March 2018   |   Volume 16   |   Issue 3

Linear-Stapled Gastrointestinal Anastomosis

in this issue

in this issue

Top 5 Viral Dermatoses in Cats

Optic Neuritis

Blood Smear Platelet Evaluation & Interpretation

Nutritional Management in a Senior Cat with Weight Loss

Top 5 Gastrointestinal & Hepatobiliary Antibiotics

Top 5 Corticosteroids for Use in Emergency Settings

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Linear-Stapled Gastrointestinal Anastomosis

Daniel J. Lopez, DVM, University of Guelph

Ameet Singh, DVM, DVSc, DACVS (Small Animal), University of Guelph

Daniel D. Smeak, DVM, DACVS, Colorado State University

Surgery, Soft Tissue

|Peer Reviewed

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Linear-Stapled Gastrointestinal Anastomosis

Intestinal resection and anastomosis is commonly performed in small animal practice to remove segments of bowel that are devitalized or diseased, often due to foreign material or neoplasia.1

In human and veterinary medicine, stapling devices have been developed for GI surgery, and a variety of different stapling techniques for intestinal anastomosis have been described, including1-10:

  • Everting, triangulating end-to-end anastomosis (EEA) using a thoracoabdominal linear stapler 
  • Inverting EEA using an EEA circular stapler
  • EEA using a skin stapler 
  • Antiperistaltic side-to-side (ie, functional end-to-end) anastomosis using a GI anastomosis (GIA) linear and/or cutting stapler

Stapled GIA in dogs and cats and, more recently, a technique in dogs for a stapled functional end-to-end anastomosis (SFEEA) using only a GIA stapler have also been reported.10,11 Ideally, SFEEA is used following enterectomy of the jejunum and/or ascending duodenum based on the mobility of this portion of the small intestine. Other portions of the intestine (eg, duodenum, large intestine) are more fixed because of the short mesentery, precluding the use of this technique. 

Studies have been conducted to evaluate the technique and outcome of SFEEA in veterinary medicine.1,12-14 Potential benefits of SFEEA as compared with hand-sewn anastomosis include reduced procedure time, decreased tissue trauma, decreased intraoperative contamination, consistency and repeatability of the anastomosis, and preservation of blood supply.13-15 In addition, severe luminal disparity between 2 cut bowel ends (eg, severe segmental dilation orad to an obstructive foreign body) can be readily resolved via SFEEA. A multi-institutional retrospective study in dogs demonstrated no significant difference in anastomosis dehiscence rates or decreased procedure time with SFEEA as compared with hand-sewn anastomosis.12 

Disadvantages of SFEEA as compared with hand-sewn anastomosis include the learning curve required to perform the procedure and the inability to perform this procedure in areas of the GI tract other than the jejunum and ascending duodenum. An additional limiting factor of stapled anastomosis may be financial investment, with SFEEA instruments and staple cartridges costing 15 to 25 times more than suture costs.14 However, in some institutions, the total procedural time saved may result in equivalent overall costs between SFEEA and hand-sewn anastomosis.

Preoperative peritonitis, a serum albumin concentration less than 2.5 g/dL (25 g/L), and presence of an intestinal foreign body are classically reported risk factors for intestinal anastomosis dehiscence following hand-sewn anastomosis.16 In a retrospective study examining risk factors specifically related to SFEEA dehiscence, preoperative presence of inflammatory bowel disease, intraoperative hypotension, and resection and anastomosis involving the large intestine were identified as risk factors.14 

Preoperative peritonitis was examined and was not an identified risk factor for SFEEA, contrary to previous reports.14 Furthermore, in another retrospective study, SFEEA was found to be less likely to undergo dehiscence as compared with hand-sewn intestinal anastomosis in dogs with preoperative septic peritonitis.1

With proper instruction, SFEEA has been demonstrated to be a reliable tool for surgeons and may be useful during emergency situations to decrease operative time in unstable patients when a rapid anastomosis is required and to potentially decrease dehiscence risk in patients with septic peritonitis.13,14

Surgical Stapler Functionality

Before performing a linear-stapled intestinal anastomosis, the surgeon should become familiar with the GIA stapling device used for SFEEA (Figure 1). The GIA stapler is a linear/cutting stapling device composed of 2 interlocking halves. When fired via a push-bar handle, the device applies 4 staggered rows of B-shaped titanium staples while a knife blade cuts between the 2 rows of double staple lines (Figure 2). The knife blade stops cutting approximately 8 mm before the last staple at the tip of the fork. 

Staple cartridges for the directional stapling technology (DST) series GIA stapler come in different lengths and closed staple heights. The color of the cartridge corresponds to the closed staple height. Blue staple cartridges (1.5-mm closed staple height) are typically used in small animals for SFEEA. White (1-mm closed staple height) and green (2-mm closed staple height) staple cartridges are also available but are not routinely used for SFEEA.

STEP-BY-STEP

STAPLED FUNCTIONAL END-TO-END ANASTOMOSIS


WHAT YOU WILL NEED

  • Standard surgical instrument kit
  • Balfour retractor
  • GIA stapler (60-mm and/or 80-mm or 100-mm for medium-to-large–breed dogs) and blue staple cartridges that correspond in length to the stapler
  • Doyen intestinal forceps (atraumatic; 2 pairs)
  • DeBakey thumb forceps (2 pairs)
  • Traumatic forceps (eg, Rocheter-Carmalt; 1 pair)
  • Suture material (3-0 monofilament, absorbable)

STEP 1

Anesthetize the patient and place in dorsal recumbency. Administer antimicrobial therapy (eg, cefoxitin [30 mg/kg IV for clean-contaminated surgery]) 30 minutes before incision and every 90 minutes thereafter until skin closure; of note, recent data suggest that q4h administration of cefoxitin is also acceptable.17 Clip, prepare, and drape the ventral abdomen for aseptic surgery.

Perform a ventral midline exploratory laparotomy and remove the falciform ligament to improve abdomen exposure, then place a Balfour retractor. Explore the abdomen thoroughly in a systematic fashion, and isolate the affected intestinal segments with multiple layers of saline-soaked laparotomy sponges. Perform an enterectomy and, if indicated, submit for histopathologic evaluation.

Author Insight

An initial pair of Doyen forceps (gripping the portion of bowel to remain intact) can help with intestinal manipulation and resection and anastomosis, and traumatic forceps (gripping the portion of bowel to be removed) can help limit surgical-site contamination. When placing Doyen forceps, only one ratchet should be used to prevent devitalization of tissue. Although the initial Doyen forceps are placed at the traditional site of hand-sewn anastomosis, this portion of tissue will be removed after SFEEA completion.


STEP 2

After resecting the affected intestine, milk the intestinal contents orally and aborally to the Doyen forceps (A). Place a second pair of Doyen forceps approximately 10 cm orally and aborally to the first set of Doyen forceps (B). This technique is employed to minimize contamination when using the stapling devices for anastomosis, as the initially placed pair of forceps will be removed on staple application.

Proximal and distal segments of the jejunum occluded by Doyen forceps at the site of resection (A). The resected portion of the intestine was removed from the surgical site with Rochester-Carmalt (ie, traumatic) forceps attached (not pictured). Proximal and distal jejunal segments of the intestine with second Doyen forceps placed approximately 10 cm away from the initial Doyen forceps (B; black arrows)
Proximal and distal segments of the jejunum occluded by Doyen forceps at the site of resection (A). The resected portion of the intestine was removed from the surgical site with Rochester-Carmalt (ie, traumatic) forceps attached (not pictured). Proximal and distal jejunal segments of the intestine with second Doyen forceps placed approximately 10 cm away from the initial Doyen forceps (B; black arrows)
Proximal and distal segments of the jejunum occluded by Doyen forceps at the site of resection (A). The resected portion of the intestine was removed from the surgical site with Rochester-Carmalt (ie, traumatic) forceps attached (not pictured). Proximal and distal jejunal segments of the intestine with second Doyen forceps placed approximately 10 cm away from the initial Doyen forceps (B; black arrows)
Proximal and distal segments of the jejunum occluded by Doyen forceps at the site of resection (A). The resected portion of the intestine was removed from the surgical site with Rochester-Carmalt (ie, traumatic) forceps attached (not pictured). Proximal and distal jejunal segments of the intestine with second Doyen forceps placed approximately 10 cm away from the initial Doyen forceps (B; black arrows)

Proximal and distal segments of the jejunum occluded by Doyen forceps at the site of resection (A). The resected portion of the intestine was removed from the surgical site with Rochester-Carmalt (ie, traumatic) forceps attached (not pictured). Proximal and distal jejunal segments of the intestine with second Doyen forceps placed approximately 10 cm away from the initial Doyen forceps (B; black arrows)


STEP 3

Place 2 stay sutures (eg, 3-0 polydioxanone) into the cut ends of each intestinal segment on the mesenteric border. Once the stay sutures have been applied, remove the first pair of Doyen forceps directly at the cut bowel ends; leave the second pair in place until the stapled anastomosis is complete. Use the stay sutures to elevate the bowel ends and to facilitate insertion of each fork of the GIA stapler (A). It is important to ensure symmetrical apposition of the antimesenteric border of the intestine before locking the stapler. The authors recommend apposition of the antimesenteric borders of the bowel because this can help minimize incidence of trauma to the vascular supply on the mesenteric border.

Two stay sutures have been placed  at the mesenteric border of the jejunum, and the initially placed Doyen forceps have been removed (A). The stay sutures are elevated to allow for insertion of the individual forks of the GIA stapler into the lumen of both jejunal ends. The GIA stapler is engaged and locked, ensuring symmetrical apposition of the antimesenteric border and terminal end of the jejunum (B). The GIA stapler is then fired. The stay sutures (black arrows) can be noted. 
Two stay sutures have been placed  at the mesenteric border of the jejunum, and the initially placed Doyen forceps have been removed (A). The stay sutures are elevated to allow for insertion of the individual forks of the GIA stapler into the lumen of both jejunal ends. The GIA stapler is engaged and locked, ensuring symmetrical apposition of the antimesenteric border and terminal end of the jejunum (B). The GIA stapler is then fired. The stay sutures (black arrows) can be noted. 
Two stay sutures have been placed  at the mesenteric border of the jejunum, and the initially placed Doyen forceps have been removed (A). The stay sutures are elevated to allow for insertion of the individual forks of the GIA stapler into the lumen of both jejunal ends. The GIA stapler is engaged and locked, ensuring symmetrical apposition of the antimesenteric border and terminal end of the jejunum (B). The GIA stapler is then fired. The stay sutures (black arrows) can be noted. 
Two stay sutures have been placed  at the mesenteric border of the jejunum, and the initially placed Doyen forceps have been removed (A). The stay sutures are elevated to allow for insertion of the individual forks of the GIA stapler into the lumen of both jejunal ends. The GIA stapler is engaged and locked, ensuring symmetrical apposition of the antimesenteric border and terminal end of the jejunum (B). The GIA stapler is then fired. The stay sutures (black arrows) can be noted. 

Two stay sutures have been placed  at the mesenteric border of the jejunum, and the initially placed Doyen forceps have been removed (A). The stay sutures are elevated to allow for insertion of the individual forks of the GIA stapler into the lumen of both jejunal ends. The GIA stapler is engaged and locked, ensuring symmetrical apposition of the antimesenteric border and terminal end of the jejunum (B). The GIA stapler is then fired. The stay sutures (black arrows) can be noted. 

