the only diagnosis given during the admission, despite the collateral history of 3 weeks of symptoms prior to her fall. Symptoms continued, and several weeks later, she was again seen in A&E and referred to stroke clinic due to confusion (being unable
Jonathan Brown and Luqman Sardar
Victoria John, Philip Evans, and Atul Kalhan
nausea and confusion ( 3 ) to seizures and coma in profound hyponatraemia (Na + <115 mmol/L, normal range 135–145 mmol/L) ( 4 ). Development of neurotic–psychotic symptoms secondary to an electrolyte imbalance is a well-established and extensively
Bidhya Timilsina, Niranjan Tachamo, Prem Raj Parajuli, and Ilan Gabriely
consequence of the intake of calcium supplements or calcium-containing antacids and is also known as calcium-alkali syndrome ( 3 ). Case presentation A 74-year-old woman presented to the Emergency Department (ED) with progressive lethargy, confusion
Catarina Roque, Ricardo Fonseca, Carlos Tavares Bello, Carlos Vasconcelos, António Galzerano, and Sância Ramos
-year-old woman presented to the emergency department with confusion, nausea and vomiting on the 26th of April 2014. The complaints had started 4 weeks earlier. She was not able to report her own history, a family member did so. She had type 2 diabetes
Navira Samad and Ian Fraser
primarily neurologic and reflect the changes in cerebral hydration in response to changing serum sodium concentration. Symptoms can range from subtle confusion, gait disturbances and attention deficit in chronic cases to seizures coma and obtundation in the
Katia Regina Marchetti, Maria Adelaide Albergaria Pereira, Arnaldo Lichtenstein, and Edison Ferreira Paiva
months prior to the described events with bloating, weakness, lack of appetite, nausea, weight loss, dyspnea and edema of the lower limbs. In the preceding 3 months, her general condition had worsened, and she experienced episodes of mental confusion and
Pooja Sahni, Nitin Trivedi, and Abdulkadir Omer
-month history of recurrent symptoms (once a week) of sweating, headache and confusion occurring 2 h after meals. She reported no symptoms during fasting state. The fingerstick blood sugar readings during these symptoms were 35 mg/dL, 38 mg/dL and 48 mg
A Veltroni, G Zambon, S Cingarlini, and M V Davì
Medicine Department of an Italian peripheral hospital. In the previous 2 weeks, the patient reported recurrent symptoms referring to hypoglycaemia (blurred vision, diaphoresis and confusion), mainly occurring 2–3 h after meal and resolving with food
Adriana de Sousa Lages, Isabel Paiva, Patrícia Oliveira, Francisco Portela, and Francisco Carrilho
due to a second-degree atrioventricular block (Mobitz type II) and severe aortic valve disease was admitted to the 1st time to our emergency department (ED) due to acute prostration and confusion. At that time, a plasma glucose level of 50 mg/dL was
Mawson Wang, Catherine Cho, Callum Gray, Thora Y Chai, Ruhaida Daud, and Matthew Luttrell
We report the case of a 65-year-old female who presented with symptomatic hypercalcaemia (corrected calcium of 4.57 mmol/L) with confusion, myalgias and abdominal discomfort. She had a concomitant metabolic alkalosis (pH 7.46, HCO3 - 40 mmol/L, pCO2 54.6 mmHg). A history of significant Quick-Eze use (a calcium carbonate based antacid) for abdominal discomfort, for 2 weeks prior to presentation, suggested a diagnosis of milk-alkali syndrome (MAS). Further investigations did not demonstrate malignancy or primary hyperparathyroidism. Following management with i.v. fluid rehydration and a single dose of i.v. bisphosphonate, she developed symptomatic hypocalcaemia requiring oral and parenteral calcium replacement. She was discharged from the hospital with stable biochemistry on follow-up. This case demonstrates the importance of a detailed history in the diagnosis of severe hypercalcaemia, with MAS representing the third most common cause of hypercalcaemia. We discuss its pathophysiology and clinical importance, which can often present with severe hypercalcaemia that can respond precipitously to calcium-lowering therapy.
- Milk-alkali syndrome is an often unrecognised cause for hypercalcaemia, but is the third most common cause of admission for hypercalcaemia.
- Calcium ingestion leading to MAS can occur at intakes as low as 1.0–1.5 g per day in those with risk factors.
- Early recognition of this syndrome can avoid the use of calcium-lowering therapy such as bisphosphonates which can precipitate hypocalcaemia.