Opening the Lines of Communication: The BluePearl Portal
We all know communication is one of the most important – and most frequently overlooked – aspects of veterinary medicine.
Good communication is especially vital between primary care veterinarians and specialty and emergency teams. When there are clear and easily accessible opportunities to share information, everyone benefits – especially the patient.
Of course, nothing can replace the value of a one-on-one conversation. But in today’s hectic world, that’s not always possible. That’s why we’ve developed the BluePearl Portal. This online feature gives our referring vets 24/7 password-protected access to 12 months of patient records with the click of a mouse.
Most of you refer to BluePearl hospitals that offer the Portal. For those who don’t, it will be coming to your area soon.
To access the Portal, either click through an email sent to you with your patient’s records or use your practice’s username and password on the login page. To find the login page from any computer or mobile device, go to BluePearl’s website, bluepearlvet.com, and click on the button on the top right of the page that says “For veterinarians.” Forgot your username or password? Just click on “help” at the bottom of the login screen – or give us a call.
The Portal gives you access to your patients’ medical records, both past and present, including:
- Appointment schedules and check-in and check-out history
- Labs and prescriptions
- Images and imaging reports
- Surgery and discharge reports
For those of you who have been using the feature, we’ve made some enhancements to the referral function based on your feedback. For example, referrals made via the Portal now are kept right in your account for quick reference.
Of course, whether or not you use the Portal is entirely up to you. We know that many of you prefer telephone conversations, faxes or all of the above. Our goal is to make communication as easy and beneficial as possible for you.
If you have questions or concerns — or you’d like to offer some feedback on how we can communicate better with you – we’d love to hear from you. Feel free to reach out to your local BluePearl hospital or send an email to email@example.com. We always look forward to hearing from you.
Jen Welser, DVM, DAVCO
Chief Medical Officer
BluePearl Veterinary Partners
Where is the Rhythm Coming From?
Dr. Kursten Pierce
BluePearl in Massachusetts
Arrhythmias, especially ventricular arrhythmias, can be life-threatening if not treated in a timely manner and with the right antiarrhythmic medication. Choosing an appropriate antiarrhythmic therapy depends on the type of arrhythmia, including origin (supraventricular vs. ventricular), arrhythmogenic mechanism, metabolic status of patient (evaluate for electrolyte imbalances), presence of underlying structural heart disease and/or congestive heart failure, and the patient’s co-morbidities.
Depending on the degree of tachycardia, it may be difficult to sort out the origin of the arrhythmia. Clues for distinguishing between supraventricular (SVT) and ventricular tachycardia (VT) can include evaluation of the QRS duration, morphology and cycle length regularity (AV conduction). SVT is a rapid rhythm (heart rate (HR) >180-200 bpm) originating from above the ventricles and typically has a narrow complex (QRS < 70 ms dogs, < 40ms cats). VT is a wide complex tachycardia (HR > 160 -180 bpm) originating from an ectopic ventricular focus. Other important clues to help better classify the arrhythmia include whether there is a constant QRS morphology (monomorphic) or a beat-to-beat variation in appearance (polymorphic) and whether the cycle length is normal (constant R-R interval) or irregular (variable R-R intervals).
It is important to rule out sinus tachycardia, which may be characterized by a regular rhythm with heart rate > 160 bpm with visible P waves on ECG and a constant PR interval. There may be a ramp up and slow down of the arrhythmia, which may respond to a vagal maneuver (ocular pressure, carotid sinus massage) and result in gradual slowing on the HR. Patients who are in pain, shock, hypovolemic, anemic, excited or CHF may exhibit sinus tachycardia; the underlying cause should be treated with no specific antiarrhythmic treatment.
