To prevent movement and to facilitate the surgical exposure, neuromuscular blocking agents are generally used. These drugs are competitive or noncompetitive inhibitors of the neurotransmitter acetylcholine at the neuromuscular junction. The only noncompetitive inhibitor used clinically is succinylcholine. This drug rapidly binds to the nicotinic receptors and produces depolarization at the neuromuscular junction, clinically manifesting as fine-muscle fasciculations occurring about 30 to 60 seconds after injection. Succinylcholine cannot be reversed, but has a short duration of action (<10 minutes) because it is quickly hydrolyzed in the plasma by cholinesterase. Because of rapid onset and short duration of action, succinylcholine is frequently used to facilitate endotracheal intubation when it must be accomplished quickly, or when quickly regaining neuromuscular function is beneficial.
All other clinically useful muscle relaxants are termed competitive inhibitors and do not cause depolarization when they attach at the neuromuscular junction (nondepolarizing). Because these agents compete with endogenous acetylcholine, the block produced is in direct proportion to the concentration of the agent relative to the concentration of acetylcholine. If the concentration ratio is low enough, competitive relaxants can be reversed if the concentration of acetylcholine is artificially elevated. Acetylcholine concentration can be increased by giving a drug that blocks its metabolism, an anticholinesterase (e.g., neostigmine). The neuromuscular blocking agent is still present, but motor function returns if the acetylcholine concentration is high enough to overwhelm the blocking agent. There is a ceiling to which anticholinesterase drugs can safely elevate circulating acetylcholine; above this threshold, a novel selective relaxant binding agent, suggamadex, may be used to reverse the effects of specific nondepolarizing neuromuscular blocking drugs (rocuronium and vecuronium). Using anticholinesterases to reverse neuromuscular relaxants is not analogous to using naloxone to reverse the effects of opioids. The reversal agent neostigmine does not compete or combine with the relaxant.
Unfortunately, there are systemic consequences to increasing the plasma concentration of acetylcholine. Acetylcholine is the predominant neurotransmitter in the preganglionic sympathetic and parasympathetic nervous systems and in the postganglionic parasympathetic nervous system. For this reason, an anticholinergic drug (atropine or glycopyrrolate) must be given with the anticholinesterase to prevent the undesirable effects of a generalized acetylcholine overdose. Given these side effect profiles of anticholinesterase drugs, the selective relaxant binding agent suggamadex – recently approved for use in the US – offers new promise for reversing high levels neuromuscular blockade. The common neuromuscular blocking drugs and their doses, durations, and side effects are listed in Table 13-2; common regimens of reversal agents are shown in Table 13-3.
Postoperative residual neuromuscular blockade is now recognized as a common problem after routine administration of nondepolarizing muscle relaxants. The evaluation of depth of muscle relaxation is a subjective process based upon empirical pharmacokinetics or visual inspection of a patient’s peripheral nerve response to an artificial electrical stimulation. During peripheral nerve stimulator monitoring, two electrode patches are placed on the patient’s skin along the course of a peripheral nerve which innervates a distinct and observable muscle group. Commonly used monitoring locations include the ulnar nerve, ophthalmic branch of the facial nerve, or the posterior tibial nerve. Next, the electrodes are connected to a hand-held device which delivers four short transcutaneous bursts of electricity, ranging from 10 to 100 mA every 0.5 seconds, hence the term “train-of-four monitoring.” A clinician visually inspects the response to each electrical stimulation. In a patient without any pharmacologic neuromuscular blockade, the strength of the fourth muscle response (or “twitch”) matches that of the first. In the face of complete pharmacologic competitive inhibition of neuromuscular transmission, no muscular twitches are observed at all. At varying levels of neuromuscular blockade in between, the fourth, third, or second twitch may be absent. Due to competitive blocking of the neuromuscular junction nicotinic receptor, each incremental stimulation results in a weaker response because of increasingly limited receptors available for stimulation. The ratio between the strength of the fourth twitch and the first twitch is known as the train-of-four ratio. During normal neuromuscular transmission, the ratio is 1. Historically, a ratio of 0.7 was considered adequate muscular strength for extubation. However, more recent literature suggests that a ratio between 0.7 and 0.9 still exposes the patient to significant risks of atelectasis, hypoxemia, aspiration, pneumonia, and possibly reintubation. In routine practice, a clinician is incapable of assessing a concept as precise or nuanced as train-of-four ratio. As a result, the number of twitches observed is typically reported, that is, 0/4, 1/4, 2/4, 3/4, 4/4. A patient with 3/4 or 4/4 twitches is capable of responding to cholinesterase inhibitors and return to normal function. A patient with 0/4, 1/4, or 2/4 is unlikely to respond to cholinesterase inhibitors with full return of muscular strength. Data from multiple centers have demonstrated that a significant proportion of patients demonstrated residual neuromuscular blockade of <0.9 in the recovery room despite reversal.
