Ammonia

January 26, 2006

Suzie can you be roused from this sleep easily?? Or is it deep?? Does your Mom and Dad have a key to your house?? If not get one made for them. Contact your family Doctor..This is important Suzie really and truly important and very scary hon!!! Kathy Boosuzie <suzieandsandy@...> wrote: Hi, The infectious disease guy I see (Dr Idiot) wants me to go down east - I haven't asked where cause I'm really not interested in a transplant. I've got an appointment with him in April & will ask at that time where he wants to send me. It won't be anywhere in the States, that's for sure, OHIP - the Ontario health program - won't

pay for me to go to the States when comparable tx is available here & it is. I'm thinking of going for the assessment just to find out how my liver feels. The past few days I've done nothing but sleep - wake up for a few minutes then back to sleep. I've never done that before - anyone have an idea what's going on? HUGS, SuZieKathy Brunow

January 26, 2006

Hey , I've seen a GI doc a few times lately - mainly for the endoscopy which came out good - no varicies . He told me the doc I'm seeing knows a lot more than he does about HCV. The infectious diseases guy seems to want to hand me off to the GI since he thinks I won't jump when he say hop. I really don't like the guy. Me & Sir SpYke the Fuzzy do O K. He wakes me up whenever his dish is empty so don't worry, I'm up every six to eight hours (depending on his appetite) How does ESLD feel? I don't feel all that bad, a little foggy sometimes & tired all the time but no pain or

anything. I don't feel bad at all just tired. SuZie <kcmija@...> wrote: Hi, Here in the states ID Dr's are great,but I wouldn't go to one for Hep C.I know we are talking about different country's so Im just talking from some experience and off the top of my head.please don't take any offense. The best option here is a Hepatolagist,a GI specialist that has specialized again in Hepatitis.Most here might insist on a transplant or not treat.They can be jerks. There are some Hematologist(blood

specialist) that are very good and also some great Internal Medicine Dr's that are very Knowledgeable. I don't know how much choice you have there,I've heard it takes forever to get tests and have seen many Canadians come to the states for treatment or different kinds of tests. You say you don't want a transplant but it sounds like your end stage.Do you have close family?If not here in the states you would be in trouble,support is important. Here I would suggest at least a good sympathetic Family Dr. that would treat you Pallatively. Wish you the best Re: Ammonia Sorry Kathy-Boo I was referring to the area around Hamilton or is it Guelph ? Whatever, it's still quite a ways from you. I get the impression I'd have to be closer than that. You are definitely NOT nobody. Hugs, SuZieKathy Brunow <kathy-boo@...> wrote: Suzie want you mean you don't know any one down here!! I'm down here!! In Milwaukee WI, just down from you..Heck when we go to deer camp we are just across the lake from you!!!We get a lot of Canadas Transplant people here!!! No kidding..But hey I respect your descion you know.. It is after all you liver hon!! But I am not NOBODY!!!! Kathy Kathy Brunow Next time I'm coming back as a cat

Next time I'm coming back as a cat

January 26, 2006

What's the big deal people?? I'm sleeping, not comatose. I've got an appointment with my family doc next week & I will tell her all about it, I promise. SuZieKathy Brunow <kathy-boo@...> wrote: Suzie can you be roused from this sleep easily?? Or is it deep?? Does your Mom and Dad have a key to your house?? If not get one made for them. Contact your family Doctor..This is important Suzie really and truly important and very scary hon!!! Kathy Boosuzie <suzieandsandy@...> wrote: Hi, The infectious disease guy I see (Dr Idiot) wants me to go down east - I haven't asked where cause I'm really not interested in a transplant. I've got an appointment with him in April & will ask at that time where he wants to send me. It won't be anywhere in the States, that's for sure, OHIP - the Ontario health program - won't pay for me to go to the States when comparable tx is available here & it is. I'm thinking of going for the assessment just to find out how my liver feels. The past few days I've done nothing but sleep - wake up for a few minutes then back to sleep. I've never done that before - anyone have an idea what's going on? HUGS,

SuZie Kathy Brunow

Next time I'm coming back as a cat

January 26, 2006

Well suzie I felt foggy most of the time and slept constantly,don't remember much pain.Go with the Dr you get along the best with,we can help you train Him/Her what they need to know.

