By Uday B. Nanavaty, MD
Subarachnoid hemorrhage (sah) is a common, life-threatening disorder in which critical care may play an important role in obtaining a positive outcome. Aneurysmal bleeding is the most common cause of acute subarachnoid hemorrhage. There are some data to suggest that care provided by a specialized neurocritical care unit may improve outcomes in acute neurological and neurosurgical conditions, suggesting further that intensivists may play an important role in coordinating the care of patients with SAH, whether they are undergoing surgical repair.
Epidemiology and Pathophysiology
The incidence of SAH rises with age with median age of around 50 years. There are some data to suggest that the disorder is more common in females and that perhaps African Americans are more likely to suffer from SAH. More than 25,000 patients suffer from SAH every year in North America and unfortunately, 10,000 or so die before reaching the hospital. Of the patients who make it to the hospital, more than half will die or be severely disabled, further highlighting the need for critical approach to their problems.
Most SAH (more than 80%) result from rupture of a saccular aneurysm. The anterior cerebral circulation is the site of the aneurysm in more than 80% of cases. Other causes of SAH include arteriovenous malformations and trauma. In about 10% of the patients, no cause can be identified even after several different diagnostic approaches.
It is thought that an attenuated tunica media and lack of external elastic lamina in intracranial arteries are primarily responsible for the increased incidence of aneurysm formation inside the cranial vault. Shear forces arising at branching of intracranial vessels are thought to be responsible for the development and rupture of an aneurysm. Factors that increase the shear forces or hinder the repair from an injury further contribute to the process. Hypertension, smoking, and alcohol consumption are considered to be modifiable risk factors. Family members of patients with SAH have more than a 4-fold increase in incidence of SAH and screening of family members with more than one affected member in the family is often suggested. Patients with autosomal dominant polycystic kidney disease have increased incidence of SAH and unruptured aneurysms. Whether patients with Marfan’s syndrome or Ehler-Danlos syndrome also have higher incidences of SAH is not clear.
Once an aneurysm or arteriovenous malformation ruptures, blood leaks into the subarachnoid space. Due to the limited space in the intracranial vault, the intracranial pressure (ICP) rises rapidly, resulting in a reduction in cerebral perfusion pressure. Distal blood supply is reduced due to vasospasm and clot formation locally. As the blood clot is resolved, further vasospasm may occur, and fibrinolysis is thought to contribute to rebleeding. Hypothalamic dysfunction develops for unclear reasons and results in altered cardiovascular and respiratory functions.
Those patients who are not comatose from a massive hemorrhage often describe development of "the worst headache of my life." Nausea and vomiting from rising ICP are other common manifestations. Some patients may present with a "warning leak," a milder headache and are often misdiagnosed in the clinic with other common types of headache. Rarely, patients may present with ischemic stroke-type symptoms, but CT scan often reveals SAH, preventing them from getting thrombolytic therapy, that can be fatal if administered to a patient with SAH.
Nuchal rigidity is common. Cranial nerve palsy, often affecting the lateral rectus muscle of the eyes, is seen in more severe cases. Focal neurological deficits in the setting of SAH portend more severe disease, and loss of consciousness is considered ominous, especially if the patient is deeply comatose.
Several different classification schemes have been described. Two most commonly used are summarized in the Tables. Hunter and Hess classes I and II are considered good grades. Classes IV and V portend a very poor prognosis, even with active therapy. These classification schemes help identify patients who may need referral to a specialized center, as well as providing good prognostic information.
CT scan of the head is very sensitive at detecting SAH. It is positive in more than 90% of the cases, in the first 24 hours. After 24 hours, its ability to detect recent bleeding declines drastically. In those circumstances, a lumbar puncture can be used to demonstrate xanthochromia in the cerebrospinal fluid, after first making sure by a CT scan that cerebral herniation is not imminent. Once the initial diagnosis is established, further diagnostic tests are performed to localize site of the aneurysm. Conventional angiography is considered standard in most institutions, and if contraindicated, CT angiography or magnetic resonance angiography can be used.
