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Perianesthetic Considerations

courtney-peck-ecc-webCourtney Peck, DVM, DACVECC
www.angell.org/emergency
emergency@angell.org
781-902-8400
MSPCA-Angell West, Waltham

Over the past decade, there have been significant advances in the use of analgesia and anesthesia in veterinary medicine. Routine sedation and anesthesia have become progressively more familiar and safer, and as a result, they are widely used in our patient population. While the vast majority of sedated or anesthetized pets recover without incident, potentially preventable complications continue to occur. Nonfatal complications occur more frequently than fatal complications, but nonfatal complications are also underreported in veterinary literature.  The incidence of nonfatal complications has been reported to range from 2 to 10%. The most commonly reported complications involve the respiratory, cardiovascular, renal, gastrointestinal, and neurologic systems. Recognizing these risks and incorporating preemptive perianesthetic strategies into our daily practice will ultimately reduce potential adverse outcomes in patients undergoing sedation and/or anesthesia.

Anti-emetics

Many of the commonly used drugs for sedation/anesthesia stimulate the central emesis centers (chemoreceptor trigger zone, vomiting center). Opioids (hydromorphone, oxymorphone, morphine, fentanyl) commonly will cause nausea, regurgitation, and vomiting; however, alpha-2 agonists (medetomidine, xylazine) are also noted to act as emetics. The risk of regurgitation in dogs without predisposing factors has been reported to range between 0.42% and 5.5%. A recent study (Lamata et al, Vet Anaesth and Analgesia, 2012) found that dogs undergoing orthopedic surgery were 26.7 times more likely to regurgitate compared to dogs undergoing diagnostic procedures. Interestingly, dogs that weighed more than 40 kilograms were five times more likely to regurgitate than those weighing less than 20 kilograms. Gastroesophageal reflux, which is often clinically silent and can lead to significant esophageal mucosal damage, has been reported in 16% to 60% of dogs. Even in otherwise healthy and stable patients, the administration of sedation or anesthetic drugs increases the risk of regurgitation and vomiting as well as sequelae such as aspiration pneumonia. These adverse effects can increase morbidity and mortality in pets.

Anti-emetic therapy such as maropitant (Cerenia) has been shown to reduce nausea and vomiting in dogs receiving hydromorphone. When given subcutaneously 60 minutes prior to administration of pre-anesthetic doses of hydromorphone, maropitant significantly reduced nausea and vomiting (Hay Kraus, JAVMA 2014). Use of pre-anesthetic anti-emetic therapy is strongly recommended to prevent perianesthetic nausea, gastroesophageal reflux, regurgitation, and vomiting.

Compassion-dog-Pets-peoplePre-oxygenation

The most common respiratory complications reported in association with veterinary anesthesia are hypoxemia (PaO2 < 60 mmHg) and hypoventilation/hypercapnia (PaCO2 > 60 mmHg). Previously reported rates of respiratory complications ranged from 0.35 to 0.5%; however, a more recent study (Redondo et al 2007) found 60% of anesthetized dogs experienced hypoventilation, and 16% experienced hypoxemia. Use of supplemental oxygen increases a patient’s PaO2 and enhances oxygen delivery to tissues. Pulse oximetry is an easy and non-invasive way to monitor a patient’s oxygenation status and response to oxygen supplementation. Any patient that has the potential to experience hypoxemia in the perianesthetic period (brachycephalic breeds, underlying airway or pulmonary pathology, pregnant individuals) should be pre-oxygenated for at least 5 minutes prior to induction. Continuous monitoring of the SpO2 (or PaO2) should be implemented in sedated/anesthetized patients, as well as during recovery.

Hypothermia

There are many predisposing factors and causes for hypothermia in the perianesthetic period; in human medicine, prolonged post-operative hypothermia is associated with increased mortality. A large surface area to mass ratio, prolonged preparation time, inadequate patient warming, homeostatic depressant effects of general anesthesia, length of anesthesia, and length of procedure are all contributing factors to the disruption of thermoregulation. Hypothermia results in multiple consequences, including alterations in vasoconstriction, coagulation, cardiac function, hepatic function, renal function, CNS function, and wound healing.

