Species Specific Anaesthesia - Horses PDF

SPECIES SPECIFIC ANAESTHESIA - HORSES MIMV 3rd year – 1st semester 15 October 2024 Ricardo Felisberto, DVM, Dipl. ECVAA, MRCVS  CLINICAL EXAMINATION Pertinent history should be obtained from the caregivers: Age Vaccination status Concomitant i...

SPECIES SPECIFIC ANAESTHESIA - HORSES MIMV 3rd year – 1st semester 15 October 2024 Ricardo Felisberto, DVM, Dipl. ECVAA, MRCVS  CLINICAL EXAMINATION Pertinent history should be obtained from the caregivers: Age Vaccination status Concomitant illnesses and treatments Clinical examination: thoracic auscultation; mucous membranes colour and capillary refill time, peripheral pulses strength and synchronic with heart beats. Horses are driven by their sympathetic nervous system (fight or flight response) – they tend to try to escape if they are in a strange environment Chemical restraint is usually essential for horses as physical restraint can be difficult  HEART MURMURS Physiological murmurs: Become more intense after mild exercise; located over the aortic and pulmonic valves. Systolic grade I to II soft murmurs Can also occur in anaemic horses due to lower blood viscosity; and hyperdynamic cardiovascular state due to increased sympathetic outflow in sepsis. Young racehorses: Usually have tricuspid and mitral valve regurgitation Usually low grade systolic murmurs The heart is hypertrophied with exercise, but the valve leaflets do not grow further, therefore, the valves become leaky as the valve rings stretch Aortic regurgitation: Occurs in middle aged to older animals. Diastolic murmur over aortic region or systolic over mitral valve region. Left ventricle becomes volume overloaded (due to aortic regurgitation), gets hypertrophied (eccentric), the chamber dilates, leading to secondary mitral valve regurgitation. Bounding pulses occur, due to diastolic run-off of blood from the aorta back to the left ventricle (large pulse pressure, or difference between systolic and diastolic pressure)  HEART MURMURS Mitral valve regurgitation: Systolic murmur over the mitral valve region May be secondary to bacterial endocarditis Tricuspid regurgitation may develop due to pressure overload on the right heart as a consequence of volume overload on the left heart. Tricuspid regurgitation: Systolic murmur over the tricuspid valve Can be physiologic in racehorses, but may be secondary to mitral valve regurgitation or to other causes of pulmonary hypertension (as chronic respiratory disease) Right atrial enlargement can develop and lead to the development of atrial fibrillation Ventricular septal defects: Pansystolic murmur; systolic ejection murmur is also heard over the pulmonic valve Common congenital defect in small pony breeds (Shetlands, Welsh section A) Often located in the membranous portion of the interventricular septum beneath the tricuspid valve area on the right side. Left to right shunting of blood through the defect causes the loudest murmurs  SEDATION AND PREMEDICATION The sedation or premedication plans should consider the patient’s temperament and degree of excitement Try to calm the patient as much as possible (calm environment!) Use other routes rather than IV if difficult to handle (IM or oral transmucosal) Patient’s physiological condition (concurrent illness, pregnancy) Available personnel and their experience (ability to help) Facilities and environment Degree of sedation / duration of effect Your own familiarity with the drugs Patients weight  SEDATION AND PREMEDICATION Consider what are the procedures: Sedation for clipping (excessive sweating is not ideal – avoid too much α2 agonists) Sedation for boxing or travelling: duration of the journey Sedation for laryngeal endoscopy (excessive α2 agonists = may lead to reduced laryngeal movement) Sedated horses are not to be trusted, they may still be rousable and hurt you and the staff. Consider training the horse to be minimally restrained in a box before the elective procedures If the horse is too temperamental, any procedure should be performed under general anaesthesia Consider the legislation (licensed products): Allowed annex: Regulation - 37/2010 - EN - EUR-Lex (europa.eu) Essential list: Regulation - 122/2013 - EN - EUR-Lex (europa.eu)  PHENOTHIAZINES Acepromazine: Licenced for horses in the EU injectable and oral gel (0.01 – 0.05 mg/kg) Unpredictable sedative / anxiolytic effect; can be improved with addition of opioid and/or α2 agonist Long onset of action 20minutes after IV; if IM or oral transmucosal 30 – 40 minutes (leave the animal undisturbed) Long duration of action (6h), but sedation may last for only 2h Produces hypotension due to α1 antagonistic effects Reduces locomotor activity caused by opioids (due to acepromazine anti-dopaminergic effects) According to CEPEF 2002: reduces anaesthesia-related mortality, due to: Sedative effects (smooths induction, maintenance and recovery from anaesthesia) Improves cardiovascular function (reduces cardiac afterload due to vasodilation, which improves cardiac output and muscle perfusion) Anti-arrhythimic effect (reduces myocardial sensitization to catecholamines effects) Anti-inflammatory and anti-spasmodic effects May cause priapism in 