September 2018   |   Volume 16   |   Issue 9

Eosinophilia Causes in Cats

in this issue

in this issue

Diagnosing Constipation, Obstipation, & Megacolon in Cats

Intrahepatic Splenosis in a Labrador Retriever

Diuretics Commonly Used in Dogs & Cats

Guidelines for Emergency Patient Referral

Differential Diagnosis: Hypoglycemia

Phenylpropanolamine

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Diagnosing Constipation, Obstipation, & Megacolon in Cats

Glenn A. Olah, DVM, PhD, DABVP (Feline), Winn Feline Foundation, Albuquerque Cat Clinic, Albuquerque, New Mexico

Internal Medicine

|Peer Reviewed

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Diagnosing Constipation, Obstipation, & Megacolon in Cats
Clinician's Brief
Clinician's Brief
Clinician's Brief
Clinician's Brief
*Megacolon is suggestive of neuromuscular dysfunction.

CKD = chronic kidney disease, DM = diabetes mellitus, DSS = dioctyl sodium sulfosuccinate, FeLV = feline leukemia virus, FIP = feline infectious peritonitis, FIV = feline immunodeficiency virus, IBD = inflammatory bowel disease, NE = nasoesophageal

References

For global readers, a calculator to convert laboratory values, dosages, and other measurements to SI units can be found here.

All Clinician's Brief content is reviewed for accuracy at the time of publication. Previously published content may not reflect recent developments in research and practice.

Material from Digital Edition may not be reproduced, distributed, or used in whole or in part without prior permission of Educational Concepts, LLC. For questions or inquiries please contact us.


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Intrahepatic Splenosis in a Labrador Retriever

Akaterina Davros, DVM, Fort Collins Veterinary Emergency and Rehabilitation Hospital, Fort Collins, Colorado

Kate KuKanich, DVM, PhD, DACVIM (SAIM), Kansas State University

Kelli Almes, DVM, DACVP, Kansas State University

Katherine Tucker-Mohl, VMD, Diagnostic Imaging, P.C., Aurora, Colorado

Megan Wilson, DVM, First Coast Veterinary Specialists, Jacksonville Beach, Florida

Emily Klocke, DVM, DACVS, Kansas State University

Internal Medicine

|Peer Reviewed

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Intrahepatic Splenosis in a Labrador Retriever

Figure 1 Ultrasonographic appearance of a cavitary mass measuring >10 cm in the left liver on initial presentation. Area of mass demonstrated by arrows

Sophie, a 9-year-old spayed Labrador retriever, was presented to the internal medicine service for abdominal distension. She had a clinical history of acute hemoabdomen, splenectomy, and benign hemangioma on splenic histopathology 2 years prior to presentation. One month prior to presentation, the owners noted that Sophie was gaining weight and that her abdomen appeared larger than usual. Abdominal radiographs obtained by the primary veterinarian revealed a large mid-abdominal mass. She was up-to-date on vaccinations and received routine flea, tick, and heartworm preventives.

Physical Examination Findings

Sophie was bright, alert, and responsive, with normal vital signs. The only abnormal examination findings were abdominal distension and a large and palpable left-sided cranial abdominal mass.

Diagnosis

Mild leukocytosis (17.3 × 103/μL [17.3 × 109/L]; reference range, 4.3-13.6 × 103/μL [4.3-13.6 × 109/L]) and mild regenerative anemia (hematocrit, 33% [reference range, 40%-57%]; reticulocytes, 150 000/μL [150 × 109/L]) were noted. The remainder of the CBC, coagulation profile, and serum chemistry profile were within normal limits. Abdominal ultrasonography demonstrated a large (>10 cm in diameter) hepatic mass (Figure 1) originating from the left aspect of the liver that contained numerous variably sized anechoic regions and mild anechoic peritoneal effusion. Two smaller masses were visible in the hepatic parenchyma (Figure 2). Ultrasound-guided fine-needle aspiration of the large hepatic mass was performed, and cytology showed evidence of previous hemorrhage and mild extramedullary hematopoiesis. Ultrasound-guided biopsies were not considered safe because of the risk for hemorrhage due to the cavitated nature of the masses. The top differential diagnosis was malignant neoplasia (eg, hemangiosarcoma, histiocytic sarcoma, hepatic adenocarcinoma); benign (eg, hemangioma) or infectious (eg, fungal or parasitic) lesions were considered possible but unlikely. Thoracic radiographs were unremarkable. 

Ultrasonographic appearance of a second hepatic mass measuring 5.7 cm on initial presentation. Area of mass demonstrated by arrows
Ultrasonographic appearance of a second hepatic mass measuring 5.7 cm on initial presentation. Area of mass demonstrated by arrows

Figure 2 Ultrasonographic appearance of a second hepatic mass measuring 5.7 cm on initial presentation. Area of mass demonstrated by arrows

Figure 2 Ultrasonographic appearance of a second hepatic mass measuring 5.7 cm on initial presentation. Area of mass demonstrated by arrows

TOP DIFFERENTIAL DIAGNOSIS:

MALIGNANT HEPATIC NEOPLASIA

Treatment & Long-Term Management

Although neoplasia was suspected, it could not be confirmed without histopathology. The owners elected for abdominal exploratory surgery to attempt either complete mass resection or debulking with biopsy for histopathology. The owners were prepared to consult with the oncology team following surgery if neoplasia was confirmed. Three liver masses and one mass adhered to the linea alba with omental adhesions were removed, leaving smaller masses and irregularities throughout the liver. The largest mass (11 cm), located in the left medial liver lobe, was firm and vascular and interspersed with pockets of unclotted blood. The left medial liver lobe containing the largest liver mass, 2 additional liver masses, and a mass adhered to the linea alba with omental adhesions were all removed, leaving smaller masses and irregularities throughout the liver. On histopathologic examination, the hepatic masses were found to be composed of red pulp, extramedullary hematopoietic tissue, rare white pulp, and smooth muscle trabeculae (Figure 3). The mass associated with the linea alba was also composed of ectopic splenic tissue, with similar components, consistent with splenosis. No evidence of neoplasia was seen. Recovery was uneventful, and the patient was discharged 2 days postoperatively. 

Histopathology of hepatic mass with compressed hepatocytes (star) and splenic red pulp (diamond). Necrosis can be seen in the lower left corner. 
Histopathology of hepatic mass with compressed hepatocytes (star) and splenic red pulp (diamond). Necrosis can be seen in the lower left corner. 

Figure 3 Histopathology of hepatic mass with compressed hepatocytes (star) and splenic red pulp (diamond). Necrosis can be seen in the lower left corner. 

Figure 3 Histopathology of hepatic mass with compressed hepatocytes (star) and splenic red pulp (diamond). Necrosis can be seen in the lower left corner. 

Prognosis & Outcome

Abdominal radiographs taken 3 months postoperatively were unremarkable. Sophie experienced a brief episode of vomiting 4 months postoperatively, and packed cell volume (PCV) was 34%; however, ultrasonography was not performed, and she recovered without therapy. Five months postoperatively, she was clinically normal, and a routine recheck identified a PCV of 39%. Ultrasonography at this time identified a 10.5-cm cavitated mass in the right liver near the porta hepatis (Figure 4) and an 8.6-cm hepatic mass with similar appearance to the presurgical ultrasound findings; hemoabdomen was not present. Although recurrence of hepatic splenosis was suspected, hemangiosarcoma or other neoplasia could not be ruled out. Cytology revealed extramedullary hematopoiesis.

Ultrasonographic appearance of 10.5-cm cavitated mass in the right liver lobe near the porta hepatis on recheck examination 5 months postoperatively. The mass was suspected to be a recurrence of hepatic splenosis, and cytology was consistent with extramedullary hematopoiesis; however, biopsies for histopathology were not pursued. Area of mass demonstrated by arrows
Ultrasonographic appearance of 10.5-cm cavitated mass in the right liver lobe near the porta hepatis on recheck examination 5 months postoperatively. The mass was suspected to be a recurrence of hepatic splenosis, and cytology was consistent with extramedullary hematopoiesis; however, biopsies for histopathology were not pursued. Area of mass demonstrated by arrows

Figure 4 Ultrasonographic appearance of 10.5-cm cavitated mass in the right liver lobe near the porta hepatis on recheck examination 5 months postoperatively. The mass was suspected to be a recurrence of hepatic splenosis, and cytology was consistent with extramedullary hematopoiesis; however, biopsies for histopathology were not pursued. Area of mass demonstrated by arrows

Figure 4 Ultrasonographic appearance of 10.5-cm cavitated mass in the right liver lobe near the porta hepatis on recheck examination 5 months postoperatively. The mass was suspected to be a recurrence of hepatic splenosis, and cytology was consistent with extramedullary hematopoiesis; however, biopsies for histopathology were not pursued. Area of mass demonstrated by arrows

