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PubMed2005

Chest wall necrosis and death secondary to hydrochloric acid infusion for metabolic alkalosis.

Central line complications are common, and extravasation injuries related to infusion of caustic substances have been previously described. Although hydrochloric acid has been used for many years to treat metabolic alkalosis, there have been no reported fatal complications. We report the case of a 53-year-old female who received a fatal chemical burn due to extravasation from a subclavian central venous catheter of hydrochloric acid infused to correct severe metabolic alkalosis. This case illustrates the hazards of the infusion of caustic substances through central lines and underscores the importance of constant vigilance regarding line positioning and changes to the surrounding tissues when infusing these substances.

Alkalosis↗
PubMed2000

Separation of trace amounts of palladium (II) with crown ether from hydrochloric acid and potassium thiocyanate media.

A new method for the separation of trace amounts of palladium from hydrochloric acid and potassium thiocyanate media has been established based on the formation of an ion-pair complex of palladium thiocyanate anion Pd(SCN)4(2-) and the cationic potassium complex of dicyclohexyl- 18-crown-6 (DC18C6) in chloroform. The effect of various factors (solvent, crown ether, potassium thiocyanate, hydrochloric acid, reagent concentration, shaking time, phase volume ratio, composition of the extracted species, foreign ions, etc.) on the extraction and back-extraction of palladium has been investigated. The method can be combined with subsequent FAAS determination of palladium. The procedure was applied to determine palladium traces in chloroplatinic acid and rhodium chloride.

Journal Article↗
PubMed1975

Postoperative metabolic alkalosis and acute renal failure: rationale for the use of hydrochloric acid.

Metabolic alkalosis secondary to chloride depletion, especially following gastrointestinal surgery and associated with acute renal failure, is a frequent clinical occurrence. Management of the resultant acid-base disturbance mandates chloride replacement. The presence of oliguria limits the choice of accompanying cation. The use of intravenous hydrochloric acid to correct and maintain proper chloride balance, secondary to external gastric fluid losses, is recommended as a straightforward approach. Two brief case synopses are presented. Both patients, florid examples of profound chloride depletion, required large amounts of intravenous hydrochloric acid. The options regarding the choice of chloride solution, hazards involved, and a simplified schema of replacement therapy are presented. Combined gastrointestinal and renal dysfunction create unusual biochemical and clinical alterations and may result in a complex management problem.

Acute Kidney Injury↗
PubMed2001

[A case of disseminated intravascular coagulopathy (DIC) and multiple organ failure (MOF) after ingestion of hydrochloric acid].

Ingestion of caustic materials causes systemic damages and requires treatment in an intensive care unit. This report presents a case of disseminated intravascular coagulopathy (DIC) and multiple organ failure after ingestion of hydrochloric acid in an attempted suicide. The patient was admitted to the emergency ward within 1 hr after ingestion of 60 ml of 35% hydrochloric acid. Initial blood examination suggested hemolysis without anemia or thrombocytopenia. Arterial blood gas analysis exhibited evident metabolic acidosis with hypoxia. Two hours after ingestion, severe hemolysis, anemia, thrombocytopenia emerged with abnormal results from clotting and fiblinolysis tests, and a diagnosis of DIC was made. Subsequently, conjugate deviation and severe bleeding diathesis appeared. No evidence for gastrointestinal bleeding and brain hemorrhage was obtained in our abdominal echography and brain computed tomography, respectively. In spite of vigorous suppurative therapy including transfusion of blood, fresh frozen plasma, and catecholamines, the patient expired 29 hrs after ingestion. Autopsy was not carried out. Rapid progressive DIC as an acute complication of acid ingestion must be born in mind.

Acidosis↗
PubMed1986

Role of endogenous prostaglandins in duodenal alkaline response to luminal hydrochloric acid or arachidonic acid in conscious dogs.

Duodenal secretion of HCO-3 and luminal release of PGE2 were measured in conscious dogs. The results show that the HCO-3 secretion is closely correlated with the luminal release of PGE2 and that both the HCO-3 and the PGE2 outputs increase dose-dependently after topical application of hydrochloric acid or arachidonic acid. Indomethacin reduced basal HCO-3 and PGE2 release and prevented their increase in response to hydrochloric acid or arachidonic acid. We conclude that mucosal PGE2 plays an important role in the alkaline secretion from the duodenum.

Animals↗
PubMedDate not supplied

[Hydrolysis of lorazepam with hydrochloric acid. Qualitative and quantitative analysis of byproducts of hydrolysis].

Results of the identification of some additional products in the hydrochloric acid hydrolysis of lorazepam are reported, together with some quantitative results about the hydrolysis products under varying circumstances. It appeared that the amount of byproducts was reduced by applying hydrochloric acid of good quality and further on hydrolysis time had to be short.