1 out of 10 000 stallions (due to vasodilation of the corpus cavernosum, and relaxation of the penile retractor muscle) May end up in penile amputation Requires massage, hydration, diuretics, mechanical support, benzatropine may also help  BENZODIAZEPINES Diazepam (0.01 – 0.2 mg/kg); Midazolam (0.01 – 0.2 mg/kg); Zolazepam + tiletamine Considered to be cardiovascular and respiratory system safe drugs (at higher doses may cause respiratory depression) Reduce anaesthetic agent requirements May cause dis-inhibition (increased uncoordinated movement / ataxia), thus they tend not to be used for standing sedation Useful adjunct for ketamine induction of anaesthesia (to promote muscle relaxation and avoid excessive muscle contraction induced by ketamine) Foals: are less bothered or stressed if incoordination is induced, and attain recumbency calmly after benzodiazepines. Anti-convulsive drugs Antagonist: flumazenil (short half-life, may need to be repeated) 0.01 mg/kg IV  α2-AGONISTS Sedative, analgesics with muscle relaxant properties Licenced in horses: xylazine (0.25 – 1.1 mg/kg IV); detomidine (0.005 – 0.08 mg/kg IV or IM); romifidine (0.025 – 0.1 mg/kg IV) Medetomidine and dexmedetomidine (0.0035 – 0.01 mg/kg IV) Administer doses of the lower end to large breeds as they are more sensitive / allometric scaling should be used (larger breeds = relatively smaller body surface areas and slower metabolic rates) Reliable sedation (but still rousable), characterised by ptosis, head-lowering, drooping of lower lip, ataxia, penile protrusion. Addition of an opioid enhances sedation Muscle relaxation (ataxia) – may interfere with evaluation of laryngeal paralysis General anaesthetics sparing effect Analgesia (similar mechanism to opioids) Endocrine effects (reduce insulin, hyperglycaemia, reduced anti-diuretic hormone release thus increased diuresis) Causes sweating Uterine muscle contraction (↑ uterine pressure) and reduced uterine blood flow (induces foetal stress): In non-gravid uterus, xylazine causes higher intra-uterine pressure; romifidine has the lowest effect. In gravid uterus detomidine (0.02 mg/kg) reduces electrical activity of the uterine muscle (intra-uterine pressure doesn’t increase). But all α2-agonists are not recommended for pregnant mares at the last third of prengnancy (unless clenbuterol 800 ng/kg IV is administered, which reduces the α2-agonists effects) Reduces GI motility (ileus) (reduced gut perfusion), but analgesia may avoid ileus development Hypothermia due to suppressed thermoregulation α2-agonist Xylazine Detomidine Romifidine Dose (IV) 1 mg/kg 0.015 mg/kg 0.08 mg/kg Onset of action 3 minutes 5 minutes 5 minutes Duration of action 20 minutes 80 minutes > 80 minutes Sedation +++ ++ + Muscle relaxation ++ +++ + Ataxia ++++ ++++ + Analgesia ++++ ++++ + Sweating Difficult to predict Intra-uterine pressure ++++ ++ + (non-gravid) Duration of intra-uterine + ++ + pressure Intra-uterine pressure ++++ -/+ ++ (gravid)  α2-AGONISTS Clinical uses: Continuous rate infusion to maintain sedation, analgesia, muscle relaxation for standing procedures Xylazine: 0.5 mg/kg/h; Detomidine: 0.005 – 0.02 mg/kg/h; Romifidine: 0.02 – 0.04 mg/kg/h; Medetomidine: 0.003 – 0.005 mg/kg/h. Premedication: to smooth induction, maintenance and recovery from anaesthesia. Top up at recovery can prolong recovery allowing enough time for elimination of the inhalant anaesthetic from the body, reducing chances of ataxia and dysphoria. Romifidine leads to delayed recovery of swallowing reflex, thus if you administer romifidine on recovery, don’t wait until the horse swallows to remove the ETT.  α2-AGONISTS Epidural administration: Can be administered with opioids, local anaesthetics. Causes analgesia, and prolongs blockade of local anaesthetics effects There is also systemic absorption from the epidural space, thus, ataxia may still develop even if they administered alone. Xylazine is greater analgesic than detomidine, possibly due to its α1-agonist effects too (local vasoconstriction = delayed systemic absorption + maintenance of high concentration of drug in epidural space → prolonged effect). Dose: 0.17 – 0.35 mg/kg +/- lidocaine 0.22 mg/kg  α2-AGONISTS Complications of α2-agonists: Hypertension and baroreflex bradycardia; if bradycardia is severe, can administer antagonist followed by anticholinergic (atropine, glycopyrrolate or hyoscine) In animals in shock, the cardiovascular effects of α2 agonists may cause severe tissue hypoperfusion Respiratory obstruction (prolonged sedation and head down = nasal oedema and obstruction) Diuresis (inhibition of antidiuretic hormone release) Sweating Ataxia (muscle weakness or relaxation) Increased intrauterine pressure Reduced GI motility (ileus) Large breeds are more sensitive to α2 agonists, therefore, lower doses must be administered  α2-AGONISTS Antagonism: The α2 agonists can be antagonised in case there are unwanted complications following their administration. However, by antagonising their unwanted effects, we also antagonise the analgesic effects Atipamezole (0.05 mg/kg IM or slow IV), has been used in horses, but it is not licenced, but it is in the essential list of drugs that can be