Re: Ammonia

Sorry Kathy-Boo I was referring to the area around Hamilton or is it Guelph ? Whatever, it's still quite a ways from you. I get the impression I'd have to be closer than that. You are definitely NOT nobody.

Hugs,

SuZieKathy Brunow <kathy-boo@...> wrote:

Suzie want you mean you don't know any one down here!! I'm down here!! In Milwaukee WI, just down from you..Heck when we go to deer camp we are just across the lake from you!!!We get a lot of Canadas Transplant people here!!! No kidding..But hey I respect your descion you know.. It is after all you liver hon!! But I am not NOBODY!!!! Kathy

Kathy Brunow

Next time I'm coming back as a cat

January 26, 2006

Why are you scaring us..I know what your going though.. And it is obvious you haven't a clue.. Why???Tell us!!! Why don't you care???Do you even read want is being posted of this subject!!!! Then I won't say any more..I will not resond in any way any more ok!!! And Deb I am sorry so spouting off.. Yell at me later OK...suzie <suzieandsandy@...> wrote: What's the big deal people?? I'm sleeping, not comatose. I've got an appointment with my family doc next week & I will tell her all about it, I promise. SuZieKathy Brunow

January 27, 2006

Kathy Boo, Sorry if I'm worrying you but I've read the stuff on ESLD & don't think I'm there yet. I'm not jaundiced, no ascites or malnutrition. I do have edema, & encephalopathy and my blood doesn't clot very well any more but my LFTs haven't changed much(of course they've always been high). I'm sorry you're worried but I feel fine. How can I tell for sure if there's something wrong? What do you guys think I should be doing besides going for the transplant assessment? Love you all, SuZieKathy Brunow <kathy-boo@...> wrote: Why are you scaring us..I know what your going though.. And it is obvious you haven't a clue.. Why???Tell us!!! Why don't you care???Do you even read want is being posted of this subject!!!! Then I won't say any more..I will not resond in any way any more ok!!! And Deb I am sorry so spouting off.. Yell at me later OK...suzie <suzieandsandy@...> wrote: What's the big deal people?? I'm sleeping, not comatose. I've got an appointment with my family doc next week & I will tell her all about it, I promise. SuZie Kathy Brunow

Next time I'm coming back as a cat

January 27, 2006

Hiya SuZie,

When I have a long day some times I will sleep for the next 2 days. My record is 54 hours straight only getting up to pee.

Do you have any problems with neuropathy? Muscle tremors? Day/Night reversal?

Allan with 2 L's

RE: Re: Ammonia

Kathy Boo,

Sorry if I'm worrying you but I've read the stuff on ESLD & don't think I'm there yet. I'm not jaundiced, no ascites or malnutrition. I do have edema, & encephalopathy and my blood doesn't clot very well any more but my LFTs haven't changed much(of course they've always been high).

I'm sorry you're worried but I feel fine. How can I tell for sure if there's something wrong? What do you guys think I should be doing besides going for the transplant assessment?

Love you all,

SuZieKathy Brunow <kathy-boo@...> wrote:

Why are you scaring us..I know what your going though.. And it is obvious you haven't a clue.. Why???Tell us!!! Why don't you care???Do you even read want is being posted of this subject!!!! Then I won't say any more..I will not resond in any way any more ok!!! And Deb I am sorry so spouting off.. Yell at me later OK...suzie <suzieandsandy@...> wrote:

What's the big deal people?? I'm sleeping, not comatose. I've got an appointment with my family doc next week & I will tell her all about it, I promise.

