Understanding intracranial hypertension

Evaluation of ICP in the operating room

Treatment of intracranial hypertension

Management of Cerebral Aneurysm Rupture

Pre-exposure rupture

Neurophysiologic monitoring

Intraoperative rupture (IOR)

Temporary clips and cerebral protection

Bleeding During Excision of Spinal Cord Tumor

Preoperative evaluation

Intraoperative management

INTRODUCTION

As technology in both anesthesia and neurosurgery advances, the need for a systems-based approach to operative procedures has become critical to the success of each operation. Strategies to improve safety and outcome in the OR environment must include effective and efficient communication among all physicians and personnel. Impediments to this level of communication in the OR include stress, differing knowledge base, and a steep hierarchy, among others. The aviation industry has successfully addressed deficits in information exchange, prompting the healthcare industry to adopt similar best practices. One of the more effective communication methodologies responsible for reducing error in the cockpit is the checklist.

In this chapter, we have introduced and discussed several critical intraoperative scenarios that demand coordinated responses from the neurosurgical and anesthetic teams. The physiologic rationale for appropriate action is presented in the context of efficient communication. We conclude each scenario with a simple checklist that can serve as a prompt to ensure human error remains at a minimum and to empower all members of the team to take ownership of their roles within this hierarchical structure.

I. INTRACRANIAL AND BLOOD PRESSURE MANAGEMENT DURING INTRACRANIAL HEMATOMA EVACUATION

The intraoperative interaction between the neurosurgeon and the anesthesiologist requires communication that is at once clear, engaging, and open. During operative neurosurgical procedures, special attention to multiple factors on the part of the anesthesiologist is necessary to ensure that the patient does well from a neurologic standpoint. The anesthesiologist’s management of both ICP and blood pressure (BP) in these cases goes beyond the general anesthesia protocol for general surgery procedures. Specifically, the control of increases in ICP and BP during the evacuation of an intracranial hematoma is a very important illustration of the necessity for close collaboration between the neurosurgeon and the anesthesiologist. To accomplish this, the anesthesiologist should focus on the following:

Understanding of ICP dynamics

Evaluation of ICP in the OR

Treatment of intracranial hypertension
 

A. Intracranial hypertension

1. The Monro–Kellie hypothesis states that the sum of the intracranial volumes of blood, brain, cerebrospinal fluid (CSF), and other components (such as tumor, hematoma, and abscess) is stable. An increase in one of these components results in an equal decrease in another component or the pressure inside the intracranial compartment will begin to rise. The normal ICP in adults is < 10 to 15 mm Hg. Intracranial hypertension produces pressure gradients that, if not treated emergently, result in herniation of brain tissue. Often, Cushing’s Triad can be used as an indicator of elevated ICP before the actual measurement of ICP. The hallmarks of Cushing’s Triad are hypertension, bradycardia, and respiratory irregularities. Intracranial hypertension can be caused by traumatic brain injury (TBI) with resultant cerebral edema, hyperemia, mass lesions (such as epidural and subdural hematoma), intraparenchymal hemorrhage, hemorrhagic contusion, foreign body, and depressed skull fracture. Other etiologies include hydrocephalus, hypoventilation, systemic hypertension, and venous sinus thrombosis. Specifically, when intracranial hematoma is the cause of the elevation in ICP, the goal is to ensure that tight control of ICP and BP is coupled with urgent removal of the mass lesion.

2. It is also important to ensure that cerebral blood flow (CBF) is not compromised to the point of neuronal loss, infarction, or even brain death. However, CBF is difficult to quantify as it requires specialized equipment for careful measurement at the bedside. In addition, assessment of intracranial dynamics by means of CBF is a relatively complex undertaking. While increasing ICP may be associated with decreases in CBF, other physiologic changes occur as well. Mean arterial pressure (MAP) may increase as the ICP increases. The cerebral vascular resistance (CVR) adjusts to the increase in MAP with a decrease in cerebral perfusion pressure (CPP), the difference between the MAP and the ICP, until vasodilatation reaches its peak, which usually occurs when CPP ≤ 50 mm Hg. An appropriate expedient is to view CPP as a predictor of CBF. Because of cerebral autoregulation, the mechanism whereby large changes in systemic BP produce only small changes in CBF, CPP would have to drop to below 40 mm Hg in the normal brain before CBF is impaired. This is the lower limit of autoregulation. In TBI, ICP ≥ 20 mm Hg may be more harmful than changes in CPP as long as CPP > 60 mm Hg.

