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Laura Jackson

Articles, General

Complete Blood Count (CBC): Decoding the Numbers and What They Mean for Your Patients

The CBC is more than just numbers on a report — it’s a snapshot of your patient’s cellular health. It represents the dynamic interplay between peripheral cellular demand and the bone marrow response, mediated by various hormonal, neural and cytokine stimuli. And as a veterinary clinical pathology resident, I’ve come to appreciate the depth of information the humble CBC provides. Let’s break it down and explore how to interpret these values with confidence.

 

 

 

What Makes Up a CBC, and Where Do These Cells Come From?

A CBC evaluates the three major cellular components of blood: red blood cells (RBCs), white blood cells (WBCs), and platelets. But understanding these cells starts with their origins in the bone marrow.

  • Red Blood Cells (RBCs): These originate from erythropoietic precursors in the bone marrow, maturing under the influence of erythropoietin (EPO). EPO production ramps up in response to hypoxia, regulated by hypoxia-inducible factors. Immature RBCs, or reticulocytes, are released into circulation, where they complete maturation. While dogs, cats, and pigs readily release reticulocytes into circulation, horses retain them in the marrow, and healthy cattle and goats rarely have circulating reticulocytes.

 


RBC maturation. Image adapted from Veterinary Haematology, A Diagnostic Guide and Colour Atlas, John W. Harvey.

 

  • White Blood Cells (WBCs): These include:
    • Neutrophils: Mature from myeloblasts through promyelocytes, myelocytes, metamyelocytes and bands, becoming segmented neutrophils. This process takes 6–9 days, with bone marrow storing ~7x the number of circulating neutrophils.
    • Eosinophils and Basophils: Similar maturation pathways to neutrophils, with lineage distinctions becoming apparent at the myelocyte stage. Interleukin-5 released by activated T-helper cells drives eosinophil maturation.

 

Granulocyte maturation. Image adapted from Veterinary Haematology, A Diagnostic Guide and Colour Atlas, John W. Harvey.

 

    • Lymphocytes: Derived from common lymphoid progenitors. B cells mature in the bone marrow, while T cells migrate to the thymus. Both undergo rigorous selection to ensure self-tolerance; failures here can lead to immune-mediated diseases.

 

  • Platelets: Produced by megakaryocytes in the bone marrow, each generating 1,000–3,000 platelets. Their production is stimulated by thrombopoietin (TPO), and their appropriate function is critical for primary haemostasis.

 

What Does My CBC Tell Me?

The CBC provides quantitative data about the blood’s cellular components. Paired with a blood smear, it paints a complete picture of haematological health, offering insights into immune function, oxygen-carrying capacity, clotting ability, and bone marrow activity.

Key Parameters and Their Clinical Significance

  1. Red Blood Cell Indices

 

 

 

