Coma and Delayed Emergence
Roger S. Mecca
CASE SUMMARY
You are asked to see a 72-year-old man who has been in the postanesthesia care unit (PACU) for 60 minutes following a total hip replacement under spinal anesthesia with intrathecal bupivacaine and morphine, along with intravenous sedation with midazolam. During placement of the prosthesis, the patient became very agitated and complained of discomfort. This led his intraoperative anesthesia provider to induce a general endotracheal anesthetic that incorporated fentanyl, isoflurane, and vecuronium. Placement of the prosthesis was extremely difficult, and the amount of blood lost throughout the case was significant.
Upon review of the patient’s chart, a history of diabetes, hypertension, atrial fibrillation, and stable angina is noted. Physical examination reveals an unconscious, spontaneously ventilating patient with small, poorly reactive pupils, a carotid bruit on the right, and a subtle, holosystolic murmur at the left sternal border. His blood pressure is 20% below his chronic baseline, and his arterial oxygen saturation has varied between 97% and 93% on supplemental oxygen in the PACU. He has a central venous catheter in his right internal jugular vein. The patient does not respond at all to verbal stimulation and only twitches his arms feebly in response to a firm tactile stimulus.
The PACU nurse asks you how much longer it will take for the patient to regain consciousness. The orthopedic surgeon wants you to assure the family that, in fact, he will emerge from anesthesia. How would you assess the etiology of his state of unconsciousness to answer these questions?
What Is the Impact of a Prolonged State of Unconsciousness?
In current practice, emergence from anesthesia is more rapid and predictable than ever before, owing to such factors as the significant refinements in anesthesia and surgical techniques, the deployment of shorter-acting intravenous agents and lower solubility inhalational anesthetics, and the use of depth of anesthesia indicators, such as end-expired volatile agents and processed electroencephalogram (EEG) monitoring. In spite of these advances, some patients still exhibit a significantly depressed state of consciousness after surgery. For most of these individuals, persistent sedation resolves during the early recovery interval without intervention; however, occasionally a patient will not regain consciousness as expected. Evaluation and treatment of prolonged unconsciousness after anesthesia is one of the most perplexing and anxiety-provoking challenges presented to a practitioner during postoperative care.
To quickly complete a thorough and accurate analysis of prolonged unconsciousness, an organized and consistent approach should be utilized that addresses potential problems in order of their likelihood and their impact on the patient’s well-being. These measures will expedite the identification and resolution of the etiology of delayed emergence and minimize the chances of adverse outcomes.
Prolonged unconsciousness after anesthesia can be caused or exacerbated by a large number of adverse physical conditions. Unfortunately, most of these conditions are progressive and generate time-sensitive morbidity, and can be life-threatening if not addressed promptly.1,2,3 Many of these conditions are also easily reversible without permanent injury if discovered and treated early in their clinical course.
▪ RESPIRATORY SYSTEM
A state of unconsciousness poses a variety of secondary risks that are independent of the underlying etiology. For example, factors that depress the central nervous system (CNS) sufficiently to produce unconsciousness usually also depress, to some degree, the centers that are responsible for regulating ventilation. An unconscious patient’s awareness of ventilation and volition to breathe are undoubtedly impaired. Central monitoring of changes
in lung volume is also blunted by a reduced level of consciousness. The medullary respiratory center near the fourth ventricle primarily regulates the partial pressure of carbon dioxide in arterial blood (PACO2) by monitoring the pH concentration in the cerebrospinal fluid. Any factor that interferes with the sensitivity of this center encourages the “acceptance” of a higher than usual PACO2, thereby leading to hypoventilation and respiratory acidemia. Even a moderate level of somnolence, as occurs during normal sleep, will result in some degree of hypercarbia and a reduction of serum pH.
in lung volume is also blunted by a reduced level of consciousness. The medullary respiratory center near the fourth ventricle primarily regulates the partial pressure of carbon dioxide in arterial blood (PACO2) by monitoring the pH concentration in the cerebrospinal fluid. Any factor that interferes with the sensitivity of this center encourages the “acceptance” of a higher than usual PACO2, thereby leading to hypoventilation and respiratory acidemia. Even a moderate level of somnolence, as occurs during normal sleep, will result in some degree of hypercarbia and a reduction of serum pH.
