Disorders of the renal tract can often lead to biochemical abnormalities, due the kidneys being the predominant organ of this system. 1 Common disorders of the renal tract often present with a metabolic acidosis due to the renal handling of various electrolytes, and the specific cellular pump mechanisms within the kidney. However, the metabolic acidosis is usually a high-anion gap acidosis due to the accumulation of phosphate and sulphate ions within the plasma, leading to a depletion in serum bicarbonate. We present a patient with an iatrogenic disorder of the genitourinary tract that presented with a severe normal anion gap acidosis, and serum biochemistry that demonstrated the potential use of calculating the strong ion difference.

An 81-year-old male presented with to the Emergency Department with urinary retention subsequent to passing blood clots. His urine-flow had been becoming increasingly difficult over the past few months, and he had a recent history of being treated with antibiotics for a urinary tract infection by his General Practitioner. He had a background medical history of benign prostatic hypertrophy, and ischaemic heart disease, although he had not reported any cardiovascular symptoms for many years. He was extremely independent and actively engaged in farming. There was no history of recent trauma to the abdomen or bladder, and his history. It was felt that his presentation was due to haemorrhagic cystitis subsequent to his urinary tract infection 2, since although he did not have coronary artery stents, he was receiving dual antiplatelet therapy. His urinary retention was treated by insertion of a three-way catheter with the aim of performing continuous bladder irrigation to eradicate the bladder of any current blood clots, and his dual antiplatelet therapy was ceased to prevent the formation of further blood clots. It was noted that the insertion was technically difficult with blood being seen at the urethral meatus during the procedure, which was likely due to his worsening benign prostatic hypertrophy, and he was subsequently transferred to the urology ward.

48 hours after admission it was noticed that he was feeling increasingly breathless, and complaining of chest discomfort. He received a Medical Emergency Team review two hours after this documentation for worsening shortness of breath and hypoxaemia, with a respiratory rate of 35 breaths/min and a SpO₂ of 91% on 10 litres/minute oxygen via a Hudson mask. Clinical examination revealed bi-basal medium intensity inspiratory crepitations and scrotal odema. His first arterial blood-gas analysis is shown in Table 1, demonstrating a significant normal anion gas acidosis, which was not explained by the 2500 ml of intravenous 0.9% sodium chloride he had received over the previous 48 hours.

On inspection of his urinary irrigation chart, calculations suggested that he had received 10 litres entering via the afferent limb, but only 3 litres fluid recorded exiting via the efferent limb of the circuit, although at the time it was unclear if it was not excreted from his urinary tract or if the recording on the ward was incorrect. With calculations difficult to fully ascertain, it was felt that the most likely diagnosis was pulmonary odema due to fluid overload, which was confirmed on chest x-ray, which showed bilateral opacification predominantly in the upper lobe vasculature. His bladder-irrigation was ceased, and was treated with intravenous frusemide and was transferred to the Intensive Care Unit for ongoing treatment of the pulmonary odema with non-invasive ventilation. On arrival in the Intensive Care Unit, his shortness of breath had worsened and a repeat arterial blood-gas (column 2 of Table 1), showed a worsening of his biochemical profile. It was suspected that there was a conduit from the in-dwelling catheter to his systemic circulation, which was initially thought to result from a vascular-cystic interface, similar to the pathogenesis of TURP (transurethral resection of prostate) syndrome. TURP syndrome is a rare but life-threatening complication of TURP procedure, which leads to systemic fluid overload and rapid hyponatraemia, due to absorption of the fluids used to irrigate the bladder during the operation into the prostatic venous sinuses. 3

However, a closer look at his arterial blood-gas analysis demonstrated a significant normal anion-gap academia, and his Strong Ion Difference calculations are shown below. Strong ions are ions that dissociate completely at a certain pH in a particular solution. In blood, this is at a pH 7.4. Strong cations are: Na⁺, K⁺, Ca²⁺, Mg²⁺, whereas strong anions are: Cl^- and SO₄^2-. Strong Ion Difference is the difference between the concentrations of strong cations and strong anions which = (Na⁺ + K⁺ + Ca²⁺ + Mg²⁺) – (Cl^– – L-lactate – urate). Abbreviated this = (Na⁺) – (Cl^–), and the overall effect on the base excess is SID – 38 (the normal sodium-chloride difference). The other parameter that has to be considered is ATOT, which is the total plasma concentration of inorganic phosphate, serum proteins and albumin (weak non-volatile acids), and is most affected by the serum albumin concentration. Using the abbreviated forms of the Strong Ion Difference equations, which take into account the effect on the base excess of hyperchloridaemia and hypoalbuminaemia, 4 the calculated base excess is -13, which exactly matches the base excess that was found on the ABG.