When placement is deemed adequate, lock and fire the forks, creating the side-to-side opening between the bowel lumens (B). After firing, disengage and remove the forks. Carefully inspect the anastomosis site to ensure proper staple placement, which is dependent on passage of the staple fully through both layers of the adjacent intestinal wall and on consistent closure of the B-shaped staple on the opposite tissue edge. 

Author Insights

Caution should be exercised when using this stapling technique for anastomosis in cases in which the intestinal wall is severely thickened (eg, inflammatory bowel disease), as the closed blue cartridge staple leg length (1.5 mm) may not be long enough to completely capture both intestinal walls.14 In cases of severely thickened intestines, hand-sewn anastomosis is recommended.

Future obstruction at the site of anastomosis is a potential long-term risk, with one report documenting subsequent obstruction in 4.3% of SFEEAs.18 The authors routinely use a GIA 60 stapler for the first half of the SFEEA; in their clinical experience, a GIA stapler of longer working length, although not harmful, does not appear to be beneficial in preventing subsequent obstruction. Further investigation in this area is needed.


STEP 4

Using the previously placed stay sutures for handling the intestinal segments, place the GIA stapler (with a new loaded cartridge) perpendicular to the lumen of the intestine. Before locking, offset the staple rows from the lumens portion using 2 pairs of DeBakey thumb forceps. This prevents the initial staple lines from being stacked on top of each other, which could prevent complete engagement of the staples through both walls of the terminal end of the SFEEA. Lock and fire the stapler. The authors generally aim to leave 1 mm to 3 mm of tissue beyond the edge before firing the GIA stapler. The GIA stapler will automatically transect the bowel, resulting in a 2-row stapled edge creating the “waist.” The remaining tissue at the terminal end of the SFEEA does not need to be oversewn.

The 2 previously placed stay sutures are gently distracted to maintain tension on the intestine. A GIA stapler (of appropriate length) is engaged and locked over the terminal end of the intestine. Approximately 3 mm of tissue extends beyond the proposed staple line, and no tissue extends past the 0 mark of the GIA stapler, ensuring a complete terminal seal. If tissue extends past the 0 mark of the GIA stapler, a stapler of longer working length should be used. The stapler is fired, resulting in a stapled terminal end of the intestine and transection of the remaining distal portion, including the stay sutures. The 2 staple lines of the GIA line should be offset (white arrows) to ensure staple engagement of all tissues.
The 2 previously placed stay sutures are gently distracted to maintain tension on the intestine. A GIA stapler (of appropriate length) is engaged and locked over the terminal end of the intestine. Approximately 3 mm of tissue extends beyond the proposed staple line, and no tissue extends past the 0 mark of the GIA stapler, ensuring a complete terminal seal. If tissue extends past the 0 mark of the GIA stapler, a stapler of longer working length should be used. The stapler is fired, resulting in a stapled terminal end of the intestine and transection of the remaining distal portion, including the stay sutures. The 2 staple lines of the GIA line should be offset (white arrows) to ensure staple engagement of all tissues.

The 2 previously placed stay sutures are gently distracted to maintain tension on the intestine. A GIA stapler (of appropriate length) is engaged and locked over the terminal end of the intestine. Approximately 3 mm of tissue extends beyond the proposed staple line, and no tissue extends past the 0 mark of the GIA stapler, ensuring a complete terminal seal. If tissue extends past the 0 mark of the GIA stapler, a stapler of longer working length should be used. The stapler is fired, resulting in a stapled terminal end of the intestine and transection of the remaining distal portion, including the stay sutures. The 2 staple lines of the GIA line should be offset (white arrows) to ensure staple engagement of all tissues.

Author Insight

The GIA 60 stapler is often too short to adequately engage all tissues when closing the terminal end of the SFEEA in medium-to-large–breed dogs; in such patients, a GIA 80, 90, or 100 stapler is recommended.


STEP 5

Two simple interrupted, prolonged absorbable monofilament sutures should be placed just below the base (ie, point of the “V” intersecting GIA staple line) of the anastomosis to minimize tension on the staple line (A). These sutures should aim to capture submucosa for holding power (B).

Two simple interrupted, prolonged absorbable monofilament sutures are placed at the SFEEA base  (A; white arrow) to minimize tension on the staple line. Completed SFEEA, with a demonstration of the flow of ingesta through the SFEEA (B; white arrows)
Two simple interrupted, prolonged absorbable monofilament sutures are placed at the SFEEA base  (A; white arrow) to minimize tension on the staple line. Completed SFEEA, with a demonstration of the flow of ingesta through the SFEEA (B; white arrows)
Two simple interrupted, prolonged absorbable monofilament sutures are placed at the SFEEA base  (A; white arrow) to minimize tension on the staple line. Completed SFEEA, with a demonstration of the flow of ingesta through the SFEEA (B; white arrows)
Two simple interrupted, prolonged absorbable monofilament sutures are placed at the SFEEA base  (A; white arrow) to minimize tension on the staple line. Completed SFEEA, with a demonstration of the flow of ingesta through the SFEEA (B; white arrows)

Two simple interrupted, prolonged absorbable monofilament sutures are placed at the SFEEA base  (A; white arrow) to minimize tension on the staple line. Completed SFEEA, with a demonstration of the flow of ingesta through the SFEEA (B; white arrows)


STEP 6

Remove the laparotomy sponges from the surgical field. With a new pair of sterile surgery gloves, use a separate sterile closure pack to complete the laparotomy. Lavage the abdomen thoroughly with sterile saline. Using a monofilament absorbable suture, close the mesenteric defect in either an interrupted, cruciate, or continuous pattern. Avoid damaging adjacent vasculature supplying the anastomosed bowel in the mesentery. Drape the omentum over the anastomosis site before closing the abdominal incision in a routine fashion, and perform a routine closure of the abdomen.

DST = directional stapling technology, EEA = end-to-end anastomosis, GIA = gastrointestinal anastomosis, SFEEA = stapled functional end-to-end anastomosis<

References and Author Information

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.


Top 5 Viral Dermatoses in Cats

Liora Waldman, BVM&S, CertSAD, MRCVS, Veterinary Dermatology & Allergy Center, Haifa, Israel

Alexander Werner Resnick, VMD, DACVD, Animal Dermatology Center

Dermatology

|Peer Reviewed

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Top 5 Viral Dermatoses in Cats

Figure 1 Hyperkeratotic hyperpigmented plaque on the nose, muzzle, and chin of a cat infected with papillomavirus

Viral dermatoses in cats are rare diseases caused by direct viral cytopathic effects in the skin. Viral infections are diagnosed using techniques such as PCR, immunohistochemistry, and in situ hybridization. Presented below are the authors’ top 5 feline viral dermatoses most likely to be encountered in veterinary practice.

1

Papillomavirus

Papillomavirus influences cell growth and differentiation and may cause cancer.1 Although in general the viruses are species-specific, human and bovine papillomaviruses have been detected in cats.2 Four feline papillomaviruses have been completely sequenced. FcaPV-2 is the most frequently isolated from cat lesions1,3,4 and was found on the skin of 52% of cats in one study.5 FcaPV-2 and FdPV-3 are closely related to canine PV-1 and canine PV-7,3 respectively.

Papillomavirus causes the following dermatoses in cats:

  • Viral plaques are uncommon and are seen as single or grouped round-to-oval scaly, gray, tan, or black papules or plaques with hyperkeratosis (Figure 1, above).6 They are neither pruritic nor painful and may be present anywhere on the body. In healthy cats, they may resolve spontaneously.2 In immunosuppressed cats (eg, those with FIV, FIP, FeLV, or neoplasia; those receiving glucocorticoid treatment), resolution occurs after treating the primary cause. Demodex cati mites might be found in the lesions.1,6-9
  • Bowenoid in situ carcinoma (BISC; ie, Bowen’s disease) is often a progression from viral plaque. It presents as hyperpigmented macules or crusted plaques that may ulcerate. The face, neck, and limbs are predisposed, but lesions can be seen anywhere on the body.3 Cutaneous horns may be present.10 BISC can progress to squamous cell carcinoma with metastases.11 Ultraviolet light does not affect neoplastic transformation (Figure 2).2,8,9
Ulceration, bleeding, alopecia, and hyperkeratotic plaques on the face of a cat with Bowen’s disease caused by papillomavirus infection
Ulceration, bleeding, alopecia, and hyperkeratotic plaques on the face of a cat with Bowen’s disease caused by papillomavirus infection

FIGURE 2 Ulceration, bleeding, alopecia, and hyperkeratotic plaques on the face of a cat with Bowen’s disease caused by papillomavirus infection

FIGURE 2 Ulceration, bleeding, alopecia, and hyperkeratotic plaques on the face of a cat with Bowen’s disease caused by papillomavirus infection

  • Cutaneous papilloma is rare and appears as a single pedunculated or cauliflower-like hyperkeratotic lesion, smaller than 0.5 cm, at any body site.2,8
  • Oral papilloma is also rare. Only 2 cases have been reported, found on the tongue as small, multifocal, soft, pink, raised, flat-topped lesions.12
  • Feline sarcoid is seen in cats in rural areas and is likely caused by bovine papillomavirus.13 Sarcoid lesions are firm, round, single masses that can ulcerate and occur mainly on the nose, upper lip, and digits. They do not metastasize but may recur after excision.8-10
  • Basal cell tumors are uncommon and usually appear as a soft, mobile, painless, dermal mass with some surface scaling. A novel papillomavirus similar to FcaPV-314 has been identified.
  • Papillary squamous cell carcinoma is seen on the head as hornlike crusted masses.6
  • Fibrosarcoma and apocrine gland cysts are rarely associated with papillomavirus.2,15

Diagnosis is made via histopathology, PCR (swab more sensitive than formalin fixed tissue1), immunohistochemistry, in situ hybridization, or electron microscopy.9,10

Treatment of oral papilloma and single plaques may include excision, cryosurgery, electrosurgery, or CO2 laser ablation. Some plaques might regress following control of the primary problem. Imiquimod can be effective for plaques and BISC within 3 to 4 weeks. Lesions can recur when treatment is discontinued.8,10 Side effects may include local erythema and, occasionally, systemic effects (eg, nausea, vomiting, myalgia, fever, hypotension).16 Interferon-α (IFNα; 30 units PO q24h) has been reported to be effective.10

2

Feline Herpesvirus 1

FHV-1 primarily causes facial dermatitis affecting the nasal planum, muzzle, bridge of nose, and periocular skin (Figure 3), but it can occur at other sites.17-19 Recent upper respiratory infection, stress, and/or glucocorticoid therapy may precede onset.

Twelve-year-old domestic shorthair cat with FHV-1 dermatitis
Twelve-year-old domestic shorthair cat with FHV-1 dermatitis

FIGURE 3 Twelve-year-old domestic shorthair cat with FHV-1 dermatitis

FIGURE 3 Twelve-year-old domestic shorthair cat with FHV-1 dermatitis

Facial lesions may start unilaterally with vesicles, erythema, and alopecia. Due to intense pruritus, lesions may become ulcerated and crusted.