  • RBC Count, Haemoglobin (Hb), and Haematocrit (HCT):
    • HCT and PCV should give a similar result, but they are obtained differently. HCT is calculated by the analyser as ([RBC x MCV] / 10) and is therefore susceptible to artifacts affecting these indices (see below). PCV is the direct measure of the packed RBC fraction and is performed manually. This will still be affected by haemolysis (due to loss of the cells you are counting!)
    • These values indicate whether anaemia is present. HCT is typically ~3x Hb, and any mismatches exceeding 5% will be picked up and explored by your pathologist. Discrepancies are often caused by sample interference (e.g., lipemia or haemolysis).
    • Histogram analysis can identify whether analysers are misclassifying giant platelets as small RBCs or microcytes as platelets.
  • Mean Corpuscular Volume (MCV):
    • We use the Sysmex XN-V analyser. The Sysmex directly measures MCV using hydrodynamic focusing, forcing individual RBCs into a single file line which is passed through a laser beam. Increased MCV can indicate regeneration (reticulocytes are bigger than mature RBCs) or breed-specific macrocytosis (e.g., poodles). Decreased MCV may suggest iron deficiency, portosystemic shunts, or breed-specific traits (e.g., Akitas), and can also reflect in vitro cell shrinkage in hyponatraemic patients (think osmosis).
  • Mean Corpuscular Haemoglobin (MCH) & Mean Corpuscular Haemoglobin Concentration (MCHC):
    • MCH is the amount of Hb per red blood cell [(Hb/RBC) x10], and so does not account for the volume of the cell.
    • MCHC is calculated as [(Hb/HCT) x 100], which accounts for the cell volume (since HCT is calculated using MCV). Both MCH and MCHC are susceptible to the interferences which affect Hb and RBC count (e.g., lipemia falsely elevates Hb).
  • Red Cell Distribution Width (RDW):
    • Reflects anisocytosis. Elevated RDW often accompanies regenerative anaemia or recent blood transfusions, for example.
  • Reticulocyte Count:
    • A critical marker of bone marrow activity. In mild anaemia, even a “normal” reticulocyte count might signal regeneration. Manual reticulocyte counts are often necessary for cats due to the persistence of punctate reticulocytes; aggregate reticulocytes provide a clearer indication of recent bone marrow activity.
  • Nucleated RBCs (nRBCs):
    • Indicates accelerated turnover. Their presence in peripheral blood reflects the bone marrow’s attempt to meet increased demand, but it may also signify marrow disruption or extramedullary haematopoiesis.
  • Retic-He:
    • A marker of iron availability. This is an early warning for iron restricted haematopoiesis and would be low in developing iron deficiency anaemia. However, it is relatively non-specific and is commonly low in patients with neoplasia, immune mediated disease and inflammation.

 


RBC histogram created by direct current sheath flow detection. Cells which are between 40 and 150fL are classified as RBCs. The small peak to the left of the x-axis represents platelets.

 

 

  1. White Blood Cell Indices
  • Total WBC Count and Differential:
    • Many laboratory analysers will use more than one method to generate accurate total WBC counts, but nRBCs can falsely elevate these if not excluded manually. A blood smear review remains vital, and manual differential count would be performed if there are unusual changes such as neutrophil toxicity or atypical cells.
  • Neutrophil Count:
    • Neutrophilia suggests inflammation or stress (corticosteroid response). The presence of band neutrophils (left shift) signals increased inflammatory demand and can make it challenging for the analyser to accurately gate these populations.
  • Monocyte Count:
    • Elevated counts often accompany chronic inflammation but can also reflect stress.
  • Eosinophil Count:
    • Eosinophilia may point to parasitic, allergic, or paraneoplastic conditions.

 

WBC DIFF plot generated by the Sysmex XN-V. The plot on the left is from a healthy dog whilst the plot on the right is from a dog with marked toxic change and a left shift. The overlapping of the clouds indicates that the analyser is not able to confidently gate the different cell populations, and we should interpret the cell counts with caution.

 

 

  1. Platelet Parameters
  • Platelet Count:
    • Our analysers use two methods to count platelets: impedance (PLT-I) and optical (PLT-O). PLT-O uses fluorescent markers to identify platelets and tends to better mitigate the effects of platelet clumping, which can cause pseudothrombocytopenia. A blood smear review is essential to confirm platelet numbers and evaluate morphology.
    • Differentials for thrombocytopenia include consumption (usually mild reductions), immune-mediated destruction (marked reductions) and decreased production (e.g. bone marrow or infectious diseases).
  • Platelet Volume (MPV):
    • Larger platelets suggest increased turnover, as seen in recovery from thrombocytopenia or bone marrow stimulation.

 

PLT histogram illustrates the impedance method. Cells which are between 10 and 40fL are classified as PLTs. The large peak to the right of the x-axis are RBCs.

 

Why Is the CBC Useful?

