Permanent transvenous cardiac pacing

Transvenous cardiac pacing is a commonly employed treatment for symptomatic bradyarrhythmias in dogs. Medical management of these conditions has not proven to be successful leaving pacing as the only viable alternative. The technique of pacemaker implantation is not difficult, but successful pacemaker therapy requires an understanding of electrophysiology, cardiac fluoroscopic anatomy, pacemaker instrumentation, and programming. Proper patient selection and identification of the underlying rhythm disturbance is essential to a successful clinical outcome. This article discusses the indications, equipment, techniques, complications, and outcome of permanent transvenous cardiac pacing.     

Transvenous pacemaker placement in a dog with atrioventricular block and persistent left cranial vena cava

The case reported herein describes the placement of a permanent transvenous pacemaker in an older dog with a previously undiagnosed persistent left cranial vena cava (PLCVC) and recent onset symptomatic third-degree atrioventricular (AV) block. On presentation the dog was found to have atrial flutter and third-degree AV block and echocardiography demonstrated evidence of chronic valvular disease and pulmonary arterial hypertension. The persistent left cranial vena cava was discovered via angiography when difficulties were encountered with pacemaker placement. Successful right ventricular pacing necessitated passage of the lead through the coronary sinus. The attendant complications in pacemaker placement in the presence of a PLCVC are well-described in man but, to the authors' knowledge, have not been described in companion animals.     

Successful resuscitation from cardiac arrest associated with extradural lidocaine in a dog

BACKGROUND: Extradural lidocaine exerts several adverse effects which are seldom fatal. While cardiac arrest following extradural lidocaine injection has been reported in human beings, it has not hitherto been reported in dogs. OBSERVATIONS: The emergency management of a dog with complete urethral obstruction is described. We intended to perform vaginoscopy and cystostomy under extradural lidocaine anaesthesia, but cardiac asystole occurred a few minutes after injection. Resuscitation was successful. About 20 minutes later cardiac arrest recurred, and was treated successfully. The dog remained hypothermic for approximately 7 hours. Complete recovery without neurological deficit occurred the next day and the dog remained normal for at least 3 months. The probable cause of the problem was cranial lidocaine dispersion causing a drop in cardiac preload and cardiac arrest. The successful neurological outcome was attributed to early diagnosis and effective treatment. Hypothermia may have conferred cerebral protection during ischemia. CONCLUSIONS: Extradural local anaesthetic administration is not without risk and the technique should be tailored to individual animals. Constant monitoring is required to detect potentially fatal complications and increase the likelihood of successful outcome.     

Follow-up of troponin I concentration in dogs with atrioventricular block and dual-chamber pacing in a case-matched study

Background

Increased cardiac troponin I (cTnI) concentration has been reported in dogs with atrioventricular (AV) block before and shortly following pacemaker implantation. The role of AV dyssynchrony, age, or concurrent cardiac disease on cTnI concentration remains unknown.

Xylitol intoxication associated with fulminant hepatic failure in a dog

Objective: To describe a case of xylitol intoxication causing fulminant hepatic failure in a dog. Case summary: A 2.5‐year‐old castrated male English Springer Spaniel weighing 26 kg, was presented after ingestion of half of a loaf of bread containing the sweetener xylitol. Toxic effects of the xylitol in this dog included vomiting, mild hypoglycemia and fulminant hepatic failure. Clinical management of acute hepatic failure and subsequent coagulopathy with supportive care and fresh frozen plasma is described. The dog was discharged 3 days after admission after a full clinical recovery. New or unique information provided: This paper describes the clinical consequence and successful treatment of fulminant hepatic failure in a dog following ingestion of xylitol.     

Treatment of accidental ethanol intoxication with hemodialysis in a dog

Objective – To describe the successful treatment of accidental ethanol intoxication with hemodialysis in a dog. Case Summary – A 1.5‐year‐old female intact mixed breed dog was presented in a comatose state believed to be due to ethanol intoxication. The initial 9 hours of supportive care treatment were complicated by multiple seizures and hypothermia, and resulted in only minimal improvement in the dog's level of consciousness. Hemodialysis was implemented and resulted in rapid clinical recovery, corresponding to a rapid decline in serum ethanol concentration. New or Unique Information Provided – To the authors' knowledge, this is the first reported case of using hemodialysis to treat accidental ethanol intoxication in a dog. The patient's initial serum ethanol concentration was higher than those previously reported for cases of accidental ethanol intoxication in dogs, and the serum ethanol concentration was shown to rapidly decline during hemodialysis. Treatment with hemodialysis for severe ethanol intoxication was effective in this case and may be able to decrease morbidity and mortality in some cases.     

Peliosis hepatis and hemoperitoneum in a dog with diphacinone intoxication

Objective: To describe the clinical course of a dog presented with peliosis hepatis and hemoperitoneum in concert with anticoagulant rodenticide intoxication.
Case summary: A 7.75-year-old spayed female Shetland Sheepdog presented with clinical signs consistent with hypovolemia, hemoperitoneum, and a history of bright green stool 3 days before the onset of clinical signs. Initial packed cell volume/total solids were consistent with acute hemorrhage. A coagulation profile showed prolongation in activated clotting time and prolongation of both prothrombin and activated partial thromboplastin time, suggesting abnormal coagulation. Abdominal hemorrhage persisted in the face of normalization of the hemodynamic status and coagulation profile, and treatment with Vitamin K₁. Abdominal ultrasound revealed multiple patchy hypoechoic areas throughout the caudate liver lobe. An exploratory laparotomy was performed 24 hours after presentation and revealed the caudate liver lobe as the source of the hemorrhage. Histopathologic examination of a specimen of the liver was consistent with peliosis hepatis. Toxicologic testing identified diphacinone levels in the blood consistent with anticoagulant rodenticide intoxication. Postoperative recovery was uneventful, and within 48 hours the dog was discharged. The dog returned to full function and a hepatic ultrasound performed 15 months postoperatively showed no significant abnormalities.
New or unique information provided: Exposure to anticoagulant rodenticides may be associated with the development of peliosis hepatis in dogs.     

