History
An 11-year-old 37.2-kg (81.8-lb) castrated male Labrador Retriever was referred for splenectomy and eyelid mass excision. Five days earlier, the dog had been evaluated by the referring veterinarian because of possible fecal incontinence and for prescriptions for preventatives against heartworm, fleas, and ticks. At that time, the owners did not report any other medical problems; however, the referring veterinarian identified substantial splenomegaly, a small mass on the dog's left upper eyelid, an acrochordon on the left hind limb, a subcutaneous lipoma (size not recorded) on the right lower aspect of the abdomen, and a firm, flat mass with irregular margins on the skin overlying the lateral aspect of the right shoulder. The owners reported that the shoulder mass had been present since birth. The referring veterinarian also identified signs of pain with palpation of the dog's lumbar spine and hip joints and with flexion of the stifle joints bilaterally. The dog had mild crepitus but no effusion in both stifle joints. Results of a CBC and serum biochemical analyses were within reference limits, except for a high serum total bilirubin concentration (1.0 mg/dL; reference range, 0.0 to 0.9 mg/dL) and low alkaline phosphatase activity (12 U/L; reference range, 23 to 212 U/L). Results of a screening test for vector-borne diseasesa indicated exposure to an Anaplasma sp. Thoracic and abdominal radiography were performed, and findings indicated no radiographic abnormalities in the thoracic cavity but a large mass that had soft tissue opacity in the cranioventral aspect of the abdomen and that displaced the stomach and spleen craniodorsally and the intestines caudally. In addition, abdominal radiography revealed low serosal detail.
On referral examination the day of surgery, the dog appeared bright, alert, and responsive. Results of venous blood gas analyses were within reference limits, the PCV was 42% (reference range, 41% to 58%), and plasma concentration of total solids was 6.8 g/dL (reference range, 5.0 to 8.0 g/dL).
An 18-gauge, 3-cm IV catheter was placed in the dog's right cephalic vein and fitted with a T-connector extension. The dog was premedicated with hydromorphone (0.05 mg/kg [0.02 mg/lb], IV), followed 10 minutes later with maropitant citrate (1.0 mg/kg [0.45 mg/lb], IV). Supplemental O2 (3.0 L/min) was administered by face mask, and the dog was instrumented with lead II ECG. The dog had ventricular bigeminy, a heart rate (HR) of 89 beats/min (reference range, 60 to 100 beats/min), and strong, regular femoral pulses. General anesthesia was induced with ketamine hydrochloride (2.0 mg/kg [0.9 mg/lb], IV bolus) followed immediately with propofol (1.4 mg/kg [0.6 mg/lb], IV) titrated slowly to effect. A laryngoscope was used to facilitate intubation with a cuffed 11-mm endotracheal tube. The cuff was inflated with air until no audible leak was heard while manually maintaining a positive inspiratory pressure of 15 cm H2O. End-tidal CO2 concentration (measured with side-stream capnography), indirect mean arterial blood pressure (MAP; oscillometric measurement with a medium-sized cuff on the left forelimb), and O2 saturation of hemoglobin (measured with pulse oximetry) were monitored with a multiparameter monitor.b The dog was allowed to breathe spontaneously throughout the anesthetic event, and end-tidal CO2 concentration never exceeded 48 mm Hg (reference range, 35 to 45 mm Hg). Esophageal temperature was monitored continuously.c Ventricular bigeminy resolved following intubation, and a normal sinus rhythm with an HR of 121 beats/min was recorded. The dog was positioned in dorsal recumbency for surgical preparation (clipping of the fur and cleaning of the ventral midline from the pubis to the xiphoid process), and a lubricating ophthalmic ointmentd was applied to both eyes.
The initial MAP measurement (58 mm Hg; reference range, 89 to 131 mm Hg) indicated hypotension; therefore, administration of isoflurane was delayed, and the dog's depth of anesthesia was monitored by repeated assessment of jaw tone and palpebral reflexes. A bolus of 6% hydroxyethyl starch solution (1.6 mL/kg [0.7 mL/lb], IV) was administered manually over 2 minutes. Ten minutes after induction of anesthesia, the dog was transferred to the operative theater, where lactated Ringer solution (5.0 mL/kg/h [2.3 mL/lb/h], IV) was administered with an IV sete and fluid pumpf throughout the surgical procedures. Cefazolin (22 mg/kg [10 mg/lb], IV) was administered slowly, and the dog's body temperature was supported throughout surgery by means of a circulating water blanketg placed on the operating table and a forced warm air deviceh placed over the dog, cranial to the surgical field during splenectomy, and over the torso during the eyelid mass removal.
