This is a 9 year old Mix breed, Female spayed dog who presented for a wellness exam. There are no abnormal clinical signs. On physical exam an arrythmia was asuculted, but no murmur. An ECG confirmed frequent VPC’s. Mexilitine was intitiated. The arrythmia completely resolved on Mexilitine. An echo was performed to look for a primary cause of the VPC’s. The echo was normal. An abdominal ultrasound was recommended to screen for secondary causes of the VPC’s. The large renal cyst was found on the US exam.
This is a 9 year old Mix breed, Female spayed dog who presented for a wellness exam. There are no abnormal clinical signs. On physical exam an arrythmia was asuculted, but no murmur. An ECG confirmed frequent VPC’s. Mexilitine was intitiated. The arrythmia completely resolved on Mexilitine. An echo was performed to look for a primary cause of the VPC’s. The echo was normal. An abdominal ultrasound was recommended to screen for secondary causes of the VPC’s. The large renal cyst was found on the US exam.
Does anyone think the renal cyst could be the cause of the arrythmia or a coincidence? Would you aspirate the contents? consider surgery?
This patient was aggressive and difficult and absoultely would require sedation for a sampling procedure. The primary clinician was concerned about sedation due to the VPC’s that were present prior to Mexilitine therapy.
Thanks!
Comments
Is the patient hypertensive
Is the patient hypertensive and/or azotemic?
In people activation of the renin-angiotensin-aldosterone system occurs in cystic renal disease due to decreased nitric oxide production as well as cyst expansion and intra-renal ischemia. With increasing cyst size, further activation of the renin-angiotensin-aldosterone system occurs, blood pressure increases and a vicious cycle ensues with enhanced cyst growth and hypertension ultimately leading to end-stage renal disease.
The blood work was normal
The blood work was normal with no azotemia. Not hypertensive.
Trying to decide if we should consider FNA or surgery or just monitoring?
This case reminds me of a
This case reminds me of a post I made some time ago.
https://sonopath.com/forum/polycystic-kidney-disease
My sons dog had a similar looking renal cyst. I tried to drain it- but the material was very thick and I could not actually get it reduced. It seemed to resolve over time on its own- but every once in a while he shows signs of pain. I never recall him having an arrhythmia. I may have to recheck him next week. His kidney numbers have always been fine. I evaluated both kidneys and he does have small cysts in both kidneys- so he has polycystic kidney disease.
Below is a small paragraph from “Kittelsons Textbood of Cardiovascular Medicine” listing some of the causes of PVC’s. If there is no other indication of obvious cystic disease you may want to consider surgery to remove the cyst.
If you have not had a cardiologist evaluate the EKG strip- you may want to have this done. Bundle Branch Blocks can sometimes look a bit similar- both left and right.
Another thought- I often wonder what the effect of pain is on the cardiac conduction system.
Causes. Ventricular premature depolarizations can occur in many settings. They are rare in normal dogs and cats. They are common in hospitalized patients, occurring, for example, after trauma, after surgery, in association with gastric-dilatation volvulus, and secondary to systemic disease. VPDs are common in the presence of anesthetic agents. One of the most common situations is to observe ventricular bigeminy following the administration of a thiobarbiturate.1 VPDs also occur in dogs and cats with primary myocardial disease. Doberman pinschers and Boxers with dilated cardiomyopathy commonly have VPDs present on an ECG.
The reason for VPDs in many patients is clear. Dogs and cats with primary myocardial disease have myocardial damage that can produce reentry, abnormal automaticity, or triggered activity. Determining the exact mechanism responsible is impossible from a surface ECG. Understanding how myocardial toxins, such as anesthetic agents, can produce VPDs is easy. These arrhythmias are exacerbated by administration of catecholamines and vagolytic agents.2,3 Dogs with gastric dilatation-volvulus have regions of microscopic ischemia in their myocardium, probably associated with hypovolemia.4 The reason for VPDs in other patients is unclear. Dogs with systemic disease, abdominal disease, or prostatitis develop VPDs with no evidence of cardiac disease other than the arrhythmia. Acid-base and electrolyte disturbances may exacerbate the arrhythmias in these patients but are not severe enough in the vast majority of patients to produce VPDs.