A complicated hospitalization following dilute ammonium chloride ingestion.

INTRODUCTION: Unintentional ingestions of dilute (<7.5%) cleaning solutions containing ammonium chloride typically do not cause serious harm. We present a case of an intentional ingestion of a dilute ammonium chloride solution resulting in significant morbidity. CASE REPORT: A 60-year-old woman with bipolar disorder presented one hour after an intentional ingestion of approximately 15 fluid ounces (500 mL) of an algae and odor humidifier treatment containing a total of 2.25% ethyl ammonium chloride. Initial complaints included nausea with a single episode of nonbilious, nonbloody emesis, mild shortness of breath, and chest and epigastric pain. Physical exam was remarkable for bilateral wheezing and epigastric tenderness. An emergent endoscopy demonstrated a Grade 2b caustic injury in the esophagus and a Grade 3b injury in the stomach. Due to persistent cough, copious oral secretions, and worsening hoarseness, the patient was intubated and admitted to the ICU. Her course was complicated by mild hypotension, nonanion gap metabolic acidosis, and oliguria treated successfully with intravenous (IV) fluids. She also developed bilateral pneumonias later in the hospital course. Bedside bronchoscopy showed laryngeal edema and mucosal injury to the segmental level. The patient underwent tracheostomy on hospital day 6. An upper GI swallow study revealed poor esophageal motility in the mid- to lower third of the esophagus. The patient gradually tolerated oral fluids and on hospital day 20 had her tracheostomy tube removed. The patient was subsequently transferred to the psychiatric ward on hospital day 22. CONCLUSION: Intentional ingestions of dilute ammonium chloride solutions can cause serious injury to the gastrointestinal tract and pulmonary systems, which can result in a complicated and prolonged hospitalization.

High prevalence of diffuse parenchymal lung diseases among Turkish tinners.

The objective is to investigate the prevalence of parenchymal lung diseases among tinners. Twenty-four tinners who signed an informed consent form in the Gaziantep area were the subjects of this study. Demographics, spirometric test results, and high resolution computed tomography (HRCT) scans were obtained for all the tinners. Out of 24 tinners, eleven tinners (46%) had HRCTs consistent with DPLD. Of these 11 subjects, HRCT findings were consistent with respiratory bronchiolitis interstitial lung disease in nine, usual interstitial pneumonia pattern in one, and non-specific interstitial pneumonia in one. HRCT patterns consistent with DPLDs are significantly prevalent among Turkish tinners. This is the first field study reporting this occupational lung hazard in tinners. Future research is needed to uncover the underlying mechanisms.

Hypokalemic metabolic acidosis attributed to cough mixture abuse.

This report describes a patient with mixed normal anion gap hyperchloremic metabolic and respiratory acidosis associated with hypokalemia attributed to cough mixture abuse. Metabolic acidosis was likely related to an overdose of ammonium chloride, whereas respiratory acidosis was probably related to the effect of hypokalemia on respiratory muscles, causing hypoventilation. Hypokalemia was caused by a transcellular shift of potassium induced by ephedrine and pseudoephedrine. Both ammonium chloride and ephedrine were probably present in the cough mixture obtained by our patient as an over-the-counter medication. Physicians should be aware of the potential for cough mixture abuse to cause major electrolyte disturbances that may carry the risk for major cardiac arrhythmias, particularly in youth.

Acute zinc chloride ingestion in a child: local and systemic effects.

A 16-month-old boy ingested liquid zinc chloride/ammonium chloride soldering flux. He developed severe local burns, metabolic acidosis, hepatic damage, hyperamylasemia, lethargy, and hypertension. Peak measured plasma zinc was 1,199 micrograms/dL. Because of persistent signs of systemic toxicity, he was chelated with dimercaprol (BAL) and EDTA. Although clinical improvement was noted coincident with the initiation of chelation, there was no apparent increase in urinary zinc excretion. Scarring in the gastric antrum necessitated an antrectomy. The child recovered without other apparent complications.

[The intraerythrocytic acid-base status in dogs]. / Untersuchungen zum intraerythrozytären Säure-Basen-Status beim Hund.

The determination of the intracellular acid-base state is reported in this paper, using erythrocytic haemolysate in dogs as an example. Reference values are given for 217 clinically healthy dogs. The effects of various selected stages of illness and additional stresses on the erythrocytic acid-base equilibrium are reported and compared with acid-base changes in the blood. The metabolic acidosis observed may occur earlier and be stronger in the intracellular space than in the blood. There seems to be a closer correlation between a disturbed intraerythrocytic acid-base equilibrium and the degree of clinical symptoms than between the (commonly investigated) acid-base changes in the blood and the clinical presentations. The investigation of the blood alone does not provide a satisfactory indication of the patient's acid-base state and of the necessity for treatment.

[Antidotal effect of Stenoloma chusanum(L.) Ching against arsenic and ammonium].

The antidotal effect of four extracts from Stenoloma chusanum on acute poisoning of mice caused by arsenic and ammonium chloride was observed. The result shows: extracts B and C can reduce the mortality of mice remarkably, while extract C can raise the tolerance of mice by raising their LD50 from 31.1 +/- 4.3 mg/kg to 38.2 +/- 5.9 mg/kg. In the case of the mice poisoned by ammonium chloride, the four extracts can also reduce the mortality, but make no significant difference as compared with the control group statistically (P greater than 0.05).

Ammonium chloride poisoning in chronic renal disease.

A 58-year-old woman with a long history of renal stone disease and urinary tract infection presented to the emergency room with exhaustion and air hunger. Laboratory data confirmed profound metabolic acidosis. Unduly large quantities of bicarbonate and potassium were required for correction of the deficits. She had been taking 6 g daily of ammonium chloride as a urine-acidifying agent for a period of six months in addition to agents directed against urinary tract infection. The combination of impaired renal function and effective hydrogen ion loading resulted in profound systemic acidosis. The metabolic derangements associated with the administration of ammonium chloride and its use as a therapeutic agent are discussed.