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or a myocardial infarction

in a patient with type 2 diabetes on an SGLT2 inhibitor .

INITIAL PRESENTATION

THE clinical presentation of DKA is

initially driven by marked hyperglycaemia

leading to characteristic polyuria , excessive thirst , polydipsia and signs of dehydration ( see figure 5 ). However , with the development of systemic acidosis , other non-specific clinical features , including fatigue , malaise , nausea , vomiting and abdominal pain , are superimposed . The onset of DKA is often rapid and can easily be confused with acute gastroenteritis or even an acute abdomen requiring surgical attention . It is important to always consider ketoacidosis in the differential diagnosis of any patient with diabetes who presents with abdominal symptoms , even if their glucose levels are not obviously elevated .

Patients with ketoacidosis may also experience shortness of breath and Kussmaul respiration , as a respiratory compensation to acidosis .

Neurological status in patients with DKA may vary from full alertness to a profound lethargy , somnolence , confusion , delirium , and eventually loss of consciousness and coma .

Some patients can detect the unusual smell of acetone on their breath . For those practitioners who are able to smell acetone , it resembles the smell of rotting apples , ‘ pear drops ’, or nail polish remover .

The presentation of EKA in non-diabetic individuals is often milder and less precipitous in nature . Unlike DKA that often appears suddenly in those with type 1 diabetes , EKA can evolve over several days of illness and fasting .

Figure 3 . A ketogenic diet aims to increase blood ketones in healthy adults to greater than 0.5mmol / L .

Often its symptoms are masked by ( or indistinguishable ) from those of the triggering intercurrent illness , such as infection , dehydration or a myocardial infarction ( see box 2 ), meaning that consideration of ketoacidosis can be easily forgotten in the haste to deal with the trigger event . As infection is a common precipitant of ketoacidosis , it might be anticipated that many patients with EKA could be febrile . However , patients with ketoacidosis can have a normal body temperature or mild

hypothermia , despite a coexisting infection . It is therefore important to also consider underlying infection in patients presenting with ketoacidosis , even in the absence of fever .

DIAGNOSING KETOACIDOSIS IN ADULTS

IT is recommended that all primary

care practices have access to pointof-care capillary blood glucose and ketone monitoring meters and strips

( see figure 6 ). 19 An abnormally elevated blood ketone concentration is 0.6mmol / L or greater . However , patients with ketoacidosis usually have critically elevated capillary or blood ketone concentrations of greater than 1.5mmol / L . 20 The presence of elevated ketones in the urine can also be used . However , the urine test only measures acetoacetate , it is not quantitative , and interpretation may be confounded by coexisting dehydration and oliguria ( associated with hyperglycaemia ),

which may delay testing , diagnosis and treatment .

In DKA , blood glucose levels are also elevated ( greater than 11.1mmol / L ), while in EKA , blood glucose levels are in the normal range ( less than 11.1mmol / L ).

Once in hospital , a diagnosis of ketoacidosis is confirmed by a venous blood pH less than 7.3 and / or a serum bicarbonate less than 15mmol / L . Some countries also use the presence of elevated anion gap as part of their diagnostic criteria .