Liquid ammonia injury

The toxic effects of a gas depend on the time of exposure, concentration and its chemical nature. Pressurized liquids and gases exert an additional cold thermal injury and this may complicate the clinical picture. A patient who had an accidental exposure to liquid ammonia over a prolonged period, manifesting in cutaneous, respiratory and ocular damage in addition to a severe cold thermal injury (frostbite) with a fatal outcome is presented. The patient had flaccid quadriparesis and episodes of bradycardia, which has not been reported previously. These manifestations raise the possibility of the systemic toxicity in patients with prolonged exposure to ammonia.     

Effect of cortical-medullary gradient for ammonia on urinary excretion of ammonia

Previous studies suggested that a portion of ammonia secreted into the proximal tubule may diffuse directly from Henle's loop into the medullary collecting duct. Since water is absorbed along the course of the descending portion of the loop, it was proposed that the concentration of ammonia increased in loop fluid, and that rapid diffusibility of the free base would facilitate the delivery of ammonia into medullary interstitium where a high level could be maintained by the countercurrent exchange process. In this schema it was proposed that there was an ammonia concentration gradient between medullary structures and cortex, and recovery of ammonia by the medullary collecting duct due to the low pH in tubule fluid at that site. The present study was designed to evaluate this hypothesis by estimating ammonia concentrations in medullary and cortical tissue, and by correlating medullary levels with secretion rate into the inner medullary collecting duct. In control animals the concentration of total ammonia (NH4+ + NH3+) in inner medullary vasa recta was 9.2 +/- 1.5 mumoles/ml, a level 100-fold higher than the cortical level of 0.10 +/- 0.01. During acute acidosis the medullary level rose to 22.5 +/- 2.7 mumoles/ml, but in acute acidosis during mannitol infusion the level fell to 8.0 +/- 1.2. The rate of ammonia secretion into inner medullary collecting duct fluid correlated directly with medullary vasa recta ammonia concentration. These data provide evidence for a steep ammonia concentration gradient between the medulla and cortex, and suggest that the diffusion gradient across collecting duct epithelium governs the rate of the addition of ammonia to collecting duct fluid.     

Inhalation of ammonia vapour

Eight men were admitted to hospital following exposure to gaseous ammonia at a local factory. They were divided into three groups, according to their clinical condition. The clinical findings, chest radiographs and treatment are discussed. One case was very severely injured. His management is discussed in detail. He required mechanical ventilation, positive end expiratory pressure and tracheostomy. The toxic effects of ammonia gas are discussed. A review of the literature is included. It was concluded that ammonia is an extremely irritant gas, capable of producing severe damage to all levels of the respiratory tract which may result in clinical impairment of respiratory function, ranging from mild to fatal. Prolonged respiratory support may be required. Superinfection may cause a late deterioration in those severely affected.     

Acute toxicity of ammonia to Artemia sp.]

The acute toxicity of total ammonia-N, (NH3 + NH4+), and un-ionized ammonia-N, NH3-N, on newly hatched Artemia nauplii and Artemia adults was measured in 24, 48, 72, and 96-h semi-static bioassays system. There was a significant difference (P < 0.05) in medial lethal concentrations (LC50) obtained during the tests. The LC50 values on nauplii ranged from 650 mg/l, in 24-h, to 399.1 mg/l total ammonia-N, in 96-h, while the LC50 values on adults ranged from 1290.4 mg/l to 600.5 mg/l total ammonia-N, in the same period. Two methods for calculations of un-ionized ammonia toxicity are analyzed and discussed.     

Role of ammonia in the induction of renal hypertrophy

Recent experiments from our laboratory have documented the importance of ammonia as a modulator of renal cell growth in vitro. Ammonia induces renal hypertrophy by increasing the rate of protein synthesis and decreasing the rate of protein degradation. These results have led to the hypothesis that an increase in renal ammoniagenesis contributes to renal growth in several seemingly unrelated clinical disorders. In chronic hypokalemia and metabolic acidosis, mitochondrial ammoniagenesis is stimulated directly. During protein loading, uninephrectomy, and diabetes mellitus, renal ammoniagenesis may be stimulated by an increase in single-nephron glomerular filtration rate (SNGFR).     

Relationship of renal ammonia production and potassium homeostasis.

Renal ammonia production appears to be intimately related to potassium homeostasis, and the two may comprise the components of a closed loop regulatory system. Studies with both intact organisms and in vitro systems indicate that potassium depletion stimulates and chronic potassium-loading suppresses renal ammonia production. An increase in ammoniagenesis has been shown to decrease potassium excretion. These observations suggest that changes in potassium modulate ammonia production, which in turn maintains hydrogen ion homeostasis and influences potassium excretion. Potassium depletion increases rat renal cortical ammonia production by altering metabolism in fashion identical to metabolic acidosis, but there is no convincing evidence that both processes are mediated by similar changes in either cellular hydrogen ion or potassium concentration. By contrast, potassium-loading, which depresses ammonia production, appears to affect primarily the outer medulla, a region that is not influenced by potassium depletion. Thus, potassium-loading apparently affects different portions of the renal tubule than depletion does, but the specific mechanism and physiologic significance of the different sites of action is unknown.     

