July / August 2021   |   Volume 19   |   Issue 5

Breed-Specific Considerations to Avoid Adverse Drug Effects

in this issue

in this issue

Top 5 Breed-Specific Considerations to Avoid Adverse Drug Effects

Enteral & Parenteral Nutrition in the Intensive Care Unit

Canine Pelvic Limb Amputation

Electrocution Emergency in a Puppy

Differential Diagnosis: Hypernatremia

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Claro CB JulyAug 2021

Enteral & Parenteral Nutrition in the Intensive Care Unit

Daniel L. Chan, DVM, DACVECC, DACVN, DECVECC, MRCVS, The Royal Veterinary College, University of London, London, England

Nutrition

|Peer Reviewed

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Enteral & Parenteral Nutrition in the Intensive Care Unit

Nutritional support is essential for critically ill patients in the intensive care unit and should be included as part of the standard of care, as there are potentially serious consequences of malnutrition. Effective nutritional management strategies can alleviate the risk for development of malnutrition and associated morbidities.1,2

Inadequate food intake, GI dysfunction, and metabolic changes can cause malnourishment in hospitalized patients not supported with nutritional interventions. Critically ill patients catabolize lean body mass during periods of food and nutrient deprivation, emphasizing the need for nutritional support2; this is also the case in obese patients, as critically ill patients with inadequate food intake preserve fat stores but catabolize lean body tissue.2 Cats do not downregulate gluconeogenesis or proteolysis during low protein intake.3 Continued loss of lean body mass can result in negative effects on wound healing, immune function, and, ultimately, clinical outcomes.2,4 Conversely, adequate energy substrates, protein, essential fatty acids, and micronutrients support wound healing and tissue repair.

Nutritional Assessment

Nutritional support carries a risk for complications (eg, hyperglycemia, electrolyte shifts, aspiration pneumonia), but these can be minimized through careful patient selection, nutritional assessment, and sound nutritional planning. A nutritional assessment should be performed through systematic evaluation to identify patients that require immediate nutritional support.5 Patients with obvious signs of malnutrition, >10% body weight loss, ≥3 days poor food intake, and prolonged illness should be given urgent nutritional support.5

Cardiovascular status should be stable and electrolyte, fluid, and acid-base abnormalities should be corrected before nutritional support is provided.

Nutritional Plan

A nutritional plan should include the anticipated duration of nutritional support, which largely depends on clinical judgment. The best route of nutrition (enteral or parenteral) should be determined, with the enteral route considered first when possible. If enteral feedings are not tolerated (when part or all of the GI tract is not functional [eg, with motility disorders]), parenteral nutrition can be considered so the patient is not without nutrition for >3 days. Nutrition should be introduced gradually, and target levels should be reached in 48 to 72 hours, except in patients at risk for refeeding syndrome.

Calculating Energy Needs

Resting energy requirement (RER) is the number of calories required to maintain homeostasis while the patient is at rest.2,4 RER is calculated as 70 × body weight in kg0.75. In patients that weigh 4.4 to 66 lb (2-30 kg), 30 × body weight in kg + 70 can be used to approximate energy needs. RER has historically been multiplied by an illness factor between 1.1 to 2 to account for increases in metabolism associated with different conditions and injuries. Recently, less emphasis has been placed on these subjective illness factors, and current recommendations include using RER as a starting point and adjusting based on the response to feeding.6

Although definitive studies determining the precise nutritional requirements for critically ill patients have not been performed, some recommendations are available. It is generally accepted that hospitalized dogs should be supported with 4 to 6 g of protein/100 kcal (15%-25% of total energy requirements) and cats should be supported with ≥6 g of protein/100 kcal (25%-35% of total energy requirements).5,7 Patients with poor protein tolerance (eg, those with hepatic encephalopathy) should receive reduced amounts of protein (dogs, ≈3 g/100 kcal; cats, 4 g/100 kcal).7 Patients with hyperglycemia or hyperlipidemia may also require decreased amounts of carbohydrates and lipids, respectively, when provided with parenteral nutrition.

Enteral Nutrition

Enteral nutrition is usually preferable, as it helps maintain GI structure and function. Nasoesophageal/nasogastric, esophagostomy, and gastrostomy feeding tubes are commonly used in dogs and cats. Considerations for various feeding tubes should be reviewed (Table). Guidance on placement of feeding tubes is available (see Suggested Reading).

Most complications with feeding tubes include tube occlusion and localized irritation at the tube exit site.8,9 More serious complications include infection at the exit site or, rarely, complete tube dislodgment and peritonitis with a gastrotomy tube (proper stoma require 10 days to form). Risk for complications can be reduced by using the appropriate tube, through proper food selection and preparation, and with careful monitoring.8,9

Feedings are generally administered every 4 to 6 hours, and feeding tubes should be flushed with 5 to 10 mL (based on size of patient and tube) of water before and after each feeding to minimize obstruction of the tube. At discharge, the number of feedings should be reduced to 3 to 4 times per day to help facilitate pet owner compliance.

A volume of 5 to 10 mL/kg per individual feeding is generally well-tolerated but can vary by patient. Enteral diets are mostly composed of water (most canned foods are already >75% water); thus, the amounts of fluids administered parenterally (including water from pre- and postfeeding flushes) should be adjusted to avoid volume overload. Premature removal of tubes can be prevented by using special collars (eg, Elizabethan) and wrapping the tube securely. Care should be taken to avoid tightly wrapping the tube, as this could lead to patient discomfort and even compromise proper ventilation.

TABLE

CONSIDERATION FOR DIFFERENT TYPES OF FEEDING TUBES

Feeding Tube Typical Duration of Use Advantages Disadvantages
Nasoesophageal Short-term (<5 days) Inexpensive, easy to place, no anesthesia required Requires complete liquid diet, prone to being dislodged
Esophagostomy Extended (weeks to months) Inexpensive, simple to place, can accommodate high-calorie semiliquid diets Requires brief anesthesia, prone to becoming obstructed, incision can become inflamed or infected
Gastrostomy Extended (weeks to months) Can accommodate high-calorie semiliquid diets Requires general anesthesia for placement, endoscopic placement requires special equipment, tube displacement can result in peritonitis

 

Parenteral Nutrition

Indications for parenteral nutrition include persistent vomiting, severe malabsorptive disorders, and severe ileus. Safe administration of IV nutrition requires a dedicated catheter placed using an aseptic technique; this should only be provided by a 24/7 care facility where close monitoring can be provided.7 Long catheters composed of silicone, polyurethane, or tetrafluoroethylene are recommended for use with parenteral nutrition to reduce the risk for thrombophlebitis.7 Most parenteral nutrition solutions contain a carbohydrate (dextrose), protein (amino acids), and fat (lipids) source. The proportions of each component in the admixture are determined based on the required energy and protein needs of the patient. Detailed instructions for formulation of parenteral nutrition admixtures are available.7 Compounding parenteral nutrition admixtures requires special equipment and is commonly sourced from human hospitals. Alternatively, there are a few commercially available, ready-made, 3-in-1 solutions (Figure) that provide 40% to 70% of a patient’s RER (depending on the size of the patient) when administered at 2 to 4 mL/kg/hour; these solutions contain ≈20 mmol/L of potassium and therefore cannot be administered at higher rates.7 The osmolarity of these solutions can vary, but solutions of <600 to 750 mOsmol/L can be suitable for peripheral administration.7

A commercially available, ready-made, 3-in-1 solution that contains dextrose, amino acids, and lipid emulsion can be used as an alternative to compounding parenteral nutrition with specialized equipment. The solution can be mixed just prior to use by squeezing the bag.
A commercially available, ready-made, 3-in-1 solution that contains dextrose, amino acids, and lipid emulsion can be used as an alternative to compounding parenteral nutrition with specialized equipment. The solution can be mixed just prior to use by squeezing the bag.

FIGURE A commercially available, ready-made, 3-in-1 solution that contains dextrose, amino acids, and lipid emulsion can be used as an alternative to compounding parenteral nutrition with specialized equipment. The solution can be mixed just prior to use by squeezing the bag.

FIGURE A commercially available, ready-made, 3-in-1 solution that contains dextrose, amino acids, and lipid emulsion can be used as an alternative to compounding parenteral nutrition with specialized equipment. The solution can be mixed just prior to use by squeezing the bag.

Monitoring & Reassessment

Daily monitoring of body weight in patients supported with nutritional interventions is recommended. However, fluid shifts should be accounted for when changes in body weight are evaluated; thus, BCS assessment is also important. Using RER as the patient's caloric requirement as a starting point, the number of calories provided may need to be increased (typically by 25% if well-tolerated) to meet the patient's changing needs. In patients unable to tolerate prescribed amounts, reducing amounts of enteral feedings and supplementing feed with parenteral nutrition should be considered.

Possible complications of parenteral nutrition include thrombophlebitis and metabolic disturbances (eg, hyperglycemia, electrolyte shifts, hypertriglyceridemia). Avoiding serious complications associated with parenteral nutrition requires early identification of problems and prompt action. Frequent monitoring of vital signs, catheter exit sites, and routine serum chemistry profiles can help identify developing problems. Persistent hyperglycemia while the patient is receiving nutritional support may require adjustment to the nutritional plan (eg, decreasing dextrose content in parenteral nutrition) or administration of regular, short-acting insulin.

Continual reassessment can help determine when to transition the patient from assisted feeding to voluntary consumption of food. Nutritional support should only be discontinued when the patient can consume ≈75% of their RER without support. In patients receiving parenteral nutrition, the transition to enteral nutrition should occur over at least 12 to 24 hours, depending on tolerance of enteral nutrition.

References

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

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

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


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Hill's CB JulyAug 2021

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CareVet CB JulyAug 2021

Differential Diagnosis: Hypernatremia

Todd Archer, DVM, MS, DACVIM, Mississippi State University

Internal Medicine

|Peer Reviewed

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Differential Diagnosis: Hypernatremia

Following are differential diagnoses for animals presented with hypernatremia.

Hypotonic fluid losses (hypovolemia)

  • Extrarenal fluid losses
    • Cutaneous losses
    • GI losses (vomiting, diarrhea)
    • Third space losses
  • Renal fluid losses
    • Drug use (eg, furosemide, corticosteroids)
    • Osmotic diuresis
    • Renal disease

Pure water losses (normovolemia)

  • Diabetes insipidus (central or nephrogenic)
  • Inadequate water intake
    • Defect in thirst mechanism
    • Inadequate access
    • Neurologic disease
  • Increased insensible fluid losses (panting, fever, elevated environmental temperature)

Sodium gain (hypervolemia)

  • Hyperaldosteronism
  • Iatrogenic causes via IV fluids (hypertonic saline administration, sodium bicarbonate)
  • Increased sodium ingestion (play dough, paint ball toxicity, salt water)

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

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

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


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Imoxi CB JulyAug 2021

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iM3 CB JulyAug 2021

Canine Pelvic Limb Amputation

James Howard, DVM, MS, DACVS, The Ohio State University College of Veterinary Medicine, Columbus, Ohio

Kristen French-Kim, DVM, The Ohio State University

Stephen C. Jones, MVB, MS, DACVS-SA, The Ohio State University

Nina Kieves, DVM, DACVS, DACVSMR, CCRT, The Ohio State University College of Veterinary Medicine, Columbus, Ohio

Surgery, Soft Tissue

|Peer Reviewed

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Canine Pelvic Limb Amputation

Pelvic limb amputations are palliative salvage procedures used for end-stage diseases, including complex fractures or chronic complications with previous repairs, appendicular neoplasia, extensive trauma, chronic nonhealing wounds, or appendicular neuropathies (eg, brachial plexus avulsion). Some amputations are necessary due to the pet owner’s financial constraints. However, surgeons are encouraged to exhaust all options prior to limb amputation while also educating owners about the risks, complications, and prognosis for each specific clinical case.

The midfemoral amputation technique protects male genitalia with favorable cosmesis but can cause a greater likelihood of muscle atrophy and pressure sores. Amputation by coxofemoral joint disarticulation, however, obviates the risk for delayed muscle atrophy and has favorable cosmesis. This procedure provides a predictable outcome and reduces the likelihood of pressure sore development, thereby improving postoperative recovery and at-home incision management as compared with the midfemoral technique.

Complete presurgical orthopedic and neurologic examinations are necessary. Dogs undergoing pelvic limb amputation adapt through increased tarsal range of motion in the contralateral limb, coupled with increased range of motion of the cervicothoracic and thoracolumbar vertebrae.1 It is important to explain to owners that, although amputations typically have a good prognosis, increased BCS negatively correlates with quality-of-life scores.2 Preoperative surgical preparation varies based on patient size, although the landmarks used are identical regardless of patient size (see Step 1). Owners should be informed that extensive removal of the patient’s hair coat prior to surgery is necessary and that regrowth will take some time.

