Elevated ICP and HTN Emergencies

THE CLINICAL CHALLENGE

Elevated intracranial pressure (ICP) poses a direct threat to the viability and function of the brain by limiting blood flow and oxygen delivery. In head trauma, elevated ICP has been clearly associated with worse outcomes. The problems associated with elevated ICP may be compounded by many of the techniques and drugs used in airway management, because they may cause further elevations of ICP. In addition, victims of multiple traumas may present with hypotension, thus limiting the choice of agents and techniques available. This chapter provides the basis for an understanding of the problems of increased ICP and the optimal methods of airway management in this patient group.

When increased ICP occurs as a result of an injury or medical catastrophe, the brain’s ability to regulate blood flow (autoregulation) over a range of blood pressures is often lost. In general, ICP is maintained through a mean arterial pressure (MAP) range of 80 to 180 mm Hg. Elevation in ICP often is a sign that autoregulation has been lost. In this setting, excessively high or excessively low blood pressure could aggravate brain injury by promoting cerebral edema or ischemia. Hypotension, even for a very brief period, is especially harmful. Hypotension and hypoxia have been shown to be independent predictors of mortality and morbidity in patients with traumatic brain injury (TBI).

Cerebral perfusion pressure (CPP) is the driving force for blood flow to the brain. It is measured by the difference between MAP and ICP, expressed as the formula:

CPP = MAP − ICP

It is clear from this formula that excessive decreases in MAP, as might occur during rapid sequence intubation (RSI), would decrease CPP and contribute to cerebral ischemia. Conversely, increases in MAP, if not accompanied by equivalent increases in ICP, may be beneficial because of the increase in the driving pressure for oxygenation of brain tissue. It is generally recommended that the ICP be maintained <20 mm Hg, the MAP between 100 and 110 mm Hg, and the CPP near 70 mm Hg. There are a number of confounding elements that may increase ICP during airway management.

Reflex Sympathetic Response to Laryngoscopy

The reflex sympathetic response to laryngoscopy (RSRL) is stimulated by the rich sensory innervation of the supraglottic larynx. Use of the laryngoscope, and particularly the attempted placement of an endotracheal tube, results in a significant afferent discharge that increases sympathetic activity to the cardiovascular system mediated through direct neuronal activity and release of catecholamines. More prolonged or aggressive attempts at laryngoscopy and intubation result in greater sympathetic nervous system stimulation. This catecholamine surge leads to increased heart rate and blood pressure, which significantly enhances cerebral blood flow (CBF) at the apparent expense of the systemic circulation. These hemodynamic changes may contribute to increased ICP, particularly if autoregulation is impaired; therefore, it is desirable to mitigate this RSRL. Gentle intubation techniques (including the use of experienced operators and video laryngoscopy devices) that minimize airway stimulation and pharmacologic adjuncts (e.g., β-blockade and synthetic opioids) have been studied to accomplish this mitigation.

Evidence is mixed regarding the use of lidocaine to blunt the hemodynamic response to laryngoscopy. Studies in patients without cardiovascular disease have failed to show effect. Other studies have shown variable results with respect to hemodynamic protection, with some appearing to demonstrate benefit and others showing none. As a result, lidocaine is not recommended, currently, for the mitigation of the RSRL associated with emergency intubation.

The short-acting β-blocker esmolol, in contrast, has consistently demonstrated the ability to control both heart rate and blood pressure responses to intubation. A dose of 2 mg per kg given 3 minutes before intubation has been shown to be effective. Unfortunately, administration of β-blocking agents in emergency situations may be problematic for several reasons. Even a short-acting agent, such as esmolol, may exacerbate hypotension in a trauma patient, or confound interpretation of a decrease in the blood pressure immediately following intubation. For these reasons, although esmolol is consistent and reliable for mitigation of RSRL in elective anesthesia, it is generally not used for this purpose for emergency intubation.

Fentanyl at doses of 3 to 5 µg per kg has also been shown to attenuate the RSRL associated with intubation. Although a full sympathetic blocking dose of fentanyl is 9 to 13 µg per kg, the recommended dose of fentanyl for physiologic optimization during emergency RSI is 3 µg per kg and should be administered as a single dose over 60 seconds. This technique permits effective mitigation of the RSRL, with greatly reduced chances of apnea or hypoventilation before sedation and paralysis (see Chapter 20).

Several studies have investigated the potential advantages of flexible endoscopic intubation over direct laryngoscopy, working on the premise that these techniques minimize tracheal stimulation and thus the RSRL. Results of these studies are mixed and do not permit any conclusions recommending one technique over the other. In a controlled operating room setting, the insertion of the endotracheal tube into the trachea is more stimulating than a routine laryngoscopy.

