Anesthetic complications can rapidly become emergencies if not identified and rectified. The most effective way to deal with anesthetic complications is to prevent them through (1) appropriate patient stabilization; (2) anesthetic and analgesic drug and dosage selection; (3) anesthetic equipment preparation; (4) pre-, post-, and intraoperative patient support; and (5) physiologic monitoring. This article provides an overview of the most common and\/or critical anesthesia-related complications, with tips for complication identification, prevention, and treatment or correction.<\/p>\n
Take-Home Points<\/strong><\/p>\n <\/div><\/div><\/p>\n Many anesthetic drugs can impair the physiologic function of vital organ systems, potentially leading to anesthesia-related complications. Patient factors, including extremes of age (i.e., neonatal<\/a>, geriatric<\/a>), presence of disease, and extremes of body weight and size, can also contribute to complications during anesthesia, as can duration of anesthesia.1<\/sup> Surgical procedure, approach, and invasiveness, along with patient positioning, can exacerbate some anesthesia-related complications. Although most complications generally have minimal impact on the patient when recognized and corrected early, the ultimate complication is anesthesia-related death, the rate of which is higher in dogs and cats than in humans.1<\/sup><\/span><\/p>\n The most effective way to deal with anesthetic complications is to prevent them through appropriate patient stabilization based on the patient\u2019s American Society of Anesthesiologists<\/a> status; anesthetic and analgesic drug and dosage selection (<\/span>BOX 1<\/b><\/span>); anesthetic equipment preparation; pre-, post-, and intraoperative patient support; and physiologic monitoring.4<\/sup><\/span><\/p>\n To decrease the likelihood of both sudden arousal and the tendency to lean toward excessive anesthetic depth, administer preanesthetic sedatives and provide robust analgesia. This allows a more stable plane of anesthesia at a lower inhalant mean alveolar concentration.3<\/sup> It is also recommended to have a dose of an injectable induction drug available so that if the patient undergoes arousal, an appropriate plane of anesthesia can be regained more rapidly and safely instead of \u201cbagging down\u201d with inhalants until the patient stops moving. <\/div><\/div>\n Complications involving the central nervous system (CNS), respiratory system, and cardiovascular system are among the most common anesthetic complications and are generally the most immediately life-threatening. Thus, physiologic monitoring and support are focused on these systems. However, anesthesia can directly or secondarily affect all organ systems, primarily through decreased oxygen delivery. Supporting the CNS, respiratory system, and cardiovascular system supports other organ systems (e.g., renal, hepatic) by ensuring adequate oxygen delivery. Physiologic monitoring greatly improves anesthetic safety, and the best monitor is a trained veterinary nurse who watches the patient and responds to concerning physiologic trends\u2014often before they become complications. Vigilant monitoring in the recovery period is critical for anesthetic safety and should continue until the patient is awake and responsive with normal physiologic parameters. (<\/span>BOX 2<\/b><\/span>).<\/span><\/p>\n Along with any of the physiologic concerns discussed in this article, common recovery complications include \u201crough\u201d recoveries. Any patient vocalizing or with uncoordinated movement (thrashing) for more than 1 to 2 minutes (less, if violent) should receive sedatives, analgesics, or, most commonly, both to prevent self-injury. Pain is often a major contributor. <\/div><\/div>\n Excessive anesthetic depth is a dangerous complication that is often not recognized until it results in other complications, primarily hypotension and hypoventilation. Excessive anesthetic depth during the maintenance phase of anesthesia can also contribute to a prolonged anesthesia recovery.