A CBC helps to answer critical questions like:

  • Is the anaemia regenerative or non-regenerative?
    • Regenerative anaemia favours underlying haemorrhage or haemolysis (e.g. IMHA).
    • Non-regenerative anaemia often indicates chronic disease, iron deficiency, or bone marrow disorders (e.g., precursor-targeted immune-mediated anaemia [PIMA]).
  • What’s driving the leukocyte changes?
    • Inflammatory leukograms feature a neutrophilia and monocytosis, often with toxic change and left shifts. Stress leukograms may have a concurrent lymphopenia, and toxic changes are not present. Eosinophilia prompts investigation for parasites, allergies, or neoplasms.
  • What about platelets?
    • Mild thrombocytopenia could reflect consumption, whilst severe thrombocytopenia raises suspicion for immune-mediated thrombocytopenia (IMTP). Thrombocytosis might accompany inflammation or iron deficiency.
  • Are multiple lineages affected?
    • Bicytopenia or pancytopenia signals potential bone marrow involvement. Neutropenia and thrombocytopenia typically precede anaemia due to the longer lifespan of RBCs. Bone marrow aspiration is helpful to identify whether the marrow is responding appropriately, and may reveal underlying causes, such as leukaemia, infection (e.g., Ehrlichia, Leishmania), or immune mediated destruction (e.g., PIMA).
    • Concurrent anaemia and thrombocytopenia can create a chicken or egg dilemma – which came first? This is why a detailed clinical history is vital.

Personal Reflections on the CBC

The CBC is a powerful diagnostic tool, but the analyser is not foolproof. Throughout my residency I have learned to identify and flag erroneous results caused by factors such as RBC agglutination, hyponatraemia or sample lipemia. Identifying these unusual results and working out the mechanisms behind the error has encouraged me to gain a deeper understanding of how haematology analysers work, as well as the importance of assessing dot plots and the meaning behind the lesser-known indices which are often overlooked. Each case builds a richer understanding of the nuances in haematology.

Final Thoughts

Interpreting a CBC is both an art and a science. Each value tells a story, and together, they reveal the body’s dynamic response to health and disease. By combining analyser results, blood smear reviews, and clinical context, we can uncover the deeper narratives within our patients and provide them with the best possible care.

Next time you receive a CBC report, take a moment to appreciate the wealth of information it offers. And remember, when in doubt, look at the smear — it might just surprise you.

 

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Articles, Case Studies

Case Study: 15-Year-Old Domestic Shorthair Cat with Multiple Myeloma

Signalment

A 15-year-old domestic shorthair cat, neutered male, presented to the clinic for evaluation of lethargy, weight loss, and reduced appetite. The cat had a known history of heart failure, which was managed with medication. During physical examination, mild dehydration was noted along with pallor of the mucous membranes. There was no evidence of lymphadenopathy, however osteolytic bone lesions of the spinal vertebrae were present on radiography.

Clinical Presentation and Laboratory Findings

The initial laboratory workup revealed several abnormalities. The cat had a marked hyperglobulinemia with a globulin level of 160 g/L, accompanied by a markedly low albumin-to-globulin (AG) ratio of 0.1, indicating a hyperproteinaemia state driven by an elevated globulin fraction. Blood tests also revealed moderate azotaemia, which could be a result of renal impairment either due to hyperproteinaemia or as an independent comorbidity in this older cat. Additionally, a moderate neutrophilia was noted, alongside mild non-regenerative anaemia, which is often associated with chronic inflammation or neoplasia.

Cytologic Findings

Fine-needle aspirates were taken from the liver and spleen to further investigate the hyperglobulinemia and other laboratory abnormalities. Cytologic evaluation of the spleen revealed a large population of discrete cells with moderate pleomorphism, eccentric nuclei, and deeply basophilic cytoplasm. These cells exhibited moderate anisocytosis and anisokaryosis and occasional binucleation. Occasional mitotic figures were seen. A similar cytologic picture was observed within the liver. The cytological findings were consistent with plasma cell neoplasia.

