduced rebleeding) is at least partially offset by the disadvantages of early surgery²⁶⁸ (see above)

2. outcomes seem worse when surgery is performed between days 4-10 after SAH (the “vasospastic interval”) than if performed early or late

IMMINENT ANEURYSM RUPTURE

Findings that may herald impending aneurysm rupture include:

1. progressing cranial nerve palsy e.g. development of 3rd nerve palsy with p-comm aneurysm (traditionally regarded as an indication for urgent treatment) (see page 1056)

2. increase in aneurysm size on repeat angiography

3. beating aneurysm sign²⁶⁹: pulsatile changes in aneurysm size between cuts or slices on imaging (may be seen on angiography, MRA, or CTA)

30.8. General technical considerations of aneurysm surgery

The goal of aneurysm surgery is to prevent rupture or further enlargement of the aneurysm, while at the same time preserving all normal vessels and minimizing injury to brain tissue and cranial nerves. This is usually accomplished by excluding the aneurysm from the circulation with a clip across its neck. Placing the clip too low on the aneurysm neck may occlude the parent vessel, while too distal placement may leave a so-called “aneurysmal rest” which is not benign (see below).

See Intraoperative aneurysm rupture below for general measures to reduce the risk of this complication during surgery.

Aneurysmal rest

When a portion of the aneurysm neck is not occluded by a surgical clip, it is referred to as an aneurysmal rest. A “dogear” occurs when a clip is angled to leave part of the neck at one end, and obliterates the neck at the other. Rests are not innocuous, even if only 1-2 mm, because they may later expand and possibly rupture years later, especially in younger patients²⁷⁰. The incidence of rebleeding was 3.7% in one study, with an annual risk of 0.4-0.8% during the observation period of 4-13 yrs²⁷¹. Patients should be followed with serial angiography, and any increase in size should be treated by reoperation or endovascular techniques if possible.

BOOKING THE CASE - CRANIOTOMY: FOR ANEURYSM

Also see defaults & disclaimers (page v).

1. position: (depends on location of aneurysm), radiolucent head-holder

2. intraoperative angiography (optional)

3. equipment: microscope (with ICG capability if used)

4. blood: type and cross 2 U PRBC

5. post op: ICU

6. consent (in lay terms for the patient - not all-inclusive):

A. procedure: surgery through the skull to place a permanent clip on the base of the aneurysm to prevent future bleeding, intraoperative angiogram, possible placement of external (ventricular) drain, possible lumbar drain

B. alternatives: nonsurgical management, endovascular treatment only for aneurysms that are candidates

C. complications: (usual craniotomy complications - see page v) plus (the following are not really complications of surgery but are possible developments) post-op vasospasm, hydrocephalus, formation of new aneurysms

SURGICAL EXPOSURE

To avoid excessive brain retraction, surgical exposure requires sufficient bony removal and adequate brain relaxation (see below).

BRAIN RELAXATION

More critical for ACoA and basilar tip than for easier to reach aneurysms such as pcomm or MCA…. Techniques include:

1. hyperventilation

2. CSF drainage: provides brain relaxation and a field dry of CSF, and removes blood & blood breakdown products. ✖ CSF drainage before opening the dura is associated with an increased risk of aneurysmal rebleeding (see page 1043)

A. ventriculostomy: risks include seizures, bleeding from catheter insertion, infection (ventriculitis, meningitis), possible increased risk of vasospasm

1. placed pre-op in cases of acute post-SAH hydrocephalus (see page 1044)

2. placed intra-op

B. lumbar spinal drainage (see below)

C. intraoperative drainage of CSF from cisterns

3. diuretics: mannitol and/or furosemide. Although proof is lacking, lowering ICP by this or any means may theoretically increase the risk of rebleeding²⁷²

Lumbar spinal drainage

May be inserted with Tuohy needle following induction of anesthesia (to minimize BP elevation), prior to final positioning. CSF is gradually withdrawn by the anesthesiologist only after the dura is opened (to minimize chances of intraoperative aneurysmal bleeding), usually a total of 30-50 cc are removed in ≈ 10 cc aliquots.

Risks include¹²⁹: aneurysmal rebleeding (≤ 0.3%), back pain (10%, may be chronic in 0.6%), catheter malfunction preventing CSF drainage (< 5%), catheter fracture or laceration resulting in retained catheter tip in the spinal subarachnoid space, post-op CSF fistula, spinal H/A (may be difficult to distinguish from post-craniotomy H/A), infection, neuropathy (from nerve root impingement with needle), epidural hematoma (spinal and/or intracranial).

CEREBRAL PROTECTION DURING SURGERY

PATHOPHYSIOLOGY OF CEREBRAL ISCHEMIA

The cerebral metabolic rate of oxygen consumption (CMRO₂) (see page 1010) arises from neurons utilizing energy for two functions: 1) maintenance of cell integrity (homeostasis) which normally accounts for ≈ 40% of energy consumption, and 2) conduction of electrical impulses. Occlusion of an artery produces a central core of ischemic tissue where the CMRO₂ is not met. The oxygen deficiency precludes aerobic glycolysis and oxidative phosphorylation. ATP production declines and cell homeostasis cannot be maintained, and within minutes irreversible cell death occurs; a so-called cerebral infarction. Surrounding this central core is the penumbra, where collateral flow (usually through leptomeningeal vessels) provides marginal oxygenation which may impair cellular function without immediate irreversible damage. Cells in the penumbra may remain viable for hours.

CEREBRAL PROTECTION BY INCREASING THE ISCHEMIC TOLERANCE OF THE CNS

1. drugs that mitigate the toxic effects of ischemia without reducing CMRO₂

A. calcium channel blockers: nimodipine, nicardipine, flunarizine

B. free radical scavengers: superoxide dismutase, dimethylthiourea, lazaroids, barbiturates, Vitamin C

C. mannitol: although not a cerebral protectant per se, it may help re-establish blood flow to compromised parenchyma by improving the microvascular perfusion by transiently increasing CBV and decreasing blood viscosity

2. reduction of CMRO₂

A. by reducing the electrical activity of neurons: titrating these agents to a isoelectric EEG reduces CMRO₂ by up to a maximum of ≈ 50%

1. barbiturates: in addition to reducing CMRO₂, they also redistribute blood flow to ischemic cortex, quench free radicals, and stabilize cell membranes. For dosing of thiopental, see below

2. isoflurane (see page 2): shorter acting and less myocardial depression than with barbiturates

B. by reducing the maintenance energy of neurons: no drugs developed to date can accomplish this, only hypothermia has any effect on this. Below mild hypothermia, extracerebral effects must be monitored (see page 880)

1. even mild hypothermia (core temperatures down to 33° C) has beneficial effects

2. moderate hypothermia: 32.5-33° C has been used for head injury

3. deep hypothermia to 18° C permits the brain to tolerate up to 1 hour of circulatory arrest

4. profound hypothermia to < 10° C allows several hours of complete ischemia (the clinical usefulness of this has not been substantiated)

ADJUNCTIVE CEREBRAL PROTECTION TECHNIQUES USED IN ANEURYSM SURGERY

1. systemic hypotension

A. usually used during final approach to aneurysm and during manipulation of aneurysm for clip application

B. theoretical goals

1. to reduce turgor of aneurysm facilitating clip closure, especially with atherosclerotic neck

2. to decrease transmural pressure (see page 1044) to reduce the risk of intraoperative rupture

C. danger of hypoxic injury to other organs and brain (including areas of impaired autoregulation as well as normal areas). Because of this, some surgeons avoid this method

2. “focal” hypotension: using temporary aneurysm clips (specially designed with low closing force to avoid intimal injury) placed on parent vessel (small perforators will not tolerate temporary clips without injury)

A. used in conjunction with methods of cerebral protection against ischemia

B. may be combined with systemic hypertension to increase collateral flow

C. the proximal ICA can tolerate an hour or more of occlusion in some cases, whereas the perforator bearing segments of the MCA and the basilar apex may tolerate clipping for only a few minutes

D. in addition to the risk of ischemia, there is the risk of intravascular thrombosis and subsequent release of emboli upon removal of the clip

3. circulatory arrest, utilized in conjunction with deep hypothermia

A. candidates include patients with large aneurysms that contain significant atherosclerosis and/or thrombosis that impedes clip closure and a dome that is adherent to vital neural structures

SYSTEMATIC APPROACH TO CEREBRAL PROTECTION²⁷³

The following factors may mandate the use of temporary clips (and associated techniques of cerebral protection): giant aneurysm, calcified neck, thin/fragile dome, adherence of dome to critical structures, vital arterial branches near the aneurysm neck, intraoperative rupture. Aside from giant aneurysms, most of these factors may be difficult to identify pre-op. Therefore, Solomon provides some degree of cerebral protection to all patients undergoing aneurysm surgery.

1. spontaneous cooling is permitted during surgery, which usually results in a body temperature of 34° C by the time that dissection around the aneurysm begins

2. if temporary clipping is utilized

A. if a long segment of the ICA is being trapped, administer 5000 U IV heparin to prevent thrombosis and subsequent emboli

B. < 5 mins temporary clip occlusion: no further intervention

C. up to 10 or 15 mins occlusion: administer thiopental 5 mg/kg loading bolus, followed by drip infusion titrated to burst suppression on compressed spectral array EEG

D. > 20 mins occlusion: not tolerated (except possibly ICA proximal to pcomm), terminate operation if possible and plan repeat operation utilizing

1. deep hypothermic circulatory arrest (see above)

2. endovascular techniques

3. bypass grafting around the segment to be occluded

POSTOPERATIVE ANGIOGRAPHY

Due to the fact that unexpected findings (aneurysmal rest, unclipped aneurysm, or major vessel occlusion) were seen on 19% of post-op angiograms (the only predictive factor identified was a new post-op deficit, which signalled major vessel occlusion) the use of routine post-op angiography has been recommended²⁷⁴.

SOME DRUGS USEFUL IN ANEURYSM SURGERY

propofol (Diprivan®)DRUG INFO

May be used to achieve burst suppression²⁷⁵ with shorter duration of action than other barbiturates. Results are preliminary, further investigation is needed to demonstrate the degree of neuroprotection. Has been reported at doses 170 μg/kg/min for neuroprotection²⁷⁶ (if tolerated) but this may be risky. May also be used as a continuous drip for sedation (see page 24), and for ICP management (see page 885). Reverses rapidly upon discontinuation (usually within 5-10 minutes).

SIDE EFFECTS: possible anaphylactic reaction with angioneurotic edema (angioedema) of the airways²⁷⁷, Propofol Infusion syndrome (see page 25).

