Example reports

Pathologica-generated reports using SI or conventional units for canine cases

• Biochemistry results only

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  Example report: Biochemistry data only

  8 year old, Female neutered, Cross breed

  Intermittent vomiting, vaccinated, polyuria-polydipsia (PUPD)

  Analytical Check

  There may be EDTA artifact. Repeat testing may be indicated for accurate measurement of some test parameters.

  Biochemistry

  Test	Result	Ref.	Units
  TP	5.8	5.4 - 8.2	g/dL
  Alb	3.2	2.5 - 4.4	g/dL
  Glob	2.6	2.3 - 5.2	g/dL
  Na	146	138 - 160	mmol/L
  K	5.0	3.7 - 5.8	mmol/L
  tCa	8.2	8.6 - 11.8	mg/dL
  Phos	7.5	2.9 - 6.6	mg/dL
  BUN	18.5	2.5 - 8.9	mg/dL
  Cre	3.0	0.3 - 1.4	mg/dL
  ALT	19	10 - 118	U/L
  ALP	40	20 - 150	U/L
  tBil	0.2	0.1 - 0.6	mg/dL
  Glu	75	60 - 110	mg/dL
  Amy	1800	200 - 1200	U/L

  Analysis

  The azotaemia supports renal failure, given the significant increase in BUN (18.5) and creatinine (3.0). The hyperphosphataemia (7.5) also then reflects renal failure. The increased amylase in this instance is likely then due to reduced renal clearance too.

  Given the potassium (5.0) together with the decreased calcium (8.2), anti-coagulant contamination (eg. EDTA) may be a consideration. However, in this instance, acid-base disturbances and the resulting anion gap (eg. ethylene glycol toxicity, lactic acidosis) may be more likely.

  Recommendations

  Abdominal imaging for renal changes would be recommended. Additional urinanalysis would more fully evaluate renal function. If significantly hypersthenuric (USG > 1.030) pre-renal failure is likely, classically USG being even higher. Given supportive clinical signs, differentials would then include dehydration or cardiac disease. If however isosthenuric (USG 1.008-1.012) and significantly proteinuric (ratio > 0.5), intrinsic renal failure and chronic disease (eg: chronic interstitial nephritis or neoplasia, primary or secondary) are more likely. The urinanalysis should include sediment microscopy and bacterial culture, even though the failure to detect bacteria does not exclude pyelonephritis.

  This analysis, especially urinary sediment for any significant crystalluria (eg: calcium oxalate monohydrate) would support a toxicosis, as well as expected acidic urine for a metabolic acidosis. Similarly, fresh serum/plasma testing may be warranted to exclude the possible EDTA contamination.

  Disclaimer: This analysis applies only to the data inputted and is not a clinical diagnosis.

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• Haematology results only

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  Example report: Haematology data only

  2 year old, Male, Springer Spaniel

  Lethargic, Inappetant

  Analytical Check

  The markedly increased MCV may be agglutination artifact. Repeat testing may be indicated for accurate measurement of some test parameters.

  Haematology

  Test	Result	Ref.	Units
  RBC	0.9	5.5 - 8.5	1012/L
  Hgb	36	120 - 180	g/L
  HCT	12	37 - 50	%
  MCV	114	60 - 77	fL
  MCH	22.0	19.5 - 24.5	pg
  MCHC	300	310 - 390	g/L
  RDWc	22.2	14.0 - 20.0	%
  PLT	284	165 - 500	109/L
  MPV	7.5	3.9 - 11.1	fL
  WBC	96.1	6.0 - 17.0	109/L
  Neu	69.1	3.0 - 12.0	109/L
  Lym	0.5	1.0 - 4.8	109/L
  Mon	5.3	0.2 - 1.5	109/L
  Eos	0.0	0.0 - 0.8	109/L
  Bas	0.0	0.0 - 0.4	109/L

  Analysis

  The anemic pattern supports hemolysis with expected regeneration, given no clinical bleeding (eg: hematuria, epistaxis, hematemesis) is evident nor biochemically supported (eg: panhypoproteinemia). Whilst often primary and idiopathic, due to immune-mediated destruction, an underlying infectious trigger or oxidative damage are possible differentials.

  The markedly increased mean cell volume (MCV) is often in part regenerative, but to this degree can also be artefactual due to erythrocyte agglutination. This then falsely increases the hematocrit (HCT), so monitoring the hemoglobin (Hb) during therapy can be more accurate.

  The noted leucocytosis is commonly seen due to concurrent systemic inflammation but can also be seen with infectious etiologies. The lymphopenia in this instance is non-specific and may well relate to endogenous stress.

  Recommendations

  If there are no specific external signs, then internal imaging (abdominal and thoracic) would be recommended for an inflammatory trigger of the anemia (eg: pancreatitis). Potential infectious etiologies depend in part on travel history and vector-borne risk, but would commonly include parasites and bacteria (eg: Ehrlichia and Babesia). These may be visible in the smear within the white and red cells, respectively, but specific PCR testing would be warranted for their exclusion.

  Given no recent exogenous drug exposure (eg: penicillins), an ingested toxin would remain a consideration. These are often oxidative (eg: zinc, onion, garlic), with resulting erythrocyte changes, such as eccentrocytosis and Heinz body formation being evident within the blood smear.

  Polychromasia and/or anisocytosis would also be expected in the blood smear. If the hemolysis is otherwise immune-mediated, spherocytosis, ghost cells and/or erythrocyte agglutination are often seen. If there is agglutination (microscopic), in-saline testing of the EDTA sample would be recommended to confirm and exclude rouleaux formation.

  Given the MCV in this case, macroscopic agglutination may be visible and justify repeat analysis after in-saline dilution for more accurate assessment of erythrocyte parameters.

