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The Minimum Data Base

Haematology, Chemistry and Urinalysis

The standard minimum database includes a complete blood cell count (CBC) or hematology with peripheral blood film review, serum biochemistry, and urinalysis.

Many cases of neurological dysfunction with a metabolic etiology have significant and sometimes specific minimum database abnormalities. However, many animals with diseases restricted to the central nervous system do not present with specific minimum database findings. Regardless, this information can be useful in detecting concurrent and potentially unrelated systemic diseases and may direct further investigation.

Infectious and sterile inflammatory disease processes demonstrate non-specific hematological changes and some biochemical abnormalities. Neoplastic and toxic disease processes may also manifest hematological, biochemical, and urinalysis changes.

Specific microscopic abnormalities may be present in peripheral blood or urine sediment in some cases, such as disseminated fungal/pseudofungal infection, vector-borne infections, acute canine distemper viremia, multiple myeloma, other lymphoid neoplasia, ethylene glycol intoxication, and lysosomal storage diseases.

In the emergency patient with primary neurological disease, data from “bedside tests” such as total protein and packed cell volume can reveal abnormalities that require prompt treatment.

Packed cell volume and Total protein

The brain relies solely on aerobic metabolism and is therefore very susceptible to hypoxic damage. It is crucial to maintain an adequate concentration of circulating hemoglobin to ensure adequate delivery of oxygen to the tissues. In cases of head trauma and raised intracranial pressure from any cause, the brain is especially vulnerable. Thus, early correction of low circulating hemoglobin concentration will optimize oxygen delivery to the brain.

Plasma proteins play an important role in maintaining colloid osmotic pressure (COP) and thus vascular volume, in addition to their other homeostatic functions. Animals with low protein levels are at risk of developing edema, so fluid therapy must be tailored to their needs.

PCV and TP measurements are easily performed. Ensure that the samples are taken into the correct volume of anticoagulant, are spun for the appropriate duration and always ensure that the refractometer is calibrated. When there are concerns that a patient has raised intracranial pressure (ICP), and blood tests are required, consider sampling from a large intravenous catheter at the time of placement or from other peripheral veins. Always avoid jugular occlusion when blood sampling in emergency patients.


Inadequate glucose supply to the brain, neuroglycopaenia, can directly lead to CNS signs. These include altered mentation, weakness and recumbency, ataxia, alterations in vision, and seizures. Before overt neurological signs, pacing, restlessness and vocalization may be evident. These are not however consistent signs. There is some evidence that chronic hypoglycemia, as is seen in insulinoma cases, may result in the upregulation of cerebral glucose uptake associated with the preservation of neurological function. Hyperglycaemia may result in neurological signs and severe hyperglycaemia may manifest as hyperglycaemia-hyperosmolar syndrome, a complication of diabetes mellitus. 


The primary electrolytes that we consider relevant in disease processes in the neurological patient are sodium (Na+), potassium (K+), calcium (Ca2+), magnesium (Mg2+), and chloride (Cl).  Hydrogen carbonate (HCO3−) is addressed in the blood gas analysis section. There is a subtle and complex electrolyte balance between the intracellular and extracellular compartments.  Electrolytes may enter or leave the cell membrane through various ion channels. The maintenance of osmotic gradients of electrolytes is important. Such gradients affect and regulate the hydration of the body, and blood pH, and are critical for nerve and muscle function. Various mechanisms exist in living species that keep the concentrations of different electrolytes under tight control. The major extracellular ions are sodium (Na+) and chloride (Cl-). The major intracellular ions are potassium (K+) and magnesium (Mg2+)


Normal animals deprived of water for considerable periods of time can become severely hypernatraemic. The loss of low sodium fluid through vomiting, diarrhoea or polyuria may also cause hypernatraemia. In the primary neurological patient the most common cause is probably central diabetes insipidus which may occur secondary to traumatic brain injury, pituitary masses and has been reported in granulomatous meningoencephalitis, hydrocephalus and CNS lymphoma. 

