Anesthesia and Restraint of the Horse during Laparoscopy and Thoracoscopy

Minimal Invasive Surgery in Standing Horses: Chemical Restraint

Minimal invasive surgery can be successfully performed in standing horses (Fig. 1), once a desirable degree of sedation has been achieved through the use of tranquilliser and sedative drugs, and their combination with opioids. There are many sedative and tranquillisers available for use in horses, but in some countries access to these drugs may be limited. This article will describe some of the commonest means of chemical restraint. For insertion of trocars, local anesthetic drugs, such as lidocaine, can be infiltrated into the abdominal or thoracic wall at the point of trocar insertion.

Figure 1. Laparoscopic surgery on a standing horse sedated with detomidine and methadone. Dept. of Large Animal Surgery, Veterinary Medical Faculty, Leipzig, Germany.

Tranquillisers

Acepromazine

Alone, acepromazine may not provide enough sedation for surgical procedures and certainly does not provide analgesia. Acepromazine can be combined with a number of opioids to intensify the degree of sedation, and for analgesia. Draught horses may be more sensitive to the action of tranquillisers and it has been recommended that the dose is reduced to half of the recommended dose for other horses. The incidence of priapsim in male horses is of the order 1:10,000, but it is advisable to avoid using acepromazine in breeding stallions.

Sedatives

Alpha2 Adrenergic Agonists

Drugs such as xylazine, detomidine and romifidine can successfully be used to sedate horses for standing surgery. The onset of action is within 1 - 3 minutes when administered intravenously. These drugs produce transient hypertension and bradycardia, followed by mild hypotension. Effects on the respiratory system are mild, but care should be taken in horses with upper airway obstruction because the muscle relaxing properties of the alpha2 adrenergic agonists can exacerbate the condition. Xylazine provides the shortest duration of effect (30 - 60 minutes), and the duration of effect from detomidine is longer (60 - 150 minutes). Analgesic effects usually last approximately half of the duration of the sedative effects. Alpha2 adrenergic agonists also produce more muscle relaxation than acepromazine, and horses sedated with alpha2 adrenergic agonists tend to become ataxic. A better effect (reduced ataxia, improved analgesia and sedation) can be obtained if the alpha2 adrenergic agonists are combined with an opioid.

Opioids

These drugs provide analgesia and sedation in combination with either acepromazine or alpha2 adrenergic agonists. They are best not used alone since they can produce excitement in some horses. There are two classes of opioids commonly used in horses. The partial agonist group comprises of butorphanol and the older drug pentazocine, whereas the agonist group consists of morphine, methadone and meperidine (pethidine). Both groups of drugs should be used in combination with tranquillisers and sedatives.

Combinations

Combinations of acepromazine with an opioid tend not to provide as much sedation as alpha2 adrenergic agonist combinations, but may not cause as much ataxia. Most clinicians select a combination of alpha2 adrenergic agonist with an opioid. In lengthy procedures it may be better to select a long acting alpha2 adrenergic agonist (detomidine, romifidine) in combination with a long acting opioid (methadone, morphine, butorphanol). When the shorter acting xylazine is used in combination with morphine or methadone, some excitement may be observed as the xylazine effects wear off, another half dose of xylazine can be administered at this point. The cardiopulmonary effects of xylazine (0.66 mg/kg) and morphine (0.66 mg/kg) include a 25% decrease in cardiac output during the first 30 minutes, but this returns to normal after 45 minutes. Arterial blood gases do not change significantly. Combinations of xylazine/butorphanol may not induce as much central nervous system depression, but a similar degree of analgesia is produced compared to the xylazine/morphine combination. With this mixture, a decrease in cardiac output is produced which lasts for less than 15 minutes, and no adverse effects on the respiratory system. The detomidine (1.1 mg/kg)/butorphanol (0.1 mg/kg) combination has been found to produce reliable sedation and analgesia with no significant adverse effects on the cardiopulmonary systems. Detomidine (0.01 mg/kg)/morphine (0.1 mg/kg) combinations have been found to produce more cardiovascular side effects and may be less reliable. In difficult horses, a combination of acepromazine, alpha2 adrenergic agonist and opioid may be used, the use of acepromazine may also reduce the incidence of dysphoria during the waning effects of the alpha2 adrenergic agonist. For lengthy procedures a jugular catheter should be placed and intravenous fluid therapy administered at 5 ml/kg/hr.

Equine General Anesthesia

There are a number of valuable textbooks available that describe equine anesthesia in depth and the salient points as regards minimal invasive surgery will be described in this article. The reader should consult texts on equine anesthesia for further details if necessary. As with any patient to be anesthetised, a full physical examination, bodyweight measurement and history from the owner should be obtained in order to ascertain the health status of the horse. The health of the patient has a great influence on successful outcome from anesthesia. The cardiopulmonary systems should be thoroughly examined as these systems are placed under much stress during anesthesia, and their ability to compensate for physiological derangements should be assessed.

Laparoscopic surgery requires that the gastrointestinal system is emptied as much as possible and many horses are fasted for as long as 24 hours. Since this duration of fasting represents an abnormal state for a horse used to grazing there may be problems with acid/base balance and postoperative complications such as colic. By not starving the animal, however, the surgical procedure may become more difficult and take more time, thus increasing the risk of complications from general anesthesia.