Table 13-2 Common Neuromuscular Blocking Drugs and Reversal Agents
Table 13-3 Drugs for Antagonizing Nondepolarizing Neuromuscular Blockadea
The use of subjective train-of-four monitor is inferior to objective acceleromyography, a calibrated device used to accurately establish the train-of-four ratio. It requires careful calibration and setup, and access to the patient’s arm and hand. Although clinically effective at eliminating the limitations of subjective train-of-four monitoring, its use remains limited because of the time spent in set up, and an underappreciation of the frequency of residual neuromuscular blockade. It has been promoted by patient safety experts, and is beginning to demonstrate increased penetration in Europe.
In addition to the limitations intrinsic to nerve monitoring devices themselves, nerve monitoring must be performed with caution, as muscles in the body are not equally sensitive to muscle relaxants. The diaphragm is most resistant to neuromuscular blockade, whereas the neck and pharyngeal muscles that support the airway are most sensitive. It is possible for an intubated patient to spontaneously ventilate and even to produce a large negative inspiratory effort and yet develop complete airway obstruction when extubated because of the effects of residual muscle relaxant on the upper airway muscles.
As described earlier, a novel class of compounds known as selective relaxant binding agents, – currently comprised of only one FDA-approved drug, suggamadex – may serve to revolutionize the practice of neuromuscular blockade and its reversal. Such compounds are able to rapidly reverse the effects of profound levels of muscle relaxation (0/4 twitches) created by steroidal nondepolarizing muscle relaxant agents such as rocuronium, vecuronium, or pancuronium. Rather than attempting to increase the concentration of acetylcholine, these agents physically bind free muscle relaxant molecules within a cyclodextrin ring structure. This decreases the concentration of free muscle relaxant and allows acetylcholine to function normally at the neuromuscular junction. The cyclodextrin–muscle relaxant combination is then eliminated via the kidney. This offers the ability to rapidly (<3 minutes) reverse profound muscle relaxation as surgical conditions warrant.2 This will enable profound relaxation during wound closure, and then immediate reversal of blockade just prior to extubation. Its significant expense, approximately $US 200 for a single dose of reversal of deep blockade, has limited its use.
Opioids (Narcotics) and Other Intravenous Analgesics
Table 13-4). Opioids produce profound analgesia and respiratory depression. They have no amnesic properties, minimal direct myocardial depressive effects, and no muscle-relaxant properties. Opioids can produce significant hemodynamic effects indirectly by releasing histamine or blunting the patient’s sympathetic vascular tone because of analgesic properties. The latter effect depends on the degree of sympathetic tone that is present at baseline. Acutely injured patients may be hypovolemic and in pain, with high sympathetic tone and peripheral vascular resistance. Patients in this condition can experience dramatic drops in systemic blood pressure with minimal doses of opioids. For this reason, it is important to titrate narcotics in small incremental doses. Because of the lack of direct myocardial depression and the absence of histamine release with the synthetic opioids, they are frequently used as the primary anesthetic in combination with an amnesic agent and a muscle relaxant in patients with significant myocardial dysfunction.Narcotics and synthetic analogues belong to the class of drugs called opioids. The most commonly used drugs in this family are morphine, fentanyl, and hydromorphone. Since the mid-1980s, a series of synthetic opioids have been developed with fentanyl as the prototype. More recently developed synthetics (sufentanil, alfentanil, and remifentanil) are more potent and of varying duration (
When opioids are titrated intravenously, patients first become apneic because of the respiratory depressive effect (shifting the CO2 response curve), but they still breathe on command. As the dose increases, patients become apneic and unresponsive.