Chromatography, Gas↗
PubMed1986

Comparison of pancreatic exocrine secretion via endogenous secretin by intestinal infusion of hydrochloric acid and monocarboxylic acid in anesthetized piglets.

The secretory response of the exocrine pancreas via endogenous secretin (IRS) by intraduodenal instillation of hydrochloric acid (HCl) and various monocarboxylic acid solutions was studied in anesthetized piglets. The secretion induced by HCl solutions of various concentrations containing 250 mM NaCl occurred when pH of the solutions was lower than 1.5. After instillation of the HCl solution of pH 1.0, juice flow and protein output increased 26 times and 9 times, respectively, as compared with basal levels. Such pancreatic responses paralleled an increase in plasma IRS concentration in the portal vein. The pancreatic response induced by a lactic acid solution occurred when pH of the solutions was lower than 3.8. The juice flow and protein output stimulated by a lactic acid solution of 250 mM and pH 2.0 were 16 and 8 times higher than the basal levels. The responses to the lactic acid solution of pH 2.0 increased concentration dependently, and were followed by an increase in IRS concentration in the portal vein. The pancreatic exocrine responses induced by other monocarboxylic acid solutions (250 mM) of pH 2.0 were in the following order: formic acid greater than lactic acid greater than pyruvic acid much greater than acetic acid greater than butyric acid greater than propionic acid. Lactamide, an analogous substance of lactic acid, did not evoke any pancreatic secretion. The results indicate the possibility that pancreatic exocrine response induced by HCl is dependent upon hydrogen ion, while the response induced by monocarboxylic acid is not always dependent on dissociation constant of acid.

Anesthesia↗
PubMed1982

[Antacids: A comparison of their in vitro neutralizing capacity in hydrochloric acid and in acidified peptone solution (author's transl)].

Using a simple and reproducible in vitro-test the neutralizing capacity of different liquid commercial antacids was measured at pH 2.0 and at pH 3.5 in diluted hydrochloric acid and in acidified peptone solution. In peptone solutions corresponding to postprandial gastric juice, antacids containing aluminum hydroxide and aluminate forming components demonstrated a marked loss in their neutralizing capacity when compared to peptone free hydrochloric acid as control. This loss in buffering capacity is dependent on the reaction time, the pH of the reaction mixture, the concentration of peptone in the solution and the amount of aluminum in the different antacid compounds. Furthermore the neutralizing capacity of aluminum hydroxide is also diminished by dibasic organic acids which mimicked fasting gastric juice in the experiment. The different availability of neutralizing potency of aluminum hydroxide containing antacids in acid and in acidified peptone solution will need to be considered when antacids are recommended for the treatment of patients with peptic ulcer disease.

Aluminum Hydroxide↗
PubMed1998

Intravenous lidocaine attenuates acute lung injury induced by hydrochloric acid aspiration in rabbits.

BACKGROUND: Neutrophils play a crucial role in the pathogenesis of acid-induced acute lung injury. Lidocaine inhibits the function of neutrophils. This study aimed to determine whether lidocaine attenuates acute lung injury induced by hydrochloric acid (HCl) instillation. METHODS: In study 1, rabbits were divided into four groups (n = 7 each). Lung injury was induced by intratracheal HCl (0.1 N, 3 ml/kg) in two groups. The other two groups received saline intratracheally. Lidocaine given intravenously (2 mg/ g bolus + 2 mg x kg(-1) x h(-1) infusion) was started 10 min before intratracheal instillation in one HCl and one saline group, and saline was given intravenously in the other two groups. In study 2, rabbits (four groups of seven animals each) received HCl (0.1 N, 3 ml/kg) intratracheally. Treatment with intravenous lidocaine was started 10 min before, 10 min after, or 30 min after acid instillation, or saline was given intravenously 10 min before instillation. RESULTS: In study 1, HCl caused deterioration of the partial pressure of oxygen (PaO2), lung leukosequestration, decreased lung compliance, and increased the lung wet-to-dry weight ratio and albumin, interleukin-6 (IL-6), and IL-8 levels in bronchoalveolar lavage fluid. Lidocaine pretreatment attenuated these changes. Hydrochloric acid increased superoxide anion production by neutrophils and caused morphologic lung damage, both of which were lessened by lidocaine. In study 2, lidocaine given 10 min after acid instillation was as effective as pretreatment in PaO2, lung mechanics, and histologic examination. However, PaO2 changes in lidocaine 30 min after injury were similar to those in saline given intravenously. CONCLUSIONS: Intravenous lidocaine started before and immediately after acid instillation attenuated the acute lung injury, in part by inhibiting the sequestration and activation of neutrophils.

Anesthetics, Local↗
PubMed1983

Analytical methods based on transformations with hydrochloric acid.