Follow-up abdominal ultrasonography and blood work were performed every 2 to 3 months postoperatively. Sophie underwent a unilateral arytenoid lateralization for laryngeal paralysis (11 months after splenosis diagnosis) and a gastropexy after gastric dilatation-volvulus (1 year after splenosis diagnosis), both without complication. She was clinically stable 14 months postoperatively, with a PCV of 36%, no evidence of hemoabdomen or thoracic metastasis, and a stable appearance of the hepatic masses, with the largest mass measured at 9.85 cm. She continued long-term treatment with Yunnan Baiyao (500 mg PO q8h) for potential hemostatic effect.1

Splenosis is a rare complication of splenic trauma or rupture leading to implantation of splenic tissue onto vascular sites in the abdomen or intravascular seeding from surgical splenectomy. Whereas in humans splenosis typically occurs 5 to 10 years after splenectomy,2 in dogs, splenosis has been diagnosed concurrently with a splenic lesion3 or 2 to 5 years after trauma or splenectomy.4-8 Prior to Sophie’s diagnosis, intrahepatic splenosis had been reported in 5 dogs,4-8 and splenosis had been reported in the pancreas,3 mesentery,6,7 abdominal wall,6,7 diaphragm,7 and jejunum6 of dogs. Splenosis can be an incidental finding6 but more often has been reported with inappetence, weight loss, lethargy, weakness, abdominal distension, and/or abdominal pain in dogs.3-5,7,8 Two dogs had hemoabdomen secondary to rupture of intrahepatic splenosis lesions.7,8 Although splenosis is benign in nature, true prognosis and recurrence rate are unknown due to the rarity of this condition. Two of the 5 patients in the literature were euthanized at or around the time of diagnosis, and the remaining 3 cases were reported to have survived at least 5, 8, and 10 months postdiagnosis.4,6,7 Sophie’s survival of at least 14 months (at the time of this article’s publication) provides important prognostic information. In contrast, median survival for hemangiosarcoma after surgery and chemotherapy is 6 months.

Intrahepatic Splenosis at a Glance

  • If an abdominal mass is palpated, abdominal radiography and ultrasonography can help further characterize the mass, but prognosis should not be decided on imaging appearance alone.
  • Thoracic radiography is recommended to look for pulmonary metastasis prior to laparotomy.
  • If removing a large vascular mass, the clinician should be prepared to transfuse the patient.
  • All surgically excised masses should be submitted for histopathologic examination.
  • Hepatic splenosis is rare, and further prognostic information is needed. Repeating abdominal ultrasonography every 1 to 3 months is suggested to monitor for recurrence.

The Take-Home

Splenosis should be considered a differential diagnosis for hepatic or abdominal masses in dogs with a history of splenic trauma or splenectomy. Not all cavitated hepatic masses in older, large-breed dogs are neoplastic. Histopathology is required to assess whether neoplasia is present so that appropriate treatment options and prognosis can be determined.

PCV = packed cell volume

References

For global readers, a calculator to convert laboratory values, dosages, and other measurements to SI units can be found here.

All Clinician's Brief content is reviewed for accuracy at the time of publication. Previously published content may not reflect recent developments in research and practice.

Material from Digital Edition may not be reproduced, distributed, or used in whole or in part without prior permission of Educational Concepts, LLC. For questions or inquiries please contact us.


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Phenylpropanolamine

Phenylpropanolamine

Julie K. Byron, DVM, MS, DACVIM, The Ohio State University

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Phenylpropanolamine

Phenylpropanolamine is an α1-adrenergic agonist used to increase smooth muscle tone in the urethra of dogs with urethral sphincter mechanism incompetence (USMI). It is widely available in approved veterinary products and is often the first-line choice for treatment of urinary incontinence secondary to USMI.1 Phenylpropanolamine is well tolerated, but specific adverse effects make it less appropriate in some patients, particularly those with or at risk for hypertension. 

MECHANISM OF ACTION

  • Phenylpropanolamine is a synthetic sympathomimetic amine that acts primarily at α receptors with some β effect, as well as in the CNS.2
    • Although the drug’s effect on continence has been thought to come primarily from the stimulation of α receptors in urethral smooth muscle, there is evidence that phenylpropanolamine also stimulates β receptors in the bladder, leading to increased detrusor relaxation and lower bladder pressures during the storage phase of micturition (see Physiology of Micturition).3 

Physiology of Micturition

Storage Phase

During the normal storage phase, stretch receptors in the bladder wall send afferent signals along the pelvic nerve, which activate a reflex arc through the hypogastric nerve to the urethra. Norepinephrine is released by postganglionic neurons to activate β-adrenergic receptors in the bladder wall, allowing for relaxation and continued filling. Norepinephrine also stimulates α1-adrenergic receptors in the urethra and causes contraction of the circular and longitudinal smooth muscle surrounding the urethra, thus preventing urine leakage.

In addition to smooth muscle tone, the somatic-mediated contraction of the striated muscle surrounding the urethra is also important for maintenance of continence. With sudden increases in abdominal pressure, afferent signals travel up the pelvic nerve and initiate efferent signals down the pudendal nerve, releasing acetylcholine and activating nicotinic cholinergic receptors, thus causing contraction of the striated muscle.

Voiding Phase

During initiation of voiding, stretch receptors send afferent signals along the pelvic nerve and cranial to the pontine micturition center. Signals from the cerebral cortex and the hypothalamus are processed to determine if the situation is appropriate for initiation of micturition; if so, signals are sent down the pelvic nerve, leading to release of acetylcholine at the postganglionic parasympathetic neurons. Acetylcholine binds to receptors and stimulates bladder smooth muscle contraction. At the same time, inhibitory signals are sent to the sympathetic reflexes, and the urethra relaxes, allowing for normal emptying.

CLINICAL APPLICATIONS & EFFICACY

  • Phenylpropanolamine is primarily used to increase urethral tone in spayed dogs with acquired urinary incontinence secondary to USMI.
    • Studies have shown resolution or improvement of incontinence in 85% to 90% of female dogs with USMI.4
  • Phenylpropanolamine can also be used in cats, but there is little evidence of its efficacy.
    • Anecdotal evidence suggests that many cats with urinary incontinence have underlying urogenital malformations and that the incidence of USMI is likely low.
  • Dosages up to 2 mg/kg PO q8-12h are considered safe in patients without comorbidities that can predispose to hypertension or in patients that are vulnerable to negative effects of increased cardiac preload (eg, mitral valve insufficiency).
    • Otherwise healthy dogs receiving higher doses are at risk for clinically significant elevations in blood pressure.5
  • There is anecdotal evidence that phenylpropanolamine may become less effective over time in some patients and require dose escalation.
    • This may be due to downregulation of adrenergic receptors, but this is unproven.
    • When maximum doses are reached, an estrogen (eg, estriol, diethylstilbestrol) can be added to improve continence.
  • There has been speculation that phenylpropanolamine and estrogens have a synergistic effect.
    • Only one study of this effect has been performed and did not support this theory6; however, further studies should be conducted to evaluate the interaction of these drugs.
  • Anecdotally, patients with intolerance to higher doses of phenylpropanolamine may be maintained on lower doses with the addition of an estrogen (eg, diethylstilbestrol, estriol) at a standard dose.

MONITORING & ADVERSE EFFECTS

  • The nonspecific nature of phenylpropanolamine can lead to potential for adverse effects from stimulation of the sympathetic nervous system, including hypertension, agitation, sleeplessness, and decreased appetite.7
    • Most adverse effects are mitigated by decreasing the dose or discontinuing use of phenylpropanolamine.
  • A recent study showed that dogs receiving standard oral doses of 1 and 2 mg/kg q12h experienced increases in systolic, diastolic, and mean blood pressure, as well as compensatory decreases in heart rate.5
    • Of note, changes were not outside normal parameters and therefore are unlikely to be clinically significant.
  • Phenylpropanolamine should be used with caution in patients with hypertension, with diseases predisposed to hypertension (eg, hyperadrenocorticism, chronic kidney disease, pheochromocytoma, hyperthyroidism), or with conditions sensitive to increased cardiac preload.
    • Blood pressure should be monitored 2 hours postadministration (at the time of maximal blood levels and smooth muscle effect) and can be evaluated after a single dose.5,8
    • The author recommends initial blood pressure measurement and twice-yearly rechecks in healthy patients and monitoring every 3 to 4 months in patients at risk for hypertension.

USMI = urethral sphincter mechanism incompetence

References

For global readers, a calculator to convert laboratory values, dosages, and other measurements to SI units can be found here.

All Clinician's Brief content is reviewed for accuracy at the time of publication. Previously published content may not reflect recent developments in research and practice.

Material from Digital Edition may not be reproduced, distributed, or used in whole or in part without prior permission of Educational Concepts, LLC. For questions or inquiries please contact us.


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Characteristics of Granulocytic Anaplasmosis in Dogs

Janet Foley, DVM, MS, PhD, University of California, Davis

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Characteristics of Granulocytic Anaplasmosis in Dogs

In the Literature

Chirek A, Silaghi C, Pfister K, Kohn B. Granulocytic anaplasmosis in 63 dogs: clinical signs, laboratory results, therapy, and course of disease. J Small Anim Pract. 2018;59(2):112-120.