Preoperative antibiotics (eg, cefazolin [22 mg/kg IV], ampicillin/sulbactam [30 mg/kg IV]) should be routinely administered at induction and every 90 minutes during surgery. However, because routine amputations are classified as clean procedures, postoperative antimicrobial stewardship should be considered before continuing antibiotics. In most cases, unless there is noticeable pyoderma surrounding the incision site, antibiotics are not necessary postoperatively. Preoperative epidurals, intraoperative perineural injections, liposomal encapsulated bupivacaine during closure, and/or placement of an indwelling pain-soaker catheter in the superficial tissues should be considered. Perioperative analgesics are necessary. Additional IV and oral analgesics should be administered during the postoperative period for 10 to 14 days depending on the patient’s comfort level. Injectable opioids (eg, morphine, methadone, fentanyl) can be administered immediately following surgery and later (next day following pain assessment) transitioned to oral NSAIDs for the duration of the recovery period. 

Routine postoperative exercise restriction and incision care, including use of cold and warm compresses, are standard. NSAIDs, ancillary analgesics, and anxiolytics are routinely provided for at-home care.


STEP-BY-STEP

PELVIC LIMB AMPUTATION


WHAT YOU WILL NEED

  • Soft tissue surgery pack, including Mayo scissors, Metzenbaum scissors, forceps, a variety of hemostats, and right-angle forceps (optional)
  • Electrocautery
  • ± Hatt spoon
  • Monofilament suture (4-0 to 0, depending on patient size)
    • Polydioxanone suture for vessel ligation, muscle apposition, and deep subcutaneous closure (4-0 to 2-0)
    • Poliglecaprone 25 suture for superficial subcutaneous closure (4-0 to 3-0)
    • Nonabsorbable monofilament suture (eg, polybutester [4-0])
  • Local anesthetic for perineural injection (recommended doses should not be exceeded)
    • Ropivacaine (0.5% or 0.75%): 1-3 mg/kg (dogs) and 1-2 mg/kg (cats)
    • Bupivacaine (0.25% or 0.5%): 1-2 mg/kg (dogs) and 1 mg/kg (cats)
  • Syringes and needles for perineural injections (syringe size depends on recommended doses; a 25-gauge needle is recommended for perineural injections)
  • 4 x 4 or 3 x 3 gauze sponges and laparotomy sponges to control hemorrhage

STEP 1

Clip hair from the level of the umbilicus, dorsally 2 to 5 cm past dorsal midline, ventrally 5 cm past ventral midline, around the entire inguinal and abdominal region, circumferentially around the pelvic limb to the level of the hock, from the perineal region, and from the base of the tail. If the patient has evidence of current soft stool or diarrhea, use an anal purse string suture. Wrap the limb distal to the hock in sterile bandage material during draping, and place the patient in lateral recumbency with the affected limb upward and the limb draped routinely.

Clinician's Brief

STEP 2

To ensure adequate skin is available for closure, identify the lateral incision (dashed line), which begins at the level of the cranial flank fold and (in a gentle arc) reaches its most distal point approximately halfway down the length of the femur, meeting the caudal flank fold near the ischiatic tuberosity. Also, identify the medial incision (solid line), which mirrors the lateral incision but is slightly more proximal.

Clinician's Brief

STEP 3

Abduct the limb to begin the medial dissection. Using right-angle forceps, incise the subcutaneous tissue and underlying deep femoral fascia with a combination of sharp and blunt dissection. Approach the femoral triangle by palpating the medial aspect of the pelvic limb and feeling for a short, tight muscular band (ie, the pectineus muscle).

Author Insight

The femoral triangle provides passage of the femoral artery, femoral vein (Figure A; solid arrow), and saphenous branch of the femoral nerve to the pelvic limb. When dissecting vessels, blunt dissection using right-angle forceps should be used in a parallel orientation to the long axis of the vasculature (Figure B). This technique reduces the risk for accidental vessel rupture or penetration.

Boundaries of the femoral triangle are:

  • Cranial: Caudal sartorius muscle
  • Caudal: Pectineus muscle; easiest to palpate to find the triangle (Figure A; dashed arrow)
  • Lateral: Vastus medialis, pectineus, and iliopsoas muscle
  • Medial: External abdominal oblique muscle
Clinician's Brief
Clinician's Brief

STEP 4

Dissect the femoral artery, vein (Figure A), and saphenous branch of the femoral nerve. Triple ligate each vessel. Place a single transfixing and circumferential suture on the side of the vessel that will remain with the patient, then place another single circumferential suture on the side of the vessel that will remain with the amputated limb to prevent back-bleeding. Transect the vessels between the transfixing suture that will stay with the patient and the circumferential suture that will prevent back-bleeding (Figure B). To provide local nerve blocks, insert the needle into the perineural sheath and inject a small amount of ropivacaine or bupivacaine. A small “bleb” will form. Wait 3 minutes, then transect the nerve distal to the injection site.

Author Insight

Large arteries and veins should always be ligated with a transfixing suture and 2 circumferential sutures. This is common practice in medium to large dogs. Arteries and veins in small dogs and cats can be ligated with 3 circumferential sutures only; 2 sutures always stay with the patient side of the vessel and one will be removed with the amputated limb to prevent back-bleeding.

Clinician's Brief
Clinician's Brief

STEP 5

Work cranially and caudally to transect the cranial and caudal bellies of the sartorius (solid arrows), pectineus (dashed arrow; this can be transected at its origin, midbelly, or insertion), adductor (Ad), and gracilis (Gr) muscles midfemur. Once the medial circumflex femoral artery and vein or the deep branch of the medial circumflex femoral artery and vein* are encountered, ligate using the same technique described in Step 4. (The semimembranosus [Sm] is labeled for orientation.)

Palpate the lesser trochanter of the femur, then transect the iliopsoas (Ili) midbelly or at its insertion.

Clinician's Brief

Author Insights

Only the extrinsic pelvic limb muscles (ie, those that attach the limb to the pelvis) need to be transected. Excessive dissection of the quadricep muscles can prolong surgical time and increase the risk for complications.

The femoral nerve courses through the iliopsoas muscle before exiting the muscle belly and penetrating the rectus femoris and vastus medialis. The femoral nerve can be injected with ropivacaine or bupivacaine and transected.

*The vascular bundle is located caudal to the femoral artery and vein, medial to the pectineus muscle, and lateral to the iliopsoas [Ili] muscle.

STEP 6

Palpate the medial joint capsule (dashed arrow), and sharply incise into it following the anatomy of the acetabular cup. Once the joint capsule is open, disrupt the ligament of the head of the femur with a scalpel blade, Mayo scissors, or Hatt spoon. (The iliopsoas [Ili] muscle is identified with the solid arrow for orientation.)

Clinician's Brief

Author Insight

The limb should be put through range of motion to isolate the coxofemoral joint to guide the incision into the joint capsule.


STEP 7

Adduct the limb for the lateral aspect of the muscular attachments. Transect the tensor fasciae latae (TFL) muscle at its distal aspect and the associated fascia lata (FL) near midfemur. In the same plane of dissection, transect the biceps femoris (BF) and caudal crural adductor (CCA) near the level of the midfemur. Do not transect the sciatic nerve, which is deep in the muscles, prior to injecting local anesthetic, as unnecessary neuropathic postoperative pain can cause patient discomfort.

Clinician's Brief

Author Insight

The biceps femoris arises from the ventrocaudal aspect of the sacrotuberous ligament and ischial tuberosity, allowing the proximal portion of the transected muscle belly to reflect dorsally, thus facilitating dissection and midbelly transection of the semitendinosus (St) and semimembranosus (Sm) muscles.

Clinician's Brief
Clinician's Brief

STEP 8

As the dorsal reflection of the biceps femoris muscle exposes the greater and third trochanteric region of the femur (improving visualization of the superficial, middle, deep gluteal, and deeper piriformis muscle insertion sites), transect each close to its insertion.

Reflect the superficial gluteal and piriformis muscles dorsally, and bluntly dissect the underlying fascia to isolate the caudal gluteal artery, vein, and sciatic nerve (previously transected) that are adjacent to each another. Triple ligate the caudal artery and vein separately.


STEP 9

At the caudal aspect of the hip, locate the gemelli (Ge) muscles; the bellies are bisected by the tendon of the internal obturator (IO) muscle. Transect the gemelli muscles midbelly along with the tendon of the internal obturator muscle.

Dorsally and ventrally reflect the gemelli muscle bellies to expose the underlying external obturator muscle, then transect it midbelly. Simultaneously transect only the rectus femoris, as it is the only muscle of the quadriceps group attached to the pelvis.

At the dorsal aspect of the acetabulum, incise the remaining portion of the joint capsule (curved arrow) with the small articularis coxae muscle. Ligate the underlying branch of the lateral circumflex femoral artery.

At the caudal aspect of the limb, isolate the abductor cruris caudalis (scissors under muscle in image), and transect it midbelly.

Clinician's Brief

STEP 10

Identify the iliopsoas muscle by its close proximity to the parent femoral nerve. If the saphenous branch of the femoral nerve has not already been transected, transect the parent femoral nerve. To free the cranial and ventromedial aspect of the limb, abduct the limb, transect any remaining iliopsoas muscle attachments, and ligate any remaining branches of the medial circumflex femoral vessels.

Caudal to the iliopsoas muscle, isolate the adductor longus and quadratus femoris muscles, and transect each muscle at midbelly.

Complete the ventral incision into the joint capsule. Use monopolar electrocautery to maintain hemostasis.

Gently abduct the limb to expose the head of the femur. Transect any remnants of the ligament of the head of the femur to complete the coxofemoral disarticulation. Remove the limb from the body.

Clinician's Brief

Author Insight

Smaller branches of the medial circumflex femoral artery are in close proximity to the ventral aspect of the joint capsule.


STEP 11

Prior to closure, inspect the surgical field for bleeding and plan to prevent dead space. Lavage the surgical field with warm saline to minimize the potential for postoperative infection.


STEP 12

Start deep muscle closure. Appose the muscle bellies to protect the acetabulum and the transected ends of the femoral artery, vein, and nerve. Use either a continuous or interrupted suture pattern (arrows) with absorbable suture material (suture size, 3-0 to 0, depending on patient size).

Clinician's Brief

STEP 13

Close the subcutaneous tissue layer routinely. If desired, place an indwelling pain-soaker catheter in the superficial tissues for postoperative administration of local analgesics—do not place in the closure of the incision. Triangular protrusions of skin (ie, “dog ears”) may form at the termination of the suture lines. If there is excessive skin in this area, it can be removed and closed routinely. Smaller “dog ears” can be corrected with multiple geometric correction techniques including placement of an apex cutaneous suture, removing the dog ear with a fusiform shape extending from the original incision, or removing a triangular-shaped portion of skin extending from the incision, among others.

Author Insight

Throughout closure, care must be taken to ensure there is enough skin for closure. Any excess skin should be excised to prevent excess dead space.


STEP 14

Perform skin or intradermal closure using either a continuous or interrupted pattern (suture size range, 4-0 to 3-0, depending on patient size).

Clinician's Brief

Author Insight

Staples are not recommended due to discomfort and increased inflammation but may be considered with longer incisions in larger dogs.

References

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

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

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


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Elanco Trio CB JulyAug 2021

Esophageal Hiatal Size in Brachycephalic Breeds

Lisa Corti, DVM, DACVS, CCRP, North Shore Veterinary Surgery, Andover, Massachusetts, North Shore Community College, Danvers, Massachusetts

Surgery, Soft Tissue

|Web-Exclusive

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Esophageal Hiatal Size in Brachycephalic Breeds

In the literature

Conte A, Morabito S, Dennis R, Murgia D. Computed tomographic comparison of esophageal hiatal size in brachycephalic and non-brachycephalic breed dogs. Vet Surg. 2020;49(8):1509-1516.


FROM THE PAGE…

The gastroesophageal junction (GEJ) is an important anatomic region composed of intrinsic and extrinsic components that help prevent gastroesophageal reflux (GER). These components (ie, lower esophageal sphincter [LES], esophageal hiatus [EH], diaphragmatic crura) work to create a high-pressure zone at the GEJ that prevents GER. In humans, enlargement of the EH has been correlated with sliding hiatal hernia, decreased LES pressure, and increased frequency of GER.1,2 The aim of this retrospective study was to characterize the EH via CT evaluation in brachycephalic and nonbrachycephalic dogs and to determine whether a difference exists that may predispose brachycephalic breeds to GER and sliding hiatal hernia.

Medical records of pet dogs that received thoracic and abdominal CTs were reviewed and divided into 2 groups. Group 1 consisted of brachycephalic breeds presented for upper airway, respiratory, and gastroesophageal conditions. Group 2 was composed of nonbrachycephalic breeds presented for reasons unrelated to respiratory or gastroesophageal conditions. Axial images of the EH in each dog were combined to determine the circumference; a ratio of the cross-sectional areas of the EH and descending aorta (Ao) was then calculated (ie, EH:Ao ratio). Absolute EH measurements were also compared in weight-matched dogs from both groups.

Dogs in group 1 had a significantly higher EH:Ao ratio than dogs in group 2. This difference reflected significantly larger EH areas and smaller Ao dimensions in dogs in group 1. Further comparison of the weight-matched groups revealed that group 1 had a significantly larger EH area as compared with group 2.