If a narrow complex tachycardia is identified and sinus tachycardia has been ruled out, there may be evidence of atrial activation (P’, flutter, or fibrillation waves) that can provide evidence for determining the type of SVT. Keep in mind that atrial waves may be hidden in the previous ST segment or T wave, especially at faster heart rates. There may be an abrupt onset and termination of the arrhythmia, usually with a single beat. Treatment of SVT is mostly aimed at slowing AV nodal conduction. Common types of SVT include atrial fibrillation (irregularly irregular R-R intervals, absence of P waves, +/- fibrillation waves) and atrial flutter (typically regular R-R intervals, saw-toothed oscillations). Other types of SVT include focal atrial tachycardia (FAT) or an accessory pathway (OAVRT), where an early P wave (P’ wave) or delta wave (wave seen on the upstroke of the QRS indicating ventricular pre-excitation) with short PQ interval may be visualized, respectively. If SVT is causing hemodynamic compromise such as poor perfusion (weak femoral pulses, pale mucus membranes) or collapse, emergency medications include IV diltiazem, esmolol or procainamide. In general, SVT is rarely life-threatening and is managed with oral medications such as diltiazem (first choice), digoxin, sotalol or amiodarone. Typical doses for treating atrial fibrillation and atrial flutter are diltiazem (Dilacor®) ER 1-3 mg/kg PO BID and digoxin 0.003 -0.005 mg/kg PO BID (do not exceed 0.25 mg PO BID).
If a wide complex tachycardia is present, when in doubt treat for ventricular tachycardia as this is life-threatening arrhythmia that can lead to ventricular fibrillation and death. The exception for a wide complex tachycardia not being ventricular in origin would be atrial fibrillation in conjunction with a bundle branch block. In this scenario, treating for VT with lidocaine (2 mg/kg IV bolus) will not cause harm to the patient. A common approach to treating VT includes administering lidocaine IV boluses (2mg/kg) to convert to sinus rhythm and if successful start on a lidocaine CRI at 50 mcg/kg/min. Generally, 3 doses are administered before determining that the lidocaine was unsuccessful. If this occurs, procainamide IV boluses (2 mg/kg IV repeated up to 4-6 times) can be administered and followed by a CRI. Procainamide is effective for conversion for VT as well as SVT. If the VT is refractory to lidocaine and procainamide administration and the dog is able to receive oral medications, sotalol 1-3 mg/kg can be administered; however, if that patient is hemodynamically compromised then amiodarone should be administered by IV (1-2 mg/kg IV boluses (up to 3-5 mg/kg) followed by a CRI. Oral antiarrhythmic drugs used to maintain sinus rhythm and control ventricular arrhythmias include sotalol, mexiletine, beta-blocker such as atenolol in combination with mexiletine, or amiodarone. Sotalol and amiodarone are class III antiarrhythmics and work well for patients with a combination of supraventricular and ventricular arrhythmias.
Antiarrhythmics that are negative inotropes (diltiazem, sotalol, beta-blockers) should be used with caution in patients with poor contractile function or in active congestive heart failure. Amiodarone should be avoided or used with caution in patients with thyroid disease and liver disease as side effects include thyroid dysfunction and hepatopathy (both of which are reversible with discontinuation of the drug).
When choosing appropriate antiarrhythmic therapy, one should take into account the type and origin of the arrhythmia (+/- mechanism of the arrhythmia), patient’s metabolic status, underlying structural heart disease and other co-morbidities.
Let the Liver Live
A portosystemic shunt (PSS) is an aberrant vessel or vessels that shunts blood from the portal vascular system to the systemic vascular system. This causes blood flowing from the GI tract, pancreas, and spleen to bypass the liver where it would normally be “processed” and redirects this blood flow directly to the heart and systemic vasculature. The liver never has the opportunity to remove toxins absorbed by the GI tract, release anabolic hormones into the circulation in response to portal constituents, or process nutrients such as fatty acids and proteins for efficient use by the body. Growth and development of the organs of the body are frequently compromised.
Most congenital shunts are the result of a single aberrant vessel. Extrahepatic shunts are more common in small breed dogs, whereas intrahepatic shunts are more common in large breed dogs. The condition is often hereditary, especially in Yorkshire terriers. Portosystemic shunts have also been reported in cats.
Portosystemic shunts are most commonly diagnosed in young animals, although they have been found in animals as old as 10 years of age. Clinical signs may be subtle. Intermittent gastrointestinal upset, lethargy, stunted growth, pica, or neurologic signs such as circling, head pressing or seizures may be seen. In many patients the first abnormality noted may be a slower than expected recovery from anesthesia. Dysuria (from urate bladder stones) or even mild elevations in the liver values on routine blood work in clinically normal dogs are reasons to consider the possible presence of a PSS.