FROM THE PAGE …

This study examined medical records of 974 dogs from Germany with clinical signs suggestive of granulocytic anaplasmosis (GA). Dogs were included in the study if they tested positive for GA via real-time PCR with no comorbidities that could potentially confuse whether signs and laboratory test results were attributable to Anaplasma phagocytophilum. Sixty-three dogs met the study criteria and were included in the analysis.

Clinical signs in affected dogs included lethargy and reduced activity, fever, lameness, and pain on joint palpation. Of importance, 13% of dogs had hemorrhage consisting of petechiae, gingival bleeding, epistaxis, pulmonary or vaginal hemorrhage, fresh fecal blood, or hematoma; these signs were often associated with thrombocytopenia. Splenomegaly and hepatomegaly were often observed. CBC findings most consistently included thrombocytopenia; 44% of dogs tested had platelet-bound antibodies. Synovial fluid of dogs with suspected polyarthritis was cellular and occasionally tested positive for GA via real-time PCR. Doxycycline was highly effective in mitigating clinical signs when used, although hematologic abnormalities took several weeks to improve. Polyarthritis and immune-mediated hemolytic anemia were indicators for treatment with steroids or cyclosporine.

The study did not include a control group; thus, it cannot be determined which of the findings might also occur in dogs without GA—and at what frequency—from the same region or with the same signalment. The study authors acknowledged that chronic infection or occult infection in dogs with less notable clinical signs was likely overlooked but indicated that dogs are more likely to be infected in particular geographic regions and during seasons of peak tick activity. Creating a clinical picture of the dog with GA can help improve diagnostic efficiency and ensure that dogs at risk receive appropriate and timely care. 


… TO YOUR PATIENTS

Key pearls to put into practice:

1

Obtaining patient travel history, which should include locations recently visited, is crucial, as risk differs across geographic regions and in forests or environments where ticks would quest. Of note, tick-borne GA is seasonal.

2

Screening should include physical examination and complete minimum database (CBC, serum chemistry profile, urinalysis) augmented with PCR testing of blood. PCR-negative results should be rechecked in a few days.

3

Although most dogs with GA respond well to doxycycline, long-term sequelae can include immune-mediated disease. Steroids should be considered when indicated.

For global readers, a calculator to convert laboratory values, dosages, and other measurements to SI units can be found here.

All Clinician's Brief content is reviewed for accuracy at the time of publication. Previously published content may not reflect recent developments in research and practice.

Material from Digital Edition may not be reproduced, distributed, or used in whole or in part without prior permission of Educational Concepts, LLC. For questions or inquiries please contact us.


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Owner Perceptions of Pet Pain

Kristyn D. Broaddus, DVM, MS, DACVS, Veterinary Services of Hanover, Mechanicsville, Virginia

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Owner Perceptions of Pet Pain

In the Literature

Simon BT, Scallan EM, von Pfeil DJ, et al. Perceptions and opinions of pet owners in the United States about surgery, pain management, and anesthesia in dogs and cats. Vet Surg. 2018;47(2):277-284.


FROM THE PAGE …

A reliable indicator of pain as perceived by pet caretakers and pet health professionals remains elusive. Perception of pain in animal patients and pain scales are generally based on human models and human experience. Because animals cannot articulate specific pain levels, pain can be overlooked in a suffering animal.

This study gauged owner perception of pet pain related to surgery and medical illness using a short (<5 minutes) questionnaire. Owners (n = 948) responded to questions regarding perception of pain in their pet, effect of pain on their pet, and the need for pain medications after specific surgical or medical therapies.

That perception of pain in pets is challenging and that pain affects quality of life were both appreciated by owners in the study. Healthcare professionals, college graduates, and respondents who had previously experienced surgery on themselves or their pet reported an elevated appreciation of the need for pain control and the need to be informed about the level of pain expected from a procedure. This group also felt it important that a board-certified anesthesiologist perform anesthesia. High-school–educated respondents were less likely to appreciate the need for analgesics after surgery. In general, owners lacked an appreciation for the need to treat medical conditions such as aural infections with pain medications.

Studies such as this underscore the need to educate pet owners on pain perception. Common beliefs, such as a pet cannot be in pain because it is still active or that pain helps ensure a pet will rest, persist. It is essential for veterinarians to provide owners with information that clarifies signs of pain in pets.


… TO YOUR PATIENTS

Key pearls to put into practice:

1

Multimodal pain therapy is important in the management of pain in pets. Local anesthetic blocks, opioid therapy, gabapentin, and NSAIDs (when appropriate) can help owners treat their pet for pain from surgical and nonsurgical conditions.

2

Due to the current opioid crisis in the United States, veterinarians are required to examine pets more frequently before refilling controlled pain medications. This can be used as an opportunity for ongoing owner education on pet comfort. 

3

Taking time to educate owners about the perception of pain in pets is invaluable. Describing how bilateral chronic otitis externa can be experienced as painful as cruciate ligament rupture is important. Describing signs of pain that owners may not appreciate (eg, lack of play, lameness, lethargy, grumpiness, inappetence) can be helpful.

Suggested Reading

For global readers, a calculator to convert laboratory values, dosages, and other measurements to SI units can be found here.

All Clinician's Brief content is reviewed for accuracy at the time of publication. Previously published content may not reflect recent developments in research and practice.

Material from Digital Edition may not be reproduced, distributed, or used in whole or in part without prior permission of Educational Concepts, LLC. For questions or inquiries please contact us.


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Changes to Cephalosporin Susceptibility Reporting

JD Foster, VMD, DACVIM, Friendship Hospital for Animals, Washington, DC

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Changes to Cephalosporin Susceptibility Reporting

In the Literature

Papich MG, Lindeman C. Cephalexin susceptibility breakpoint for veterinary isolates: Clinical Laboratory Standards Institute revision. J Vet Diagn Invest. 2018;30(1):113-120.


FROM THE PAGE …

Microbial culture and susceptibility testing is an integral part of the diagnosis and treatment of bacterial infections. The Clinical Laboratory Standards Institute (CLSI) evaluates the antibiotic concentration (ie, breakpoint) required to prevent growth of cultured bacteria, the drug’s pharmacokinetic properties, and the likelihood of clinical success for typical doses of the antibiotic to determine whether an isolate will be susceptible (S), intermediate (I), or resistant (R) to that particular drug. Cephalothin, a first-generation cephalosporin, has historically been evaluated to predict the susceptibility to all other oral drugs within that class (eg, cephalexin, cefadroxil, cephapirin). However, research has shown that cephalothin is poor at predicting cephalexin susceptibility. This limitation, combined with cephalexin’s position as the most commonly prescribed first-generation cephalosporin, highlights the need for cephalexin-specific CLSI guidelines.

This study evaluated bacterial isolates from a 4-year time span to determine minimum inhibitory concentration (MIC) breakpoints for 4 cephalosporins used in veterinary medicine (ie, cephalexin, cephalothin, cefovecin, cefpodoxime) and simulated the likelihood of successful eradication of the infection. The study results showed discrepancies in susceptibility between cephalothin and cephalexin. Most notable were the susceptibility results for the Staphylococcus pseudintermedius isolates that were positive for penicillin-binding protein 2A. Only 4.3% of these isolates had MIC values ≤2 µg/mL for cephalexin as compared with 66.3% for cephalothin. These results further confirm the poor agreement of cephalothin to predict cephalexin susceptibility, which has led the CLSI to replace cephalothin with cephalexin for testing canine isolates. 


… TO YOUR PATIENTS

Key pearls to put into practice:

1

Microbiology laboratories should replace cephalothin with cephalexin on culture and susceptibility reports.

 

2

Cephalexin at 25 mg/kg PO q12h has a 90% likelihood of clinical success in dogs when treating isolates with a MIC ≤2 µg/mL. The likelihood of success for isolates with MICs of 4 µg/mL and 8 µg/mL is only 73% and 47%, respectively. Alternative drugs should be considered at these higher MICs based on culture and susceptibility report results.

3

If a bacterial isolate is resistant to oxacillin, it should also be considered resistant to all other β-lactam drugs, including cephalexin and cephalothin. Alternative drug classes should be used to treat such infections.

For global readers, a calculator to convert laboratory values, dosages, and other measurements to SI units can be found here.

All Clinician's Brief content is reviewed for accuracy at the time of publication. Previously published content may not reflect recent developments in research and practice.

Material from Digital Edition may not be reproduced, distributed, or used in whole or in part without prior permission of Educational Concepts, LLC. For questions or inquiries please contact us.


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Feline Retroviruses

Glenn A. Olah, DVM, PhD, DABVP (Feline), Winn Feline Foundation, Albuquerque Cat Clinic, Albuquerque, New Mexico

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Feline Retroviruses

In the Literature

Spada E, Perego R, Sgamma EA, Proverbio D. Survival time and effect of selected predictor variables on survival in owned pet cats seropositive for feline immunodeficiency and leukemia virus attending a referral clinic in northern Italy. Prev Vet Med. 2018;150:38-46.


