Clinical Medicine , Emergency Medicine/Critical Care , Gastroenterology/Hepatology , Internal Medicine

Canine Pediatrics: The Vomiting Puppy

Canine Pediatrics: The Vomiting Puppy

pdf_button


Justine A. Lee, DVM, Diplomate ACVECC & ABT
VETgirl (vetgirlontherun.com)

Leah A. Cohn, DVM, PhD, Diplomate ACVIM (Small Animal Internal Medicine)
University of Missouri

JP, a 6-week-old, 3.5-kg intact male pit bull mix, presented for anorexia, vomiting, and bloody diarrhea. He had been acquired from a flea market and seemed healthy but thin.

HISTORY

The day after the owners acquired JP, the puppy began vomiting and, the following day, he had diarrhea. On day 4, JP was presented to the primary care veterinarian, who evaluated him for progressive listlessness, anorexia, continued vomiting, and bloody diarrhea.

The owners stated that JP had 2 littermates at the flea market that were not as playful as JP. They also confirmed the puppies had not received any vaccinations.

SNAP Parvo Test (idexx.com) results were positive, and JP was referred to another facility that had an isolation unit and provided 24-hour care.

PHYSICAL EXAMINATION

The physical examination findings of JP upon presentation to the referral facility are listed in Table 1.

JP also had bloody diarrhea staining his ventral abdomen and hindlimbs. He vomited just after palpation. While JP was able to stand with support, he was extremely weak.

T1509F03_Table01

DIAGNOSTIC APPROACH

Peripheral IV access was attempted but, due to JP’s volume-depleted state, multiple attempts at cephalic catheterization failed. An 18-gauge, 6-cm catheter was placed into the left jugular vein, allowing a minimal volume of blood to be obtained for analysis of packed cell volume (PCV), total solids (TS), blood urea nitrogen (BUN) (Azostix, usa.healthcare.siemens.com), blood glucose (BG), and blood smear. Fecal flotation was performed on voided stool.

Depending on available resources and the financial limitations of the owners, diagnostics can follow 3 tiers of diagnostic evaluation (see Levels of Diagnostic Evaluation).

Levels of Diagnostic Evaluation

GOLD

Blood Analysis

  • Complete blood count, with smear evaluation
  • Serum biochemical profile
  • Venous blood gas (eg, acid–base, electrolytes)

Fecal Analysis

  • Fecal flotation
  • Direct fecal smear
  • Parvoviral fecal antigen*

Imaging

  • Abdominal radiography/ultrasonography

Other

  • Colloid osmotic pressure
  • Blood pressure

SILVER

Blood Analysis

  • Complete blood count, with smear evaluation
  • Serum biochemical profile
  • Venous blood gas (eg, acid–base, electrolytes)

Fecal Analysis

  • Fecal floatation
  • Parvoviral fecal antigen

Other

  • Blood pressure

BRONZE

Blood Analysis

  • Packed cell volume and total solids
  • Blood smear evaluation
  • Serum biochemical profile or venous blood gas (eg, acid–base, electrolytes), along with blood glucose and blood urea nitrogen

Fecal Analysis

  • Parvoviral fecal antigen

* If result is negative but parvovirus is still suspected, perform polymerase chain reaction on feces.

Initial Analysis

  • Initial laboratory tests revealed:
    • BG concentration of 36 mg/dL (pediatric [6- to 8-weeks old] reference interval, 134–272 mg/dL)
    • PCV of 40% (pediatric [6- to 8-weeks old] reference interval, 27%–36%)
    • TS of 4.8 g/dL (pediatric [6- to 8-weeks old] reference interval, 3.9–4.2 g/dL)
    • BUN level of 30 to 40 mg/dL (pediatric [6- to 8-weeks old] reference interval, 14–15.5 mg/dL).
  • Blood smear revealed fewer neutrophils than expected, with mild toxic change; this was grossly estimated to be a white blood cell count of 2000 to 3000 (cells/mcL) on 100× magnification. Approximately 10 platelets per high power field were seen on 1000×; this was estimated to be a platelet count of 100,000 to 150,000 (cells/mcL).
  • High numbers of Toxocara canis eggs were identified in the stool.
  • Doppler blood pressure measurement was attempted, but proved difficult due to the small size of the puppy (pediatric [6- to 8-weeks old] reference range, approximately 112 mm Hg).1

Further Analysis

After initial treatment, blood was collected in low-volume tubes for routine complete blood count (CBC) and serum biochemical profile (Table 2).