Early surgical therapy is gaining acceptance in United States as the standard approach. Most patients with Hunt and Hess grades I and II SAH undergo early surgical intervention. Although the outcome is poor in patients who are at grades IV or V at presentation, many centers report good outcomes in as many as 20% of such patients, making referral to a tertiary center worthwhile especially for younger patients without much underlying medical disease. Decompressive craniectomy has been reported to be effective at rescuing some of the poor-grade patients in their early part of hospitalization.
The biggest contributor to mortality in patients who present alive is rebleeding from the aneurysm. Studies suggest 4% risk of bleeding in first 24 hours and 1-2% per day thereafter up to 14 days. If the aneurysm is not repaired, therapy of vasospasm further increases the risk of bleeding, making early repair a priority. Rebleeding is suspected when neurological status deteriorates or if ICP rises acutely, if monitoring is being performed.
In most centers, a good-grade patient will have an early definitive treatment to repair the aneurysm. Most centers favor surgical repair especially for large aneurysms. Endovascular therapies are also performed in centers with active interventional neuroradiology programs. Long-term success of such endovascular therapy is not very well defined, further favoring a surgical approach. A combined approach with coiling or embolization followed by surgical repair of arteriovenous malformations is also performed.
Surgical repair also helps to establish better monitoring and control of ICP. The timing of surgery is controversial, but most centers opt for first 3 days or delay the surgical repair to after 10-14 days.
Antifibrinolytic therapy to prevent rebleeding has not been shown to benefit overall outcome and may increase the risk of vasospasm, hence such therapies as tranexamic acid or aminocaproic acid are not routinely used in the United States.
Vasospasm and Cerebral Ischemia
Development of vasospasm and secondary cerebral ischemia is another leading cause of mortality and morbidity in patients with SAH. Extravascular blood and the products of its dissolution are considered irritant for cerebral vessels, giving rise to cerebral vasospasm. Local factors also contribute to vasospasm, although they are not necessarily the only factors as the vasospasm may be diffuse or may involve cerebral arteries away from the site of the ruptured aneurysm.
Transcranial measurement of the velocity of blood flow using the Doppler effect to detect asymptomatic vasospasm is common. Rather than going by an absolute velocity to define vasospasm, it is more helpful to follow trends. A persistent upward trend in transcranial Doppler (TCD) velocity is suggestive of vasospasm. It is important to remember that TCDs are not very accurate at detecting changes in velocity in the posterior circulation; hence one has to follow clinical examination as well. A deteriorating clinical status with rising flow velocity by TCD is sufficient to make a diagnosis of vasospasm. If the clinical condition is deteriorating and TCDs are negative, angiography remains the gold standard to detect vasospasm.
Nimodipine, a calcium channel blocker with selective CNS vasodilatory effects, has been shown in randomized, controlled trials to improve the mortality and morbidity in SAH. Although the incidence of vasospasm remains the same on nimodipine, it is thought that this agent prevents vasospasm in smaller vessels thereby improving the cerebral blood flow.
If vasospasm is detected in a single vessel, and especially if it is detected during angiography, endovascular therapy can be used, either in the form of balloon angioplasty of the affected vessel or in the form of papaverine infusion locally. If the local therapy fails or if diffuse vasospasm is detected, "HHH" therapy is instituted. The components of HHH therapy include Hypervolemia, Hypertension, and Hemodilution. Although the studies are not conclusive and experts argue on either using it or abandoning it, some or all components are used widely in critical care. Circulatory volume is expanded with the use of isotonic saline. Hypertension is generated, especially if the patient is hypotensive, by using dopamine, norepinephrine, neosynephrine, or isoproterenol depending upon the underlying comorbidities that the patient may have. Hemodilution is achieved concomitantly to maintain hematocrit in the range of 30-35. In appropriate settings, invasive monitoring is recommended to further optimize HHH therapy, as patients may develop rebleeding or pulmonary edema if they are not closely monitored.
Patients can develop vasospasm any time between 3 and 14 days following the initial bleed. Nimodipine therapy in the dose of 60 mg every 4 hours is started within the first 96 hours, and it is continued for 4-6 weeks. Hypotension remains the common side effect of Nimodipine therapy.
