The management of patients with SAH focuses on the anticipation, prevention and management of these secondary compliations;
Early complications include: rebleeding, hidrocephalus e seizures (within 1-3 days);
During the first 1-2 weeks after hemorrhage, patients are at risk of delayed ischemic deficits (vasospasm, autoregulatory falure and intravascular volume contraction);
Intracranial aneurysms account for 85% of cases of nontraumatic SHA;
Other causes of SHA include bleeding from other vascular malformations (arteriovenous malformations), Moyamoya Syndrome, coagulopathy and rarely extension of an intracerebral hematoma;
In up to one fifth of cases, no source of bleeding is identified;
Incidence of rupture is only 2-20 of 100.000 individuals per year, hemorrhage is more frequent in women than men (ratio 3:2);
Peak rupture rates occur between the ages of 50 and 60 years;
Risk factors for SAH include hypertension, cigarette smoking, heavy alcohol consumption and a history of SAH in first-degree relatives;
The majority of aneurysms are found in the circle of Willis;
Only about 15% of aneurysms occur in the posterior (vertebro-bailar) circulation;
The most common sites of ruptured aneurysms are the takeoff of the posterior communicating artery from the internal carotid artery (41%), anterior communicating artery anterior cerebral artery (34%), and middle cerebral artery (20%);
The classic presentation: severe headache ("worst headache of my life"), nausea, vomiting and syncope followed by a gradual improvement in level of consciousness;
Focal neurologic signs are unusual but may occasionally be seen due to mass effect from a giant aneurysm, parenchymal hemorrhage, subdural hematoma or a large localized subarachnoid clot;
In addition, third and sixth cranial nerve palsies may be present because of aneurysmal compression of nerve or increased intracranial pressure, respectively;
Seizures at onset may be reported, but it is not clear how many of theses episodes represent true epileptic events vs. abnormal posturing;
Initial and evaluation Management: suspected SAH focus on aieway evaluation, early computed tomography imaging, blood pressure control, serial assessment of neurologic function and preparation for angiography;
The patient's clinical status is assessed using the Hunt and Hess Scale and World Federation of Neurologic Surgeons Scale
World Federation Of Neurological Surgeons Scale
Hunt and Hess Scale - Symptoms ___________________________________________________________________________________________________
Grade
Grade I Asymptomatic or mild headache (E.G 15 ), Motor Deficit: Absent
Grade II Moderate to severe headache, nuchal rigidity, with or without cranial
nerve deficits (E.G. 14 - 13), Motor Deficit: Absent
Grade III Confusion, lethargy, or mild focal symptoms (E.G. 14 ), Motor Deficit : Present
Grade IV Stupor and/or hemiparesis (E.G. 12 - 07 ), Motor Defict: Present or Absent
Grade V Comatose and/or extensor posturing (E.G. 06 - 03), Motor Deficit: Present or Absent
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A noncontrast CT scam within 24 hours detects > 95% of SHA;
CT may be falsely negative if the volume of bood is very small, if the hemorrhage occurred several days prior, or if the hematocrit is extremely low;
The amount of subarachnoid blood is graded and is an important predictor of vasospasm risk.
The modified Fisher computed tomography rating scale _________________________________________________________________________________
Grade 1 - Minimal or diffuse thin subarachnoid hemorrhage without intraventricular hemorrhage (IVH), indicating low risk for symptomatc vasospasm;
Grade 2 - Minimal or thin subarachnoid hemorrhage with IVH;
Grade 3 - (Thick cisternal clot without IVH), indicating intermediate risk for symptomatic vasospasm; and
Grade 4 - (Cisternal clot with IVH), indicating high risk for symptomatic vasospasm.
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Early hydrocephalus is suggested by enlargement of the third ventricle and of the temporal horns of the lateral ventricles;
If CT is normal and suspicion of SAH remains strong, a lumbar puncture should be performed;
The presence of xanthochromia may be helpful in distinguishing a traumatic lumbar puncture from a true SAH especially if it detected by spectrophotometry;
Conventional catheter angiography remains the gold standard for detection of intracranial aneurysms and should be performed as soon as practical to facilitate early rapair of the rupture aneurysm;
CT angiography has recently improved to the point where some centers use it as the primary test to identify an aneurysm;
Magnetic resonance imaging techniques are rapidly advancing to this point as well;
Angiography fail to demonstrate the cause of nontraumatic SAH in ~15% to 20% of case;
If the patient is the lethargic or agitated, management of the airway should be addressed.
Consideration should be given to facilitate performing safe and rapid angiography;
To prevent aneurysmal re-rupture, hypertension requires prompt treatment;
Analgesic alone may be effective;
The preferred agents include labetalol, B-blockers, hydralazine, and nicardipine;
A notable exception to vigorous treatment of hypertension is when hydrocephalus is present.