T1509F03_Table02

CBC Results

  • Marked lymphopenia and neutropenia were seen, typical of parvoviral enteritis.
  • Relative hemoconcentration was likely due to severe dehydration. Low PCV due to age and/or anemia due to gastrointestinal (GI) bleeding may become evident after fluid therapy.

Biochemistry Results

  • JP’s hypoglycemia was more severe than could be attributed to age, cachexia, and decreased food intake.
  • Cholesterol is often lower in puppies than adult dogs.
  • Electrolyte depletion was attributed to vomiting and diarrhea.
  • Low albumin and total protein levels were most likely caused by protein loss through the GI tract, including via GI bleeding.
  • Hypocalcemia was at least partially related to severe hypoalbuminemia.
  • Increased alkaline phosphatase, bilirubin, and phosphorus were most likely related to a combination of age and illness.

DIAGNOSIS

Cormorbidities

In this patient, canine parvovirus infection had been diagnosed before referral. Additional comorbid conditions may include infection with another virus (eg, coronavirus), intestinal parasitism, intestinal bacterial infection or overgrowth (eg, Escherichia coli, Salmonella species, Campylobacter species, Clostridia species), intussusception, or foreign body.

Sepsis & Hypovolemic Shock

The presence of hypovolemic shock and sepsis—caused by dehydration, leukopenia, and intestinal bacterial translocation—is the most life-threatening condition present in JP. Associated hypoglycemia, hypoalbuminemia, and electrolyte or acid–base disturbances must be addressed.

Should Oxygen Be Given During Initial Resuscitation? While JP was tachypneic—likely secondary to hypovolemia—he was not dyspneic and his lung sounds were clear. Therefore, supplemental oxygen was probably not necessary but could have been provided until normoxemia was confirmed. However, for a neonate (< 2 weeks of age), oxygen therapy would be recommended.

TREATMENT APPROACH

Therapy for Hypovolemic Shock

  • Due to the life-threatening hypoglycemia, JP received an initial IV bolus of 0.5 g/kg dextrose (3 mL of 50% dextrose diluted in 7 mL of 0.9% saline over 1 minute).
  • Aggressive fluid therapy was indicated due to the extreme dehydration and hypovolemic shock (see Fluid Therapy Plan).
  • A bolus of 120 mL (34 mL/kg) of warmed lactated Ringer’s solution was administered over 15 minutes, followed by 33 mL/H (10 mL/kg/H) of lactated Ringer’s solution with 5% dextrose and potassium chloride supplementation.
  • A colloid was administered in addition to the crystalloid.

BG was measured every 6 H, with glucose supplementation adjusted as necessary to maintain normoglycemia.

Fluid Therapy Plan

T1509F03_Box2

  1. Expand intravascular volume and treat shock with IV bolus of fluids; JP received a 120-mL bolus (30 mL/kg). Volume resuscitate the patient appropriately based on clinical signs of improved:
    • Pulse quality
    • Heart rate
    • Mentation
    • General perfusion parameters.
  2. Correct estimated dehydration: JP’s estimated dehydration was 12%. The remaining deficit was corrected over 12 H.
    • 3.5 kg (body weight) × 0.12 (dehydration) = 420 mL fluid deficit
    • 420 mL (original deficit before fluid bolus) – 120-mL bolus fluid volume = 300 mL
    • 300 mL (remaining deficit)/12 H = 25 mL/H
  3. Provide for estimated ongoing loss: JP had frequent diarrhea and vomiting, with an estimated loss of 75 mL Q 24 H; therefore, 75 mL/24 H = 3.1 mL/H
  4. Provide maintenance fluids; fluid requirements for puppies vary with age (Table 3).6,7 For JP, fluid requirements were:
    • 3.5 kg (body weight) × 80 mL Q 24 H = 280 mL Q 24 H
    • 280 mL /24 H = 11.7 mL/H
  5. Consider colloidal support (see Table 2):
    • VetStarch (abbottanimalhealth.com): 2 mL/kg/H
    • 3.5 kg (body weight) × 2 mL/kg/H = 7 mL/H

T1509F03_Table03

Crystalloid fluid rate for the first 12 hours—after the initial fluid bolus—was calculated by considering:

Replacement (25 mL/H) + ongoing losses (3.1 mL/H) + maintenance (11.7 mL/H) = 39.8 mL/H

Colloid volume was subtracted (39.8 mL/H – 7 mL/H), which equaled a crystalloid fluid rate of 33 mL/H.