Iatrogenic hypernatraemia can result from excess NaCl administration, either orally or via intravenous fluids (e.g hypertonic saline or sodium bicarbonate). Serum sodium in excess of 180 mEq/l (mmol/L) may be associated with neurological signs such as head pressing, stuporous, progressing to coma, seizures and death. Hypernatraemia causes free water to move out of the cell into the relatively hyperosmolar extracellular space, leading to a decreased cell volume. This results in the formation of intracellular osmolytes in order to replenish cell volume – complete compensation can take 24 hours. These osmolytes must be considered during the management of hypernatraemia.

Patients with hypernatraemia have a free water deficit, and should be managed as such, aiming to reduce serum sodium by no more than 0.5 mEq/L/hour (mmol/L/hour). Rapid drops in plasma sodium concentration (and therefore osmolality) cause a rapid movement of free water back into the intracellular space. Overly rapid correction will result in cellular swelling – i.e., neuronal oedema because the osmolytes are broken down relatively slowly. 


Hyponatraemia is relatively uncommon in critically ill dogs and cats, but neurological patients with head trauma or intracranial masses, particularly pituitary lesions may be predisposed to developing it. Dogs and cats with hyponatraemia almost always have free water retention rather than an absolute sodium deficit. When serum sodium falls below 120 mEq/L(mmol/L) or falls rapidly, clinical signs may be evident. These include obtundation, seizures, head pressing, coma and death.

Hyponatremia itself produces brain edema, because it causes free water to move into the relatively hyperosmolar cell. This may result in increased intracranial pressure which potentially leads to subsequent neuropathological sequelae or death. When serum sodium decreases, the brain prevents further cellular swelling by extruding intracellular electrolytes and organic osmolytes, a process almost fully achieved after 48 hours. Conversely, during the subsequent increase in serum sodium, reestablishment of intracerebral osmolytes occurs but their reuptake is more delayed (+/- 5 days). Rapid or excessive correction of this hyponatraemia can be followed by development of brain demyelinating lesions (central pontine myelinolysis also known as osmotic demyelination syndrome). This is a result of neuronal shrinking as water moves out of the cell during correction of hyponatraemia – i.e., as extracellular osmolality increases, water is drawn into the extracellular space. Guidelines suggest that sodium should not be corrected at a rate greater than 0.5 mEq/L/hour.

Other Biochemical Assays

Specific analytes can be measured in the serum of neurologic patients, either if indicated by abnormalities identified by the minimum database tests or for therapeutic monitoring (e.g. thyroid hormone level, anticonvulsant serum concentration). Commercial laboratories can perform many of these tests; however, test availability and sample handling needs may vary with each laboratory. Local commercial laboratories should be contacted for their specific sample handling requirements.


Bedside urinalysis tests include urine specific gravity (USG) and a dipstick. Cytology, culture and further tests including urine protein:creatinine ratio may be indicated in the diagnosis and management of specific diseases. Urine volume depends on hydration status and renal concentrating ability and is inversely related to the USG. Urine concentration will affect the depth of the colour. Cloudy red urine that clears after centrifugation is seen when RBCs (hematuria) are present. Dark red to brown color may be due to haemoglobinuria or myoglobinuria. Yellow-brown, greenish-yellow, or dark brown urine may be due to bilirubinuria. Other urine colours may result from certain drug therapies. 

Urine is normally clear. Semen, mucus, and lipid may cause turbidity in normal urine. Increased numbers of cells, crystals, casts, or organisms can increase the turbidity of urine in disease conditions. An unpleasant odor may indicate sepsis. Animals with ketosis/ ketoacidosis may have urine with an acetone odor.

Urinalysis in conjunction with USG is a useful indicator of renal perfusion and volume status in an animal with previously normal renal and endocrine function. An elevated USG and a low urine output suggest hypovolaemia.

