ABC and EVD. You must optimize cerebral perfusion pressure (CPP) for all poor-grade SAH

The clinical and radiographic presentation of this case is consistent with poor grade (initially Hunt and Hess [HH] grade IV, which quickly progressed to grade V while in transit to the tertiary care center) acute aneurysmal SAH. Airway, breathing, and circulation (ABC) have all been addressed, although the BP is high at this time. The very first step in managing this patient is ventricular drain, the second step is ventricular drain, and the third step is ensuring that the ventricular drain you have just placed is working (ie, draining bloody cerebrospinal fluid [CSF] adequately when the drain is open, and maintaining good waveforms when the drain is clamped). After ABC, placing external ventricular drain (EVD) is the most crucial, lifesaving, important early step for managing patients with high-grade acute SAH with poor mental status and IVH. The presence of IVH complicates the natural course of both intracerebral hemorrhage (ICH) as well as SAH cases. IVH is often associated with development of an acute obstructive hydrocephalus, which may lead to vertical eye movement impairment and depressed level of arousal by its mass effect on the thalamus and midbrain. IVH is also associated with elevated intracranial pressure (ICP), which lowers the CPP (by the principle of the equation, CPP = MAP – ICP) if the mean arterial pressure (MAP) remains constant. Moreover, IVH has been reported to be an independent risk factor for increased risk of developing symptomatic vasospasm. The mass effect and cerebral edema may rapidly progress to herniation syndrome and death. As such, the presence of IVH has been recognized as a significant risk factor for poor outcome for both ICH and SAH.^1-3 Placing an EVD provides two benefits: (1) reliable (as long as the catheter tip is in the right location to provide appropriate ICP waveforms without obstructing the ventricular catheter by any blood clot) measurements of the ICP and (2) therapeutic drainage of the CSF in order to alleviate the intracranial hypertension (Figure 1-2). Placement of an EVD may not be necessary in a low-grade ([HH] grade 1-2) SAH patient if IVH is not severe and hydrocephalus is not present. In a high-grade patient, however, even if hydrocephalus is not seen in the first CT scan, if the patient has bled significantly (ie, a thick basal cistern SAH clot with classic Fisher group 3 and a modified Fisher grade 3 or 4; more on this below), placement of an EVD is often required.

It is important to note that the presence of IVH does not necessarily mean the ICP is abnormally elevated, and the placement of an EVD alone may not always lead to an improved outcome even if the high ICP responds favorably to opening and lowering of the drain.⁴ In the past, there were concerns regarding the potential harmful effect of EVD placement in treating the acute hydrocephalus in SAH patients. These concerns were mainly focused on the theoretical impact of suddenly lowering the ICP by EVD placement and eliminating the tamponade effect on a ruptured aneurysmal wall, leading to an increased risk of rebleeding in the acute phase. However, clinical studies have failed to prove such a hypothesis, and there is not sufficient evidence to believe that the CSF diversion by an EVD in treating acute hydrocephalus after SAH results in a higher incidence of rerupturing of the unsecured aneurysms.^5,6 It is wise, however, to avoid aggressively lowering the drain level immediately after placement. For example, leaving the EVD open at about 15 cm above the level of the external auditory meatus is reasonable before securing the aneurysm. In managing SAH cases, whether or not to place an EVD is occasionally debatable. For instance, a patient with low-grade (eg, HH I or II) SAH who is awake, follows commands with normal strength, and has no IVH, no acute hydrocephalus, and either absent or minimal volume of SAH (eg, classic Fisher groups 1 to 2) is not a candidate for EVD placement. On the other hand, a patient with a high HH grade and Fisher group 3 SAH, plus the radiographic evidence of severe IVH and acute hydrocephalus, who exhibits a progressively worsening level of arousal needs emergent placement of an EVD (classic indication for ABC and EVD). These are extreme ends of the clinical spectrum of SAH, and the timing and indication for EVD could be debated for the cases that are somewhere between these two extreme case scenarios. Acute hydrocephalus with IVH and clinical signs and symptoms of intracranial hypertension are all good indications for placing EVDs. It is also important to remember that even if the patient does not have any of the indications mentioned above, if the treating physician believes that there is a reasonable probability of developing these signs and symptoms in the near future, EVD placement should be considered. (Technical details and further management strategies are discussed in Chapter 22.) Despite the lack of “level 1” evidence of randomized data for improved outcomes, the use of an EVD is important because it can be helpful in managing ICP and CPP and often is lifesaving in certain SAH patients.

Changing Neurologic Status After EVD Placement

Placement of an EVD frequently results in a significant improvement in neurologic status. Comatose patients may start to localize to painful stimulation and may even open their eyes. Although this is not always seen, when it happens, it may possibly indicate a favorable outlook (eg, a patient who presents with HH grade V after aneurysmal SAH wakes up after EVD placement and begins to follow verbal commands: if this patient remains awake and continues to follow commands throughout the course of his or her illness, then the patient is behaving at a low-grade HH [ie, grades I to III], not like a grade V patient who presents with and remains in coma).