After being positioned in the operative theater, the dog had an MAP of 82 mm Hg. General anesthesia was maintained with isoflurane (1.5% to 3.0% vaporizer setting) delivered in O2 (0.5 to 2.0 L/min) through an adult coaxial rebreathing circuit (a universal F circuit). Isoflurane concentrations were adjusted as indicated depending on the anesthetic requirements of the dog. Lidocaine hydrochloride (2 mg/kg, IV bolus, followed by 50 μg/kg/min [22.7 μg/lb/min], IV constant rate infusion) was administered with a syringe pump. The splenectomy was performed without complications. The lidocaine dose rate was decreased to 25 μg/kg/min (11.4 μg/lb/min) after closure of the midline abdominal incision and before repositioning the dog into sternal recumbency for excision of the eyelid mass.
Onto the eye with the eyelid mass, a generous amount of lubricating ophthalmic ointment was applied, and the skin of the eyelid was aseptically prepared with a dilute iodine solution. During the 5 minutes between repositioning the dog from dorsal to sternal recumbency and the start of eyelid mass excision, no changes in the dog's vital signs were observed. However, simultaneous to the start of the eyelid mass excision, the dog's HR and MAP rapidly declined from 121 beats/min and 88 mm Hg, respectively, to 35 beats/min and 71 mm Hg, respectively, and the dog's esophageal temperature was 36.2°C (97.3°F; reference range, 38.3° to 39.2°C [101.0° to 102.5°F]). Immediately, the surgeon was advised to halt manipulations of the palpebra, and atropine sulfate (20.0 μg/kg [9.1 μg/lb], IV) was administered. Instead of an improved HR as expected, second-degree atrioventricular block with ventricular escape beats was noted. An additional dose of atropine (10.0 μg/kg [4.5 μg/lb], IV) was administered. Gradually, the atrioventricular block and bradycardia resolved, and the dog's HR and MAP increased to 100 beats/min and 82 mm Hg, respectively. The palpebral surgery was completed within 5 minutes. The dog recovered from anesthesia uneventfully and was discharged from the hospital after 48 hours of postoperative monitoring in the intensive care unit. Histologic results confirmed that the splenic mass was a hematoma and that the eyelid mass was a meibomian gland adenoma.
Question
What was the cause of this dog's sudden episode of severe bradycardia and concomitant hypotension?
Answer
The sudden development of severe bradycardia and concomitant hypotension was presumed to have occurred secondary to an oculocardiac reflex (OCR).
Discussion
Occurrence of OCRs is a risk of ophthalmic surgery in dogs.1,2 The ophthalmic and maxillary nerves are branches of the trigeminal nerve (ie, the fifth cranial nerve) and together provide sensory innervation to the eyelids, whereas the auriculopalpebral nerve is a branch of the facial nerve that provides motor innervation to the upper eyelids. With the OCR, which is one of the most commonly discussed trigeminovagal reflexes in the veterinary literature, sensory afferent nerve endings of the frontal and lacrimal nerves, each branching from the ophthalmic nerve, project to the sensory nucleus of the trigeminal nerve, forming the afferent pathway of the reflex arc. Primary afferent fibers synapse with interneurons that connect with the efferent pathway in the motor nucleus of the vagus nerve. Cardioinhibitory efferents that originate within the motor nucleus of the vagus nerve terminate in the myocardium, and vagal nerve stimuli provoke negative chronotropic and inotropic responses. As a result, the OCR manifests as bradycardia in response to excitation of the sensory fibers of the eye and eyelids. In severe cases, bradycardia may progress to asystole if rapid intervention does not occur.2
Bradycardia observed in the dog of the present report may have been caused by the stimulation of the ophthalmic branch of the trigeminal nerve owing to manipulation of the left upper eyelid during the surgery to excise a mass on the eyelid. A local anesthetic was not applied before the procedure; therefore, the dog may have been predisposed to a vagal response to the palpebral surgery. Although positional changes in anesthetized patients can lead to changes in cardiovascular function and bradycardia, ≥ 5 minutes without changes in vital signs had elapsed between when the dog of the present report was repositioned and when its severe bradycardia and concomitant hypotension occurred. Thus, patient repositioning was considered a much less likely cause, and we believe that an OCR best explained the sudden cardiovascular episode.