FROM THE PAGE …

Feline immunodeficiency virus (FIV) can cause an acquired immune deficiency syndrome, predisposing cats to other infections. However, most naturally FIV-infected cats do not develop a severe clinical syndrome, especially if appropriate husbandry and healthcare are provided.1-3

Feline leukemia virus (FeLV) is more pathogenic than FIV. Cats with FeLV frequently succumb to fatal diseases associated with FeLV infection (eg, bone marrow suppression leading to nonregenerative anemia, secondary infections, neoplasia), resulting in decreased life expectancy in these cats.4

This retrospective cohort study aimed to estimate survival times and evaluate select predictor factors on survival in cats that tested positive for FIV antibodies and/or FeLV antigen. Of the 816 cats tested, 117 (14.3%) tested positive for infection, of which 60 were FIV positive, 46 were FeLV positive, and 11 were both FIV and FeLV positive. Seroprevalence rates for FIV, FeLV, and FIV–and-FeLV–coinfected cats were thus 7.4%, 5.6%, and 1.4%, respectively.

Survival data agreed with previous studies.2,3,5-9 Survival time for FIV-infected cats was not statistically different as compared with retrovirus-negative cats. Median survival times for FeLV-infected and FIV–and-FeLV–coinfected cats were significantly shorter (714 days and 77 days, respectively) as compared with retrovirus-negative and FIV-infected cats (3960 days and 2040 days, respectively). Median age at diagnosis for FIV-infected cats (5 years) was higher than for FeLV- infected cats (2 years), and median age of coinfected cats was 7 years. Despite shorter survival times, some cats with FeLV and cats with FIV and FeLV lived much longer than their respective median survival times (as long as 8.5 years and 4.9 years, respectively). The wide survival time distribution highlights that FeLV infection is not necessarily suggestive of an immediate death, and clinicians should assess FeLV-infected and coinfected cats case by case. Only reduced RBC count was shown to correlate negatively with median survival time in all retroviral-infected cats.


… TO YOUR PATIENTS

Key pearls to put into practice:

1

FIV and FeLV infection should not be considered indicative of pending death in infected cats.

 

2

FeLV infection is often more pathogenic and progresses more rapidly than does FIV infection. As represented in this study, causes of death in FeLV-infected cats may primarily be due to lymphoma and, less commonly, anemia. FeLV and FIV coinfection likely results in more severe and rapidly progressive disease.

3

Only reduced RBC counts at time of FIV and FeLV diagnosis have been shown to be a negative prognostic indictor for survival; in this study, FeLV-infected cats with reduced RBC counts at diagnosis had a death ratio 3.5 times higher than FeLV-infected cats with normal RBC counts at diagnosis. Thus, blood counts should be evaluated at diagnosis and all follow-up examinations for retrovirus-infected cats.

References

For global readers, a calculator to convert laboratory values, dosages, and other measurements to SI units can be found here.

All Clinician's Brief content is reviewed for accuracy at the time of publication. Previously published content may not reflect recent developments in research and practice.

Material from Digital Edition may not be reproduced, distributed, or used in whole or in part without prior permission of Educational Concepts, LLC. For questions or inquiries please contact us.


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Nonazole Wipes for Malassezia spp-Associated Dermatitis

William Oldenhoff, DVM, DACVD, Madison Veterinary Specialists in Monona, Wisconsin

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Nonazole Wipes for <em>Malassezia</em> spp-Associated Dermatitis

In the Literature

Sjöström Y, Mellor P, Bergvall K. A novel non-azole topical treatment reduces Malassezia numbers and associated dermatitis: a short term prospective, randomized, blinded and placebo-controlled trial in naturally infected dogs. Vet Dermatol. 2018;29(1):14-e7.


FROM THE PAGE …

Malassezia spp-associated dermatitis (MAD) is a common skin condition in dogs that often contributes to the exacerbation of atopic dermatitis. Treatment with an azole is generally the standard of care. Although likely uncommon, there have been reports of decreased susceptibility to azoles,1-3 creating a need for additional therapeutic options for MAD.

This study* assessed a commercially available nonazole solution. Eighteen dogs with MAD on at least 2 paws were recruited. Each dog was its own control. In a blinded fashion, the test solution was applied daily to one affected paw, and placebo was applied daily to the other. The dogs were rechecked 2 weeks after enrollment. Malassezia spp numbers were compared between the initial visit and the recheck.  The owners also reported pruritus levels for each paw both before and after the trial.

There was significant reduction in Malassezia spp numbers in the test-solution group as compared with the placebo group. Owners reported improvement in pruritus of both the placebo-treated paw and the test-solution–treated paw. No significant difference in pruritus levels was observed between the 2 groups at the end of the study. 


… TO YOUR PATIENTS

Key pearls to put into practice:

1

The nonazole wipes used in this study show promise as an additional tool to treat Malassezia spp overgrowth on canine paws; however, this product is not currently available in the United States. Further trials are also needed to compare this product with existing azole products.

2

Although yeast numbers decreased significantly in the actively treated paw, owners reported improved pruritus in both placebo and test-solution–treated paws. One potential explanation is that some of these dogs may have been atopic in addition to having MAD. It is possible that the topical treatments removed pollens and thus improved atopic pododermatitis and improved pruritus regardless of change in Malassezia spp numbers. This highlights the value of wiping the paws of any dog with pododermatitis. 

3

Malassezia spp are part of the normal flora; overgrowth is typically secondary to some primary disease process (eg, allergy, endocrinopathy). Dogs with Malassezia spp overgrowth should also be evaluated for primary conditions. Treatment of the primary disease process may prevent secondary yeast overgrowth from developing.

*This study was partially supported by Orion Pharma Animal Health, Sollentuna.

References

For global readers, a calculator to convert laboratory values, dosages, and other measurements to SI units can be found here.

All Clinician's Brief content is reviewed for accuracy at the time of publication. Previously published content may not reflect recent developments in research and practice.

Material from Digital Edition may not be reproduced, distributed, or used in whole or in part without prior permission of Educational Concepts, LLC. For questions or inquiries please contact us.


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Research Note: Personality & Pain Assessment in Dogs

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Pain control is a key element of animal welfare, and behavior scales are often used for quantification. Personality, defined as individual differences in behavior that are stable over time and across contexts, can affect behavior assessment scales. This study investigated whether extraversion and neuroticism (as measured by the Monash Canine Personality Questionnaire-Revised) are associated with differences in behavioral and physiologic responses to pain induced by routine neutering in dogs. Results indicated that more highly extraverted dogs had significantly higher pain scores, whereas neuroticism was not associated with physiologic or behavioral pain responses. Owners’ ratings of their dog’s pain tolerance were not found to be a reliable predictor of pain response.

Source

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Differential Diagnosis: Hypoglycemia

Shanna Hillsman, LVMT, University of Tennessee

M. Katherine Tolbert, DVM, PhD, DACVIM (SAIM), Texas A&M University

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Differential Diagnosis: Hypoglycemia

Following are differential diagnoses, listed in order of likeliness, for patients presented with hypoglycemia.

  • Spurious (eg, storage artifact)
  • Neonates (typically <6 weeks of age; normal finding or related to another condition [eg, portosystemic shunt])
  • Toy-breed puppy (can occur in healthy puppies when fasting or if no access to nursing)
  • Exogenous insulin overdose
  • Hepatic failure
  • Portosystemic shunt
  • Hypoadrenocorticism
  • Sepsis
  • Systemic inflammatory response syndrome
  • Insulinoma
  • Xylitol toxicity
  • Paraneoplastic syndrome (eg, leiomyoma/leiomyosarcoma, hepatoma)
  • High-intensity exercise
  • Pituitary dwarfism
  • Glycogen storage disease
  • Renal glucosuria
  • Polycythemia
  • Oleander toxicity
  • Amphetamine-dextroamphetamine toxicity
  • Trypanosoma congolense infection (only in specific geographic regions)

References

For global readers, a calculator to convert laboratory values, dosages, and other measurements to SI units can be found here.

All Clinician's Brief content is reviewed for accuracy at the time of publication. Previously published content may not reflect recent developments in research and practice.

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Top 5 Causes of Eosinophilia in Cats

Glenn A. Olah, DVM, PhD, DABVP (Feline), Winn Feline Foundation, Albuquerque Cat Clinic, Albuquerque, New Mexico

Clinical Pathology

|Peer Reviewed

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Top 5 Causes of Eosinophilia in Cats

Eosinophils are polymorphonuclear, granulocytic leukocytes involved in the initiation and propagation of inflammatory responses that act as modulators of innate and adaptive immunity.1 Normal eosinophil blood count typically measures between 0 and 1500/μL and may vary based on the instrumentation and methodology used (eg, reference laboratory vs in-house).2,3 Eosinophilia is a state in which blood eosinophil levels are above the normal reference interval.