At present, based on the best available evidence, it seems advisable to administer 3 µg per kg of fentanyl intravenously (IV) 3 minutes before administration of the induction and neuromuscular blocking agents (NMBAs) to mitigate the RSRL for patients who may be intolerant to spikes in heart rate, vascular sheer forces, or ICP. Fentanyl should not be administered to patients with incipient or actual hypotension or to those who are dependent on sympathetic drive to maintain an adequate blood pressure for cerebral perfusion. In such cases, the ensuing hypotension may cause further central nervous system injury. In addition to pharmacologic maneuvers to reduce RSRL, intubation should be performed in the gentlest manner possible, limiting both the time and intensity of laryngoscopy.

Reflex ICP Response to Laryngoscopy

Laryngoscopy may also increase the ICP by a direct reflex mechanism not mediated by sympathetic stimulation of the blood pressure or heart rate. The details of this reflex are poorly understood. Insertion of the laryngoscope or endotracheal tube may, therefore, further elevate ICP, even if the RSRL is blunted. Although it would be desirable to blunt this ICP response to laryngoscopy in patients at risk for having elevated ICP, literature related to the use of lidocaine for this purpose is mixed, at best. Given how specific the timing and dosage of lidocaine needed to be even in studies where an effect was shown, and how cognitive and staff resources could be used maximizing patients’ safety in other ways prior to intubation (such as optimizing hemodynamics, improving preoxygenation, etc.), we no longer recommend lidocaine as a pretreatment medication in an attempt to blunt this response or for any other purpose during emergency airway management.

ICP Response to Neuromuscular Blockade

Succinylcholine (SCh) itself may be capable of causing a mild and transient increase in ICP. Studies have shown that this increase is temporally related to the presence of fasciculations in the patient but is not the result of synchronized muscular activity leading to increased venous pressure. Rather, there appears to be a complex reflex mechanism originating in the muscle spindle and ultimately resulting in an elevation of ICP. One recent study challenged the claim that SCh causes an elevation of ICP, and SCh remains a commonly used NMBA for management of patients with elevated ICP because of its rapid onset and short duration. Although we recommended in earlier editions of this manual the routine use of a defasciculating agent when SCh is administered to a patient with elevated ICP, we no longer advocate this practice. There is insufficient evidence to support the use of a defasciculating agent, and it adds unnecessary complexity.

Neuromuscular blockade with nondepolarizing agents such as rocuronium is becoming more common, and recent registry data suggests nearly half of all emergency RSIs are now performed with rocuronium. At doses of 1.0 to 1.2 mg per kg, ideal intubating conditions at 60 seconds are similar to SCh. Because rocuronium does not carry a risk of elevating ICP and is not associated with hyperkalemia, it is a viable option for neuromuscular blockade in brain injury. One important note is that the duration of paralysis with rocuronium is much longer than that with SCh (about 1 hour at 1 mg per kg) and is dose-dependent. If a shorter duration of paralysis is desirable, SCh should be considered.

Choice of Induction Agent

When managing the patient with potential brain injury, it is important to choose an induction agent that will not adversely affect CPP. Ideally, one would like to choose an induction agent that is capable of improving or maintaining CPP and providing some cerebral protective effect by decreasing the basal metabolic rate of oxygen utilization of the brain (CMRO₂). This effect can be likened to decreasing myocardial oxygen demand in the ischemic heart. Etomidate is a short-acting imidazole derivative that exhibits this beneficial cerebroprotective profile with the added benefit of hemodynamic stability. In fact, etomidate is the most hemodynamically stable of all commonly used induction agents except ketamine (see Chapter 21). Its ability to decrease CMRO₂ and ICP and its remarkable hemodynamic stability make it the drug of choice for patients with elevated ICP.

In the past, ketamine has been avoided in patients with known elevations in ICP because of the belief that it may elevate the ICP further. Several case series in spontaneously breathing patients with known cerebral spinal fluid (CSF) outflow obstructions, which contained no control groups, formed the basis for this concern. The evidence regarding this phenomenon is mixed, however, and more recent data suggests that ketamine is safe for use in head injury (discussed in Chapter 21). Ketamine may in fact increase cerebral perfusion. In patients with elevated ICP and hypotension, ketamine’s superior hemodynamic stability, on balance, argue for its use. In the hypertensive patient, etomidate is preferred owing to the possibility that ketamine can increase MAP.

APPROACH TO THE AIRWAY

RSI is the preferred method for patients with suspected elevated ICP because it provides protection against the reflex responses to laryngoscopy and rises in ICP. The presence of coma should not be interpreted as an indication to proceed without pharmacologic agents or to administer only a NMBA without a sedative induction drug. Although the patient may seem unresponsive, laryngoscopy and intubation will provoke the reflexes described previously if appropriate sympatholytic and induction agents are not used. Following appropriate assessment and preparation, as described in Chapters 2 and 20, the sequence in Box 34-1 is recommended for patients with elevated ICP.