Differential diagnoses include allergy (eg, food, atopy) and eosinophilic plaque.19 Diagnosis is made via histopathology, revealing eosinophils, neutrophils or lymphoplasmacytic dermatitis, necrosis, or ulceration with intranuclear inclusion bodies. PCR from fresh biopsy (preferably in saline, not formalin) should be submitted for definitive diagnosis.19,20

Treatment options include famciclovir (90-125 mg/kg q8-12h19,20), recombinant feline interferon ω (1.5 million units/kg perilesionally and SC for 2-3 weeks) or recombinant feline interferon-α (1 million units/m2 SC 3 times per week).21 Topical idoxuridine, cidofovir, or trifluridine is used to treat ulcerative keratitis. Vaccination can protect cats from developing lesions.

3

Feline Calicivirus

Feline calicivirus is an RNA virus that is shed via ocular, nasal, and oral secretions.10,22

Dermatologic signs may include ulcers on the nasal philtrum, lips, tongue, gingiva, and paws10; swollen feet; facial skin erosions, especially of the nose; and ventral pustules (Figure 4).21

Ulceration with crusting on the nose, philtrum, muzzle, and upper lip of a calicivirus-infected cat. Image courtesy of Stephen White, DVM
Ulceration with crusting on the nose, philtrum, muzzle, and upper lip of a calicivirus-infected cat. Image courtesy of Stephen White, DVM

FIGURE 4 Ulceration with crusting on the nose, philtrum, muzzle, and upper lip of a calicivirus-infected cat. Image courtesy of Stephen White, DVM

FIGURE 4 Ulceration with crusting on the nose, philtrum, muzzle, and upper lip of a calicivirus-infected cat. Image courtesy of Stephen White, DVM

Differential diagnoses include nasal ulceration (eg, from FHV-1, squamous cell carcinoma, other neoplasia, Cryptococcus spp, Sporothrix schenckii, or mosquito hypersensitivity), and ulceration of the paws (eg, from pox virus, papillomavirus, FeLV, malignancy, plasma cell pododermatitis).

Treatment with antibiotics might be needed if secondary bacterial infection develops. Oral glucocorticoids may be beneficial to treat oral ulceration.

4

Feline Pox Virus

Feline pox virus dermatitis, caused by cowpox virus, is a rare disease seen primarily in Europe and West Asia. Cats are infected by hunting rodents (the natural hosts), typically in rural areas. Lesions occur mostly on the head, ears, neck, and legs. Primary lesions may look like bite wounds, nodules, plaques, crusted papules, ulcers, abscesses, or cellulitis (Figures 5 and 6). Pruritus is variable. Crust-covered, ulcerated papules and nodules typically develop within 1 to 3 weeks. Oral ulceration can lead to anorexia. Fever, conjunctivitis, and pneumonia may develop.10,23,24

Pox virus is zoonotic, especially in immunosuppressed humans.

Differential diagnoses include bacterial and fungal infections, neoplasia (mast cell tumor, lymphoma), and granuloma. Diagnosis is made via biopsy (eosinophilic intracytoplasmic inclusion bodies), serology, PCR, immunohistochemistry, or virus isolation.

Most patients recover without complications. Treatment may include antibacterial drugs for secondary infections and supportive treatment. Glucocorticoids are contraindicated.

5

Feline Leukemia Virus

FeLV, a retrovirus, causes giant-cell dermatosis10,25 with pruritus, ulceration, and crusting lesions—mainly on the head, neck, and face (Figure 7) but occasionally on the extremities or footpads, trunk, and mucocutaneous junctions of the anus and/or prepuce. Cutaneous horns may be seen.10

Thirteen-year-old FeLV-positive cat with alopecia, mildly seborrheic dermatitis, and excoriations on the ventral neck
Thirteen-year-old FeLV-positive cat with alopecia, mildly seborrheic dermatitis, and excoriations on the ventral neck

FIGURE 7 Thirteen-year-old FeLV-positive cat with alopecia, mildly seborrheic dermatitis, and excoriations on the ventral neck

FIGURE 7 Thirteen-year-old FeLV-positive cat with alopecia, mildly seborrheic dermatitis, and excoriations on the ventral neck

Differential diagnoses include evident pruritus caused by allergy (eg, food, atopy), Notoedres cati, Cheyletiella spp, or Demodex spp; or crusted lesions caused by exfoliating dermatitis, pemphigus foliaceus, drug reaction, systemic lupus erythematosus, or seborrhea. Diagnosis is made via histopathology (giant-cell dermatoses), serology, or PCR.10,25,26

BISC = Bowenoid in situ carcinoma

References and Author Information

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.


Optic Neuritis

Thomas Chen, DVM, DACVO, University of Tennessee

Anansa Persaud, DVM, Long Island Veterinary Specialists, Plainview, New York

Ophthalmology

|Peer Reviewed

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Optic Neuritis
Figure 1 Optic neuritis in a dog. The optic nerve and its associated blood vessels are hazy with indistinct borders, as the vessels are elevated relative to the retinal blood vessels surrounding the nerve.

Optic neuritis is a rare but serious condition that can result in acute blindness or visual deficits in one or both eyes.1,2 Prompt diagnosis and treatment are necessary to recover vision, and evaluation for neurologic, infectious, and/or neoplastic disease may also be warranted.1,3,4

Clinical Signs

In cases of bilaterally affected animals, owners often report suspected vision loss based on a clinical history of the pet bumping into walls or objects, missing treats, or having difficulty with stairs. Astute owners of pets with unilateral disease may report more subtle changes (eg, visual deficits, anisocoria with the dilated pupil in the affected eye).

Absent menace responses, with absent pupillary light reflexes and mydriatic pupils, are usually noted on ophthalmic examination.1,5 Further vision testing (eg, visual placement testing, maze) can help confirm lack of vision. 

A thorough fundic examination is crucial for including optic neuritis in the list of diagnostic differentials. The optic nerve head most often appears swollen, hyperemic, or elevated (Figure 1). Chorioretinitis with associated focal retinal detachment or edema, hemorrhage, or white or gray foci can also be present adjacent to or near the optic nerve head. Rarely, inflammation can also occur posterior to the optic nerve head (retrobulbar) and therefore cannot be appreciated except with advanced imaging (eg, MRI).5

Diagnosis

Optic neuritis is often diagnosed by confirmation of blindness and pupillary light reflex deficits and visualization of an abnormal optic nerve head on fundic examination. Other important rule outs for blindness can include diffuse retinal detachment (in contrast to focal detachment proximal to the optic nerve head) and sudden acquired retinal degeneration syndrome. Retinal detachment can also be diagnosed on fundic examination, whereas sudden acquired retinal degeneration syndrome can only be confirmed with an electroretinogram. Performing a complete neurologic examination and obtaining a thorough history are also recommended to assess for concurrent neurologic signs that might be suggestive of meningoencephalitis.

Causes

Optic neuritis in dogs is most often the result of immune-mediated and/or inflammatory brain disease, which together comprise approximately 80% of optic neuritis cases in a study of 96 dogs.1 Other causes in dogs include infection or neoplasia. Optic neuritis in cats occurs secondary to infectious6-9 or neoplastic causes,5 with no reports of immune-mediated causes or incidence rates for all causes in cats.

Immune-Mediated

Immune-mediated optic neuritis appears to be the most common diagnosis in dogs.1,5 The optic nerve is a direct extension of the CNS; therefore, inflammatory brain disease can extend to or focally involve the optic nerves, usually bilaterally. Meningoencephalitis of unknown etiology (MUE; or, when confirmed histologically, subtyped more specifically as granulomatous meningoencephalitis [GME]) is one such condition10 and has been categorized by neurologists as ocular GME when inflammation involves the optic nerves, either alone or with concurrent MUE/GME signs.11

In contrast, veterinary ophthalmologists have historically considered optic neuritis (in patients without concurrent neurologic clinical signs) a separate clinical entity from MUE.2 A difference in signalment in canine patients with isolated involvement of the optic nerves has been reported; MUE patients were typically female small-breed dogs, whereas isolated optic neuritis patients were often male medium-to-large–breed dogs.1 The exact relationship or difference between the syndromes, if it exists, has not yet been definitively determined. 

Whether a manifestation of MUE or isolated immune-mediated optic neuritis, definitive diagnosis often requires an MRI and CSF tap while also ruling out other infectious or neoplastic diseases; however, many owners often decline advanced imaging or CSF taps due to cost or availability.1

Infectious Disease

Infectious diseases, with tropism for or involvement of the CNS, have also been reported to cause optic neuritis. Infectious optic neuritis usually manifests as an extension of more generalized or multifocal meningoencephalitis or from ocular and orbital involvement. Fungal disease in particular can involve the orbit or neighboring areas (eg, nasal or sinus cavities) and may result in subsequent involvement and inflammation of the optic nerve.1,12 Viral diseases (eg, distemper, tick-borne encephalitis virus, feline infectious peritonitis) affect the nervous tissue directly or indirectly via damage from host immune responses. These diseases can also result in uveitis (both anterior and posterior) or chorioretinitis (not necessarily associated with the optic nerve), the presence of which should raise clinical suspicion of infectious disease as compared with immune-mediated meningoencephalitis.

In dogs, optic neuritis has been reported with distemper virus, tick-borne encephalitis virus, ehrlichiosis, Toxoplasma gondii or Neospora caninum infections, and fungal disease (eg, aspergillosis, cryptococcosis, histoplasmosis, blastomycosis).1,13-20 In cats, T gondii infections, feline infectious peritonitis, and systemic fungal disease (ie, histoplasmosis, cryptoccosis) have been reported with optic neuritis.6-9,17,21

Infectious disease testing should be conducted based on clinical suspicion from history and signalment (eg, unvaccinated animal, use of tick preventives), geography (for fungal disease), tick exposure, and exploratory bloodwork.

Neoplasia

Primary optic nerve tumors, including optic nerve meningioma and gliomas, have been reported, although they are rare.1,5,22,23 Orbital neoplasia can also affect the optic nerve. In a case series involving 53 neoplastic cases, carcinomas were seen most commonly (30%), followed by sarcomas (20%), lymphoma (15%), and presumptive meningiomas (17%).5 Carcinomas and sarcomas were noted to occasionally arise from neighboring areas of the orbit (ie, frontal bone or sinus, nasal cavity, maxilla) that extended into the orbit with involvement of the optic nerve.

Extension of Orbital Disease

Optic neuritis may also occur secondary to orbital inflammation, including retrobulbar cellulitis and/or abscessation, which can be associated with infection, neoplasia, foreign body, or dental disease.5,8,19,24-28 If inflammation is severe or near enough to the optic nerve, compression or inflammation of the optic nerve can result in subsequent blindness. Clinically, these conditions can be observed as change in the position or placement of the eye (eg, enophthalmia, exophthalmia), protrusion of the third eyelid, and/or difficulty or pain on opening of the mouth, with periocular swelling and inflammation. Optic neuritis secondary to orbital or retrobulbar inflammation can be unilateral depending on the laterality of the primary disease (eg, unilateral in bacterial retrobulbar cellulitis).

Treatment & Prognosis

Ultimately, treatment of optic neuritis depends on the underlying cause. Because immune-mediated causes largely predominate, treatment typically involves short-term immunosuppressive doses of steroids (Figure 2). Partial or full return of vision was noted in approximately 30.6% (22/72) of dogs in one study1 and 64% (7/11) of dogs in another.4 Return of vision 1 to 2 weeks after initiating therapy for acute blindness has been noted (author experience).