Enlarged EH may be an additional anatomic difference that could explain why brachycephalic dogs have an increased risk for GER, sliding hiatal hernia, regurgitation, and aspiration pneumonia.3-5 This study did not assess EH function, and it is unknown whether enlarged EH alone leads to decrease in pressure across the GEJ. Of clinical importance is the increased risk brachycephalic breeds have for anesthetic complications, most commonly regurgitation and aspiration pneumonia.3,4 Many premedications and inhalant anesthetics decrease LES tone and gastric pH, which can further increase the risk for GER.6-9 Prolonged fasting for general anesthesia and surgery is also a risk factor for GER in humans10 and dogs.9,11 It is thus prudent to consider administration of antacids, prokinetics, and antiemetics—along with avoidance of prolonged fasting and use of certain anesthetic drugs—to help maintain LES tone, improve gastric motility, and decrease gastric secretions and acidity in brachycephalic dogs undergoing general anesthesia.3-5,8,9,11


…TO YOUR PATIENTS

Key pearls to put into practice:

1

Brachycephalic dogs are at increased risk for GER, sliding hiatal hernia, regurgitation, and aspiration pneumonia. Enlarged EH may be a contributing factor.

2

Brachycephalic dogs undergoing general anesthesia have higher morbidity and mortality rates than nonbrachycephalic dogs. Careful selection of anesthetic drugs, rigorous monitoring throughout the perioperative and postanesthetic periods, and quick staff intervention in case of a postoperative complication are required.

3

Pre-emptive treatment with antacids, prokinetics, and antiemetics may improve anesthetic outcomes in brachycephalic dogs. Consideration should be given to feeding a canned food meal at half the daily rate ≈3 hours prior to surgery.

References

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

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

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


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Phnotix CB JulyAug 2021

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WVC CB JulyAug 2021

Research Note: Machine Learning Algorithm for Diagnosing Hypoadrenocorticism in Dogs

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Canine hypoadrenocorticism (CHA) is a life-threatening condition that affects 3 out of every 1000 dogs. CHA mimics many disease processes, including kidney, hepatic, and GI disease. Prognosis is excellent with appropriate treatment. This study used machine learning methods to aid in the diagnosis of CHA.  Results of CBC and serum chemistry profiles were collected from 908 control dogs and 133 dogs with confirmed CHA and used as data for the machine algorithms. The model showed a sensitivity of 96.3% and specificity of 97.2%. Although prospective studies are needed to validate these methods, they demonstrated diagnostic performance similar to resting cortisol values (regardless of glucocorticoid or mineralocorticoid deficiency status) and employed an easy-to-use graphic interface.

Source

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: Postpyloric Feeding in Dogs with Acute Kidney Injury

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Enteral nutrition (EN) is the most physiologic way to provide nutrition in severely ill, anorectic, and vomiting dogs. This study evaluated a novel technique for placing an esophagojejunal feeding tube (E-tube) in dogs with severe acute kidney injury (AKI). Randomized patients (n = 20) were given 18-Fr E-tubes or a postpyloric feeding tube, which consisted of an 8-Fr jejunostomy tube introduced through the E-tube and guided endoscopically past the pylorus for placement in the jejunum. Dogs with a PPF were fed a commercial-soluble veterinary diet via automatic pump-driven administration; dogs with an E-tube were fed a blended GI–renal canned diet with a manual syringe. The jejunostomy tube was safe and well-tolerated, allowing EN to be started at an early stage of treatment and enabling rapid attainment of the full feeding target. Protein-energy wasting still occurred in both groups despite nutritional support, suggesting increased feeding targets or qualitative changes in diet composition are needed in dogs with AKI.

Source

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

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Nestle CB JulyAug 2021

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Nocita CB JulyAug 2021

Research Note: Serum Cytokine Concentrations & Canine Osteosarcoma

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Osteosarcoma (OS) in dogs accounts for 80% to 90% of primary bone tumors and is used as a natural model for human OS because of many disease similarities. The systemic immune response to OS appears to affect disease progression and/or tumor suppression. This study investigated serum cytokines in healthy dogs as compared with dogs that had OS at the time of diagnosis. Interleukin (IL)-8 and IL-12p40 were increased in dogs with OS as compared with healthy dogs. IL-8 is produced in response to infection and inflammation; OS cell lines express excess amounts of the deltaNp63 isoform, which increases IL-8 and promotes tumor vessel growth and invasion. In contrast, IL-12 is linked to antitumor responses. These results reflect those found in similar human studies and contribute to the knowledge of immunologic changes seen in OS.

Source

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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Nexgard CB JulyAug 2021

How Appearance Can Influence Pet Owner Perception

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

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How Appearance Can Influence Pet Owner Perception

In the literature

Bentley E, Kellihan H, Longhurst C, Chun R. Effect of attire on client perceptions of veterinarians. Vet J. 2020;265:105550.


FROM THE PAGE…

This study surveyed 505 pet owners regarding their perceptions of clinicians based on attire. Respondents reviewed photos of faceless Caucasian men and women in both blue surgical scrubs and business casual attire—with and without an added white coat—and rated their comfort interacting with and perceived competence of clinicians. Higher levels of comfort and competence were associated with surgical scrubs versus business casual clothing. Addition of a white coat increased comfort level.

Because this study was limited to an academic specialty hospital in the midwestern United States, results may differ with other clinics and/or demographics. Faces were not visible, but skin tone was suggestive of a Caucasian demographic; this may also affect individual implicit bias and judgment. In addition, business attire can vary (eg, in style, color, fit, cleanliness, functionality) among individuals, possibly affecting perceptions. 

The experience of veterinary patients should also be considered. Whereas a white coat enhanced owner opinion, patients may experience “white coat syndrome,” in which fear, anxiety, and hypertension are associated with the presence of a white coat. Although this concept is extrapolated from human medicine, absence of a white coat may reduce stress in veterinary patients that have had a previously negative experience with a human in a white coat. 


…TO YOUR PATIENTS

Key pearls to put into practice:

1

Although owners should not base opinions on clothing in place of actions and/or communication skills, first impressions can be lasting, and an owner’s first impression may be based on the clinician’s profile photo on the clinic’s website. It is both acceptable and professional to be photographed in a white coat and scrubs.

2

Clothes worn in the clinic should fit well and be clean, tidy, and functional. An extra set of clothing should be kept in the clinic in case of unexpected staining events. This is especially true for white coats, which can be easily stained and should be disinfected, cleaned, and pressed regularly. Wearing the same white coat between patients can increase the risk for infection.

3

A clinic dress code may be beneficial. Regardless of the attire worn, it should be consistent among all staff members and should be universally decided on based on the culture of the clinic and its clientele. Staff with a similar appearance can indicate a professional and unified team that reflects quality care.

References

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

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

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


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Nutramax CB JulyAug 2021

Osteosarcoma Immunotherapy for More Days at Home

Oncology

|Sponsored

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Osteosarcoma Immunotherapy for More Days at Home
Sponsored by ELIAS

Osteosarcoma accounts for ≤85% of all primary bone tumors in dogs.1-4 Unfortunately, there have been relatively few advancements to create better outcomes for patients suffering from this cancer. In addition, once the current standard of care (ie, amputation plus chemotherapy for patients with limb tumors) fails, there is little hope of survival. That’s why studying ELIAS Cancer Immunotherapy (ECI) has been exciting for Jeffrey N. Bryan, DVM, MS, PhD, DACVIM (Oncology), professor of oncology at University of Missouri, and member of the ELIAS Animal Health Scientific Advisory Board.5

ECI is the only 2-step immunotherapy in veterinary medicine and has the potential to match or exceed the current standard of care while reducing or eliminating the need for chemotherapy. A form of precision medicine, ECI incorporates both a vaccine pretreatment made from the patient’s cancer cells and an activated “killer” T-cell immunotherapy. The vaccine introduces mutated proteins to the immune system that serve as markers for which cells to eliminate. This generates anticancer lymphocytes that circulate in the blood. After the 3-vaccine pretreatment, the anticancer lymphocytes are harvested from the patient’s blood. ELIAS activates and expands them before they are transfused back into the patient (see ECI Treatment Protocol).

ECI TREATMENT PROTOCOL

ECI requires fewer appointments as compared with chemotherapy; this and a close partnership between the primary care veterinarian and specialist make the ECI treatment process easier on the client—and the patient.

  • BEFORE ECI: The primary care veterinarian refers the patient to a veterinary oncologist for aseptic tissue harvesting before amputation. Leaving the limb intact for the oncologist is critical to ensure the collection of viable, plentiful cancer cells. The oncologist performs therapeutic amputation and cell collection before sending tissue to ELIAS for vaccine preparation. ELIAS ships the vaccines back to the oncologist.
  • WEEKS 1-3: The oncologist administers 3 intradermal injections a week apart with the autologous vaccinations prepared from the collected tissue to generate the appropriate immune response. The injection must be intradermal rather than SC to ensure proper presentation to the immune system.
  • WEEK 5: The patient visits a specialty apheresis center for leukapheresis, a procedure in which the immune-stimulated T cells are collected from the patient’s blood. The oncologist sends these T cells to ELIAS, where technicians prepare the T-cell product, then ship it back to the oncologist.
  • WEEK 6: The oncologist performs activated T-cell infusion.
  • WEEKS 7-8: The primary care veterinarian or oncologist performs follow-up interleukin-2 injections. These SC injections are well tolerated and require no specialty training to administer.

Results Backed by Data

Safety and efficacy results support the value of ECI.6 Dr. Bryan and his team completed a single-arm, 14-dog pilot study examining ECI osteosarcoma treatment in dogs with no concurrent use of chemotherapy.6 ECI showed better survival outcomes than did other treatment options in previous studies.6-8 Dogs receiving ECI survived an average of 415 days, with 5 surviving past 730 days, which exceeds most median survival times historically reported for patients receiving amputation plus chemotherapy.6 Few other trials show this proportion of osteosarcoma patients living this length of time (ECI Trial Results: Powerful Potential).5,6,8 Dr. Bryan noted it was rewarding to give patients a better-than-average survival rate and create a greater proportion of long-term survivors.5-8

ECI Hits the Treatment Target

Using the patient’s cancer cells to introduce the patient’s particular mutations to the immune system is a well-developed anticancer therapy but, by itself, is rarely successful.5 Coupling autologous cancer vaccination with activated T-cell therapy is unique to ECI. As a result, ECI provides the following potential benefits over chemotherapy and standalone autologous cancer vaccination5:

  • Eliminates both dividing and dormant cells. Chemotherapy targets rapidly dividing cells to prevent metastatic disease. Osteosarcoma likely includes a large population of metastatic cells not rapidly dividing at the time of treatment. With ECI, cells do not have to be dividing to be eliminated. Instead, they need only to express the mutated abnormal proteins typical of osteosarcoma.
  • Produces durable protection. Although the underlying immunologic mechanisms involved in ECI are still being investigated, it is possible that the process initiates a population of memory cells that remain in the system.6 If cancer cells express the same proteins again, which they tend to do, the immune system can continue to suppress the cancer over time.
  • Powerfully activates cell-killing T cells. When cancers reach a measurable size, they tend to contain a potently immunosuppressive microenvironment that protects them from immune attack. Autologous vaccination educates the immune system that cancer cells are abnormal; however, that re-education alone is not enough to overcome the immunosuppressive environment. Literature has shown that most autologous cancer vaccines have failed to induce strong and durable antitumor immunity.9 The combination of autologous vaccination and T-cell therapy is critical and associated with the clinical success observed with ECI.
  • Provides more days at home. The benefits of ECI extend beyond potential treatment success. Chemotherapy often causes severe adverse effects, whereas those associated with ECI are low-grade and transient.6 In addition, chemotherapy tends to require longer duration of therapy as compared with ECI; therefore, ECI requires fewer trips to the veterinarian and allows for more time in the comfort of home.

Referring Veterinarians Play an Active Role

When a primary care veterinarian diagnoses cancer, the next step is to identify the specific cancer type. Aspiration cytology with ALP staining supports the likelihood of bone for tumor origin; this can be performed through radiography to determine tumor location, then through removal of cells with a 22-gauge needle for cytology.

Instead of making amputation the first response, clinicians should consider taking some time to speak with owners about their long-term goals.

Many veterinarians follow an osteosarcoma diagnosis with immediate leg amputation; ELIAS recommends changing this approach. Immediate amputation eliminates the opportunity to treat with immunotherapy, including ECI. Instead of making amputation the first response, clinicians should consider taking some time to speak with owners about their long-term goals. ECI can provide an alternative to chemotherapy. If owners are interested in ECI, preserving the limb and tumor on the body is vital for ample collection of live cancer cells. With ECI, the specialist performs the amputation, immediately harvesting the tumor and sending the cancer cells to ELIAS for autologous vaccine generation.

