Over-the-counter antacids linked to severe hypokalaemia in the context of threatened preterm labour.

A healthy multiparous woman presented at 35 weeks and 4 days' gestation with threatened preterm labour on multiple occasions. An incidental finding of severe hypokalaemia (2.4 mmol/L) was detected on routine blood tests. The cause of this hypokalaemia was not initially obvious. It was eventually linked to overuse of over-the-counter antacids for pregnancy-associated heartburn. The patient was managed with parenteral and then oral electrolyte replacement which corrected a pH of 7.55, bicarbonate of 36.7 mEq/L and a base excess 13.1. In this case report we consider whether hypokalaemia could be linked to uterine irritability and threatened preterm labour, whether antacids were being abused in the context of an eating disorder and the importance of taking a full drug history.

Reversible cerebral vasoconstriction syndrome (RCVS) caused by over-the-counter calcium supplement ingestion.

A 59-year-old woman was found unresponsive at home. Initial neurologic examination revealed aphasia and right-sided weakness. Laboratory results demonstrated a serum calcium level of 17.3 mg/dL (corrected serum calcium for albumin concentration was 16.8 mg/dL). Extensive workup for intrinsic aetiology of hypercalcemia was unrevealing. Further discussion with family members and investigation of the patient's home for over-the-counter medications and herbal supplements revealed chronic ingestion of calcium carbonate tablets. CT angiogram of the brain revealed multifocal intracranial vascular segmental narrowing, which resolved on a follow-up cerebral angiogram done 2 days later. These findings were consistent with reversible cerebral vasoconstriction syndrome.Appropriate blood pressure control with parenteral agents, calcium channel blockade with nimodipine and supportive care therapies resulted in significant improvement in neurologic status. By discharge, patient had near-complete resolution of neurologic symptoms.

Paradoxical hypomagnesemia caused by excessive ingestion of magnesium hydroxide.

Excessive ingestion of magnesium may lead to hypermagnesemia even without kidney dysfunction. Several cases of development of hypermagnesemia after overdose of magnesium hydroxide have been reported. Although magnesium hydroxide is widely used as laxative, its overdose may induce diarrhea, which is followed by excessive magnesium loss. I report a case of paradoxical hypomagnesemia developed after excessive ingestion of magnesium hydroxide. A 39-year-old woman was presented to the emergency department complaining of severe watery diarrhea and carpopedal spasm after ingesting a handful of magnesium hydroxide tablets. The laboratory tests detected hypomagnesemia, hypocalcemia, and normokalemia. Calcium gluconate was given to the patient, but her symptom did not improve shortly. The symptom disappeared spontaneously 2 days after the watery diarrhea subsided. This case shows that overdose of magnesium hydroxide, which leads to massive diarrhea, might induce hypomagnesemia unexpectedly. This case also suggests that it should be treated, as well as typical magnesium deficiency.

Severe hypokalaemic metabolic alkalosis following ingestion of gaviscon.

INTRODUCTION: Uncommon metabolic abnormalities in the emergency department could be a result of drug overdose due to uncommon agents. CASE REPORT: A 35-year-old male presented to the emergency department with a Glasgow Coma Scale (GCS) of 3/15 and a normal pulse rate and blood pressure. Subsequent questioning after recovery revealed he had ingested 2 L of Gaviscon over the preceding 48 hours. He had normal haematology, liver, and renal function during admission. The electrocardiogram showed T wave inversion in the inferior leads on admission. Arterial blood gas on air was: pH 7.54, HCO3 50 mmol/L (50 meq/L), Chloride 66 mmol/L, anion gap was 19, pO2 11 kPa (82.5 mmHg), and pCO2 8 kPa (60 mmHg). Serum sodium was 127 mmol/L and serum potassium was 1.6 mmol/L. His GCS improved within one hour of admission with supportive care, and his serum potassium and bicarbonate improved within 24 hours. He subsequently made a full recovery. Discussion. Bicarbonate ingestion in the form of Gaviscon(R) and vomiting made this patient alkalotic, and simple supportive care provided effective management with a complete recovery. CONCLUSION: This case illustrates how a severe metabolic alkalosis can result from a significant ingestion of Gaviscon, and that such presentations can give rise to diagnostic dilemma.

Severe metabolic alkalosis due to baking soda ingestion: case reports of two patients with unsuspected antacid overdose.

Oral ingestion of baking soda (sodium bicarbonate) has been used for decades as a home remedy for acid indigestion. Excessive bicarbonate ingestion places patients at risk for a variety of metabolic derangements including metabolic alkalosis, hypokalemia, hypernatremia, and even hypoxia. The clinical presentation is highly variable but can include seizures, dysrhythmias, and cardiopulmonary arrest. We present two cases of severe metabolic alkalosis in patients with unsuspected antacid overdose. The presentation and pathophysiology of antacid-related metabolic alkalosis is reviewed.

Undisclosed self-medication--a clinical pitfall.

Over-the-counter medication may produce side-effects or precipitate hospital admission. Our patient's self-medication, initially not admitted, led to much mental and physical morbidity.

[Chronic bismuth poisoning with encephalopathy and dementia]. / Chronische Wismutintoxikation mit Enzephalopathie und Demenz.

A 58-year-old woman developed severe progressive dementia. Markedly impaired memory, apraxia and abnormal behaviour with psychotic components suggested Alzheimer's syndrome. But there were atypical signs, namely abnormal coordination, occasional tremors and dysarthria. A search for a possible toxic cause was at first unsuccessful, but by chance a "gastric power" containing 0.1 g of bismuth gallate per gram of powder, was found in her night-table. The patient had taken it regularly over years, at a dosage of up to 1.5 g daily, to combat gastric acidity. Six days after stopping the drug the blood bismuth level was 70 micrograms/l, which within 1-2 months fell to 9 micrograms/l. After 4 1/2 months in hospital the patient was discharged in a good general condition and with normal intellectual function.

[The radiological findings in poisonings by metals]. / Hallazgos radiológicos en intoxicaciones por metales.

We present four cases of heavy metal poisoning (mercury, lead, bismuth and arsenic) in which plain chest and/or abdominal assisted in the differential diagnosis of the clinical picture manifested upon admission at our Emergency Department. The patients suffering from mercury, lead, and bismuth poisoning recovered some weeks after treatment was started. However, the patient with arsenic trioxide poisoning developed cardio-circulatory collapse leading to death three days after admission.