administered to horses (EN 122/2013) Vatinoxan: It is a peripheral α2-receptor antagonist that doesn’t cross the blood brain barrier; thus, preventing the cardiovascular effects of the α2-agonists. Only licensed in dogs (Zenalpha®)  ANAESTHESIA Risk factors reported in horses: Size: larger horses = difficult to handle; risk of fractures are higher; higher risks of neuropathy or myopathy; higher risk for the development of hypoxaemia especially if at dorsal recumbency; more sensitive to drugs (relative overdose); also weight estimation may not be accurate. Breed: Draught horses (higher risk of developing spinal cord Malacia; myopathy); quarter horses (hyperkalaemic periodic paralysis); Welsh ponies (high prevalence of ventricular septal defects); Thoroughbred horses (high chances of fractures on recovery due to their fitness and temperament) Temperament: flighty horses will try to stand up quickly and run, this may lead to rough recoveries. Sex: stallions may have rough recoveries or develop priapism with ACP; pregnant mares are sensitive to α2-agonists. Age: young animals – immature physiology, higher risk of hypothermia; older horses – higher chances of osteoporosis and muscle weakness on recovery. Surgical time: long procedures = long recoveries and higher chances of complications. Time of the day of the procedure: out of hours procedures = less available staff, junior untrained staff, fatigue. Anaesthetic agents: lack of premedication = higher risks; Acepromazine = reduces mortality; isoflurane vs halothane = no major differences regarding mortality Health status: sick animals = higher mortality.  PREPARATION FOR ANAESTHESIA Clinical history, examination. Blood work baseline (PCV and TP at least). Food restriction: Horses cannot vomit, but they do regurgitate / develop reflux. Recommended starvation is 4 to 6h prior to anaesthesia with free access to fresh water , but there isn’t a consensus It is important to avoid a large stomach which can splint the diaphragm against the lungs (compression atelectasis) + stomach rupture when the horse falls on induction. Place IV catheter (jugular vein) Apply a specific theatre head collar Remove shoes to protect box floor and staff involved Mouth wash to remove debris Personal protective equipment Pre-anaesthetic medications (NSAIDs; Antibiotics IV) Premedication  INDUCTION OF ANAESTHESIA Safe induction area (padded box; soft ground; squeeze-gated padded induction area; padded tilt-table; on a Sling). Quality of induction is entirely dependent on: area; equipment; personnel and calm environment. Usually injectable option for adults; inhalant agents induction is an option for foals. Few licenced and authorised induction agents in horses (ketamine; midazolam; diazepam; thiopental; propofol)  INDUCTION OF ANAESTHESIA Ketamine: Dissociative agents with inhibitory and stimulatory effects at different parts of the CNS Takes 2 minutes for peak effect after IV injection Scheduled 2 drug (controlled, needs to be locked away and record keeping) Adequate sedation must be achieved prior to ketamine induction (otherwise, induction can be rough) → alpha 2 agonist-based premedication is essential Tap horses ears and make soft noise to see if horse reacts (minimal reaction = ideal for induction) Dose 2-3 mg/kg IV Co-induction: Diazepam or midazolam (0.02 – 0.05 mg/kg IV) (immediately before ketamine) Guaiphenesin (30 – 100 mg/kg) produces minimal cardiovascular depression as benzodiazepines. Apnoea may follow ketamine induction or irregular apneustic breathing (long inspiration short expiration) Minimal cardiovascular depression due to stimulation of sympathetic system (animals in shock = only negative inotropy effects) Maintenance of cranial nerves reflexes. Anaesthesia duration after IV bolus = 10 – 20 minutes Produces active metabolite (norketamine) that can produce dysphoria on recovery if larger ketamine doses were administered Causes analgesia Can increase intracranial and intraocular pressure  INDUCTION OF ANAESTHESIA Thiopental: Ultra-short acting barbiturate Suffers tautomerism once administered (enol to keto form, keto being the lipid soluble form that crosses the blood brain barrier) Very irritant to the tissues if administered outside the vessels Dose: 3 – 5 mg/kg IV Co-induction: can also be done with benzodiazepines and guaiphenesin Fast induction time, takes seconds to peak effect; induction therefore can be rough. Post-induction apnoea is likely to occur Minimal cardiovascular effects (hypotension and arrhythmias are more profound and likely to occur in hypovolaemic patients) Cranial nerves reflexes are lost Duration of anaesthesia following a single bolus (20 – 30 minutes) Does not provide analgesia Slow metabolism by means of redistribution (important to return of consciousness)  INDUCTION OF ANAESTHESIA Propofol: Substituted phenol that produces unconsciousness by acting on the GABAA receptors in the CNS. Rapid metabolism hepatic and extra-hepatic Large volumes to induce anaesthesia in horses (difficult to administer large volume and expensive) Induction and recovery from anaesthesia may not be good Dose: 2 – 5 mg/kg IV Co-induction: with guaiphenesin has been reported (but not with