Once ECI has been initiated, the general practitioner plays a critical role as the patient’s advocate and care team leader. ECI creates a treatment and communication loop among the primary care veterinarian, oncology specialist, and pet owner and also allows the primary care veterinarian to be highly involved in the treatment process (ECI Trial Results: Powerful Potential). The specialist completes the more intricate aspects of the procedure while the primary care veterinarian manages most of the patient monitoring without the complexities and risks of handling cytotoxic drugs.

Clinician's Brief

Because the primary care veterinarian can be highly involved in supporting the patient through the immunotherapy process, they remain integral to communicating with the pet owner; thus, clients are more likely to contact the primary care veterinarian with questions. They are also likely to return to the primary care veterinarian for vital follow-up visits and any monitoring required (eg, blood tests, radiography). ELIAS Animal Health has resources to guide primary care veterinarians before, during, and after ECI treatment, and practitioners are always welcome to contact ELIAS directly for support.

Hope for Dogs & Their Owners

Hearing their dog has cancer of any kind is scary for pet owners. ECI allows veterinarians to help owners of dogs with osteosarcoma decide which options will give their dog the best chance at long-term survival. Although no veterinarian can definitively predict a treatment outcome, data show that immunotherapy tends to result in the highest chance of long-term remission and lowest rate of recurrence across all cancer types.9 The ECI trial produced 5 long-term survivors (ie, ≈415 days).5-8

Conclusion

The potential benefits of ECI are significant. Patients bounce back from treatments quickly, and after treatment completion, the only follow-ups required are periodic rechecks. In addition, patients can potentially experience longer survival times, as well as fewer appointments and more days at home when receiving ECI as compared with other treatments,5 which can be a major benefit to pet and owner quality of life.

This article was created with the help and expertise of Jeffrey N. Bryan, DVM, MS, PhD, DACVIM (Oncology), professor of oncology at University of Missouri, and member of the ELIAS Animal Health Scientific Advisory Board. Dr. Bryan’s research interests include targeted imaging and therapy and cancer epigenetics and epidemiology. His clinical interests include novel therapy for lymphoma, targeted radiopharmaceutical imaging and therapy, and cancer immunotherapy.

References

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

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

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


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CVM Conference CB JulyAug 2021

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Layers of Multi CB JulyAug 2021

Local Anesthetic Blocks of the Distal Limbs for Dermatologic Procedures

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

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Local Anesthetic Blocks of the Distal Limbs for Dermatologic Procedures

In the Literature

Douglas H, Welsh S, Barr C. Clinical techniques in veterinary dermatology: regional anaesthesia of the canine and feline distal limb. Vet Dermatol. 2021;32(1):90-e17.


FROM THE PAGE …

The distal limb is a common site for dermatologic procedures for both therapeutic and diagnostic purposes. The analgesic protocol should include local anesthesia.

This study reviewed and described the technique of administering regional anesthesia (using either 2% lidocaine or 0.5% bupivacaine) in the distal limbs of dogs and cats. The authors recommend sedation with general anesthesia if necessary (eg, in aggressive patients). The local anesthetic is injected circumferentially around the limb, targeting the major nerves of the distal limb. The manus (ie, distal part of the thoracic limb) is innervated by the radial and median nerves. The pes (ie, distal part of the pelvic limb) is innervated by branches of the common fibular (peroneal) and tibial nerves.

The limb should first be clipped and aseptically prepared. At each injection site, the skin should be tented. On the dorsal aspect of the thoracic limb, the injection is made immediately proximal to the carpus—starting medial to the dewclaw—targeting the superficial branches of the radial nerve and the dorsal branch of the ulnar nerve. On the palmar aspect of the thoracic limb, injection is made on either side of the accessory carpal pad, targeting the median and ulnar nerves. In the pelvic limb, injection is made just distal to the tarsometatarsal joint on both dorsal and plantar aspects, targeting the superficial fibular nerve dorsally, the deep fibular nerve dorsolaterally, and the tibial nerve on the plantar aspect.

Prior to starting the procedure, a maximum dose for the anesthetic should be calculated. For lidocaine, the maximum dose is 6 to 10 mg/kg in dogs and 3 to 5 mg/kg in cats. For bupivacaine, the maximum dose is 2 mg/kg in dogs and 1 to 1.5 mg/kg in cats. A small-gauge needle should be used to inject a bleb of anesthetic after aspiration to ensure the needle is not in a vessel prior to injection. The typical total volume used in dogs weighing <11 lb (5 kg) and in cats is 0.5 mL. In dogs weighting >11 lb (5 kg), typical total volumes used are 1 to 3 mL for both dorsal and palmar blocks. The total dose should be divided between the injection sites; the anesthetic can be diluted with 0.9% saline if additional volume is needed.


… TO THE PATIENT

Key pearls to put into practice:

1

Regional nerve blocks are useful in reducing the amount of sedation needed for a procedure. A ring block of the distal extremity is useful for any painful procedure involving the foot (eg, biopsy or clipping a painful claw). Pet owners may be more comfortable with a procedure when they know that local and regional anesthesia will be used to reduce the amount of sedation needed.

2

The desired time of onset (lidocaine, 10-15 minutes; bupivacaine, 20-30 minutes) and duration of activity (lidocaine, 1-3 hours; bupivacaine, 4-12 hours) should be considered when deciding which local anesthetic agents to use.

3

To avoid toxicity, it is important to calculate the maximum drug dose to ensure the total doses are below the high end of the range.

 

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

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

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


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Cardalis CB JulyAug 2021

Dental Disease in Central Bearded Dragons

Thomas H. Boyer, DVM, DABVP (Reptile & Amphibian), Pet Hospital of Penasquitos, San Diego, California

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Dental Disease in Central Bearded Dragons

In the Literature

Mott R, Pellett S, Hedley J. Prevalence and risk factors for dental disease in captive central bearded dragons (Pogona vitticeps) in the United Kingdom. J Exotic Pet Med. 2020;36:1-7.


FROM THE PAGE…

This study represents the first large-scale investigation of risk factors for the prevalence of dental disease in one of the most common captive reptiles—the central bearded dragon (Pogona vitticeps). Data from 20 veterinary clinics in the United Kingdom showed dental abnormalities in half of the examined population of central bearded dragons (n = 304). Only 24.8% of dragons with dental disease exhibited clinical signs, and all of these had advanced dental disease. Central bearded dragons, like chameleons, have acrodont teeth (ie, laterally compressed triangular teeth directly ankylosed to the mandibles and maxilla).1 During development, the pulp of the teeth is lost to a mineralized matrix that fuses teeth to bone.1 In these lizards, teeth are permanent and not replaced throughout life; this is unlike the pleurodont dentition of most other lizards.2 Also unlike other lizards, the gingiva of acrodont lizards does not attach at the base of the teeth; instead, a thin layer of stratified squamous epithelium covers exposed mandibular and maxillary bone, which is predisposed to bacterial colonization.3,4 Acrodonts also lack periodontal ligaments,1 and the authors state that although periodontal disease has been widely described in acrodont reptiles, dental disease is likely a better descriptor.

The authors graded dental disease as normal (grade 0: clinically normal, no dental disease); mild (grade 1: staining of teeth and exposed bone only; grade 2: mild tartar development, gingival erythema); and advanced (grade 3: moderate tartar development, gingival erythema and recession; grade 4: severe tartar buildup, severe gingival erythema and recession, osteomyelitis of jawbones; grade 5: end-stage disease, severe tartar buildup, severe gingival recession, osteomyelitis, pathologic fractures).

The percentage of central bearded dragons with dental disease increased from 11.5% in those <1 year of age to 36.9% in those 1 to 3 years of age and to 86.8% in those >8 years of age. There were significant associations among dental disease, increasing age, being under- or overweight, and concurrent disease. There was also a strong significant association between fruits in the diet and dental disease, with an odds ratio of 2.68; 66% of central bearded dragons with fruits in the diet had dental disease. In contrast, there was no significant association between vegetables in the diet and dental abnormalities or disease. The authors suggested eliminating fruits from the diet, as the high sugar content and acidity of fruits may contribute to dental disease. 


… TO YOUR PATIENTS

Key pearls to put into practice:

1

Thorough oral examination and dental grading are always indicated in central bearded dragons. Dental disease increases with age, but dental cleaning can reduce disease, especially with early detection.

2

Tartar initially supports gram-positive aerobic cocci that shift over time to anaerobic gram-negative bacteria and spirochetes.5 Fungal infections are less common.

3

In central bearded dragons, diagnosis and treatment of dental disease involve anesthesia with tracheal intubation; cytology; dental radiography; curettage of calculus, gingival sulci, and infected bone with a dental ultrasonic scaler; surgical removal of granulomas; long-term antibiotics—based on aerobic culture and susceptibility testing—that include anaerobic coverage; pain medication; and swabbing or flushing of the labial bones with 0.05% chlorhexidine or oral cleansing gels.5

References

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

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

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


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Vaccines CB JulyAug 2021

Reliability of Refractometers in Measurement of Urine Specific Gravity in Dogs

Anne Barger, DVM, MS, DACVP, University of Illinois

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Reliability of Refractometers in Measurement of Urine Specific Gravity in Dogs

In the literature

du Preez K, Boustead K, Rautenbach Y, Goddard A, Hooijberg EH. Comparison of canine urine specific gravity measurements between various refractometers in a clinical setting. Vet Clin Pathol. 2020;49(3):407-416.


FROM THE PAGE …

Urinalysis is a valuable diagnostic tool that consists of a combination of diagnostic tests, including gross evaluation of urine, urine chemistry, sediment examination, and specific gravity. Urine specific gravity (USG) is a critical component of urinalysis and minimum database; it allows for assessment of the ability of renal tubules to dilute or concentrate glomerular filtrate.1 USG is used in combination with physical examination findings and serum chemistry profile values in the diagnosis of renal disease.

Urine osmolality is considered the gold standard for determining the concentration of the urine. Urine concentration is measured by determining the freezing point of the urine, which decreases with increasing solute in the urine. However, it is impractical to measure urine osmolality in clinical practice, and use of a refractometer to measure USG has been shown to be comparable with measurement of osmolality.2 All refractometers are not necessarily equal, and there have been studies to evaluate their reliability.2,3 One study compared 5 different refractometers (including 1 digital and 2 feline-specific) and found proportional negative bias among them.3 A second study compared USG measured on canine urine obtained via 4 refractometers with results of measured osmolality2; refractometers included 2 optical and 1 digital refractometer, and 3 of 4 were found to be comparable. These studies collectively suggest that comparing results among refractometers could present some clinical challenges.

In this study, the authors evaluated results from 4 different refractometers and evaluated the variability among different users performing USG measurements. Similar to an earlier study,2 this study showed excellent correlation among refractometers, although one showed constant and proportional biases. Minimal variation of the other refractometers was not clinically relevant. In addition, correlation among users was exceptional. In contrast to other studies, this study found that some refractometers could be used interchangeably and do not appear to have clinically relevant variation and users of variable clinical training could accurately interpret refractometer results with limited training.


…TO YOUR PATIENTS

Key pearls to put into practice:

1

USG is an important component of urinalysis, and certainty of accurate results is crucial.

 

2

Although this study found excellent agreement between categorization of patient urine concentrations and azotemia, a single USG value should not be used alone; further diagnostics and repeated USG measurements should be performed to confirm categorization of urine concentration and azotemia.

3

Measurement of USG by different users, regardless of experience level, did not appear to result in clinically relevant differences, which is important in clinical practice where various members of staff may be reading USG values.

References

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

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

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


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Adequan CB JulyAug 2021

Research Note: Species Identification of Sepsis-Associated Bacteria

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Early identification of the causative agent of bacteremia in a septic patient is critical. Standard bacterial culture takes ≥48 hours, and accuracy can be subject to variations in methodology. Matrix-assisted laser desorption/ionization time of flight mass spectrometry (MALDI-TOF MS) is a new method of identifying bacteria by their unique protein fingerprints. Results are usually available in ≈20 minutes. This study evaluated whether MALDI-TOF MS is a reliable tool for use in dogs and cats. Aseptically collected dog and cat blood was inoculated with reference samples of 6 common sepsis-inducing bacteria into a liquid blood-culture medium, which was then analyzed. Species identification obtained through MALDI-TOF MS as compared with classical microbiologic analysis was identical for all 72 samples tested. Investigators concluded that MALDI-TOF MS is reliable for identifying sepsis-inducing bacteria in dogs and cats.

Source

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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PVD CB JulyAug 2021

NSAIDs, Cats, & Anesthesia: Are the Kidneys at Risk?

Berit Fischer, DVM, DACVAA, CCRP, Crown Veterinary Specialists Lebanon, New Jersey

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NSAIDs, Cats, & Anesthesia: Are the Kidneys at Risk?

In the literature

Kongara K, Cave N, Weidgraaf K, Dukkipati VSR. Effect of non-steroidal anti-inflammatory drugs on glomerular filtration rate and urinary N-acetyl-β-D-glucosaminidase activity in cats after dental surgery. Vet Anaesth Analg. 2020;47(5):631-636.


FROM THE PAGE…

Although NSAIDs can alleviate postoperative pain in healthy cats, potential adverse effects on kidney perfusion often discourage use of these drugs in analgesic protocols.