Ultrasound demonstrating an irregular tortuous shunt vessel
Ameroid rings placed around the shunting vessel slowly squeeze the vessel obstructing blood flow.
Bile acid testing should be considered in any patient with clinical signs or blood work abnormalities compatible with a PSS. An excessively high postprandial bile acid value (usually greater than 100 mg/dl) should prompt a search for a PSS.Imaging is typically performed to confirm the presence of a PSS. Radiographs often show a small liver but otherwise are unremarkable. In our experience, ultrasound examination of the abdomen has been very sensitive (80-92% sensitivity) for identifying PSSs. Ultrasound has also proven useful for identifying other hepatic diseases, concurrent intra-abdominal abnormalities, and urate bladder stones. Urate bladder stones will not typically appear on routine radiographs.
Other imaging methods used to confirm the presence of a PSS include portal scintigraphy (the visualization of portal vascularity via radioactive dye injected into the spleen), CT scanning and mesenteric portography (the intraoperative injection of radiopaque dye into a portal vessel for radiographic viewing). In some patients, an exploratory surgery will be performed based on the patient’s signalment, clinical signs and blood work alone.
Surgery is the treatment of choice for a single PSS. Attenuation of the shunting vessel utilizing an ameroid ring or cellophane band placed around the shunting vessel, or insertion of intravascular coils into the vessel is the preferred method of surgical treatment. The goal is to slowly decrease the volume of blood flowing through the shunt vessel over time. Complete and immediate ligation of the shunting vessel is no longer recommended due to complications of portal hypertension, i.e. excessive backpressure within the portal circulation.
Patients with extrahepatic shunts typically do well with shunt attenuation; 80-85% of patients achieving a successful outcome. By contrast, intrahepatic shunts can be difficult to reach and have a success rate of generally 50%. Cats also do not do as well following shunt attenuation.
Unfortunately, attenuation of the shunting vessels is not without potential sequelae. Acute hemorrhage, disseminated intravascular coagulopathy (DIC), hypotension, ascites, hypoglycemia and seizures have all been described. Long-term complications may also develop after surgery including chronic portal hypertension, inadequate attenuation of the shunt, and progressive liver disease due to concurrent portal vein hypoplasia.
Another congenital condition characterized by the microvascular shunting of blood within the liver, either in conjunction with macroscopic shunts or as a primary entity, can mimic a PSS. This abnormality was initially called hepatic microvascular dysplasia (HMD), but more recently this condition has been termed portal atresia. Since there is no shunt vessel to attenuate, medical management is the only treatment option.
A Clinical Approach to the Belly of the Beast
Adam R. Lancaster, DVM, DACVECC
BluePearl in Michigan
A patient with an acute abdomen can typically be identified by the presence of acute abdominal pain. Other signs such as vomiting and diarrhea may also be present. General causes of abdominal pain include distention of a hollow viscus or organ capsule, ischemia, traction and inflammation. Any of these causes may progress to necrosis and loss of organ function. There are numerous causes of acute abdominal pain including intestinal obstruction, septic peritonitis, hemoabdomen, pancreatitis, uroabdomen, gallbladder disease or rupture, GDV and ileus. This is not an exhaustive list but rather some of the more common causes.
Once a patient has been identified as having acute abdominal pain, a primary survey of the patient should be completed. At this point, it is important to recognize and treat shock and other concurrent injuries quickly. Following initial stabilization, a thorough diagnostic evaluation should be performed to identify the underlying cause of the abdominal pain. A full physical examination should be performed and a careful and detailed abdominal palpation may occasionally locate the specific area of pain, such as a loop of intestine, the prostate, kidney or an abdominal mass. Frequently a specific area cannot be identified and additional diagnostics may need to be performed.