30.8.1. Intraoperative aneurysm rupture

EPIDEMIOLOGY

Reported rates of intraoperative aneurysm rupture (IAR) range from ≈ 18% in the cooperative study (1963-1978)²⁷⁸ to 40% in a more recent series²⁷⁹. Although rupture rate may be higher in early surgery than with late surgery²⁷⁹, other series found no difference²⁸⁰.

Morbidity and mortality for patients experiencing significant IAR is ≈ 30-35% (vs. ≈ 10% in the absence of this complication), although IAR may primarily affects outcome when it occurs during induction of anesthesia or opening of dura²⁷⁹.

For aneurysm rupture during coiling, see page 1060.

PREVENTION OF INTRAOPERATIVE RUPTURE

Presented as a list here to be incorporated into general operative techniques.

1. prevent hypertension from catecholamine response to pain:

A. insure deep anesthesia during headholder pin placement and skin incision

B. consider local anesthetic (without epinephrine) in headholder pin-sites and along incision line

2. minimize increases in transmural pressure: reduce MAP to slightly below base-line just prior to dural opening

3. reduce shearing forces on aneurysm during dissection by minimizing brain retraction:

A. radical removal of sphenoid wing for circle of Willis aneurysms

B. reduce brain volume by a number of mechanisms: diuretics (mannitol, furosemide), CSF drainage through lumbar subarachnoid drain at the time of dural incision, hyperventilation

4. reduce risk of large tear in aneurysm fundus or neck:

A. utilize sharp dissection in exposing aneurysm and in removing clot from around aneurysm

B. whenever possible, completely mobilize and inspect aneurysm before attempting clip application

DETAILS OF INTRAOPERATIVE RUPTURE

Rupture can occur during any of the three following stages of aneurysm surgery²⁸¹:

A. initial exposure (predissection)

1. rare. Brain can become surprisingly tight even when bleeding seems to be into open subarachnoid space. Usually carries poor prognosis

2. possible causes:

A. vibration from bone work: dubious

B. increasing transmural pressure upon opening the dura

C. hypertension from catecholamine response to pain (see above)

3. management tactics:

A. have anesthesiologist radically drop BP

B. control bleeding (with anterior circulation aneurysms) by placing temporary clip across ICA as it exits from cavernous sinus, or if not possible then compress ICA in patient’s neck through drapes

C. if necessary to gain control, resect portions of frontal or temporal lobe

B. dissection of the aneurysm: accounts for the majority of IARs, two basic types:

1. tears caused by blunt dissection

A. tends to be profuse, proximal to the neck, and difficult to control

B. do not attempt definitive clipping unless adequate exposure has been achieved (which is usually not the case with these tears)

C. temporary clipping: this step is often necessary in this situation, after the temporary clip is in place return the MAP to normal and administer neuroprotective agent (e.g. propofol)

D. once the temporary clip is in place, it is better to take a few extra moments to improve the exposure and apply a well placed permanent clip instead of hastily clipping and trying to restore circulation

E. microsutures may need to be placed to close any portion of the tear that extends onto the parent vessel

2. laceration by sharp dissection

A. tend to be small, often distally on fundus, and usually easily controlled by a single suction

B. may respond to gentle tamponade with a small cottonoid

C. may shrink down with repeated low current strokes with the bipolar (avoid the temptation to use continuous high current)

C. clip application: bleeding at this point is usually due to either

1. inadequate exposure of aneurysm: clip blade may penetrate unseen lobe of aneurysm. Similar to tears caused by blunt dissection (see above). Bleeding worsens as clip blades become approximated

A. prompt opening and removal of clip at the first hint of bleeding may minimize the extent of the tear

B. utilize 2 suckers to determine if definitive clipping can be done, or what is more common, to allow temporary clipping (see above)

2. poor technical clip application: tends to abate as clip blades become approximated. Inspect the blade tips for the following:

A. to be certain that they span the breadth of the neck. If not, a second longer clip is usually applied parallel to the first, which may then be advanced

B. to verify that they are closely approximated. If not, tandem clips may be necessary, and sometimes multiple clips are needed

30.9. Aneurysm recurrence after treatment

Incompletely treated aneurysms may increase in size and/or bleed. This includes aneurysms that are clipped or coiled where there is still aneurysm filling, as well as a persistent aneurysm rest or a neck (see page 1061). While most aneurysm rests appear to be stable, there is a small subset that may enlarge or rupture²⁸².

Additionally, even an aneurysm that has been completely obliterated may recur, and therefore one has to consider the durability of treatment. The risk of recurrence of a completely clipped aneurysm is ≈ 1.5% at 4.4 years²⁸².

Table 30-12 Follow-up schedule for treated aneurysms

Perform indicated study at the following times after treatment
Coiled aneurysms	Clipped aneurysms
Study: CTA or gad-MRA*	Study: CTA
6 mos	1 year
1.5 years	5 years
3.5 years	every 10 years thereafter
? every 5-10 years (as with clipped aneurysms)

* gad-MRA indicates gadolinium MRA which is more sensitive here than TOF-MRA (see page 132). Use the same modality for each follow-up to facilitate accurate comparison

FOLLOW-UP AFTER ANEURYSM TREATMENT

Based on the above, together with the small risk of de novo aneurysm formation²⁸², there is a trend to indefinitely follow patients with known aneurysms. One suggested follow-up schedule is shown in Table 30-12.

30.10. Aneurysm type by location

30.10.1. Anterior communicating artery aneurysms

The single most common site of aneurysms presenting with SAH²⁸³. May additionally present with diabetes insipidus (DI) or other hypothalamic dysfunction.

CT SCAN

SAH in these aneurysms results in blood in the anterior interhemispheric fissure in essentially all cases, and is associated with intracerebral hematoma in 63% of cases²⁸⁴. Intraventricular hematoma is seen in 79% of cases, with the blood entering the ventricles from the intracerebral hematoma in about one third of these. Acute hydrocephalus was present in 25% of patients (late hydrocephalus, a common sequelae of SAH, was not studied).

Frontal lobe infarcts occur in 20%, usually several days following SAH²⁸⁴. One of the few causes of the rare finding of bilateral ACA distribution infarcts is vasospasm following hemorrhage from rupture of an ACoA aneurysm. This results in prefrontal lobotomy-like findings of apathy and abulia.

ANGIOGRAPHIC CONSIDERATIONS

Essential to evaluate contralateral carotid, to determine if both ACAs fill the aneurysm. If the aneurysm fills with one side only, it is desirable to inject the other side while cross compressing the side that fills the aneurysm to see if collateral flow is present. Also, determine if either carotid fills both ACAs, or if each ACA fills from the ipsilateral carotid injection (may permit trapping, see below).

If additional views are needed to better demonstrate aneurysm

Try oblique 25° away from injection side, center beam 3-4 cm above lateral aspect of ipsilateral orbital rim, orient x-ray tube in Towne’s view. A submental vertex view may also visualize the area but the image may be degraded by the amount of interposed bone.

SURGICAL TREATMENT

Approaches

1. pterional approach: the usual approach (see below)

2. subfrontal approach: especially useful for aneurysms pointing superiorly when there is a large amount of frontal blood clot (allows clot removal during approach)

3. anterior interhemispheric approach²⁸⁵: ✖ contraindicated for anteriorly pointing aneurysms as the dome is approached first and proximal control cannot be obtained (see below)

4. transcallosal approach

PTERIONAL APPROACH

Side of craniotomy:

A right pterional craniotomy is used with the following exceptions (for which a left pterional crani is used):

1. large ACoA aneurysm pointing to right: left crani exposes neck before dome

2. dominant left A1 feeder to aneurysm (with no filling from right A1): left crani provides proximal control

3. additional left sided aneurysm

See Pterional craniotomy on page 159 for positioning, etc. (use shoulder roll, rotate head 60° from vertical, see Figure 7-7, page 159). Craniotomy is as shown in Figure 7-9, page 160 (slightly more frontal lobe needs to be exposed than, e.g. for a p-comm aneurysm).

Lumbar drain (if IVC not already inserted) assists with brain relaxation.

MICROSURGICAL DISSECTION

Dissect down sylvian fissure with gentle retraction of frontal lobe away from base of skull. Olfactory nerve visualized first, then optic nerve. Open arachnoid over carotid and optic cistern and drain CSF. Elevate temporal tip, coagulate any bridging temporal tip veins that are present, and expose ICA.

Follow the ICA distally, looking for A1 (exposure of this allows temporary clipping in event of rupture). If the A1 take-off is too high, it may be hidden and would require excessive retraction to expose. Options to increase exposure include

1. gyrus rectus resection: a 1 cm long gyrus rectus cortisectomy is performed²⁸⁶ just medial to the olfactory tract. Helps find the ipsilateral A1 and often ACoA and A2. This is also helpful for downpointing aneurysms because it permits visualization of the contralateral A1 before exposing the dome of the aneurysm (for proximal control). May lead to neuropsychiatric deficits. A subpial resection is performed with preservation of the small arterial branch that is consistently located here

2. fronto-temporal-orbital-zygoma removal

3. splitting the sylvian fissure: about 50% of experts do this routinely

4. ventricular drainage

Once found, A1 is followed until the ipsilateral A2 is identified. Then the contralateral A2 is identified and is followed proximally until the contralateral A1 is exposed. The a-comm is usually encountered in the process.

Critical branches to preserve: recurrent artery of Heubner; small ACoA perforators (may be adherent to aneurysm dome). If the aneurysm cannot be clipped, it may be trapped by clipping both ends of the ACoA only if each ACA fills from the carotid on its own side.

Post clipping, some authors recommend fenestrating the lamina terminalis in an effort to reduce the need for post-op shunting.

ANTERIOR INTERHEMISPHERIC APPROACH²⁸⁵

Involves minimal brain retraction.

More suitable for an aneurysm that points straight up, but even with this proximal control is poor.

Position: supine with the neck extended ≈ 15°. A transverse skin incision is made in a skin crease in the lower forehead. The authors²⁸⁵ describe using a 1.5 inch trephine craniotomy in the midline just superior to the glabella. Alternatively, better advantage of the dural opening may be possible with a more rectangular opening. The dural flap is hinged on the superior sagittal sinus. The depth of the aneurysm is ≈ 6 cm from the dura. Proximal control of the A1 branch of the ACA is difficult with this approach.