Urine SG may also provide additional information to support a diagnosis of endocrine disease. Dogs with Cushing’s syndrome and central or nephrogenic diabetes insipidus (DI) are often hyposthenuric (can be isosthenuric).Central DI may occur with pituitary neoplasia, after head trauma or craniectomy. Secondary nephrogenic DI is very common and is caused by a failure of the kidney to respond to vasopressin. Other differential diagnoses that must be considered when USG is inappropriately low include chronic renal failure and ethylene glycol toxicity, which also results in the formation of calcium oxalate monohydrate crystals. 

Note that many drugs including steroids, diuretics, phenobarbitone and alpha 2 agonists can have effects on USG.

Differentials for myoglobinuria include seizures, crush injury and severe muscle disease (e.g. necrotizing myopathy).

Urine samples obtained by catheterisation may have red cell, epithelial cell, lubricant and bacterial contamination. Free catch samples are also non-sterile. Cystocentesis samples may contain red cells but are indicated where urinary culture is required. Urine is unstable and must be analyzed promptly.  It should be collected in clean or sterile containers and if not analyzed within a short period of time, it should be refrigerated. Cold urine should be allowed to return to room temperature prior to analysis to avoid a false increase in specific gravity. Precipitates may form in urine as it cools, and cold may interfere with some chemical tests. Always ensure that refractometers are calibrated prior to use.

Dipstick analysis

Dipsticks are labile. They must be kept dry, in well-capped jars, and used prior to the expiration date for accurate results. Prolonged exposure to air may cause false positive tests for glucose and false negative tests for occult blood.

  1. Urine pH. 

Acidic urine is caused by increased acid excretion or production (increased protein catabolism, metabolic or respiratory acidosis, paradoxical aciduria with alkalosis). Alkaline urine is caused by increased alkali excretion or production (decreased protein catabolism, cystitis due to urea-splitting bacteria, prolonged storage at room temperature, metabolic or respiratory alkalosis). Urine pH is not an accurate indicator of systemic acid/base balance.

2. Protein. 

Urine protein results always must be interpreted in conjunction with specific gravity. A small amount of protein normally is present in urine and may be detected in concentrated urine. Many false positive protein tests occur, especially with alkaline urine. The protein test mainly detects albumin on the dipstick. Physiologic pre-renal proteinuria may result from excessive muscular exertion, convulsions, or excess protein ingestion. Pathologic proteinuria may be pre-renal (hemoglobinuria, myoglobinuria), renal (glomerular or tubular), or post-renal (urogenital hemorrhage or inflammation). 

3. Glucose

Glucose, an abnormal finding in urine, occurs when blood glucose levels exceed the renal threshold for reabsorption. Glucosuria with hyperglycaemia occurs in diabetes mellitus, dextrose administration, or secondary to catecholamines or glucocorticoids. Glucosuria without hyperglycaemia may occur when hyperglycaemia is transient or in selective renal proximal tubule dysfunction. Urine containing glucose is an excellent culture medium for bacteria.

4. Ketones

Ketonuria occurs when ketone production exceeds the renal tubular absorption capacity. Dipsticks are semi-quantitative only. The urine ketone test detects acetoacetate, but not beta hydroxybutyrate. False positive test results may occur if urine is highly pigmented. False negative test results are uncommon in fresh urine but may occur where urine has been standing due to the volatility of ketones.

Ketonuria may occur in diabetic ketoacidosis,, pregnancy, ketosis, insulinoma  glycogen storage disease or starvation.

5. Hemoprotein (occult blood). 

Haemoproteinuria may result from increased RBCs (haematuria, especially dilute urine with lysed RBCs), haemoglobinuria, or myoglobinuria. Sediment evaluation may differentiate haematuria from haemoglobinuria and myoglobinuria. Typically, red urine supernatant indicates haemoglobin or myoglobin. Haemoglobinuria is often accompanied by haemoglobinemia.

6. Bilirubin. 

Dogs with concentrated urine may have trace to 1+ bilirubinuria; they have a lower renal threshold for bilirubin than do other species, and canine renal epithelium also can conjugate and excrete bilirubin (especially in male dogs). 