In that situation blood presure should be addressed after the hydrocephalus is treated;
Cardiacs abnormalities are common in the first 48 hours: ECG, T-waves or cerebral T-waves, ST segment depression , and prolonged QT segments are frequent, cardiac enzymes are often mildly elevaded,and arrhythmias are very common but typically benign;
In rare cases, the cardiac abnormities are much more severe: myocardical contractility may be markedly impaired, leading to a fall in cardiac output (CO). This condition has been referred to as "stunned myocardium", and may also includ an element of neurogenic pulmonary edema;
The management is similar to other causes of acute pump failure with inotropic agents, diuretics, hight concentrations of oxygen, and positive end-expiratory pressure;
Troponin levels eleveted is surprisingly transient ad completely reversed in a few days;
Early Critical Care Management
Continuous electrocardiogram minitoring;
Serial neurologic examinations;
Frequent determinations of blood pressure;
Electrolytes;
Body weight;
Fluid balance;
Transcranial Doppler (TCD);
Adequate hydration with isotonic saline;
Aspects of oxygenation;
Management fever;
Glucose control;
Nutrition are covered elsewhere;
Anticonvulsants
It appears that short term (3 day) use during the perioperative period does not increase risk of seizures;
"Three-day phenytoin prophylaxis is adequate after subarachnoid hemorrhage. - Chumnanvej S - Neurosurgery - 01-JAN-2007; 60(1): 99-102; discussion 102-3 (MEDLINE is the source for the citation and abstract of this record ): "CONCLUSION: A 3-day regimen of PHT prophylaxis is adequate to prevent seizures in subarachnoid hemorrhage patients. Drug reactions are significantly reduced, but seizure rates do not change. Short-term PHT administration may be a superior treatment paradigm".
Steroids
A recent Cochrane review concluded that there is no evindece of a beneficial or adverse effect of corticosteroids in patients with SAH;
Rebleeding
The risk of rebleeding is highest immediately following hemorrhage (4% to 6% over the first 24 hours) and over the next few days declines;
Short term (3-day) use of antifibrinolytics may prevent rebleeding without increased risk of vasospasm;
Cough, valsalva should be minimized;
Headache should be controlled;
Agitated patients should be sedated with short-acting agents to the pointof drowsiness, but should remain responsivefor assessment of neurologic status;
Outcome in a large prospective controlled trial found that for patients appropriate for either modality, 4-year outcome was better with endovascular coiling (de Oliveira JG, Beck J, Ulrich C, et al: Comparison between clipping and coiling on the incidence of cerebral vasospasm after aneurysmal subarachnoid hemorrhage: A systematic review and mata-analysis. Neurosurg Rev 2007; 30:22-30 & 84. Diringer MN: To clip or to coil acutely ruptured intracranial aneurysms: Up date on121–125);
The study has generated considerable controversy. Follow up ofpatients enrolled in this study revealedthat patients treated with endovascularcoiling were 6.9 times more likely to undergo retreatment over a mean interval 21 months because of aneurysm recurrenceofor rebleeding (Campi A. Ramzi N, Molyneux Aj, et al: Retreatment of rupture cerebral aneurysms in patients randomized by coiling or cliping in the International Subarachnoid Aneurysm Trial (ISAT). Stroke 2007; 38: 1538-1544
Hydrocephalus
Early hydrocephalus occurs in 20% to 30% of patients and is often accompanied by intraventricular blood;
Clinical improvement is seen in the majority after external ventricular drainage;
Hydrocephalus rates are not different in patients undergoing clipping or endovascular
treatment of their aneurysms;
Hidrocephalusdevelops in about one fourth of surviving patients and is associated witho lder age, early ventriculomegaly, ventricular hemorrhage, poor clinical conditionon presentation, and female gender.
Later Complications
Hyponatremia and Intravascular Volume Contraction (Smith M: Intensive care management of patients with subarachnoid haemorrhage. (Curr Opin Anaesthesiol 2007; 20:400–407, Diringer MN: Neuroendocrine regulation of sodium and volume following subarachnoid hemorrhage. Clin Neuropharmacol 95;18:114–126 & Wijdicks EFM, Vermeulen M, ten Haaf JA, et al: Volume depletion and natriuresis in patients with a ruptured intracranial aneurysm. Annals Neurol 1985; 18:211–216);
There are disturbances of humoral and neural regulation of sodium, intravascular volume, and water in SAH that lead to intravascular volume depletion and hyponatremia,sometimes referred to as cerebral salt wasting (Diringer MN: Neuroendocrine regulation of sodium and volume following subarachnoid hemorrhage. Clin Neuropharmacol 1995;18:114–126 & Diringer MN: Management of sodium abnormalities in patients with CNS disease.Clin Neuropharmacol 1992; 15:427–447);
Hyponatremia can frequently be managed with restriction of free water by giving only isotonic intravenous fluids, minimizing oral liquids, and using concentrated enteral feedings;
Persistent hyponatremia9 can be treated by utilizing mildly hypertonic solutions(1.25%–3.0% saline) as the sole intravenous fluid;
Vasospasm
Pathologic changes occur in intracranial arteries following SAH that thicken the wall, narrowt he lumen, and impair relaxation (Seifert V, Stolke D, Reale E: trastructural changes of the basilar artery following experimental subarachnoid haemorrhage. Amorphological study on the pathogenesis ofelayed cerebral vasospasm. (Acta Neurochir(Wien) 1989; 100:164–171);