In-clinic diagnostics may include PCV/TS, BUN, blood smear, venous blood gas and electrolyte levels, abdominal radiographs, abdominal ultrasound, and abdominal fluid analysis and cytology. PCV/TS should be performed on all patients with acute abdomen. Increases in PCV/TS suggest dehydration. A high PCV with low or normal TS may indicate hemorrhagic gastroenteritis. Patients with bleeding into the abdomen may have low PCV, TS or both. In acute hemorrhage, the TS will often decrease before the PCV due to splenic contraction. If a patient is found to have a bloody fluid in the abdomen, the fluid PCV/TS should be compared to a peripheral sample.
Hypoglycemia is often associated with sepsis or non-septic systemic inflammatory response syndrome (SIRS). Identification of hypoglycemia warrants immediate treatment as well as an aggressive diagnostic plan to identify the underlying cause. A venous blood gas may reveal acidosis or electrolyte abnormalities. Many cases of acidosis are from lactic acidosis from hypoperfusion and are best treated with fluid resuscitation. The presence of hyperkalemia may indicate kidney dysfunction or bladder rupture among other things.
Abdominal radiographs are indicated for any animal with abdominal pain. Any number of radiographic abnormalities may be present based on the underlying cause. Specific abnormalities to look for include evidence of peritoneal or retroperitoneal effusion, free gas in the abdomen, a mass effect or GI distention (either generalized or segmental). Peritoneal effusion typically causes a loss of serosal detail or may be more of a “ground glass” appearance, especially in the cranial abdomen associated with pancreatitis. Retroperitoneal effusion may occur secondary to inflammatory diseases of the kidney or bleeding of renal or adrenal masses. Retroperitoneal effusion occurs as “streaky” areas typically just caudal to the kidneys in the retroperitoneum. Free gas in the abdomen can be identified by pockets of gas that do not coincide with a gas-containing structure. This is most easily seen between the stomach or liver and the diaphragm. You may also see two walls of the stomach indicating gas on the inside and outside of the stomach. The presence of free gas indicates rupture of a hollow viscus or the presence of gas-producing bacteria within the abdomen. The presence of free gas in the abdomen is a clear indication for abdominal exploratory.
Segmental gaseous or fluid distention of the small bowel suggests intestinal obstruction. Generalized small bowel distention suggests small intestinal ileus or a distal GI obstruction. Localized small bowel distention is not a definitive finding for obstruction but should prompt further investigation if an obvious foreign body is not evident. This may include repeat radiographs, abdominal ultrasound or an upper GI contrast study.
An abdominal focused assessment with sonography for trauma (AFAST) is a useful diagnostic tool for all patients with severe abdominal pain. It allows for rapid identification of peritoneal effusion and increases the sensitivity of abdominocentesis for fluid evaluation. If fluid is identified an attempt to obtain a sample for analysis and cytology should be made. Generally speaking, effusions can be grouped into one of three categories:
|Fluid Type||Protein level||Cell Count||Common Causes|
|Transudate||TP <2.5 g/dl||<500 cells/µl||Hypoalbuminemia, portal venous obstruction|
|Modified transudate||TP 2.5-5.0 g/dl||300-5500 cells/µl||Many including CHF, liver disease, neoplasia|
|Exudate||TP >3 g/dl||5000-7000 cells/µl||Septic peritonitis, pancreatitis, bile peritonitis|
Other specific types of effusion may also be diagnosed based on various chemistries that can be performed on the fluid. These include septic peritonitis, bile peritonitis and uroabdomen. The chart below summarizes some of these findings:
|Septic peritonitis||Fluid lactate >2 mmol/L higher than blood|
Fluid glucose >20 mg/dl lower than blood
|Caution: very inflammatory exudates may mimic septic peritonitis|
Confirm via presence of intracellular bacteria on cytology
|Uroabdomen||Fluid creatinine >2x the blood creatinine|
Fluid potassium >1.4x the blood potassium
|Bile peritonitis||Fluid bilirubin >2x the blood bilirubin||May also see bile crystals or intracellular bile on cytology|
Cytology should also be performed on all samples to look for evidence of bacteria or neoplastic cells.
Generally speaking treatment will be based on the underlying condition and may be medical or surgical management. Surgical management is required in cases with confirmed (or highly suspected) septic peritonitis, bile peritonitis, GDV, mesenteric torsion, persistent abdominal hemorrhage or small intestinal obstruction. Uroperitoneum is often managed surgically but may be medically managed in some cases. Fluid therapy, pain medications, antibiotics and supportive care and monitoring make up the bulk of management of these cases.