7. Urobilinogen should not be relied upon in dogs and cats. 

Normal ranges:

Urine specific gravity is one of the most important tests in a urinalysis and should be done using refractometry (DO NOT use dipstick tests for specific gravity). Turbidity of the urine can affect the specific gravity (usually increase it). Ideally urine should first be centrifuged and the supernatant used for determination of specific gravity. 

Normal specific gravity values vary widely (usually between 1.015 and 1.045, up to 1.065+ in cats) depending on hydration status and water intake. 

Cat urine contains different solutes than dog urine; therefore, some refractometers have separate scales for cat urine to adjust for this. Specific gravity must be evaluated in light of BUN/creatinine values and hydration status. Abnormal substances such as glucose and proteins may falsely increase the specific gravity.

Tests of Haemostasis

Animals with defects in hemostasis may present with neurological signs secondary to hemorrhage; for example, spinal cord or brain parenchymal bleeding secondarily to Angiostrongylus infection or anti-coagulant toxicity. In addition, there is some evidence that traumatic brain injury may itself result in coagulopathy, at least in humans. Defects in platelet numbers or function may be related to the presenting clinical signs; for example, thrombocytopenia in disseminated intravascular coagulation (DIC), or may be due to an unrelated disease process, for example thrombocytopathia in Von Willebrand’s disease. 

Animals with primary hemostatic disorders may present with petechiae or ecchymoses and spontaneous hemorrhage from mucosal surfaces. This may include hyphema, hematuria, epistaxis and melena. However they commonly present in a similar manner to animals with defects of secondary hemostasis, which are characterized by multiple hematomas, bruises (subcutaneous bleeding), hemorrhage into joints and body cavities. Acquired disorders, for example DIC, do not fit this description because of the multiple abnormalities often present. There should be a systemic approach to the assessment of hemostasis and this should be based on the clinical and neurological examinations.

Clinical relevance

Thrombocytopenia is a common finding in critically ill patients and results from either lack of platelet production, sequestration, consumption or destruction. It is important to determine the underlying cause of the thrombocytopenia, to determine whether the platelet count is low enough to warrant therapy and then to act accordingly. 

Thrombocytopathia may also be present, and may be inherited, such as with Von Willebrand’s disease or acquired, either as a result of drug administration or secondary to other disease processes, such as neoplasia. 

Coagulopathies result from defects in the coagulation cascade. They may be either acquired, (e.g., DIC, hepatopathies, pharmacologic administration of anti-coagulants and vitamin K or rodenticide toxicity) or they may be inherited. The extrinsic (tissue factor) and common pathways of the coagulation cascade can be assessed by determining prothrombin time (PT),  the intrinsic (contact activation) and common pathways by determining the activated partial thromboplastin time (APTT).

Testing and normal ranges

Platelets should always be counted manually on a smear. Sampling (for example clumping) and laboratory artefacts can give erroneous results. Greyhounds tend to have lower numbers of platelets and Cavalier King Charles spaniels may have macroplatelets. In cats, there is an overlap in size between platelet and red blood cells, potentially leading to inappropriate platelet counts with automated cells counters.

Normal platelet counts are 200 000 – 800 000 cells/µL, which equates to 8-15 platelets per (x100) high power field. Platelet counts below 20 000 - 50 000 cells/µL may lead to clinical bleeding. 

Buccal mucosal bleeding times (BMBT) should be performed in any animal where a primary haemostatic defect is suspected. Normal BMBT in the dog is under 4.3 minutes and in the cat, 2.5 minutes. A prolonged BMBT time in a patient with normal platelet number confirms a thrombocytopathia.

Activated clotting time (ACT) is a screening test for the intrinsic and common pathways of the coagulation cascade. Blood (2mL) is drawn into a pre-warmed commercial tube that contains diatomaceous earth, after discarding the first few drops of blood. The sample is placed in a 37°C heating bath and inverted every 10 seconds.  ACT is the time to first clot formation. ACT is relatively insensitive - it is not abnormal until one factor is less than 10% of normal concentrations or multiple factor deficits are present.  