benzodiazepines) Fast onset (30-90 seconds) Can induce post-induction apnoea that lasts for 120 seconds usually Cardiovascular depression is more profound than thiopental Cranial nerves reflexes are lost Duration of anaesthesia following an IV bolus = 20 – 30 minutes No analgesia Rapid metabolism  INDUCTION OF ANAESTHESIA Inhalant anaesthetic induction: Lower blood solubility agents (Sevoflurane) may be better for a faster induction of anaesthesia with inhalant anaesthetic agents May be stressful for the patient (↑ catecholamines) CEPEF study indicates a higher anaesthesia-related mortality with induction of anaesthesia using inhalant anaesthetic agents (but at the time of the study halothane was the most used agent for inhalant anaesthesia, and this sensitises the myocardium to the arrhythmogenic effects of catecholamines; and drops cardiac output profoundly)  POST-INDUCTION CARE Monitor vital signs (as soon as possible) Place ETT asap Move patient onto the table on the required recumbency (care on how to position the horse: allow even weight distribution, and support non-dependent limbs so there is not totally over the dependent limb; over overextension of the head and limbs to avoid neuropraxia) Protect the eyes from debris and disinfectant products Initiate maintenance of anaesthesia Consider balanced analgesia: NSAIDs α2-agonists Opioids Locoregional anaesthesia  MAINTENANCE OF ANAESTHESIA Maintenance with injectable / inhalant Provide loco-regional anaesthesia techniques to allow a balanced anaesthetic Inhalational anaesthesia: Requires expensive equipment (breathing system; vaporiser; anaesthesia machine; carbon dioxide absorbent) Not easy to transport for field anaesthesia ETT is essential Oxygen supplementation is essential Depth of anaesthesia may be easier to change than with injectable agents Hypoxic pulmonary vasoconstriction is inhibited which may contribute to worsening of the ventilation perfusion mismatch  MAINTENANCE OF ANAESTHESIA Total intravenous anaesthesia (TIVA): Minimal equipment required Easy to perform in field anaesthesia Does not imply supplementation with oxygen, but it is recommended ETT is not essential, oxygen supplementation can be administered via nasal cannula Depth of anaesthesia is slower to change Drugs can be expensive Ventilatory support may be necessary Hypoxic pulmonary vasoconstriction is maintained as it is for the cardiovascular function which leads to reduction of the chances of ventilation perfusion mismatch and hypoxaemia Example: acepromazine 0.03 mg/kg IM + romifidine 0.08 mg/kg IV + butorphanol 0.03 mg/kg IV + ketamine 2.5 mg/kg IV + Midazolam 0.06 mg/kg; maintenance with IV bolus of ketamine 1/3 or ½ of the original ketamine and xylazine doses.  MAINTENANCE OF ANAESTHESIA TIVA (triple drip): Ketamine + Guaiphenesin + α2-agonists: Solution created to maintain anaesthesia after it has been induced with injectable agents Limit TIVA anaesthesia for 90 minutes to avoid accumulation of active metabolites (norketamine) which may make recovery from anaesthesia of poor quality. Plus care when administering doses >150 mg/kg of guaiphenesin as it is toxic, and excessive catechol production leads to excitable recoveries too.  MAINTENANCE OF ANAESTHESIA Supplemental Intravenous anaesthesia (SIVA): Consists in administration of analgesics (alpha-2 agonists, opioids, lidocaine, ketamine alongside other injectable or inhalant anaesthetics) → to produce a balanced anaesthesia. Requires ETT to enable mechanical ventilation Requires the use of infusion pumps or syringe drives (may not be feasible for field anaesthesia) Drugs administered have a sparing effect on inhalant or injectable agents, which reduces their negative effects on the cardiovascular and respiratory systems If using lidocaine infusion, stop 30 minutes before anaesthesia recovery, because otherwise it can cause ataxia during recovery.  MONITORING Horses should be monitored with standard monitoring: Electrocardiogram Pulse oximetry Capnography Spirometry Invasive or non-invasive blood pressure monitoring Inhaled and exhaled inhalant agents Temperature NMJ function if neuromuscular blockade has been administered Cardiac output if available (lithium dilution or transoesophageal doppler) In addition, check the patient regularly for signs of anaesthesia depth (nystagmus, palpebral reflexes, neck and pectoral muscles tension)  MONITORING CNS / reflexes: Eye position is unreliable for indication of anaesthesia depth Palpebral reflex (spontaneous movement usually maintained), but brisk blinking = may be too superficial. Perineal reflex / anal tone = to high = too superficial Ketamine → maintains CNS reflexes  MONITORING Cardiovascular system: Susceptible to depression induced by anaesthetic agents (particularly volatile agents → cardiovascular support is frequently required Hypotension is frequent (+++ if inhalant anaesthesia and horses in dorsal recumbency) Horses have a large cardiac reserve, thus, if sympathetic tone increases = heart rate may not increase, the stroke volume increases instead. This means that Heart rate is not a good indicator that the horse is too superficial or too deep, but blood pressure is. To avoid