30.10.2. Distal anterior cerebral artery aneurysms

Aneurysms of the distal anterior cerebral artery (DACA) (i.e. the ACA distal to the ACoA) are usually located at the origin of the frontopolar artery, or at the bifurcation of the pericallosal and callosomarginal arteries at the genu of the corpus callosum. Aneurysms located more distally are usually posttraumatic, infectious (mycotic), or due to tumor embolus²⁸⁷. DACA aneurysms are often associated with intracerebral hematoma or interhemispheric subdural hematoma²⁸⁸ since the subarachnoid space is limited here. Conservative treatment of DACA aneurysms is often associated with poor results. Un-ruptured DACA aneurysms have a higher incidence of bleeding than unruptured aneurysms in other locations. These aneurysms are fragile and adherent to the brain, which predisposes to frequent premature intraoperative rupture.

On arteriography, if both ACAs fill from a single sided carotid injection, it may be difficult to make the important determination as to which ACA feeds the aneurysm. Multiple aneurysms are commonly associated with DACA aneurysms.

TREATMENT

Mycotic aneurysms should be treated as outlined on page 1082.

Aneurysms up to 1 cm from the ACoA may be approached through a standard pterional craniotomy with partial gyrus rectus resection.

Aneurysms > 1 cm distal to the ACoA up to the genu of the corpus callosum, including those of the pericallosal/callosomarginal bifurcation, may be approached surgically by a basal frontal interhemispheric approach²⁸⁹ via a frontal craniotomy using a bicoronal skin incision. The patient is positioned supine with the neck slightly extended, positioned vertically or just a few degrees to the left. A right sided craniotomy is preferred in most instances (exception: aneurysm dome buried in the right cerebral hemisphere making retraction hazardous), but should cross to the contralateral side by a couple centimeters. It must be taken all the way to the floor of the frontal fossa to permit exposure of the anterior cerebral artery for proximal control. The craniotomy extends ≈ 8 cm above the supraorbital ridge in order to provide leeway in circumnavigating veins bridging to the superior sagittal sinus. The dural flap is based on the superior sagittal sinus. If the sinus needs to be mobilized, it may be divided low anteriorly.

ACA aneurysms distal to the genu of the corpus callosum may also be approached by an interhemispheric approach using a unilateral skin incision. For these, the patient’s neck is not extended, and a parasagittal craniotomy is used that doesn’t need to be as low on the frontal fossa. The cingulate gyri may be difficult to separate, and care must be taken because excessive retraction may pull the cingulate gyrus off the dome of the aneurysm and produce premature rupture.

Ideally, A2 proximal to the aneurysm should be identified initially for proximal control and then followed distally to the aneurysm. When this is not possible, dissection should follow distal ACA branches proximally, towards the aneurysm, taking care not to disturb the aneurysm. Often, a portion of the cingulate gyrus may need to be removed and sometimes up to 1-2 cm of the anterior corpus callosum may need to be divided.

Surgical complications: Prolonged retraction on the cingulate gyrus may produce akinetic mutism that is usually temporary. The pericallosal arteries are small in caliber and may be atherosclerotic, which together increases the risk of occlusion of the parent artery with the aneurysm clip.

30.10.3. Posterior communicating artery aneurysms

May occur at either end of p-comm; that is at the junction with the PCA, or more commonly at the junction with carotid (typically points laterally, posteriorly, and inferiorly). May impinge on the third nerve in either case and cause third nerve palsy (ptosis, mydriasis, “down and out” deviation) that, is not pupil sparing in 99% of cases.

ANGIOGRAPHIC CONSIDERATIONS

Vertebral artery (VA) injection is necessary to help evaluate the p-comm artery:

1. if the p-comm is patent: determine if there is a “fetal circulation” where the posterior circulation is fed only through the p-comm

2. determine if the aneurysm fills from VA injection

If additional views are needed to better demonstrate aneurysm

Try paraorbital oblique 55° away from injection side, center beam 1 cm posterior to inferior portion of lateral rim of ipsilateral orbit, orient x-ray tube 12° cephalad.

See Pterional craniotomy on page 159 for positioning, etc.. For the more common aneurysm at the ICA-p-comm junction, rotate head 15-30° from vertical, see Figure 7-7, page 159. Craniotomy is as shown in Figure 7-9, page 160 (less frontal lobe needs to be exposed than for an ACoA aneurysm).

MICROSURGICAL DISSECTION

Ultimately, the major vector of retraction will be on tip of temporal lobe (less on frontal lobe than in ACoA aneurysm), but the initial approach will be more anterior to reduce risk of intraoperative rupture.

1. dissect down sylvian fissure, retract frontal lobe and come down on optic nerve

2. cautiously elevate temporal tip (aneurysm may be adherent to temporal tip and/or to tentorium), coagulate bridging temporal tip veins if necessary

3. incise arachnoid membrane along the optic nerve from anterior to posterior

4. open arachnoid and drain CSF to gain relaxation

5. start to dissect carotid at anterior margin (at junction with optic nerve) and work towards the posterior margin of carotid where the aneurysm is located (isolating the carotid gives proximal control)

The aneurysm dome usually points laterally, posteriorly and inferiorly, and is encountered before and usually blocks visualization of the p-comm. The aneurysm frequently projects behind the tentorial edge which then obscures the dome.

Critical branches to preserve: anterior choroidal artery, posterior communicating artery (p-comm). If necessary, the p-comm may be sacrificed (e.g. included in clip) without deleterious effect in most cases if there is not a fetal circulation.

30.10.4. Carotid terminus (bifurcation) aneurysms

ANGIOGRAPHIC CONSIDERATIONS

If additional views are needed to better demonstrate aneurysm

Try oblique 25° away from injection side, center beam 3-4 cm above lateral aspect of ipsilateral orbital rim, orient x-ray tube in Towne’s view. Also may try submentovertex view.

See Pterional craniotomy on page 159 for positioning, etc. (rotate head 30° from vertical, see Figure 7-7, page 159). Craniotomy is as shown in Figure 7-9, page 160.

30.10.5. Middle cerebral artery (MCA) aneurysms

The following considers MCA aneurysms of the M1-M2 junction (“trifurcation” region, although this is not a true trifurcation, see page 98).

SURGICAL TREATMENT

APPROACHES

1. trans-sylvian approach through a pterional craniotomy: the most common

2. superior temporal gyrus approach²⁹⁰:

A. advantages: minimizes brain retraction, possible reduced vasospasm from manipulation of proximal vessels

B. disadvantages: proximal control difficult, slightly larger bone flap, possible increased risk of seizures

PTERIONAL APPROACH

See Pterional craniotomy on page 159 for positioning, etc. (rotate head 45° from vertical, see Figure 7-7, page 159).

CRANIOTOMY

Craniotomy is as shown in Figure 7-9, page 160. Less frontal lobe needs to be exposed than for, e.g. for an ACoA aneurysm (distance “B” in Figure 7-9 only needs to be ≈ 1 cm). The height “H” of the bony opening should be ≈ 5-6 cm (larger than for circle of Willis aneurysms).

MICROSURGICAL DISSECTION

Dissect down sylvian fissure with major vector of retraction on tip of temporal lobe (less on frontal lobe than in ACoA aneurysm). Open arachnoid and drain CSF. Elevate temporal tip, coagulate bridging temporal tip veins, and expose the ICA for proximal control in the event of rupture.

Follow the ICA distally by splitting the sylvian fissure to expose the M1 (again, for proximal control). Although exposure for proximal control is helpful to have as a contingency, one may be able to avoid temporary clipping of the MCA in the event of intraoperative rupture by controlling bleeding with a large suction, and subsequent clip placement (since the blood flow through the MCA is not as voluminous as through the ICA, and the surgical access to these aneurysms is usually fairly unrestricted).

Critical branches to preserve: distal MCA branches, recurrent perforators from the origin of the major MCA branches.

30.10.6. Supraclinoid aneurysms²⁹¹

Applied anatomy

The carotid artery exits the cavernous sinus and enters the subarachnoid space at the dural constriction known as the carotid ring (AKA clinoidal ring). The supraclinoid portion of the carotid artery may be divided into the following segments²⁹²:

1. ophthalmic segment: the largest portion of the supraclinoid ICA. Lies between the take-off of the ophthalmic artery and the posterior communicating artery (PCoA) origin. The proximal portion of this (including the origin of the ophthalmic artery) is often obscured by the anterior clinoid process. Branches include:

A. ophthalmic artery: usually originates from the supracavernous ICA just after the ICA enters the subarachnoid space (see page 99 for variants). Enters the optic canal positioned inferolateral to the optic nerve

B. superior hypophyseal artery: the largest of several perforators supplying the dura of the cavernous sinus and the superior pituitary gland and stalk

2. communicating segment: from the PCoA origin to the origin of the anterior choroidal artery (AChA)

3. choroidal segment: from AChA origin to the terminal bifurcation of the ICA

30.10.6.1. Ophthalmic segment aneurysms²⁹³

Ophthalmic segment aneurysms (OSAs) include (NB: nomenclature varies among authors):

1. ophthalmic artery aneurysms:

2. superior hypophyseal artery aneurysms:

A. paraclinoid variant: usually does not produce visual symptoms

B. suprasellar variant: when giant, may mimic pituitary tumor on CT

PRESENTATION (EXCLUDING INCIDENTAL DISCOVERY)

OPHTHALMIC ARTERY ANEURYSMS

Arise from the ICA just distal to the origin of ophthalmic artery. They project dorsally or dorsomedially towards the lateral portion of the optic nerve.

Presentation:

• ≈ 45% present as SAH

• ≈ 45% present as visual field defect:

A. as the aneurysm enlarges it impinges on the lateral portion of the optic nerve → inferior temporal fiber compression → ipsilateral monocular superior nasal quadrantanopsia

B. continued enlargement → upward displacement of the nerve against the falciform ligament (or fold) → superior temporal fiber compression → monocular inferior nasal quadrantanopsia

C. in addition to near-complete loss of vision in the involved eye, compression of the optic nerve near the chiasm may produce a superior temporal quadrant defect in the contralateral eye (junctional scotomaAKA “pie in the sky” defect) from injury to the anterior knee of Wilbrand (nasal retinal fibers that course anteriorly for a short distance after they decussate in the contralateral optic nerve²⁹⁴)

• ≈ 10% present as both

SUPERIOR HYPOPHYSEAL ARTERY ANEURYSMS

Originate in the small subarachnoid pocket medial to the ICA near the lateral aspect of the sella. The direction of enlargement is dictated by the size of this pocket and the height of the lateral sellar wall, resulting in two variants: paraclinoid & suprasellar.

Suprasellar variant may actually grow to a size large enough to compress the pituitary stalk and cause hypopituitarism and “classic” chiasmal visual symptoms (bilateral temporal hemianopsia).

ANGIOGRAPHIC CONSIDERATIONS

A notch can often be observed in the in the anterior, superior, medial aspect of giant ophthalmic artery aneurysms due to the optic nerve²⁹⁵.