Deeper levels of unconsciousness exert a proportionally greater degree of ventilatory depression and respiratory acidemia. A patient’s hypoxic ventilatory drive, which responds to changes in partial pressure of oxygen in arterial blood (PaO2), is usually more sensitive to depression from drugs and other factors than the PACO2 drive. Therefore, hypoventilation secondary to unconsciousness can also lead to hypoxemia. In severe cases of respiratory center depression, hypoventilation or complete apnea can quickly progress to severe hypoxemia or end-stage respiratory acidemia, leading to death.
In unconscious patients, decreased tone and coordination of the pharyngeal and laryngeal musculature promotes the increase of upper airway resistance to gas flow; such a reduction in upper airway patency increases the chances that hypoxemia and/or hypercarbia will develop in spontaneously ventilating patients. The likelihood of obstructive, negative-pressure pulmonary edema is also increased. In extreme cases, augmented resistance can progress to complete upper airway obstruction.
Beyond the impact on airway patency, a depressed consciousness also impairs the protective reflexes of the airway. The probability of postoperative regurgitation and aspiration is increased in an unconscious patient, especially if the patient is left in a supine position with the head in the midline.
▪ IMPAIRED REFLEXES
A patient in an unconscious state is also prone to incidental injuries in the postoperative care environment. For example, an unconscious patient is unable to acknowledge and respond to pain from entrapment of skin folds or contact of body parts with rigid surfaces; this condition can lead to pressure necrosis in tissues, compartment syndromes, peripheral nerve damage, or myoglobinuria with renal impairment. The possibility of positioning-related and fall-related injuries varies inversely with the level of consciousness in postoperative patients. For example, the shifting of oxygen equipment placed on the face of an unconscious patient can cause corneal abrasion. Prolonged unconsciousness after anesthesia and surgery can mask the symptoms of an evolving surgical complication or a threatening unrelated condition and, consequently, can delay diagnosis and treatment. For example, a patient in an unconscious state cannot acknowledge abdominal pain from a ruptured viscus or lower extremity paralysis from an evolving epidural hematoma. Neither will such a patient exhibit agitation caused by metabolic acidemia or nausea, nor can disorientation secondary to cerebral hypoperfusion be assessed.
▪ AUTONOMIC AND SYMPATHETIC NERVOUS SYSTEMS
Factors that depress the CNS sufficiently to prolong unconsciousness will also depress centers that regulate the autonomic nervous system; therefore, sympathetic nervous system responses are blunted to pain, noxious sensations, and changes in systemic blood pressure, arterial pH, and other physiologic variables. Attenuation of sweating and tachycardia caused by hypoglycemia in an anesthetized patient is a well acknowledged example of this phenomenon.
▪ EXPENDITURE OF MEDICAL RESOURCES
Other aspects of delayed emergence impact medical risk and expenditure of resources. Prolonged unconsciousness lengthens the time that the patient spends in a postanesthesia care setting, thereby increasing staff costs due to the amount of care and observation that the patient requires. While attending to an unconscious patient, the health care team may provide less coverage to other postanesthesia patients, and therefore, additional staff may be required, further adding to hospital costs. In addition to expenditure of resources, these modifications diminish the efficiency and overall safety of postanesthesia care. Workplace safety for postanesthesia staff is also an issue. Because unconscious patients cannot participate in self-care, they must be positioned and moved by staff members, which increases the exposure of staff members to injury during lifting or fall prevention.
How Can A State of Prolonged Unconsciousness Be Generally Assessed?
Two general issues need to be addressed when deciding whether a postoperative patient is exhibiting prolonged unconsciousness after anesthesia. The first involves differentiating whether the patient is truly unconscious, merely asleep, or exhibiting a disordered sensorium.