Opioids are primarily analgesic and not amnesic. Patients can be totally aware and have substantial recall of conversations despite appearing completely anesthetized. All opioids can be reversed with naloxone. The duration of action of naloxone can be shorter than that of the opioid, and patients must be observed carefully for renarcotization after they have been treated with naloxone. Naloxone reversal of opioids can be dangerous because the agent acutely reverses not only the analgesic effects of the opioid but also the analgesic effects of native endorphins. Naloxone treatment has been associated with acute pulmonary edema and myocardial ischemia and should not be used electively to reverse the effects of a narcotic. It is appropriately used in an emergency situation when the airway is poorly controlled and the patient is not ventilating because of an opioid overdose.
Table 13-4 Analgesics
3 Due to dose-dependent direct myocardial depression and peripheral vasodilation, propofol can produce significant hypotension when IV induction doses are administered. It also produces significant pain on injection in peripheral veins. Pain can be diminished or eliminated by pretreatment with IV lidocaine via the vein to be used for propofol administration. Propofol is insoluble in aqueous solution and therefore comes dissolved in a lipid emulsion that has the associated risk of bacterial contamination. Once a vial of propofol is opened, it is not recommended that it be used after 12 hours.Propofol is a lipid-soluble substituted isopropyl phenol that produces a rapid induction of anesthesia in 30 seconds followed by awakening in 4 to 8 minutes after a single bolus. Intravenous propofol can effectively produce total anesthesia (for less stimulating procedures), including amnesia, some analgesia, and some degree of muscle relaxation. Propofol is unique because it is rapidly cleared through hepatic metabolism to inactive metabolites in a way that the patient becomes alert soon after cessation of the infusion. However, as the duration and dose of the maintenance infusion is increased, the time to return to consciousness is also significantly increased. This context-sensitive half-life of propofol must be incorporated into expectations of a “quick wake-up.” Propofol has direct antiemetic properties and is a valid alternative to inhalational anesthetics in patients who have demonstrated a history of prolonged, refractory postoperative nausea and vomiting. It has an important role in intensive care units when used as a continuous infusion sedative at dosages of 25 to 50 μg/kg/min. However, prolonged infusions have been associated with a lethal metabolic derangement known as propofol infusion syndrome, characterized by a profound metabolic acidosis and cardiovascular compromise.
Ketamine is a phencyclidine derivative that produces anesthesia characterized by dissociation between the thalamus and limbic systems. Induction of anesthesia is achieved within 60 seconds after IV injection of 1 to 2 mg/kg or within 2 to 4 minutes of intramuscular (IM) injection of 5 to 10 mg/kg. Patients appear to be in a cataleptic state in which their eyes remain open with a slow nystagmic gaze. The drug produces intense amnesia and analgesia but has been associated with unpleasant visual and auditory hallucinations that can progress to delirium. The incidence of these problems can be significantly reduced if benzodiazepines are also administered with the drug. At low doses (0.1 to 0.2 mg/kg IV or 2 mg/kg IM), patients continue to spontaneously ventilate, but cannot be expected to protect the airway should vomiting occur. At higher doses, ketamine acts as a respiratory depressant and produces complete apnea. Ketamine also has direct and indirect sympathetic nervous system stimulatory effects, which can be useful in hypovolemic patients. These effects are diminished or absent in patients who are catecholamine depleted. The sympathetic stimulatory effect increases myocardial oxygen consumption and intracranial pressure, and ketamine is relatively contraindicated in patients with ischemic heart disease or space-occupying intracerebral lesions. Owing to its analgesic properties and relatively preserved respiration, ketamine is frequently used as an IV analgesic during debridement procedures, at doses listed in Table 13-4. IM ketamine (1 to 2 mg/kg) is also very useful for sedating patients who are difficult to manage (e.g., combative or cognitively disabled patient), so IV access can be obtained. Ketamine’s most frequent use is in subanesthetic doses as part of multimodal analgesic regimens hoping to minimize the use of opioids. For procedures requiring general anesthesia that may have significant postoperative opioid requirements, a preincision ketamine bolus dose with a low-dose intraoperative infusion may be associated with improved acute and chronic pain outcomes.4
Amnesics and Anxiolytics
Benzodiazepines are the primary class of agents used as amnesics and anxiolytics. The prototype drug, diazepam, has been more recently replaced by its water-soluble analog of shorter duration, midazolam. Lorazepam also belongs in this family of agents, but because it has a very long duration of action, it is not routinely used intraoperatively. Lorazepam has intensive care unit applications (Table 13-5). Benzodiazepines produce anxiolysis and some degree of amnesia, but have no analgesic properties. Intraoperatively, midazolam is always used in conjunction with an opioid or inhalation agent. Midazolam can be used in combination with the short-acting opioid fentanyl to produce conscious sedation for minor procedures. Benzodiazepines can produce apnea and have synergistic adverse effects with narcotics. Very small doses of midazolam and fentanyl can quickly produce an unconscious apneic patient. As with all anesthetics, benzodiazepines used as IV agents for sedation should be given in small incremental doses to achieve the desired effect. A reversal agent is also available for benzodiazepines (flumazenil). The recommended dosages of these drugs and the reversal agents appear in Table 13-5.
