The risk of death from disease or related surgery is usually greater than the risk of death from anesthesia. However, anesthesia involves the controlled administration of potentially toxic drugs and thus carries a risk of organ dysfunction and damage, delayed recovery, and death. Mistakes are not necessarily reversible, and death can occur suddenly, and often without warning when patients are not appropriately monitored.

The goal of anesthetists should be to manage the risks associated with anesthesia and the perioperative period, affording patients the best chance of a successful outcome. Risk management is a term developed by the insurance industry and adopted by the healthcare industry to describe processes used to prevent injury, litigation, and financial loss. The real aim of this process is to use analysis of adverse events to prevent similar injuries to subsequent patients.

Risk management starts with an unbiased and nonjudgmental review and analysis of all “critical events” causing real or potential patient harm. The next step is formation or modification of standard operating procedures. For example, in aviation, accident investigation begins with discovery of the facts by an independent board (National Transportation Safety Board) and then analysis and publication of the findings. There is also an anonymous reporting system (Aviation Safety Reporting System) that involves the documentation and analysis of events that were considered hazardous by the participants but did not lead to an accident. These aviation review procedures provide a model for the improvement of anesthesia safety in both human and veterinary medicine. A commitment to the highest quality patient care will ultimately lead to the routine performance of such analyses by medical providers.

Advances in medical technology and pharmacology, as well as the increase in training of anesthesiologists, veterinarians, and licensed technicians, have done much to decrease the inherent risks associated with anesthesia. The risk of anesthetic-related death in people is estimated at between 1:10,000 and 1:200,000. The rate of anesthetic-related death among dogs and cats anesthetized in private practice has been assessed at approximately 0.1%. When interpreting studies of comparative anesthetic-related morbidity and mortality, it should be remembered that the definitions of the anesthetic period may vary and often include additional surgical and disease risk factors.

Based on clinical experience, the small animal patients that are associated with a high risk of adverse outcome from anesthesia and surgery include geriatric (especially hyperthyroid) cats; posttrauma cases with pulmonary pathology, hemothorax, or pneumothorax or pulmonary hemorrhage; and cases of acute head trauma and severe intra-abdominal hemorrhage. Patients requiring a high level of care and commitment to achieve a good outcome include neonates; those with low body weight or morbid obesity; and patients undergoing portosystemic shunt occlusion or cardiac, intracranial, or intraocular surgery.

Hemorrhage and fluid loss

Blood loss during surgery may be insidious or obvious. Body fluids may also be lost during surgery to transudation, sequestration, or evaporation. Extravasation of fluid to a nonfunctioning or sequestered edema space is commonly referred to as loss to the third space, the first and second spaces being the intracellular and extracellular spaces. These losses may reduce circulating blood volume significantly. Regardless of cause or route of loss, a decrease in circulating blood volume is not well tolerated by anesthetized patients.

Quantifying blood loss is important but can be difficult, so the severity of hemorrhage is often assessed by its impact on the patient. Severe blood loss causes tachycardia, reduced arterial pressure, pale mucous membranes, decreased pulse pressure, and decreased area under the arterial pulse wave. Packed cell volume decreases only during resuscitation or as fluid shifts into the vascular space, but base deficit increases as changes in bicarbonate and venous pH correlate with blood volume lost. Physiological responses to blood loss may be blunted or masked by anesthetic and anesthetic adjunctive drugs (e.g., alpha₂ agonists or high doses of fentanyl), further emphasizing the need for appropriate monitoring for early detection and correction of hypovolemia.

Shed blood can be replaced with crystalloids or colloids (e.g., plasma, hemoglobinbased oxygen-carrying solutions, dextrans, whole blood, or a combination of these solutions). In most situations, hypertonic solutions do not seem to have a distinct advantage over isotonic crystalloid solutions. Crystalloid solutions such as lactated Ringer’s, Plasmalyte (Baxter, Deerfield, IL), or Normosol (Hospira, Lake Forest, IL) are usually administered at threefold the volume of shed blood, as a rough guideline for resuscitation. The main advantage of crystalloid solutions is their low cost. Colloid solutions such as whole blood, plasma, hydroxyethyl starch, and hemoglobin-based oxygen carriers can be used as a substitute for crystalloids. Hemoglobin-based oxygencarrying solutions (e.g., Oxyglobin, OPK Biotech LLC. Cambridge, MA) are relatively expensive, but have a long shelf life and do not require crossmatching. The use of colloids has the advantage of sustaining colloid osmotic pressure while preserving plasma volume, but has the disadvantage of being more expensive than crystalloid solutions.

Acute hemorrhage of greater than 20% of the blood volume or a decline in pack cell volume to less than 20% because of the combined effects of blood loss and crystalloid fluid administration can be treated with an appropriate mass of red blood cells by either transfusion of whole blood or packed red cells. Red blood cells are preferred because of the need for restoring adequate hemoglobin concentrations to carry oxygen to the tissues. Smaller amounts of surgical hemorrhage, not associated with severe decreases in the hemoglobin concentration, can be managed with crystalloids (e.g., lactated Ringer’s) or colloids rather than red blood cells.

