Page 1138 - Hall et al (2015) Principles of Critical Care-McGraw-Hill

CHAPTER 84: Cerebrovascular Disease 777

ventricular wall abnormalities. The management of these patients typi- and nurses well-versed in the neurologic examination and recognition
cally requires invasive hemodynamic monitoring and treatment with of subtle deficits. The patients with the highest incidence of vasospasm
ionotropes such as dobutamine. If clinical vasospasm develops in these are those with Hunt-Hess grades III through V and Fisher Scale of 3.
patients prior to the resolution of cardiogenic shock, management can These patients are often monitored in the ICU (days 3-10). Clinically
become very difficult. vasospasm presents as a decline in the global level of function or a focal
Pulmonary Complications Pulmonary complications are seen in almost one- neurologic deficit. Patients may initially appear “less bright” and then
fourth of all patients with SAH. They include pneumonia (arising from become progressively less alert and finally comatose. The focal deficits
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acute or subacute aspiration, commonly with nosocomial organisms), mimic those seen in ischemic stroke. Middle cerebral artery vasospasm
cardiogenic pulmonary edema, neurogenic pulmonary edema, and can produce hemiparesis, and if left-sided, aphasia or if right-sided,
pulmonary embolism. Management of severe pulmonary edema with neglect. Anterior cerebral artery vasospasm often manifests as abulia or
refractory hypoxia usually involves positive pressure ventilation and lower extremity weakness. The focal deficits wax and wane and there-
diuretics; however, diuretics may not be appropriate for neurogenic fore are not reported by all observers. The symptoms are exacerbated by
pulmonary edema if there is relative intravascular volume depletion. In hypovolemia or hypotension.
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these cases, hemodynamic monitoring via a pulmonary artery catheter Transcranial Doppler ultrasonography detects changes in the blood
or via transpulmonary thermodilution may be warranted. flow velocity in the proximal portion of the major cerebral vessels. Very
high flow velocities (>200 cm/s) in the middle cerebral and intracranial
Postoperative Management: Knowledge of the intraoperative surgical carotid arteries are closely correlated with angiographic vasospasm,
and anesthetic course facilitates the postoperative care of SAH patients. while low flow velocities (<120 cm/s) suggest a low likelihood of vaso-
Large doses of mannitol may have been administered to shrink the spasm. Furthermore, a Lindegaard ratio (MCA/extracranial ICA mean
brain and facilitate retraction. This measure can result in postoperative velocity ratio) which is greater than 6 is also highly predictive of severe
hypovolemia. If temporary clipping of cerebral vessels was required, vasospasm. Patients with rapidly rising velocities are considered to
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hypothermia and/or large doses of barbiturates may have been employed be at highest risk for developing clinical vasospasm; therefore, a trend
and the risk of focal ischemia exists. These maneuvers may also delay is frequently more useful than isolated values. Transcranial Doppler
emergence from anesthesia and add to the systemic complications of has several limitations. High-flow velocities can be due to increased
hypothermia. The decision to extubate a postoperative patient must blood flow rather than narrowing of the blood vessel; however, this can
take these factors into consideration with the understanding that keep- be corrected for by calculating the Lindegaard ratio instead of using
ing the patient on mechanical ventilation further increases their risk for velocities. Distal segments of the major arteries cannot be evaluated.
medical complications including ventilator-associated pneumonia. If the The technique is also operator dependent and adequate “acoustic win-
aneurysm is successfully treated, many practitioners will accept higher dows” are required. Therefore, transcranial Doppler velocities should
blood pressures in the postoperative period in anticipation of vasospasm not be used in isolation as an indication for the initiation of aggressive
(see below). treatments—the clinical course must be considered as well. Given the
limitations of transcranial Doppler, other imaging modalities have been
Hyponatremia and Intravascular Volume Contraction: A total of 30% to explored and further developed. These include CT angiography and CT
50% of SAH patients develop intravascular volume contraction and a perfusion as a recent meta-analysis suggests that these techniques offer
negative sodium balance (referred to as cerebral salt wasting) when given a high diagnostic accuracy. The major limitation though is the inability
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volumes of fluids intended to meet maintenance needs. Low intravascular to intervene which conventional angiography may provide (see below).
volume is associated with symptomatic vasospasm and must be avoided.
Hyponatremia develops in 10% to 34% of patients following SAH. Treatment of Vasospasm
Administration of large volumes (5-8 L/d) of isotonic saline prevents Hemodynamic Augmentation Hemodynamic augmentation for the treatment
hypovolemia, but patients may still develop hyponatremia. The degree of of vasospasm has been referred to as hemodilution hypervolemic hyper-
hyponatremia appears to be related to the tonicity rather than the volume tensive therapy (“triple H therapy”) or as hypervolemic hypertensive
of fluids administered. Thus, administration of large volumes of isotonic therapy (HHT). The pathophysiologic rationale is based on the high
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saline and restriction of free water are usually effective at limiting hypona- rate of spontaneous hypovolemia, the association of hypovolemia with
tremia and preventing hypovolemia. In SAH patients with hyponatremia, delayed ischemic deficits, and the loss of autoregulation of cerebral blood
the volume of fluids should never be restricted; instead only free water flow in this population.
intake should be limited. Hypertonic saline solutions and fludrocortisone Most centers continue aggressive hydration during the period of
may be required in severe or refractory cases. vasospasm risk. Some will increase the rate of fluid administration if
transcranial Doppler velocities are rising. The indication for starting
Vasospasm: The term vasospasm was originally used to refer to segmen- aggressive hemodynamic augmentation is usually the onset of clinical
tal or diffuse narrowing of large conducting cerebral vessels. Recently, symptoms of delayed ischemic deficit. Early descriptions of this therapy
this term has taken on multiple meanings. It may refer to angiographic emphasized the role of volume expansion, as many of these patients had
findings, to increased transcranial Doppler velocities, or to delayed not been aggressively hydrated before the onset of symptoms. However, if
ischemic deficits. Angiographic and transcranial Doppler vasospasm intravascular volume has been maintained before the onset of symptoms,
occurs in 60% to 80% of patients, whereas clinical vasospasm (or delayed further volume expansion may not be helpful. The optimal intravascular
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ischemic deficit) occurs in 20% to 40% of patients. volume is unknown, and achieving cardiac filling pressures that optimize
The pathogenesis of vasospasm is complex. Several molecular cardiac output has been advocated.
mechanisms that are involved in the development of vasospasm have When symptoms persist despite optimal intravascular volume,
been described in animal models and confirmed in human samples vasoactive drugs are administered, with a goal of either raising mean
including inflammation, the presence of degradation blood products, arterial pressure (MAP) or augmenting cardiac output in order to
nitric oxide signaling, and calcium signaling. All of these mechanisms improve cerebral perfusion. In most cases, patients will require moni-
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appear to be time-dependent as these pathological changes develop in toring via an arterial line and with either pulmonary artery catheter or
a delayed fashion after exposure to subarachnoid blood and are self- transpulmonary thermodilution hemodynamic monitoring. The most
limited. In addition to changes in the large conducting cerebral vessels commonly used agents to increase blood pressure are norepinephrine,
that traverse the subarachnoid space, small-vessel reactivity may be dopamine, and phenylephrine. Caution must be employed when using
impaired as well. dopamine alone, because of a high incidence of tachyarrhythmias.
Monitoring for Vasospasm Serial neurologic assessments are essential in moni- When using phenylephrine one must be aware that it tends to decrease
toring for vasospasm. These must be performed frequently by physicians cardiac output, especially in those patients with impaired cardiac

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