post-anaesthetic myopathies a mean arterial blood pressure (MAP) should remain above 70 mmHg in the hope to maintain muscle perfusion during general anaesthesia. Padded bed, correct positioning, duration of anaesthesia and use of ino-dilators (dobutamine) may contribute to reduce the risk of myopathy development  MONITORING Respiratory system: Intra-operative hypoxaemia and hypercapnia are common abnormalities in horses under anaesthesia and especially in dorsal recumbency. Horses have a large respiratory reserve, so in if high sympathetic nervous system output = respiratory rate does not increase, but larger tidal volume develops. So, RR is not a good indicator of anaesthesia depth in horses, but tidal volume is. Ketamine can induce apneustic breathing (long inspiratory time) Hypoxaemia is caused by: Low inspired FiO2 (failure in supply oxygen; or supply hypoxic mixture) Hypoventilation especially if the horse is no receiving supplemental oxygen (carbon dioxide displaces oxygen in the alveoli reducing its availability to oxygenate blood) Obstruction; malposition of ETT; splinting of the diaphragm; reduced respiratory muscles tone. Diffusion impairment (thickening of the alveolar – pulmonary capillary interface leads to less oxygen uptake into circulation) Ventilation/perfusion mismatch: areas poorly ventilated and highly perfused (atelectasis or intrapulmonary shunt); areas highly ventilated and poorly perfusion (alveolar dead-space) Plus, lower cardiac output; inhibition of the hypoxic pulmonary vasoconstriction Intracardiac shunt (cardiac congenital defect) Atelectasis can be due to: Airway closure due to lower Functional Residual Capacity (FRC) Compression Absorption In horses there is contribution of all these 3 mechanisms V/Q mismatch can be worsened by: Low cardiac output Inhibition of the hypoxic pulmonary vasoconstriction (which constricts vessels in poorly ventilated areas to shunt blood into better ventilated areas)  MONITORING Management of hypoxaemia: Increase fraction inspired of oxygen (remember iso-shunt equation; the higher the shunt fraction, the less efficacious it is to improve hypoxaemia with increased FiO2). Mechanical ventilation with the use of positive end-expiratory pressure (this may distend further the opened alveoli [worsening the ventilation/perfusion mismatch due to increase alveolar dead-space], and not be enough to open the collapsed alveoli) → better if applied from the beginning of the anaesthesia Bronchodilators (salbutamol inhaled; clenbuterol IV) by dilating bronchi may avoid collapse of alveoli, but its not guaranteed. These drugs also improve cardiovascular function and may cause vasodilation of pulmonary vasculature, thus improving perfusing of well-ventilated lung, thus reducing V/Q mismatch Support cardiovascular system to improve cardiac output and pulmonary perfusion.  RECOVERY The goal is to return the horse from unconsciousness to standing up as smoothly as possible. According to CEPEF 26% of anaesthesia-related deaths were caused by fractures on recovery and 7% by post-anaesthetic myopathy (both manifested on recovery). There is no such gold-standard method for recovery of horses; it is mainly based on facilities, equipment, personnel experience. It is said that the optimal time for a horse to stand up is 30 minutes per each hour under anaesthesia (e.g., if 1h under GA = 30 minutes recovery time) Usually, recovery following inhalant anaesthesia is usually shorter than for TIVA. However, TIVA techniques may preserve better the cardiovascular function, thus avoiding impairment of muscle perfusion; in addition, it also inhibits the stress response. The temperament, health status, pain, fluid and electrolyte deficits will also contribute to recovery quality.  RECOVERY Complications: Myopathy Peripheral Neuropathies Spinal cord malacia Orthopaedic trauma Ocular trauma Upper airway obstruction Post-operative colic Hyperkalaemic periodic paralysis IV catheters-related problems Pulmonary microemboli  RECOVERY Myopathy: Related with ischaemic injury to the affected muscles (any muscle can be affected) Can also contribute to muscle weakness and pain on recovery which may cause fractures Dependent muscles: will withstand body weight on them → increases intracompartmental pressure → compromise of blood flow → ischaemic injury → myocytes swelling and muscle oedema which further compromises oxygenation. Triceps, supraspinatus, infraspinatus, pectoral, brachiocephalic, longissimus dorsi, semitendinosus, semimembranosus and deltoids are at risk of high intracompartmental pressure. To minimise muscle ischaemia: Allow MAP higher than intracompartmental pressure to allow muscle blood flow (if MAP is 70 mmHg, and intracompartmental pressure is 35 mmHg, thus the perfusion pressure is 35 mmHg allowing blood flow) + adequate positioning Non-dependent muscles: can also suffer ischaemia if MAP is not high enough to allow blood flow towards them.  