If additional views are needed to better demonstrate aneurysm

Try oblique 25° away from injection side, center beam 3-4 cm above lateral aspect of ipsilateral orbital rim, orient x-ray tube in Towne’s view. Try submentovertex view.

SURGICAL TREATMENT²⁹¹

OPHTHALMIC ARTERY ANEURYSMS

If necessary, the ophthalmic artery may be sacrificed without worsening of vision in the vast majority. Clipping a contralateral ophthalmic artery aneurysm is not technically difficult, and is not uncommonly required as OSAs are often multiple.

The aneurysm arises from the superomedial aspect of the ICA just distal to the ophthalmic artery origin, and projects superiorly.

Cutting the falciform fold early decompresses the nerve, and helps minimize worsening of visual deficit from surgical manipulation.

For unruptured aneurysms, drill off anterior clinoid via an extradural approach before opening dura to approach neck; for ruptured aneurysms, this may not be as safe.

In most cases, a side-angled clip can be placed parallel to the parent artery along the neck of the aneurysm.

SUPERIOR HYPOPHYSEAL ARTERY ANEURYSMS

If necessary, the superior hypophyseal artery on one side may be clipped without demonstrable deleterious effect (due to bilateral supply to stalk and pituitary). Clipping a contralateral superior hypophyseal aneurysms is not really feasible.

With a usual pterional approach, the carotid artery is usually encountered first, and with large aneurysms is usually bowed laterally towards the surgeon. Clinoidal removal is usually required. The entire ICA wall may appear to be involved, and it may necessitate temporary ICA clipping (with cerebral protection) to reconstitute the ICA using encircling clips parallel to the parent vessel.

30.10.7. Posterior circulation aneurysms

(See page 1074 for basilar tip aneurysms). Clinical syndrome of SAH in the posterior fossa is indistinguishable from that due to anterior circulation aneurysms except for possible increased tendency towards respiratory arrest and subsequent neurogenic pulmonary edema²⁹⁶. Vasospasm following posterior fossa SAH may be more likely to cause midbrain symptoms than vasospasm due to SAH elsewhere.

HYDROCEPHALUS

In Yamaura’s series²⁹⁷, 12% of patients required external ventricular drainage (EVD) following posterior fossa SAH to remove bloody CSF causing hydrocephalus, and 20% eventually required permanent ventricular shunt.

30.10.7.1. Vertebral artery aneurysms

Traumatic vertebral artery aneurysms (VAA) (AKA dissecting aneurysms) are more common than non-traumatic VAAs. The following discussion concerns non-traumatic VAA.

Most VAAs arise at the VA-PICA junction. Other sites: VA-AICA, VA-BA.

ANGIOGRAPHIC CONSIDERATIONS

Angiography of VAA should assess the contralateral VA for patency in case of the need to trap the aneurysm. Allcock test (vertebral artery injection with carotid compression) may be used to assess patency of circle of Willis. Test occlusion with a balloon catheter can determine if patient will tolerate occlusion (a double lumen balloon will even allow measurement of distal back pressure).

PICA ANEURYSMS

For PICA anatomy, see Figure 5-20, page 102. For arteriogram, see Figure 5-21, page 103.

Comprise ≈ 3% of cerebral aneurysms. 3 common sites:

1. VA at the VA-PICA junction²⁰⁹:

A. saccular aneurysms: most commonly at the distal (superior) angle. An aneurysm in this location should be suspected with a CT showing blood predominantly in the 4th ventricle²¹⁸ (aneurysmal dome may adhere to foramen of Luschka; rupture fills the ventricles with little subarachnoid blood visible on CT). The level is as varied as the PICA origin, and ranges from as low as the foramen magnum to as high as the pontomedullary junction. Most VA-PICA aneurysms lie in the anterolateral portion of the medullary cistern²⁹⁸, anterior to the first dentate ligament²⁹⁹. However, the PICA origin may sometimes lie in the midline or across it

B. fusiform aneurysms: usually the result of prior arterial dissection: see page 1163

2. PICA aneurysms distal to the VA-PICA junction: tend to be fragile and often develop multiple hemorrhages in a relatively short period, should be treated promptly, even when discovered incidentally

3. fusiform VA aneurysms involving PICA

ANGIOGRAPHIC CONSIDERATIONS

If additional views are needed to better demonstrate aneurysm

Try paraorbital oblique 55° away from injection side, center beam on foramen magnum, orient x-ray tube 12° cephalad.

TREATMENT

Options:

1. direct aneurysmal clipping is the preferred treatment

2. endovascular coil embolization: not as effective as clipping for relief of symptoms due to brainstem or cranial nerve compression

3. choices for unclippable and uncoilable aneurysms (e.g. fusiform, giant, or dissecting aneurysms) include:

A. proximal (hunterian) VA ligation³⁰⁰ which must be distal to the PICA origin to prevent severe morbidity or mortality³⁰¹

B. occlusion of the VA distal to the PICA origin (usually done endovascularly)

C. midcervical VA occlusion (allows collateral flow through suboccipital muscular branches) e.g. endovascular Amplatzer plug

One approach to the VA-PICA junction is via a low extreme-lateral p-fossa approach. However, if the aneurysm is too far anterior to the brain stem, it may be totally out of vision or reach. Also, since these aneurysms usually project posteriorly and superiorly, the critical PICA will be directly in harms’ way. Direct lateral approach more directly exposes the aneurysm³⁰² through a lateral suboccipital transcondylar approach.

Position: options include sitting position (less frequently used, see Sitting position, page 153) or lateral oblique (“park bench”).

Lateral oblique position

Position: side of involved PICA is up, thorax elevated ≈ 15°. Head inline with the thorax, neck slightly flexed, and slightly rotated 20° toward the floor (away from the side of the aneurysm). Upper shoulder depressed with adhesive tape. Lumbar spinal subarachnoid catheter placed, allows CSF drainage once dura is opened.

Options for skin incision:

Avoid opening too far laterally, otherwise the muscle mass impedes vision^{303 (p 1747)}.

1. paramedian vertical incision } from just above superior nuchal line to C2 vertebra²⁹⁸

2. midline vertical incision (hockey stick) } from just above superior nuchal line to C2 vertebra²⁹⁸

3. “sigmoid” incision starting 2 cm medial to mastoid notch, and curving to midline at level of C1 arch³⁰⁴

Craniectomy: lateral exposure of bone to the base of the mastoid, medially crossing the midline. Need not be quite as high as the transverse sinus. The foramen magnum is removed to its lateral margin. Removing the posterior arch of C1 from midline to the sulcus arteriosus (under VA) may help with proximal VA exposure³⁰⁴ but is not usually necessary³⁰⁵.

Dural opening: K-shaped dural opening with a linear incision across the band at the foramen magnum (some patients have a sinus known as the arcuate sinus here that may require vascular clips).

Approach: first, gain proximal control of the VA where it first becomes intradural (in case of aneurysmal rupture). Retract cerebellum superiorly (caution: aneurysm dome may be adherent). Follow VA up from point where it enters dura; PICA origin then encountered usually just at neck of aneurysm (PICA origin may be confused for continuation of VA). Dissection must spare branches of pharyngeal filaments of spinal accessory nerve and lower filaments of vagus. May place temporary clip on VA proximal to PICA. Permanent clip usually placed between the fibers of IX & X above and XI below. It is better to leave a small residual aneurysm than to risk compromising PICA³⁰⁵.

Postoperative care: when neuropraxia of the lower cranial nerves is likely (in cases of difficult dissection or traction applied during clipping) the patient is kept intubated overnight. Patients who do not tolerate extubation at this point are immediately reintubated and elective tracheostomy is scheduled. Tracheostomy is maintained until the neuropraxia resolves.

30.10.7.2. Vertebrobasilar junction aneurysms

Saccular aneurysms located where the two vertebral arteries join often form at the location of a basilar artery fenestration (basilar fenestration aneurysm).

ANGIOGRAPHIC CONSIDERATIONS

If additional views are needed to better demonstrate aneurysm

Try oblique 15° away from injection side, center beam on foramen magnum, orient x-ray tube 25° Towne. Try submentovertex view.

CT-angiogram may be helpful as an adjunct because it can opacify both vertebral arteries simultaneously (not generally feasible with catheter angiogram).

SURGICAL APPROACHES

1. suboccipital approach: for most; performed in lateral oblique position

2. subtemporal-transtentorial approach if the vertebrobasilar junction is high; performed in supine position

Suboccipital approach in lateral oblique position

NB: the side of approach must be chosen based on angiogram, as the extreme tortuosity of the VAs may cause the aneurysm of one VA to lie on the contralateral side of the brain stem.

Position: thorax elevated ≈ 15°. Head inline with the thorax, neck slightly flexed, and slightly rotated away from side of aneurysm. Upper shoulder depressed with adhesive tape. Spinal drain placed for CSF drainage, opened only once dura is opened.

30.10.7.3. AICA aneurysms

ANGIOGRAPHIC CONSIDERATIONS

If additional views are needed to better demonstrate aneurysm

Try AP or submentovertex view, center beam on nasion, orient x-ray tube 15° caudad.

30.10.8. Basilar bifurcation aneurysms

AKA basilar tip aneurysms. The most common posterior circulation aneurysm. Comprise ≈ 5% of intracranial aneurysms.

PRESENTATION

Most present with SAH indistinguishable from SAH due to anterior circulation aneurysmal rupture. Enlargement of the aneurysm prior to rupture may rarely compress the optic chiasm → bitemporal field cut (mimicking pituitary tumor), or occasionally may compress the third nerve as it exits from the interpeduncular fossa → oculomotor nerve palsy²⁹⁶.

CT/MRI SCAN

May occasionally be seen on CT or MRI as round mass in region of suprasellar cistern. With SAH, tend to see blood in interpeduncular cistern with some reflux into 4th (and to a lesser extent, third and lateral) ventricle. Occasionally may mimic pretruncal nonaneurysmal SAH (see page 1085).

ANGIOGRAPHY

Dome usually points superiorly. Should evaluate flow through posterior communicating arteries (may require Allcock test) in case trapping is required. Need to assess the height of the basilar bifurcation in relation to the dorsum sella (see Approaches below).

If additional views are needed to better demonstrate aneurysm

Try oblique 25° away from or towards injection side, center beam 3-4 cm above lateral aspect of ipsilateral superior orbital rim, orient x-ray tube 25° Towne. Try submentovertex view.