If the reduction in flow is severe enough, ischemia and infarction follow (Powers WJ, Grubb RL Jr, Baker RP, et al.Regional cerebral blood flow and metabolism in reversible ischemia due to vasospasm. Determination by positron emission tomography. J Neurosurg 1985; 62:539–546)
Monitoring for vasospasm typically consists of serial neurologic exams, serial measurement of blood flow velocities byTCD (Transcranial Doppler Ultrasonography) and catherter angiogtaphy (Sloan MA, Haley EC Jr, Kassell NF, et al: Sensitivity and specificity of transcranial doppler ultrasonography in the diagnosis of vasospasm following subarachnoid hemorrhage, Neurology 1989; 39:1514–1518 62. Sekhar LN, Wechsler LR, Yonas H, et al: Value of transcranial Doppler examination in the diagnosis of cerebral vasospasm after subarachnoid hemorrhage. Neurosurgery 1988; 22:813–821);
Neurologic signs may be vague, such as a global decline in responsiveness, or consist of focal deficits such as hemiparesis, hemiplegia, abulia, or language disturbance that may wax and wane;
The utility of other imaging modalities, like perfusion computed tomography, Xenon computed tomography, diffusion weighted magnetic resonance imaging, and single photon emission computed tomography in detecting vasospasm is under investigation;
The utility of other imaging modalities: perfusion computed tomography, Xenon computed tomography, diffusion weighted magnetic resonance imaging and single photon emission computed tomography;
Cerebral microdialysis, which involves measuring extracellular cerebral fluid levels of glucose, glutamate, lactate, and pyruvate, and brain tissue oxygen tension monitoring may offer promise (Skjoth-Rasmussen J, Schulz M, Kristensen SR, et al: Delayed neurological deficits detected by an ischemic pattern in the extracellular cerebral metabolites in patients with aneurysmal subarachnoid hemorrhage.
J Neurosurg 2004; 100:8–15 116. Sarrafzadeh AS, Sakowitz OW, Kiening KL,
et al: Bedside microdialysis: A tool to monitor cerebral metabolism in subarachnoid hemorrhage patients? Crit Care Med 2002; 30:1062–1070
117. Schulz MK, Wang LP, Tange M, et al: Cerebral microdialysis monitoring: Determination of normal and ischemic cerebral metabolisms in patients with aneurysmal subarachnoid hemorrhage. J Neurosurg 2000; 93:808–814);
Management of Vasospasm
Nimodipine is safe, cost-effective, and reduces the risk of poor outcome and secondary ischemia;
Hypotension is infrequent, especiallyif patients are well hydrated;
Dips in blood pressure following nimodipine administration may be more of a problem, and administering small the vasopressors;
The use of prophylactic hypervolemia is more controversial;
The amount of blood in the subarachnoidspace is a strong predictor of vasospasm;
Other approaches under investigation include insertion of prolonged release implants impregnated with vasodilators (papaverine and nicardipine), enoxaparin (126), and prophylactic transluminal balloon angioplasty;
The use of triple-H therapy (hypervolemia, hypertension, and hemodilution) stems from numerous clinical observations noting improvement in patients’ clinical symptoms following induced hypertension and volume expansion;
(Muench E, Horn P, Bauhuf C, et al: Effects of hypervolemia and hypertension on regional cerebral blood flow, intracranial pressure, and brain tissue oxygenation after subarachnoid hemorrhage. Crit Care Med 2007; 35:1844–1851)
Endovascular techniques frequently play a role in the aggressive treatment of vasospasm.
They include transluminal angioplasty and intra-arterial infusion of vasodilators;
Transluminal balloon angioplasty is very effective at reversing angiographic spasm of large proximal vessels and produces a sustained reversal of arterial narrowing
Major complications occur in 5% of procedures and include vessel rupture, occlusion, dissection, hemorrhagic infarction, and hemorrhage from unsecured aneurysms;
A recent prospective controlled trial of prophylactic angioplasty in patients at high risk for
vasospasm did not show any improvement in outcome;
Intra-arterial papaverine has an immediate and dramatic effect on blood vessels, but reversal of clinical deficits is variable;
In most centers, use of papaverine has been abandoned because of its short-lived effect and complications including increased intracranial pressure, apnea, worsening of vasospasm,
neurologic deterioration, and seizures;
This has led to the growing use of intraarterial nicardipine, verapamil, nimodipine, and milrinone as alternatives to papaverine;
A number of potential new therapies are currently under active investigation, including an endothelin antagonist, magnesium, and statins;
Two small prospective controlled trials have found a reduction in delayed ischemia neurologic deficits and symptomatic vasospasm with statin therapy;
A prospective, randomized controlled trial of intravenous magnesium found a nonsignificant trend toward better outcome;
Clazosentan, a selective endothelin A receptor antagonist, was evaluated in a randomized, double-blind, placebo-controlled, multicenter phase IIa study, and it was found that it reduced
the frequency and severity of angiographic vasospasm, a phase III study is underway.