The horse will require aseptical placement of a suitable 14G or 12G over-the-needle catheter into a jugular vein prior to induction of anesthesia. Whether the catheter is placed before premedication or after depends on the temperament of the horse. Alpha2 adrenergic agonists are a good choice for premedication and which one to use largely reflects clinician preference. This author still prefers to use intravenous xylazine to premedicate (Fig. 2), but will switch to intramuscular detomidine in difficult horses. Since intramuscular use of alpha2 adrenergic agonists can produce variable effects, the horse may require a further dose of the drug administered intravenously to achieve a suitable degree of sedation.

Figure 2. Sedated horse in padded induction room after xylazine (0.5 mg/kg bwt IV).

Any suitable anesthetic induction regime can be used and the dosages can be obtained from Table 2. Although the use of guaifenesin helps to relax the horse through its action on skeletal muscle especially if the horse is to be hoisted (Fig. 3), its use may accentuate the intraoperative hypotension which occurs in many anesthetised horses. Therefore, the clinician should be aware of this and have suitable treatment for hypotension regimes ready. Ketamine is probably the commonest induction agent used in horses following adequate sedation from premedicant drugs (Fig. 4).

Figure 3. Horse receiving 5 % guaifenesin to effect (until there is swaying on the hind-end) prior to administration of ketamine for induction of anesthesia.

Figure 4. Horse after induction of anesthesia with ketamine (2 mg/kg bwt IV).

To prolong anesthesia for lengthy procedures it is better to use inhalational anesthesia such as halothane or isoflurane. The airway is protected with the use of an endotracheal tube and oxygen is administered as a carrier gas for the anesthetic agent thereby increasing the safety of anesthesia. Positive pressure ventilation can be provided by squeezing the rebreathing bag, or with the use of a ventilator. Ideally, monitoring of patient vital signs and anesthetic depth should involve an experienced clinician or technician, and include the use of direct blood pressure measurement, capnography, and measurement of hemoglobin/oxygen saturation.

Capnoperitoneum and General Anesthesia in the Horse

Carbon Dioxide as the Insufflation Gas

Carbon dioxide is often used as the insufflating gas because it does not support combustion and can therefore be used with electrocautery, unilke nitrous oxide or air. Nitrous oxide or nitrogen may also produce dangerous gas emboli, whereas carbon dioxide is more soluble and the risk of gas embolism is decreased. Carbon dioxide, however, because of its high solubility is rapidly absorbed across the body cavity lining and is transported in the circulation in the same way as endogenous carbon dioxide. It is therefore excreted at the level of the lungs and can produce a state of hypercarbia if pulmonary ventilation is not adequate. In the spontaneously breathing conscious patient, the respiratory drive within the brain is stimulated and hypercapnia is not a problem, unless abdominal distenstion is severe. Under anesthesia, however, positive pressure ventilation is necessary in order to maintain normocapnia. Hypercapnia may have detrimental effects by by increasing the amount of circulating catecholamines. Catecholamines may produce cardiac arrhythmias in the presence of cardiac sensitising anesthetic agents such as halothane. Direct effects of carbon dioxide on vascular smooth muscle produce vasodilatation and increased blood loss at the operating site. The uptake of carbon dioxide into the circulation is dependent on the gas' solubility and the perfusion of the peritoneal lining, and not on the rate of insufflation. Most carbon dioxide absorption and hemodynamic changes occur in the first fifteen minutes of insufflation.

The Physical Effects of Capnoperitoneum

Administering a gas into the abdominal cavity causes more cranial movement of the diaphragm and enhances the formation of areas of atalectic lung which can decrease the state of oxygenation of the patient. The use of intermittent positive pressure ventilation is important in order to maintain a state of normocapnia, but the use of a ventilator may decrease venous return to the heart therefore this may need to be addressed with the use of intravenous fluid therapy (10 - 20 ml/kg/hr). The abdominal pressure should be kept to a minimum as increasing abdominal pressure causes more distention which will cause hypoventilation in spontaneously breathing patients. It is recommended that intra-abdominal pressure should not increase beyond 20 mmHg, and should preferably be kept around 12 - 15 mmHg in horses.

A capnogram is useful to follow trends in anesthetised patients, but end-tidal CO2 values may not accurately reflect arterial CO2 values and a capnogram may not be accurate enough to guide ventilation. It has been found that anesthetised horses without capnoperitoneum have a PaCO2 - PACO2 gradient in the order of 11 mmHg. With capnoperitoneum this gradient can increase to over 15 mmHg in horses. It is therefore recommended that arterial blood gas analysis be used to help make decisions on anesthetic management in horses with capnoperitoneum.

The above effects can result in hypoxemia and hypercarbia, therefore high inspired O2 concentrations should be used in anesthetised horses. Hypercarbia can be exaggerated by the administration of CO2 into the abdomen.