Table 13-5 Anxiolytics and Amnesics (Benzodiazepines)
Local anesthetics constitute a class of drugs that temporarily block nerve conduction by binding to neuronal sodium channels. As the concentration of the local anesthetic increases around the nerve, autonomic transmission will be blocked first, followed by sensory transmission, and then motor nerve transmission. These drugs can be injected locally into tissue to produce a field block, around peripheral nerves to produce a specific dermatomal block, around nerve plexuses to produce a major conductive block, or into the subarachnoid or epidural space to produce extensive neuraxial blockade. All the methods have been used to assist in the provision of an alternative form of balanced anesthesia by supplementing analgesia and muscle relaxation.
Adverse consequences associated with the use of local anesthetics fall into three categories: acute central nervous system toxicity due to excessive plasma concentration, hemodynamic and respiratory consequences due to excessive conduction block of the sympathetic or motor nerves, and allergic reactions. Whenever a local anesthetic is injected, there can be inadvertent intravascular injection or an overdose of the drug because of rapid uptake from the tissues. Overdose can produce seizures, as well as cardiovascular collapse from ensuing arrhythmias. Complications can be minimized by withdrawing before injection to avoid an intravascular injection and limiting dosages to the safe range (Table 13-6).
Table 13-6 Local Anesthetics
5 Because the level of sympathetic block is two to six dermatomal levels higher than the sensory block, it is often difficult to obtain a high spinal sensory level without approaching a total sympathectomy. For this reason, spinal or epidural techniques can present a prohibitively high risk in patients with severe flow-dependent cardiovascular disease.When local anesthetics are administered for a spinal or epidural block, they produce a progressive blockade of the sympathetic nervous system, which produces systemic vasodilation. Sympathetic nerves travel along the thoracolumbar region with the first four thoracic branches, including the cardiac sympathetic accelerators. A sympathetic blockade of this entire region produces a characteristic profound systemic vasodilatation and bradycardia. This condition is referred to as total sympathectomy, and the hypotension that ensues is usually below the minimal cerebral perfusion pressure required to maintain consciousness. Affected patients are bradycardic, hypotensive, unconscious, and usually apneic. This disastrous situation is easily remedied if treated quickly with a vasopressor (phenylephrine or ephedrine) and atropine or small doses of epinephrine (increments of 10 μg for an adult). If not treated promptly, the situation proceeds to cardiac arrest. In this emergency situation, the treatment of high doses of epinephrine is 10 to 40 μg/kg, or 1 to 4 mg for an adult. The doses of epinephrine are higher than in a usual cardiac arrest because of the total sympathectomy.
Local anesthetics are chemically divided into two groups: esters and amides. The esters (2-chloroprocaine and tetracaine) produce metabolites that are related to p-aminobenzoic acid and have been associated with allergic reactions. Amides (lidocaine and bupivacaine) are rarely associated with allergic reactions. If an allergic reaction does occur, it is most likely due to the preservative (methylparaben) used in multidose vials of lidocaine.