 

 

Diagnosis and Discussion: Plasma Cell Neoplasia in Cats

Multiple myelomas are plasma cell neoplasms that originate in the bone marrow and infiltrate other organs, whilst solitary plasma cell tumours in organs other than bone marrow are plasmacytomas.  Neoplastic plasma cells secrete abnormal immunoglobulins which appear as a monoclonal spike on protein electrophoresis. Diagnostic criteria for multiple myeloma, initially outlined by MacEwen and Hurvitz in 1977 for dogs, require at least two of four specific indicators: (1) paraproteinemia or monoclonal gammopathy, (2) radiographic evidence of osteolytic bone lesions, (3) Bence Jones proteinuria (abnormal immunoglobulin light chains in urine), and (4) greater than 5% neoplastic plasma cells in the bone marrow. In this case, cytologic evidence of an atypical plasma cell proliferation in both the liver and spleen, alongside a marked hyperproteinaemia and presence of osteolytic lesions is strongly suggestive of multiple myeloma, although bone marrow samples were not obtained for confirmation.

Clinical signs of multiple myeloma are non-specific and can include lethargy, anorexia and weight loss. Initial work up may reveal renal impairment, anaemia and osteolytic lesions. However, osteolytic bone lesions, a hallmark of multiple myeloma in dogs, are less frequently observed in cats. An azotaemia (as seen in this case) may reflect existing renal compromise or reduced glomerular filtration rate secondary to hyperviscosity syndrome.

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Articles, Case Studies

Case of the Month: Hepatocutaneous Syndrome in a Cavalier King Charles Spaniel

Clinical history

Chucky was presented to the primary veterinary care practice with a 1 month history of hyperkeratosis, crusting and erythema of the skin of all four paws. A previous canine biochemical profile conducted at VPG revealed significantly elevated alkaline phosphatase (ALP), alanine transaminase (ALT), glutamate dehydrogenase (GLDH) and bile acids. A small liver was detected on abdominal ultrasound.

Histology

Haired skin from the feet and an additional lesion in the perianal region were sampled by the veterinarian, fixed in formalin and submitted to VPG for histopathological examination.

The epidermis (surface layer of the skin) was markedly thickened in the samples. Specifically this comprised a thick keratin layer with retention of nuclei (parakeratosis) and overlying this, a prominent neutrophilic crust, an oedematous and pale stratum spongiosum (middle epidermal layer) and a prominently proliferative basal cell layer. This created a distinct ‘red, white and blue’ pattern, colloquially termed the ‘French flag’ sign by pathologists. Surface bacterial colonies were also seen. Some mild separation or splitting through the pale stratum spongiosum was observed (‘necrolysis’). The underlying dermis was variably inflamed with mixed infiltrates of neutrophils, lymphocytes and plasma cells. Adnexa were largely unaffected.

hepatocutaneous syndrome

Figure 1. Low magnification image of the skin. The epidermis is markedly thickened (black arrow heads). The underlying dermis is mildly oedematous and inflamed (white arrow heads).

hepatocutaneous syndrome

Figure 2. Higher magnification of the epidermal surface reveals a markedly thickened stratum corneum, expanded by parakeratosis  and neutrophilic infiltrates (red). The middle layer is pale and swollen with intracellular and intercellular oedema (white). The basal and suprabasilar layers are hyperplastic (blue). Surface colonies of bacteria are present.

 

Interpretation: 

Superficial necrolytic dermatitis (SND) or ‘hepatocutaneous syndrome’

More information on superficial necrolytic diagnosis: 

Superficial necrolytic dermatitis (SND; also known as hepatocutaneous syndrome) is a necrotising skin disease, most commonly seen in older dogs, but is rarely recognised in cats (1). It is a rare and poorly understood disease, usually associated with a poor prognosis. Most cases reported are associated with an underlying metabolic liver disease or pancreatic neuroendocrine neoplasia [2].

