Life-threatening hyperkalemia from cream of tartar ingestion.

INTRODUCTION: Cream of tartar (potassium bitartrate) has a long history as a cooking aid and medicinal purgative. Despite containing large amounts of potassium, there are no well-documented cases of it causing toxicity. We report two cases in which intentional ingestions of cream of tartar resulted in life-threatening hyperkalemia. In addition, we briefly review the use of cream of tartar as a historical purgative. CASE REPORTS: In both cases, individuals ingested a large quantity of cream of tartar in an effort to "clean themselves out". They manifested similar initial symptoms (vomiting), abnormal serum potassium (>8.0 mmol/L), and EKG's with peaked T waves. Both patients were treated for hyperkalemia and recovered without complication. A search for articles on an academic internet database failed to identify any cases specifically dealing with ill effects of potassium bitartrate and numerous websites continue to purport its beneficial health effects. CONCLUSION: Ingestion of cream of tartar can potentially result in life-threatening hyperkalemia.

Findings of biopsy-proven chronicity and end-stage renal failure associated with oral sodium phosphate solution.

Bowel purgatives containing oral sodium phosphate (OSP) solution are used frequently in general practice and they have the potential of causing acute kidney injury especially in patients with some identified risk factors. Kidney injury may lead to chronicity and end-stage renal disease. Here we present, with renal biopsy findings, an elderly patient suffering from end-stage renal failure due to OSP solution.

Severe hypermagnesemia as a result of excessive cathartic ingestion in a child without renal failure.

A 14-year-old girl was referred to our hospital with lethargy and hypotension and was found to have a serum magnesium level of 14.9 mg/dL after having received an magnesium hydroxide (Magnesie Calcinee) for 7 days because of constipation. She was lethargic, her blood pressure was 70/40 mm Hg, and electrocardiogram revealed prolonged corrected QT interval and first-degree atrioventricular block. She has no renal dysfunction. Emergency hemodialysis after her condition ameliorated, her serum magnesium levels returned to normal. The present case suggests that massive oral magnesium ingestion with severe constipation and ileus may result severe hypermagnesemia without renal dysfunction.

Destroyed lung due to aspiration of phenolphthalein.

A 76-year-old female, presented with a recurrent cough and haemoptysis after an aspiration of a 'grain de Valls'. Chest radiography and computed tomography demonstrated an atelectasis of the medial segment of the right middle pulmonary lobe. Bronchoscopy was negative for any malignancy but the onco-PET-scan showed a pathologic hypermetabolic lesion in the right middle lobe. A lobectomy was performed and pathology revealed a 'destroyed lung' with images of foreign body reactions and microabscesses without any sign of malignancy. Postoperatively, clinical improvement with complete resolution of the symptoms was observed. With this case report we demonstrate the irritative and clastogenic characteristics of phenolphtalein, the main active ingredient of the 'grain de Valls'. This case also illustrates an example of a false positive PET-scan.

Fatal acute sodium phosphate enemas intoxication.

We describe a patient who died as a result of severe hypocalcaemia and hyperphosphatemia after treatment with a sodium-phosphate enema. Physicians should be aware of the risk when using these enemas, even in normal doses, especially in elderly patients without signs of renal failure, as in our patient.

Acute phosphate nephropathy following oral sodium phosphate bowel purgative: an underrecognized cause of chronic renal failure.

The findings of diffuse tubular injury with abundant tubular calcium phosphate deposits on renal biopsy are referred to as nephrocalcinosis, a condition typically associated with hypercalcemia. During the period from 2000 to 2004, 31 cases of nephrocalcinosis were identified among the 7349 native renal biopsies processed at Columbia University. Among the 31 patients, 21 presented with acute renal failure (ARF), were normocalcemic, and had a history of recent colonoscopy preceded by bowel cleansing with oral sodium phosphate solution (OSPS) or Visicol. Because the precipitant was OSPS rather than hypercalcemia, these cases are best termed acute phosphate nephropathy. The cohort of 21 patients with APhN was predominantly female (81.0%) and white (81.0%), with a mean age of 64.0 yr. Sixteen of the 21 patients had a history of hypertension, 14 (87.5%) of whom were receiving an angiotensin-converting enzyme inhibitor or angiotensin receptor blocker. The mean baseline serum creatinine was 1.0 mg/dl, available within 4 mo of colonoscopy in 19 (90.5%) patients. Patients presented with ARF and a mean creatinine of 3.9 mg/dl at a median of 1 mo after colonoscopy. In a few patients, ARF was discovered within 3 d of colonoscopy, at which time hyperphosphatemia was documented. Patients had minimal proteinuria, normocalcemia, and bland urinary sediment. At follow-up (mean 16.7 mo), four patients had gone on to require permanent hemodialysis. The remaining 17 patients all have developed chronic renal insufficiency (mean serum creatinine, 2.4 mg/dl). Acute phosphate nephropathy is an underrecognized cause of acute and chronic renal failure. Potential etiologic factors include inadequate hydration (while receiving OSPS), increased patient age, a history of hypertension, and concurrent use of an angiotensin-converting enzyme inhibitor or angiotensin receptor blocker.