Most clinically available biochemical tests lack the sensitivity to detect early kidney damage, making it difficult to identify direct cause-and-effect relationships. In research settings, measurement of glomerular filtration rate (GFR) is an effective but time-consuming method to detect acute kidney injury (AKI).1 N-acetyl-β-D-glucosaminidase (NAG) is a novel, highly specific urine biomarker for renal damage that is predictive of AKI in humans and has been shown to rapidly increase in cats and dogs receiving nephrotoxic drugs.2

In this clinical trial, healthy cats were administered carprofen (n = 8), meloxicam (n = 8), or saline (n = 8) SC at the time of preanesthetic medication prior to routine dental prophylaxis. GFR was measured in all 3 groups, and urinary NAG activity was measured in the meloxicam and saline groups 4 hours before and 24 hours after the dental prophylaxis. The goal was to determine whether NSAIDs produced changes in GFR and NAG indicative of AKI. Results demonstrated no significant differences in GFR among the 3 groups or in NAG between the meloxicam and saline groups at either time point. The authors concluded that preanesthetic administration of carprofen or meloxicam did not result in appreciable renal dysfunction in healthy, normotensive cats during the trial period.

It is important to note that NSAID-associated AKI is rarely caused by direct nephrotoxic effects. Rather, it is related to the kidneys inability to increase renal perfusion via prostaglandin-mediated vasodilation in times of hemodynamic instability (eg, hypotension).3 Because no cats in the trial had mean arterial blood pressure below that expected to stimulate prostaglandin release, NSAID-related renal damage was not anticipated.


…TO YOUR PATIENTS

Key pearls to put into practice:

1

Based on this trial, preanesthetic administration of carprofen to healthy, normotensive cats is not associated with changes in GFR that might indicate the presence of renal tubular damage. Preanesthetic administration of meloxicam to healthy, normotensive cats is also not associated with changes in GFR or NAG that might indicate the presence of renal tubular damage.

2

Hypotension is a common and not always predictable complication of anesthesia. The mechanism of NSAID-associated AKI suggests that administration before anesthesia in hypotensive patients may leave the kidneys vulnerable. 

3

Until further studies elucidate risk in anesthetized, hemodynamically compromised patients, cautious use of preanesthetic administration of NSAIDS in cats is recommended.

References

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

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

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


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Profender CB JulyAug 2021

Prevalence of Problematic Behaviors in Dogs

John J. Ciribassi, DVM, DACVB, Chicagoland Veterinary Behavior Consultants, Schereville, Indiana

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Prevalence of Problematic Behaviors in Dogs

In the literature

Didehban N, Borujeni MP, Avizeh R, Mosallanejad B. Problematic behaviors in companion dogs: a survey of their prevalence and associated factors. J Vet Behav. 2020;39:6-13.


FROM THE PAGE …

Behavior problems are a leading reason companion animals (particularly dogs) are relinquished to shelters.1 It can be helpful to ask pet owners specific behavior-related questions during visits to the clinic so veterinary staff can better recognize behavior problems and increase the likelihood that the behavior can be managed.

In this study, owners (representing 401 dogs) visiting a university veterinary hospital in southwest Iran for wellness care were surveyed. Thirteen problematic behaviors were identified, and owners reported ≥1 behavior problem in 86% of dogs; this is similar to the prevalence seen in a separate study performed in the United States.2

Problems identified in this study included excessive activity, fearfulness, destructiveness, roaming, house soiling, excessive barking, coprophagy, withdrawal, mounting/humping, and aggression toward unfamiliar humans, familiar humans, owners, and other dogs. Fearful behavior was more common in small, adult, and female dogs. Aggressive behaviors were more likely in adult dogs and outdoor dogs, whereas indoor dogs showed more fear, withdrawal, and mounting behaviors.


…TO YOUR PATIENTS

Key pearls to put into practice:

1

Owners should be provided with a brief questionnaire that asks about recognized behavior issues in their pet and whether they would like assistance with the problem (see Suggested Reading).3

 

2

Owner concerns should be addressed during routine consultation. Consult time can be increased if a behavior concern is known in advance. For concerns brought up spontaneously during the visit, a brief discussion of the problem can be held; significant concerns may warrant another visit so the issue can be more fully addressed.

3

Staff should be trained to handle screening and initial discussions with owners and to offer advice regarding basic behavior problems (eg, house soiling, destructive behavior). A full behavior consultation can be scheduled for more in-depth issues (eg, fears, phobias, aggression), or patients can be referred to a qualified veterinary behaviorist.

4

Critical behavior topics (eg, house training, puppy biting, proper play, destructive behavior), puppy class recommendations for dogs 8 to 14 weeks of age, and grooming techniques should be addressed at puppy visits.

References

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

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

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


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AHS CB JulyAug 2021

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Galliprant CB JulyAug 2021

Research Note: Role of Bisphenol A in Feline Hyperthyroidism

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Bisphenol A (BPA) is frequently used in the production of food and beverage containers. BPA is thought to be an endocrine disruptor in humans and it has been suggested to play a role in feline hyperthyroidism. Previous studies identified canned food as a risk factor for hyperthyroidism. This study assessed clinicopathologic data from 69 clinically healthy cats ≥7 years of age and compared them with serum BPA concentrations. All samples had measurable BPA levels. There was no association between BPA and thyroid levels. Further research in cats with hyperthyroidism is warranted.

Source

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

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

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


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Zoetis CB JulyAug 2021

Owner (Mis)Perceptions of CPR

Janine M. Calabro, DVM, DACVECC, Friendship Hospital for Animals, Washington, D.C.

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Owner (Mis)Perceptions of CPR

In the literature

Oberholtzer JA, Hofmeister EH. Perception of small animal cardiopulmonary resuscitation of owners presenting to a small animal teaching clinic including a large first opinion service. J Vet Emerg Crit Care. 2020;30(4):411-417.


FROM THE PAGE…

Although pet owners at the clinic may be asked whether they want cardiopulmonary resuscitation (CPR) performed if their pet goes into cardiac arrest, public perception of CPR survival rates may be inaccurate. This study used a questionnaire to evaluate owner perceptions of CPR; questions included owner demographics, CPR knowledge, reasons for choosing versus declining CPR, and estimated CPR success rates and costs, as well as whether owners work in healthcare and whether owners watch medical television shows. Pet age and species were also included.

Of the 296 surveys analyzed, almost all owners (92%) provided an appropriate basic definition of CPR. Most respondents (76%) had previously taken a human CPR training course, 11% possessed knowledge of how to perform CPR on a dog or a cat, and 67% elected to have CPR performed on their pet at the current visit if necessary. Owners overestimated the likelihood of survival to discharge from the hospital as compared with reports in current literature, and those that elected CPR estimated lower costs associated with resuscitation as compared with owners that declined CPR. Respondents who watched television medical dramas estimated higher rates of survival to hospital discharge. Most respondents (76%) wanted the clinician to make the CPR decision in the event of an arrest, and 82% also wanted to discuss CPR status at the veterinary clinic visit.

This study identified inaccurate perceptions and knowledge gaps regarding CPR among pet owners. Considering the vast majority of respondents expressed interest in discussing CPR status with their clinician, clinicians can help by educating owners, thus enabling them to make better-informed decisions.


…TO YOUR PATIENTS

Key pearls to put into practice:

1

Owners may have inaccurate perceptions about survival rates following CPR.

 

2

It is important to educate owners about CPR, including costs and anticipated outcomes, so they can provide truly informed consent.

 

3

The Reassessment Campaign on Veterinary Resuscitation (RECOVER) initiative has created evidence-based guidelines for small animal CPR (see Suggested Reading); these guidelines are being updated.

Suggested Reading

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

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

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


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AVMA CB JulyAug 2021

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Arthrex CB JulyAug 2021

Histologic Subtypes and Clinical Outcomes in Canine B-Cell Lymphoma

Davis Seelig, DVM, PhD, DACVP, University of Minnesota

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Histologic Subtypes and Clinical Outcomes in Canine B-Cell Lymphoma

In the literature

Wolf-Ringwall A, Lopez L, Elmslie R, et al. Prospective evaluation of flow cytometry characteristics, histopathologic diagnosis and clinical outcome in dogs with naive B-cell lymphoma treated with a 19-week CHOP protocol. Vet Comp Oncol. 2020;18(3):342-352.


FROM THE PAGE…

Canine B-cell lymphoma consists of multiple histologically and biologically distinct subtypes, but it is often treated as a single disease with doxorubicin-based, multiagent chemotherapy protocols. Although retrospective studies have reported the prognostic importance of subtype,1,2 clinical importance has not been directly studied in standardized prospective clinical trials.

Identification of subtypes traditionally requires lymph node removal, histopathology, immunohistochemistry, and review by a veterinary pathologist trained in hematopathology. However, because of the time, invasiveness, and cost associated with this approach, a diagnosis of canine lymphoma is more routinely made using fine-needle aspiration and cytology. Because cytology can provide both prognostic and subtyping information, it is increasingly combined with flow cytometry, which can provide rapid and clinically relevant diagnostic and prognostic information for many different subtypes of canine lymphoma.

This study sought to examine the influence of subtype on outcome in dogs with B-cell lymphoma treated with a standardized chemotherapeutic protocol (n = 64), as well as the use of flow cytometry to identify histologic subtype. Flow cytometry was able to diagnose 100% of B-cell lymphoma cases but was unable to identify clear phenotyping differences between the different B-cell lymphoma subtypes.

This study also confirmed that nodal B-cell lymphoma in dogs is a clinically heterogenous disease and there are infrequent subtypes (eg, marginal zone lymphoma) with inferior objective response rates and decreased median survival times as compared with diffuse large B-cell lymphoma; these rates were comparable with some forms of T-cell lymphoma.


…TO YOUR PATIENTS

Key pearls to put into practice:

1

Canine lymphoma comprises a broad group of individual diseases, including clinically slow subtypes with prolonged survival times (>600 days) that do not require systemic chemotherapy. Other subtypes are aggressive, with survival times <200 days.

2

A multimodal approach is important for diagnosing canine lymphoma. Flow cytometry can provide significant prognostic information that may help guide diagnostic and therapeutic decisions.

References

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

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

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


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Vetriscience CB JulyAug 2021

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Douxo CB JulyAug 2021

Top 5 Breed-Specific Considerations to Avoid Adverse Drug Effects

Katrina Mealey, DVM, PhD, DACVIM, DACVCP, Washington State University

Michael H. Court, BVSc, PhD, DACVAA, Washington State University

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Top 5 Breed-Specific Considerations to Avoid Adverse Drug Effects

Adverse drug effects can increase morbidity and mortality in dogs, cause emotional stress for pet owners, and increase cost of care. Many (but not all) adverse drug effects can be predicted and therefore prevented. Genetic testing can be used to help identify possible drug effects and determine whether dose adjustments or alternative drug therapies are needed.

Following are the top 5 adverse drug effects that are more likely to occur in specific dog breeds, according to the author.

1

MDR1 Mutation & Enhanced Susceptibility to CNS Toxicity (Primarily in Herding Breeds)

P-glycoprotein, encoded by the multidrug sensitivity gene (MDR1 gene, also known as ABCB1 gene), functions as a drug transport pump at the blood-brain barrier, preventing potentially toxic compounds from gaining access to the brain.1 The MDR1 gene mutation (ABCB1-∆) results in production of dysfunctional P-glycoprotein and affects many herding breed dogs (Table 1) and some nonherding breeds.2 Drugs that are P-glycoprotein substrates achieve higher brain concentrations in dogs with the MDR1 mutation (heterozygous or homozygous) than in dogs without the mutation.1 When P-glycoprotein substrate drugs exert CNS effects, those effects are more pronounced in dogs with the MDR1 mutation unless the dosage is decreased appropriately.1,3 Thus, dose reductions should be made when possible or an alternative drug should be selected. A nuclear scintigraphy study demonstrated that wild-type MDR1 homozygotes (MDR1 normal/normal) have a fully functional blood-brain barrier with essentially no radioactivity in the brain, whereas MDR1 mutant homozygotes (MDR1 mutant/mutant) have brain radioactivity levels comparable with surrounding tissue, demonstrating a dysfunctional blood-brain barrier with respect to P-glycoprotein substrates (Figure 1).1 Although many P-glycoprotein substrate drugs (Table 2) exert CNS effects and cause neurologic toxicity in dogs with the MDR1 mutation, some do not and can therefore be administered at usual dosages. MDR1 genotyping should be performed to identify at-risk dogs prior to treatment with P-glycoprotein substrate drugs.4

Nuclear scintigraphic images of the brain and surrounding tissue in collies after IV injection of the radiolabeled P-glycoprotein substrate sestamibi (99mTc-sestamibi). P-glycoprotein restricts 99mTc-sestamibi entry into brain tissue of the MDR1 wild-type dog (A), whereas lack of P-glycoprotein allows 99mTc-sestamibi to enter brain tissue of the MDR1 mutant/mutant dog (B).
Nuclear scintigraphic images of the brain and surrounding tissue in collies after IV injection of the radiolabeled P-glycoprotein substrate sestamibi (99mTc-sestamibi). P-glycoprotein restricts 99mTc-sestamibi entry into brain tissue of the MDR1 wild-type dog (A), whereas lack of P-glycoprotein allows 99mTc-sestamibi to enter brain tissue of the MDR1 mutant/mutant dog (B).