A recent multicenter retrospective study2 suggests that although the prevalence of OCR in dogs undergoing enucleation is low (7/145 [4.8%]), local anesthetics administered as a preoperative retrobulbar block may be useful in preventing OCR during surgical manipulation of the eye and surrounding tissues in dogs. The authors further recommended that in the presence of an OCR, surgery is best halted until a positive response to treatment with an anticholinergic is observed.2
The dog in the present report also had ventricular bigeminy during the approximately 5 minutes of preoxygenation before induction of anesthesia; however, the condition resolved after induction and intubation. The occurrence of ventricular arrhythmias in dogs with splenic masses, such as the dog in the present report, has been previously studied.3–6 In addition, a recent study7 of autonomic nervous system imbalances and potential sympathetic stimulation by splenic masses in 12 dogs undergoing splenectomy for splenic masses shows that dogs with no ventricular premature complexes (VPCs) in the preoperative period (n = 6) rarely had VPCs during the postoperative period, whereas those with preoperative VPCs (6) also had markedly more VPCs during the postoperative period. The investigators further reported that dogs with more frequent VPCs had lower HR variability indices and higher plasma concentrations of catecholamines than did dogs with fewer VPCs (suggesting that splenic masses may stimulate the splenic nerve and thereby excite the sympathetic nervous system) and that the dogs with fewer preoperative VPCs had higher parasympathetic tone than did their counterparts.7 In the dog of the present report, ventricular bigeminy may have resulted from such an autonomic nervous system imbalance. Resolution of the dog's ventricular bigeminy following induction may have been caused by the sympathomimetic effect of ketamine on the autonomic nervous system. Alternatively, a positive chronotropic response may have resulted from a baroreceptor response to the vasodilation and hypotension following administration of propofol8 or a sudden decrease in venous return secondary to a positional change from sternal to dorsal recumbency. Enhanced vagal tone may have also predisposed the dog in the present report to an OCR at the time of eyelid surgery.
The paradoxical response by the dog in the present report to an initial injection of atropine could have been explained by the effect of atropine on presynaptic muscarinic acetylcholine receptors, which are believed to be involved in the negative feedback regulation of acetylcholine release from cardiac parasympathetic fibers.9 Interruption of this negative feedback loop causes increased secretion of acetylcholine and decreased HR. Additionally, stimulation of postsynaptic muscarinic acetylcholine receptors at the sinoatrial node may lead to activation of potassium channels, causing hyperpolarization of membranes and decreasing excitability of sinoatrial cells.
Findings in the dog of the present report further underscored the risk of OCR in dogs undergoing ophthalmic surgery and the need for patient monitoring to include ECG and ideally alternate means of pulse monitoring to allow rapid diagnosis of severe bradycardia. Continuous and diligent monitoring of anesthetized patients and efficient communication between the anesthesiologist and surgical team are key in mitigating such complications.
Acknowledgments
The author thanks Dr. John D. Anastasio for his intellectual assistance with the present report and Mr. Glenn Lesher for his invaluable technical assistance.
Footnotes
SNAP 4DX Plus, Idexx Laboratories Inc, Westbrook, Me.
SurgiVet Advisor, Smiths Medical, Saint Paul, Minn.
Thermocouple, Smiths Medical, Saint Paul, Minn.
Soothe lubricant eye drops, Bausch and Lomb Inc, Bridge-water, NJ.
PlumSet, ICU Medical Inc, San Clemente, Calif.
Plum infusion pump, Hospira Inc, Lake Forest, Ill.
Adroit Medical Systems, Loudon, Tenn.
Bair Hugger, Arizant Healthcare Inc, Eden Prairie, Minn.
References
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