▪ VERBAL AND TACTILE STIMULATION
For purposes of this discussion, unconsciousness can be defined as the absence of any meaningful, directed
response to ordinary levels of verbal or non-noxious tactile stimulation.4 If a patient can be aroused with gentle tactile stimulation, mumbles a vague verbal response to a question, and/or purposefully withdraws an extremity from a mildly uncomfortable physical stimulus, he or she is not unconsciousness but is merely somnolent. Similarly, if a patient is combative or exhibits confusion or disorientation, he or she is not unconscious but likely exhibiting an unusual emergence reaction. However, if no response to verbal interaction is forthcoming, and only a deep reflex response to a painful tactile stimulus is elicited, a patient should be considered unconscious.
response to ordinary levels of verbal or non-noxious tactile stimulation.4 If a patient can be aroused with gentle tactile stimulation, mumbles a vague verbal response to a question, and/or purposefully withdraws an extremity from a mildly uncomfortable physical stimulus, he or she is not unconsciousness but is merely somnolent. Similarly, if a patient is combative or exhibits confusion or disorientation, he or she is not unconscious but likely exhibiting an unusual emergence reaction. However, if no response to verbal interaction is forthcoming, and only a deep reflex response to a painful tactile stimulus is elicited, a patient should be considered unconscious.
▪ RATE OF EMERGENCE
The second issue involves estimating the reasonable period in which the patient is expected to regain consciousness after the anesthetic, taking into consideration the specific conditions of the situation at hand. Obviously, there is an acceptable interval after the termination of general or regional anesthesia with deep sedation during which decreased responsiveness is expected. The amount of time that a patient requires to regain consciousness after anesthesia is terminated depends on the following factors:
Type and duration of anesthesia and surgery
Type and dosage of agents employed
Timing of final doses and discontinuation of agents
The occurrence and severity of unexpected events
Many factors that are intrinsic to each patient also affect the rate of emergence; therefore, establishing the acceptable duration of unconsciousness post anesthesia is a highly individualized judgment that depends on the clinical circumstances. Nevertheless, it is possible to predict an interval within which a vast majority of patients will regain consciousness after a reasonably conducted anesthetic. Most patients emerging from general anesthesia should regain consciousness and react purposefully to verbal and tactile stimuli within 15 minutes of admission to the PACU. (For practical purposes, ignore the 5 to 10 minutes that usually elapse between the discontinuation of a general anesthetic and admission to the PACU. Doing so expands the actual interval to 20 to 25 minutes after the cessation of anesthetic delivery.) Even a patient who is highly sensitive to the residual sedative effects of anesthetic agents should respond to verbal or tactile stimuli within 30 minutes of admission to the PACU (35 to 40 minutes after cessation of anesthesia). A state of unconsciousness that persists for more than 30 minutes after admission to the PACU is considered prolonged and should be aggressively evaluated.
▪ MEDICAL HISTORY
An initial assessment of a patient’s medical history can help elucidate the cause of prolonged unconsciousness (see Table 25.1). This is particularly important when the practitioner performing the postoperative examination was not involved in the intraoperative anesthetic and is not familiar with the patient’s condition before induction of anesthesia.
TABLE 25.1 Medical History Pertinent to the Differential Diagnosis of Prolonged Unconsciousness | ||||||||||||||||||
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A review of the admission history and physical examination, the preanesthesia evaluation, and other sources, such as inpatient progress notes, nursing notes, or referral forms can yield invaluable insight. During this review, assess whether preexisting factors are contributing to the patient’s state of unconsciousness such as level of mental dysfunction or any history of epilepsy or trauma-related seizure disorder. Take special note of preexisting medical conditions that can impact CNS function, such as cerebral vascular disease, transient ischemic attacks, stroke, intracranial tumor, cerebral aneurysm, or previous head trauma. The presence of supraventricular dysrhythmias such as atrial fibrillation or flutter should lead one to consider the possibility of cerebral thromboembolism secondary to migration of atrial clots. A history of congenital heart disease, septal defect, endocarditis, or heart murmur may point toward paradoxical cerebral embolization with thrombus, vegetations, air, or fat. Cirrhosis, chronic hepatitis, or other disorders of liver function may indicate an element of hepatic encephalopathy. Chronic metabolic conditions, electrolyte disorders, or inborn errors of metabolism can certainly affect the level of consciousness, particularly if exacerbated by intraoperative conditions.
