This can be performed by the dedicated laboratory technician ( Skelly , 2018 ). A free-flow urine sample can be collected and the test performed in-house , with a result available within minutes .
The three main ketone bodies found in the urine are beta-hydroxybutyrate , acetate and acetoacetate . These are produced by the liver and used as an energy source when glucose is not readily available . Commercial dipsticks are available for the testing of ketones in the urine , but they only detect the presence of acetate and acetoacetate , not beta-hydroxybutyrate ( VetsNow , 2013 ).
Boag ( 2012 ) states that beta-hydroxybutyrate is produced in larger quantities than the other acids when the body is in a state of hyperfusion and shock , so the presence of this acid will allow a more clear diagnosis of DKA . If the ketones present are beta-hydroxybutyrate but are not detected , it is possible to dilute the urine 1:9 with hydrogen peroxide to turn the betahydroxybutyrate to acetoacetate to make the ketones detectable ( VetsNow , 2013 ).
Urinalysis is a crucial part of the diagnosis and should include specific gravity , sediment examination and general dipstick evaluation , as well as a ketone-specific dipstick . A urine culture is generally advised to test for an underlying urinary tract infection and is considered essential if the sediment examination is suggestive of infection . Diabetic patients are particularly prone to urinary tract infections , which can lead to destabilisation of the diabetes resulting in DKA ( VetsNow , 2013 ). It is crucial , during the diagnostics stage , to try to identify the underlying cause of the condition , which will need to be corrected alongside the acidosis .
DKA patients commonly present with azotaemia . This is often prerenal secondary to dehydration . The nature of the azotaemia ( renal or prerenal ) can be assessed by performing a specific gravity ( SG ) measurement on the urine . However , due to diabetes leading to osmotic diuresis enhanced by ketonuria , the urine SG results cannot be completely relied on to be precise . Due to the condition and complicating factors , the patient will commonly have a urine SG of > 1.020 ( Boag , 2012 ).
A blood gas analysis should be performed to allow quantification of the blood acidity ( Boag & Nichols , 2011 ). A blood gas analyser is used to measure blood pH , partial pressure of oxygen , partial pressure of carbon dioxide , bicarbonate levels , base excess and saturation of haemoglobin with oxygen . These parameters are used to indicate metabolic disturbances ( Boag & Nichols , 2011 ). Initial and continuous blood glucose measurements will need to be taken throughout the treatment process . The normal blood glucose range is 3.3 – 6 mmol / l ( Irwin-Porter , 2011 ). A patient in DKA will have a blood glucose higher than the normal range ( Gear & Mathie , 2011 ).
In both cats and dogs , hyperglycaemia is often accompanied by stress . This may lead to confusion in the diagnosis of DM . When assessing blood glucose , it is beneficial to take a series of samples once the patient is settled to allow complete monitoring . In a routine blood-glucose curve these samples would usually be taken over 8 – 12 hours , at 2-hourly intervals , but the more critical patient would benefit from more regular sampling . Skelly ( 2018 ) states that there is no cutoff value to distinguish between stress and true DM , but it is rare for stress alone to cause a blood glucose of > 20 mmol / l .
The blood samples can be taken via ear prick or venous sampling . An ear prick would be perfectly acceptable for a one-off sample . However , for continuity , it would be advisable to take venous samples , as ear-prick samples can differ depending on the patient ' s tissue perfusion . When necessary , venous sampling can be performed with a needle and syringe or , for better patient care , a central line can be placed . This would allow for continuous blood sampling without the need to frequently insert a needle into the patient .
Care of the patient
Intravenous fluid therapy is required in all DKA patients , due to the dehydration that comes secondary to diuresis from hyperglycaemia ( Battaglia & Steele , 2016 ). If the patient arrives in shock , over 48 hours of aggressive fluid therapy should be given to replace deficits in addition to maintenance fluids and ongoing losses ( Battaglia & Steele , 2016 ). The fluid supplementation given over 24 hours can be calculated based on :
Deficit ( ml ) = percentage dehydration (%) × weight ( kg ) × 10
+ Maintenance ( ml ) = 50 ml × weight ( kg ) + Ongoing losses
Ongoing losses will be individual to each patient depending on ongoing gastrointestinal losses and renal losses from osmotic diuresis ( Boag , 2012 ). Hypovolaemia severity can be assessed by different clinical signs , which can be seen in Table 3 .
When using fluid therapy to assist in the management of DKA , the correction of the acidosis and dehydration is the primary concern , alongside the patient being on insulin therapy ( Skelly , 2018 ). The choice of fluid therapy is dependent on the hydration status and electrolyte status of the patient , but there are no published studies comparing the efficacy of different fluid types in critically ill diabetic patients . Although some clinicians recommend 0.9 % sodium chloride ,
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