Although general anesthesia is employed for millions of surgical procedures each year in the United States, many operations can be performed safely using neuraxial blockade. The two primary neuraxial techniques, a “single-shot” spinal and continuous epidural catheter, can be used for lower extremity and lower abdominal procedures. In both techniques, a small dose of local anesthetic is administered near spinal nerve roots in order to temporarily ablate sensory input from the peripheral somatic and visceral structures. In the case of a spinal anesthetic – also known as a subarachnoid block – the intrathecal sac surrounding the cauda equina at vertebral interspace L2-L3 or below is located using a sterile, small-caliber needle (25 gauge typically). Once cerebrospinal fluid is observed in the hub of a needle, 1 to 2 mL of preservative-free local anesthetic (typically bupivacaine or lidocaine) is injected into the intrathecal space. The needle is then completely withdrawn. This local anesthetic serves to directly inactivate efferent and afferent transmission at the nerve roots it comes in contact with. Because local anesthetics are not specific to specific nerve fiber types, blockade of sensory, motor, and sympathetic nerves occurs. The spread of local anesthetic within the subarachnoid space is primarily determined by three factors: (a) the vertebral interspace accessed, (b) the density of the local anesthetic in relation to the density of cerebrospinal fluid (a concept known as baricity), and (c) the position of the patient during injection and immediately thereafter. In order to eliminate the risk of needle puncture of the spinal cord, subarachnoid blocks are only performed below L2-L3 in adults and L3-L4 in children. The local anesthetic solution may be combined with vasoconstrictors such as epinephrine or opioids such as fentanyl or morphine in order to increase the density or duration of the sensory blockade. Surgical anesthesia ranging from 1 to 2 hours can be achieved using a subarachnoid block. Because of concerns regarding permanent nerve damage, intrathecal catheters are typically not used.6,7 As a result, most subarachnoid blocks are “single-shot” techniques that cannot be redosed.
In the case of epidural techniques, the nerve roots are blocked outside the thecal sac in potential space between the ligamentum flavum and dura mater. This space is accessed sterilely using a 19-gauge introducer needle and a loss of resistance technique. Once the space is identified, a 21-gauge catheter is inserted into the space via the introducer needle and the needle is removed. After testing to reduce the likelihood of inadvertent intravascular or intrathecal placement of the catheter, the epidural catheter can be taped in place. Because the epidural catheter can be left in place for several days, redosing is possible. Dilute local anesthetics combined with vasoconstrictors or opioids are the mainstay of epidural therapy. Epidural neuraxial techniques can be used for surgical anesthesia, as an adjunct to general anesthesia, or for postoperative pain relief. Epidural catheters can be placed in the thoracic or lumbar regions because the intrathecal sac is not being accessed; associated dermatomal spread and analgesia is observed. Epidural techniques often fail to result in a dense sacral nerve root blockade, so this may be a poor choice for surgical anesthesia at or below the knee.
PERIPHERAL NERVE BLOCKADE
Peripheral nerve blockade (PNB) has been used for surgical anesthesia of the extremities since the days of intravenous regional anesthesia described by Bier in 1908. PNB differs from neuraxial techniques in that it targets peripheral nerves after they have formed from the combinations of nerve roots. Upper extremity, lower extremity, and visceral peripheral nerves are targets of these peripheral nerve blocks. Much like neuraxial blockade, PNB can be used to achieve intraoperative surgical anesthesia, intraoperative analgesia as an adjunct to general anesthesia, or for postoperative analgesia. Use of long-acting local anesthetics or placement of an indwelling continuous catheter provides long-term (16 hours to several days) pain relief. The effective use of PNB requires excellent communication between the anesthesiologist and surgeon to ensure that the planned surgical procedure site(s) and any other sources of procedural stimulation (e.g., tourniquet) are adequately addressed by the block. A specific preoperative planning discussion to match the planned surgical procedure to a feasible dermatomal distribution of blockade is essential. Even when blockade of a dermatomal distribution specific to a surgical procedure is feasible, a PNB may be contraindicated if a neurologic examination performed at or near the surgical site in the early postoperative period is necessary.