Same dog as in after a month of prednisone and cytarabine treatment. The margins around the optic nerve are still indistinct but much improved. Vessels overlying the nerve can be clearly seen and are in the same plane as the surrounding retinal blood vessels.
Same dog as in after a month of prednisone and cytarabine treatment. The margins around the optic nerve are still indistinct but much improved. Vessels overlying the nerve can be clearly seen and are in the same plane as the surrounding retinal blood vessels.

Figure 2 Same dog as in after a month of prednisone and cytarabine treatment. The margins around the optic nerve are still indistinct but much improved. Vessels overlying the nerve can be clearly seen and are in the same plane as the surrounding retinal blood vessels.

Figure 2 Same dog as in after a month of prednisone and cytarabine treatment. The margins around the optic nerve are still indistinct but much improved. Vessels overlying the nerve can be clearly seen and are in the same plane as the surrounding retinal blood vessels.

Recurrence has been noted in 2 cases at 15 and 18 months after successful treatment and at 2 weeks after tapering steroids.1 For optic neuritis that is suspected to be occurring secondary to MUE, treatment recommendations by neurologists generally entail life-long administration of steroids and/or immunomodulatory agents.11

Immunosuppressive doses of steroids can be detrimental if an underlying infection is present and may mask clinical signs or delay diagnosis if an underlying neoplastic disease is present. Any indication of orbital disease should be closely investigated before initiating steroidal treatment. Ideally, infectious disease should be ruled out, with specific testing conducted before initiating steroidal treatment, and an MRI and CSF tap performed to definitively rule in immune-mediated optic neuritis. However, if regaining vision is a priority and immune-mediated disease is suspected, empiric treatment with steroids can be initiated, as long as owners are educated regarding the risks.

Specific treatment for infectious disease or neoplasia will vary depending on the causative or suspected causative agent. Prognosis varies depending on CNS involvement and severity of primary disease but, for vision, is generally considered poor.

References and Author Information

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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Gabapentin & Fear in Cats

Karen Lynn C. Sueda, DVM, DACVB, VCA West Los Angeles Animal Hospital

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Gabapentin & Fear in Cats

In the Literature

Pankratz KE, Ferris KK, Griffith EH, Sherman BL. Use of single-dose oral gabapentin to attenuate fear responses in cage-trap confined community cats: a double-blind, placebo-controlled field trial. J Feline Med Surg. 2017. doi:10.1177/1098612X17719399


FROM THE PAGE …

Trap-neuter-return programs are used extensively for population control among unowned community cats. During trapping and perioperative cage confinement, cats may experience high levels of stress and self-inflicted trauma. Gabapentin, an anticonvulsant used in the treatment of neuropathic pain, has been shown to reduce anxiety in rats and humans.1,2 Although gabapentin’s anxiolytic properties have not been studied in cats, pharmacokinetics studies have reported excellent oral bioavailability and a wide margin of safety with single-dose administration.3

In a double-blind, placebo-controlled study, the behavior of 53 unowned community cats estimated to be older than 4 months were individually cage trapped, confined, and observed during a regional trap-neuter-return program. Following baseline behavior observation, cats were randomly assigned to receive one of 3 oral suspension treatments: low-dose gabapentin (50 mg/cat), high-dose gabapentin (100 mg/cat), or placebo. During baseline and 1, 2, 3, and 12 hours posttreatment, each cat’s stress score, global sedation score, and respiratory rate were determined. Additionally, a facial injury score was assigned at baseline, 12 hours posttreatment, and during sterilization surgery. After 12 hours, cats were anesthetized and underwent sterilization.

Gabapentin doses ranged from 9.2-47.6 mg/kg. Cats receiving either low- or high-dose gabapentin had significantly lower stress scores 2 and 3 hours posttreatment as compared with controls. There were no significant differences between low- and high-dose group stress scores at any time. All 3 groups exhibited a decline in respiratory rate over the 3 hours after treatment. No significant differences in sedation scores were observed for any group at any time. Facial injuries were observed in all groups and did not vary over time. No adverse events attributable to gabapentin were noted; all cats successfully and uneventfully underwent anesthesia and sterilization surgery. Hypersalivation was observed in 4 cats (placebo, 2; low-dose, 1; high-dose, 1).


… To Your Patients

Key pearls to put into practice:

1

In cats, single-dose gabapentin (50-100 mg/cat) may result in decreased stress, but not necessarily sedation, 2 to 3 hours after oral administration.

 

2

Gabapentin may be safely administered before anesthesia and routine surgery in healthy patients older than 4 months.  

3

Oral administration of a liquid suspension of gabapentin is generally well tolerated, although hypersalivation may occur in some patients.

References and Author Information

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.


Screening Obstructed Cats

Zenithson Y. Ng, DVM, MS , University of Tennessee

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Screening Obstructed Cats

In the Literature

Neri AM, de Araújo Machado LH, Guimarães Okamoto PT, et al. Routine screening examinations in attendance of cats with obstructive lower urinary tract disease. Top Companion Anim Med. 2016;31(4):140-145.


From the Page …

Feline obstructive lower urinary tract disease (FLUTD) diagnosis is based on history of stranguria, palpation of a firm distended bladder, and presence of ischuria.1 Metabolic and hemodynamic abnormalities often result and should be documented before anesthesia is administered for unobstruction. This study described a standardized diagnostic protocol and results from 26 male cats that were presented for urethral obstruction. 

In addition to history and physical examination, a minimum database (ie, blood pressure measurement, ECG, serum chemistry profile, blood gas analysis) was collected. Urine for urinalysis was collected from 17 cats via cystocentesis. Despite concerns regarding cystocentesis in obstructed cats, no adverse effects were reported. 

Cats that were obstructed for more than 36 hours had greater hemodynamic and metabolic abnormalities than did cats obstructed for less than 36 hours. Arrhythmias were noted in 15.38% of cats with a serum potassium greater than 8.5 mEq/L; a previous study found arrhythmias were not correlated directly with the magnitude of electrolyte abnormalities.2 Despite hyperkalemia being a common finding in this population, bradycardia was infrequent (7.69% of cats). The authors proposed that sympathetic activation from stress and pain may have masked bradycardia, which would have typically been present. 

Most cats (69.24%) were normotensive, but ionized calcium levels were significantly lower in normotensive cats as compared with hypertensive cats. This is concerning because calcium concentration has been shown to be lower in nonsurvivors as compared with survivors.3 Therefore, it cannot be assumed that normotensive patients are metabolically stable, as these cats had more significant laboratory changes as compared with hypertensive cats. Less than half of these cats (46.15%) were able to be unobstructed via urethral catheterization; the remaining cats (53.85%) were surgically unobstructed via perineal urethrostomy.

This proposed protocol of clinical screening examinations during early treatment of obstructed cats provides a dynamic assessment that can be monitored continually as therapy is instituted.


… To Your Patients

Key pearls to put into practice:

1

Prepare owners by communicating clearly that failure to correct obstruction via urethral catheterization is common and warrants surgical intervention.

 

2

Normal heart rate and blood pressure do not rule out laboratory abnormalities. Electrolytes should be measured in all patients, even for normotensive patients and in the absence of bradycardia. 

3

Hypothermia is a common clinical finding and may reflect the magnitude of urinary obstruction and associated clinicopathologic abnormalities.

References and Author Information

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.


Another Tool for Detecting Benign Prostatic Hyperplasia

Bruce W. Christensen, DVM, MS, DACT, University of California, Davis

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Another Tool for Detecting Benign Prostatic Hyperplasia

In the Literature

Pinheiro D, Machado J, Viegas C, et al. Evaluation of biomarker canine-prostate specific arginine esterase (CPSE) for the diagnosis of benign prostatic hyperplasia. BMC Vet Res. 2017;13:76. doi:10.1186/s12917-017-0996-5


FROM THE PAGE …

Nearly all intact male dogs eventually develop benign prostatic hyperplasia (BPH). Although most will show no clinical signs and therefore will not require treatment, some may exhibit hemospermia, hematuria, tenesmus, dysuria, prostatomegaly, poor semen quality, infertility, and serosanguinous urethral discharge not associated with urination. Diagnosis of prostatic disorders typically relies on clinical history, physical examination (including digital rectal examination), ultrasonography, and prostatic cytology. Use of canine prostate-specific arginine esterase (CPSE) as a biomarker that can reliably and specifically increase with the development of BPH in dogs has been promoted.

In this study, 60 intact dogs were divided into 2 groups (BPH [n = 29; median age, 9 years] and nonBPH [n = 31; median age, 5 years]) based on prostatic cytology obtained from fine-needle aspiration or prostatic massage. Clinical history, physical examination, ultrasonographic evaluation, and CPSE values were all recorded. Differences between CPSE concentrations in BPH and nonBPH groups were compared, and correlations between CPSE and other variables were measured. A significant difference in median CPSE levels was detected between BPH and nonBPH groups. Significant positive correlations were detected between mean CPSE levels and age or prostatic volume, as well as clinical examination findings, ultrasonographic findings, and positive cytology results. The high sensitivity of CPSE demonstrated in this study justifies the addition of this assay to the list of tools for the diagnosis of canine BPH. The specificity, however, was lower, with roughly 10% of false-positive results.


… To Your Patients

Key pearls to put into practice:

1

A strong correlation between elevated CPSE concentrations and all 3 traditional diagnostic procedures (ie, clinical examination, ultrasonographic evaluation, cytology) suggests that, as with most other medical investigations, definitive diagnoses are most confidently made when incorporating and noting agreement among multiple diagnostic approaches.

2

Cytology remains the gold standard for diagnosis of any prostatic disorder. Cytology can be best and—in most cases—easily obtained through manual stimulation of ejaculation, with separation of the prostatic (ie, third) fraction. In cases in which this method is not possible, prostatic massage or ultrasound-guided fine-needle aspiration may be employed. 

3

CPSE is a sensitive test for canine BPH and can be used as an adjunctive diagnostic test if clinical examination and ultrasonographic evaluation are inconclusive, if diagnostic prostatic cytology cannot be obtained, and/or if quantitative pre- and posttreatment evaluations are desired.

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.


Intervertebral Disk Herniation: In-House Postoperative Rehabilitation

Jason Bleedorn, DVM, DACVS, University of Wisconsin–Madison

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Intervertebral Disk Herniation: In-House Postoperative Rehabilitation

In the Literature

Hodgson MM, Bevan JM, Evans RB, Johnson TI. Influence of in-house rehabilitation on the postoperative outcome of dogs with intervertebral disk herniation. Vet Surg. 2017;46(4):566-573.


From the Page …

In dogs, intervertebral disk herniation (IVDH) is a common and disabling condition that, in severe cases, often requires surgical decompression. Postoperative rehabilitation is often recommended and employed to facilitate a safe and efficient functional recovery; however, despite its widespread popularity and availability, few outcome data exist regarding dogs.