FIGURE 1 Nuclear scintigraphic images of the brain and surrounding tissue in collies after IV injection of the radiolabeled P-glycoprotein substrate sestamibi (99mTc-sestamibi). P-glycoprotein restricts 99mTc-sestamibi entry into brain tissue of the MDR1 wild-type dog (A), whereas lack of P-glycoprotein allows 99mTc-sestamibi to enter brain tissue of the MDR1 mutant/mutant dog (B).

FIGURE 1 Nuclear scintigraphic images of the brain and surrounding tissue in collies after IV injection of the radiolabeled P-glycoprotein substrate sestamibi (99mTc-sestamibi). P-glycoprotein restricts 99mTc-sestamibi entry into brain tissue of the MDR1 wild-type dog (A), whereas lack of P-glycoprotein allows 99mTc-sestamibi to enter brain tissue of the MDR1 mutant/mutant dog (B).

TABLE 1

DOG BREEDS KNOWN TO CARRY THE MDR1 MUTATION24-26

Breed     Approximate Frequency (%)
Collie 70
Windsprite* 65
Australian shepherd (all sizes) 50
McNab 30
Silken windhound 30
English shepherd 15
Shetland sheepdog 15
German shepherd dog 10
Herding crossbreed 10
Crossbreed 5
Old English sheepdog 5
Border collie <5
*Formerly longhaired whippet

TABLE 2

DRUGS & THEIR POTENTIAL ADVERSE EFFECTS IN DOGS WITH THE MDR1 MUTATION1-3,12,13

  Drug Category Specific Agent
Neurologic toxicity    
  Analgesic Butorphanol
  Sedative Acepromazine
  Antiparasitic (macrocyclic lactones)*

Doramectin

Eprinomectin

Ivermectin

Milbemycin

Moxidectin

Selamectin

  Antiparasitic (octadepsipeptide) Emodepside
  GI (antidiarrheal) Loperamide
  GI (antiemetic) Ondansetron
Other toxicities (eg, myelosuppression, GI)  

 

  Chemotherapeutic (antibiotic/antineoplastic agents)

Doxorubicin

Actinomycin D

  Chemotherapeutic (vinca alkaloids)

Vincristine

Vinblastine

Vinorelbine

  Chemotherapeutic (taxanes)

Paclitaxel

Docetaxel

  Immunosuppressant Cyclosporine
*Should only be administered at label doses; label doses for heartworm prevention undergo safety studies in dogs with the MDR1 mutation as required by the FDA.

2

Deficiency in Greyhounds & Other Sighthounds

Greyhounds recover more slowly than other dog breeds after receiving certain injectable anesthetic drugs (eg, thiopental, thiamylal, propofol).5,6 Accumulating evidence suggests this is largely due to decreased liver expression of cytochrome P450 2B11 (CYP2B11; a major drug-metabolizing enzyme) in affected dogs.7 CYPB11 metabolizes a range of anesthetic drugs, including propofol, ketamine, midazolam, and medetomidine.7-9 A mutation in the CYP2B11 gene (CYP2B11-H3) that decreases CYP2B11 expression in vitro was recently identified in greyhounds and certain other sighthound breeds.10 The mutation has higher prevalence in American Kennel Club-registered greyhounds than in National Greyhound Association-registered greyhounds.10 This difference may be a consequence of selective breeding for different purposes (ie, conformation vs racing speed). CYP2B11-H3 was also identified in >50% of the sighthound breeds that were evaluated, as well as in some nonsighthound breeds at a lower prevalence (Table 3).10 Although in vivo validation studies are still needed, CYP2B11 genotyping might aid in identification of individual dogs likely to demonstrate prolonged effects when receiving drugs that require the CYP2B11 enzyme for efficient elimination.

TABLE 3

DOG BREEDS KNOWN TO HARBOR THE CYP2B11-H3 MUTATION10

Breed CYP2B11-H3 Frequency (%)
Sighthounds  
Greyhound (American Kennel Club-registered) 59
Rhodesian ridgeback 28
Borzoi 26
Greyhound (National Greyhound Association-registered) 17
Italian greyhound 11
Whippet 11
Scottish deerhound 11
Silken windhound 7
Spanish sighthound 6
Windsprite* 5
Ibizan hound 3
Other breeds  
Golden retriever 12
Border collie 8
Labrador retriever 6
Crossbreed 2
*Formerly longhaired whippet

3

MDR1 Mutation & Enhanced Susceptibility to Drugs Eliminated via Biliary Excretion (Chemotherapeutics & Other Drugs)

Adverse drug effects caused by the MDR1 gene mutation are not limited to neurologic toxicity. Because P-glycoprotein actively transports substrate drugs into the bile, dogs with the MDR1 mutation have decreased biliary clearance of those drugs normally eliminated via biliary excretion (Figure 2), resulting in increased overall drug exposure.11 Affected dogs experience susceptibility to associated adverse effects when the drugs are administered at recommended dosages. This effect has been documented with vincristine (bone marrow suppression),12 cyclosporine A (immunosuppression),13 doxorubicin (bone marrow suppression, GI toxicity; anecdotal), and others. Affected dogs should receive decreased dosages of these drugs as previously described.14 MDR1 genotyping should be performed to identify at-risk dogs prior to treatment with P-glycoprotein substrate drugs.4

Nuclear scintigraphic images of the ventral abdomen of an MDR1 wild-type dog (A) and an MDR1 mutant/mutant dog (B) 2 hours after IV injection of the radiolabeled P-glycoprotein substrate sestamibi (99mTc-sestamibi). P-glycoprotein efficiently pumps 99mTc-sestamibi into the gallbladder in the MDR1 wild-type dog (arrowhead). In stark contrast, biliary excretion is essentially nonexistent in the MDR1 mutant/mutant dog (arrow).
Nuclear scintigraphic images of the ventral abdomen of an MDR1 wild-type dog (A) and an MDR1 mutant/mutant dog (B) 2 hours after IV injection of the radiolabeled P-glycoprotein substrate sestamibi (99mTc-sestamibi). P-glycoprotein efficiently pumps 99mTc-sestamibi into the gallbladder in the MDR1 wild-type dog (arrowhead). In stark contrast, biliary excretion is essentially nonexistent in the MDR1 mutant/mutant dog (arrow).

FIGURE 2 Nuclear scintigraphic images of the ventral abdomen of an MDR1 wild-type dog (A) and an MDR1 mutant/mutant dog (B) 2 hours after IV injection of the radiolabeled P-glycoprotein substrate sestamibi (99mTc-sestamibi). P-glycoprotein efficiently pumps 99mTc-sestamibi into the gallbladder in the MDR1 wild-type dog (arrowhead). In stark contrast, biliary excretion is essentially nonexistent in the MDR1 mutant/mutant dog (arrow).

FIGURE 2 Nuclear scintigraphic images of the ventral abdomen of an MDR1 wild-type dog (A) and an MDR1 mutant/mutant dog (B) 2 hours after IV injection of the radiolabeled P-glycoprotein substrate sestamibi (99mTc-sestamibi). P-glycoprotein efficiently pumps 99mTc-sestamibi into the gallbladder in the MDR1 wild-type dog (arrowhead). In stark contrast, biliary excretion is essentially nonexistent in the MDR1 mutant/mutant dog (arrow).

4

Delayed Postoperative Bleeding in Greyhounds & Other Sighthounds

Significant and occasionally life-threatening postoperative bleeding that starts 24 to 48 hours following surgery has been identified as a significant health concern in greyhounds.15 Clinical studies suggest the incidence of delayed bleeding can range from 26% following routine gonadectomy16 to ≤67% following limb amputation for osteosarcoma.17 Current evidence indicates reduced α2-antiplasmin activity in the plasma of affected dogs, suggesting that bleeding may be secondary to enhanced fibrinolysis of newly formed clots.18,19 Both retrospective and placebo-controlled prospective studies have established the effectiveness of treatment with epsilon aminocaproic acid (EACA; Table 4), an antifibrinolytic drug, for preventing delayed bleeding via increased clot strength.16,17 Anecdotal evidence suggests Scottish deerhounds are also susceptible to delayed postoperative bleeding and may benefit from preventive antifibrinolytic treatment (EACA or tranexamic acid).20 A breed-based predisposition to this condition has not yet been reported, but it is likely caused by a mutation in a gene that regulates fibrinolysis. Although current recommendations are to treat all affected breed dogs, genetic testing for the putative mutation could be used to identify individual dogs that would benefit from prophylactic antifibrinolytic treatment. Identifying dogs of affected breeds that do not require treatment (ie, those that lack the mutation) could also minimize the potential risk for adverse effects of antifibrinolytic drugs (eg, thromboembolism).

TABLE 4

EACA DOSE RATES CURRENTLY USED FOR THE PREVENTION OF DELAYED POSTOPERATIVE BLEEDING IN GREYHOUNDS27 & SCOTTISH DEERHOUNDS20

Dog Weight EACA Dose*
55-79 lb (25-35 kg) 500 mg (1 tablet)
80-104 lb (36-47 kg) 750 mg (1.5 tablets)
>105 lb (>47 kg) 1,000 mg (2 tablets)
*EACA tablets are administered PO every 8 hours for 5 days starting on the day of surgery.

5

Sulfonamide Hypersensitivity in Doberman Pinschers

Hypersensitivity to sulfonamides can manifest as fever, keratoconjunctivitis sicca, hepatotoxicity, skin eruptions, blood dyscrasias, and/or arthropathy and may lead to a mortality rate of 21% in Doberman pinschers.21 Doberman pinschers have been reported to be particularly predisposed to sulfonamide hypersensitivity, but this is not limited to this breed.22 A recent study identified an association between a mutation in the cytochrome b5 reductase (CYB5R3) gene and sulfonamide hypersensitivity.23 This mutation was determined to be overrepresented in Doberman pinschers and in dogs of other breeds that experienced sulfonamide hypersensitivity reactions. Although CYB5R3 encodes a drug-metabolizing enzyme, this enzyme does not appear to be directly involved in the metabolism of sulfonamides.23 Instead, it is likely to be linked to a polymorphism that is directly involved in sulfonamide clearance. When possible, sulfonamides should be avoided in Doberman pinschers.

Conclusion

The physical characteristics of certain dog breeds can provide clues for breed-specific susceptibility to certain adverse drug reactions. Genotyping for specific variants can be used to inform appropriate drug selection and/or dosage modifications. Preventive treatment with EACA or tranexamic acid should be considered in greyhounds and Scottish deerhounds undergoing major surgery after assessment of the risks and benefits to individual dogs.

References

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

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

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


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WSAVA CB JulyAug 2021

New Diagnostic Test for Dogs with Chronic Gastrointestinal Signs

Internal Medicine

|Sponsored

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New Diagnostic Test for Dogs with Chronic Gastrointestinal Signs
Sponsored by Antech Diagnostics

GI signs (eg, vomiting, diarrhea, inappetence) are common presenting complaints in veterinary patients.1 When these signs become chronic (lasting >14 days), they can impact both patient and pet owner quality of life. Obtaining a definitive diagnosis for the cause of chronic GI signs can be difficult, expensive, and sometimes invasive.

Chronic enteropathy (CE) describes GI conditions causing clinical signs lasting >14 days.2 These signs, including vomiting, diarrhea, inappetence, borborygmi, flatulence, nausea, abdominal pain, and weight loss, result from uncontrolled intestinal inflammation,3 which creates compromise in the mucosal barrier and loss of immunologic tolerance to antigens (ie, food, bacteria) in the GI tract. Antibodies to these antigens are formed, perpetuating inflammation.

CE can be subclassified based on response to treatment as food-responsive enteropathy (FRE), antibiotic-responsive enteropathy (ARE), immunosuppressant-responsive enteropathy (IRE), or nonresponsive enteropathy (NRE).3 In >50% of CE cases, dogs have FRE, which can be successfully treated with a novel protein or hydrolyzed diet.3

Although the terms are used interchangeably, CE and inflammatory bowel disease (IBD) are not the same.2,3 CE is used in the absence of histopathology, whereas inflammation must be demonstrated on histopathology to make a diagnosis of IBD.2,3 Immunosuppressant medications are required to treat true IBD.

CE is used in the absence of histopathology, whereas inflammation must be demonstrated on histopathology to make a diagnosis of IBD.

Because of the potential adverse effects of immunosuppressants and the invasiveness and expense of obtaining biopsies, a novel diagnostic test for CE/IBD can aid in the investigation of chronic GI signs and benefit both patients and pet owners.

Case Presentation

Luna, a 5-year-old spayed Labrador retriever crossbreed, is presented for chronic, intermittent diarrhea that has been nonresponsive to medical management. She is up to date on vaccinations and flea/tick and heartworm prevention.