  With the leucocytosis, the blood smear assessment may confirm toxic changes within the neutrophils or reactive changes in the mononuclear cells to support inflammation. It would also discriminate nucleated red cells from lymphocytes and could exclude an atypical mononuclear cell population for pathological review. Intracellular infectious agents may also be evident (eg: Ehrlichia).

  Disclaimer: This analysis applies only to the data inputted and is not a clinical diagnosis.

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• Biochemistry and haematology values, combined with clinical signs

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  Example report: Biochemistry and haematology data, combined with clinical signs

  4 year old, Male, Golden Retriever

  Clinical history includes: Vomiting, Unvaccinated, Scavenging, Acute illness.
  No clinical report of: Jaundice, Collapsing, Cavity effusion, Dehydration.

  Analytical Check

  In this instance, the calculated hematocrit (HCT) appears falsely decreased. This is often due to in vitro relative EDTA effects or altered MCV due to specific disease processes. Repeat sampling could then be indicated to exclude EDTA effects, if not otherwise noted in the sample analysed (eg: over or underfilled). Otherwise the blood smear examination should reveal significant microcytosis and/or macroplatelets.

  Biochemistry

  Test	Result	Ref.	Units
  TP	7.7	5.4 - 8.2	g/dL
  Alb	2.7	2.5 - 4.4	g/dL
  Glob	5.0	2.3 - 5.2	g/dL
  Na	149	138 - 160	mmol/L
  K	3.7	3.7 - 5.8	mmol/L
  tCa	2.2	2.2 - 3.0	mmol/L
  Phos	3.7	0.9 - 2.1	mmol/L
  Urea	62.3	2.5 - 8.9	mmol/L
  Cre	710	27 - 124	umol/L
  ALT	285	10 - 118	U/L
  ALP	356	20 - 150	U/L
  tBil	8	2 - 10	mmol/L
  Glu	5.1	3.3 - 6.1	mmol/L
  Amy	700	200 - 1200	U/L

  Haematology

  Test	Result	Ref.	Units
  RBC	7.0	5.5 - 8.5	1012/L
  Hgb	160	140 - 180	g/L
  HCT	37	35 - 52	%
  MCV	68	60 - 77	fL
  MCH	22.0	19.5 - 24.5	pg
  MCHC	350	310 - 390	g/L
  RDWc	17.0	14.0 - 20.0	%
  PLT	300	165 - 500	109/L
  MPV	7.5	3.9 - 11.1	fL
  PCT	0.35	0.2 - 0.5	%
  PDWc	38.6	38 - 40	%
  WBC	19.0	6.0 - 17.0	109/L
  Neu	16.5	3.0 - 12.0	109/L
  Lym	1.0	1.0 - 4.8	109/L
  Mon	0.8	0.2 - 1.5	109/L
  Eos	0.1	0.0 - 0.8	109/L
  Bas	0.0	0.0 - 0.1	109/L

  Analysis

  The azotaemia supports evidence of renal failure, given the increase in BUN (62.3) and creatinine (710), which could be at least in part, pre-renal in this instance. The hyperphosphataemia (3.7) also then reflects renal failure. The haematology is non-specific but consistent with systemic stress, likely renal-related in this instance. The leukogram is non specific, however the neutrophilia could relate to systemic inflammation or infection (eg. Leptospira infection, pyelonephritis).

  The recent clinical onset would support acute renal failure due to circulatory collapse or potentially nephrotoxin ingestion (eg: ethylene glycol).

  The relative hepatic enzymatic increases indicate hepatic parenchymal disease, which could include biliary-associated pathology such as cholangiohepatitis. They could also result from a chronic (primary) hepatitis though, often presumptively immune-mediated and idiopathic, but in some cases can be copper-associated. Alternatively, the hepatopathy could result from any cause of hepatocyte damage or severe hepatocyte vacuolation, such as an infectious process of the parenchyma (eg: Leptospirosis, Adenovirus, etc, especially if unvaccinated) or an ascending infection from the GI system, neoplasia (primary or secondary), a toxic hepatic insult or significant endocrinopathy. With the known scavenging behaviour, an acute toxic insult may remain a differential. Given the concurrent renal and hepatic disease, Leptospirosis is a primary differential for initial further investigations. More rarely, multiorgan neoplasia, such as lymphoma or disseminated histiocytic sarcoma, can present similarly.

  Recommendations

  Urinanalysis would more fully evaluate renal function, especially urinary specific gravity and sediment analysis for any significant crystalluria (eg: calcium oxalate) as well as expected acidic urine if acidotic (eg: metabolic such as ingested metaldehydes). If poorly concentrating (such as SG 1.013 - 1.030), acute-on-chronic renal disease may be more likely.

  Abdominal ultrasound could further evaluate the cause of the renal failure, as well as identifying any concurrent disease (eg. GI disease) if clinical signs are otherwise non-specific.

  Hepatic imaging is then recommended with potentially aspiration of any focal lesions or significant sonographic changes in the parenchyma. Otherwise, prior coagulation screening (PT and APTT) would be indicated for more invasive biopsying and histopathology. Fresh tissue sampling could also be considered for further testing, such as toxin measurement, qPCR and/or culture. Further more sensitive evaluation of hepatic function via pre and post prandial bile acids could also be considered. However, this does not discriminate the type of hepatic disease. Additionally in this instance measurement of specific ingested toxins would be a consideration on fresh tissue (eg: biopsy, blood, urine). Given the lack of a vaccinal response, initial Leptospira screening via serology could be undertaken, with a positive and even rising titre supporting likely Leptospirosis.

  Disclaimer: This analysis applies only to the data inputted and is not a clinical diagnosis.

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