Portable machines are available for the assessment of PT and APTT. It is important that the correct methodology is followed to prevent erroneous results. Normal values are supplied by the manufacturer. It is an excellent screening test but false positives do occur in both the PT and APTT test, and some defects of the extrinsic pathway will not be detected. It is prudent to validate all abnormal results by conventional methodology.

D-dimers are fibrin split products that indicate the activation of thrombin and plasmin. Several “bedside tests” have been developed involving various technologies.  They are reasonably sensitive but not specific tests for DIC.


Ammonia is elevated in animals with significant liver disease or porto-systemic shunts.  Whilst less sensitive than bile acids for the detection of hepatic dysfunction, the presence of an elevated circulating ammonia concentration warrants immediate treatment. Hyperammonaemia may contribute to the clinical signs of hepatic encephalopathy, and thus appropriate treatment can produce a marked clinical improvement. Samples intended for ammonia measurement must be collected in anticoagulant (ethylenediamine tetra-acetic acid (EDTA) or heparin) and put on ice. Plasma should be harvested and refrigerated within 30 minutes of collection. The ammonia concentration should be determined within 60 minutes of collection. Samples intended for ammonia measurement should not be frozen. Ammonia will degrade with freezing. Hyperammonaemia is implied if pathologic ammonium biurate crystalluria is present.

Bile acids

Bile acids are a direct test of liver function that may be useful in cases of suspected hepatic dysfunction and prior to treatment with medications that are potentially hepatotoxic, such as phenobarbital. Fasting bile acids alone are diagnostically adequate in most situations, except for portosystemic vascular anomalies. In patients with portosystemic vascular anomalies, the preprandial serum bile acids concentration is typically normal or mildly elevated. The postprandial sample is typically moderately to markedly elevated. In severe hepatobiliary disease/hepatic failure, the serum bile acids concentration is typically moderately to markedly elevated in both the pre- and postprandial samples. Bile acids do not predict the severity of portosystemic vascular anomalies or hepatic disease. Additional testing will be needed for definitive diagnosis.

Interpretation of pre- and postprandial bile acids may be confused by the timing of bile acids release from the gall bladder, their intestinal transit time and their intestinal absorption. The gall bladder may contract prematurely - not on schedule with the postprandial blood sample. There may be delayed gastric emptying of the meal and, therefore, delayed gall bladder contraction - not on schedule with postprandial sample. There may be delayed intestinal transit time and, therefore, delayed absorption of bile acids.

CSF Lactate and acute phase proteins in CSF and serum

Increased CSF lactate by small-volume point-of-care analyser has been observed in approximately half of the dogs with CNS inflammatory disease and meningoencephalitis of unknown origin. In dogs with seizures, CSF lactate >2.5 mmol/l may help predict structural epilepsy. With inflammatory or neoplastic diseases, CSF lactate is higher than with idiopathic or unknown epilepsy.

Measurement of positive acute phase proteins (e.g. C-reactive protein, alpha-2 macroglobulin, serum amyloid A, haptoglobin, alpha-1 acid glycoprotein) in serum and CSF has been applied to the diagnosis and management of steroid-responsive meningitis-arteritis in dogs. C-reactive protein concentration and that of other positive acute phase proteins may be useful when evaluating and monitoring treatment of steroid-responsive meningitis-arteritis cases. In suspected cases of discospondylitis, serum C-reactive protein has been shown to be a more sensitive predictor than fever, leucocytosis, neutrophilia and hyperglobulinaemia. Results should be interpreted judiciously. C-reactive protein and other positive acute phase proteins elevations are non-specific biomarkers. Elevations are routinely detected with most systemic inflammatory, infectious, autoimmune, neoplastic and some metabolic diseases or, in the case of haptoglobin, with endogenous or exogenous hypercortisolemia.

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