URINARY TRACT INFECTIONS (UTIs)
Urine Trouble: Confronting the Complicated UTI
Lauren Devine, DVM, DACVIM
BluePearl in Washington
In this time of increasing antibiotic resistance, the World Health Organization named November 14-20, 2016 as World Antibiotic Awareness week. Complicated urinary tract infections have become an increasing issue in veterinary medicine as more pets are managed for long-term diseases. Repeated use of antibiotics in dogs and cats with recurrent urinary tract infections can result in development of antibiotic resistance. How can we control the spread of resistance and improve our patient’s quality of life? Understanding the root of the problem, the cause of the infection, is often key to appropriate treatment.
Urinary tract infections develop when the host defense mechanisms are overcome by bacterial virulence factors to allow adhesion of bacteria to the urothelium, which in turn promotes persistence and proliferation of the bacteria. The lifetime incidence of UTIs in dogs is around 14%, and the incidence in cats much lower, especially young cats. Most of these infections are caused by Escherichia coli and easily curable. Cases in which rapid, durable cures are not achieved through a standard short course of antibiotics require more diagnostics and management. Determining the type of complicated urinary tract infection may be helpful for management, but is often challenging.
Reinfection occurs when one UTI is cleared and another occurs due to a different isolate. This isolate may or may not be a different bacterial species. These infections are most commonly observed shortly after curing the initial infection. Common anatomic abnormalities resulting in reinfection include vulvar recession/hooding, ectopic ureters, vaginal bands (vestibulovaginal remnants) or prostatic cysts/abscesses. Urine retention and/or incontinence may also contribute to re-infection. Urinary tract infections have been frequently associated with systemic diseases such as hyperadrenocortism, diabetes mellitus, the use of immunosuppressive medications and cancer.
A relapsed UTI occurs when the same bacterial isolate is identified following effective treatment of one UTI. It is often indicative of a persistent nidus that protects bacteria from antibiotic exposure and permits recolonization once the pressure is removed (discontinuation of the antibiotic). The site of nidus may be host tissue such as renal parenchyma, prostate, thickened urinary bladder wall, urinary bladder mass (neoplasia vs polypoid cystitis), or the uroepithelium itself. Alternatively, foreign objects can be the site of nidus such as uroliths or intraluminal suture.
Persistent UTIs occur when the infection has failed to clear despite appropriate therapy. These infections are documented through a positive urine culture during or within 1 week of discontinuation of antibiotics. These infections may be caused by medication factors (dose, duration or noncompliance), bacterial factors (sequestration, resistance) or host factors (impaired host defenses, anatomic or physiologic abnormalities).
Strains of uropathogenic E.coli (UPEC) have recently emerged to possess both virulence factors and significant drug resistance. Additionally, UPEC has been demonstrated to invade urothelial cells, which permits the development of long-lived reservoirs protected from host immunologic defenses and antimicrobial exposures. This in turn plays a significant role in persistent and relapsing infections.
Since differentiating reinfection, relapse and persistent urinary tract infections can be challenging; a thorough physical examination and systemic evaluation is warranted in most cases. This includes full blood work (CBC, serum chemistry) and urine evaluation (urinalysis and urine culture). If the presence of a urinary bladder mass is suspected, a midstream urine culture may be obtained and interpreted in light of the collection method. Imaging of the urinary tract is often necessary to ensure there are no overt anatomic abnormalities. Radiography and ultrasonography provide complementary information. Abdominal radiographs, in general, are better at determining the number and location of urinary stones. On the other hand, ultrasound is a more useful diagnostic technique to evaluate renal, urinary bladder and prostate structure. Additional diagnostics such as cystoscopy may be necessary to evaluate for ectopic ureter and/or vaginal bands. Urinary bladder wall biopsies may also be collected at the time of cystoscopy for culture and histopathology.