During the remaining period of hospitalization, and after the dehydration deficit had been replaced, fluid rate was decreased to reflect only maintenance needs and ongoing losses.

Therapy for Parvovirus & Sepsis

JP was treated with symptomatic and supportive care (see Typical Supportive Therapies for Parvoviral Enteritis), including provision of warmth and zinc oxide barrier therapy to prevent moist dermatitis.

Due to sepsis secondary to leukopenia, antibiotic therapy was initiated (IV initially; then PO once vomiting abated). A potent antiemetic was initiated to treat nausea and minimize risk for aspiration pneumonia.

The supportive medications and nutrition JP received are outlined in Table 4; daily in-hospital monitoring for parvovirus patients is described in Table 5.

T1509F03_Table04

T1509F03_Table05A

Typical Supportive Therapies for Parvoviral Enteritis

  • Crystalloid fluids, along with dextrose and potassium chloride supplementation as needed
  • Colloidal support, such as VetStarch, hetastarch, or plasma
  • Antiemetics, such as maropitant, dolasetron, or metoclopramide
  • Gastric protectants, such as famotidine or pantoprazole
  • Parenteral antibiotic therapy while hospitalized (eg, ampicillin/sulbactam, cefoxitin)
  • Antidiarrheals, such as probiotics or metronidazole
  • Analgesics, such as buprenorphine and lidocaine
  • Nutritional support, such as nasogastric tube feeding (if oral feeding refused) or mirtazapine

 

Other Therapeutic Options: Worth It?

In the past, fresh or fresh frozen plasma from recovered dogs had been suggested to provide antiparvoviral antibodies. Recent studies, however, have demonstrated no beneficial effect of this method and shown that even recently recovered animals have minimal anti-canine parvovirus antibody concentrations.8,9 Moreover, such treatment may prime the dog for future transfusion reactions later in life.

Equine endotoxin antiserum, recombinant human granulocyte-stimulating factor, and antiviral agents (eg, oseltamivir) have not been shown to improve survival or outcome.10-12 In small studies, use of feline interferon has been weakly associated with improved survival; however, this agent is not readily available in veterinary hospitals in the U.S.13,14

Ongoing Supportive Care

JP’s vital parameters improved markedly over the first few hours of therapy. By the following day, he subjectively looked less nauseated and had less abdominal pain. A temporary nasogastric feeding tube was placed at that time for nutritional support, with sporadic gastric suctioning to measure residual gastric volume. By day 4, JP was ingesting small amounts of meat-based baby food, and the nasogastric tube was removed. JP was dewormed with fenbendazole and discharged later that day.

PROGNOSIS

JP was discharged on day 4, and the owner was taught how to administer medications and encourage JP to eat. The primary care veterinarian performed a recheck examination 3 days later, and reported that JP was acting and eating normally at that time.

The prognosis for canine parvovirus infection is fair to good. Perhaps surprisingly, severity of neutropenia is not a negative prognostic factor; rather, severity of dehydration and lymphopenia may be instead.15 Recently, several studies have evaluated other measures that may affect prognosis.16-18

A study from Colorado State University compared standard in-hospital treatment versus a modified outpatient treatment (using volume resuscitation followed by SC fluid therapy and supportive care), with recent survival rates of 80% to 90% reported with treatment.19 Both protocols can be successful, with a slightly lower survival rate in outpatients.19

Hospitalization with intensive therapy was initially indicated for JP due to his severe hypoglycemia, dehydration, and shock, but a modified outpatient protocol (SC fluids, antiemetics, antibiotics) may be a good alternative for less severely affected patients or clients with financial limitations.