Eosinophilia in cats is most often associated with parasitic infestation or hypersensitivity reactions (ie, allergies).4,5 Tissue sites most commonly affected by hypersensitivity conditions include the skin, lungs, and/or GI tract.6 Transient epinephrine-induced excitement may lead to mild eosinophilia in conjunction with lymphocytosis and mild neutrophilia. Prolonged survival and increased numbers of eosinophils may also be seen in patients with hypereosinophilic syndrome, some neoplastic conditions, and/or paraneoplastic syndromes.7-9

Eosinophils—with or without accompanying peripheral eosinophilia—have 3 primary features, including:

  • Role as a vital host defense against helminthic parasitic infections
  • Frequent presence in allergic disorders (eg, asthma, atopy, food allergies)
  • Nonspecific, destructive, and cytotoxic effects against both the pathogen and the host

Following are the author’s 5 most common causes of eosinophilia in cats.

1

Internal & External Parasitism

Eosinophilia associated with parasitic infestations in cats includes those caused by Gl helminths (eg, Toxocara cati, Toxascaris leonina, Strongyloides stercoralis, Ancylostoma spp), filarial helminths (eg, Dirofilaria immitis), respiratory helminths (eg, Aelurostrongylus abstrusus, Eucoleus aerophilus, Paragonimus kellicotti), ectoparasites (eg, fleas, ticks, mites, mosquitoes), and, rarely, protozoa (eg, Giardia duodenalis, Coccidia spp, Isospora spp, Toxoplasma gondii, Tritrichomonas foetus).10,11

Internal and external parasites may cause clinical signs ranging from subclinical infections to serious disease. Clinical signs commonly depend on the body system that is parasitized (eg, diarrhea, vomiting, failure to thrive, or weight loss with GI parasites; anemia, lackluster coat, or skin lesions with flea infestation). Clinically significant parasitism can affect any cat but depends on age (with increased prevalence and incidence in kittens), general health and immune function, geographic location, and lifestyle (with increased risk to outdoor cats, feral cats, and cats that hunt).

Eosinophil function contributes to the host’s defense against helminth infection.12 The large size of helminths precludes phagocytosis. Eosinophils adhere to a variety of tissue-invading helminth larvae coated with immunoglobulins, then degranulate and secrete soluble factors, which kill larvae.12-16 Migrating parasites that have been in prolonged contact with host tissue are more likely to induce peripheral eosinophilia, as are migrating stages of ascarids, hookworms, lungworms, and heartworms.17-22 Rather than persisting long-term, peripheral eosinophilia may be present for only a few weeks after helminth endoparasite infection or for a few months after heartworm infection.17,18,22,23 A low intestinal parasite burden may not even induce peripheral eosinophilia.23

One report showed no difference in mean eosinophil counts in 62 cats with endoparasitism as compared with 122 cats with a negative fecal examination for endoparasite ova.4 Although sensitivity of fecal flotation methods can vary approximately 13% to 100% depending on the exact method and combination of methods used (eg, zinc sulfate centrifugation, saturated sodium chloride, spontaneous sedimentation, formol-ether technique) and on presence of particular endoparasites,24 absence of peripheral eosinophilia does not rule out parasitic infection. However, presence of peripheral eosinophilia in combination with other diagnostic information (eg, fecal ova or helminth larvae noted in fecal analysis, elevated serum liver parameters with liver flukes, respiratory signs with migrating larva or lungworms) is supportive of presence of clinically significant parasitic infection.

2

Feline Allergic Dermatitis

Allergic inflammation is an inappropriate immune response that arises from polarization of T cells toward a Th2 immune-mediated response. Greater expression of Th2 cytokines, along with downregulation of Th1 cytokines, is seen in allergen-challenged patients. Eosinophils are increased in number in both the serum and in skin lesions and contribute to the pathogenesis of feline allergic dermatitis. Pathogenesis involves multifaceted immune dysregulation and skin barrier dysfunction stemming from an increasingly complex interplay of genetic and environmental factors.25-27 Impaired skin integrity increases patient susceptibility to allergens and pathogens, which may lead to activation of innate and adaptive immune responses.27

Hypersensitivity may manifest as reactions to allergens derived from food ingredients, inhalants (eg, atopy), contact material, and/or fleas, lice, mites, ticks, or insect bites (eg, hymenoptera). Regardless of the inciting cause, cats with allergic dermatitis are usually pruritic, and primary skin lesions (eg, erythema, maculae, papules) are frequently present. One or more of the following cutaneous reaction patterns may be observed28,29:

  • Head, neck, and/or pinnal excoriations
  • Self-induced alopecia
  • Miliary dermatitis
  • Eosinophilic lesions, including eosinophilic plaques, eosinophilic granulomas, and indolent ulcers

Histologic or cytologic examination of pruritus-induced skin lesions and surrounding areas commonly reveals increased numbers of eosinophils and mast cells.30-32 The degree of tissue eosinophilia can correlate with the severity of skin lesions.30-32

Age at onset of allergic dermatitis signs is broad. Atopic cats have been reported to experience onset between 3 months and 12 years of age, with a mean age of approximately 2 to 3 years, and cats with food allergies have been reported to experience onset between 3 months and 11 years of age, with a mean age of 4 to 5 years.33-35 Various studies have reported that approximately 38% to 46% of allergic cats developed signs before 2 to 3 years of age.34,36 No particular breed or sex predilection has been firmly established for atopy,34 although some studies have noted an increase of atopy in purebreed and female cats.32 Higher risk for food allergies has been noted in Siamese, Siamese crossbreeds, and Birmans.34 Positive treatment responses to atopic dermatitis therapy have been reported with cyclosporine (100%), systemic glucocorticoids (55%), and allergen-specific immunotherapy (57%), and a partial-to-good response has been reported with antihistamines (67%).35 Avoidance of allergens is recommended.

Flea infestation, the most common cause of allergic dermatitis in cats, may be accompanied by peripheral eosinophilia in approximately 13% to 20% of allergic cats.37 Peripheral eosinophilia may be identified in 20% to 50% of cats with food allergies. Concurrent GI signs, including frequent bowel movements, vomiting, diarrhea, and/or flatulence, may be exhibited.33,34

3

Feline Asthma

Feline asthma is a result of a reaction to inhaled aeroallergens provoking a type 1 hypersensitivity reaction characterized by eosinophilic airway inflammation and bronchoconstriction.38 Although their clinical presentations may be similar, chronic bronchitis and asthma have different etiologies. Chronic bronchitis may arise from previous airway insult (eg, smoke, toxins, infections)—leading to permanent lung damage—and is dominated by neutrophilic inflammation of the lower airways accompanied by edema and hypertrophy of the respiratory mucosa and excessive mucus production. Although asthma is dominated by eosinophilic airway inflammation (≥17% eosinophils in bronchial lavage cytology) and bronchoconstriction, excessive mucus production and bronchial wall edema are often present to varying degrees.39,40

Hallmark characteristics of asthma include reversible airway inflammation, bronchoconstriction causing obstruction/airflow limitation, and airway hyperresponsiveness.39

Long-term asthma can lead to irreversible airway remodeling (including bronchiectasis, fibrosis, and/or emphysema), lung hyperinflation, and airway trapping. Cats with asthma are usually young to middle-aged, and no sex predilection has been identified, although middle-aged (ie, 2-8 years) female cats and some Oriental breeds appear to be overrepresented.38 Asthma is estimated to affect approximately 1% of the general domestic cat population and possibly as many as 5% of the Oriental cat population.39,41 Clinical presentation includes various combinations of coughing, expiratory wheezing, tachypnea, exercise intolerance, and respiratory distress characterized by an expiratory respiratory pattern.41-44

Clinical signs of heartworm-associated respiratory disease may appear similar to asthma; therefore, heartworm serum antibody/antigen tests may be helpful in ruling out heartworm infection.38,39,45,46 However, heartworm tests have poor sensitivity because antibody and antigen blood levels may only be transient and can be easily missed. Appropriate fecal analysis (eg, direct, float, centrifugation, Baermann technique for Aelurostrongylus abstrusus) should be performed in cats with lower respiratory disease signs if intestinal parasite larval lung migration is suspected and in cats that live in or have visited lungworm-endemic areas.