Critical angiographic features to assess: On angiogram or CTA:

1. general features: see page 1039

2. orientation: determines whether surgery is an option. Posteriorly pointing aneurysms obscure perforators which may be adherent to the aneurysm, making surgery more difficult

3. patency of PCAs & SCAs

4. patency and size of p-comms

A. diameter of p-comm > 1 mm is needed to support collateral flow (expert opinion)

B. to determine if the P1’s can be sacrificed

C. P-comm patency and size is important for endovascular treatment as a potential route for deployment of horizontally oriented stent extending from P1 to contralateral P1306, 307

D. which can facilitate temporary clipping, or sacrifice, or placement of stents.

5. height of the aneurysm relative to the posterior clinoid process which will affect the selection of surgical approach^{308, 309} (the range of height of the posterior clinoid is 4-14 mm³⁰⁹)

A. supraclinoidal: aneurysm neck > 5 mm superior to posterior clinoid process

B. clinoidal: aneurysm neck within 5 mm of posterior clinoid process

C. infraclinoidal: aneurysm neck > 5 mm inferior to posterior clinoid process

SURGICAL TREATMENT

TIMING

Initial experience tended to favor allowing basilar tip aneurysms to “cool-down” for ≈ 10-14 days after SAH before attempting surgery to permit cerebral edema to subside. More recently, early surgery for these aneurysms has been advocated as for anterior circulation aneurysms³¹⁰ (see Timing of aneurysm surgery, page 1060). However, some surgeons still recommend waiting ≈ 1 week³¹¹, and most would agree that if there are obvious technical difficulties because of size, configuration or location of the aneurysm, that early surgery may not be appropriate. Also, if during the craniotomy it becomes apparent that cerebral edema is impairing the exposure, the operation should be aborted and attempted again at a later date.

APPROACHES

1. right subtemporal craniotomy (classical approach of Drake): approached through the incisura or division of the tentorium. Most basilar tip aneurysms are probably best approached via pterional approach (see below) except for posteriorly pointing aneurysms

A. advantage:

1. less distance to basilar tip

2. may be better than pterional approach for aneurysms projecting posteriorly or posteroinferiorly³¹¹

B. disadvantages:

1. requires temporal lobe retraction (minimized with lumbar drainage, mannitol, and possibly zygomatic arch section³¹²)

2. poor visualization of contralateral P1 segment and thalamoperforators

2. pterional approach (described by Yasargil): trans-Sylvian (see below)

A. advantages:

1. little or no retraction on temporal lobe (unlike subtemporal approach)

2. better visualization of both P1 segments and thalamoperforators

3. other aneurysms, e.g. of the anterior circulation, can be dealt with at the same sitting

B. disadvantages:

1. increases reach to aneurysm by ≈ 1 cm compared to subtemporal

2. requires wide splitting of the sylvian fissure

3. operating field is narrower than subtemporal approach

4. perforators arising from the posterior aspect of P1 may not be visible

3. modified pterional craniotomy: may allow trans-sylvian or subtemporal approach³¹¹. The craniotomy is taken further posteriorly than a standard pterional craniotomy

4. orbitozygomatic approach: allows access to portions of the basilar artery below the bifurcation. May be augmented by removal of the top of the clivus

Optional resection of the temporal tip will increase exposure of either approach. Unlike most anterior circulation aneurysms, securing proximal control is very difficult.

If the basilar bifurcation is high above the dorsum sella, then more retraction is required on a subtemporal approach than for a normal bifurcation height (near the dorsum sella). A high bifurcation is dealt with on a trans-sylvian approach by opening the sylvian fissure more widely, or by a subfrontal approach through the third ventricle via the lamina terminalis³¹³. A low bifurcation may require splitting the tentorium behind the 4th nerve.

PTERIONAL APPROACH³¹⁴

Risks include: oculomotor palsy in ≈ 30% (most are minimal and temporary).

Approach is from the right unless:

1. additional left sided aneurysm (e.g. p-comm aneurysm) which could be treated simultaneously by a left sided approach

2. aneurysm points to the right

3. aneurysm is located to the left of midline (the operation is more difficult when the aneurysm is even just 2-3 mm contralateral to the craniotomy)³¹¹

4. patient has right hemiparesis or left oculomotor palsy

See Pterional craniotomy on page 159 for general information. Rotate the head ≈ 30° off the vertical so that the malar eminence points directly upward (see Figure 7-7, page 159). Slight neck flexion is used for low-lying aneurysms, slight extension for high ones. Craniotomy is as shown in Figure 7-9, page 160, with aggressive removal of the sphenoid wing. The sphenoid wing and the orbital roof may be reduced with a drill. The posterior clinoid can be removed to improve exposure.

Approach

The sylvian fissure is split until the take-off of the proximal M1 from the carotid terminus is identified. The approach is medial to the ICA (between the ICA and optic nerve) when this space is ≥ 5-10 mm. If the ICA is close to the optic nerve, an approach lateral to the ICA may be used, aided by medial retraction of the ICA/M1 segment (see Figure 7-10, page 161). Here, the exposure is limited by the height of the M1 branch above the skull base, and if the basilar tip height above the skull base greatly exceeds this, clipping via this approach is not feasible²⁹⁷.

The 3rd nerve is identified. Also the p-comm and the anterior choroidal artery (AChA) are located as they arise from the posterior surface of the ICA (to differentiate between them: the p-comm origin is proximal to that of the AChA, p-comm courses perpendicular to Liliequist’s membrane whereas AChA courses obliquely into the crural cistern). The p-comm is followed posteriorly through Liliequist’s membrane which is opened revealing the prepontine cistern. The p-comm is followed until it joins the PCA at the P1/P2 junction. If p-comm is absent, follow the third nerve back to find where it emerges between PCA and SCA. P1 is followed proximally to the basilar bifurcation region where the contralateral P1 and both SCAs are identified. Caudal dissection of Liliequist’s membrane exposes the interpeduncular cistern with proximal BA (this exposure is critical for proximal control of BA in the event of aneurysmal rupture).

Thalamoperforating arteries (ThPAs) arise from the distal p-comm and proximal PCA, and often compromise the access. Early poor results with clipping of basilar tip aneurysms has been attributed to sacrificing these vessels, which produces lacunar infarcts in the thalamus, midbrain, subthalamic, and pretectal regions. If hypoplastic, the p-comm may be divided between clips to improve exposure (preserving the ThPAs which will then arise from the stumps). Similarly, a hypoplastic P1 may be divided if the PCA fills from the p-comm. If the ThPAs make it impossible to clip the aneurysm, some may have to be sacrificed, which is best done at their origin. Fortunately, there are some anastomoses³¹⁵ and thus they are not entirely end-arteries as originally thought.

OUTCOME

If the aneurysm is not giant, then these may be as safe to clip as anterior circulation aneurysms. Overall mortality is 5%, and morbidity is 12% (mostly due to injury to perforating vessels)²³.

30.10.9. Basilar trunk aneurysms

Most aneurysms of the basilar trunk are fusiform in morphology. Surgical access for these is extremely difficult.

30.11. Post-op orders for aneurysm clipping

1. admit PACU, transfer to ICU (neuro unit if available) when stable

2. VS: q 15 min x 4 hrs, then q 1 hr. Temperature q 4 hrs x 3 d, then q 8 hrs. Neuro check q 1 hr

3. activity: bed rest (BR) with HOB elevated 20-30°

4. knee high TED hose and pneumatic compression boots

5. I & O q 1 hr (if no Foley: straight cath q 4 hrs PRN bladder distension)

6. incentive spirometry q 2 hrs while awake (do not use following transsphenoidal surgery)

7. IVF: NS + 20 mEq KCl/L @ 90 ml/hr

For extubated patients

8. diet: NPO except minimal ice chips and meds as ordered

9. O₂: 2 L per NC

For intubated patients

8. diet: NPO. NG tube to intermittent suction. May clamp for 1 hour after meds given

9. ventilator orders

For all patients

10. meds:

A. H₂ antagonist, e.g. ranitidine 50 mg IVPB q 8 hrs

B. Keppra® (levetiracetam): 500 mg PO or IV q 12 hours. Maintain therapeutic AED levels for 2-3 months post-op for most supratentorial craniotomies

C. Cardene® drip: titrate to keep SBP < 160 mm Hg and/or DBP < 100 mm Hg (use cuff pressures, may use A-line pressures if they correlate with cuff pressures)

D. analgesics: fentanyl (unlike morphine, does not cause histamine release. Lowers ICP) 25-100 mcg (0.5-2 ml) IVP, q 1-2 hrs PRN

E. acetaminophen (Tylenol®) 650 mg PO/PR q 4 hrs PRN temperature > 100.5° F (38 C)

F. mini-dose heparin or enoxaparin {for DVT prophylaxis (no difference in heparin-induced thrombocytopenia with these 2 agents³¹⁶)}

G. calcium channel blockers (see admitting orders page 1042): nimodipine (Nimotop®) 60 mg PO/NG q 4 hrs or 30 mg q 2 hrs to avoid dips in BP. May be given IV where available

H. continue prophylactic antibiotics if used: (e.g. cefazolin (Kefzol®) 500-1000 mg IVPB q 6 hrs x 24 hrs, then D/C)

11. if available, transcranial doppler to monitor MCA, ACA, ICA, VA and BA velocities and Lindegaard ratio (see page 1048) {typical protocol is 3 x per week)

12. labs:

A. CBC once stabilized in ICU and q d thereafter

B. renal profile once stabilized in ICU and q 12 hrs thereafter

C. ABG once stabilized in ICU and q 12 hrs x 2 days, then D/C (also check ABG after any ventilator change if patient on ventilator)

13. call M.D. if any deterioration in crani checks, for T > 101° (38.5 C), sudden increase in SBP, SBP < 120, U.O. < 60 ml/2-hrs

30.12. Unruptured aneurysms

Unruptured intracranial aneurysms (UIA) includes incidental aneurysms (those that do not produce any symptoms and are discovered incidentally) and aneurysms that produce symptoms other than those due to hemorrhage (e.g. pupillary dilatation due to third nerve compression). UIA merit consideration for treatment since the outcome from SAH with or without surgery is poor even under the best of circumstances. About 65% of patients die from the first SAH³¹⁷, and even in patients with no neurologic deficit after aneurysm rupture, only 46% fully recover, and only 44% return to their former jobs¹. Estimated prevalence of incidental aneurysms is 5-10% of the population¹.

PRESENTATION

See items other than “rupture” in Presentation of aneurysms, page 1055.

NATURAL HISTORY

Risk of bleeding from UIA differs from aneurysms that have ruptured. True risk is not known with certainty. The largest, most detailed study to date is the ISUIA³¹⁸.

Σ	There appears to be 2 distinct types of aneurysms: those that rupture, and those that tend to remain stable. Most UIAs seen in the clinic fall into the latter group

Spontaneous thrombosis of unruptured aneurysms may occur rarely (see page 1058).