Critical illness-related corticosteroid insufficiency in a dog with septic shock

Objective – To describe a case of hydrocortisone-responsive hypotension and critical illness-related corticosteroid insufficiency (CIRCI) in a dog with septic shock.
Case Summary – A dog with aspiration pneumonia developed septic shock with pressor-refractory hypotension. A standard ACTH stimulation test was performed that showed a blunted cortisol response consistent with CIRCI. Reversal of shock was achieved within 2 hours of hydrocortisone administration, and complete weaning from pressors was accomplished over the subsequent 8 hours. The patient recovered and was discharged from the hospital. An ACTH stimulation test performed 1 month after hospital discharge showed normal adrenal responsiveness consistent with resolution of CIRCI.
New or Unique Information Provided – This case is the first published report of hydrocortisone-responsive hypotension and transient CIRCI associated with naturally occurring septic shock in a dog.     

Transient neuromyopathy after bromide intoxication in a dog with idiopathic epilepsy

A seven-year old Australian Shepherd, suffering from idiopathic epilepsy under treatment with phenobarbitone and potassium bromide, was presented with generalised lower motor neuron signs. Electrophysiology and muscle-nerve biopsies revealed a neuromyopathy.The serum bromide concentration was increased more than two-fold above the upper reference value.Clinical signs disappeared after applying diuretics and reducing the potassium bromide dose rate. This is the first case report describing electrophysiological and histopathological findings associated with bromide induced lower motor neuron dysfunction in a dog.     

Acute polyneuromyopathy with respiratory failure secondary to monensin intoxication in a dog

Objective

To describe a successfully managed case of polyneuropathy and respiratory failure secondary to presumed monensin intoxication.

Case Summary

A 9‐month‐old Australian Shepherd was evaluated for progressive generalized weakness and respiratory distress. Several days preceding presentation, the dog was seen playing with a monensin capsule, and had free access to a barn where the product was stored and where chewed capsules were subsequently found. The dog was presented with flaccid tetraparesis, hyperthermia, and severe respiratory distress. Bloodwork and urinalysis revealed marked increase in serum creatine kinase concentration and presumed myoglobinuria. Cardiac troponin I level was markedly increased. Management included mechanical ventilation for 5 days, fluid‐therapy, active cooling, antimicrobial therapy, analgesia, gastroprotectants, antiemetics, enteral feedings, continuous nursing care, and physiotherapy. Intravenous lipid rescue therapy was administered with lack of improvement in respiratory function and muscle strength. The patient completely recovered and was discharged after 12 days of hospitalization.

New or Unique Information Provided

Monensin intoxication should be considered in the differential diagnosis of acute polyneuromyopathy and respiratory failure in dogs with access to this compound. Respiratory failure secondary to monensin intoxication does not necessarily carry a poor prognosis if mechanical ventilation can be provided as a bridge until return of respiratory function is achieved.     

Baclofen intoxication in a dog successfully treated with hemodialysis and hemoperfusion coupled with intensive supportive care

Objective: To describe a case of confirmed baclofen intoxication in a dog that was successfully treated with hemodialysis and hemoperfusion (HD/HP) and to report the serum baclofen kinetics. Case summary: A 2.5‐year‐old, 23 kg, spayed female Brittany Spaniel‐mix was treated after ingesting 21‐52 mg/kg of baclofen. The dog was comatose and was receiving manual ventilation at the time of presentation. Extracorporeal HD/HP was started 10 hours after admission. Within 3 hours of starting HD/HP the dog began initiating breaths and was extubated 18 hours after admission. Serial serum samples that were obtained during the first 24 hours of hospitalization were later analyzed for baclofen concentrations. The dog had elevated creatine phosphokinase and liver enzymes that correlated with an agitated recovery period. The dog had thrombocytopenia that resolved by 10 days after presentation. New or unique information provided: HD/HP shortened the baclofen serum elimination half‐life from 5 to 1.5 hours in the initial 2 hours of treatment. The intrinsic elimination rate constant (K_intr) for this dog was 0.138/hour and the total elimination rate constant (K_tot) during the first 2 hours of HD/HP treatment was 0.458/hour. In this dog, HD/HP was an effective method for rapidly decreasing serum baclofen concentration after an acute overdose.     

Combined corneal lipid and calcium degeneration in a dog with hyperadrenocorticism: a case report

Corneal degeneration may occur with a deposition of lipids or calcium, or both. Calcareous and lipid degeneration may be either primary or secondary, associated with systemic diseases such as primary hyperlipidemia, hyperlipidemia associated with hyperadrenocorticism, and hypothyroidism. The authors report a case of bilateral corneal lipid and calcium degeneration in a 7-year-old female Poodle with hyperadrenocorticism. The condition worsened with Lysodren therapy but responded to surgical excision.