This retrospective study compared clinical outcomes and complications using in-house rehabilitation in dogs (n = 87) following surgical decompression for single-site IVDH. Rehabilitation commenced at a median of 2 weeks postoperatively and consisted of treadmill (land/underwater), laser, and active and passive manual therapies collectively for a median of 12 days and 49 treatments. A control group (n = 161) received laser therapy, passive range-of-motion exercises, and cryotherapy during the immediate postoperative hospitalization period only. At minimum, dogs were examined daily while hospitalized, 10 to 14 days postoperatively, and 4 to 6 weeks postoperatively.

Preoperative neurologic scores were similar between groups. More dogs returned to full neurologic function with rehabilitation (33%) as compared with control dogs (9%). However, mean time to ambulation was faster in control dogs (14 days) as compared with rehabilitation dogs (28 days). Dogs without deep pain were analyzed separately, and outcomes were similar. The complication rate was higher in control dogs (29%) as compared with rehabilitation dogs (16%) and included surgery for recurrent disk extrusion in 3 control cases and one rehabilitation case.

Study results were somewhat difficult to decipher. Dogs with a consistent rehabilitation program experienced a greater return to normal function and fewer complications. In-house rehabilitation allows for frequent examination by rehabilitation specialists and veterinarians to guide an individualized plan and to identify and manage complications. Greater gains would be anticipated, as other studies in human and veterinary medicine have demonstrated. Time to ambulation was prolonged with rehabilitation, likely because of the retrospective study design and inconsistent follow-up in these cases.


… To Your Patients

Key pearls to put into practice:

1

Early diagnosis and intervention in dogs with IVDH are critical. Surgical decompression should be considered in severe cases, especially for nonambulatory patients.

 

2

Prognosis for return to function following surgery is greater than 85% with deep pain perception and approximately 50% without pain.1,2

 

3

Communication between veterinarians and rehabilitation specialists is important for development of a rehabilitation plan based on individualized patient assessment and goals.

 

4

Multimodal rehabilitation strategies may be beneficial and may include active standing exercises, weight-shifting, and proprioceptive activities and, when appropriate, passive joint mobility, cold laser, and treadmill walking.

References and Author Information

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.


Research Note: Canine Vision & Color Blindness

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To test the hypothesis that canine vision is dichromatic in nature and resembles that of human red–green color blindness, researchers used a modified version of a human color blindness test (Ishihara test) to evaluate an orienting response (ie, movements of the eyes, head, and body) to movements of a colored target in the dog’s visual field. Results of this study support the hypothesis, providing a direct comparison with color vision in humans and potentially opening the door for the development of new techniques to assess color vision in animals.

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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Research Note: Palmitoylethanolamide & Homeostasis

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Palmitoylethanolamide (PEA) is a bioactive lipid involved in maintaining and restoring cellular homeostasis. The effect of ultramicronized PEA (PEA-um) on mast cells was measured in an ex vivo skin model of canine atopic dermatitis. Cultured skin biopsy samples were treated with either 10 µg/mL or 100 µg/mL of compound 48/80 (ie, a secretagogue that causes mast cell degranulation), with or without 30 µM PEA-um. Exposure to PEA-um before and during a 72-hour treatment period with 10 µg/mL or 100 µg/mL of compound 48/80 caused a marked-to-significant decrease in degranulating mast cells, histamine content, and vasodilation.

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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Venous Access in Dogs with Cardiovascular Collapse

Marie Holowaychuk, DVM, DACVECC, Critical Care Vet Consulting, Calgary, Alberta, Canada

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Venous Access in Dogs with Cardiovascular Collapse

Figure An IO catheter is inserted into the humerus of a canine cadaver using an automatic rotary insertion device. Image courtesy of Marie K. Holowaychuk, DVM, DACVECC

In the Literature

Allukian AR, Abelson AL, Babyak J, Rozanski EA. Comparison of time to obtain intraosseous versus jugular venous catheterization on canine cadavers. J Vet Emerg Crit Care. 2017;27(5):506-511.


FROM THE PAGE …

Obtaining IV access can be difficult in veterinary patients with cardiovascular collapse or after cardiopulmonary arrest. In such situations, rapid IV access is imperative to facilitate administration of IV fluids and cardiopulmonary resuscitation medications.

This study compared 2 methods of obtaining rapid vascular access in dogs: intraosseous (IO) catheterization of the humerus via an automatic rotary insertion device and IV catheterization via a jugular venous cutdown. Canine cadavers were used as a model for cardiopulmonary arrest; cadavers were placed in lateral recumbency in the emergency room, with all necessary materials in their normal locations, to simulate a hospital CPR setting. An assistant was available to hold off the vein or stabilize the leg for catheterization.

Four categories of catheter placers participated in the study: a veterinary technician specialist certified in emergency medicine, an experienced emergency and critical care specialist, a first-year emergency and critical care resident, and a final-year veterinary student on the emergency and critical care rotation. Verbal instructions on how to perform jugular venous cutdown and place an IO catheter were given. Catheter placement was timed, and fluoroscopy was used to confirm proper placement once complete.

Cadaver body weight ranged from 13.67 lb to 88.18 lb (6.2-40 kg), and median BCS was 5/9. IO catheterization was faster (median, 55.4 seconds) than IV catheterization (median, 217.3 seconds) for all catheter placers. There was no difference in time among catheter placers for IO catheterization; however, time to achieve IV catheterization varied among catheter placers (range, 55.6-614 seconds). The overall success rate for both types of catheter placements was 87.5%.


… To Your Patients

Key pearls to put into practice:

1

Venous access can be achieved faster using IO catheterization with an automatic rotary insertion device as compared with IV catheterization of the jugular vein in dogs with cardiovascular collapse.    

2

IO catheterization time is not affected by catheter placer experience, whereas jugular catheterization using venous cutdown requires practice and is performed more quickly by experienced personnel.  

3

IO catheterization using an automatic rotary insertion device does not require an incision and enters the medullary cavity of the bone, where vascular collapse does not occur.

 

4

The selected IO catheter length must be sufficient to reach the medullary cavity to ensure successful placement.

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.


IV Fluid Bag Contamination

Amanda Cavanagh, DVM, DACVECC, Colorado State University

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IV Fluid Bag Contamination

In the Literature

Guillaumin J, Olp NM, Magnusson KD, Butler AL, Daniels JB. Influence of hang time and location on bacterial contamination of intravenous bags in a veterinary emergency and critical care setting. J Vet Emerg Crit Care. 2017;27(5):548-554.


FROM THE PAGE …

To avoid fluid contamination and subsequent bloodstream infection in humans, the Centers for Disease Control and Prevention recommends discarding IV fluids within 24 hours of initial use.1 However, these guidelines were developed when glass IV fluid bottles were more likely to become contaminated during manufacturing due to poor quality control. No updated guidelines for hospitalized humans have been published, nor have veterinary guidelines been published.

The purpose of this study was to determine the bacterial contamination rate of IV fluid bags and their fluid while hanging in the veterinary emergency room or intensive care unit. This experimental study mimicked a clinical environment in which IV fluid bags were punctured multiple times during reutilization. IV fluid bags were hung near sinks and open supply bins in the emergency room and intensive care unit for 11 days (ie, days 0-10). Each day, the bags were punctured 3 times with sterile needles; of note, the study design purposefully called for not disinfecting the injection port. The investigators then cultured the bags’ access ports and fluid on days 0, 2, 4, 7, and 10. By day 7, 31.1% of access ports and 4.4% of fluids were contaminated. Port contamination was more likely if bags were located near a sink. No fluids were contaminated on days 0 or 2, which indicated that fluid contamination occurred between days 2 and 4.

IV fluids will support bacterial growth if contaminant bacteria are introduced to the bag, which puts patients at risk for bloodstream infections.2


… To Your Patients

Key pearls to put into practice:

1

Swabbing access ports with a saline-soaked cotton swab mechanically removes greater than 99% of microorganisms; using 70% ethanol increases microbe eradication.3

 

2

IV fluid bags should not be used as a source of saline flush solutions because of the risk for contamination. Commercially available prefilled saline syringes can decrease the risk for bacterial contamination and subsequent catheter-related bloodstream infection.4

3

Fluid administration sets should be replaced every 4 to 7 days.5 Administration sets used to deliver blood products or parenteral nutrition should be replaced every 24 hours.6 There are no recommendations for the frequency of fluid bag replacement, but bags should at least be replaced with each administration set change. The same fluid bag should not be used in more than one patient.6

References and Author Information

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.


Electrosurgery vs Cold Instruments in Midline Abdominal Incisions

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

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Electrosurgery vs Cold Instruments in Midline Abdominal Incisions

In the Literature

Meakin LB, Murrell JC, Doran ICP, et al. Electrosurgery reduces blood loss and immediate postoperative inflammation compared to cold instruments for midline celiotomy in dogs: a randomized controlled trial. Vet Surg. 2017;46(4):515-519.


FROM THE PAGE …

Concerns that healing after electrocautery is inferior as compared with healing after sharp dissection with cold instruments have been reported. Historically, a rodent model showed reduced tensile strength in abdominal incision healing with electrocautery use.1 However, in most wound healing models, electrocautery has been used in coagulation mode, which is more destructive than lower voltage cutting mode. In addition, due to species differences, a direct correlation cannot be proven from rodents to dogs without direct examination. 

Use of a polar instrument to create a parapatellar incision (ie, cutting mode) and to pinpoint individual vessels (ie, coagulation mode)
Use of a polar instrument to create a parapatellar incision (ie, cutting mode) and to pinpoint individual vessels (ie, coagulation mode)

FIGURE 1 Use of a polar instrument to create a parapatellar incision (ie, cutting mode) and to pinpoint individual vessels (ie, coagulation mode)

FIGURE 1 Use of a polar instrument to create a parapatellar incision (ie, cutting mode) and to pinpoint individual vessels (ie, coagulation mode)

This study examined routine sharp excision with scalpel blade and scissors versus electrocautery in cutting mode to create a midline abdominal incision from skin through the linea alba in 120 dogs. Dogs were evaluated in hospital at 24 and 48 hours postoperation for pain and incisional complications. Wound healing was found to be similar, with reduced blood loss documented in the electrosurgery group. Electrocautery was associated with significantly less incision redness at 24 hours postoperation as compared with cold instrument technique. Both groups were similar thereafter.

Use of a bipolar instrument for delicate tissue dissection and individual vessel coagulation. Bipolar has only one mode.
Use of a bipolar instrument for delicate tissue dissection and individual vessel coagulation. Bipolar has only one mode.

FIGURE 2 Use of a bipolar instrument for delicate tissue dissection and individual vessel coagulation. Bipolar has only one mode.

FIGURE 2 Use of a bipolar instrument for delicate tissue dissection and individual vessel coagulation. Bipolar has only one mode.

Although more precise evaluation of wound healing and follow- up would have been beneficial, this study can be helpful in providing assurance regarding the safe use of electrosurgery in routine abdominal incisions. This information is especially useful for anemic or coagulopathic patients, in which blood conservation is paramount. Caution should always be taken with the use of cautery to avoid excessive tissue damage. Pairing electrosurgery alongside traditional cold instruments likely leads to an optimal solution, maximizing the benefits of both techniques.


… To Your Patients

Key pearls to put into practice:

1

Electrosurgery can be monopolar or bipolar. Monopolar requires a grounding source, typically a ground plate placed under the patient. A grounding plate must be adequately placed to avoid serious cautery burns. The bipolar type is self-grounding through the forceps tips and is typically more precise. Tips must be 1 mm apart to work appropriately.