During the initial evaluation, the owner notes that Luna vomits bile 2 to 3 times per month. These episodes do not seem to be associated with a particular time of day or event. The owner notes that her bowel movements have been softer over the past few weeks, progressing to liquid stool. A fecal flotation is performed and is negative for ova and parasites. The owner elects to try a short course of a probiotic and bland diet.

At the recheck appointment 1 month later, her owner reports that her stool consistency has improved but has not returned to normal. She is eating well and has resumed her normal adult maintenance diet. She has an appropriate BCS of 4 out of 9 but has lost 5 lb since her annual wellness examination 3 months prior. The physical examination is otherwise unremarkable.

Based on her chronic GI signs, a diagnostic investigation is recommended. Fecal flotation, diarrhea PCR panel, and Giardia spp antigen results are negative. CBC, serum chemistry, urinalysis, and thyroxine (T4) levels are within normal limits. Abdominal radiography does not suggest structural disease or GI obstruction.

What Comes Next?

The owner is offered a choice to pursue a treatment trial for CE, start a hypoallergenic diet trial, or continue the diagnostic investigation, which would include abdominal ultrasonography, resting cortisol, Precision PSL, and Texas A&M GI panel. This approach is typically preferred for any patient with chronic GI signs that is clinically unstable, may have severe clinical signs, and/or may have hypoalbuminemia.3

Obtaining biopsies allows diffuse neoplasia such as lymphoma to be ruled out; however, biopsies are invasive and expensive and carry anesthesia-associated risks.

The owner is interested in pursuing further diagnostics in the hopes of obtaining a more definitive diagnosis. The owner is advised that a definitive diagnosis of IBD is based on histopathology obtained via endoscopy (partial-thickness biopsy) or exploratory laparotomy (full-thickness biopsy).3 Obtaining biopsies allows diffuse neoplasia such as lymphoma to be ruled out; however, biopsies are invasive and expensive and carry anesthesia-associated risks. In addition, there are often minimal changes to the treatment plan when results are received, as histopathology cannot differentiate FRE from ARE and IRE and does not always correlate with severity of clinical signs.2

As an alternative next step, the owner is offered a novel serum-based diagnostic test from Antech Diagnostics.

A New Diagnostic Option

Antech’s CE/IBD assay is a rapid and affordable blood test that evaluates 3 serologic biomarkers to help distinguish CE/IBD from other causes of chronic GI signs, guide therapy, and monitor response to treatment. The test has high sensitivity (86%) and specificity (94%) for CE and IBD.2 Owners should be aware that their pet may still need additional diagnostics with this test and that the gold-standard diagnostic for IBD remains histopathology.

The assay is an ELISA test for:

  • Antiporin IgA (ACA): An antibody produced in response to the outer membrane protein C (OmpC) of Escherichia coli.2 With increased intestinal permeability, bacteria can translocate and proliferate, resulting in production of ACA.2,4 ACA is the single best marker to differentiate CE/IBD from other causes of GI disease in dogs.2,4
  • Anti-calprotectin IgA (ACNA): An additional marker of intestinal inflammation2
  • Antigliadin IgA (AGA): An antibody to gliadins, a component of gluten.2 In some types of CE, gliadins can cross the intestinal epithelial barrier due to increased permeability, resulting in AGA production. Presence of AGA indicates possible food sensitivity.2

Assay results are either “consistent with CE/IBD” or “not consistent with CE/IBD,” based on biomarker levels.2,4,5 If results are not consistent with CE/IBD, additional diagnostics should be pursued to determine the cause of chronic GI signs. If results are consistent with CE/IBD and the patient is stable, treatment for presumptive CE/IBD can be pursued. However, if the patient is not stable, further diagnostics should be pursued while continuing supportive care.

In addition to the combined results, biomarker levels can help direct treatment. Each biomarker has an interpretive range of values that can determine if the level is low, intermediate, or high.2 For instance, a gliadin-free diet should be considered in cases of elevated AGA, even if results are not consistent with CE/IBD.2,5 If AGA is low, a dietary trial with any novel protein or hydrolyzed diet can be pursued. Elevated ACA suggests prebiotics and probiotics may be useful, as this is a marker of bacterial proliferation.2

This test can be used in patients with intermittent or persistent GI signs lasting >14 days, patients with acute GI signs and documented weight loss (suggesting chronicity), and monitoring of patients undergoing treatment using serial testing.2,4

Case Results

Assay results are consistent with CE/IBD. ACA is 52.6 and considered high (>40 EU/ mL), ACNA is 8.9 and considered intermediate (6-15 EU/mL), and AGA is 90.8 and considered high (>60 EU/mL). The client agrees to a dietary trial with a gliadin-free novel protein diet. Because ACA is also elevated, pre- and probiotic therapy are also instituted.

If there is no improvement in biomarkers with dietary trial alone, further diagnostics and abdominal imaging should be considered if not already performed.

Patients should be retested 2 to 4 weeks after starting initial treatment to evaluate therapeutic response.2,5 A decrease in ACA and ACNA values is indicative of reduced intestinal inflammation, and decreased ACA levels are indicative of reduced bacterial proliferation. In cases of elevated AGA, improvement should be expected after starting a gliadin-free diet if clinical signs are due, at least in part, to food sensitivity. If there is no improvement in biomarkers with dietary trial alone, further diagnostics and abdominal imaging should be considered if not already performed. Biopsies should be collected prior to starting immunosuppressant medications.

Luna is retested 4 weeks after starting the dietary trial, prebiotics, and probiotics. ACA is 22.4 and considered intermediate (15-40 EU/mL), ACNA is 5.2 and is now low (<6 EU/mL), and AGA is 51.8 and considered intermediate (50-60 EU/mL). Her stool is normal, and she has gained 3 lb. The owner declines further diagnostics and elects to continue the diet trial alone and retest again in 1 month to monitor response to treatment.

Conclusion

The Antech CE/IBD Assay is an affordable, rapid, and noninvasive test that can aid in the diagnosis of CE and IBD in dogs. Use of the assay can help increase client compliance in obtaining a definitive diagnosis and following treatment recommendations and provides an objective way to monitor response to therapy for each patient. It may also reduce the need for the invasive diagnostics required to obtain histopathology samples.

ADDITIONAL RESOURCE

For a canine GI diagnostic algorithom, visit brief.vet/antech-IBD-algorithm

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.


Simplifying Treatment of Urinary Incontinence

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Simplifying Treatment of Urinary Incontinence
Sponsored by PRN Pharmacal

Urinary incontinence secondary to urethral sphincter mechanism incompetence (USMI) is a common issue seen in as many as 1 out of 5 spayed dogs.1 Although PROIN® has historically been an invaluable option for such dogs, twice-daily dosing can be inconvenient and problematic for many pet owners, as experienced by Annie’s owners.

Follow Annie’s case to see how she and her owners overcame this struggle.

Annie’s Case

Annie, a 6-year-old female spayed golden retriever, was diagnosed with USMI by her primary veterinarian. Annie was initially prescribed PROIN® (phenylpropanolamine HCl, 2 mg/kg PO every 12 hours for 4 weeks); however, her owners struggled to give the medication every 12 hours due to their work schedules. Her owners noted that PROIN® had improved Annie’s incontinence when they were able to give it regularly but were concerned that 12-hour dosing was not sustainable.

1  Questions
Multiple Choice Questions
Score 0/1

PROIN®’s mechanism of action

1/1  Questions
Score
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How does PROIN®’s mechanism of action differ from that of other common treatment options for USMI?
Select one of the above choices.
1/1  Questions
Multiple Choice Questions
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Unlike diesthylstilbestrol and estriol, which are synthetic estrogens, phenylpropanolamine HCl (PROIN ER™ or PROIN®) is a sympathomimetic, which increases contraction of the urethra and urinary bladder neck. It is FDA-approved specifically for urinary incontinence secondary to USMI/urethral sphincter hypotonus. Unlike other urinary incontinence therapeutics, it can also be used successfully in male dogs.2 Although PROIN® requires twice-daily dosing, PROIN ER™, an extended-release formulation that allows for once-daily administration, was created to overcome this very issue experienced by pet owners.2 PROIN ER™ is a convenient and effective once-daily treatment for USMI that works through a patented, extended-release formulation to improve muscle tone around the urethral sphincter throughout the dosing period, decreasing the risk for urinary accidents.2

1  Questions
Multiple Choice Questions
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Which of the following is not true of PROIN ER™?

1/1  Questions
Score
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Which of the following is not true of PROIN ER™?
Select one of the above choices.
1/1  Questions
Multiple Choice Questions
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PROIN ER™ extended-release technology results in steady absorption of the drug, allowing for safe and effective concentrations throughout the day.2 A multicenter clinical field trial of 104 dogs with USMI showed that 75 dogs remained well-controlled after receiving PROIN ER™ for 28 days, and 19 dogs showed improvement in signs of incontinence as compared with when receiving PROIN®.2 In another study, 82.2% of dogs readily consumed PROIN ER™ with or without a small meal.3 PROIN ER™ comes in 4 convenient strengths: 18 mg for dogs weighing 10 to 20 lb (4.5-9 kg), 38 mg for dogs weighing 21 to 40 lb (9.5-18 kg), 74 mg for dogs weighing 41 to 80 lb (18.5-36 kg), and 145 mg for dogs weighing 81-125 lb (36.7-56 kg).2

Because PROIN® worked well for Annie with no noticeable adverse effects, her veterinarian offered to switch her to PROIN ER™. Upon switching, Annie’s incontinence remained resolved. Her owners were much happier with the more convenient, once-daily dosing.

Transitioning to PROIN ER™ requires only a simple dosage adjustment. The dosage for PROIN ER™ is 2-4 mg/kg PO every 24 hours as compared with 1-2 mg/kg PO every 8 to 12 hours for PROIN. No washout period is required.2

PROIN ER™ is a convenient option to manage a common problem. At appropriate dosages, its efficacy is high, and potential adverse effects are minimal. Further, PROIN ER™ can treat a broader range of patients than some other urinary incontinence therapeutics can, making it an easier treatment to prescribe in-house and keep in the clinic’s inventory.2,3

For full prescribing information, as well as, efficacy and safety information, please visit the PRN Pharmacal website at PRNPharmacal.com

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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Electrocution Emergency in a Puppy

Jennifer Good, DVM, DACVECC, University of Georgia

Emergency Medicine & Critical Care

|Peer Reviewed|Web-Exclusive

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Electrocution Emergency in a Puppy

Clinical History & Signalment

Charlie, a 6-month-old, intact male crossbreed dog, was presented to an emergency clinic for suspected electrocution after chewing on an electric cord. On the day of presentation, Charlie’s owners found him collapsed on the floor next to a connected (ie, plugged in) power strip and a shredded cord. He was conscious but appeared dull and painful around the face. His owners immediately brought him to the veterinary emergency clinic. Prior to this incident Charlie had been a healthy puppy.

Physical Examination

On physical examination, Charlie was quiet but alert and responsive. Temperature was normal, but pulses were rapid and weak; heart rate was 180 bpm, indicating tachycardia. Mucous membranes were pale pink with a capillary refill time of 3 seconds. Charlie was panting and had slightly increased respiratory effort. Ulcerated burns were appreciated at the commissures of the lips and across the dorsum of the tongue. Cardiothoracic auscultation did not reveal any murmurs or arrhythmias, but increased bronchovesicular sounds and soft crackles were appreciated bilaterally in the caudal pulmonary fields.

Radiograph showing air bronchograms consistent with noncardiogenic pulmonary edema (arrows). Atelectasis, which would be evident with shifting of the heart to the left or right, is not present.
Radiograph showing air bronchograms consistent with noncardiogenic pulmonary edema (arrows). Atelectasis, which would be evident with shifting of the heart to the left or right, is not present.

FIGURE 1 Radiograph showing air bronchograms consistent with noncardiogenic pulmonary edema (arrows). Atelectasis, which would be evident with shifting of the heart to the left or right, is not present.

FIGURE 1 Radiograph showing air bronchograms consistent with noncardiogenic pulmonary edema (arrows). Atelectasis, which would be evident with shifting of the heart to the left or right, is not present.

Diagnostics

Blood pressure was decreased (85 mm Hg) on Doppler ultrasound. Oxygen saturation was initially 92% but increased to 98% with flow-by oxygen supplementation via mask (4 L/minute). Initial blood work showed mild hyperlactatemia (3.1 mmol/L; reference range, 0-2.5 mmol/L), packed cell volume of 54%, and total solids at 6.8 g/dL. Chest radiography was performed with oxygen supplementation and revealed a moderate to severe caudodorsal interstitial to alveolar lung pattern (Figures 1 and 2).