Development of acute hydrocephalus is also a common cause of change in mental status in patients with SAH. It is easily detected by CT scan. Most patients undergoing surgical repair will have some form of ventricular drainage to control the hydrocephalus. Ventriculostomy performed without definitive repair of the aneurysm increases the risk of rebleeding by suddenly reducing intracranial pressure.
Cardiac and Pulmonary Abnormalities
The cardio pulmonary abnormalities are thought to result from hypothalamic dysfunction associated with SAH. Most patients with SAH will have EKG abnormalities, especially in the form of T-wave inversion and prolongation of the QT interval. It is important to rule out SAH if a patient presents to the emergency room with coma and an EKG suggestive of acute ischemia.
Although focal abnormalities are not common, some patients may develop globally reduced left ventricular function and may need inotropic support before recovering. Subendocardial necrosis is often seen in necropsies and it is suggested that severe local vasospasm from sympathetic overstimulation may cause such changes. Consistent with that, many patients will have elevation of biomarkers suggestive of myocardial infarction without really having occlusive coronary artery disease.
Neurogenic pulmonary edema may develop in the setting of SAH. Again, in such patients, it is important to ensure that cardiac function is adequate, as pulmonary edema from neurogenic causes can have a normal, low, or even high pulmonary artery occlusion (wedge) pressure. Hence, invasive monitoring with pulmonary artery catheter-directed therapy may be needed in order to optimize cardiopulmonary function. Management of most cardiac and pulmonary abnormality is symptomatic, as most of the dysfunction improves over time if neurological status improves.
Hyponatremia in patients with SAH may be secondary to the syndrome of inappropriate antidiuretic hormone (SIADH) or due to cerebral salt wasting from increased production of atrial natriuretic peptide. It is important to correct the hyponatremia to maintain an isotonic environment, but the usual approach of fluid restriction is not appropriate as that may worsen the vasospasm. Hypervolemia must be maintained with administration of hypertonic saline if necessary. Treatment of cerebral salt wasting involves replacement of lost fluids with isotonic saline.
Other traditional critical care issues such as steps to prevent gastrointestinal bleeding, deep venous thrombosis, and prevention of nosocomial infections, along with appropriate nutritional support, should be addressed. In patients with focal neurological deficits, seizure prophylaxis is often recommended. Families may need support during this often-tragic event in the life of their loved ones.
The mortality from SAH is highest in the first 24 hours of the event, and more than 25% of patients will not make it to the hospital alive. Further, patients who present with higher grades of Hunter and Hess classification (grades IV and V) have a very poor prognosis. Of the patients who present alive, the mortality rate approaches 40%, and a further 20% will suffer from severe disability. In spite of the overall poor prognosis, a large body of literature favors an aggressive approach, especially for young and otherwise healthy patients.
In summary, critical care physicians play an important role in the management of patients with SAH. Coordination of care among the intensivist, neurosurgeon, neurologist, neuroradiologist, and other health care providers is important for the optimum outcome. Research continues in the area of finding further medical miracles such as a recent report of a platelet activating factor receptor antagonist to be safe and perhaps efficacious; however, hours of painstaking attention to detail at the bedside are more likely to produce more "miraculous" saves than an ever elusive "magic bullet."
Severity of Subarachnoid Hemorrhage; Modified Hunter and Hess Classification
Asymptomatic or minimal headache and minimal nuchal rigidity
Moderate to severe headache and nuchal rigidity, no focal neurological deficits except for cranial nerve palsy
Drowsiness, confusion, or mild focal deficits
Stupor, hemiparesis, early decerebrate type posturing, vegetative disturbances
Deep coma, moribund appearance, decerebrate rigidity
|Severity of Subarachnoid Hemorrhage; World Federation of Neurological Surgeons Classification|
|WFNS Grade||GCS* Score||Motor Deficit|
|IV||7-12||Present or Absent|
|V||3-6||Present or Absent|
* GCS = Glasgow Coma Scale
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