Diagnosis and Clinical Presentation

DKA usually develops over a short period of time, generally in less than 24 h. There may have been some antecedent days with general malaise and poor metabolic control. Depending on the degree of hyperglycaemia, the history will include symptoms of polydipsia and polyuria. Specific symptoms depend on precipitating factors and co-morbidity. Physical examination may reveal poor skin turgor, hyperventilation (Kussmaul), hypotension, tachycardia and impairment of mental status. Many patients have infection, but patients may present with normothermia or even hypothermia due to peripheral vasodilation caused by the acidemia.

Prompt diagnosis and initial treatment rests on: (i) careful clinical examination, (ii) determination of plasma glucose, (iii) measurement of ketones in blood or urine, (iv) measurement of plasma potassium and other electrolytes and (v) assessment of acidemia. If glucose is high and blood/urine ketones are markedly elevated, DKA is likely and fluid and insulin therapy can usually be initiated, unless the patient is severely hypokalaemic (<3.5 mmol/L). If potassium is very low supplementation must be given before insulin therapy. However, rehydration should not be delayed whilst waiting for a potassium measurement.

The next diagnostic steps usually include arterial gas analysis, blood electrolytes (including anion gap), serum lactate (if there is doubt about the cause of the acidemia), complete blood cell count, biochemical assessment of liver and renal function, blood and urine cultures, myocardial biomarkers (if there is suspicion of a myocardial infarction), ECG and chest X-ray. In this context it is advantageous that most modern gas analysers also readily provide potassium concentrations. Another recent advantage is the advent of bedside ketone body monitors. It is thus nowadays possible to have quick and reliable measures of 3-hydroxybutyrate concentrations in blood [17], as opposed to unreliable measurements of acetoacetate in urine or time-consuming conventional laboratory methodology of the past. Diagnostic criteria are shown in Table 1.

Despite potassium depletion, serum potassium is typically either normal or elevated due to water deficiency and an intra- to extracellular shift caused by insulin deficiency and acidemia. Patients with potassium in the low range have severe total body potassium deficiency and should receive vigorous replacement therapy guided by cardiac monitoring. Sodium concentrations can be normal or low, due to osmotic shifts. It can be calculated that for every 3 mmol/L rise in plasma glucose the plasma sodium falls by 1 mmol/L. Thus there is often a real hypernatremia and the sodium levels will always rise as the glucose is brought under control. A majority of patients will have leukocyto-sis, which correlates with ketone body levels rather than with the presence of infection. There is also a water deficit of around 10% of body weight. Non-specific elevations of amylase and liver enzymes are common.

Differential diagnoses include all other causes of acidosis. It should be emphasised that many acute medical conditions induce stress ketosis and may be associated with acidosis. DKA is a metabolic aci-dosis characterised by a high anion gap and varying degrees of respiratory compensation. It is therefore crucial to obtain measures of ketone body concentrations and arterial gas analysis. If there is a major discrepancy between the extent of the ketonaemia and the acidemia, then lactate measurements are warranted. Starvation ketosis and alcoholic ketoaci-dosis can usually be identified by clinical history. Other conditions causing metabolic acidosis include lactic acidosis and intoxication with sali-cylate, methanol, ethylene glycol (antifreeze) and paraldehyde. The clinical picture may be blurred whenever the acidosis is aggravated by renal failure or respiratory failure. In addition DKA may imitate other diseases. High levels of potassium may cause ECG changes suggestive of myocar-dial infarction, and elevation of myocardial enzymes and biomarkers may occur in the absence of clear myocardial infarction [18]. DKA may also mimic an acute abdomen, particularly in younger patients.

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