The natural history and treatment results are influenced by³¹⁹ (see Surgical outcome below):

1. patient factors:

A. history of previous SAH from a separate aneurysm³¹⁸ significantly increases the risk of rupture of an UIA

B. patient age

C. concurrent medical conditions

2. aneurysm characteristics³¹⁸

A. aneurysm size: the most important predictor for future rupture (see below) except (for unknown reasons) in patients with prior SAH from another source

B. location: p-comm, vertebrobasilar/posterior cerebral, and basilar tip UIAs were more likely to rupture

C. morphology

3. surgical capabilities

A. experience of the surgical team

B. possibly by ancillary services available

An estimate for UIA is ≈ 1% per year. The risk of bleeding in patients with multiple aneurysms was higher (6.8%) than for patients with single aneurysms (2.3%)³²⁰.

Aneurysm size: Risk of rupture appears critically dependent on aneurysm diameter³²¹. Estimated annual risk of rupture of aneurysms of diameter < 10 mm is 0.05% (range: 0-4%)^{208, 318A} and is lower than for diameters ≥ 10 mmwhich is 1% (range: 0.46-1.54%)^{318, 322} (this seems paradoxical since the mean diameter of aneurysms on post-rupture angiograms is 7.5 mm; this may be due to a shrinkage of aneurysms following rupture). The rupture rate was 6% in the first year with giant (≥ 2.5 cm) UIAs. Furthermore, aneurysms are not static, and have been shown to increase in size on serial angiograms³²³.

A. selection bias may play a role in lowering the apparent SAH rate as follows: enlarging aneurysms (which have increased risk of rupture) may produce symptoms and may be preferentially referred for surgery, and the inclusion of cavernous carotid aneurysms (which rarely cause SAH)

SURGICAL OUTCOME

There are no prospective randomized studies of treatment natural history vs. treatment options³¹⁹, and most data are either from personal series or are retrospective. Summary of 260 patients show no surgical mortality, and morbidity of 0-10.3% (6.5% major and 8% minor morbidity in the multicenter study)¹. A recent study found surgical mortality of 2.3% at 30-days, and 3.8% at 1 year³¹⁸. A meta-analysis found 2.6% case fatality³²⁴.

Operative morbidity was mild in 5%, moderate to severe in 6%³²⁴. Morbidity also increased with aneurysm size (2.3% for diameter < 5 mm, 6.8% for 6-15 mm, and 14% for 16-25 mm)³¹⁸. Morbidity also varied with location(4.8% for p-comm, 8.1% for MCA, 11.8% for ophthalmic, 15.5% for anterior communicating, and 16.8% for carotid bifurcation). Morbidity also increases with patient age (6.5% for age < 45 yrs, 14% for age 45-64, and 32% for age > 64)³¹⁸.

MANAGEMENT

To understand the calculation of cumulative risk for aneurysmal rupture, see page 1100 for a discussion of this issue related to AVMs which also pertains to aneurysms.

Decision analysis

Requires data about the natural history (see above), life expectancy, and morbidity and mortality of SAH and aneurysm surgery.

In one such study³²⁵, using the values shown in Table 30-13, the result obtained was that a life expectancy of 12 more years is the break-even point, i.e. if the patient is not expected to live for 12 more years, then non-surgical management is a better choice than surgery (this result involves numerous assumptions and estimations; e.g. 5% “risk aversiveness” (intermediate) relates to patient’s fears of immediate surgical risk vs. risk of rupture spread over many years). Another analysis of various scenarios for a 50 year old female found that treatment was cost effective for UIAs that were symptomatic, ≥ 10 mm diameter, or with a previous history of SAH³²⁶.

Table 30-13 Data used in decision analysis of management of unruptured aneurysms³²⁵

	Typical value	Range
annual risk of rupture*	1%	0.5-2%
3 month mortality of SAH	55%	50-60%
serious morbidity after SAH	15%	10-20%
surgical morbidity & mortality	2% & 6%	4-10%

* this is an intermediate risk for aneurysms 6-10 mm diameter (NB: size may change; small aneurysms may grow)

Management recommendations based on aneurysm size

Numerous recommendations have been made for a critical size above which an un-ruptured aneurysm should be considered for surgery, and have included 3 mm^{322, 5} mm^{327, 7} mm³²⁸, and 9 mm²⁰⁸. And again, the patient’s expected longevity must be taken into account. One proposal is to promptly treat unruptured aneurysms ≥ 10 mm, to repair those measuring 7-9 mm in young and middle-aged patients, and to follow smaller aneurysms with serial angiography³²⁹.

Summary of the American Heart Association Stroke Council recommendations

Table 30-14 summarizes factors favoring treatment made based on a review of the literature³¹⁹ (only level IV and V evidence was found, and therefore only grade C recommendations can be made (i.e. an array of potential actions, any of which could be considered appropriate)^{330, 331}). Patients for whom expectant management is elected should have periodic CT, MRA or selective contrast angiography seeking changes in aneurysm size or configuration. Symptomatic large or giant aneurysms carry increased risk of treatment.

In all treatment decisions, coexisting medical conditions must be taken into account.

Table 30-14 Factors favoring treatment of UIAs

Factor	Features favoring treatment
patient age	young age (risk of SAH accumulates with time)
previous SAH	UIA in patient with previous SAH due to another aneurysm
aneurysm location	basilar apex
aneurysm size	small UIAs approaching 10 mm in size, and in particular UIAs ≥ 10 mm size
aneurysm configuration	UIAs with daughter aneurysm or other unique hemo-dynamic featrures
family history	family members with aneurysms or aneurysmal SAH
symptomatic aneurysms	development of new symptoms related to mass effect may indicate enlargment and urgent treatment is recommended
changes on follow-up studies	enlargment or change in configuration

Recommended follow-up for UIAs

Σ	Annual follow-up TOF-MRAs are recommended for most incidental aneurysms that are not treated. Intervention is indicated for any documented growth.

Background: The morbidity from catheter arteriograms is probably too high to recommend them for this purpose. CTA is more accurate than MRA, but involves iodine contrast and radiation. A TOF-MRA (not gadolinium-MRA) has no known risks and does not involve radiation.

Unfortunately, most aneurysms rupture without demonstrable enlargement on follow-up. Aneurysms do not grow at a constant rate, and it may take several years to appreciate a millimeter of increased size on MRA. Over a 47 month median follow-up, only 10% of aneurysms enlarged on follow-up MRA³³². Larger aneurysms (≥ 8 mm original diameter) more frequently showed growth³³². An aneurysm showing any growth should be treated (it is not really known if enlargement is associated with increased risk of rupture, but there are probably few situations like this where the physician would be willing to wait and see).

UNRUPTURED CAVERNOUS CAROTID ARTERY ANEURYSMS

Most cavernous carotid artery aneurysms (CCAAs) develop on the horizontal segment of the artery.

Presentation:

1. CCAAs may be discovered incidentally

A. on arteriography for other reason

B. on MRI

C. occasionally on CT

2. when symptomatic:

A. usually present with:

1. headache

2. cavernous sinus syndrome (see page 1204): primarily produces diplopia (due to ophthalmoplegia). Classically the third nerve palsy from enlarging CCAA will not produce a dilated pupil because the sympathetics which dilate the pupil are also paralyzed^{85 (p 1492)}

3. those that expand through the carotid ring into the subarachnoid space may cause monocular blindness²⁹¹

B. rarely, pain (retro-orbital or pain mimicking trigeminal neuralgia^{220, 221}) or a carotid-cavernous fistula (CCF) are the sole manifestation

C. when CCAAs rupture, they usually produce a CCF

D. life threatening complications are rare, but may be more common with giant intracavernous aneurysms³³³. Manifestations include:

1. SAH^{333, 334} } especially CCAAs that straddle the carotid ring^A

2. arterial epistaxis from rupture into sphenoid sinus (usually with traumatic aneurysms, see page 1081) } especially CCAAs that straddle the carotid ring^A

3. emboli

A. subarachnoid extension of CCAAs may be indicated by “waisting” of the aneurysm on angiography³³⁶

Indications for treatment:

1. unruptured CCAAs: the natural history is not precisely known

A. symptomatic: patients with intolerable pain or visual problems³³⁵

B. giant aneurysms: especially those that straddle the clinoidal ring^A

C. aneurysms that enlarge on serial imaging

D. controversial: incidental aneurysms in the distribution of a stenotic carotid artery for which carotid endarterectomy is indicated. There has been no evidence that doing the endarterectomy increases the risk of rupture, and, as indicated above, most ruptures are not life threatening and so the carotid disease should be treated according to it’s own merits

2. ruptured CCAAs:

A. emergent treatment for cases with epistaxis or SAH

B. urgent treatment for CCFs with severe eye pain or threat to vision

Treatment options for CCAAs:

Treatment of small incidental intracavernous CCAAs is not generally indicated³¹⁹.

For other unruptured CCAAs, options include detachable coils in an attempt to thrombose the aneurysm (see page 1058). This results in reduction of mass effect in ≈ 50%. Open surgical treatment is rarely appropriate. Aneurysms that rupture and produce a carotid-cavernous fistula may be treated by endovascular occlusion (see page 1113).

30.13. Multiple aneurysms

Multiple aneurysms are present in 15-33.5% of cases of SAH¹. In one study of multiple factors, hypertension was found to be the most important one associated with multiplicity³³⁷.

When a patient presents with SAH and is found to have multiple aneurysms, the following may be clues as to which aneurysm has bled:

1. epicenter (center of greatest concentration) of blood on CT or MRI^{53, 56}

2. area of focal vasospasm on angiogram

3. irregularities in the shape of the aneurysm (so-called “Murphy’s tit”)

4. if none of the above help, then suspect the largest aneurysm

5. NB: in one series, the most common cause of post-op bleeding in 93 patients with multiple aneurysms was felt to be from rebleeding of the original aneurysm that ruptured that was actually missed on initial angiogram³³⁸

30.14. Familial aneurysms

The role of inheritance in the development of intracranial aneurysms (IA) is well established for disorders such as polycystic kidney disease, and connective tissue disorders such as Ehlers-Danlos type IV, Marfan syndrome, and pseudoxanthoma elasticum (see Conditions associated with aneurysms, page 1057).

Additional cases of IAs in identical twins^{339, 340} as well as familial aggregations of IAs without a recognized inherited disorder have also been reported but are felt to be rare (it has been estimated that < 2% of IAs are familial³⁴¹). Most reported cases consist of only 2 family members with IAs, and these are most commonly siblings³⁴². Analysis of case reports reveals that when IAs occur in siblings they tend to occur at identical or mirror image sites, and in comparison to sporadic IAs, familial IAs tend to rupture at a smaller size and at a younger age, and that the incidence of anterior communicating artery aneurysms is lower³⁴³. It has been postulated that IAs occurring in siblings may represent a distinct population of IAs³⁴⁴.