Cardiac dysrhythmia

Most dysrhythmias are caused by preexisting medical conditions, administration of premedications, anesthesia induction and maintenance agents, and surgical stimulation. Dysrhythmias require treatment if they reduce cardiac output, cause sustained tachycardia, or are likely to initiate dangerous ventricular dysrhythmias.

Canine gastric dilation/volvulus, splenic tumors, or multiple traumas often precipitates dysrhythmias that may require treatment prior to induction of anesthesia. Dysrhythmias following gastric dilation/volvulus presumably have their origin in acid–base imbalance, electrolyte disturbance, myocardial ischemia, circulating cardiac stimulatory substances, and/or autonomic nervous system imbalance. Treatment involves correcting phy siological abnormalities and administering lidocaine or procainamide. It is absolutely imperative that ventricular premature contraction s (VPCs) be differentiated from ventricular escape beats before administration of antiarrhythmic drugs, because suppression of an escape rhythm can cause immediate asystole and death. If the sinus rate is low, an intravenous atropine injection of 0.02mg/kg may increase the sinus rate and invoke overdrive suppression, which may inhibit the dysrhythmia. VPCs and ventricular tachycardia resulting from a traumatized myocardium are commonly treated during the perioperative period with lidocaine or procainamide. If possible, surgery should be delayed 2–4 days or until the dysrhythmias have subsided.

Several popular drugs used as preanesthetic medication can predispose patients to conduction abnormalities. Atropine or glycopyrrolate can cause sinus tachycardia and increase myocardial work and oxygen consumption. Phenothiazine tranquilizers reportedly predispose the heart to sinus bradycardia, sinus arrest, and, occasionally, first-degree and second-degree heart block, although it has also been shown to protect against VPCs. Xylazine may cause bradycardia and second-degree atrioventricular blockade and decreases the epinephrine threshold for VPCs. The μ-receptor agonist opioids morphine, hydromorphone, fentanyl, and oxymorphone will also precipitate a slowing of heart rate via increased vagal efferent activity. The anesthesia induction agents thiopental and ketamine have been reported to increase the likelihood of dysrhythmia formation after epinephrine administration during halothane anesthesia. This multidrug interaction has also been described for thiopental and isoflurane.

Other factors responsible for the development of the dysrhythmias during the surgical period include altered arterial carbon dioxide partial pressure (PaCO₂), altered PaO₂, altered pH, and autonomic reflexes from surgical manipulation, as well as central nervous system disturbances and cardiac disease. Because most perioperative dysrhythmias do not seriously affect cardiac output, treatment can be discrete. Changing to a different inhalation anesthetic, using intermittent positive pressure ventilation or increasing the depth of anesthesia may eliminate the dysrhythmia. Other treatments for controlling ventricular dysrhythmias include correcting blood gas abnormalities or administering a small quantity of intravenous lidocaine (0.5 mg/kg) or procainamide (1.0mg/kg).

Allergic reactions involving anesthetics are uncommon but could occur after sensitization to a drug. Allergic or anaphylactic reactions are mediated by the immune system. They are more commonly associated with repeated exposure to an allergen, but cross-reactivity may be seen with some preexisting allergies (e.g., allergies to eggs and to egg proteins in propofol). Anaphylactic reactions following thiopental administration have been reported. Intravenous injection of the intravenous contrast agent diatrizoic acid (Hypaque, Amersham Health, Princeton, NJ) has caused tachypnea, bronchoconstriction, and mucoid diarrhea in dogs. Allergic reactions are treated with intravenous fluids, antihistamines, and corticosteroids. Epinephrine should be administered in severe reactions accompanied by severe bronchoconstriction or cardiovascular collapse. Many unexpected responses to anesthetic and anesthetic adjunctive drugs have been labeled as “allergies” by veterinarians; however, proper diagnosis is crucial because it may have serious ramifications for future anesthetic delivery.

Successful treatment of cardiac arrest requires early diagnosis. Because of its high metabolic requirements, the brain is the organ most susceptible to hypoxia or ischemia. Serious brain injury develops after only 4–5 minutes of cardiac arrest. The brain injury can be multifactorial, including the rapid loss of high-energy phosphate compounds during ischemia, cell structural damage during reperfusion, progressive brain hypoperfusion especially in certain areas, and suppression of protein synthesis in selectively vulnerable neurons. Once the diagnosis of cardiac arrest has been confirmed, all efforts must be toward restoration of effective oxygen delivery and reestablishing a heartbeat. Cardiopulmonary resuscitation (CPR) with external cardiac massage appears to be ineffective in protecting the brain from injury and should be only part of the initial resuscitation protocol. If not quickly successful, time should not be wasted with external CPR in lieu of more effective, but more invasive, internal techniques.