Plus-Hex CLINICAL
ABSTRACT Diabetic ketoacidosis ( DKA ) is a severe , potentially life-threatening metabolic disorder that occurs secondary to diabetes mellitus ( DM ), a commonly managed condition in veterinary patients .
DKA can occur when DM has not yet been detected , when it is diagnosed but poorly controlled , or when a concurrent illness has caused destabilisation .
This article will provide an in-depth understanding of the pathophysiology of DKA , how it is diagnosed and what is involved in stabilising these patients .
Keywords diabetic ketoacidosis , insulin , diabetes mellitus , ketones , blood glucose , fluid therapy
Pathophysiology
During normal function , beta cells within the pancreas secrete insulin when they are stimulated by rising glucose levels in the blood . Insulin works to drive glucose from the blood and into cells to provide the body with a source of energy . Diabetes mellitus ( DM ) occurs when there is a lack of insulin and therefore a lack of glucose reaching the cellular level . It may occur due to immune destruction of the insulin-producing cells , or when insulin is produced but the body does not respond to it correctly . Gear [ 1 ] states that the immune destruction of insulin-producing cells is seen mainly in dogs , whereas insulin resistance is more commonly seen in cats , often due to obesity .
A deficiency in insulin causes cell starvation and , if left untreated , will result in the breakdown of body fat to provide energy . During the breakdown of fat , fatty acids are released and enter the circulation and are then transported to the liver , where they are metabolised into acidic ketone bodies , which are used as a source of cellular energy instead of glucose . The accumulation of these acidic ketones , when not entirely used by the body for energy , causes a reduction of the pH of the blood . This results in metabolic acidosis . At this point , the patient will present seriously ill and require intensive hospital treatment [ 2 ] .
Diagnosis
Clinical signs of diabetic ketoacidosis ( DKA ) include hyperglycaemia , ketonaemia , glucosuria and ketonuria . Tabor [ 3 ] states that measuring blood glucose , ideally using a point-of-care glucometer , is the first step towards diagnosis . In the absence of insulin driving glucose into the cells , it remains in the bloodstream , causing hyperglycaemia . In cases of uncontrolled DM , the liver continues to release glucose for cellular energy , which exacerbates the existing hyperglycaemia .
There are three ketone bodies : acetate , acetoacetate and beta-hydroxybutyrate . Beta-hydroxybutyrate is the principal ketone and is of particular importance when confirming ketonaemia , but it can be assessed only by an external laboratory and may not prove helpful in an emergency situation . In the absence of betahydroxybutyrate measurement , urine dipsticks will detect acetate and acetoacetate and can be used to estimate plasma ketones . Galloway [ 2 ] states that ketones detected using this method should be considered abnormal .
It must be remembered that ketone bodies alone are not an indicator of DM as they will be present in any form of increased fat catabolism or starvation [ 4 ] . Therefore , detection of ketone bodies along with other clinical signs , such as hyperglycaemia , is indicative of DKA . Ketones are described as very low renal threshold substances ( the threshold indicates the level a substance reaches in the blood before the kidneys start to remove it ). As a result , significant accumulations of ketones will spill into the urine for excretion from the body and are considered abnormal if detected on urinalysis . Ketonuria can be an early and significant indication that the patient is developing ketonaemia and acidosis . As urinary tract infections are considered a common cause of the destabilisation of DM , Tabor [ 3 ] suggests collecting a urine sample through cystocentesis to ensure that culture testing can be carried out .
If available , blood gas analysis is carried out to confirm acidosis . The normal pH of blood is between 7.35 and 7.45 . In some cases , this parameter can remain normal while compensatory mechanisms continue to work [ 3 ] . In cases of DKA , there will be a marked decrease in the pH value , with a reading of < 7.1 requiring aggressive treatment to correct the metabolic derangement [ 3 ] . Galloway [ 2 ] suggests that if the patient ' s electrolytes and acid – base cannot be assessed it is advisable to have the patient referred .
The goals of treatment in the DKA patient are to correct acidosis , dehydration and electrolyte deficits ; prevent further ketone accumulation ; and treat underlying factors contributing to DM instability . Nutritional support will also be necessary .
Fluid therapy
Niessen [ 5 ] suggests that intravenous fluid therapy ( IVFT ) is the priority treatment for patients presenting with DKA and should be administered before insulin therapy is started . The aim is to correct hypovolaemia and dehydration , improve perfusion and stabilise electrolyte abnormalities . IVFT will also promote the excretion of ketones from the body , and will correct acidosis and decrease blood glucose levels by dilution [ 5 ] .
Hypovolaemia and dehydration are not the same but often present together . When a fluid deficit occurs within the interstitial and intracellular compartments ,
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