B. Measurement of ICP

1. While various methodologies for measuring ICP are available, the gold standard is the external ventricular drain (EVD) or ventriculostomy. Depending on the rapidity of evacuation from the field to the hospital, EVDs are indicated for management of severe TBI when the Glasgow Coma Scale (GCS) score ≤ 8 after cardiopulmonary resuscitation and there is either an abnormal computed tomographic (CT) scan of the brain or a normal CT scan with ≥ 2 risk factors including age > 40 years, systolic BP < 90 mm Hg, and decerebrate or decorticate posturing on motor exam.

2. ICP waveforms

a. The ICP waveform is affected by BP and respiratory patterns. Specifically, alterations in the normal ICP tracing are derived from small pulsations transmitted from the systemic BP to the intracranial cavity. These BP pulsations are superimposed on slower oscillations caused by the respiratory cycle. In mechanically ventilated patients, the superior vena cava pressure increases during inspiration, which reduces venous outflow from the cranium, causing an elevation in ICP.

b. Pathologic waveforms appear as the ICP increases, cerebral compliance decreases, arterial pulses become more pronounced, and venous components disappear. Pathologic waveforms include Lundberg A, B, and C types. Lundberg A waves or plateau waves are ICP elevations to > 50 mm Hg lasting 5 to 20 minutes. These waves are accompanied by a simultaneous increase in MAP, but it is not clearly understood if the change in MAP is the cause or effect. Lundberg B waves or pressure pulses have an amplitude of 50 mm Hg and occur every 30 seconds to 2 minutes. Lundberg C waves have an amplitude of 20 mm Hg and a frequency of four to eight per minute; they are seen in the normal ICP waveform, but high-amplitude C waves may be superimposed on plateau waves. Regardless of the waveform, if the ICP > 20 mm Hg, the anesthesiologist should alert the neurosurgeon of the elevation to determine how and when to proceed.

C. Treatment of intracranial hypertension

The current practice for managing intracranial hypertension is to use an ICP of 20 to 25 mm Hg as the upper limit of normal. If the patient has an EVD, it is important to zero the transducer at the level of the external auditory canal as this approximates the level of the foramen of Monroe. The following ways to control ICP should be initiated by the anesthesiologist:

1. Elevate the head to approximately 30 degrees.

2. Ventilate to normocarbia: arterial carbon dioxide tension (PaCO₂) of 35 to 40 mm Hg.

3. Hyperventilate to PaCO₂ of 30 to 35 mm Hg if ICP > 20 to 25 mm Hg.

4. Use sedation and pharmacologic paralysis with thiopental, propofol, or fentanyl and a non-depolarizing muscle relaxant.

5. Drain 3 to 5 mL CSF if a ventriculostomy is present.

6. Give mannitol, 0.25 to 1 g/kg; then 0.25 g/kg every 6 hours; increase dose if needed and serum osmolality < 320 mOsm/L

a. Mannitol increases the osmolality of the blood relative to the brain, which in turn pulls water from the brain to the intravascular compartment to restore osmolar balance.

b. Furosemide is often given concomitantly as it induces systemic diuresis, decreases CSF production, and reduces cerebral edema by enhancing water transport. In other words, furosemide reduces ICP without increasing cerebral blood volume (CBV) or blood osmolality.

7. Control fever, which can cause brain swelling; maintaining normothermia decreases the cerebral metabolic rate for oxygen consumption (CMRO₂)

8. Increase MAP.

9. Infuse 3% hypertonic saline (HS) in boluses of 250 mL.

II. MANAGEMENT OF CEREBRAL ANEURYSMAL RUPTURE

The preoperative or IOR of a cerebral aneurysm is one of the most catastrophic events that can occur in the OR environment. The incidence of IOR has been documented to range between 11% and 19% with the majority of ruptures occurring during either dissection or clipping of the aneurysm. The clinical outcome after rupture during the predissection interval is poor in that only one of four patients survives. Thus, the lines of communication between the surgical team and the anesthesia team need to be open and reciprocal even before the patient enters the OR. Factors that predispose to premature rupture and appropriate preventive/management techniques can be organized into a checklist to facilitate communication and strategic planning.

A. Pre-exposure rupture is associated with a high morbidity and mortality. Thus, continual communication between the anesthesiologist and the neurosurgeon is essential. For example, destabilization of the BP before the surgical incision can be the cause of premature rupture. Painful procedures may trigger swings in systolic pressure. Abrupt changes in intracranial dynamics, especially when associated with placement of a lumbar subarachnoid drain or a ventriculostomy, may also lead to premature rupture of the aneurysm.

1. The goal of anesthetic and surgical management

Related posts:

Anesthetic Management of Head Trauma Anesthetic Management of Diagnostic Neuroradiology Ischemic Cerebrovascular Disease Improving Neurologic Recovery from Cerebral Ischemia Traumatic Brain Injury, Stroke, and Brain Death Pediatric Neuroanesthesia

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