Case study: Jess

Diagnostic plan

In view of the relative bradycardia and clinical signs consistent with hypovolaemia and dehydration the following actions were taken: intravenous access was obtained, blood samples for laboratory testing were collected before any treatment, blood pressure was measured (100mmHg systolic) and intravenous fluids were administered via boluses to address the hypovolaemia and more slowly to address dehydration.  

Blood samples were used for full haematology, serum biochemistry and measurement of electrolytes. Ideally urinalysis would have been performed but the bladder was relatively empty at presentation. 

Results of laboratory tests

The red blood cell and platelet counts were within normal limits. There was leukopenia due to neutropenia.
Serum biochemistry revealed mild elevations of SDMA, urea and creatinine, hypoproteinaemia due to hypoalbuminemia and hypoglobulinaemia and hypocholesterolaemia and sodium to potassium ratio was within normal limits.

Interpretation of laboratory test results

The normal platelet count excludes thrombocytopenia as a cause of the gastrointestinal bleeding. Coagulation times were not assessed but could have been useful to exclude other systemic bleeding causes before considering the possibility of an intestinal or infectious cause. 

Neutropenia can indicate lack of production, overwhelming consumption/utilisation or destruction of neutrophils. It is worth bearing in mind that the lymphocyte and eosinophil counts were within reference intervals (absence of a stress leukogram) despite the collapsed state of the dog. 

The mild azotaemia and elevated SDMA could be secondary to dehydration/hypovolaemia (pre-renal) or reflect renal or post renal causes. Pre-renal was considered likely given the clinical examination and history. Urinalysis would have been helpful to further assess this, however the bladder was too small to obtain a sample and fluids had already been given at the referring practice. The fluid therapy before referral may have impacted on the blood results at presentation. 

In this case, the hypoalbuminaemia most likely reflected the loss of albumin due to acute gastrointestinal bleeding, however loss due to an underlying protein losing enteropathy cannot be excluded. Protein loss via the urogenital tract or decreased hepatic synthesis would typically result in hypoalbuminemia without hypoglobulinaemia. 

Further investigations

Although electrolyte concentrations were normal, the relative bradycardia, lack of stress leukogram, mild azotaemia and collapse led to clinical concern for hypoadrenocorticism. An ACTH stimulation test was performed and revealed undetectable levels of cortisol pre and post administration of intravenous tetracosactide (Dechra) at 5µg/kg confirming the presence of hypocortisolaemia. Since the electrolytes were normal at presentation, it was unclear whether this dog needed mineralocorticoid in addition to glucocorticoid supplementation. Aldosterone was therefore measured on the pre and post ACTH samples; both aldosterone results were subnormal indicating lack of response to stimulation thus confirming a lack of mineralocorticoid production. Primary hypoadrenocorticism /Addison’s disease was diagnosed. 

In view of the acute haemorrhagic diarrhoea and leukopenia which are unusual in Addison’s disease, (Snead et al, 2011), a SNAP Parvo test (Idexx) was performed which was negative. Other infectious causes of acute haemorrhagic diarrhoea were considered as the hypoproteinaemia and neutropenia were more severe than typically seen in Addison’s disease and there was an outbreak of Leptospirosis locally at the time. Leptospirosis serology was performed using the original blood sample (acute period) revealing no significant elevation in the antibody titres of the serovars tested. However, the PCR test (EDTA blood sample) detected the presence of DNA confirming acute infection with pathogenic leptospires. 

Once Jess was clinically stable, abdominal ultrasound was performed which showed moderate distension of the caecum and colon with anechoic fluid. Although the overall wall thickness was within normal limits, there were diffuse changes in the jejunal wall layering (muscularis and submucosal layers). The jejunal lymph nodes were slightly enlarged and irregular but were considered most likely to be reactive. The adrenal gland measurements were slightly smaller than normal. 

In view of the ultrasonographic findings and the report of chronic diarrhoea, serum TLI, cobalamin (vitamin B12) and folate were measured to assess intestinal function; decreased cobalamin and folate suggestive of diffuse small intestinal disease and malabsorption were present.

Diagnostic tests