2

Monopolar cautery has 2 modes: cutting and coagulation. Electrocautery in cutting mode is best for focal tissue dissection, whereas coagulation mode is best for individual bleeding vessels. Monopolar cautery requires a relatively dry field, whereas bipolar tolerates more fluid.

3

The use of traditional cold instruments, along with varying amounts of electrocautery, is likely beneficial to most surgical patients. Sharp skin and linea alba incisions can be paired with electrocautery in the subcutaneous region to achieve the benefits of both techniques.

References and Author Information

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.


Do Backyard Chickens Pose Any Health Risks to Humans?

Casey Barton Behravesh, MS, DVM, DrPH, DACVPM, Centers for Disease Control and Prevention, Atlanta, Georgia

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Do Backyard Chickens Pose Any Health Risks to Humans?

Owners of backyard chickens and other poultry (eg, ducks, geese, turkeys) should be made aware of the risks these pets pose to humans and take basic biosecurity steps to protect against zoonotic disease transmission. Backyard poultry can appear healthy and clean but can carry Salmonella spp or Campylobacter spp.1-3 Eggs and habitats can also become contaminated.1-3

Zoonotic diseases that backyard poultry may spread to humans include salmonellosis, campylobacteriosis, and avian influenza viruses. Since the 1990s, numerous widespread outbreaks of human Salmonella spp infections linked to contact with backyard chickens have been documented in the United States.4 Some humans—including children younger than 5 years, humans with weakened immune systems, humans 65 years of age or older, and pregnant women—are at higher risk for serious illness from poultry-borne zoonotic diseases.

Salmonellosis & Campylobacteriosis

Symptoms of salmonellosis or campylobacteriosis include diarrhea (which may be bloody), fever, and/or abdominal cramps. In cases of severe infection, hospitalization may be required and infection may spread from the intestines to the bloodstream and other body sites, which can be life threatening. Infection generally lasts up to one week.

Avian Influenza Viruses

Avian influenza viruses (ie, diseases caused by infection with avian influenza Type-A viruses) occur naturally among wild aquatic birds worldwide and can easily spread and infect domestic poultry and other avian and animal species.5 Wild aquatic birds (eg, ducks, geese) can be infected with avian influenza viruses but appear healthy; however, some of these viruses can cause serious illness and death in domestic poultry (eg, chickens, ducks, turkeys). Infected birds can carry viruses in saliva, mucus, and feces.5

Avian influenza viruses can infect humans via inhalation or contact with the eyes, nose, or mouth.5 Avian influenza in humans has ranged from mild to severe. Signs and symptoms include fever, cough, sore throat, runny or stuffy nose, muscle or body aches, fatigue, headaches, conjunctivitis, diarrhea, nausea, vomiting, and difficulty breathing. Humans in close or prolonged unprotected contact with infected birds or contaminated environments are thought to be at greater risk for infection, and some humans—including children younger than 5 years, humans with weakened immune systems, humans 65 years of age or older, and pregnant women—are at greater risk for serious illness from avian influenza virus infections. Most reported avian influenza infections in humans have occurred after unprotected contact with infected birds or contaminated surfaces.6

Prevention

Veterinarians should advise owners of backyard chickens and/or other poultry about zoonotic risks and how to reduce the risk for disease transmission: 

  • Hands should always be washed thoroughly with soap immediately after touching poultry or anything in their habitat. 
    • Adults should supervise handwashing by young children.
    • Hand sanitizer should be used if soap and/or water are unavailable. 
  • Poultry should not be allowed to enter homes, especially areas where food or drinks are prepared, served, or stored. 
  • Owners should designate a pair of shoes to wear while caring for poultry and avoid bringing those shoes into the home. 
  • Children younger than 5 years, those with weakened immune systems, pregnant women, and adults 65 years or older should not handle or touch chicks, ducklings, or other live poultry. 
  • Food or drink should not be consumed in areas where poultry live or roam. 
  • Birds and other poultry should never be kissed or snuggled, and touching of the face or mouth after handling birds should be avoided until hands can be washed. 
  • Equipment or materials used to raise or care for live poultry (eg, cages, feed or water containers) should be cleaned outside the home.

References and Author Information

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

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Nutritional Management in a Senior Cat with Weight Loss

Marjorie L. Chandler, DVM, MS, MANZCVS, DACVN, DACVIM, MRCVS, University of Edinburgh

Kara M. Burns, MS, MEd, LVT, VTS (Nutrition), Olathe, Kansas

Gregg K. Takashima, DVM, WSAVA Global Nutrition Committee Series Editor

Nutrition

|Peer Reviewed

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Nutritional Management in a Senior Cat with Weight Loss
Figure The patient showing muscle and weight loss

THE CASE

A 14-year-old neutered male British Burmese cat (Figure) was presented for a routine geriatric examination. Although he had a good appetite, his weight had decreased from 10.1 lb (4.6 kg) to 9.1 lb (4.14 kg) over the past year. 

History

The owner reported that the cat had become less active over the past year, had been sleeping on the floor instead of the couch as he had previously preferred, and may have been urinating increased volumes.

The patient’s diet comprised a combination of commercial adult maintenance dry cat food fed ad libitum and canned cat food fed at approximately 1.8 oz (≈50 g) per feeding twice a day. He had outdoor access only to a fenced garden; to the owner’s knowledge, the cat neither hunted nor scavenged. His appetite was good and unchanged over the past year.

The household included another cat, which was fed from a separate bowl; however, the cats often finished one another’s food, so the exact amount the presenting cat ate could not be determined.

Physical Examination 

The cat’s muscle condition score had not been evaluated or recorded the previous year, but mild-to-moderate muscle mass loss is currently evident. BCS, which was 7/9 the previous year, was 6/9 on examination. BCS is an estimate that was designed with healthy adult cats; elderly or ill cats may lose muscle mass (ie, sarcopenia) and retain fat (eg, inguinal fat pads) and therefore are more difficult to score accurately. 

The patient was bright and alert, with normal mucous membranes, thoracic auscultation, and abdominal palpation. Respiratory rate was 28 breaths per minute, and heart rate was 180 bpm with synchronous pulses. Blood pressure was 140 mm Hg. Rectal temperature was 100.6°F (38.1°C). He had decreased mobility because of previously diagnosed arthritis in both elbows; some joint thickening was noted, but no crepitus was observed.

Diagnostic Results

Hematology results were within reference ranges. 

Urine specific gravity was 1.029; dipstick results were negative for all parameters. Urine culture results were negative. Urine protein:creatinine ratio was 0.18 (reference range, <0.2). Abnormalities in the serum chemistry profile included elevated blood urea nitrogen and elevated glucose without glucosuria (Table). Fructosamine levels were within reference range. 

Table

Serum Chemistry Results

Test Result Reference Range
Blood urea nitrogen 34.2 mg/dL (12.2 mmol/L) 8.1-27.4 mg/dL (2.9-9.8 mmol/L)
Creatinine 1.57 mg/dL (139 µmol/L) 0.45-2.0 mg/dL (40-177 µmol/L)
Glucose 178 mg/dL (9.86 mmol/L) 71-159 mg/dL (3.94-8.83 mmol/L)
Fructosamine 201 µmol/L 159-295 µmol/L
Total T4 2.95 µg/dL (38 nmol/L) 1.48-5.05 µg/dL (19-65 nmol/L)
SDMA 27.4 µg/dL (1.37 µmol/L) 0-21.4 µg/dL (0-1.07 µmol/L)

Elevated serum glucose without glucosuria and fructosamine within the reference range is likely a transient rise from stress. Because British Burmese are at risk for diabetes mellitus, fructosamine evaluation was possibly justified, although the glucose value is not consistent with polyuria and/or polydipsia resulting from diabetes mellitus.

The patient’s mild azotemia was likely due to prerenal causes (eg, subclinical dehydration), early kidney disease, or both. 

DIAGNOSIS:

CHRONIC KIDNEY DISEASE & PRESUMPTIVE OSTEOARTHRITIS

In addition to osteoarthritis, the patient was diagnosed with International Renal Interest Society (IRIS) Stage 1, nonproteinuric, normotensive chronic kidney disease (CKD).1 

Cats with early-stage CKD may be able to concentrate urine more than a dog at the same stage; therefore, the cat’s urine specific gravity did not rule out CKD.

Nutritional Management

Nutritional management can be more challenging in senior pets (ie, those >7 years of age) because they often have several concurrent disorders; however, nutritional management should be considered for senior patients with CKD and weight loss and may be helpful in arthritis cases. Nutritional management for feline IRIS Stage 1 CKD is less clear-cut than for later stages, but there are some key guidelines (see Feline IRIS Stage 1 CKD Guidelines).1

Feline IRIS Stage 1 CKD Guidelines1

  • Adequate fluid intake can prevent dehydration. Feeding canned food and providing multiple accessible water sources may help with hydration. Water bowls should be easily accessible, especially for cats with arthritis, and should be separate from the food bowl and the litter box.
  • A palatable diet can help prevent further weight loss. 
  • Phosphorus should be restricted to decrease renal secondary hyperparathyroidism. 
  • Excess sodium should be avoided. 
  • Acidifying diets should be avoided, as metabolic acidosis may be present.
  • Water-soluble vitamin supplementation can replace vitamins lost in urine. 
  • High-quality protein (ie, proteins with a high percentage of amino acids), possibly in reduced amounts, can decrease azotemia.

Recommendations vary regarding dietary phosphorus restriction in patients with early CKD; however, the diet should not be high in phosphorus. A nonacidifying, low-sodium diet with increased water-soluble vitamins is appropriate. Although low-sodium diets are not associated with hypertension in cats, high salt is associated with hypokalemia and possibly an increase in serum creatinine, blood urea nitrogen, and phosphorus. The amount of protein to provide at IRIS Stage 1 is controversial. This patient—like many older cats—has muscle loss, so restriction should initially not be excessive, and a high-quality protein (ie, with a high percentage of essential amino acids) should be fed.2 Omega-3 fatty acids may help improve survival time in patients with CKD,3 improve arthritis signs,4 and improve cognition in older cats.5

Transitioning to a new diet should be done slowly, with both the old and new diets offered initially. For this patient, the diets were mixed; however, some clinicians may recommend offering each diet separately based on the proportions an individual cat will accept. In some cases, it may take weeks to transition a cat to a new diet. Warming a canned diet to just below body temperature may be helpful. Maropitant can help with nausea and vomiting, and mirtazapine can help stimulate appetite.

For this patient, a commercial diet formulated for older cats is appropriate. A senior diet can be a good transition diet for cats with early stages of CKD. Many senior diets are lower in phosphorus and sodium and are less acidic than maintenance diets. Potassium content should be high, as there will be increased renal loss. Antioxidants are often added to help enhance immune and cognitive function and increase longevity. Oxidative damage may be present in renal disease, and antioxidants may have a beneficial effect on this stress.6

A diet with functional lipids (fish oil), antioxidants (vitamins C and E), l-carnitine, botanicals (vegetables), highly bioavailable protein, and amino acid supplements was shown to improve symmetrical dimethylarginine (SDMA) in older cats.7 A dose of EPA and DHA of 50-100 mg/kg has been suggested, as long as it does not affect diet palatability.7 Older cats should have an energy-dense diet (4-4.5 kcal/g dry matter). Caloric intake should only be restricted in obese cats.