Patients with HH grade V have extremely poor prognosis. Many physicians and surgeons disclose such a poor prognosis to the patient’s family, and this disclosure often leads to withdrawal of life-sustaining care prior to any treatment. Although the decision to treat or not to treat should be made based on the prognosis and in the best interest of the patient, the initial prognosis is mostly based on the bedside neurologic assessment. Physicians should be aware that the patient’s clinical status may dramatically change after placement of an EVD, which has significant implications for the prognosis.⁷ When a patient with high-grade SAH is stuporous or comatose, it is difficult to determine whether such exam is due to hydrocephalus and IVH or to the initial injury, which is independent of the hydrocephalus and/or IVH. Thus, it would be prudent to wait until the initial resuscitation (ABC and EVD) is completed before making any predictions.

There are several SAH grading systems worth mentioning here. In 1967, Hunt and Hess reported 275 consecutive patients who were treated at the Ohio State University over a 12-year period. They believed that the intensity of the meningeal inflammatory reaction, the severity of neurologic deficit, and the presence or absence of significant systemic disease should be taken into account when classifying SAH patients. From their original manuscript, their grading system (which is now known and widely used as the Hunt and Hess Grade) was a classification of patients with intracranial aneurysms according to surgical risk (Table 1-1).⁸

Higher grades are associated with increased surgical risk for the repair of ruptured intracranial aneurysms. The Hunt and Hess original report included the presence of significant systemic disease (such as “hypertension, diabetes, severe arteriosclerosis, chronic pulmonary disease, and severe vasospasm seen on angiography”) as a negative sign, and the presence of such disease resulted in placement of the patient in the next less favorable (higher surgical risk) grading category.⁸ This grading system is not flawless as it can be challenging sometimes to differentiate between categories. For example, consider a patient with SAH with mild headache and nuchal rigidity compared with another patient with moderate headache and nuchal rigidity (which means grades I and II, respectively, according to the original HH grading system). The only differentiating variable here would be the intensity of the headache, which can be problematic because the intensity of headache is subjective, and patients often cannot differentiate mild from moderate headache (most people would describe a “very bad” headache and cannot provide specific details).

This criticism had been actually predicted, and the original authors mentioned it in their journal article: “It is recognized that such classifications are arbitrary and that the margins between categories may be ill-defined.”⁸ For this reason, it has been pointed out that the HH system has poor interobserver reliability and reproducibility.⁹ Nevertheless, the HH grading system is widely used, and numerous studies have shown that the higher grade (or sometimes called poor grade, which usually refers to HH grades IV and V) is associated with a poor outcome.^10-13

Another grading system to consider is the one that is the most universally accepted system for patients presenting with an altered level of consciousness: the Glasgow Coma Scale (GCS). In 1975, Jennet and Bond, from the University of Glasgow, reported a scale called Assessment of Outcome After Severe Brain Damage, a Practical Scale (Table 1-2).¹⁴

The GCS is a more general grading system and was not developed specifically for SAH patients. However, studies show that for patients with aneurysmal SAH, the initial GCS score has positively correlated with long-term outcome.¹⁵

In 1988, the World Federation of Neurosurgical Societies (WFNS) developed a grading system that incorporated both the GCS and bedside neurologic assessment focusing on any focal deficit (Table 1-3).¹⁶

The HH and WFNS grading systems are by far the two most commonly used systems for grading patients with acute aneurysmal SAH. Despite the frequently raised criticisms regarding the interobserver variability, the HH grade is used even more commonly than the WFNS scale (71% of reported studies from 1985 to 1992 used the HH grade compared with 19% that used the WFNS scale),^17,18 and both grading systems have been shown to correlate reasonably well with the long-term outcome.¹⁹

In 1980, Fisher and colleagues reported the relationship between the amount of SAH and the risk of developing severe vasospasm (defined as delayed clinical symptoms and signs; Table 1-4).²⁰

The Fisher group’s grading system is based on the description of CT findings, mainly focusing on the actual volume of blood in the subarachnoid space. There is a linear relationship between the amount of hemorrhage and the rate of developing symptomatic vasospasm.²⁰ This grading system has been extensively studied and there are numerous clinical studies validating its usefulness.^21-25 In multiple studies, the risk of developing symptomatic cerebral vasospasm appears to increase along with the increasing amount of acute hemorrhage in the subarachnoid space. Although original report by Fisher et al does describe the low risk of vasospasm, there is a clearly observed risk of vasospasm even for patients with minimal blood in the subarachnoid space and for those with intraparenchymal or intraventricular hemorrhage.²⁰

It is important to understand that the Fisher scale actually did report some incidence of vasospasm in groups 1, 2, and 4. Group 3 had the highest incidence of vasospasm, but other groups also had vasospasms, just much lower in frequency.²⁰ Like all other grading systems, the Fisher scale is not without limitations. There have been concerns in the literature reporting a low correlation between the Fisher grade and the incidence of symptomatic vasospasm (one recent study showed about 50% correlation between the Fisher grade and vasospasm).²⁶ Another criticism about the Fisher scale is its inevitable interpersonal variability in assessing the estimated blood volume. Also, according to the scale, all cases of CT of the head showing SAH with greater than 1 mm of vertical thickness is categorized as grade III, but this includes vast majority of patients with SAH who may not in fact have the same risk of developing vasospasm.^26,27