Lethal iatrogenic hypermagnesemia.

The administration of magnesium is an effective therapeutic option in such conditions as preeclampsia, ischemic heart disease, cardiac arrhythmia, and asthma. It has also been used as a cathartic in the treatment of constipation. As a medical therapy, magnesium enjoys an acceptable safety record. Because magnesium is almost exclusively excreted in the urine, significantly elevated levels of magnesium are typically anticipated only in patients with renal dysfunction. With wider application, emerging reports suggest that additional factors such as intestinal hypomotility and chronic constipation should be considered before using magnesium to avoid toxicity.

Extreme hyperphosphatemia and acute renal failure after a phosphorus-containing bowel regimen.

Phosphate intoxication, manifested by hypocalcemic tetany and acute renal failure, may complicate bowel-cleansing preparations which contain phosphate. These preparations are commonly used to prepare patients for various gastrointestinal procedures. Often, patients who receive these regimens are at increased risk of phosphate intoxication from diseases which slow gastrointestinal transit or decrease renal excretion (renal insufficiency). We present a patient who developed oliguric acute renal failure from severe phosphate intoxication associated with a phosphate-containing bowel-cleansing regimen.

Laxative poisoning: toxicological analysis of bisacodyl and its metabolite in urine, serum, and stool.

An 11-year-old boy was hospitalized because of severe diarrhea (over 5 L/day). The child survived; however, the diarrhea continued while he was given intravenous fluids and his electrolyte balance was closely supervised. Based on observation of the patient and his family in the hospital, surreptitious administration of a poison by his mother was suspected, and toxicological analysis was carried out on stools from the boy and on medicine administered to him by his mother. Bisacodyl, a cathartic with a direct effect on the colon, was detected in the medicine, and a metabolite of bisacodyl was present in the stool. We devised a sensitive and reliable method to quantitate the bisacodyl metabolite in urine and serum. The sample was incubated with beta-glucuronidase at 37 degrees C for 2 h; bisacodyl metabolite was extracted with tert-butyl methyl ether, then derivatized by methylation, and subjected to gas chromatography-mass spectrometry. Bisphenol A was used as an internal standard. The calibration curve was linear in the concentration range from 2 to 1000 ng/0.2 mL, and the lower limits of detection were 1 ng/0.2 mL for the urine and 2 ng/0.2 mL for the serum. As concentrations of bisacodyl metabolite in the urine and serum of the patient were clearly defined, perhaps such investigations are warranted before extensive clinical therapy is prescribed.

Magnesium toxicosis in two horses.

Magnesium sulfate, a saline laxative, is often used for treatment of intestinal impactions in horses. Clinical signs of hypermagnesemia are an uncommon complication following oral administration of magnesium sulfate. Overdose of magnesium sulfate in combination with renal insufficiency, hypocalcemia, or compromise of intestinal integrity may predispose horses to magnesium toxicosis. Establishment of diuresis with fluids and IV administration of calcium may provide successful treatment of magnesium toxicosis in horses.

Acute hypermagnesemia after laxative use.

We present the case of a patient in whom hypotension, sudden cardiopulmonary arrest, and coma developed after a massive dose of a seemingly harmless cathartic agent. The diagnosis of hypermagnesemia was made 9 hours after the patient's admission, when the serum magnesium concentration was 21.7 mg/dL (8.9 mmol/L). The patient's condition improved with IV calcium, saline solution infusion, and cardiorespiratory support. The elimination half-life of magnesium in this case was 27.7 hours. Few cases have been reported in which patients have survived with serum levels greater than 18 mg/dL (7.4 mmol/L). This case provides evidence that hypermagnesemia may occur in patients with normal kidney function. The diagnosis of hypermagnesemia should be considered in patients who present with symptoms of hyporeflexia, lethargy, refractory hypotension, shock, prolonged QT interval, respiratory depression, or cardiac arrest.

Munchausen syndrome presenting as hemophilia: a convenient and economical "steal" of disease and treatment.

Munchausen's syndrome and Munchausen's syndrome by proxy (MSBP) can cause many conditions, including bleeding problems, seizures, failure to thrive and others. We report here an unusual case in which a mother presented to the hospital for her hemophiliac son's failure to thrive, subsequently for her own self-inflected mutilating wounds, and finally for self-induced simulation of her son's hemophiliac bleeding and arthritic complications.

Fatal methemoglobinemia caused by inadvertent contamination of a laxative solution with sodium nitrite.

We describe two cases of fatal methemoglobinemia resulting from ingestion of laxative solution inadvertently contaminated with sodium nitrite. Postmortem toxicological examination revealed methemoglobin levels in excess of 75% in both patients--a level that is uniformly fatal. The laxative solution was found to contain sodium nitrite instead of sodium sulphate at a concentration of 15 g/l. The pathophysiology of methemoglobinemia and a review of other reported cases of toxic methemoglobinemia are presented. Marked cyanosis in the face of intact cardiorespiratory function should alert the physician to the possibility of toxic methemoglobinemia.