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References and Author Information

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.


Blood Smear Platelet Evaluation & Interpretation

Lisa M. Pohlman, DVM, MS, DACVP, Kansas State University

Clinical Pathology

|Peer Reviewed

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Blood Smear Platelet Evaluation & Interpretation

In most laboratories and veterinary practices, platelet concentration is determined via automated analysis. However, there are several variables that can affect accuracy of results, the most common of which, in the author’s experience, is platelet clumping. Platelet clumps must be identified on a blood film to avoid potential misdiagnosis of thrombocytopenia.

Analyzers that use impedance methodology can also produce erroneous results when platelet size overlaps with RBC size, causing large platelets to be counted as RBCs; this can result in a falsely decreased platelet concentration and misdiagnosis. This can occur in any animal that produces large platelets but is particularly common in cats, as their platelet size is similar to their RBC size.1,2

Estimation of the platelet concentration from a blood film should be performed in the monolayer using 100× objective (ie, 1000× magnification). A well made blood film with even distribution of platelets throughout the monolayer is essential. If platelet clumps are present, the platelet estimation will be falsely decreased to an unknown degree, depending on the amount of clumping. However, estimation using the method provided should help to provide the minimum concentration of platelets present.

First, the entire film should be examined for clumps. Then, at least 10 fields within the monolayer should be reviewed to determine the average number of platelets per 1000× magnification field. The number observed should be multiplied by 15 000 to get the lower end of the reference interval and then by 20 000 to determine the upper end of the reference interval.2

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Although individual laboratory reference values vary, healthy dogs and cats typically have 150 000 to 500 000 platelets/µL (150 x 109 to 500 x 109 platelets/L). For the purposes of this article, less than 150 000/μL (150 x 109/L) is indicative of thrombocytopenia and greater than 500 000/μL (500 x 109/L)  is indicative of thrombocytosis. Of note, the purpose of this exercise is to demonstrate the method of platelet estimation; because the images in this exercise are square, they may not be representative of the number of platelets seen in an entire 1000× magnification field. All films are stained with modified Wright’s Stain.

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References and Author Information

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.


Top 5 Gastrointestinal & Hepatobiliary Antibiotics

Craig B. Webb, PhD, DVM, DACVIM (Small Animal), Colorado State University

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Top 5 Gastrointestinal & Hepatobiliary Antibiotics

Antibiotic use in GI and hepatobiliary disease should be judicious, purposeful, and, ideally, directed by culture and susceptibility results when appropriate. These conditions are often chronic or recurring, and repeated courses of ineffective or unnecessary antibiotic “trials” could result in the emergence of antibiotic-resistant organisms. Injudicious use of common antibiotics can also be associated with significant alterations in the microbiota, risking both immediate and far-reaching deleterious consequences.1 

The author considers enrofloxacin, metronidazole, and tylosin to be the antibiotics most deserving of thoughtful consideration in the treatment of GI conditions in dogs and cats. Metronidazole and enrofloxacin are also frequently used in the treatment of hepatic disease. Amoxicillin–clavulanic acid and neomycin are additional important antibiotics for pharmacotherapy of hepatobiliary conditions.

1

Enrofloxacin

Enrofloxacin is a fluoroquinolone with broad-spectrum bactericidal activity against aerobic bacteria. Its mechanism of action is believed to be inhibition of bacterial DNA-gyrase, which then prevents DNA supercoiling and synthesis.2 Enrofloxacin also has efficacy against Escherichia coli.

Enrofloxacin represents a unique collective effort of the veterinary profession to successfully identify a specific therapy targeting a defined condition (ie, histiocytic ulcerative colitis [HUC; Figure 1] in boxers) that previously had been almost always terminal. This accomplishment serves as an example of the effort that should inform all areas of antibiotic use in small animal medicine,3-6 particularly because of the therapeutic difficulties now presented by antibiotic resistance. Before enrofloxacin was identified as an effective treatment for HUC, most boxers with this disease were euthanized because immunosuppressive therapy was unable to slow the rapid progression of the condition. Invasive E coli was identified as the causal agent, and remission was correlated with eradication of intramucosal E coli organisms following treatment with enrofloxacin (5-10 mg/kg PO q24h for 6-8 weeks).7-9 Cases of HUC in which enrofloxacin was a critical component of successful therapy have also been reported in French bulldogs, an English bulldog, and several other nonboxer breeds.10-12 It is crucial to note that treating dogs with enrofloxacin before obtaining a definitive diagnosis of HUC has been associated with antimicrobial resistance and a poor clinical outcome.13

Histopathology and Periodic Acid-Schiff (PAS) stain of a sample obtained from a dog with histiocytic ulcerative colitis
Histopathology and Periodic Acid-Schiff (PAS) stain of a sample obtained from a dog with histiocytic ulcerative colitis

FIGURE 1 Histopathology and Periodic Acid-Schiff (PAS) stain of a sample obtained from a dog with histiocytic ulcerative colitis

FIGURE 1 Histopathology and Periodic Acid-Schiff (PAS) stain of a sample obtained from a dog with histiocytic ulcerative colitis

E coli is one of many potential enteropathogenic bacteria associated with GI disease in dogs and cats; however, according to the ACVIM Consensus Statement on enteropathogenic bacteria, the disease is uncomplicated and self-limiting in most cases, molecular identification is sophisticated but causality is extremely elusive, and the injudicious use of antibiotics in GI disease may cause more harm than benefit.14

The most common adverse effects of enrofloxacin are GI in nature, including vomiting, diarrhea, and loss of appetite. Enrofloxacin should not be used in young, growing dogs because of the risk for cartilage damage. Enrofloxacin should be avoided in patients with seizure disorders and used at a reduced dose in patients with a significant loss of renal or hepatic function. Enrofloxacin should not be used at dosages greater than 5 mg/kg/day in cats because of the retinotoxicity reported in this species.2

2

Metronidazole

Metronidazole is a bactericidal antibiotic that targets anaerobes; it is also an antiprotozoal agent used frequently to treat Giardia spp infection. It is one of the most common nonspecific antidiarrheal drugs prescribed in veterinary medicine.15,16 Metronidazole has been shown to have immunomodulatory effects in mice (in vitro) and in humans, and these properties often are cited as justification for its use as a nonspecific GI immunosuppressive agent.17-19 However, recent work in a model of sepsis failed to identify any impact of metronidazole on systemic innate immune responses in humans.20

The veterinary profession’s understanding and appreciation for the importance of the microbiota for GI health and immune function is increasing, along with concern over the untargeted use of antibiotics and their potential for contributing to dysbiosis, and metronidazole is a key component of this discussion. Metronidazole (12.5 mg/kg PO q12h for 14 days) has been shown to reduce some pathogenic bacteria (eg, fusobacteria) and increase some beneficial bacteria (eg, bifidobacteria) but also significantly decrease the bacterial composition and diversity of the microbiota of healthy dogs.21 Composition and diversity are thought to be central components of a healthy microbiome. Recent studies have demonstrated significant dysbiosis and decreased microbiota diversity in dogs with both acute diarrhea and inflammatory bowel disease.22,23

Metronidazole has been used in the treatment of a number of veterinary diseases but most often in combination with other therapeutic agents, making it difficult to assess the efficacy of the antibiotic alone. Metronidazole (15-20 mg/kg PO q12h for 7-17 days) was found to effectively resolve diarrhea in an outbreak of Clostridium difficile-toxin–positive dogs at a small animal teaching hospital.24 In a recent report, metronidazole (10 mg/kg PO q12h for 5 days) was used in combination with trimethoprim–sulfamethoxazole in Labrador retriever puppies presented for anorexia, hematemesis, and hematochezia and diagnosed with Isospora spp infection. All puppies recovered completely.25 In another report, metronidazole (10-15 mg/kg PO q12h for 6 weeks) was used in combination with prednisolone in a group of dogs presented for diarrhea and vomiting with hypoalbuminemia and hypocobalaminemia. Colonoscopy and histopathology showed lipogranulomatous lymphangitis, and fluorescent in situ hybridization (FISH) analysis disclosed invasive bacteria in 20% of the cases. Remission was achieved in 8 of the 10 dogs.26 Another paper, however, reported that combining metronidazole (10 mg/kg PO) with prednisone was no more effective as induction therapy for dogs with inflammatory bowel disease than using prednisone alone.27 A 2007 paper described the use of metronidazole (10 mg/kg PO q12h for 2 weeks) as part of a triple antimicrobial therapy in dogs with chronic vomiting and gastric Helicobacter spp infection. Vomiting frequency was reduced by 86%.28

Exposure to antibiotics, including metronidazole or fluoroquinolones, markedly increases the risk for new-onset inflammatory bowel disease, specifically Crohn’s disease, especially in children.29 Of increasing concern is the emergence of metronidazole-resistant organisms,30 as was demonstrated in one study that found metronidazole-resistant C difficile isolates in dogs with GI disorders.31 Metronidazole is frequently prescribed for treatment of hepatic encephalopathy in dogs and cats, but controlled clinical trials evaluating the effectiveness of this therapy in veterinary patients have not been conducted.32

3

Tylosin

Tylosin is a macrolide antibiotic thought to bind 50S ribosomes and inhibit protein synthesis. It is frequently used as adjunct treatment for diarrhea in veterinary patients with a variety of diseases. A specific GI condition in dogs termed tylosin-responsive diarrhea has been identified in middle-aged, large-breed dogs with chronic diarrhea that resolves rapidly following tylosin treatment but returns just as quickly with the cessation of tylosin treatment.33 A subsequent study found that the combination of tylosin (20 mg/kg PO q24h for 10 days) and a highly digestible canned food diet effectively controlled chronic diarrhea for at least 3 months in a group of beagles.34 In a randomized placebo-controlled clinical trial in dogs, recurrent diarrhea that had previously resolved with tylosin treatment responded to tylosin again in 85% of cases (25 mg/kg PO q24h for 7 days).35 Later work suggested that a dose as low as 5 mg/kg PO q24h for 7 days may be just as effective in cases of relapsing diarrhea.36 In a translational study, a 10-day course of tylosin significantly improved diarrhea, decreased colonic inflammation, and decreased serum C-reactive protein levels in rhesus macaques with chronic diarrhea.37

Tylosin (20-22 mg/kg PO q24h for 14 days) may resolve diarrhea because it increases concentrations of Enterococcus spp- and E coli-like organisms while decreasing fusobacteria and Bacteroidales in the jejunum of healthy dogs.38 A study of dogs with recurrent tylosin-responsive diarrhea found that tylosin administration significantly increased Enterococcus spp in those dogs with diarrhea that resolved following administration of tylosin (25 mg/kg PO q24h for 7 days).39

Like metronidazole, tylosin is often used for properties believed to be immunomodulatory. Although tylosin has not been shown to demonstrate such properties, studies of the macrolide antibiotic tilmicosin in large animals suggest that it has immunomodulatory and anti-inflammatory properties.40 Tylosin is one of the most frequently prescribed medications for dogs with inflammatory bowel disease.41

4

Amoxicillin–Clavulanic Acid

Amoxicillin–clavulanic acid is a bactericidal aminopenicillin with a β-lactamase inhibitor. Penicillins act by inhibiting cell wall synthesis. Adverse effects are rarely serious, although GI signs (eg, anorexia, vomiting, diarrhea) are relatively common.