In light of these concerns, Claassen et al’s group, from Columbia University, proposed another grading system (Table 1-5): the modified Fisher scale (mFS).^28,29

Note that the mFS incorporates the presence or absence of IVH, and if a patient has IVH, even if there is no blood in the subarachnoid space, the scale is 2 (as opposed to 1 [no blood seen] or 4 [minimal SAH and the presence of intraparenchymal hemorrhage or IVH] in the original Fisher scale). This scale emphasizes that the presence of IVH increases the risk of developing symptomatic vasospasm. This emphasis is stronger but not completely different from that of the Fisher scale, because the original Fisher scale does report some incidence (although low) of vasospasm in those with IVH and absent or minimal SAH. Furthermore, the mFS uses a subjective description and coding of the hemorrhage by the use of “thick” or “thin” clots in the subarachnoid space, and the description of IVH does not take the exact amount of IVH into account (this scale takes the “presence” versus the “absence” of IVH into account, not how much IVH there is). The mFS emphasizes the importance of IVH, and it also highlights how the amount of hemorrhage once again plays an important role. Its grading system is easy and intuitive (unlike the classic Fisher scale in which group 4 actually has a lower incidence of vasospasm than lower grades), as the scale goes from 0 to 4, and the higher grade has the higher risk of developing delayed cerebral ischemia (DCI).

In order to minimize the interobserver variability in assessing the estimated volume of blood in the subarachnoid space, a volumetric quantification of Fisher grade 3 has been proposed and studied by Friedman and colleagues from the Mayo Clinic.³⁰ However, although quantification of SAH may provide a more accurate assessment of the volume of blood in the subarachnoid space, it requires manual outlining of the hemorrhage volume, which can be time consuming and less reliable.

In 2011, Ko and colleagues, from Columbia University, reported a study of volumetric analysis of SAH using a MIPAV (Medical Image Processing, Analysis, and Visualization; version 4.3; National Institutes of Health [NIH]) software package that automatically outlines the hemorrhage on CT at the click of a button.³¹ This quantification analysis showed that patients with a higher volume of cisternal plus IVH clot burden developed a greater risk of developing DCI and poor outcome at 3 months (Figure 1-3).

It also validated the modified Fisher scale as a reasonable grading system in predicting DCI that can be done easily at the bedside. However, it is important to note that although both the Fisher scale and the mFS have demonstrated the association between blood burden and DCI, a question still remains: Do the location and exact thresholds of blood volume matter? Ko and colleagues reported.³¹

Klimo and Schmidt have eloquently summarized a historical review of the literature on the relationship between the CT findings and the rate of developing cerebral vasospasm after aneurysmal SAH using different scales.³²

The first battle in high-grade SAH: The battle against elevated ICP

The early phase of high-grade SAH is often complicated by the presence of ICP crisis. An ICP value out of the normal range (0-20 mm Hg) is considered abnormal, but the ICP alone as an absolute value may not always signify the need for an urgent treatment. A good example would be people with pseudotumor cerebri and high ICP who perform normal daily activities. ICP also rises when patients cough or are suctioned. Such an increase, if it is induced and transient, does not necessarily require any treatment. In the setting of acute, high-grade SAH, however, abnormally elevated ICP is a major concern owing to its direct, negative impact on the CPP. With persistently low or decreasing CPP, a certain degree of ischemic insult is inevitable. A step-by-step algorithm for managing refractory ICP crisis is outlined below. This is a recommendation that reflects the latest medical treatment available in the literature.

With all other factors that are known to influence the ICP being constant, increasing the MAP leads to increased CPP. Increased CPP and blood flow may result in increased cerebral blood volume. Increased cerebral blood volume could lead to any one of the following scenarios:

1. 
   

   Development of vasoconstriction would occur if autoregulation is intact in response to increased blood volume delivered. Such vasoconstriction may result in a decrease in ICP.

   
   
2. 
   

   No vasoconstriction would occur if autoregulation is impaired (pressure–volume breakdown). Because blood volume is increased, there may be a further increase in the ICP.

   
   
3. 
   

   A mixed picture of all of the above as different parts of the brain have either impaired or intact autoregulation at a point prior to the pressure–volume breakdown.

It is important to emphasize that increasing the BP with phenylephrine may either increase or decrease the ICP. Clearly, if the MAP is too low to the point that the patient is in a state of shock, it makes sense to increase the MAP in order to maintain adequate end-organ perfusion. However, if the MAP is already 90 mm Hg, then increasing the MAP to 130 mm Hg with phenylephrine may have a deleterious effect on the ICP. Finally, it is important to remember that every effort needs to be made to avoid the worst combination that is associated with devastating results: systemic hypotension and uncontrolled ICP.