A patient may be using medications on a chronic basis that can depress the level of consciousness or lead to unusual cross-reactions with agents administered during surgery. For example, baclofen taken preoperatively or given during a procedure can significantly impair the postoperative level of consciousness.5,6 Postanesthesia arousal can also be affected by the use of herbal medications, such as St. John’s wort.7 If possible, also assess the nutritional status and look for alcohol or
other substance abuse. A history of deafness occasionally explains an emerging patient’s lack of response to verbal stimuli. Finally, scrutiny of events that occurred in the immediate interval before surgery is important. In trauma patients or those requiring emergency surgery, the possibility of unrecognized head injury, asphyxia, or exposure to carbon monoxide, environmental toxins, or ingested poisons should be evaluated.
other substance abuse. A history of deafness occasionally explains an emerging patient’s lack of response to verbal stimuli. Finally, scrutiny of events that occurred in the immediate interval before surgery is important. In trauma patients or those requiring emergency surgery, the possibility of unrecognized head injury, asphyxia, or exposure to carbon monoxide, environmental toxins, or ingested poisons should be evaluated.
▪ PERIOPERATIVE EVENTS
With respect to the surgical procedure, reviewing documentation that clarifies the patient’s peri-induction state of responsiveness and behavior helps elucidate whether unrecognized acute intoxication with drugs or alcohol is a contributing factor. The time and amount of sedative or hypnotic drugs administered for premedication should be noted, being especially vigilant for longer-acting sedatives given orally or rectally, because these exhibit a delayed peak effect and a much longer duration of action than parenterally administered, shorter-acting sedatives.
A review of the actual anesthesia record is critical:
Check for any documentation describing the patient’s mental status just before the induction of anesthesia.
Assess the amount and timing of medications administered during surgery, such as sedatives and opioids, particularly those causing significant CNS depression.
Evaluate the duration, concentration, and discontinuation time of inhalational anesthetics, especially when one of the more soluble agents is utilized in high concentrations for a long period or if it is continued through the end of surgery as a strategy for extubation or transport under a deep level of anesthesia.
Note any unusual intraoperative events such as transient airway obstruction, periods of low arterial oxygen saturation, prolonged decreases in systemic blood pressure, dysrhythmias, or blood loss.
Discussing the patient’s intraoperative course (see Table 25.2) with the anesthesia provider often helps elucidate a perspective that may not be evident from the anesthesia record alone.
Knowing the patient’s mental status in the operating room at the end of surgery and upon admission to the PACU will distinguish whether unconsciousness was present in the operating room or appeared during or after transfer to the PACU. A review of the PACU admission report can be very useful in making a differential diagnosis.
▪ PHYSICAL EXAMINATION
Physical assessment of an unconscious patient is equally important in elucidating an etiology (see Table 25.3).
Vital Signs
First, assessment of basic vital signs should be completed (heart rate, rhythm, and systemic blood pressure) to qualitatively reveal the adequacy of cerebral perfusion and to help establish the level of autonomic nervous system depression. Evaluating the rate, depth, and character of spontaneous ventilation helps in assessing the degree of cerebral depression from medications, particularly if relatively large dosages of opioids were incorporated into the general anesthetic. Examining pupillary size and responses may not yield any conclusive information in determining the diagnosis of postoperative unconsciousness because medications, autonomic nervous system tone, and even eye surgery can all affect pupillary reactions during emergence.