Table

Common Bacteria Causing Bacterial Cholangitis in Dogs & Cats

Common Bacterium Class
Escherichia coli Gram-negative aerobic
Enterococcus spp Gram-positive aerobic
Clostridium spp Anaerobic
Streptococcus spp Gram-positive aerobic
Rare Bacterium Class
Enterobacter spp Gram-negative aerobic
Klebsiella spp Gram-negative aerobic
Proteus spp Gram-negative aerobic
Bacteroides spp Anaerobic

Studies published in 2007 and 2016 demonstrated that bacterial cholangitis and cholecystitis (Table), although rarely reported in the literature, should be considered in dogs and cats presented for vomiting, jaundice, and abdominal pain and/or fever.42,43 These patients commonly have an increase in liver enzyme activity, hyperbilirubinemia, an inflammatory leukogram, and ultrasonographic evidence of gallbladder abnormalities. Because antimicrobial resistance has become common with aerobic isolates, antibiotic choice should be based on culture and susceptibility testing. Sampling the bile or gallbladder wall—not the liver—results in the greatest yield for a positive culture. In these studies, metronidazole was used to treat most anaerobic infections, whereas a fluoroquinolone (eg, enrofloxacin, ciprofloxacin) or amoxicillin–clavulanic acid was used to treat most patients with aerobic infection. In the absence of antimicrobial susceptibility testing, treatment with a broad-spectrum antibiotic is indicated and may require combination of a fluoroquinolone, penicillin, and metronidazole or a fluoroquinolone and amoxicillin–clavulanic acid. Use of empiric therapy may fail because of the prevalence of antimicrobial resistance in the common isolates.42,43

According to the WSAVA International Liver Standardization Group, feline cholangitis is the predominant liver disease in cats after hepatic lipidosis.44 In cases of acute neutrophilic cholangitis, a bacterial infection is likely the inciting cause, and many of these cats are presented with significant clinical morbidity.45 Clinical signs include acute onset of vomiting, diarrhea, anorexia, and lethargy, and patients may be febrile and icteric (Figure 2). These cats may have pancreatitis and gastroenteritis as concurrent conditions (feline triaditis); aggressive supportive care along with directed antibiotic therapy may be critical to a successful outcome. Gallbladder aspiration for cytology (Figure 3) and culture has become the diagnostic test of choice in these cases, and culture and susceptibility results should dictate the choice of antibiotic.46,47 The bacteria most frequently identified in feline neutrophilic cholangitis are enteric organisms (Figure 4), including E coli, Enterococcus spp, Bacteroides spp, Clostridium spp, and Streptococcus spp.48 In lieu of culture and susceptibility results, empiric therapy with amoxicillin–clavulanic acid for 8 weeks is recommended.49

5

Neomycin

An important potential clinical consequence of decreased liver function is hepatic encephalopathy. In dogs and cats, hepatic encephalopathy is most commonly associated with portosystemic shunts (congenital or acquired), portal hypertension or liver cirrhosis (eg, from chronic copper hepatopathy), and, more rarely, acute hepatic failure (eg, from drugs and toxins). Although the pathogenesis is not completely understood, intestinal bacteria are thought to represent an important source of ammonia production, and increased systemic ammonia concentrations play a central role in this condition.50

Urease-producing bacteria in the GI tract convert urea to ammonia. One treatment strategy uses antibiotics to change the GI microbiota in a way that decreases bacterial production of ammonia. The importance of the microbiota to ammonia production was highlighted by a study showing that probiotic therapy resulted in a significant reduction in overt encephalopathy in humans with liver cirrhosis.51 

Neomycin is a bactericidal aminoglycoside that binds to the 70S ribosomal subunit. In dogs and cats, oral neomycin (20 mg/kg PO q8-12h) is still used in conjunction with lactulose for treating hepatic encephalopathy, although, as in humans, both nephrotoxicity and ototoxicity are serious concerns. Metronidazole (7.5 mg/kg PO q8h or q12h) has been used as an alternative antibiotic in veterinary patients.2

HUC = histiocytic ulcerative colitis

References and Author Information

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.


Top 5 Corticosteroids for Use in Emergency Settings

Kiko E. Bracker, DVM, DACVECC, Angell Animal Medical Center, Boston, Massachussetts

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Top 5 Corticosteroids for Use in Emergency Settings

Corticosteroids are a diverse group of medications used to treat a wide array of illnesses. At lower dose ranges, they provide anti-inflammatory effects, whereas higher doses are immunosuppressive. These properties make them valuable tools in the emergency and critical care setting. Clinicians must be familiar with the appropriate indications for each drug, along with their relative potencies and adverse effects. Following are the author’s top 5 corticosteroids used in emergency settings.

1

Prednisone/Prednisolone

Prednisone is used for both anti-inflammatory and immunosuppressive purposes because of its effectiveness, low cost, small tablet size, innocuous taste, and variable dose sizes.

When used for anti-inflammatory effects, prednisone is administered at 0.5-1.0 mg/kg/day, often for only a few days to limit local or systemic inflammation.1-3 Inflammatory or traumatic disorders of emergency patients (eg, oropharyngeal trauma, oropharyngeal biopsy, decompensation secondary to laryngeal collapse or tracheal collapse) are often short in duration, and treatment with steroids for 2 to 3 days allows the initial insult or exacerbation to subside. In patients with transient inflammatory disorders, the common side effects of steroids (see Glucocorticoid Adverse Effects) are mild because of the relatively low dose and short duration of treatment.3 

Glucocorticoid Adverse Effects

  • Polyuria/polydipsia
  • GI ulceration
  • Increased liver enzyme activity
  • Muscle atrophy
  • Weakness
  • Insulin resistance and hyperglycemia
  • Symmetric hair loss
  • Panting
  • Polyphagia
  • Impaired wound healing
  • Hypercoagulability/thromboembolism

Immunosuppressive doses of prednisone range from 1-2 mg/kg q12h.1,4 Some overlap of the dosing ranges for anti-inflammatory and immunosuppressive effects may be noted, most likely because those effects are not entirely distinct. 

Steroids, particularly prednisone, are used to treat many autoimmune disorders, including immune- mediated hemolytic anemia, immune-mediated thrombocytopenia, and immune-mediated polyarthropathy. Because these diseases often require long-term treatment with high doses of steroids, adverse effects are more common. A second or third immunosuppressive agent is often used with prednisone to maintain immunosuppression and allow rapid reduction of prednisone doses to maintenance levels. 

Because cats and animals with severe hepatic disease have difficulty converting prednisone into the active metabolite prednisolone, some sources suggest that prednisolone may be a better choice in these patients.5,6 

2

Dexamethasone Sodium Phosphate

Dexamethasone is often used as the first-line steroid for urgent conditions because it has a rapid onset of action and can be administered parenterally.1,2 Most patients that require continued steroid therapy are switched to oral prednisone. Dexamethasone is approximately 7 times more potent than prednisone, so the prednisone dose should be approximately 7 times greater than an equivalent dexamethasone dose.1,2 For example, a patient receiving 5 mg dexamethasone would be switched to 30-35 mg prednisone. 

When using different steroids, clinicians must be careful to recognize the relative glucocorticoid potency of each drug.1,2 Dexamethasone has a longer duration of action than other steroids.1 When switching from injectable dexamethasone to an oral steroid, the oral steroid is usually started 24 hours after dexamethasone has been discontinued. Dexamethasone does not affect cortisol assays, so it can be administered to patients with suspected hypoadrenocorticism before an ACTH stimulation test or before blood is obtained for cortisol testing. However, continued use of dexamethasone (or any other steroid) will suppress the hypothalamic-pituitary-adrenal axis, which in turn will suppress endogenous cortisol concentrations.1

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Hydrocortisone

Many topical medications contain hydrocortisone as an anti-inflammatory agent. Even with topical application, some systemic absorption of hydrocortisone can occur.7 Hydrocortisone is used in shampoos and in various topical, ocular, and otic preparations to manage superficial irritation. 

Hydrocortisone is also an appropriate treatment choice for critical illness-related corticosteroid insufficiency (CIRCI; formerly relative adrenal insufficiency). CIRCI affects patients with severe sepsis that are hypotensive despite fluid therapy and vasopressor support. In some CIRCI patients, low doses of IV corticosteroids can improve blood pressure.8,9 Because there is no consensus on how best to diagnose this syndrome, an appropriate response to therapy is used as a surrogate for an objective diagnosis. The best treatment of CIRCI is not established, but hydrocortisone has been used at 0.5-1.0 mg/kg IV q6h or as a CRI at 2.5-3.0 mg/kg/day.9,10 If blood pressure improves within 24 hours of starting hydrocortisone, steroid supplementation should be continued at a tapering dose for approximately 1 week.9,10

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Methylprednisolone Sodium Succinate 

IV methylprednisolone sodium succinate (MPSS) is often administered to dogs and cats with acute spinal cord injury before and after a decompressive spinal surgery. Strong opinions for and against the use of MPSS (and other steroids) exist within the veterinary community, despite the lack of evidence to support its benefits.11,12 The human literature also shows little consensus regarding the use of MPSS for acute spinal cord injury.2 The potential benefits of MPSS are likely associated with the limitation of ischemic and oxidative damage in the area of the damaged spine.2 Side effects of aggressive MPSS therapy include diarrhea, vomiting, melena, hematemesis, and anorexia.13 MPSS should be considered only when it can be administered within 8 hours of the initial injury.2,14 The author suggests 2 protocols for administration of MPSS. Both require an initial loading dose of 30 mg/kg IV followed either by a decreased dose (15 mg/kg) in 2 hours and then 8 hours after the initial bolus or by a CRI of 5.4 mg/kg/hr for 24 hours.2

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Fluticasone

Fluticasone is the most commonly used inhaled steroid of those available.15 Because they can be delivered directly to the site of inflammation with minimal systemic absorption, inhaled steroids are used to efficiently treat inflammatory pulmonary diseases in dogs and cats (eg, asthma, chronic bronchitis, eosinophilic bronchopneumopathy).15-17

Although it can take 1 to 2 weeks for inhaled steroids to decrease inflammation, clinicians commonly begin this course of therapy at the time of diagnosis, which is often in the emergency room.15 Most of these inflammatory pulmonary conditions are initially managed with oral steroids, but treatment is switched to inhaled steroids as soon as possible to avoid side effects. Pet owners should be shown how to use the inhaler and delivery chamber (preferably species-specific) while their pet is still in the clinic to provide them with multiple opportunities for supervised practice. Hands-on instruction can increase owner confidence in performing this technique at home and can hasten the transition from oral to inhaled steroids. Fluticasone is available through human pharmacies.

Conclusion

Corticosteroids comprise a broad group of pharmacologic agents with a choice of administration routes. In the critical care setting, these drugs treat conditions ranging from allergic reactions to acute soft tissue inflammation, autoimmune disease, asthma, spinal cord injury, and vasopressor nonresponsive hypotension in sepsis. Corticosteroids cause predictable dose-dependent side effects but remain a valuable drug class for use by critical care and emergency clinicians.

References and Author Information

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