Key Points: Treating the Pediatric Patient

In critically ill neonate and pediatric patients, goals of treatment should be prioritized by the four H’s:

  • Hypovolemia/hydration
  • Hypothermia
  • Hypoglycemia
  • Hypoxemia

Fluid Therapy

  • Dehydration can rapidly progress to hypovolemia in neonates and pediatric patients; therefore, aggressive fluid therapy is warranted because these small patients can deteriorate quickly.
  • Fluid requirements for neonates and pediatric patients are much higher than those for adults.
  • In critically ill pediatric patients, fluid therapy for shock must initially be given by IV or intraosseous routes.6,7 Intraperitoneal or SC routes are not adequate due to slower absorption and, ideally, should not be used in the critically ill, dehydrated, or hypovolemic patient.
  • Colloids can be used in pediatric patients; however, keep in mind that puppies have a lower colloid osmotic pressure than adult dogs.20 If necessary, a colloid (eg, hetastarch, 1 mL/kg/H; VetStarch, 2 mL/kg/H) can be used to keep colloid osmotic pressure above 15 mm Hg. No published data are available on colloid use in neonates.

Temperature

  • Normal rectal temperature in neonates is 96°F ± 1.5°F (35.6°C ± 0.7°C) in the first week of life; then 98.6°F to 100°F (37°C to 38.2°C) in the second and third weeks of life.21
  • Adult temperatures are reached by 7 weeks of age.21
  • Careful warming should be initiated to prevent overheating.

Hypoglycemia

  • Neonates and pediatric patients are prone to hypoglycemia due to decreased glycogen stores, inefficient hepatic gluconeogenesis, and an immature glucose feedback mechanism.
  • Hypoglycemia is worsened by anorexia, ongoing losses (eg, vomiting, diarrhea), dehydration, and sepsis.
  • Frequent BG monitoring is warranted in these patients; however, the minimum amount of blood should be drawn to prevent iatrogenic anemia.

Immune System

  • In neonate and pediatric patients, the immune system is not fully mature until 3 to 6 months.
  • Poor husbandry (eg, lack of vaccination, lack of parasite prevention) often worsens clinical disease.

 

Pathophysiology of Parvovirus

Canine parvovirus (CPV) is a common and severe pathogen that affects young dogs that are unvaccinated, under-vaccinated, or immunosuppressed. The virus first emerged in dogs in the mid 1970s and has since mutated into 3 different forms: CPV-2a, CPV-2b, and, most recently, CPV-2c.

All 3 forms of CPV are environmentally stable, nonenveloped viruses transmitted via the fecal–oral route.

  • The virus initially replicates in oropharyngeal lymphoid tissues, leading to viremia; rapidly dividing cells of the GI tract, thymus, lymph nodes, and bone marrow are most affected.
  • Loss of both intestinal epithelial villous and crypt cells leads to malabsorption and increased intestinal permeability, accompanied by vomiting, diarrhea, and GI bleeding.
  • Destruction of bone marrow cells results in neutropenia and, to a lesser degree, thrombocytopenia.
  • Translocation of intestinal bacteria, complicated by neutropenia, often leads to bacteremia, endotoxemia, and sepsis.

Without treatment, CPV can be life threatening due to sepsis, severe fluid losses and electrolyte derangements secondary to anorexia, vomiting, and diarrhea. In order to ensure the best outcome, treatment should be aimed toward symptomatic supportive care, aggressive fluid therapy, antiemetics, antibiotic therapy, and nutritional support.

IN SUMMARY

Although there are differences between young and adult animals, pediatric patients can still be treated aggressively and respond well to therapy. However, clinicians must be aware of their normal physiologic and hemodynamic measures. The small size of these patients should not limit our ability to appropriately treat them.

BG = blood glucose; BUN = blood urea nitrogen; CBC = complete blood count; GI = gastrointestinal; PCV = packed cell volume; TS = total solids