While uncomplicated urinary tract infections are curable with a 7-14 day course of antimicrobial therapy, complicated urinary tract infections often require a longer duration (4-6 weeks). UTIs in cats and intact male dogs should be treated as complicated urinary tract infections. Special consideration of antimicrobial penetration into the prostate for intact male dogs is warranted (trimethoprim/sulfa, chloramphenicol and enrofloxacin). Culture-directed antimicrobial therapy is essential for the treatment of all complicated urinary tract infections. A urine culture performed 1 week into antimicrobial therapy and 1 week after discontinuation of therapy is recommended to ensure complete clearance of the organism. Management or treatment of the underlying disorder, if present, is critical to prevent recurrence and complete clearance of the organism. A good recommendation is to check a urinalysis and urine culture every 3-4 months in most chronic diseases (hyperadrenocortism, diabetes mellitus, CKD, etc.).
Due to the pervasiveness of complicated urinary tract infections both in human and veterinary medicine, a number of alternative and nonantibiotic therapies has been proposed. The most promising therapy both in women and our canine patients is cranberry extract (proanthocyanidins). Cranberry proanthocyanidins has been shown to be effective at preventing pillous adhesion of Escherichia coli to the urothelial cells in several studies of women with recurrent UTIs. A 2016 study from the “American Journal of Veterinary Research” showed a reduced recurrence of urinary tract infections in a small population of dogs treated with oral cranberry extract. Not all cranberry supplements have adequate amounts of pranthocyandins. Therefore, try to prescribe products with at least 93 mg of cranberry extract. Other alternative therapies have been proposed to reduce recurrence of complicated urinary tract infections; however, evidence for recommending these therapies is lacking.
Complicated urinary tract infections will continue to pose a treatment challenge. However, by identifying the root of the problem we may obtain better treatment and management strategies. With time, we may be able to decrease the threat of rising antibiotic resistance.
Helping the Cat Go
Recurrent constipation in cats can be frustrating to treat. There are several causes of constipation including:
- Dehydration secondary to anorexia, polyuria, or vomiting
- Perineal hernias
- Intraluminal obstructions of the colon/rectum (masses, foreign bodies, strictures)
- Extraluminal obstructions of the colon/rectum (masses, pelvic fractures, perineal hernia)
- Low fiber diets
- Idiopathic megacolon or dysautonomia
- Malformation of the spinal cord (ex. Manx cats)
In cats with prolonged, severe constipation, megacolon can develop resulting in a dilated, nonfunctioning colon. Constipation that has been refractory to medical management is termed obstipation. History, physical exam and radiographs often are used in the diagnosis of constipation/obstipation.
Many cats with mild to moderate constipation will respond to conservative medical management. Increasing dietary fiber intake (higher fiber diets such as Hill’s w/d®, Metamucil®, pumpkin pie filling) may help to soften the feces. In one study in which cats were fed a moderate fiber, psyllium-enriched, dry extruded diet (such as Royal Canin Fiber Response®), clinical remission was noted in the majority of cats, and other therapy was either not required or could often be discontinued over time.
The promotility agent, cisapride (2.5 mg p.o. TID) has occasionally proven efficacious. As cisapride is no longer available in the human market, it will need to be purchased from a veterinary compounding pharmacy. The addition of oral laxatives (lactulose syrup: 1-3 ml bid-tid, Miralax®: ¼ tsp mixed into food bid) has also been suggested. Finally, encouraging increased water consumption (water fountain, feeding canned diets) can also prove helpful. Unfortunately, most cats hate to be medicated and owner compliance is frequently inadequate for controlling the problem.
Obstipated cats typically require removal of impacted feces through enemas and/or manual extraction. Enemas should be administered slowly with a well lubricated 10-12 French rubber catheter at a dose of 5-10 mL/kg. Enemas containing phosphate are contraindicated in cats. Manually extracting the feces is done under general anesthesia. It may be necessary to do this over a period of several days to prevent prolonged anesthesia and/or perforation of the colon.
When medical management fails, a more permanent resolution of the problem can be achieved by surgically removing the diseased colon. This procedure, called a subtotal colectomy, is typically effective and associated with few complications. Most patients will experience a transient period of loose stools during the postoperative period which may last weeks to months. The need for further medical therapy and special diets is typically eliminated.