Because of the limited distribution of sympathetic blockade, PNB has a much smaller hemodynamic effect than general or neuraxial anesthesia. In addition, if general or neuraxial anesthesia can be supplanted by a PNB, the residual unwanted side effects of these anesthetics can be avoided, resulting in improved patient satisfaction, improved quality and speed of recovery, and expedited hospital/procedural center discharge. However, PNB is not without side effects; the impact of phrenic nerve motor blockade associated with specific upper extremity blocks (common with interscalene and rare with supraclavicular) may have significant consequences for patients with underlying pulmonary disease.
Historically, anatomic landmark-based identification of peripheral nerves was complemented by use of electrical stimulator needles with the hope of eliciting specific motor responses confirming correct needle placement. The technical challenges of establishing precise anatomic location percutaneously by assessing patient symptoms in response to electric stimulation of specific muscle groups are significant. Concerns regarding possible intraneural injection or vascular injury persisted for many years. However, modern anesthesia techniques now employ real-time ultrasound guidance of a PNB needle under direct visualization. Vascular structures and nerves are visualized in relation to a PNB needle in order to decrease the likelihood of intravascular or intraneural injection, increase the likelihood of an efficacious block, and minimize the dose of local anesthetic required to achieve an efficacious block. Despite direct visualization using ultrasound, PNB in adults are typically performed in the awake state to minimize the risk of intraneural injection, which may be detected via patient complaint of significant pain upon injection. PNB can be extremely difficult or contraindicated in patients with challenging body habitus, local superficial infection at the site of needle entry, significant coagulopathy, or implants near the area to be visualized or injected.
While PNB targets named major peripheral nerves resulting in both motor and sensory blockade sufficient for surgical anesthesia, field blocks target small cutaneous sensory nerve fibers, used more commonly to achieve moderate sensory blockade for postoperative analgesia. These blocks typically do not achieve sensory blockade sufficient for surgical anesthesia and must be augmented by general anesthesia or deep sedation. Procedures such as transversus abdominis plane (TAP), adductor canal, intercostal nerve, and local infiltration enable postoperative analgesia.
SEDATION ANALGESIA FOR MINOR SURGICAL PROCEDURES
There are a variety of minor surgical procedures that can be accomplished safely and comfortably with anesthesia provided by infiltration of local anesthetics (most commonly 1% lidocaine or 0.25% bupivacaine) and mild sedation/anxiolysis provided by IV agents. All IV benzodiazepines, narcotics, and other IV anesthetics produce apnea if given in a high enough dose. Because there is a substantial patient-to-patient variability in response to a given dose, IV anxiolytics must be given in small incremental doses slowly to achieve a safe sedated state. When attempting to provide appropriate sedation analgesia for a procedure, it is worth noting that inadequate infiltration of local anesthetic cannot be compensated by increased doses of IV sedatives. Such doses of sedatives as well as narcotics cannot overcome the pain associated with a surgical incision; furthermore, if large doses of narcotics are given for this purpose, a patient may quickly become apneic once the surgical stimulus ends. This is due to the fact that duration of the respiratory depression for even short-acting narcotics is much longer than the painful stimulus of the incision. Because of the potentially serious consequences of an apneic episode, the Joint Commission has required that all patients receiving sedation for minor surgical or medical procedures undergo the following8:
Figure 13-1. Classification of the patient’s upper airway based on the size of the tongue and the pharyngeal structures visible on mouth opening. Class I, soft palate and anterior/posterior tonsillar pillars, and uvula visible; Class II, tonsillar pillars and part of uvula hidden by base of tongue; Class III, soft and hard palate visible; Class IV, soft palate not visible, only hard palate visible. (Redrawn from Stoelting RK, Miller RD. Basics of Anesthesia, 5th ed. New York: Churchill Livingston; 2007:146.)