The most common radiographic change described in patients with asthma is a bronchial pattern with lung hyperinflation arising from bronchial wall thickening due to peribronchial infiltration. Focal atelectasis (typically affecting the right middle lung lobe) and/or diffuse interstitial patterns may also be seen.41,42

The most common treatment for asthma is long-term anti-inflammatory doses of corticosteroids administered orally (eg, prednisolone) or via an inhaler (eg, fluticasone). Bronchodilators (eg, terbutaline) may also be included in therapy. Other drugs such as immunomodulating agents (eg, cyclosporine) may be used, particularly in cats that do not respond well to corticosteroids23 or that develop diabetes mellitus or heart disease.47

Approximately 20% of feline asthma patients have peripheral eosinophilia, which is not correlated with the degree of airway eosinophilia.38,39,43,48 Hyperproteinemia has been reported in 33% to 50% of feline asthma cases.38,49,50

4

Eosinophilic Gastrointestinal Disease

Eosinophilic enteritis (EE) has been reported to be the second most prevalent variant of inflammatory bowel disease (IBD), only surpassed by the lymphocytic-plasmacytic form.51 Although the etiology is poorly defined, it has been hypothesized that affected cats suffer from immunologic dysregulation triggered by one or more factors, possibly including food ingredients (eg, food allergies or intolerance), dysbiosis of gut microbiota, or other factors (eg, ingestion of ectoparasites, endoparasites, excessive hair, or plant material).23 Eosinophilic IBD may also involve the stomach and/or colon.51 Diagnosis of EE is made via intestinal biopsy. Cats with primary lymphocytic-plasmacytic or lymphocytic IBD may also show subtle eosinophilic infiltrates on histopathology. In contrast, cats with EE have predominant tissue eosinophilia, variable mucosal architectural disturbances (eg, villus atrophy), and increased incidence of total intestinal wall thickening associated primarily with muscularis thickening as compared with cats with lymphocytic or lymphocytic-plasmacytic IBD.23,52 Diffuse disease is most common, but multisegmental EE has also been reported.52

No breed or sex predilections have been reported for EE in cats53,54; however, although cats of any age can be affected, the condition may be more common in mature cats (ie, 7-9 years). Clinical signs are similar to those of other forms of chronic gastroenteritis and may include vomiting, small- or large-bowel diarrhea, weight loss, and/or anorexia.53 Borborygmus, flatulence, abdominal pain, hematochezia, and mucoid stools are reported less commonly. Idiopathic EE may be solely or partially responsive to treatment with hypoallergenic diets and corticosteroids, which may be suggestive of an underlying immune disorder.52

Peripheral eosinophilia is not always present with EE but was observed in approximately 43% of cats in one study.52 If peripheral eosinophilia is associated with GI eosinophilic inflammation, other causes (eg, GI parasites, food-responsive enteropathy, intestinal neoplasia [eg, mast cell tumor, lymphoma], hypoadrenocorticism) should be ruled out.54 Parasitic infestation or dietary intolerance should be considered if moderate-to-large numbers of eosinophils are noted in intestinal biopsy samples with accompanying mild peripheral eosinophilia.53

Feline gastrointestinal eosinophilic sclerosing fibroplasia (FGESF) is a recently recognized nodular, nonneoplastic, densely fibroproliferative, eosinophil- and mast cell-rich inflammatory disease. It is thought to be a variant of EE.54-56 Its pathogenesis is unknown, but bacteria have been postulated to be an initiating factor due to their presence in 56% to 85% of cases55,57,58; however, antibiotic treatment alone is ineffective.55,57,58 Fungal infection has also been thought to be involved in the pathogenesis in some cases,59 but in other cases, no bacteria or fungi have been detected.55,56,60 Several other mechanisms (eg, penetrating wounds from a migrating foreign body, genetic eosinophil dysregulation, FHV-1, food hypersensitivity) have been proposed to be involved in the pathogenesis of FGESF.55,56 FGESF carries a guarded prognosis if untreated; however, survival times may be good in some cats, with some possibly surviving for years if they receive appropriate treatment, which includes a combination of surgery, antibiotics, and immunomodulatory drugs.57

Peripheral eosinophilia occurs more often in cats with FGESF than in cats with EE.52,55 One study reported that 58% of cats with FGESF had peripheral eosinophilia.55 If peripheral eosinophilia and an abdominal mass are observed, FGESF should be considered a differential diagnosis,57 although absence of peripheral eosinophilia alone does not rule out FGESF.57

5

Hypereosinophilic Syndrome, Neoplasia, & Paraneoplastic Syndrome

Hypereosinophilic syndrome is an uncommon systemic disorder in cats characterized by sustained eosinophilia resulting from the overproduction of eosinophils in the bone marrow and infiltration of eosinophils into multiple tissues and organs, often leading to organ damage and failure.23,61,62

Eosinophilic leukemia has been reported in cats and may be difficult to distinguish from hypereosinophilic syndrome, as each condition may represent different patterns of a similar neoplastic process.7,8 Some subtle differences in bone marrow and hematologic assessment have been reported; for example, patients with eosinophilic leukemia have been reported to have a higher myeloid:erythroid ratio in bone marrow and a higher WBC count with increased immature eosinophils. However, absolute peripheral eosinophilia is often higher with hypereosinophilic syndrome, although both conditions are typically associated with severe eosinophilia (ie, 3500-130 000/μL).

Peripheral eosinophilia may also be associated with paraneoplastic syndrome.9 Paraneoplastic peripheral eosinophilia has been observed with mast cell tumors, intestinal T-cell lymphoma, acute leukemia, and transitional cell carcinoma of the bladder and likely involves production of factors including IL-5, IL-3, and granulocyte-macrophage colony-stimulating factor by these tumors.9,63-65

Conclusion

In human medicine, it has been suggested that eosinophils have important regulatory roles in homeostasis and immunity.66-68 With an increased understanding of basic eosinophil biology, improved targeted therapies in humans—and thus, potentially, in cats—toward eosinophilic diseases may be possible.68

EE = eosinophilic enteritis, FGESF = feline gastrointestinal eosinophilic sclerosing fibroplasia, IBD = inflammatory bowel disease

References

For global readers, a calculator to convert laboratory values, dosages, and other measurements to SI units can be found here.

All Clinician's Brief content is reviewed for accuracy at the time of publication. Previously published content may not reflect recent developments in research and practice.

Material from Digital Edition may not be reproduced, distributed, or used in whole or in part without prior permission of Educational Concepts, LLC. For questions or inquiries please contact us.


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Guidelines for Emergency Patient Referral

Katherine Bennett, DVM, University of Tennessee

Christine Egger, DVM, MVSc, CVA, CVH, DACVAA, University of Tennessee

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Guidelines for Emergency Patient Referral

General practitioners generally have a rapport with pet owners and provide important primary care, including preventive medicine, diagnostics, and long-term disease treatment and control, to a variety of patients on a daily basis. However, some patients are presented with or develop conditions beyond the scope of general practice.

In these instances, practitioners may refer patients to other hospitals for more sophisticated diagnostics (eg, MRI), for consultation with a boarded specialist, or for 24-hour observation or intensive nursing care. Referral practices depend on a strong relationship with general practitioners to provide continuity of care and pet owner communication and to promote patient health and safety when a patient is transferred from one practice to another. In human medicine, good communication between the referring physician and the receiving physician, as well as between referring physician and the patient, is essential for a safe referral process and prevents poor continuity of care and delayed diagnoses.1-3 Likewise, in veterinary medicine, good communication between the general practitioner, pet owner, and specialist or referral hospital strengthens the patient care team.

Preparing the Pet Owner for Referral

Strong communication relies on the referring veterinarian as a point of reference for both the referral practice and the pet owner. When a general practitioner recommends referral, he or she should involve the pet owner in the decision: Is the owner willing to seek additional care from another facility? Does the owner have pet insurance, or would additional treatment be cost-prohibitive? Should the facility offer 24-hour care, specialty consultation, diagnostics, or a combination of these? With agreement from the owner, the referring veterinarian should then contact the referral practice to determine their preferences for the referral process.

At this time, the referral practice can ask for patient signalment and history, request the patient’s estimated time of arrival, assess the need for medication (eg, sedation, analgesia) to facilitate transport, and offer a general estimate of initial costs, which may change, depending on additional diagnostic testing after the patient is presented to the referral practice. The referring veterinarian can also inquire whether the referral practice has a transport vehicle for emergency referral cases. The referring veterinarian can use this information to help owners understand the diagnostic services or treatment provided by the referral practice.

Preparing the Patient for Referral

Documentation

The referring practice should maintain careful records of treatments and diagnostics for continuity of care. If an intravenous catheter or a bandage is placed, the date, time, and signature should be included, along with additional relevant information (Figure).

A study involving the assessment of a referral letter in a human medicine practice noted that in addition to conveying information about the patient, referral letters also reflect the diagnostic skills, communication skills, and professionalism of the doctor.3 Documentation should be succinct and detailed. Descriptors of the patient, presentation, physical examination findings, treatments, and diagnostics should be included, as should the date and time, doses, and routes of medications and fluids, when possible. In addition, physical and/or electronic copies of diagnostics (eg, imaging, blood work) should be included.

Intravenous catheter placement with informative labeling, including catheter size, date and time placed, and the veterinary team member’s initials
Intravenous catheter placement with informative labeling, including catheter size, date and time placed, and the veterinary team member’s initials

Figure Intravenous catheter placement with informative labeling, including catheter size, date and time placed, and the veterinary team member’s initials

Figure Intravenous catheter placement with informative labeling, including catheter size, date and time placed, and the veterinary team member’s initials

Medication

After the initial examination is performed by the referring veterinarian, sedation and analgesia are crucial to facilitate comfortable transport of the critical patient. The transportation time between practices will likely determine the dose and route of sedative/analgesic that is administered. Communication with the referral veterinarian should help facilitate an analgesic choice that will keep the patient comfortable without causing hemodynamic or neurologic instability before arrival at the referral practice. Drugs to consider include those that are reversible and those that will last the duration of transportation; when applicable, long-lasting antiepileptics (eg, levetiracetam, phenobarbital) and analgesics (eg, pure μ-opioid agonists) should be considered.