Radiographs showing caudodorsal alveolar pattern consistent with noncardiogenic pulmonary edema (arrows). Edema is caudodorsal and bilateral. The heart size is normal, and there is no elevation of the airways that would indicate left-sided heart enlargement. Sternal contact of the heart, which might suggest right-sided heart enlargement, is minimal.
Radiographs showing caudodorsal alveolar pattern consistent with noncardiogenic pulmonary edema (arrows). Edema is caudodorsal and bilateral. The heart size is normal, and there is no elevation of the airways that would indicate left-sided heart enlargement. Sternal contact of the heart, which might suggest right-sided heart enlargement, is minimal.

FIGURE 2 Radiographs showing caudodorsal alveolar pattern consistent with noncardiogenic pulmonary edema (arrows). Edema is caudodorsal and bilateral. The heart size is normal, and there is no elevation of the airways that would indicate left-sided heart enlargement. Sternal contact of the heart, which might suggest right-sided heart enlargement, is minimal.

Radiographs showing caudodorsal alveolar pattern consistent with noncardiogenic pulmonary edema (arrows). Edema is caudodorsal and bilateral. The heart size is normal, and there is no elevation of the airways that would indicate left-sided heart enlargement. Sternal contact of the heart, which might suggest right-sided heart enlargement, is minimal.
Radiographs showing caudodorsal alveolar pattern consistent with noncardiogenic pulmonary edema (arrows). Edema is caudodorsal and bilateral. The heart size is normal, and there is no elevation of the airways that would indicate left-sided heart enlargement. Sternal contact of the heart, which might suggest right-sided heart enlargement, is minimal.

FIGURE 2 Radiographs showing caudodorsal alveolar pattern consistent with noncardiogenic pulmonary edema (arrows). Edema is caudodorsal and bilateral. The heart size is normal, and there is no elevation of the airways that would indicate left-sided heart enlargement. Sternal contact of the heart, which might suggest right-sided heart enlargement, is minimal.

FIGURE 2 Radiographs showing caudodorsal alveolar pattern consistent with noncardiogenic pulmonary edema (arrows). Edema is caudodorsal and bilateral. The heart size is normal, and there is no elevation of the airways that would indicate left-sided heart enlargement. Sternal contact of the heart, which might suggest right-sided heart enlargement, is minimal.

DIAGNOSIS:

NONCARDIOGENIC PULMONARY EDEMA

Diagnosis

The caudodorsal, bilateral, interstitial to alveolar pattern seen on radiographs is most consistent with noncardiogenic pulmonary edema (NCPE). Other differential diagnoses typically include cardiogenic edema or pneumonia. However, because Charlie was 6 months of age with a normal heart size and no murmurs or arrhythmias auscultated, cardiogenic edema was less likely. Expected pulmonary changes to the lungs are more diffuse with fungal or viral pneumonia or more discrete with bacterial pneumonia. NCPE was most likely in this patient because of the caudodorsal, bilaterally symmetric pattern and history of presumptive electrocution.

Treatment & Management

Charlie was placed in an oxygen cage with 40% fraction of inspired oxygen, and a fluid bolus (lactated Ringer’s solution, 10 mL/kg IV) was administered over 20 minutes. Repeated blood pressure reading postbolus was 110 mm Hg. A single dose of a diuretic (furosemide, 1 mg/kg IV), a bronchodilator (terbutaline, 0.01 mg/kg SC every 8 hours),1 and an analgesic medication (methadone, 0.1 mg/kg IV every 6 hours) were administered. Oral burns were gently cleaned with a diluted oral cleansing solution, and sterile lubrication was applied to the lip commissures. Once respiratory rate and effort improved, an isotonic crystalloid (lactated Ringer’s solution, 60 mL/kg/day IV) was administered.

TREATMENT AT A GLANCE

  • Patients presented with a history of electrocution should undergo a thorough oral examination to evaluate potential burns, ulcerations, fistulas, or dental fractures.
  • Careful auscultation for any increased respiratory noise, increased effort, or distress is required.
  • Thoracic-focused assessment with sonography for trauma (ie, TFAST) examination is recommended to look for the presence of b-lines, cardiac abnormalities, or pleural fluid.
  • Fluid resuscitation with careful monitoring for increased respiratory rate and effort that may indicate edema formation is recommended in patients in hypovolemic shock.
  • Oxygen supplementation should be provided until respiratory rate and effort return to normal. 
  • Bronchodilators may be helpful in patients with respiratory distress secondary to neurogenic pulmonary edema and other forms of NCPE, although the evidence is equivocal.1
  • Pain medications for burns, wounds, and postfasciculation muscle pain are important in patients after electrocution.
  • Most cases of neurogenic pulmonary edema resolve in 1 to 3 days.

Prognosis & Outcome

Thirty-six hours following initial presentation, Charlie’s respiratory rate and effort were normal without oxygen supplementation. Recheck radiographs showed complete resolution of the former alveolar pattern. He was able to lick wet food despite his oral burns, and methadone and terbutaline were discontinued. Charlie was discharged 48 hours following presentation.

Because Charlie received care in the first few hours after the incident, the prognosis was good, as is generally the case in young patients with neurogenic pulmonary edema secondary to electrocution.

Discussion

Young patients are more prone to electrocution, as they are more likely to chew on electric cords.2 Surface burns are often noted where the electric current entered the body. Injuries are secondary to both the direct effect of the current and to transformation of the current to heat in the body. Other findings in cases of electrocution include cardiac arrhythmia, muscle spasms, spinal cord injury, and collapse.3-5

NCPE Secondary to Electrocution

NCPE secondary to electrocution is a neurogenic pulmonary edema, which is defined as acute respiratory distress triggered by a severe event that causes acute injury to the CNS. Neurogenic pulmonary edema is considered a form of acute respiratory distress syndrome (ARDS) and has its own pathophysiology as compared with other forms of acute respiratory distress syndrome.6,7 Other possible causes of neurogenic pulmonary edema include spinal cord injury, subarachnoid hemorrhage, traumatic brain injury, prolonged seizures (eg, clusters, status), and meningitis.6,8,9

NCPE can be present in several forms, including ARDS/acute lung injury (ALI), postobstructive pulmonary edema (POPE), re-expansion pulmonary edema (REPE), and neurogenic pulmonary edema. ALI and ARDS are considered the most serious manifestations of NCPE. ARDS is defined as acute-onset (<72 hours) dyspnea with pulmonary edema in the presence of a normal left heart (ie, noncardiogenic in origin), bilateral distribution on radiographs or CT, high-protein fluid in the airways, or known risk factors.1 ARDS/ALI is considered an increased permeability edema caused by injury to the pulmonary microvascular endothelial barrier and/or to the alveolar epithelium.1,10 Inflammation in the pulmonary capillaries can allow high-protein fluid to leak into air spaces.

Postobstructive Pulmonary Edema

POPE (also referred to as negative pressure pulmonary edema) typically occurs after acute upper airway obstruction (type I) or after relief of a chronic partial airway obstruction (type II).11 Type I is triggered by forceful inspiration against an obstruction or closed glottis. Increased negative pressure can result in an increase in venous return to the right side of the heart. Increased afterload secondary to negative pressure can decrease cardiac output from the left side of the heart. This combination often results in increased hydrostatic pressure, leading to pulmonary edema.11 Possible causes of type I POPE include but are not limited to choking/foreign body ingestion, strangulation, near drowning, and laryngeal paralysis.11,12 Type II is largely due to expiration against a closed airway over time (eg, brachycephalic airway syndrome, chronic stenosis). Eventually, forced expiration can cause increased pleural and alveolar pressures, resulting in reduced venous return to the right and left sides of the heart. When the obstruction is relieved with surgery, an acute drop in airway pressures typically occurs, leading to a large increase in venous return. The result is increased hydrostatic pressure leading to pulmonary edema.11,12

Re-Expansion Pulmonary Edema

REPE is rare in small animals and usually occurs after chronically collapsed lungs have been reinflated. The mechanism involves decreased surfactant in collapsed lobes, reperfusion injury, and free radical formation. The most common risk for REPE is recent repair of a chronic diaphragmatic hernia in which the lungs have been compressed over a long period of time.10

Pathophysiology

The pathophysiology of neurogenic pulmonary edema involves several mechanisms that link neurologic, cardiac, and pulmonary conditions. Any event that causes an abrupt and extreme elevation in intracranial pressure carries the greatest risk for neurogenic pulmonary edema.8 A sudden increase in intracranial pressure can result in compression, ischemia, or damage to the neuronal tissues. This increased pressure can lead to a massive sympathetic surge with release of catecholamines and subsequent vasoconstriction and hypertension,3,6,8,9 resulting in sudden and marked increase in left ventricular afterload and decreased stroke volume that results in buildup of fluid in the pulmonary vasculature. This increased fluid can cause elevated pulmonary capillary hydrostatic pressure that leads to edema.3 In addition, α-mediated pulmonary venous constriction is possible even in the absence of systemic hypertension and can result in a direct increase of pulmonary capillary pressure.13 Radiographs typically show a bilateral alveolar pattern primarily in the caudodorsal quadrant.3,9

Electrocution & Electric Burns

Treatment for electrocution should focus on controlling any sequelae to the event. Shock should be addressed first with conservative fluid boluses; judicious use of fluids is recommended because of concerns for the presence or development of NCPE; pulmonary capillaries may be leaking.3,4 Burns should be treated with standard wound management (areas should be cleaned and covered when possible).

Electric burns on the surface of mucous membranes can vary from superficial to full-thickness.3 Oral cavity burns can manifest as ulcerations but may also include dental fractures or oronasal fistulas.14 The path the electric current takes through the body is determined by the path of least resistance. Dry skin has more resistance, whereas wet skin/hair coat and mucous membranes have very low resistance and thus are typically the preferred path. An electric current can disrupt normal electrophysiologic impulses, leading to cardiac arrhythmias that should be treated as they appear with antiarrhythmics according to their chamber of origin (eg, atria vs ventricles). In addition to NCPE, respiratory distress can occur secondary to swelling of the oropharynx and/or laryngeal tissues or severe spasm of the muscles of respiration.3,15 Serum chemistry changes in these patients depend on the amount of tissue damaged by the electric burns; blood work results are usually unremarkable, but ischemia of large portions of tissue can result in hyperkalemia, myoglobinemia, myoglobinuria, severe lactic acidosis, and hypoalbuminemia.3

Resolution & Supportive Care

A hallmark of NCPE is quick resolution (usually within 48-72 hours, sometimes more quickly).3,8,15 Edema has been reported to resolve in some humans before the patient presents to the emergency room.15 Treatment should center around providing supportive care for the lungs (eg, oxygen, bronchodilators, initial diuretic therapy) and addressing any underlying issues.

Prognosis

Prognosis depends on several variables. The underlying cause of NCPE is paramount. Young, otherwise healthy patients with neurogenic pulmonary edema secondary to electrocution and no underlying disease generally have a good prognosis, whereas patients with severe ARDS secondary to pneumonia or sepsis of another origin have a far worse prognosis. These patients have ongoing, increased permeability of the pulmonary vasculature secondary to inflammation and are therefore at risk for continued leakage into the alveoli.1,3 In dogs with neurogenic pulmonary edema secondary to electrocution, prognosis also depends on voltage and type of current (ie, alternating vs direct). High voltage exposure is more serious than low voltage exposure. An alternating current can result in more muscular contractions, which prevent the victim from releasing the power source—this is especially true in humans who may grab a power source with their hands and are unable to let go.3,8,15 The degree of damage can depend on resistance of the tissues from the entry to exit points. It is important to remember that current (ie, amperage) depends on the voltage divided by the resistance of the tissue. Dry skin has a higher resistance, and mucous membranes have a low resistance; thus, voltage going through dry skin may have a lower current versus going through a mucous membrane. Therefore, even a lower voltage cord can cause more damage to wet skin or mucous membranes than to dry tissues.3 Patients with full-thickness burns, necrosis of affected tissues, severe arrhythmias, or profound neurogenic pulmonary edema are less likely to survive than those with superficial burns and mild to nonexistent pulmonary signs.3,13

TAKE-HOME MESSAGES

  • NCPE can be due to high permeability edema (ie, ARDS/ALI), postobstructive conditions, or re-expansion of chronically compressed lung lobes or can be secondary to acute, severe CNS injury.
  • Neurogenic pulmonary edema is secondary to any abrupt and severe CNS event (eg, seizures, strangulation, electrocution).
  • Neurogenic pulmonary edema is primarily due to a large sympathetic surge that can result in a massive release of catecholamines, leading to hypertension and subsequent elevated pulmonary capillary pressures. 
  • Treatment for NPE consists of oxygen supplementation, cautious fluid administration, bronchodilators, and judicious use of diuretics. In general, use of diuretics is of limited value because edema present in all forms of NCPE, including neurogenic pulmonary edema, tends to have a higher protein content. No more than 1 to 2 doses should be given due to the risk for dehydration and limited value of continued administration. Mechanical ventilation may be required in severe cases.
  • Electric shocks that penetrate tissue with low resistance (ie, wet skin or mucous membranes) can result in more serious tissue injury.
  • Prognosis for neurogenic pulmonary edema depends on the underlying cause (eg, brain tumor with intracranial bleed vs mild electrocution).

References

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

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

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


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