TABLE 25.2 Intraoperative History Pertinent to the Differential Diagnosis of Prolonged Unconsciousness | |||||||||||||||
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Response to External Stimulus
A provocative test that can be very useful in determining the source of unconsciousness is assessing the patient’s response to external stimuli. Verbal input should be sharp and loud enough to slightly startle. Although obvious, it is important to use the patient’s correct name as part of the verbal query, as a somnolent patient may ignore a verbal stimulus that he does not realize is directed toward him. Using the first name or a moniker may be more effective in eliciting a response.
If no response is elicited by verbal input, include a tactile stimulus, such as a light skin pinch, trapezius squeeze, or a sternal rub. Tactile stimulation seems to provoke a greater level of arousal than verbal stimulation,
perhaps because the sensory input is amplified through the reticular activating system. The degree of tactile stimulation should be reasonable and should cause no risk of physical injury; the use of needles or other sharp devices to generate pinprick sensation is unnecessary. As a rule of thumb, any maneuver that you would allow a colleague to apply to you at the bedside should be appropriate to apply to a patient. At this early juncture, assessment of other neurologic signs such as deep tendon reflexes or cranial nerve responses yields little value.
perhaps because the sensory input is amplified through the reticular activating system. The degree of tactile stimulation should be reasonable and should cause no risk of physical injury; the use of needles or other sharp devices to generate pinprick sensation is unnecessary. As a rule of thumb, any maneuver that you would allow a colleague to apply to you at the bedside should be appropriate to apply to a patient. At this early juncture, assessment of other neurologic signs such as deep tendon reflexes or cranial nerve responses yields little value.
TABLE 25.3 Physical Examination Pertinent to the Differential Diagnosis of Prolonged Unconsciousness | |||||||
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TABLE 25.4 General Causes of Prolonged Unconsciousness After Anesthesia | |||||||||||||
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How Do You Assess the Different Causes of Prolonged Unconsciousness?
The general causes of a prolonged state of unconsciousness after anesthesia are listed in Table 25.4.
▪ RESIDUAL EFFECTS OF ANESTHETICS
Residual sedation from anesthetic agents often contributes to prolonged unconsciousness after surgery. Generally, an unconscious state related to residual anesthesia is time-limited and characterized by a rapid and progressive lessening of depth. The rate of emergence varies with the type of anesthetics used and the specific characteristics of the individual patient. Also, prolonged unconsciousness from residual anesthesia almost always reflects the combined effects of several agents, each of which exhibits a different rate of resolution.
Opioids
Opioids are frequently implicated in producing a prolonged state of unconsciousness. The degree and duration of postoperative sedation when opioids are administered intraoperatively is related to the timing, route, and total dosage of agents administered. When long- and intermediate-acting opioids are used, the resolution of sedation is slower than that caused by residual inhalational anesthetics because opioids require hepatic metabolism and/or renal excretion for clearance. Prolonged depression is especially common after the intraoperative administration of longer-acting opioids such as morphine, meperidine, or hydromorphone. However, other opioids such as fentanyl that usually have a shorter duration of clinical action, secondary to redistribution, can also exhibit a long “tail” of sedation when high dosages or continuous infusions are administered.8 It is less likely that the shortest-acting opioids, such as alfentanil, sufentanil, and particularly remifentanil, will significantly contribute to postoperative unconscious states unless very high dosages are given over extensive periods.
Intramuscular opioid administration leads to slower uptake and prolonged action, especially in surgical patients who are hypothermic or hypovolemic. The administration of intrathecal or epidural opioids can result in the rostral spread of opioid into the cerebral ventricles, thereby resulting in unconsciousness and ventilatory depression.
Several interesting aspects of opioid pharmacology can increase their impact on prolonged unconsciousness. Some opioids are metabolized to active metabolites that prolong and add to central depression. Sedation induced by opioids is usually accompanied by a decrease in spontaneous minute ventilation that slows the washout of residual inhalational anesthetics, thereby prolonging sedation. Opioids exert a synergistic effect on the depressant properties of sedatives, leading to a greater degree of sedation than the sedative would have caused by itself. Also, when compared to other agents, the intense analgesic influence of opioids minimizes the arousal generated by postoperative pain; this effect also blunts the response to tactile stimuli and accentuates the depressant effects of sedatives or antiemetics.