Every medication administered to a patient, particularly for transportation, requires a prescription and associated prescription label. This allows the pet owner to be in possession of the medication (especially controlled substances) while transporting the patient. Depending on local state laws, many hospitals will not receive controlled substances, and prescribed medication for critical patients may not be used at the referral hospital.4

Transport

Transport of a critical patient can be difficult, especially when performed by the pet owner. Patients should be stabilized before transport, although the nature of the emergency may preclude complete stabilization. Large, open wounds should be carefully bandaged before transport. Stabilizing patients with possible fractures is ideal but may require instruction from the receiving surgeon, further promoting the importance of communication. Some larger referral hospitals may provide an ambulance service to facilitate critical patient transport. Some ambulance services may provide  oxygen administration, patient monitoring, intravenous fluid administration, and safe patient restraint for transport in addition to patient transport.5

Using appropriate protective tools for transport (ie, those that do not prevent the patient from breathing, panting, or vomiting) such as Elizabethan collars or basket muzzles can help ensure pet owner and veterinary team safety.

Maintaining patient comfort in the vehicle is essential. Patients should be placed safely in the vehicle with support for their head and neck and any other wounds or fractures. Vehicle temperature is also critical, as patients in shock can be highly susceptible to extreme heat and cold. Respiratory distress can be worsened by heat, so cool air in the vehicle is helpful to promote anxiolysis. 

TOP 5 ITEMS TO COMMUNICATE WHEN REFERRING CRITICAL PATIENTS

  • Patient signalment, presenting complaint, and relevant history
  • Initial physical examination findings
  • Treatments, such as intravenous catheter placement and fluids and medications given (including times, routes, and dosages)
  • Diagnostics (eg, radiographs, FAST examination, blood work)
  • Current patient status (eg, “stable,” “experiencing respiratory difficulty”)

Conclusion

Follow-up communication between the referring veterinarian and the referral practice is paramount to providing both continuity of care and treatment follow-through. Updates on diagnostics, findings, treatments, and patient outcome are all critical for both practices to be aware of the case progression and to facilitate an understanding of the case if the patient is returned to the referring veterinarian for additional care.

References

For global readers, a calculator to convert laboratory values, dosages, and other measurements to SI units can be found here.

All Clinician's Brief content is reviewed for accuracy at the time of publication. Previously published content may not reflect recent developments in research and practice.

Material from Digital Edition may not be reproduced, distributed, or used in whole or in part without prior permission of Educational Concepts, LLC. For questions or inquiries please contact us.


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Diuretics Commonly Used in Dogs & Cats

Diuretics Commonly Used in Dogs & Cats

David F. Senior, BVSc, DACVIM (SAIM), DECVIM-CA, Louisiana State University School of Veterinary Medicine

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Diuretics Commonly Used in Dogs & Cats

Diuretics increase tubular fluid flow rate and urine volume primarily by increasing the renal excretion of sodium and attendant anions. These characteristics allow diuretics to be useful in a number of clinical conditions (see Common Indications for Treatment with Diuretics) in which manipulation of renal function and extracellular fluid (ECF) volume and composition are indicated.

CLASSES OF DIURETICS & CLINICAL USE

Loop Diuretics

Loop diuretics, such as furosemide, bumetanide, and torsemide, inhibit the sodium-potassium-chloride (Na-K-Cl) symporter in the luminal membrane of the thick ascending limb of the loop of Henle, which induces the countercurrent multiplier effect. Inhibition of sodium reabsorption induces osmotic diuresis in more distal sections of the tubule, enhancing urinary excretion of sodium, chloride, potassium, calcium, and water. 

Furosemide

Formulations → Injectable: 50 mg/mL solution; oral solution (syrup): 10 mg/mL in 60 mL; tablets: 12.5, 50 mg

For pulmonary edema & ascites associated with congestive heart failure (CHF)1

Dose (dogs) → Injection: Start with 2 mg/kg q6-8h IV or IM; increase dose in increments of 1 mg/kg to effect (maximum, 5.5 mg/kg q6-8h); oral: up to 6 mg/kg PO q8h

Dose (cats) → Injection: Start with 0.5 mg/kg IV or IM q12h; increase dose in increments of 2.2 mg/kg to effect (maximum, 5 mg/kg q12-24h)

Maintenance dose → Oral: Start with 1 mg/kg PO every 2-3 days up to 2 mg/kg PO q8-12h, depending on response

Key Points

  • Conservative doses should be implemented initially, then adjusted to the minimum effective dose based on a target respiration rate.1
    • Ideal respiration rate varies based on the individual patient and environmental conditions and is achieved when the patient exhibits a steady, relaxed respiration pattern after stabilization.
  • Parenteral furosemide is usually only used for a short period in patients with acute fluid accumulation.
    • Single intravenous, subcutaneous, and oral administration may be equally effective to increase urine production in dogs.2
  • Also see General Comments.

For fluid retention associated with glomerular disease3

Dose (dogs only) → 1 mg/kg IV or IM q6-12h, with incremental increases of 0.5-1 mg/kg IV or IM q6-12h

Key Points

  • Use of diuretics for glomerular disease is reserved for patients with severe pulmonary edema or ascites that interferes with major organ function.3
  • Mild peripheral edema is best left untreated in these patients.
  • In patients with hypoalbuminemia, further ECF reduction with diuretics can cause severe hypovolemia and circulatory collapse.3
  • Parenteral furosemide is usually used for a short period in patients with acute fluid accumulation.3
  • Also see General Comments.

For acute management of moderate-to-severe or rapidly progressing hypercalcemia4

Dose (dogs only) → 2-4 mg/kg IV, SC, or PO q8-12h

Key Points

  • Furosemide is a temporary supportive treatment for short-term control of hypercalcemia until the primary cause can be identified and corrected.4
  • Full hydration should be maintained in patients being treated with furosemide for hypercalcemia.5
  • Furosemide is usually reserved for patients that fail to respond to solute diuresis.
  • Also see General Comments.

For prevention of cyclophosphamide-induced hemorrhagic cystitis5

Dose (dogs only) → 0.5-2.2 mg/kg PO or IV q24h

  • Shown to be effective in reducing the incidence of sterile hemorrhagic cystitis in dogs currently receiving metronomic low-dose oral cyclophosphamide6

General Comments (Furosemide)

  • Doses should be adjusted based on individual patient response.
  • Renal function and electrolytes, especially potassium, should be monitored to prevent prerenal azotemia.
  • In cats: Ototoxicity and hearing loss can occur at high doses.
  • Furosemide can potentiate the hypotensive effects of angiotensin-converting enzyme (ACE) inhibitors.
  • Severe hypokalemia and hyponatremia can develop during treatment, particularly in patients with reduced food and water intake.
  • In cats: Extreme dehydration and hypokalemia can occur when diuretics are administered long-term; careful monitoring is required.

Common Indications for Treatment with Diuretics

  • Control of pulmonary edema by mobilization of fluid: Both loop and thiazide diuretics reduce ECF volume, which in turn reduces intracapillary hydrostatic pressure, a Starling force that contributes to interstitial pulmonary edema.
  • Acute kidney injury: Manipulation of fluid electrolyte and acid-base disturbances in patients with oliguric acute kidney injury is easier if urine output can be increased with administration of mannitol and/or loop diuretics.
  • Hypercalcemia: Loop diuretics can be administered to increase renal calcium excretion, thereby addressing extreme, life-threatening hypercalcemia.
  • Control of hypertension: The reduced ECF volume and reduced plasma volume produced by loop and thiazide diuretics can render them useful as adjunct therapy to control hypertension.
  • Control of cerebral edema and glaucoma: By increasing plasma osmolality, IV boluses of mannitol can increase transfer of fluid from the intracellular fluid space and transcellular fluid space to ECF space, which can rapidly reduce cerebral swelling and intraocular pressure.
  • Calcium oxalate urolithiasis: Because thiazide diuretics can decrease urine calcium excretion, they are indicated in long-term prevention of calcium oxalate urolithiasis.
  • Nephrogenic diabetes insipidus: Loop diuretics combined with a low-sodium diet can reduce ECF volume so a greater proportion of glomerular filtrate is reabsorbed proximally, leaving less to be excreted in the absence of antidiuretic hormone activity, also known as vasopressin.
  • Prevention of cyclophosphamide-induced hemorrhagic cystitis: Concurrent administration of furosemide can reduce the likelihood of cyclophosphamide-associated sterile hemorrhagic cystitis in dogs.

Bumetanide

Formulations → Oral tablets: 0.5, 1, 2 mg; injection: 0.25 mg/mL

For cardiogenic or pulmonary edema, acute oliguric kidney failure, & moderate-to-severe hypercalcemia7-9

Dose (anecdotal; dogs, cats) → Definitive doses have not been published.