Table 13-7 Sedation Scale
1. A preprocedure evaluation including an airway examination (Fig. 13-1)
2. Appropriate monitoring: pulse oximetry as a minimum
3. Documentation of the patient’s vital signs and arterial saturation as well as the dose and timing of sedatives provided during the procedure
4. Documentation of a recovery period and a return to a safe recovered state
The preprocedure evaluation should include current medications, coexisting disease, and a brief physical examination including an evaluation of the airway. The most common drug used to provide sedation is midazolam. This is a fast-onset, relatively short-acting benzodiazepine that can be easily titrated to produce a sedated yet cooperative arousable state. It is usually given to adults in incremental doses of 1 mg (0.01 mg/kg in children). Narcotics such as fentanyl even in small doses act synergistically with benzodiazepines to cause a more sedated state with a much higher incidence of apnea. To assess the effect of the drug, a validated sedation scale can be of value. The scale used at the University of Michigan is presented in Table 13-7.9
AIRWAY EVALUATION FOR THE NONANESTHESIOLOGIST
10 Supraglottic airway devices (laryngeal mask airways) are of additional consideration, used for both definitive airway management as well as a rescue technique for failed mask ventilation or failed intubation. Limitations to supraglottic airway devices, however, include a relative lack of protection from aspiration, as well as a limited ability to provide adequate positive pressure ventilation in patients prone to airway obstruction (e.g. morbidly obese, sleep apnea). The key elements of an airway examination are an assessment of obesity, mouth opening, neck flexion and extension, Mallampati oropharyngeal classification, presence of beard, and mandibular protrusion ability (Table 13-8).11 Despite decades of research, there is no perfect combination of clinical tests to predict difficult intubation. However, the presence of abnormalities in three or more of the aforementioned elements increases the likelihood of a difficult mask ventilation and/or difficult intubation by more than eight-fold.11 In patients with multiple (three or more) airway abnormalities, the presence of a beard is an easily corrected characteristic: the patient should be asked to shave the beard in order to improve the ability to manage the airway. Assessment of oropharyngeal classification is performed by having patients open their mouth and maximally protrude the tongue without phonation. This Mallampati oropharyngeal assessment can be classified depending on whether the uvula can be completely seen (class 1), only partly seen (class 2), or not seen, with the hard and soft palate visible (class 3), or only the hard palate visible (class 4) (Fig. 13-1).12An essential skill for all clinicians is the assessment of a patient’s airway. It is important to determine how difficult it may be to obtain control of the airway if a patient requires ventilatory support. The concept of airway management should be focused on not just endotracheal intubation, but also mask ventilation. Until the airway can be secured via intubation, the patient must be supported through mask ventilation.
Table 13-8 Standard Airway Examination for Nonanesthesiologists
RISKS ASSOCIATED WITH ANESTHESIA
Because the entire purpose of surgical anesthesia is to obtund or completely block physiologic protective mechanisms, there is an underlying baseline anesthetic risk even without a surgical procedure. Fortunately, with the advent of newer agents and monitoring techniques, it is estimated that the mortality rate directly attributable to anesthesia alone has decreased from about 1 in 10,000 patients in the 1950s to as low as 1 in 200,000 or less for healthy patients today.13 Although a 1 in 200,000 risk of death or serious neurologic impairment may appear small, when dire consequences occur in a young patient undergoing a purely elective procedure, the consequences are devastating for everyone involved. When patients are placed in a condition in which they cannot breathe, there is always the possibility of a technical or judgmental error resulting in hypoxia and brain damage or death. It has been estimated that between 50% and 75% of anesthetic-caused deaths are due to human error and are preventable. Because the consequences of an anesthetic mishap are usually severe, the emotional and financial costs are high.
Historically, the most common problems associated with adverse outcomes were related to the airway and included inadequate ventilation, unrecognized esophageal intubation, unrecognized extubation, and unrecognized disconnection from the ventilator. The incidence of these problems has been significantly reduced by including capnometry and pulse oximetry in addition to other noninvasive monitors, although a cause-and-effect relation has been difficult to prove. Efforts to improve outcome can be approached at three levels: (a) reduction of the incidence of rare but catastrophic anesthetic-related problems, (b) improvement of the care and experience of every patient undergoing anesthesia and surgery, and (c) improvement of the preparation and management of patients with pre-existing medical conditions who have higher morbidity and mortality rates. The first goal has been addressed in part with improved monitoring techniques, standardized anesthesia machine checklists, and anesthesiology training. Others have been advanced by the addition of comprehensive pain management, as discussed later in this chapter. Issues of pre-existing medical disease and how they affect the anesthetic plan are also briefly discussed later in this chapter.