The administration of additional opioids in the PACU adds to the residual depression from medications that were provided intraoperatively. While determining the reason for prolonged unresponsiveness, it is appropriate to assume that the patient does not perceive significant levels of pain, and therefore, the initiation of analgesic and sedative regimens, such as loading for patient-controlled analgesia, should be delayed until the source of unconsciousness is determined. Assessing pain levels should be avoided at this time, as well as administering analgesic medications based solely on signs indicating increased sympathetic nervous system activity. Generally, a patient who generates significant tachycardia and hypertension in response to postoperative pain will also exhibit some degree of consciousness. In an unresponsive patient, these physical signs can reflect critical abnormalities of oxygenation, ventilation, systemic perfusion, or intracranial pressure. Administering opioid analgesics under these circumstances could result in the patient’s death.
To assess whether prolonged unconsciousness is related to residual opioids, small, incremental, titrated
doses of intravenous naloxone (40 µg increments) can be administered. Careful titration can reverse both ventilatory depression and sedation without precipitating the dangerous reversal of analgesia and excess sympathetic nervous system activity that can result. Unless a patient has received a massive opioid overdose, the ventilatory rate and level of consciousness will increase with a total dosage of 200 µg or less of intravenous naloxone; if unconsciousness persists, it is most likely not related to the depressant effects of residual opioids on the CNS.
doses of intravenous naloxone (40 µg increments) can be administered. Careful titration can reverse both ventilatory depression and sedation without precipitating the dangerous reversal of analgesia and excess sympathetic nervous system activity that can result. Unless a patient has received a massive opioid overdose, the ventilatory rate and level of consciousness will increase with a total dosage of 200 µg or less of intravenous naloxone; if unconsciousness persists, it is most likely not related to the depressant effects of residual opioids on the CNS.
Sedatives and Antiemetics
The administration of sedative premedication to achieve anxiolysis or amnesia can contribute to prolonged unconsciousness, particularly if long-acting sedatives (e.g., pentobarbital, hydroxyzine, promethazine, lorazepam) are administered orally, rectally, or intramuscularly. The possibility of unacknowledged “self-premedication” by patients with long-acting oral sedatives or other psychotropic medications should also always be considered. Even the judicious use of intravenous midazolam before induction can, in some patients, affect the level of consciousness in the PACU. The administration of sedatives or antiemetics as part of the anesthetic regimen likewise adds even more profound depression in the PACU, especially if given toward the end of surgery.
Parenteral medications such as propofol, short-acting barbiturates, or etomidate by frequent bolus or continuous infusion can generate high circulating serum levels and resultant redistribution of high concentrations of drug into the tissues. The delayed excretion of medication can cause or accentuate delayed awakening after discontinuation.9
Antiemetics, such as droperidol, prochlorperazine, or scopolamine, have sedative side effects that can augment the residual sedation from anesthetics. Other antiemetic agents such as dexamethasone and serotonin-blocking agents (e.g., ondansetron, dolasetron) do not exhibit significant sedative side effects, and therefore do not contribute to postoperative unconsciousness.
Evaluating the contribution of sedatives or antiemetics to prolonged unconsciousness is not quite as straightforward as evaluating the influence of opioids. If a patient has received benzodiazepines, intravenous flumazenil, a competitive benzodiazepine antagonist, can be given in titrated, incremental dosages of 0.1 mg every 2 minutes. In the perioperative setting, <1 mg is typically needed to reverse residual benzodiazepine effect. Flumazenil directly reverses the sedation caused by midazolam, diazepam, lorazepam, and other benzodiazepines, although its duration of action is relatively short. If unconsciousness due to benzodiazepines is reversed by intravenous flumazenil, it is theoretically possible that benzodiazepine’s duration could exceed that of flumazenil reversal, leading to the return of unconsciousness an hour or so after reversal. However, the dosages of benzodiazepines used in contemporary anesthesia care are low enough that the serum concentration decreases significantly during the effective duration of flumazenil. In addition, the sedative effects of other medications, such as opioids and inhalational anesthetics, also wane during this interval. Therefore, the likelihood of “re-sedation” after flumazenil reversal is insignificant, unless a benzodiazepine overdose has occurred.
