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Prompt intervention in postoperative complications reduces morbidity and mortality.
Most serious adverse events occurring immediately after surgery involve hypoxia.
Emergencies presenting after surgery are often influenced by the residual effects of anesthesia and/or surgery and require interventions unique to the perioperative period.
The Post-Anesthesia Care Unit (PACU) is a dynamic location serving a variety of patients of differing medical backgrounds that provides intensive care unit level of care for individuals recovering from anesthetic agents. The primary goal of the PACU is to provide close monitoring and support to these patients until they have returned to sufficiently normal physiological states to return to the hospital ward or to home. Because of the physiologic effects and stresses of anesthesia and surgery, the PACU is a unique location within the hospital in which emergencies of varying levels occur on a more regular basis than on the general hospital floor or in the general public.
The aim of this chapter is to provide an overview of some of the more common emergent situations encountered in the PACU and the initial steps that should be undertaken to mitigate these events and increase the chance of a favorable patient outcome. This chapter is by no means intended to be an exhaustive coverage of any of the topics herein. Most of the topics discussed here have been covered in greater detail elsewhere in this text, and I would encourage the reader to refer to the relevant chapters for more detail.
Respiratory arrest
Hypoventilation is a common concern in the PACU.[1] Many of the medications administered preoperatively (i.e. benzodiazepines, barbiturates, opioids, and other sedative hypnotics such as propofol and the potent inhaled anesthetics) depress respiratory drive. Increasing propensity towards obesity, lung disease, and obstructive sleep apnea only serves to compound this risk. A high index of suspicion should be raised for the effects of medications in contributing to post-anesthetic respiratory arrest.[2] Furthermore, hypercarbia will cause respiratory depression and possible arrest at PaCO2 greater than 40 torr, as such hypoventilation itself can cause respiratory arrest.
Immediate initiation of the American Heart Association’s Basic Life Support (BLS) protocol such as mask ventilation with 100% oxygen should occur. Any difficulty in mask ventilation by an experienced provider should prompt consideration for reintubation. Likely causes of respiratory depression should be ascertained and ruled out, starting with a review of recent medication administration with special attention paid to opioids. Consideration for measured administration of an intravenous opioid antagonist such as naloxone should be undertaken. Naloxone commonly is supplied in 0.4 mg/ml (400 mcg/ml) solution. The stock solution should be diluted 1 to 10 for a final concentration of 0.04 mg/ml (40 mcg/ml)and given in 0.5 to 1 ml aliquots every 2 to 3 minutes, titrated to the effect of return of spontaneous ventilation[3] with a rate of 12 to 14 breaths per minute. If, after a reasonably high dose has been administered, spontaneous respirations do not resume, other causes of respiratory depression such as benzodiazepine overdose or cerebral vascular accident should be considered. In this case reintubation and mechanical ventilation would be a reasonable course of action. Administration of the benzodiazepine antagonist flumazenil can be considered, but extreme care should be taken in patients on chronic benzodiazepine therapy as antagonism can precipitate withdrawal seizures. If opioid or benzodiazepine antagonism is initiated, continued close monitoring of the patient is warranted because of the difference in pharmacological half-lives of the initial agents and their respective antagonists.
Cardiac arrest/circulatory arrest
Cardiac arrest in the PACU is a rare (perioperative incidence of 19.7 per 10,000 anesthetics) but potentially devastating occurrence.[4] Upon recognition of this condition, BLS protocol with high-quality CPR should be instituted immediately as the Advanced Cardiac Life Support (ACLS) or “code” cart is retrieved. As soon as arrest events in the PACU are witnessed, immediate identification of “shockable” rhythms and early defibrillation will increase favorable patient outcomes. The American Heart Association’s ACLS protocol should be initiated without delay, but the causes of sudden cardiac arrest differ in the perioperative population than in the pre-hospital setting, and therefore a more focused assessment of the possible causes of the event can be undertaken. The generic ACLS algorithm may not be the most appropriate for perioperative patients.[4] The most common electrocardiogram (ECG) rhythms noted during perioperative arrests are bradycardia (23%), asystole (22%), ventricular tachyarrhythmias (14%), and normal (i.e. pulseless electrical activity or PEA). Common causes of arrest in perioperative patients can be divided into the categories: anesthetic, respiratory, and cardiovascular.[4]
Refer to Table 50.1 for common causes of perioperative cardiac arrest and suggested treatments.
| Causes | Treatment |
|---|---|
| Anesthetic causes | |
| Anesthetic overdose | Stop the offending medication. Administration of chemical pacemakers such as epinephrine, transcutaneous/transesophageal pacing, intubation and mechanical ventilation until return of spontaneous circulation and ventilation |
| Sympathectomy from neuraxial anesthesia | Administration of chemical pacemakers such as epinephrine, transcutaneous or transesophageal pacing, intubation and mechanical ventilation until return of spontaneous circulation and ventilation |
| Local anesthetic toxicity | Immediate intubation. Administration of lipid emulsion such as intralipid (1.5 ml/kg load followed by 0.25 ml/kg/hr), avoid epinephrine bradycardia treated with atropine. Consideration of initiation of extra corporeal membrane oxygenation (ECMO) until return of spontaneous circulation occurs |
| Malignant hyperthermia (MH) | Initiation of MH protocol, administration of dantrolene, cool patient using ice or active cooling devices |
| Drug administration error | Varies, stop offending medication, administer antagonist if available otherwise supportive measures |
| Respiratory causes | |
| Hypoxemia | Initiate oxygen therapy with 100% oxygen via bag-valve mask, strongly consider reintubation and mechanical ventilation |
| Auto-PEEP* | If intubated, increase expiratory time. Consider brief disconnect of breathing circuit to allow release of trapped air. Administer bronchodilators |
| Bronchospasm | Administer bronchodilators such as beta-agonists and nebulized racemic epinephrine |
| Cardiovascular causes | |
| Vaso-vagal reflex | Administer atropine; if unsuccessful administer epinephrine, consider transcutaneous pacing |
| Hypovolemic shock | Fluid resuscitation, control bleeding source |
| Abdominal compartment syndrome | Emergent surgical intervention, decompressive laparotomy |
| Pneumothorax | Needle decompression, chest tube insertion |
| Transfusion reaction | Cease transfusion, supportive care |
| Anaphylaxis | Administer epinephrine |
| Acute coronary syndrome (ACS) | Begin ACS protocol, urgent interventional cardiology consultation |
| Pulmonary embolism | Surgical intervention, consider ECMO |
| Prolonged QT syndrome – Torsades de pointes | Intravenous magnesium therapy, defibrillation, antiarrhythmics |
| Pacemaker failure | Transcutaneous or transesophageal pacing. |
| Severe pulmonary hypertension | Intubation and initiation of pulmonary vasodilator such as nitric oxide |
| Acute electrolyte imbalance | Correct imbalance |
* Positive end-expiratory pressure
The importance of early initiation of BLS cannot be stressed highly enough. Return of coronary perfusion is of the utmost importance for the return of cardiac function and spontaneous circulation.