The indications and best method for investigation of asymptomatic relatives of a patient found to harbor an intracranial aneurysm are controversial. Negative studies (angiography, DSA, MRA…) do not guarantee that at a later date an aneurysm will not be discovered that either subsequently developed or expanded, or was simply not detected on the initial study^345-347. Cerebral angiography is the most sensitive study, however, the risk and expense may not justify its use as a screening test in many cases. Furthermore, there is some evidence that aneurysms that rupture tend to do so shortly after their formation²⁰⁸ which would reduce the value of screening.

Screening recommendations: first-degree relatives (especially siblings) are at higher risk of harboring IAs³⁴⁸ and should undergo MRI and MRA screening. Findings suspicious for IA(s) require follow-up with four vessel arteriography to confirm suspected lesions (MRA has a high false-positive rate of ≈ 16%⁵⁸) and to rule-out additional IAs.

30.15. Traumatic aneurysms

Traumatic aneurysms (TAs) comprise < 1% of intracranial aneurysms^{349, 350}. Most are actually false aneurysms, AKA pseudoaneurysms (a rupture of all the vessel wall layers with the “wall” of the aneurysm being formed by surrounding cerebral structures³⁵¹). They may occur rarely in childhood. The mechanism of injury usually falls into one of the following groups³⁵²:

1. those arising from penetrating trauma: usually from gunshot wounds, although penetration with a sharp object (which is less common) may be more prone to cause traumatic aneurysms³⁵³

2. those arising from closed head injury: more common. Theories of pathogenesis include traction injury to the vessel wall or entrapment within a fracture. Tend to occur either:

A. peripherally

1. distal anterior cerebral artery aneurysms: secondary to impact against the falcine edge

2. distal cortical artery aneurysms: often associated with an overlying skull fracture, sometimes a growing skull fracture

B. at the skull base, usually involving the ICA in one of the following sites:

1. petrous portion } virtually always associated with basal skull fractures

2. cavernous carotid artery: } virtually always associated with basal skull fractures

a. aneurysm enlargement may cause a progressive cavernous sinus syndrome } virtually always associated with basal skull fractures

b. rupture may lead to a posttraumatic carotid-cavernous fistula (see page 1113) or to massive epistaxis in the presence of a sphenoid sinus fracture^354-356 } virtually always associated with basal skull fractures

3. supraclinoid carotid artery

3. iatrogenic: following surgery in or around the skull base, the sinuses, or orbits (including following transsphenoidal surgery³⁵⁷)

Presentation

1. delayed intracranial hemorrhage (subdural, subarachnoid, intraventricular, or intraparenchymal): the most common presentation. TAs tend to have a high rate of rupture

2. recurrent epistaxis

3. progressive cranial nerve palsy

4. enlarging skull fracture

5. may be incidental finding on CT scan

6. severe headache

Treatment

Although there are case reports of spontaneous resolution, treatment is usually recommended. ICA aneurysms at the skull base should undergo trapping or endovascular embolization. Peripheral lesions should be treated surgically with clipping of aneurysm neck, excision of the aneurysm, coiling, or wrapping if no other method is feasible.

30.16. Mycotic aneurysms

The name “mycotic” originated with Osler in whose time the term referred to any infectious process³⁵⁸ rather than the current usage which infers a fungal etiology. Currently accepted terminology favors infectious aneurysm (or bacterial aneurysm). Infectious aneurysms can, however, also occur with fungal infections³⁵⁹. Tend to form in distal (often unnamed) vessels.

EPIDEMIOLOGY & PATHOPHYSIOLOGY

• comprise ≈ 4% of intracranial aneurysms

• occurs in 3-15% of patients with subacute bacterial endocarditis (SBE)

• most common location: distal MCA branches (75-80%)

• at least 20% have or develop multiple aneurysms

• increased frequency in immunocompromised patients (e.g. AIDS) and drug users

• most probably start in the adventitia (outer layer) and spread inward

EVALUATION

Blood cultures and LP may identify the infectious organism. Table 30-15 shows typical pathogens recovered. Patients with suspected infectious aneurysm(s) should undergo echocardiography to look for signs of endocarditis.

Table 30-15 Pathogens implicated in mycotic aneurysms^{360 (p 933-40)}

Organism	%	Comment
streptococcus	44%	S. viridans (classic cause of SBE)
staphylococcus	18%	S. aureus (cause of acute bacterial endocarditis)
miscellaneous	6%	(pseudomonas, enterococcus, corynebacter…)
multiple	5%
no growth	12%
no info	14%
total	99%

TREATMENT

These aneurysms usually have fusiform morphology and are usually very friable, therefore surgical treatment is difficult and/or risky. Most cases are treated acutely with antibiotics which are continued 4-6 weeks. Serial angiography (at 7-10 days and 1.5, 3, 6 and 12 months, even if aneurysms seem to be getting smaller, they may subsequently increase³⁶¹ and new ones may form) helps document effectiveness of medical therapy (serial MRA may be a viable alternative in some cases). Aneurysms may continue to shrink following completion of antibiotic therapy³⁶². Delayed clipping may be more feasible; indications include:

• patients with SAH

• increasing size of aneurysm while on antibiotics³⁶³ (controversial, some say not mandatory³⁶²)

• failure of aneurysm to reduce in size after 4-6 weeks of antibiotics³⁶³

Patients with SBE requiring valve replacement should have bioprosthetic (i.e. tissue) valves instead of mechanical valves to eliminate the need for risky anticoagulation.

30.17. Giant aneurysms

Definition: > 2.5 cm (≈ 1 inch) diameter. Two types: saccular (probably an enlarged “berry” aneurysm) and fusiform. Comprise 3-5% of intracranial aneurysms; peak age of presentation 30-60 years; female:male ratio = 3:1.

Drake’s series of 174 giant aneurysms³⁶⁴: 35% presented as hemorrhage, with 10% showing some evidence of remote bleeding. The bleeding rate is unknown, but is probably less than the ≈ 2%/year for non-giant aneurysms.

May also present as TIAs (by reducing flow or by emboli) or as a mass. About one third have a neck amenable to clipping.

EVALUATION

Drake contends that even after thorough radiographic evaluation, actual operative visualization is the only way to definitively assess the aneurysm and its branches.

Angiogram: Often underestimates the size of the lesion secondary to thrombosed regions of the aneurysm that do not fill with contrast. CT or MRI is required to visualize the thrombosed portion.

CT scan: Frequently have a significant amount of edema surrounding the aneurysm. May see contrast enhancement of the brain surrounding the aneurysm; probably due to increased vascularity secondary to inflammatory reaction to the aneurysm.

MRI scan: Turbulence within → complicated signal on T1WI. Pulsation artifact (linear distortion radiation through aneurysm) on MRI helps differentiate giant aneurysms from solid or cystic lesions.

TREATMENT

Options include:

1. direct surgical clipping: usually possible in only ≈ 50% of cases

2. vascular bypass of aneurysm with subsequent clipping

3. trapping

4. proximal arterial ligation (hunterian ligation)

A. for vertebral-basilar aneurysms²⁴¹: results in improvement of cranial nerve deficit in ≈ 95% of patients

5. wrapping: see page 1058

30.18. SAH of unknown etiology

Recent estimates of incidence: 7-10%. This is a heterogeneous category, and a better term might be “angiogram-negative SAH” (see page 1038 for requirements to be met before considering an arteriogram to be negative). The quantity of blood on CT may predict the chances of an arteriogram disclosing a cerebral aneurysm^365-368.

Patients with angiogram-negative SAH tend to be younger, less hypertensive, and more commonly male than those with positive angiography³⁶⁶.

Possible causes of SAH with a negative angiogram include:

1. aneurysm that fails to be demonstrated in initial angiogram

A. inadequate angiography, causes include:

1. incomplete angio: see page 1038

a. must see both PICA origins (1-2% of aneurysms occur here)

b. need to cross-fill through the ACoA (see page 1038)

2. degradation of images due to

a. poor patient cooperation (e.g. from agitation). Either sedate patient (use caution in non-intubated patients) or repeat the study at a later time when patient more cooperative

b. poor quality equipment providing substandard images

B. obliteration of aneurysm by the hemorrhage

C. thrombosis of the aneurysm after SAH: see page 1058

D. aneurysm too small to be visualized³⁶⁹: although “microaneurysms” may be a source of SAH, their natural history and optimal treatment are unknown

E. lack of filling of aneurysm due to vasospasm (of parent artery or of aneurysmal orifice)

2. nonaneurysmal SAH from source that fails to show up on angiography. See page 1034 for etiologies of SAH other than aneurysm (many of which may not be demonstrated on angiography), including:

A. angiographically occult (or cryptic) vascular malformation: see page 1105

B. pretruncal nonaneurysmal SAH: see below

Risk of rebleeding

Overall rebleed rate is 0.5%/yr, which is lower than with aneurysmal SAH or rebleeding from AVMs. There is also a smaller risk of delayed cerebral ischemia (vasospasm). Neurological outcome is likewise better.

MANAGEMENT

General measures

These patients are still at risk for the same complications of SAH as with aneurysmal SAH: vasospasm, hydrocephalus, hyponatremia, rebleeding, etc. (see page 1040) and should be managed as any SAH (see page 1040). Some subgroups may be at lower risk for complications and may be managed accordingly (e.g. see Pretruncal nonaneurysmal SAH (PNSAH) below).

Repeat angiography

Yield of positive second angiogram after technically adequate negative study: 1.8-9.8%)³⁷⁰ in early (pre-CT) studies, 2-24% quoted more recently^{369, 371, 372}. CT scan findings are helpful in the decision to repeat angiography³⁷³. 70% of cases with diffuse SAH and thick layering of blood in the anterior interhemispheric fissure were associated with an ACoA aneurysm that showed up on repeat angiography³⁶⁷. The absence of blood on CT (performed within 4 days of SAH), or thick blood in the perimesencephalic cisterns alone (see below) were unlikely to be associated with a missed aneurysm.

