Clinico-laboratory and hydro-electrolytic imbalance study and therapeutic management of acute haemorrhagic gastroenteritis in German shepherd: A case report

Introduction

Canine population (Canis familiaris) exhibit great impact on the environment since its domestication about 15,000 years ago (12) and dog is the most dominant canid on earth. It is most devoted companion animal for man since long time. With the rising demand of pet the domestication is being increases in past few years with increasing cases of various infectious and non infectious diseases. Among various clinical manifestations, gastroenteritis is one of the most common multietiological (dietary, viral, bacterial, rickettsial, parasitic and miscellaneous) clinical conditions affecting the dogs of all age and breed especially growing pups (Bhat et al, 2013 and Banja et al., 2002) [1,2] . Common clinical signs include vomition, diarrhoea with or without blood, inappetence, lethargy, dehydration and anemia (Kataria et al., 2020) [3] . Dehydration and electrolyte disturbance are most important complications of gastroenteritis (Elliott, 2007) [4] and leads to mortality in many dogs. Hence present study was performed to evaluate various haematological, hepatorenal biomarker and hydroelectolytic imbalance in dog affected with acute gastroenteritis and its successful therapeutic management.

Materials and Methods

Case history and clinical examinations

Six-month-old male germen shepherded was presented to the Veterinary Clinical Complex, College of Veterinary Science, DUVASU, Mathura. Anamnesis revealed absence of scheduled vaccination, vomition (5-6 times) and bloody diarrhoea (3-4 times) since 2-3 days and oral administration of Eazypet® (combination of Praziquantel @ 50 mg, pyrental Pamoate @ 144mg and Fenbendazole @ 500 mg/kg) one week ago. Clinical examination revealed presence of reddish feces (Fig

Sampling and laboratory examinations

After detailed clinical examination, five millilitre of whole blood sample was collected from cephalic vein by using sterile plastic syringe. Two ml of blood was transferred to sterile plastic vial containing anticoagulant (3.6 mg Tripotassium EDTA) and remaining 3 mL was transferred into clot activator vial (without anticoagulant) and allowed to clot at room temperature (25±2 °C) for separation of serum via centrifugation (@ 4000rpm for 10 min). Haematological (Hb, PCV, TEC, TLC, DLC and Platelets), hepatorenal (Total protein, Albumin, ALT, BUN and Creatinine) and hydroelectolytic (Na, K and Cl) studies were performed in clinical diagnostic laboratory following standard protocol. Obtained values for all parameters were compared with standard reference values to interpret any significant difference.

Calculation of fluid requirement

Total fluid requirement was calculated as per standard protocol. Dehydration was considered as 5% based on the condition of skin elasticity and mucus membrane.

Maintenance fluid requirement (in ml) was calculated as body weight (in kg) × 30 + 70 while fluid deficit (in ml) was calculated as% dehydration× Body weight (in Kg) × 1000. Total calculated fluid was given in divided dose i.e. half in morning and then half in evening (Tello L., 2017) [5] .

Therapeutic management

Treatment was started with intravenous fluid therapy consist of ringer's lactate (200 ml, OD) and 10% dextrose normal saline (150 ml, OD) along with antiemetic (Ondansetron @ 0.2 mg/kg IV, BID), broad spectrum antibiotic (Ceftriaxone @ 30 mg/kg IV, OD), combination of vitamin B 12 , folic acid, niacinamide and vitamin-C (Eldervit ® @ 0.5 ml total dose, IV, OD), antacid (Pantoprazole @ 1 mg/kg IV, OD and Ranitidine @ 2 mg/kg, SC, OD), Hemocoagulase (Botropase @ 1 mlL total dose, IV) and oral administration of gastro protective agent (Sucralfate @ 4 ml PO, every 6 hours). Dog was clinically cured after seven days of therapy but normal appetite was regained 10 days after beginning of therapy.

Results and Discussion

All haematological parameters lie in reference range while among hepatorenal biomarkers only creatinine was lower than reference range (Table 1). Hypokalemia, hyponatremia and hypochloremia was observed (Table 1). Diversion of Hb and PCV are towards the lower range in present case may attribute to mild intestinal blood loss due to duodenal ulcers (Bhat et al., 2013) [1] while neutrophil count is towards higher side which may indicates involvement of infectious agent in the pathogenesis of gastroenteritis. Lower creatinine value may be attributed to less muscle mass or poor nutritional input (Ostermann et al., 2016) [6] . Hypokalemia and hyponatremia may be due to intestinal loss via diarrheic fluid and vomitus (Agnihotri et al., 2017; Haligur et al., 2009 and Joshi et al., 2012) [7,8,9] while hypochloremia observed in present case may be attributed to loss of chloride ions through vomition and diarrhoea (Burchell et al., 2014) [10] . Metabolic acidosis, caused by loss of bicarbonate via diarrheic fluid can be overcome by ringer's lactate solution. Ringer lactate is an isotonic crystalloid having combination of electrolyte (sodium, chloride, potassium, calcium) with sodium lactate with an osmolality of 273 mOsm/L and pH of about 6.5 (Singh et al., 2022) [11] . Conversion of lactate into pyruvate to form carbon dioxide and water which in turn produces carbonic acid and its dissociated product (bicarbonate) justify the used of ringer's lactate in present case (Gladden, 2004).

Ondansetron has antiemetic as well as antinauseant effect by inhibition of serotonin3 (5-HT3) receptors with constipation as one of the common side effect which may be beneficial in diarrheic cases (Markham and Sorkin, 1993) [13] . Altered permeability of intestine may cause nutrient loss (Marks, 2013) [14] and allow the wide verities of bacteria to absorb into circulation causing sepsis and multiple organ failure (Colbert et al., 2017) [15] . To overcome such type of outcome broad spectrum antibiotics and multivitamins are required. Excess production of gastric acid contribute to vomition, hence, use of antacid and H 2 receptor antagonist is essential to reduce gastric acid production by inhibiting proton pump on parietal cells of stomach and blocking histaminic receptors respectively. Sucralfate is basically an aluminium salt of sulfated disaccharide (sucrose sulfate) which form a complex with protein present within ulcer, hence protecting the ulcerated surface from further damage (Nakazawa et al., 1981) [16] . It also increases the mucosal concentration of prostaglandins which is important for faster mucosal healing (Candelli et al., 2000) [17] .

Acknowledgement

AcknowledgementAuthors express their gratitude to the Dean, college of Veterinary Science and Head Veterinary Clinical Complex, DUVASU, Mathura for providing necessary facilities to conduct the study.

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