Hypertension is the most common pre-existing medical disease in patients presenting for surgery and is a major risk factor for renal, cerebrovascular, peripheral vascular, and coronary artery diseases, as well as congestive heart failure (CHF). It is particularly associated with lipid disorders, diabetes, and obesity. It is these associated comorbidities that are most likely to lead to morbidity and mortality in the perioperative period, and therefore, the presence of hypertension should prompt the surgeon to review the history and physical examination for them. Hypertensive patients should be treated medically to render them normotensive before elective surgery. For elective surgical procedures, a sufficient period of time preoperatively should be allocated for antihypertensive management, as rapid correction of hypertension immediately prior to surgery is not without risk of comorbidities, including stroke and other end-organ malperfusion. In general, antihypertension medications should be continued throughout the perioperative period. However, patients treated with angiotensin receptor blockers (ARBs), such as valsartan, candesartan, losartan, or angiotensin-converting enzyme inhibitors (ACE-Is), such as lisinopril, captopril, or ramipril, who are exposed to general anesthesia, are at risk for developing profound, refractory intraoperative hypotension. This ACE-I/ARB hypotension has been treated successfully with terlipressin, vasopressin, and methylene blue.14–16 As a result, most medical centers now recommend withholding ACE-Is/ARBs the morning of surgery.17,18 Patients on concomitant diuretic therapy are at greatest risk for intraoperative hypotension requiring treatment.19,20
The incidence of hypotension and myocardial ischemia intraoperatively is higher in untreated hypertensive patients than in adequately treated hypertensive patients if the preoperative diastolic pressure is 110 mm Hg or higher.21 Inadequately treated hypertensive patients undergoing carotid endarterectomies have an increased incidence of neurologic deficits, and those with a history of prior myocardial infarctions have an increased incidence of reinfarction. Patients commonly have an elevated blood pressure on admission to the hospital. Hypertensive patients can have exaggerated responses to painful stimuli and have a higher incidence of perioperative ischemia.
Coronary Artery Disease
Much of the anesthetic preoperative evaluation has historically been focused on the detection and treatment of coronary artery disease. Coronary artery disease or its risk factors are present in about 30% of patients who undergo major surgery each year.22 It is the leading cause of death in the United States and continues to be a major cause of postoperative morbidity and mortality.23 The goal of the preoperative cardiac evaluation is to identify patients who are at increased risk of perioperative cardiac morbidity and ensure that their chronic conditions are optimized. Although perioperative cardiac events are the leading cause of death following anesthesia and surgery, it has been difficult to define patient characteristics that accurately predict a high risk of adverse outcome.24 It has been even more difficult to modify that risk effectively.25 Preoperative CHF is clearly a significant risk factor, as is recent myocardial infarction or unstable angina (Table 13-9). Diabetes mellitus (DM), atherosclerotic vascular disease, and hypertension also appear to confer risk, although less than with CHF or unstable angina. Perioperative risk in patients with valvular heart disease varies with the severity of the disease as represented by CHF, pulmonary hypertension, and dysrhythmias. Dysrhythmias are also a concern in the presence of coronary artery disease. Age and stable angina remain controversial as predictors of perioperative risk, with equal numbers of supporting and refuting studies. The value of revascularization remains controversial as well. In patients without significant pulmonary disease, the ability to climb two flights of stairs without stopping or experiencing symptoms of angina or shortness of breath is considered a good practical test of cardiac reserve. Unfortunately, many patients with ischemic heart disease have concomitant pulmonary disease or other medical problems that limit their activity. A history of myocardial infarction is important information. Large retrospective studies have found that the incidence of reinfarction is related to the time elapsed since the previous myocardial infarction.26–28 The incidence of reinfarction appears to stabilize at about 6% (50-fold higher than patient without myocardial infarction) after 6 months. The highest rate of reinfarction occurs in the 0- to 3-month period. Mortality from reinfarction, for patients undergoing noncardiac surgery (Table 13-10), has been reported to be between 20% and 50% and usually occurs within the first 48 hours after surgery.
Table 13-9 Clinical Predictors of Increased Perioperative Cardiovascular Risk (Myocardial Infarction, Heart Failure, Death)