Recommendations regarding repeat angio:

1. repeat angio after ≈ 10-14 days (allows vasospasm & some clot to resolve)^A

A. technically adequate 4 vessel angiogram is negative, and evidence for SAH is strong

B. original angio was incomplete or if there are suspicious findings

2. if CT localizes blood clot to particular area, place special attention to this area on repeat angio

3. do not repeat angio for classic pretruncal SAH (see below) or if no blood on CT

4. patients are usually kept in the hospital 10-14 days while waiting for repeat angio (to watch for and manage complication of SAH or rebleeding)

A. between 5-10 days there is decreased chance of seeing an aneurysm because of vasospasm; angiography at ≈ day 10 permits surgery to be done if needed ≈ at day 14 which is about the earliest time after the “no-op” window of day 3-12

Third arteriogram:

If the 1st 2 arteriograms are negative, and the history is suggestive of aneurysmal SAH, a 3rd arteriogram 3-6 months after SAH has ≈ 1% chance of showing a source of bleeding.

Other studies

1. imaging studies of the brain: MRI (with MRA if available) or CT (with angio-CT if available). This may visualize an aneurysm that fails to show up on angiography, and may identify other sources of SAH such as angiographically occult vascular malformation (see page 1105), tumor…

2. tests to rule-out spinal AVM: a rare cause of intracerebral SAH (see page 507)

A. spinal MRI: cervical, thoracic and lumbar

B. spinal angiography: too difficult and risky to be justified in most cases of angio negative SAH. Consider in cases with high suspicion of spinal source

Surgical exploration

Advocated by some for cases of SAH with CT findings compatible with an aneurysmal source in which a suspicious area is demonstrated angiographically³⁶⁹ with careful explanation to the patient and family of the possibility of negative operative findings.

30.19. Nonaneurysmal SAH

For etiologies of SAH other than aneurysm, see page 1034.

PRETRUNCAL NONANEURYSMAL SAH (PNSAH)

Née perimesencephalic nonaneurysmal SAH³⁷⁴. The suggestion to change the name to pretruncal nonaneurysmal SAH was proposed because improved neuroimaging techniques have shown the true anatomic localization of the blood to be in front of the brain stem (truncus cerebri) centered in front of the pons rather than perimesencephalic³⁷⁵. Blood often extends into the interpeduncular or premedullary cisterns.

A distinct entity considered to be a benign condition with good outcome and less risk of rebleeding and vasospasm than other patients with SAH of unknown etiology³⁷⁶ (no rebleeding occurred in 37 patients with PNSAH and 45 months mean follow-up³⁷⁷, nor in 169 patients with 8-51 months follow-up³⁷²; vasospasm has been reported in only 3 patients and may have been related to cerebral angiography rather than the PNSAH, and although it is low, the incidence of angiographic vasospasm may be higher than originally thought³⁷⁸).

The actual etiology has yet to be determined, but it may be secondary to rupture of a small perimesencephalic vein or capillary³⁷⁸.

Presentation

Patients may present with severe paroxysmal H/A, meningismus, photophobia, and nausea. Loss of consciousness is rare. These patients are usually not critically ill (all were grade 1 or 2), however, complications such as hyponatremia or cardiac abnormalities may occur. Preretinal hemorrhages and sentinel H/A have not occurred. CT and/or MRI demonstrate characteristic findings (see below) although it may initially be missed on CT³⁷⁸, and LP may yield bloody CSF. All have negative angiography.

Epidemiology

PNSAH has been reported to comprise 20-68% of cases of angiogram-negative SAH^{376, 379} (depending on the timing of CT, adequacy of angiography, and the definition of PNSAH). However, the true incidence is probably more in the range of 50-75%³⁷².

The reported age range is 3-70 years (mean: 50 yrs)^{372, 52-59}% are male, and pre-existing HTN was present in 3-20% of patients.

Relevant anatomy

Posterior fossa cisterns:

The perimesencephalic cisterns include: interpeduncular, crural, ambient and quadrigeminal cisterns. The prepontine cistern lies immediately anterior to the pons.

Liliequist’s membrane (LM)³⁸⁰:

Basically considered to separate the interpeduncular cistern from the chiasmatic cistern³⁸¹ (forming a competent barrier in only 10-30%). In further detail, the superior leaflet of LM (diencephalic membrane) separates the interpeduncular cistern from the chiasmatic cistern medially and from the carotid cisterns laterally^{382, 383}. The inferior leaflet (the mesencephalic membrane) separates the interpeduncular from the prepontine cistern.

The diencephalic membrane is thicker and is more often competent, effectively isolating the chiasmatic cistern. However, the carotid cisterns often communicate with the crural cisterns and in turn with the interpeduncular cistern³⁸³.

Thus, blood in the carotid or prepontine cistern is compatible with a low-pressure pretruncal source of bleeding, however, blood in the chiasmatic cistern should raise concern about aneurysmal rupture.

Table 30-16 CT or MRI criteria for PNSAH^{378, 384}

1. epicenter of hemorrhage immediately anterior to brain stem (interpeduncular or prepontine cistern) 2. there may be extension into anterior part of ambient cistern or basal part of the sylvian fissure 3. absence of complete filling of anterior interhemispheric fissure 4. no more than minute amounts of blood in lateral portion of sylvian fissure 5. absence of frank intraventricular hemorrhage (small amounts of blood sedimenting in the occipital horns of the lateral ventricles is permissible)

Diagnostic criteria

Without knowledge of the actual substrate of PNSAH, the following suggested diagnostic criteria must be viewed as empiric (adapted³⁷²):

1. CT or MRI scan performed ≤ 2 days from ictus meeting the criteria shown in Table 30-16 (later scans render the diagnosis unreliable, e.g. washout could cause an aneurysmal SAH to fit the criteria). This criteria implies that blood should be contained inferior to Liliequist’s membrane (LM) (i.e. perimesencephalic and/or prepontine cisterns). Extension into the suprasellar cistern is common. Significant amounts of blood penetrating LM to the chiasmatic, sylvian, or interhemispheric cisterns should be viewed with suspicion

2. a negative high-quality 4-vessel cerebral angiogram³⁸⁵ (radiographic vasospasm is common, and does not preclude the diagnosis nor does it mandate repeat angiography). NB: ≈ 3% of patients with a ruptured basilar bifurcation aneurysm meet the criteria of Table 30-16³⁸⁶, therefore an initial arteriogram is mandatory

3. appropriate clinical picture: no loss of consciousness, no sentinel H/A, SAH grade 1 or 2 (see Grading SAH, page 1039). Variance from this should raise suspicion of alternate pathogenesis

Repeat angiography

Controversial. Angiography carries ≈ 0.2-0.5% risk of permanent neurologic deficit in this population³⁷². Most experts agree that repeat angiography is not indicated in patients meeting the criteria of PNSAH^{371, 385} (although others recommend repeat angiography in all surgical candidates^{369, 387}). One should probably repeat the study if any uncertainty exists or if there is a history of a condition associated with increased risk of cerebral aneurysms³⁷⁸.

Treatment

Optimal treatment is not known with certainty. The low risk of rebleeding and delayed ischemia suggests that extreme measures are not indicated. The following recommendations are made^{372, 378} (period not specified):

1. symptomatic treatment

2. cardiac monitoring

3. electrolyte monitoring for hyponatremia

4. follow patient clinically (and if appropriate, with repeat imaging studies) to rule-out hydrocephalus (transient ventricular enlargement is common, however, hydrocephalus requiring shunting is rare (only ≈ 1%)³⁷²)

5. ✖ not recommended

A. hyperdynamic therapy

B. calcium channel blockers: use has not been investigated in PNSAH, but is probably not warranted due to low incidence of vasospasm

C. activity restrictions (except in cases of increasing H/A with mobilization)

D. anticonvulsants

E. reduction of blood pressure below normal

F. surgical exploration

30.20. Pregnancy & intracranial hemorrhage

Intracranial hemorrhage (subarachnoid or intraparenchymal) is a rare occurrence during pregnancy (estimated range of incidence: 0.01-0.05% of all pregnancies³⁸⁸) and yet is responsible for 5-12% of maternal deaths during pregnancy.

Intracranial hemorrhage of pregnancy (ICHOP) commonly occurs in the setting of eclampsia, and is more commonly intraparenchymal³⁸⁹ and may be associated with loss of cerebrovascular autoregulation (see page 73). Symptoms of eclampsia with or without ICHOP include H/A, mental status changes, and seizures.

A literature review of 154 reported cases of ICHOP-related SAH revealed 77% were aneurysmal and 23% were from ruptured AVM (other series show the percentage of AVMs range from 21-48%). Mortality is ≈ 35% for aneurysmal and ≈ 28% for AVM hemorrhage (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 asserted that this held true for aneurysms only³⁹⁰).

Patients with ICHOP having AVMs tend to be younger than those with aneurysm, paralleling the occurrence in the general population. One major oft-quoted study showed an increased risk of hemorrhage from AVMs during pregnancy³⁹¹ (citing an 87% hemorrhage rate), however another investigation disputes this assertion³⁹², and 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 (however, this study may suffer from significant selection bias³⁹³). Literature review³⁸⁸ found a risk of recurrent hemorrhage following ICHOP from aneurysm or AVM during the remainder of the pregnancy was 33-50%.

Management modifications for pregnant patients

1. neuroradiologic studies

A. CAT scan: with shielding of the fetus, CAT scanning of the brain produces minimal radiation exposure

B. MRI: generally felt to have low potential for complications, however, many centers will not do MRI during first trimester. The safety of gadopentetate dimeglumine (Magnevist®) has not been studied in human pregnancy (classified by FDA as a Class III drug - not recommended for use during pregnancy, but may be used if benefits outweigh potential risks)

C. angiography: with shielding of the fetus, radiation exposure is minimal. Iodinated contrast agents pose little risk to the fetus, The mother should be well hydrated during and after the study³⁸⁸

2. antiepileptic drugs: see Pregnancy and antiepileptic drugs, page 419

3. diuretics: the use of mannitol in pregnancy should be avoided to prevent fetal dehydration and maternal hypovolemia with uterine hypoperfusion

4. antihypertensives: nitroprusside should not be used in pregnancy

5. nimodipine is potentially teratogenic in animals, the effect on humans is unknown. It should be used only when the potential benefit justifies the risk

Neurosurgical management³⁸⁸

The currently recommended treatment of a ruptured aneurysm in the pregnant patient is surgical clipping. Treatment of hemorrhage from AVM is more controversial. A number of authors recommend basing the decision of treatment on neurosurgical rather than obstetrical considerations.

Obstetric management following ICHOP

Earlier recommendations were to perform C-section to avoid the hemodynamic stresses of labor and vaginal delivery, however, the risk of hemorrhage is not significantly different between vaginal delivery and C-section. Several reports have indicated that the fetal and maternal outcome is no different for vaginal delivery vs. C-section, and is probably more dependent on whether the offending lesion has been treated. 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 the use of caudal or epidural anesthesia, shortening the 2nd stage of labor, and low forceps delivery if necessary.

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