Acute anhydrous ammonia injury from accidents during illicit methamphetamine production

BACKGROUND: Anhydrous ammonia (AA), a chemical commonly used in agriculture, is a key component in illicit methamphetamine production. Although injuries associated with AA exposure are well studied, AA injuries associated with incidents during illicit methamphetamine production have not been adequately described in the literature. OBJECTIVE: This study better characterizes AA injuries occurring in an agricultural region where illicit methamphetamine production is common. METHODS: We performed a cross-sectional study based on a chart review of 49 patients who were admitted to a tertiary hospital in Illinois with known or suspected exposures to chemical agents. Indices of morbidity were compared between injuries resulting from exposure to AA and injuries from other chemicals, and between AA injuries from incidents during illicit methamphetamine production and AA injuries from other causes. RESULTS: AA was the most common cause of chemical injury (41%; n=20/49). Incidents during illicit methamphetamine production were the most common cause of AA injury (75%; n=15/20). AA injury was associated with significantly greater morbidity compared to non-AA chemical injury. In addition, methamphetamine-related AA injury was associated with significantly greater morbidity compared to non-methamphetamine-related AA injury. CONCLUSION: Chemical burns during illicit methamphetamine production were the most common cause of both chemical and AA-related injury in our agricultural population and these injuries were associated with greater morbidity during hospitalization.     

Fatal ammonia inhalation. A case report with autopsy findings

A 25-year-old refrigeration technician died 85 days after accidental massive anhydrous ammonia inhalation; the case history and autopsy findings are described. The latter included bronchiectasis and obliterative bronchiolitis, but interstitial fibrosis and emphysema were conspicuously absent. The roles of dosage, infection, and healing are discussed.     

Electrophysiology of ammonia transport in renal straight proximal tubules.

To test for electrogenic transport of ammonium ions in straight proximal renal tubules, isolated perfused tubules have been exposed to peritubular ammonium ions during continuous recording of cell membrane potential. As a result, 20 mmol/liter NH4+ leads to a rapid, reversible depolarization of the cell membrane by 9.0 +/- 0.3 mV (N = 86). This depolarization is not significantly affected by 10 mmol/liter barium or 0.1 mmol/liter amiloride on both sides of the epithelium, but is significantly blunted by omission of extracellular bicarbonate and CO2 (3.8 +/- 0.4 mV, N = 9), by 1 mmol/liter acetazolamide (4.3 +/- 0.3 mV, N = 11), by 1 mmol/liter peritubular amiloride (4.3 +/- 1.1 mV, N = 7), by 1 mmol/liter SITS (5.7 +/- 0.4 mV, N = 6), and by replacement of extracellular sodium with choline (4.7 +/- 0.5 mV, N = 8). In the presence of both amiloride (1 mmol/liter) and acetazolamide (1 mmol/liter) in the bath, the NH4+ induced depolarization is completely abolished. Furthermore, the combined omission of bicarbonate and addition of 10 mmol/liter barium eliminates the NH4+ induced depolarization. About 50% of the depolarization can be explained by enhanced electrogenic bicarbonate exit due to the intracellular alkalosis. The other 50% is explained by amiloride and barium sensitive electrogenic entry of NH4+ into the cell.     

Anhydrous ammonia burns case report and review of the literature

Chemical burns are associated with significant morbidity, especially anhydrous ammonia burns. Anhydrous ammonia is a colorless, pungent gas that is stored and transported under pressure in liquid form. A 28 year-old patient suffered 45% total body surface area of second and third degree burns as well as inhalational injury from an anhydrous ammonia explosion. Along with fluid resuscitation, the patient's body was scrubbed every 6 h with sterile water for the first 48 h to decrease the skin pH from 10 to 6-8. He subsequently underwent a total of seven wound debridements; initially with allograft and then autograft. On post burn day 45, he was discharged. The injuries associated with anhydrous ammonia burns are specific to the effects of ammonium hydroxide. Severity of symptoms and tissue damage produced is directly related to the concentration of hydroxyl ions. Liquefactive necrosis results in superficial to full-thickness tissue loss. The affinity of anhydrous ammonia and its byproducts for mucous membranes can result in hemoptysis, pharyngitis, pulmonary edema, and bronchiectasis. Ocular sequelae include iritis, glaucoma, cataracts, and retinal atrophy. The desirability of treating anhydrous ammonia burns immediately cannot be overemphasized. Clothing must be removed quickly, and irrigation with water initiated at the scene and continued for the first 24 h. Resuscitative measures should be started as well as early debridement of nonviable skin. Patients with significant facial or pharyngeal burns should be intubated, and the eyes irrigated until a conjunctivae sac pH below 8.5 is achieved. Although health care professionals need to be prepared to treat chemical burns, educating the public, especially those workers in the agricultural and industrial setting, should be the first line of prevention.     

Effect of amino acid solutions on the blood ammonia level

We have carried out several basic experiments on artificial liver support and found that the plasma free amino acid balance was lost after treatment according to this procedure. Application of fluid therapy--Using conventional amino acid preparations available on the market--Is not adequate during and after the treatment with artificial liver. Fluid therapy using mainly special amino acid preparations should have been established; preparations, named Todai Hospital fluid (THF), are intended to correct the deranged aminogram, supply nutrition and promote the improvement in symptoms. Furthermore, experimental animals with acute hepatic insufficiency of diverse severity were prepared and basic experiments were performed which these animals to see how the efficacy of THF developed. In the basic experiments, psychoneurotic symptoms and the electroencephalogram were improved with the lowering of the blood ammonia level. Clinically, THF was not only used as a therapeutic agent after treatment by artificial liver support in patients with fulminant hepatitis, but is also served as a further indication in hepatic encephalopathy accompanying chronic liver diseases in late stages. Improvement in encephalopathy was observed immediately after the administration of THF and persisted while the aminogram pattern returned to the premedication representation. There was more improvement in patients in whom ammonemia was complicated, and the blood ammonia level was reduced markedly.