Discussion

Diabetic ketoacidosis is one of the serious metabolic complications of diabetes, which consists of the triad of hyperglycaemia, ketosis, and acidosis; the diagnostic criteria being blood glucose level > 250 mg/dl, arterial pH < 7.3, bicarbonate level < 15 mEq/L, and a moderate degree of ketonaemia and ketonuria. There has been little change in the mortality rate associated with diabetic ketoacidosis despite great improvements in our understanding of its pathophysiology and treatment. During diabetic ketoacidosis, cardiovascular damage can occur as a form of (a) arrhythmias due to electrolyte imbalance, (b) adverse effects of acidosis, (c) acute myocardial infarction, and (d) pulmonary oedema.^{Reference Wasag, Gregory, Dayan and Harvey6,Reference Gandhi and Suvarna12}

Fluid and electrolyte imbalance is very common in diabetic ketoacidosis cases and manifested typically by a loss of 5–8 L of water, 400–700 mEq of sodium, 250–700 mEq of potassium, and 30–50 mEq of magnesium. However, as water loss is greater relative to electrolytes, most patients will have normal or even elevated sodium, potassium, and magnesium levels at the time of presentation, although their body stores of these elements are almost always lower than normal.^{Reference Gandhi and Suvarna12} Potassium deficit, one of the essential electrolyte imbalances seen in diabetic ketoacidosis, can lead to fatal arrhythmias. The most common cardiac arrhythmias are atrial premature contractions, atrial tachycardia with or without AV block, supraventricular tachycardia, and ventricular premature contractions. Less common are AV junctional tachycardia or escape rhythm and AV block.^{Reference Chung and Chung13} However, multiple additional factors can also cause arrhythmias, including re-entry circuits, abnormal automaticity, or triggered activity occurring within myocardial focus.^{Reference Cubbon and Kearney14} A common cause of re-entry circuits within the myocardium is electrolyte abnormalities involving calcium and potassium.^{Reference Cubbon and Kearney14}

Additionally, hypomagnesaemia and hypophosphataemia have also been associated with tachyarrhythmia such as supraventricular tachycardia.^{Reference Klevay and Milne15} During the treatment of diabetic ketoacidosis, phosphate serum levels subsequently drop profoundly as a consequence of insulin administration.^{Reference Shen and Braude16} The greater the initial acidosis, the greater the subsequent hypophosphataemia.^{Reference Shen and Braude16} Our patient had profound serum hypophosphataemia suggests an even greater total body phosphate depletion. Moreover, phosphate supplementation may precipitate hypocalcaemia.^{Reference Becker, Brown, Steranka and Drash17}

Acidosis resulting from the production of ketoacidosis is a key clinical feature found in diabetic ketoacidosis that may precipitate arrhythmias. The junctional resistance between myocardial cells is increased by about 30% if the pH falls by 0.4 units.^{Reference Kagiyama, Hill and Gettes18,Reference Marrannes, de Hemptinne and Leusen19} This reduction in conduction velocity can enable a re-entrant arrhythmia to form in a structurally normal heart in which an acidic region is present.^{Reference Garson9} However, as the acidosis was resolved in this case, this suggests that electrolyte shifts and hypophosphataemia and hypomagnesaemia are more likely to cause supraventricular tachycardia.

As almost all cases in these previous studies had a normal echocardiogram, the likely cause is an atrioventricular nodal re-entry tachycardia without an accessory pathway and can be triggered by hypo/hyperkalaemia.^{Reference Goyal, Senst, Bhyan and Zeltser20} An accessory pathway with antegrade conduction or WPW may be less likely in the differential with a normal electrocardiogram, although not entirely ruled out as antegrade conduction may be heart rate dependent. Re-entry is defined as a closed-loop circuit that develops within the myocardium and allows the action potential to self-sustain.^{Reference Goyal, Senst, Bhyan and Zeltser20} It may also fall under the category of ectopic tachycardia with atrial extra systoles, where enhanced atrial pacemaker automaticity arises from disturbed electrolytes, for example, potassium.^{Reference Ko, Deal, Strasburger and Benson21} The atrial extra systoles may have originated from metabolic derangements and then precipitated the supraventricular tachycardia.

In this case, hypokalaemia would explain both the premature atrial contractions and the supraventricular tachycardia through enhanced atrial automaticity. However, the potassium was only at the lower limits of normal at its nadir. It is important to mention that diabetic ketoacidosis can result in very rapid potassium derangements, which may be undetected where potassium levels are typically “normal” at presentation.^{Reference Ko, Deal, Strasburger and Benson21} Although serum potassium levels were generally well-controlled, intracellular potassium homoeostasis was likely to be seriously disturbed and was probably a major contributor to the genesis of the arrhythmia. Furthermore, with appropriate insulin and fluid therapy, as the acidosis reverses, potassium is concomitantly forced into the cells, resulting in a rebound of hypokalaemia.^{Reference Ko, Deal, Strasburger and Benson21} A possible hypothesis is that our patient’s low magnesium levels partook in the occurrence of supraventricular tachycardia.^{Reference Winter, Harris, Phillips and Green22} ATPase pumps in the myocardium are dependent on magnesium, and reduced magnesium alters membrane potential, irritates the myocardium, and results in an increased frequency of supraventricular beats.^{Reference Rother and Schwenk23}

Our patient was responding to adenosine as acute treatment and discharged with no anti-arrhythmic medications. Inverse, while the patient with same presentation did not respond to adenosine, flecainide was given and showed abortion of supraventricular tachycardia.^{Reference Finn, Fraser and O'Connell24}

Although diabetic ketoacidosis can cause life-threatening arrhythmias, it is usually reversible with appropriate treatment consisting of insulin and IV fluids. During treatment, it is imperative to monitor patients' electrolytes and acid–base status closely. It is recommended that electrolytes be replaced with a solution with tonicity greater than 0.45% normal saline, such as the one administrated to our patient, with the addition of potassium chloride, potassium phosphate, or potassium acetate.^{Reference Klevay and Milne25} In profoundly unwell patients with severe diabetic ketoacidosis, cardiac monitoring forms a routine part of intensive care.