Diabetic ketoacidosis (DKA) and hyponatraemia associated with beer potomania are severe diagnoses warranting intensive care level management. Our patient, a middle-aged man, with a history of chronic alcohol abuse and insulin non-compliance, presents with severe DKA and severe hyponatraemia. Correcting sodium and metabolic derangements in each disorder require significant attention to fluid and electrolyte levels. Combined they prove challenging and require an individualised approach to prevent the overcorrection of sodium. Furthermore, management of these conditions lends to the importance of understanding the pathophysiology behind their hormonal and osmotic basis.

A 40-year-old woman presented to our emergency department in an altered state following a generalised tonic-clonic seizure. On regaining consciousness, she gave a history of bleeding tendencies and menorrhagia, fatigue, nausea, vomiting and appetite loss for a long time. She had received multiple blood transfusions in the last 10 years. Investigations revealed severe hyponatraemia, transaminitis and pancytopenia, which showed cyclical fluctuations in the hospital. Hyponatraemia was attributed to a central cause owing to secondary hypothyroidism and hypocortisolism on evaluation. A diagnosis of cyclical thrombocytopenia was made by logging the trends of blood cell lines and applying the Lomb-Scargle test. Liver biopsy showed features of transfusion hemosiderosis explaining transaminitis. All of the haematological abnormalities and clinical symptoms resolved on thyroxine and corticosteroid replacement, suggesting causal association hypopituitarism with cyclical thrombocytopenia.

We report a case of severe hypokalaemia and moderate hypophosphataemia from clay ingestion. A 60-year-old woman presented with flaccid paralysis. Investigations revealed a serum potassium level of 1.8 mmol/L, phosphate level of 0.56 mmol/L and creatine kinase level of 30 747 IU/L. She had marked proximal and distal muscle weakness due to severe hypokalaemia and concurrent hypophosphataemia, which likely contributed to the onset of rhabdomyolysis. The patient subsequently admitted to significant pica, most likely secondary to an associated iron deficiency. We conclude that the ingested clay acted as a potassium and phosphate binder. Although we did not investigate the content of the clay in this case, it has been reported that clay can bind potassium in vitro and is rich in minerals such as aluminium that could play a role in the binding of phosphate, although the exact mechanism remains unclear. The patient recovered fully and outpatient follow-up at 6 months and again at 40 months confirmed no electrolyte abnormality, myopathy nor any further geophagia.

A 52-year-old man with a history of urolithiasis presents to the emergency department with a sudden, sharp, continuous right flank colicky pain. Laboratory workup demonstrates acute kidney injury with a mild hyperkalaemia. During the observation period, the patient develops an atypical broad complex sinus bradycardia and eventually short asystolic periods. This was caused by a severe therapy-resistant hyperkalaemia, wherefore emergency haemodialysis was necessary. Radiographic results showed a giant hydronephrosis with a blowout of the right kidney and an obstructing calculi of 21 mm in the distal ureter. We will discuss the mechanism of reversed intraperitoneal dialysis causing the refractory hyperkalaemia and the need of close ECG monitoring in patients where kidney blowout is considered.

Pseudohypoaldosteronism (PHA) due to obstructive uropathy, urinary tract infections and congenital urogenital malformations has been reported in the literature; however, there are no reports of PHA associated with hydrometrocolpos due to a common urogenital tract. Hydrometrocolpos is a condition resulting in distension of the vagina and uterus due to accumulation of secretions (other than blood), caused by increased oestrogenic stimulation and vaginal outflow obstruction. We report on a neonatal case of PHA caused by recurrent hydrometrocolpos presenting with vomiting and poor weight gain. There was significant hyponatraemia, hyperkalaemia, and anaemia requiring medical stabilisation prior to surgery. The mechanism by which PHA occurs in obstruction involves renal tubular dysfunction due to pressure from hydronephrosis and the release of intrarenal cytokines. In addition, there is an immature or resistant renal tubular responsiveness to aldosterone during infancy. Clinicians should be aware of this uncommon but serious presentation.