The precise pathogenesis is yet to be elucidated but is essentially a result of a ‘cutaneous nutritional deprivation’ which results in superficial skin necrosis [1]. It does partly resemble the condition necrolytic migratory erythema (NME) in human beings and could have a similar mechanism. The human NME condition is often a result of a glucagonoma with hyperglucogonaemia thought to play a role – typically associated with pancreatic neoplasia. It is likely involved with a catabolic state and dysregulation of metabolism of amino acids, proteins, zinc and essential fatty acids resulting in deficiencies [1, 3]. Reduced peptide synthesis at the epidermis may be a result of this, and hypoaminoacideamia may also increase arachidonic acid production to increase epidermal inflammation [3]. However,  pancreatic tumours are only associated with a small number of canine SND cases. In dogs, hepatic metabolic dysfunction is still likely to drive a hypoaminicadaemia through catabolism of amino acids [1, 4] with the result of a similar cutaneous insult. Other infrequent case reports indicate other causes of underlying liver damage such as a previous history of phenobarbital administration [5]. Regardless of the underlying cause, hypoaminoacidaemia appears to be consistent.

The most common clinically identified findings reported in a relatively recent review [6] were skin lesions affecting the pawpads or mucocutaneous junctions (100% of cases) and plasma hypoaminoacidaemia (100% of cases) – an amino acid profile was thus suggested by the authors [6] as a possible non-invasive aid for the diagnosis of SND. A further study [7] revealed hypoaminoacidaemia in dogs with SND was associated with marked lysinuria, essentially indicating wasting of this amino acid which is one crucial for collagen synthesis. Clinico-pathological abnormalities in one case study commonly revealed microcystosis (63%) and consistently elevated serum alkaline phosphatase activity (100 %) [8].

Diagnosis in practice

Despite the recent case series describing amino acid profiling (see above),  more often the  diagnosis of SND is made from skin biopsies of intact lesions (which have not become ulcerated or masked by secondary infection) which reveal the pathognomonic ‘red, white and blue’ skin pattern in conjunction with a liver biopsy/or clinical correlation of liver disease (such as abdominal ultrasound examination). Abdominal ultrasound of the affected animal may also help differentiate between obvious hepatic pathology or pancreatic neuroendocrine neoplasia.

Differentials clinically include autoimmune disease such as pemphigus foliaceus/SLE, zinc responsive dermatosis (which also causes parakeratosis/hyperkeratosis) and erythema multiforme [1] – these should be differentiated on histological examination.

In this case, chronic liver disease was suspected to be cause for SND although no further detailed investigation was conducted.

Treatment is typically symptomatic and supportive [1]. A recent study [9] reviews treatment regimes following diagnosis of SND.

 

References:

  1. Gross, T.L., Ihrke, P.J., Walder, E.J. and Affolter, V.K., 2008. Skin diseases of the dog and cat: clinical and histopathologic diagnosis. John Wiley & Sons.
  2. Smith, J. (2016). Superficial necrolytic dermatitis. In Vet Times [Internet]. URL: https://www.vettimes.co.uk/app/uploads/wp-post-to-pdf-enhanced-cache/1/superficial-necrolytic-dermatitis.pdf
  3. Foss, M. G., Hashmi, M. F., & Ferrer-Bruker, S. J. (2022). Necrolytic migratory erythema. In StatPearls [Internet]. StatPearls Publishing.
  4. Outerbridge, C.A., Marks, S.L. and Rogers, Q.R., 2002. Plasma amino acid concentrations in 36 dogs with histologically confirmed superficial necrolytic dermatitis. Veterinary Dermatology, 13(4), pp.177-186.
  5. March, Philip A., Andrew Hillier, Steven E. Weisbrode, John S. Mattoon, Susan E. Johnson, Stephen P. DiBartola, and Peter J. Brofman. “Superficial necrolytic dermatitis in 11 dogs with a history of phenobarbital administration (1995–2002).” Journal of Veterinary Internal Medicine 18, no. 1 (2004): 65-74.
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