RECOVERY Myopathy: Risk factors: Heavy breeds (Clydesdale, Shire, Belgian draft), not only by the heavy weight on the muscles but also due to polysaccharide storage disease in these breeds. Intraoperative hypotension and hypoxaemia Increased anaesthetic duration (>2h) Fit horses Repeated anaesthetics over a short period of time Hyperkalaemic periodic paralysis (Appaloosas and quarter horses) Clinical signs: Affected muscles are hot, swollen, painful and reduced function Reluctance to move; lameness Myoglobinuria; elevated creatine kinase, aspartate aminotransferase Ataxia, delayed recovery  RECOVERY Myopathy: Treatment: Assist horse to stand / provide appropriate padding Light exercise if clinical signs are mild IV fluid therapy to help maintaining muscle perfusion and reduce risk of renal failure due to myoglobinuria (Hartmann’s 4-6 mL/kg/h) Acepromazine 0.03 mg/kg IM or IV to promote muscle vasodilation and improve perfusion + provides anxiolysis NSAIDs +/- opioid +/- α2-agonists for analgesia; α2-agonists provide good sedation but also analgesia Mannitol 0.25 g/kg IV to reduce muscle swelling Dimethyl sulfoxide IV or topically Some practitioners apply steroidal based creams over the affected muscle and apply massage and cold therapy. Ultrasound therapy has also been applied  RECOVERY Peripheral neuropathies: Similar risk factors to myopathies. Poor padding of surgical table, and inadequate positioning contribute to neuropathies Radial, femoral, peroneal and facial nerves are mostly affected. Hyperflexion/hyperextension of the head and neck = recurrent laryngeal nerve paralysis. Clinical signs: Affected areas won’t be hot, swollen or painful Loss of motor nerve function Can delay recovery; can enhance incidence of fractures Facial paralysis is probably less dramatic than radial paralysis, but should be avoided with proper head padding Horner’s syndrome (ptosis, miosis, enophthalmos, protrusion of the nictitating membrane and sweating over the ipsilateral face and neck) Occurs due to damage of the cervical sympathetic trunk Due to multiple IV injections Transient and may respond to NSAIDs  RECOVERY Central neuropathies: Spinal cord malacia is the most frequent for of central neuropathies Associated to rapidly growing, well-muscled horses placed in dorsal recumbency Ischaemic injury of the spinal cord? Which results in haemorrhage and malacia of the grey matter (mainly in thoracolumbar area) Clinical signs: Horse is unable to stand up; forelimbs have normal strength Horse attain “dog-sitting” position Prognosis is extremely poor… usually leading to euthanasia. Cerebrocortical necrosis: Can develop up to 7 days after recovery Can lead to blindness and behavioural changes May be associated with long periods of hypoxaemia and hypotension  RECOVERY Orthopaedic trauma: Usually bone fractures from long bones, associated or not with myopathies / neuropathies Joint disarticulation / luxation can also occur. Ocular trauma: Damage to the globe and periorbital area can develop especially if the horse hits its head against the walls / floor. Corneal ulceration = consequence of abrasion of the lowermost eye against the floor surface during lateral recumbency (during ET intubation); or of the uppermost eye with disinfectant solutions.  RECOVERY Upper airway obstruction: Obstruction of the nasal passages: Horses undergoing lengthy anaesthesia and particularly in dorsal recumbency may develop nasal mucosae oedema dur to vascular congestion The congestion can be severe enough to obstruct airway, which is only noticed when ETT is removed (horses are obligatory nose breathers) How to avoid / manage: Shorter anaesthesia duration; allow head position higher than the heart to facilitate venous blood flow; apply topical vasoconstrictor in the nose (Phenylephrine 5 to 10 mg – it is short-acting so timing is important). Place a nasopharyngeal tube: can be placed unilateral or bilaterally; this allows oxygen supplementation after ET removal; and realigns the soft palate with the epiglottis. Allow recovery with endotracheal tube in place: horses tolerate well maintenance of ETT in place for recovery; make sure to secure it to the ear / halter and that the cuff is deflated to ensure the horse can breathe if the tube kinks.  RECOVERY Upper airway obstruction: Obstruction within the larynx: Due to laryngeal damage or paralysis Traumatic ET intubation can damage the arytenoid cartilages or cause oedema Damage to the recurrent laryngeal nerve can also occur and lead to laryngeal obstruction Dorsal displacement of the soft palate and epiglottic retroversion can also cause upper airway obstruction following extubation Recover the horse with the ETT in place if laryngeal issues are anticipated (following laryngeal surgery) If you notice obstruction after extubation: re-intubate (usually nasotracheal); tracheostomy Upper airway obstruction can lead to pulmonary oedema development (pink frothy fluid may come out of the nostrils + cyanotic mucous membranes) – occurs due to excessive airway negative pressure generation to overcome upper airway obstruction. Treatment: Remove obstruction Clear the airway Furosemide 1-2 mg/kg IV Dexamethasone 0.25 mg/kg IV  RECOVERY Post-operative colic: Mild signs of colic are frequently reported in horses undergoing general anaesthesia Opioids are usually blamed, but there is no direct evidence for this; other factors may play a role: Pain Stress of travelling / hospitalisation Starvation