Cardiac ischemia
The incidence of cardiac ischemia may be exacerbated by general anesthesia, owing to decrease in perfusion from cardiac depression and vasodilation that predominates with the majority of anesthetic agents. Furthermore, the depressed mental state that often occurs during the post-anesthetic period has a high likelihood of masking the subjective symptoms of cardiac ischemia (i.e. chest pain, arm pain, feelings of dysphoria, etc.). This, coupled with the low incidence of postoperative ECG, necessitates a high index of suspicion for cardiac ischemia in perioperative patients.
Indications of cardiac ischemia include chest pain, arrhythmia, tachycardia, bradycardia, hypotension, abdominal discomfort, changes in continuous ECG monitor, and cardiac arrest. Early identification and intervention is essential in patients exhibiting signs and symptoms of cardiac ischemia as sequelae of this condition are severe.
The sine qua non of evaluation of chest discomfort and signs of cardiac ischemia is the 12-lead ECG. Although changes may be seen on the continuous telemetry monitor, these are often influenced by non-standard lead placement, patient movement, etc. and cannot be considered definitive. Twelve-lead ECG is an inexpensive, rapid, and sensitive method to rule out serious or massive cardiac ischemia that allows differentiation between ischemia requiring urgent invasive intervention such as percutaneous coronary intervention (PCI) from episodes that warrant medical management alone. It is important to note that early involvement of an expert in cardiology should be sought in cases of known or suspected cardiac ischemia.[5] In cases of cardiac ischemia, early intervention should include treatments that maximize oxygen delivery to affected myocardium, decrease myocardial oxygen demand, and minimize further impairment of coronary blood flow. The traditional mnemonic for the treatment of cardiac ischemia is the MONA-B, with the corresponding letters representing Morphine, Oxygen, Nitroglycerin, Aspirin, and Beta Blockade.[5]
Morphine is recommended to control the anxiety and pain associated with cardiac ischemia, decreasing catecholamine release, tachycardia, and increased contractility associated with this state. In postoperative patients, control of the pain associated with the recent procedure is also important. Therefore, administration of the opioid pain medication most appropriate for the individual patient should be undertaken to minimize the hemodynamic effect of the pain response.[5]
Supplemental oxygen should be provided to all patients in the PACU owing to the propensity for hypoventilation after receiving general anesthetics, and is often provided in the form of nasal cannula. However, in patients with suspected or confirmed cardiac ischemia, oxygen should be provided more aggressively to obtain an arterial hemoglobin saturation of at least 90% to maximize available oxygen at the ischemic site. Oxygen therapy should be continued for 6 hours after presentation of ischemic symptoms.[5]
Nitroglycerin causes coronary vasodilation and increases coronary perfusion. It has the secondary effect of decreasing blood pressure primarily by vasodilation of the venous system with a minor effect on arterial vasodilation. The result is a net increase of myocardial perfusion with a decrease in preload, and a minor decrease in afterload, thus simultaneously increasing coronary blood flow while decreasing myocardial oxygen demand. However, nitrates should be avoided in patients with systolic blood pressure less than 90 mmHg or who exhibit a decrease in systolic blood pressure greater than 30 mmHg below their baseline. Nitroglycerin therapy is also contraindicated in patients who have taken a phosphodiesterase inhibitor within 24 hours.[5]
Aspirin therapy is a staple of the treatment of acute coronary syndrome (ACS) in non-perioperative patients, owing to its platelet-inhibiting effects.[5] In patients in the immediate postoperative period, however, it is important to weigh the benefits of aspirin’s antithrombotic effects against the possibility of increased postoperative bleeding. Perioperative Aspirin administration remains controversial. As mentioned earlier, it is important to involve the surgical team as early as possible in the care of postoperative or post-anesthetic complications so that the relative risks and benefits of antithrombotic treatment can be effectively assessed. However, in general, non-steroidal anti-inflammatory drug (NSAID) therapy should be avoided in patients who have undergone procedures in areas where a small amount of bleeding can cause excessive damage, such as neurosurgical patients.[6]
Because of the high risk of postoperative bleeding, thrombolytic therapy such as the administration of tissue plasminogen activator is most likely contraindicated in the majority of post-surgical patients. In centers where PCI is not immediately available considerations for stabilization, initiation of the above supportive measures, and transfer to a facility capable of interventional cardiac catheterization should be made. The mantra of the American Heart Association with regards to PCI is “door to needle in 30 minutes or less.”[5]
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