<\/span><\/p>\n Causes of excessive anesthetic depth include absolute overdose of anesthetic drugs, but relative overdose can also occur. Inhalant anesthesia dose, defined roughly as the minimum alveolar concentration (MAC) required to keep a patient anesthetized, is lower in neonates, geriatric patients, and many compromised patients (e.g., patients with anemia, hypercarbia, hypoxia) than in middle-aged, healthy patients.3<\/sup> Thus, the inhalant dose (and often the dose of other anesthetic drugs) should be decreased in these patients. Hypothermia also decreases the MAC, potentially by as much as 4% to 5% with every decrease in degree Celsius.3<\/sup><\/span><\/p>\n Inadequate anesthetic depth and\/or inadequate analgesia to support the level of anesthetic depth is less common but can result in sudden arousal. This complication can also lead to detrimental outcomes, and the anesthetist should always be prepared with an injectable anesthetic drug and intravenous access to quickly reanesthetize an animal if it is aroused to the point of moving or injuring itself and\/or personnel. Additional analgesia (e.g., opioid bolus, local anesthetic block, infusion of analgesic drugs) should be added if initial analgesia is deemed inadequate to prevent arousal.<\/span><\/p>\n Hypoventilation, <\/b>defined as inadequate gas exchange (i.e., removal of CO2<\/sub>\/uptake of O2<\/sub>), is a common complication that often occurs secondary to excessive anesthetic depth. Hypoventilation due to inadequate respiratory rate and\/or tidal volume (the volume of air entering the lungs during inhalation) can cause hypercarbia (which may lead to respiratory acidosis) and potentially hypoxemia (which can lead to decreased tissue oxygen delivery).<\/span><\/p>\n Causes of hypoventilation include anesthetic drugs, physical or physiologic abnormalities or changes in the patient, and equipment malfunction.<\/span><\/p>\n Almost all anesthetic drugs can cause some degree of respiratory compromise, and the degree of respiratory depression is largely dose dependent. Propofol, alfaxalone<\/a>, and all of the inhalant drugs can cause dose-dependent respiratory depression, whereas ketamine is unlikely to cause this complication.<\/span><\/p>\n Physical or physiologic abnormalities or changes <\/b>that can cause hypoventilation include those that impair the respiratory drive initiated in the CNS or gas exchange in the airways. Diseases that cause metabolic alkalosis or directly affect the CNS (e.g., primary CNS disease, cranial trauma, brain tumors) can impair the respiratory drive. Gas exchange may be impaired by upper or middle airway conditions that impede airflow to the lungs (e.g., laryngeal dysfunction, tracheal collapse<\/a>) or lower airway diseases (e.g., pneumonia) and physiologic changes such as ventilation\/perfusion (V\/Q) mismatch (e.g., pulmonary consolidation, tumors). Other factors such as obesity, pregnancy, thoracic trauma, and patient positioning can impede ventilation by impairing normal thoracic and\/or diaphragmatic movement(s).<\/span><\/p>\n Equipment malfunction that impairs gas exchange can involve any component from the endotracheal (ET) tube to the oxygen supply. Common equipment complications include kinked, plugged, malpositioned, or excessively long ET tubes; inadequate fresh gas flow; malfunctioning inspiratory\/expiratory valves in a rebreathing system; inadequate oxygen flow in a nonrebreathing system; and exhausted CO2<\/sub> absorbent.<\/span><\/p>\n A closed pop-off valve is a crisis complication, as the breathing system\u2014and the patient\u2019s respiratory system\u2014will rapidly become pressurized, causing collapse of the intrathoracic blood vessels and resulting in inadequate oxygen delivery to the myocardium and subsequent cardiac arrest. Adding a pop-off button just behind the pop-off valve can help avoid this complication (<\/span>FIGURE 1<\/b><\/span>).<\/span><\/p>\n Figure 1. Pop-off button placed between the pop-off valve and the scavenging system. When pressed, the button closes the system, allowing a positive-pressure breath to be administered by the anesthetist. When the button is no longer pressed, it automatically opens; thus, the system is never closed for longer than it takes to give a breath.<\/p><\/div>\n In conscious patients, the normal values for arterial partial pressure of carbon dioxide (Paco2<\/sub>) and end-tidal carbon dioxide (ETco2<\/sub>) are 35 to 45 mm Hg. However, mild respiratory depression under anesthesia is acceptable and values up to 55 mm Hg are tolerable in most patients. Allowing CO2<\/sub> to increase above this limit usually results in respiratory acidosis.