Blood volume can decrease in anesthetised horses due to intercompartmental fluid shifts, blood pooling in dependent areas of the body, intraoperative hemorrhage, and fluid loss from body surfaces. Hypotension can also result from decreased vasomotor tone and cardiac contractility. As explained earlier, intermittent positive pressure ventilation can decrease venous return.

With capnoperitoneum, the increase in intra-abdominal pressure can obstruct venous return in hypovolemic animals, especially if the intra-abdominal pressure is higher than 20 mmHg. Some studies, however, have indicated an increase in cardiac output during capnoperitoneum and has been attributed to redistribution of blood from abdominal organs to the central circulation, but high intra-abdominal pressures will reduce cardiac output. High intra-abdominal pressures can also increase systemic vascular resistance and therefore decrease cardiac output by increasing afterload. Higher systemic vascular resistance is again, usually observed when the intra-abdominal pressure exceeds 20 mmHg (Fig. 5).

Figure 5. Insertion of a trocar into the abdomen of an anesthetised horse.

Healthy, anesthetised horses tolerate capnoperitoneum during anesthesia fairly well, but attention should be made to ventilatory and hemodynamic support (fluid therapy, inotropes), providing high inspired concentrations of oxygen and keeping intra abdominal pressure below 15 mmHg. Fluid therapy should be provided at a rate of 10 - 20 ml/kg/hr, and inotropes such as dobutamine used at an infusion rate of 0.5 - 2 mcg/kg/min.

Head-down Tilt in the Dorsally Recumbent anesthetised Horse

Tilting anesthetised humans with capnoperitoneum to a head-down position tends to produce an increase in mean arterial blood pressure and a decrease in cardiac output (Fig. 6).

Figure 6. Laparoscopic surgery in a horse tilted head-down. Western College of Veterinary Medicine, Saskatoon, Canada.

The decrease in cardiac output is thought to be produced by activation of carotid baroreceptor reflexes. Preliminary studies in anesthetised horses with a capnoperitoneum to an intra-abdominal pressure of 12 mmHg have shown that the decrease in cardiac output produced by introducing capnoperitoneum was partially restored by tilting the horse head-down. This may have been due to increased venous return from gravitational effects and the effects of the increased intra-abdominal pressure squeezing blood from viscera into the systemic circulation. The restoration in cardiac output, however, may not be evident if higher intra-abdominal pressures are used. The weight of the abdominal organs on the diaphragm which compresses the lungs causes an increase in ventilation/perfusion mismatch and thus an increase in arterial carbon dioxide and decreased arterial oxygen partial pressures. The time the horse spends in a head down position should therefore be kept to a minimum. During lengthy procedures it is advisable to monitor arterial gases with a blood gas analyser.

Pain Control

The use of CO2 as the insufflation gas can cause postoperative discomfort in horses. This discomfort is due to the formation of carbonic acid from CO2 dissolving the fluid within the abdominal cavity. Discomfort can be eased with the use of flunixin meglumine and/or small doses of xylazine.

Complications

Head-down position

Horses undergoing head down tilt tend to develop severe congestive edema of the head (Fig. 7). Attention should be made to protection of the eye and eyelids, and consideration made for the recovery period. Nasopharyngeal tubes can be preplaced before tilt down and left in for recovery in order to provide an airway. Alternatively, the horse can be nasotracheally intubated from the start and recovered with the nasotracheal tube in place, or recovered with an orotracheal tube in place (Fig. 8).

Figure 7. Edema of the eyelids in an anesthetised horse tilted head-down for one hour.

Figure 8. Placement of a nasopharyngeal tube in a horse recovering from anesthesia. An O2 line is placed in the tube for the early recovery period.

Gas Embolism

Small amounts of insufflation gases are absorbed with little problem. If large amounts gain access to the central venous system through open venous channels, or if the splanchnic blood flow is reduced by excessive intra abdominal pressure or peripheral vasoconstriction, severe hemodynamic and respiratory compromise can occur. The presenting signs of a gas embolus are: Sudden and profound decrease in blood pressure, cardiac arrhythmias, a "mill-wheel" or other sudden heart murmur, cyanosis, pulmonary edema, and a sudden reduction in end tidal carbon dioxide. High intra abdominal pressures greater than 20 mmHg favour gas emboli formation.

Rapid intervention is important. The abdomen should be deflated, and the patient placed head down. Intravenous access to the central circulation is necessary to remove gas from the heart, or a fast thoracotomy performed in order to access the heart chambers directly to remove gas. Other conditions which may produce similar signs include: Pulmonary embolism, pneumothorax, pneumomediastinum, excessive intra abdominal pressures, and profound vasovagal reflex.

Gastric Reflux

In anesthetised patients, the increase in intra abdominal pressure may be enough to increase the risk of passive reflux of gastric contents. The airway should be secured with a cuffed endotracheal tube. A nasogastric tube may be preplaced before anesthetic induction to redirect any stomach contents away from the pharyngeal area.

Carbon Monoxide

The use of cautery under the hypoxic conditions found within the abdominal cavity can produce carbon dioxide. Studies performed in humans have found that carboxyhemoglobin concentrations do not markedly increase, but the released gases from desufflation may increase the environmental levels of carbon monoxide, therefore operating theatres should be well ventilated.