  • Because bumetanide is 25 to 50 times more potent than furosemide on a mg/mL basis, furosemide doses can be divided by 25 or 50 to arrive at a best-guess dose.7-9

Key Points

  • There seems to be little reason to use bumetanide instead of furosemide, as their modes of action are identical.
    • Furosemide is approved for use in dogs and cats; doses are anecdotal but well established in small animal medicine.
  • Extreme dehydration can occur in cats receiving long-term diuretic therapy.

Torsemide

Formulations → Oral tablets: 5, 10, 20, 100 mg; injection: 10 mg/mL

For pulmonary edema & ascites associated with CHF10

Dose (dogs, cats) → 0.2-0.3 mg/kg PO q8-24h

Key Points

  • Approximately 10 times more potent than furosemide
  • Thought to be indicated in CHF patients that prove refractory to furosemide treatment10
  • Tablet size can make oral dosing difficult in small dogs and cats; however, compounded 5 mg/mL suspension remains stable for 90 days at room temperature.9
  • Not as potassium-wasting as furosemide10
  • Longer duration of action than furosemide; single-daily dosing has proven effective in dogs with degenerative mitral valve disease.11
  • Significant dehydration can occur when cats receive long-term diuretic therapy.

Osmotic Diuretic

Mannitol is a freely filtered, nonabsorbed 6-carbon sugar that promotes osmotic diuresis via retention of sodium and water throughout the nephron, resulting in enhanced excretion of sodium, chloride, potassium, and water.

Mannitol

Formulations → 5%, 10%, 15%, 20%, 25% IV solutions

For oliguric acute kidney injury12

Dose (dogs, cats) → 0.25-1 g/kg IV (slow bolus over 10-20 minutes) of 20%-25% solution

  • If diuresis is induced within 30 to 60 minutes, continue administering at 60-120 mg/kg/hr IV CRI or 0.25-0.5 g/kg IV q4-6h.
  • If diuresis fails to develop within 60 minutes, cautiously administer an additional 0.25-0.5 g/kg IV (slow bolus over 10-20 minutes) of 20%-25% solution.

Key Points

  • Should only be administered when patients with acute kidney injury remain oliguric after complete rehydration
  • Contraindicated in cases of ethylene glycol poisoning because of the preexisting hyperosmolar state
  • Dose can be repeated once if initial administration fails to increase urine output.
    • Further administration of mannitol is contraindicated if diuresis fails to develop.
  • In dogs: Short-lived impairment of platelet function may develop after mannitol administration.13
  • Also see General Comments.

For acute glaucoma14

Dose (dogs, cats) → 0.5-1 g/kg IV (slow bolus over 10-20 minutes) of 20% solution

Key Points

  • Mannitol use is indicated in patients with acute glaucoma that is refractory to topical medication.14
  • Should be used only after correcting for fluid, electrolyte, and/or acid-base balance and if the patient is not anuric14
  • Withholding water for 1 to 4 hours after treatment is recommended.
  • Effect begins in 20 to 30 minutes and can persist for several hours.14
  • Also see General Comments.

For increased CSF pressure/cerebral edema14

Dose (dogs, cats) → 0.5 g/kg IV (20% solution; slow bolus over 15-20 minutes)

  • If required, repeat bolus at 0.5 g/kg IV q6-8h.

Key Points

  • Should only be used after correcting for fluid, electrolyte, and/or acid-base balance and if the patient is not anuric15
  • Contraindicated if ongoing intracranial hemorrhage is suspected
  • Effect begins within 30 minutes and can persist for 6 hours.15
  • Also see General Comments.

General Comments (Mannitol)

  • Fluid, electrolyte, and acid-base status must be carefully monitored.12,14
  • Contraindications include CHF, fluid overload, and pulmonary edema.12,14

Thiazide Diuretics

Thiazide diuretics, such as hydrochlorothiazide and chlorothiazide, inhibit the Na-Cl cotransport system in the early distal tubule. The consequences are similar to the action of loop diuretics in terms of increased sodium, chloride, potassium, and water excretion; however, because the effect is more distal, thiazides are not as powerful as loop diuretics and calcium excretion is reduced. 

Hydrochlorothiazide

Formulations → Oral tablets: 12.5, 25, 50 mg; oral capsules: 12.5 mg; many combined formulations with other drugs

For prevention of recurrent calcium oxalate urolithiasis16,17

Dose (dogs) → 2 mg/kg PO q12h

Dose (cats) → 1 mg/kg PO q12h

Key Points

  • Used in conjunction with appropriate diets and medications to reduce calcium excretion and relative supersaturation of urine for calcium oxalate16,17
  • Usually only added to a preventive regimen if uroliths recur, even with appropriate dietary management and potassium citrate supplementation16
  • Patients receiving long-term hydrochlorothiazide treatment should be monitored for hypercalcemia.
    • In cats: Extreme dehydration can occur when cats receive long-term diuretic therapy.17

For pulmonary edema & ascites associated with CHF18

Dose (dogs) → 1-4 mg/kg PO q12h

Dose (cats) → 1-2 mg/kg PO q12h

Key Point

  • Doses should be started at the lower dose range and gradually increased until desired clinical outcome is achieved.18

For ascites secondary to liver disease19

Dose (dogs, cats) → 0.5-1 mg/kg PO q12h (in 1:1 combination with spironolactone)

Key Points

  • Dose based on spironolactone content of the combined drug19
  • The combination of spironolactone with hydrochlorothiazide reduces renal potassium loss.20
  • Doses should be started at the lower dose range and gradually increased until desired clinical outcome is achieved.19

For systemic hypertension21

Dose (dogs only) → 1 mg/kg PO q12-24h

Key Points

  • Used as a second-choice/adjunct agent after ACE inhibitors and calcium-channel–blocking agents have been implemented
  • Hydrochlorothiazide combined with spironolactone reduces renal potassium loss.

For nephrogenic diabetes insipidus22

Dose (dogs only) → 2 mg/kg PO q12h

Key Point

  • Should be combined with a low-sodium diet to reduce urine volume

Chlorothiazide

Formulations → Tablets: 250, 500 mg; oral suspension: 50 mg/mL; lyophilized powder for injection: 500 mg

For diuretic & nephrogenic diabetes insipidus22

Dose (dogs, cats) → 20-40 mg/kg PO q12h

Key Point

  • Should be combined with a low-sodium diet to reduce urine volume

General Comments (Thiazide Diuretics)

  • Doses should be adjusted based on individual patient response.
  • Renal function and electrolytes, especially potassium, should be monitored to prevent prerenal azotemia.
  • Furosemide can potentiate the hypotensive effects of ACE inhibitors.
  • Severe hypokalemia and hyponatremia can develop during treatment, particularly in patients with reduced food and water intake.
  • Extreme dehydration and hypokalemia can occur when cats receive long-term diuretics; careful monitoring is required.
    • In cats: Ototoxicity and hearing loss can occur at high doses. 

Aldosterone Antagonist

The aldosterone antagonist spironolactone inhibits the action of aldosterone on the collecting duct. Aldosterone normally stimulates Na/K-ATPase pumps on the basolateral membrane of the collecting duct cells; without this action, the tendency of potassium to passively diffuse into the tubular lumen is reduced. Thus, spironolactone can be used in combination with either loop or thiazide diuretics to reduce renal potassium excretion.

Spironolactone

Formulations → Tablets: 10, 40, 80 mg; chewable tablets: 10, 50, 100 mg; benazepril–spironolactone tablets: 2.5 mg/20 mg, 5 mg/40 mg, 10 mg/80 mg

For adjunct treatment of CHF, ascites, & hypertension7,19,23,24

Dose (dogs) → 1-2 mg PO q24h

Dose (anecdotal; cats) → Not well documented but most likely same dose as used for dogs7

Key Points

  • Reduces potassium wasting caused by loop and thiazide diuretics
  • Adjunct treatment only23,24
  • Additional benefit of adding spironolactone to a heart failure regimen for dogs and cats beyond the potassium-sparing effect is not clear.
  • Ineffective as a sole agent to treat hypertension
  • Used in combination with furosemide, ACE inhibitors, pimobendan, and amlodipine; spironolactone may increase survival time in dogs with CHF, although the positive effects appear unrelated to any diuretic action.25

For fluid accumulation in glomerular disease7,23,24

Dose (dogs) → 1-2 mg PO q24h

Dose (anecdotal; cats) → Not well documented but most likely same dose as used for dogs7

Key Points

  • Reduces potassium wasting caused by loop and thiazide diuretics
  • Adjunct treatment only23,24

For hypokalemia associated with hyperaldosteronism in cats26

Dose (cats only) → 1-2 mg/kg PO q12h

Key Points

  • Spironolactone should be given in conjunction with oral potassium supplementation to control hypokalemia.
  • Treatment usually must be continued for life.
  • Concurrent treatment for hypertension with amlodipine or β blockers is usually indicated in patients with this condition.
  • Severe facial ulcerative dermatitis can develop in cats treated with spironolactone.27

ACE = angiotensin-converting enzyme, CHF = congestive heart failure, ECF = extracellular fluid

References

For global readers, a calculator to convert laboratory values, dosages, and other measurements to SI units can be found here.

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