<\/span><\/p>\n The main cause of hypercarbia <\/i>is hypoventilation. Other causes include failure to eliminate CO2<\/sub> due to exhausted CO2<\/sub> absorbent (rebreathing system) or inadequate oxygen flow (nonrebreathing system) and excessive production of CO2<\/sub>, as can occur with moderate to profound hyperthermia or hypermetabolic states such as malignant hyperthermia. Failure to eliminate CO2<\/sub> from the system results in \u201crebreathing\u201d of CO2<\/sub>, which can be recognized on a capnograph curve or wave by a high (><\/span>\u2009<\/span>45 mm Hg) peak and failure to return to 0 baseline (<\/span>FIGURES 2 AND 3<\/b><\/span>). All other causes of hypercarbia result in a high peak with a 0\u00a0baseline in the inspiratory pause. Hyperventilation would result in a curve with a low peak (<<\/span>\u2009<\/span>35 mm Hg).<\/span><\/p>\n Figure 2. Normal capnograph waveform. (A\u2013B) Zero baseline representing the respiratory \u201cpause\u201d between breaths. (B\u2013C) Rapid, sharp rise reflecting the exhalation of mixed dead space and alveolar gas. (C\u2013D) Alveolar plateau representing exhalation of mostly alveolar gas. (D) End-tidal CO2<\/sub> value at end of exhalation. (D\u2013E) Rapid, sharp downstroke representing inhalation.<\/p><\/div>\n Figure 3. Capnograph waveform indicating rebreathing of CO2<\/sub>. The waveform baseline stays elevated and does not return to 0.<\/p><\/div>\n If no cause can be found, this patient might require ventilator assistance throughout the anesthetic episode. This is uncommon in young, healthy patients but very common in aged or compromised patients. Ventilator assistance does not necessarily mean that a mechanical ventilator is required, since a person can easily ventilate the patient. Ventilator assistance also does not necessarily mean that total control of ventilation is necessary. Many patients can breathe on their own but need some support\u2014often 1 to 2 additional breaths per minute or even every 3 to 5 minutes will suffice. This is patient dependent, and appropriate support will be determined by monitoring.<\/div><\/div>\n The ideal arterial partial pressure of oxygen (Pao2<\/sub>) as measured by arterial blood gas is 5 times the fraction of inspired oxygen (FIo2<\/sub>). Therefore, the Pao2<\/sub> of a patient breathing room air (21% oxygen) would be roughly 105 mm Hg and that of a patient breathing 100% oxygen from the anesthesia machine would be roughly 500 mm Hg. Although values are rarely this high, the patient is not considered hypoxemic until the Pao2<\/sub> with room air decreases below approximately 80\u00a0mm Hg (absolute hypoxemia = Pao2<\/sub> <<\/span>\u2009<\/span>60 mm Hg) and below 200 to 300 mm Hg on 100% oxygen (\u201crelative\u201d hypoxemia, but not truly hypoxemic).<\/span><\/p>\n Hypoxemia is defined as oxygen saturation (Spo2<\/sub>) <<\/span>\u2009<\/span>90% in all patients, but Spo2<\/sub> should be maintained at 95% to 100% if the patient is breathing 100% oxygen (FIGURE<\/b><\/span><\/span>\u00a04<\/b><\/span>).<\/span><\/p>\n\n
Central Nervous System Complications<\/h2>\n
Excessive Anesthetic Depth<\/h3>\n
Inadequate Anesthetic Depth<\/h3>\n
Prevention of Central Nervous System Complications<\/h3>\n
\n
Treatment\/Correction of Central Nervous System Complications<\/h3>\n
\n
Respiratory System Complications<\/h2>\n
Hypoventilation<\/h3>\n
![\"\"](\"https:\/\/todaysveterinarypractice.com\/wp-content\/uploads\/sites\/4\/2024\/02\/Grubb_TVPMarApr24_AnesthesiaComplications_Fig1.png\")
<\/a>Hypercarbia<\/h3>\n
![\"\"](\"https:\/\/todaysveterinarypractice.com\/wp-content\/uploads\/sites\/4\/2024\/02\/Grubb_TVPMarApr24_AnesthesiaComplications_Fig2.png\")
<\/a>![\"\"](\"https:\/\/todaysveterinarypractice.com\/wp-content\/uploads\/sites\/4\/2024\/02\/Grubb_TVPMarApr24_AnesthesiaComplications_Fig3.png\")
<\/a>\n
Hypoxemia<\/h3>\n
![\"\"](\"https:\/\/todaysveterinarypractice.com\/wp-content\/uploads\/sites\/4\/2024\/02\/Grubb_TVPMarApr24_AnesthesiaComplications_Fig4.png\")
<\/a>![\"\"](\"https:\/\/todaysveterinarypractice.com\/wp-content\/uploads\/sites\/4\/2024\/02\/Grubb_TVPMarApr24_AnesthesiaComplications_Fig5.png\")
<\/a><\/p>\n