Reversal Agents
There are no specific reversal agents available to counteract the depressant effects of barbiturates, propofol, phenothiazines, and butyrophenones. The administration of intravenous physostigmine (1.25 mg) generates a degree of central arousal that can counteract, but not reverse, depression from sedatives, antiemetics, and other depressant medications such as baclofen.6,10,11 Application of this modality is usually not warranted unless the etiology of sedation is unclear and immediate resolution is important.
Inhalational Anesthetics
High alveolar partial pressures of residual volatile anesthetic agents can sometimes leave a patient deeply sedated early in the postoperative course. This phenomenon occurs predominantly after extended exposure to high concentrations of a more soluble agent such as isoflurane.12 During long surgical procedures, significant amounts of soluble anesthetic agents build up in tissues that have lower perfusion levels, consequently leading to a more gradual washout after discontinuation. Obese patients may be at particular risk of prolonged sedation after long procedures, given their relatively high proportion of body fat. Also, if high inspired concentrations are continued through the end of surgery to maintain bronchodilation or to facilitate a “deep” extubation, alveolar partial pressures and level of sedation will naturally be higher during the initial recovery period.
It is unlikely that low solubility agents, such as sevoflurane and desflurane, are the primary cause of persistent unconsciousness because they are eliminated very rapidly, soon after their discontinuation in the operating room. However, these agents may contribute to sedation when combined with other, longer-acting parenteral medications such as opioids. Nitrous oxide is seldom implicated, because of its low solubility and relatively weak anesthetic properties.
Considering the inevitable washout of anesthetic vapor during normal breathing, it would be unusual that the residual effects from any volatile inhalational anesthetics would be the primary cause of an unconscious state that lasts over 30 minutes after discontinuation of inhalational anesthesia. However, if the residual volatile agent should, indeed, significantly contribute to prolonged unconsciousness, then the culprit can be easily detected from breath odor or through a quantitative analysis of expired gas using standard intraoperative monitors. There are no specific agents available that will reverse residual sedation from volatile anesthetics.
If it is essential to assess whether residual inhalational anesthesia is causing prolonged unconsciousness, the administration of intravenous physostigmine can be tried to counteract the sedative effects. However, simply
allowing adequate time for the inhalational agent to wash out through alveolar ventilation will provide sufficient differentiation. If the administration of appropriate doses of naloxone, flumazenil, and physostigmine does not elicit a response, unconsciousness is not likely related to sedation from residual anesthetic medications.
allowing adequate time for the inhalational agent to wash out through alveolar ventilation will provide sufficient differentiation. If the administration of appropriate doses of naloxone, flumazenil, and physostigmine does not elicit a response, unconsciousness is not likely related to sedation from residual anesthetic medications.
Neuromuscular Relaxants
Neuromuscular agents do not have any significant sedative or analgesic properties and therefore would not exacerbate postoperative unconsciousness. Rarely, profound residual neuromuscular blockade can mimic unconsciousness during recovery by completely eliminating any voluntary motor response to verbal or tactile stimuli in a conscious but completely paralyzed patient. Although unlikely, this degree of neuromuscular blockade can occur after gross overdose with neuromuscular blocking agents or if reversal agents are omitted. Similarly, complete postoperative paralysis is conceivable in patients with unrecognized neuromuscular disease or in those exhibiting phase II blockade caused by excessive succinylcholine administration or pseudocholinesterase deficiency.
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