A 47-year-old male with chronic and treatment resistant schizophrenia, type two diabetes mellitus, hypertension, and obstructive sleep apnoea presented to the Emergency Department (ED) approximately three to four hours after an intentional ingestion of approximately 500 ml of Aldi TANDIL ULTRA Concentrate Dishwashing Liquid (Lemon Anti-bacterial 900 ml). Prior to his presentation to ED, he had four episodes of vomiting and one episode of diarrhea at home. He had a further episode of vomiting (clear-white fluid) in the ED.

His medications included clozapine, fluoxetine, rosuvastatin, metoprolol, metformin SR, dapagliflozin, gliclazide MR, and melatonin MR. Recent dose adjustments of his clozapine had been made by his psychiatrist because of increasing anxiety and behavioural problems that his supportive family were having difficulty managing. He did not have any known drug allergies. 

On examination in the ED, Glasgow Coma Scale (GCS) was 14 and he appeared diaphoretic. He was hypotensive on presentation with a blood pressure (BP) of 91/48 mmHg that responded to fluid resuscitation (BP increased to 131/74 mmHg). He was tachycardic with the heart rate of 124/min and in sinus rhythm. His oxygen saturations were 95% on room air and he was tachypneic with a respiratory rate of 32/min. His temperature was 37.3°C. There was no mucosal damage noted in oral cavity and his abdomen was soft and non-tender. 

Initial laboratory investigations showed white cell count 22 (x10^9/L), platelet 326 (x10^9/L), serum creatinine 155 µmol/L, and potassium 5.0 mmol/L. His venous blood gas revealed pH 7.322, pCO2 53.3 mmHg, HCO3 26.8 mmol/L, and lactate 6.6 mmol/L. The serum clozapine level was 378 µg/L (reference 350-600 µg/L).

After two hours in the ED, he had a further deterioration with a requirement for oxygen of 15L/minute via a non-rebreather mask to maintain oxygen saturation of 92%. This was associated with hypotension and a further reduction in his GCS to 13. His venous lactate rose to 11.3mmol/L. He had no symptoms of stridor and was transferred to the operating theatre for an awake oral fibre-optic intubation due to concern regarding potential detergent induced airway swelling. Flexible trans-nasal endoscopy revealed mild oedema affecting the arytenoid, vocal cord, aryepiglottic fold, epiglottic and supraglottic areas. The carina was visualized with bubbly secretions coating mucosa, however there was no significant airway injury or obstruction detected.

He was admitted to the Intensive Care Unit (ICU) following intubation and developed a rapidly increasing temperature and circulatory failure. Bedside Transthoracic Echocardiography (TTE) on ICU admission revealed grossly normal contracting ventricles; no large pericardial effusion; and small appearing inferior vena cava (IVC). The working diagnosis for his haemodynamic instability was that it was most likely due to hypovolaemia and not of cardiogenic aetiology. Further intravenous fluids were administered, and he was initially responsive to fluids and vasopressors.

In the first 48 hours following ICU admission, his temperature peaked at 40.8⁰C and his peak noradrenaline dose was 0.35 mcg/kg/min; concomitantly he received adrenaline (peak dose 0.08 mcg/kg/min) and fixed dose vasopressin infusion (2.4 units/hr) to provide further pharmacological circulatory support. An urgent Computed Tomography (CT) scan of his chest, abdomen and pelvis was performed which demonstrated bilateral lower lobe consolidation and no evidence of upper gastrointestinal perforation or inflammation. His electrocardiogram showed sinus tachycardia with nonspecific ST and T wave changes. A further TTE showed hyperdynamic biventricular function without significant valvular abnormalities. Microbiology results including blood and other cultures were negative.

Between 48 and 72 hours after ICU admission, he developed dark coloured urine, a rise in his serum creatinine from 152 to 269 µmol/L and a creatinine kinase of 417,500 U/L. Lactate Dehydrogenase (LDH) was elevated to 14,897 U/L. His Aspartate Transaminase (AST) increased to 3,150 U/L and Alanine Transaminase (ALT) increased to 299 U/L; these were most likely from muscle injury and there were no other features suggestive of liver injury. He also developed thrombocytopenia which was thought to be likely consumptive due to acute rhabdomyolysis and acute inflammation. Peripheral blood smear examination revealed some hyposplenic features, but no schistocytes or fragmentation. There was no evidence of disseminated intravascular coagulation or thrombotic microangiopathy. Repeat microbiology test results were also negative. Trends of temperature, inotropic and vasopressors doses are shown in Figure 1. The relevant laboratory tests and their trends are shown in Figure 2.

Circulatory support was ceased on day 10 after ICU admission. He was liberated from the invasive respiratory support on day 20 and was discharged to the ward on day 28. His last haemodialysis session occurred on day 29. His recovery was complicated by profound weakness which manifested as severe symmetric flaccid quadriparesis likely secondary to rhabdomyolysis and delayed clearance of sedatives due to his organ dysfunction. His antipsychotic medications were gradually reintroduced by the psychiatric team. His renal function recovered completely in 6 weeks with normal serum creatinine and estimated glomerular filtration rate (eGFR). He underwent gastroscopy in week 12 which was normal. He was referred to the rehabilitation unit and subsequently discharged home after spending 15 weeks in the hospital.

The product information and the safety data sheet for the detergent ingested is shown below in Table 1 and Table 2 [1].

Table 1: Detergent composition.