Or other drugs, such as α2-agonists or anti-muscarinic drugs Treatment with prokinetic / analgesics (e.g., lidocaine infusion) are essential  RECOVERY Hyperkalaemic periodic paralysis: It is an autosomal dominant genetic disease characterised by a defective sodium channel in the muscle membrane which leads to abnormal sodium and potassium movement, leading to hyperkalaemia and muscle paralysis: Associated with large influx of sodium ions and efflux of potassium ions, which leads to a persistent depolarisation of the muscle cells and generalised muscle weakness (flaccid paralysis) and hyperkalaemia. Affects mostly Appaloosa and quarter horses (familial genetic disorder) Leads to prolonged recoveries; dog-sitting position; laryngeal paralysis; respiratory muscles weakness (and respiratory muscles arrest)  RECOVERY IV catheters-related problems: Catheter cap may be dislodged, and if: The catheter is directed upwards: haemorrhage (usually not lethal as clotting limits blood loss) The catheter is directed downwards: air embolism (leads to pruritus, pulmonary oedema, agitation) Jugular vein thrombosis can also develop after a few days. Pulmonary microemboli: Can develop after orthopaedic surgery Leads to delayed recovery; sweating; distress; tachycardia; tachypnoea can develop  RECOVERY Prevent problems: Sedation during recovery (α2-agonists): extends recumbency, to allow the patient to eliminate most of the general anaesthetic drugs (mainly inhalant) and have less ataxia caused by them in the moment for standing up. E.g., romifidine ¼ of the initial premedication dose at the end of anaesthesia Oxygen supplementation: especially if the horse was hypoxaemic during anaesthesia, will provide oxygen for recovery (which requires immense muscle contraction) Via ETT; nasopharyngeal tube (by insufflation 15L/min) Oxygen demand valve can be used in apnoeic horses (apply it at the end of ETT); by pressing the blue button it allows administration of a set flow rate of oxygen from a pressurised cylinder 60 L/min or up to 120L/min depending on the valve). Then, remove valve to allow expiration. If the horse is spontaneously breathing, deflate the cuff to allow air entrainment Maintain same lateral recumbency to maintain the non-dependent lung open; If the horse was in dorsal recumbency, consider putting left lung in dependent position (as right lung is larger) Sternal recumbency: ideal for oxygenation, but difficult to achieve  RECOVERY Analgesia: Systemic (NSAIDs, Opioid, α2-agonists) and/or addition of loco-regional anaesthesia Recovery box: Ideally the recovery box should have the following characteristics: Have an area of 4 to 5 m2; well padded, compressible floor and walls made of a robust material that is resistant to high impact Have no corners to prevent the horse getting stuck when it attempts to rise Be able to be easily cleaned and disinfected Have doors secured with floor and ceiling bolts, possibly with horizontal restraining bars as well Have an observation window or platform and possibly closed-circuit television Have dimmable lighting and a controllable temperature Be close to the operating theatre and have both oxygen and suction sources Have waste anaesthetic gas scavenging Have wall rings above horse head height to allow assisted recovery, or access holes within doors to facilitate the passage of ropes Have an escape route for staff Have access to facilities to re-anaesthetise the horse in an emergency Have a ceiling hook or winch from which to hang a sling Should provide a quiet, darkened and controllable environment for the horse to recover.  RECOVERY Assisted recovery: Physical restraint Hand recovery Ropes Slings Simple sling Large animal lift Anderson sling Deflating air pillow Pool systems Hydropool Pool-raft If there are several techniques for one purpose, it's because none of them are perfect  RECOVERY Physical restraint: Anaesthetist can try to keep the horse in lateral recumbency for a long period of time. From behind the horse's head and with escape route behind you, put your body weight over horses' neck, and pull its nose up towards your chest. This will make it harder for the horse to attempt standing up You know it's time to let the horse go, when you can no longer keep the horse from lifting its head This is relatively dangerous and only experienced personnel should do it or be around to help doing it. LUCKY DAY  RECOVERY Hand recovery: Can be done to smaller horses (ponies; foals; donkeys) Use leverage on the tail and halter on the head Dangerous for the staff, only experienced staff should get involved. Rope techniques: Assisted technique using 2 ropes (mountaineering ropes, as they have an inherent stretch), one on the tail, the other on the head It supports the horse and prevents excessive movement that would unbalance the horse (it does not lift up the horse) Two metal rings must be screwed in the wall above the horses (2.5m high), through which the ropes go through (one rope per ring). 