Ultraviolet spectrophotometric methods are described for alpha-ethyl benzhydrol derivatives, 3-trifluoromethyl-alpha-ethyl benzhydrol (flumecinol), 2,5-dimethyl-alpha-ethyl benzhydrol (RGH-3395) an impurity of the latter, (1,4-di-(2,5-dimethyl-phenyl)-1,4-diphenyl-butan-1,4-diol). The methods are based on dehydrations catalysed by hydrochloric acid yielding unsaturated aromatic chromophores. The determination of 2-acetyl-3-phenyl-tetrahydro-1,2,4-oxadiazin-5-one (RGH-4615) is also based on treatment with hydrochloric acid; the chromophoric compound is a benzaldoxime derivative. The hydrochloric acid-catalysed transformation of ethynodiol diacetate to its 3,5-diene derivative enables the parent compound to be determined by gas chromatography.

Journal Article↗
PubMed1996

Hydrochloric acid inhalation: who needs admission?

Nine pharmaceutical workers were exposed to hydrochloric acid (HCl) fumes. Four were discharged with no symptoms after a 4 h observation period in the accident and emergency (A&E) department. The remaining five were admitted to the medical unit because of severe symptoms, reduced peak expiratory flow rate (PEFR), or hypoxaemia. Treatment was symptomatic and discharge followed 24 h later. Only one patient, discharged from the medical unit, developed long term airway hyper-reactivity, superimposed on a background of chronic obstructive airways disease. Thus patients who are minimally symptomatic with normal PEFR and oxygen saturation values can be safely discharged from the A&E department after a short observation period of 4 h with advice to return if dyspnoea occurs. Caution should be employed in severely symptomatic patients, those with pre-existing lung pathology or reduced PEFR, and hypoxaemic patients, where observation for at least 24 h is recommended.

Adult↗
PubMed1996

Enamel erosion resulting from hydrochloric acid tablets.

This article documents a case of severe enamel erosion caused by chewing hydrochloric acid tablets over a five-year period. Dentists must be aware that highly erosive acids are obtainable without a prescription, in this case from a health food store. They must also be alert for signs of dental erosion and identify the source of the acid.

Aged↗
PubMed1980

Effects of an intravenous infusion of hydrochloric acid on renal function in sheep.

Responses to an intravenous infusion of hydrochloric acid (150 mumol/min for three days), sufficient to induce mild acidosis, were studied in eight ewes. No changes in glomerular filtration rate or renal plasma flow were detected as blood and urine pH, plasma PCO2, plasma concentrations of hydrogencarbonate and inorganic phosphate were reduced by the acid infused. Urinary excretion of hydrogencarbonate was abolished while that of inorganic phosphate was slightly increased. The quantities of hydrogencarbonate and inorganic phosphate ions filtered and reabsorbed decreased whereas the proportion of the filtrate reabsorbed remained unaltered.

Animals↗
PubMed1983

New method for administration of hydrochloric acid in metabolic alkalosis.

In a new method for peripheral intravenous infusion of hydrochloric acid the HCl is buffered in an aminoacid solution and infused with a fat emulsion. The aminoacids and the fat emulsions are stable in the presence of HCl, and the transfusion set is resistant to the chemical actin of 0.15 mol/l HCl. Two case-reports show that HCl can be administered safely through a peripheral vein.

Alkalosis↗
PubMed2006

In vitro effects of hydrochloric acid and various concentrations of acetic, propionic, butyric, or valeric acids on bioelectric properties of equine gastric squamous mucosa.

OBJECTIVE: To compare the effects of hydrochloric acid (HCl) and various concentrations of volatile fatty acids (VFAs) on tissue bioelectric properties of equine stomach nonglandular (NG) mucosa. SAMPLE POPULATION: Gastric tissues obtained from 48 adult horses. PROCEDURES: NG gastric mucosa was studied by use of Ussing chambers. Short-circuit current (Isc) and potential difference (PD) were measured and electrical resistance (R) and conductance calculated for tissues after addition of HCl and VFAs (5, 10, 20, and 40 mM) in normal Ringer's solution (NRS). RESULTS: Mucosa exposed to HCl in NRS (pH of 1.5 and, to a lesser extent, 4.0) had a significant decrease in Isc, PD, and R, whereas tissues exposed to acetic acid at a pH of < 4.0, propionic and butyric acids at a pH of <or= 4.0, and valeric acid at a pH of <or= 7.0 induced a concentration-dependent effect on reduction in these same values. Values for Isc returned to baseline (recovery of sodium transport) after addition of calcium carbonate in tissues exposed to all concentrations of VFAs except the higher concentrations of valeric acid at a pH of <or= 4.0. Histologic examination revealed cell swelling in the mucosal layers below and adjacent to the stratum corneum in tissues exposed to HCl and VFAs at a pH of <or= 4.0. CONCLUSIONS AND CLINICAL RELEVANCE: The VFAs, especially acetic acid, in the presence of HCl at a pH of <or= 4.0 appear to be important in the pathogenesis of NG mucosal ulcers in horses.

Acetic Acid↗