Cutaneous vasoconstriction is the normal response of the body to hypothermia; this results in decreased cutaneous perfusion and extremity hypoxia. With the development of mild hypothermia (temperature 90˚F to 99˚F), catecholamine release leads to an increase in heart rate and blood pressure. Hypothermia can alter cardiovascular microcirculation, resulting in arrhythmias. Severe hypothermia (temperature below 82˚F) lowers the vascular response to catecholamines as well as baroreceptor responsiveness, leading to bradycardia, hypotension and decreased cardiac output. Hypothermia reduces hepatic metabolism, resulting in prolongation of anesthetic effects as well as delayed recovery from anesthesia. Renal effects of hypothermia include alterations in glomerular filtration rate, renal blood flow, and tubular damage in severe hypothermia. These result in renal changes ranging from a transient cold diuresis to acute kidney injury. Mild hypothermia also causes prolonged platelet aggregation, leading to increased surgical hemorrhage and potential need for transfusions. While mild hypothermia has been shown to be beneficial in protecting the CNS from ischemic injury during resuscitation, it also reduces cerebral blood flow and alters cerebral autoregulation, leading to alterations in CNS function. For every decrease in body temperature by 1.8˚F, cerebral blood flow decreases by 6 to 7%. Severe hypothermia leads to mentation changes ranging from mild depression to coma.

There are a variety of options for managing hypothermia in the perianesthetic period; combinations of these methods can be used to optimize patient care. Passive surface rewarming is used to prevent continued heat loss from a patient; placing blankets between the patient and the surface upon which they are positioned as well as over the patient will reduce heat loss by up to 30%. Active surface rewarming involves increasing the air temperature around the patient, to reduce the gradient between the patient and their surroundings and thus decrease heat loss. Active warming prior to induction of anesthesia helps to reduce heat loss during anesthesia and recovery. Methods used in this type of warming include warm water bottles, circulating warm water blankets, and forced air warming blankets. A protective barrier (such as a blanket) should always be placed between the patient and these devices to prevent thermal burns; electric heating pads should not be used due to a high incidence of burn injuries. Active core rewarming is used to provide heat internally to rapidly warm the body core. Examples of this method include warm peritoneal/pleural lavage, warm water enemas, and heated and humidified inspired air.

Maintaining normothermia, or managing hypothermia so it remains mild, are effective ways to reduce perianesthetic complications. A patient’s temperature should be monitored closely until they have reached normothermia to prevent adverse sequelae of body temperature derangements.

Patient positioning

The effect of patient positioning on respiratory function should be taken into account during the perianesthetic period. Pulmonary perfusion and ventilation are affected by gravity as well as by body positioning, with dependent lung lobes experiencing better ventilation. Atelectasis and small airway collapse caused by prolonged recumbency can exacerbate underlying pulmonary compromise and hypoxemia. Rozanski et al (Can J Vet Research 2010) evaluated the effect of body position and sedation on pulmonary function in healthy dogs, and found that right lateral recumbency decreased functional residual capacity (FRC, the volume of air within the lungs after a normal expiration) by a median of 20.4 mL/kg. Sedation alone resulted in a median decrease in FRC of 19.8 mL/kg. McMillan et al (JVECC 2009) found that patients in sternal recumbency had a significantly increased PaO2 compared with those in lateral recumbency. This improvement was due to improved pulmonary oxygen uptake. Maintaining sternal recumbency in patients during the perianesthetic period is recommended to support pulmonary function and reduce complications.

Creating and executing perianesthetic protocols which focus on anti-emetic use, pre-oxygenation, maintaining normothermia and sternal recumbency will reduce complications and patient morbidity and mortality. While we often focus on the preanesthetic and anesthetic periods as carrying the highest risk of complications, The Confidential Enquiry into Perioperative Small Animal Fatalities (CEPSAF) recently reported the post-operative period as the most common time for anesthetic-related deaths in cats, dogs and rabbits. Close, frequent monitoring of patients until recovery is complete is an essential part of perianesthetic care.

 

For more information about Angell’s Emergency/Critical Care service, please visit www.angell.org/emergency or call MSPCA-Angell West in Waltham at 781-902-8400.

 

Further reading:

Lamata C, Loughton V, Jones M et al. The risk of passive regurgitation during general anaesthesia in a population of referred dogs in the UK. Vet Anaesth Analg 2012; 39: 266-274.

Rozanski E, Bedenice D, Lofgren J et al. The effect of body position, sedation, and thoracic bandaging on functional residual capacity in healthy deep-chested dogs. Can J Vet Res 2010; 74(1): 34-39.

Armstrong S, Roberts B, and Aronsohn M. Perioperative hypothermia. JVECC 2005; 15(1): 32-37.

Brodbelt D, Flaherty D, and Pettifer G (2015). Anesthetic risk and informed consent In KA Grimm (Ed.), Veterinary Anesthesia and Analgesia (pp.11-22). Wiley Blackwell.