References

  1. Adelman RD, Wright J. Systolic blood pressure and heart rate in the growing beagle puppy. Dev Pharmacol Ther 1985; 8(6):396-401.
  2. Clinkenbeard KD, Cowell RL, Meinkoth JH, et al. The hematopoietic and lymphoid systems. In Hoskins JD (ed): Veterinary Pediatrics: Dogs and Cats from Birth to Six Months. Philadelphia: WB Saunders, 2001, pp 300-343.
  3. Earl FL, Melveger BE, Wilson RL. The hemogram and bone marrow profile of normal neonatal and weanling beagle dogs. Lab Anim Sci 1973; 23:690-695.
  4. McMichael M, Dhupa N. Pediatric critical care medicine: Physiologic considerations. Compend Contin Ed Pract Vet 2000; 22:206-214.
  5. Woldford ST, Schroer RA, Gohs FX, et al. Effect of age on serum chemistry profile, electrophoresis and thyroid hormones in beagle dogs two weeks to one year of age. Vet Clin Path 1988; 17(2):35-42.
  6. Macintire DK. Pediatric intensive care. Vet Clin North Am Small Anim Pract 1999; 29:971-988.
  7. Macintire DK. Pediatric fluid therapy. Vet Clin North Am Small Anim Pract 2008; 38:621-627.
  8. Veir JK. Canine parvoviral enteritis. In Bonagura JD, Twedt DC (eds): Kirk’s Current Veterinary Therapy XV. St. Louis: Elsevier Saunders, 2014, pp 533-535.
  9. Bragg RF, Duffy AL, Dececco FA, et al. Clinical evaluation of a single dose of immune plasma for treatment of canine parvovirus infection. JAVMA 2012; 240(6):700-704.
  10. Dimmitt R. Clinical experience with cross-protective anti-endotoxin antiserum in dogs with parvovivral enteritis. Canine Pract 1991;16(3):23-26.
  11. Duffy A, Dow S, Ogilvie G. Hematologic improvement in dogs with parvovirus infection treated with recombinant canine granulocyte-colony stimulating factor. J Vet Pharmacol Ther 2010; 33(4):352-356.
  12. Savigny MR, Macintire DK. Use of oseltamivir in the treatment of canine parvoviral enteritis. J Vet Emerg Crit Care 2010; 20(1):132-142.
  13. Ishiwata K, Minagawa T, Kajimoto T. Clinical effects of the recombinant feline interferon-omega on experimental parvovirus infection in beagle dogs. J Vet Med Sci 1998; 60(8):911-917.
  14. DeMari K, Maynard L, Eun HM, et al. Treatment of canine parvoviral enteritis with interferon omega in a placebo-controlled field trial. Vet Rec 2003; 152:105.
  15. Markovich JE, Stucker KM, Carr AH, et al. Effects of canine parvovirus strain variations on diagnostic test results and clinical management of enteritis in dogs. JAVMA 2012; 241:66-72.
  16. Kalli I, Leontides LS, Mylonakis ME, et al. Factors affecting the occurrence, duration of hospitalization and final outcome in canine parvovirus infection. Res Vet Sci 2010; 89(2):174-178.
  17. McClure V, van Schoor M, Thompson PN, et al. Evaluation of the use of serum C-reactive protein concentration to predict outcome in puppies infected with canine parvovirus. JAVMA 2013; 243(3):361-366.
  18. Kocaturk M, Martínez S, Eralp O, et al. Prognostic value of serum acute-phase proteins in dogs with parvoviral enteritis. J Small Anim Pract 2010; 51(9):478-483.
  19. Sullivan LA, Twedt DC, Boscan PL. Evaluation of an outpatient protocol in the treatment of canine parvoviral enteritis. J Vet Emerg Crit Care; in press.
  20. Koenig A. Colloid osmotic pressure in healthy puppies. IVECCS Proc, 2007.
  21. Lawler DF. Neonatal and pediatric care of the puppy and kitten. Theriogenol 2008; 70:384-392.

Author_JA LeeJustine A. Lee, DVM, Diplomate ACVECC & ABT, is the CEO and founder of VETgirl (vetgirlontherun.com), a subscription-based podcast and webinar service that offers RACE-approved veterinary continuing education. Dr. Lee recently received the 2015 NAVC Speaker of the Year Award, and is the author and editor of several veterinary textbooks, book chapters, and scientific publications. She completed her veterinary training at Cornell University, Angell Animal Medical Center (Boston), and University of Pennsylvania.

 

Author_LA CohnLeah A. Cohn, DVM, PhD, Diplomate ACVIM (Small Animal Internal Medicine), is a professor of veterinary medicine at University of Missouri in the Department of Veterinary Medicine and Surgery. Dr. Cohn earned her DVM from University of Tennessee, and completed her residency and PhD at North Carolina State University. Her clinical interests are diverse, but she especially enjoys treating pets with infectious disease. Dr. Cohn is a recent past president of the American College of Veterinary Internal Medicine.

DMCA.com Protection Status
MENU