2 people at least are required (1 per rope); relatively easy system and cheap, but requires training Useful for horses who had: Orthopaedic procedures and have heavy bandage / cast on their limb Expected weak recovery (following prolonged anaesthesia; colic surgery) However, horses may not tolerate the ropes and become stressed; ropes can get tangled or twisted if the horse is allowed to turn  RECOVERY Sling techniques: Attach the sling to the horse while still anaesthetised or heavily sedated Once the horse is looking bright and attempting to stand assistance to stand can be provided with a overhead winch Some horses may panic on the slings, thus sedation is essential (α2-agonists) If possible, train the horse pre-operatively to accept the sling Requires heavy training of the staff Simple sling: Placed under the horse's abdomen and thorax. The horse is supported in sternal by the winch and slowly allowed to bear its own weight Large animal lift: Uses a central bar which is attached to a winch, and from which the body slings are suspended The slings are passed under the horse with specific arrangements Sedation is essential, some horses calm down if a person is at their head Anderson Sling: Allows for full support of the musculoskeletal system Allows for even distribution of the weight of the horse It is hydraulically adjusted to allow more weight to be supported at the front or rear, left or right depending on the needs of the patient. Useful for horses undergoing external limb fixation (to avoid excessive weightbearing on the affected limb) Allows prolonged support (months)  RECOVERY Deflating/inflated air pillow: Deflating pillow avoids horses from lifting too soon. The pillow covers the entire floor of the recovery box and is rapidly inflated once the horse is recumbent The horse is sinking in the pillow, so, this avoids the horse from standing too soon Once the horse is fully awake, the pillow is rapidly deflated and the horse can attain sternal recumbency and then standing up Requires less staff training, but pillow is expensive and can be easily damaged (remove horse shoes) A pre-inflated pillow system can also be used; the pillows are already inflated and the horse is placed on them Once recovered, the horse can be walked out. It supports the abdomen and thorax too; but some horses can panic if they feel they are trapped, so sedation is essential. University of Ghent  RECOVERY Hydropool: Rectangular pool with adjustable floor The horse is placed on a sling and lifted into the pool while still anaesthetised With its head supported by an inflatable pillow and a rubber ring around the neck to avoid aspiration of water Slow recovery is key (provide sedation)! Once the horse regains consciousness, the floor of the pool is raised progressively so the horse weight bears more over time. Avoids repeated attempts to stand up Can cause pulmonary oedema and wound breakdown Pool-raft: At the university of Pennsylvania; the horse is positioned into a specially designed constructed inflatable raft and both the horse and the raft are placed in the pool. This avoids the horse from contacting with water (less wound breakdown); less risk of lung oedema Very expensive, requires trained staff and a well sedated and horse with good temperament Hydropool – University of Zurich Pool-raft – University of Pennsylvania  ANAESTHESIA OF FOALS Neonate: < 2weeks old. Infant: 2 to 6 weeks. Juvenile: 6 weeks to 3 to 6 months. Foals > 1 month old = physiological functions similar to adult horses (higher mortality in foals younger than 1 month old) Consider sedate the dam: If pregnant: detomidine; or another α2-agonist after clenbuterol Foals cardiac output (if neonate): Dependent mostly on heart rate, because the ventricles are less compliant, meaning they cannot expand their volume much Higher pulmonary circulation pressures, may re-open foramen ovale and ductus arteriosus leading to right to left shunt of blood and hypoxaemia. Liver metabolism is immature (prolonged drugs effects; hypoglycaemia; hypothermia) Hypothermia (due to smaller size which causes a larger surface area to body mass ratio = more heat loss); plus, they have little fat reserves (less insulation)  ANAESTHESIA OF FOALS Neonates have highly compliant chest wall, but poorly compliant or stiff lungs: Results in high work of breathing Because, the intrapleural pressure at end-expiration is equal to the atmospheric pressure as opposed to negative pressure in adults This facilitates airway collapse and low functional residual capacity They are therefore prone to develop hypoxaemia Poor capacity to excrete water in urine → prone to developing hypervolaemia Prone to GI ulcers (stress and poor GI perfusion) (avoid NSAIDs in foals younger than 6 weeks of age. Signs of GI ulceration: bruxism, salivation, dorsal recumbency  ANAESTHESIA OF FOALS Sedation in foals < 1 month old should avoid α2-agonists due to their immature cardiovascular system that may not cope with lower heart rate Sedation is usually achieved with benzodiazepine and opioid Induction of anaesthesia can be achieved with ketamine + benzodiazepine or propofol or inhalant agent mask induction Maintenance with inhalant anaesthesia as injectable anaesthesia requires heavy metabolism Recovery can be supported by hand Return the foal as quickly as possible to the dam, but make sure the foal is strong enough to walk and maintain its balance