SuZie

Kathy Brunow

Next time I'm coming back as a cat

January 27, 2006

Hey Allan, Yeah, I've got some problems there. My doctor referred me to a neurologist a few years back cause of my hand tremors & he said I have "essential neuropathy" & it would just get worse - nothing can be done. It has gotten worse, now it's jerky & I 'm dropping things a lot. I also went for a neuro-psych exam & the guy there said I was normal except for the lack of short term memory. I told him I've always scored in the upper 10% of the pop but he'd never seen me before so had no bench mark to reckon loss from. As far as day/night reversal, I've never heard of it but I worked the midnight shift (midnight to eight a m) for over twenty years. SuZieAllan W Anger Jr <allananger@...>

wrote: Hiya SuZie, When I have a long day some times I will sleep for the next 2 days. My record is 54 hours straight only getting up to pee. Do you have any problems with neuropathy? Muscle tremors? Day/Night reversal? Allan with 2 L's

Next time I'm coming back as a cat

January 27, 2006

You

did good letting your family know where you’re at with it now. That was

a big start. Did you tell your mother to come check on you if you didn’t

answer the phone?

Hugs

& kisses,

De

RE: Re:

Ammonia

Kathy Boo,

Sorry if I'm worrying you but I've read the stuff

on ESLD & don't think I'm there yet. I'm not jaundiced, no ascites or

malnutrition. I do have edema, & encephalopathy and my blood doesn't clot

very well any more but my LFTs haven't changed much(of course they've always

been high).

I'm sorry you're worried but I feel fine. How can I tell

for sure if there's something wrong? What do you guys think I should be doing

besides going for the transplant assessment?

Love you all,

SuZie

January 28, 2006

Hey De, No I haven't asked her, I'm going to talk to my niece about phoning on a regular basis, she's in nursing school at Lakehead University so she can research & understand this better. She can handle it better too, my parents are too old - they've got enough to worry about with their own health problems. I will ask (my niece) to get my Mum to come over if I don't answer the phone on schedule. It's funny tho' - I e-mailed both my sisters about everything but only one responded. Maybe she takes after our mother more than I thought they both seem to think it'll go away if they don't talk about it. Denial's a big thing in our family it seems. H & G

SuZie Motley <dmotley@...> wrote: You did good letting your family know where you’re at with it now. That was a big start. Did you tell your mother to come check on you if you didn’t answer the phone? Hugs & kisses, De

Next time I'm coming back as a cat

January 28, 2006

Hi suzie,

Down here I think we say essential or familial tremor.Peripheral neuropathy is common in Hep C and a complication of Interferon,I have it and there are meds for it.

Also globulins or an increased level can cause tremors and neuropathy.The two primary proteins in the blood are albumin and globulin.You might want to know your albumin level and globulin level.

Just want you to stay informed,if you didn't already know about that.

Re: Re: Ammonia

Hey Allan,

Yeah, I've got some problems there. My doctor referred me to a neurologist a few years back cause of my hand tremors & he said I have "essential neuropathy" & it would just get worse - nothing can be done. It has gotten worse, now it's jerky & I 'm dropping things a lot. I also went for a neuro-psych exam & the guy there said I was normal except for the lack of short term memory. I told him I've always scored in the upper 10% of the pop but he'd never seen me before so had no bench mark to reckon loss from. As far as day/night reversal, I've never heard of it but I worked the midnight shift (midnight to eight a m) for over twenty years.

SuZieAllan W Anger Jr <allananger@...> wrote:

Hiya SuZie,

When I have a long day some times I will sleep for the next 2 days. My record is 54 hours straight only getting up to pee.

Do you have any problems with neuropathy? Muscle tremors? Day/Night reversal?

Allan with 2 L's

Next time I'm coming back as a cat

January 28, 2006

Thanks - that's what I meant tremor, not neuropathy . The tremors suck big time, it's more jerky now than it was before, I keep dropping things. I've never had my globulins tested that I know of, I'll ask my doctor when I see her next week. I'm diabetic so the chiropodist checks my feet for neuropathy at least twice a year. Thanks again, SuZie <kcmija@...> wrote: Hi suzie, Down here I think we say essential or familial tremor.Peripheral neuropathy is common in Hep C and a complication of Interferon,I have it and there are meds for it. Also globulins or an increased level can cause tremors and neuropathy.The two primary proteins in the blood are albumin and globulin.You might want to know your albumin level and globulin level. Just want you to stay informed,if you didn't already know about that. ----- Original

Message ----- From: suzie Hepatitis CSupportGroupForDummies Sent: Friday, January 27, 2006 4:55 PM Subject: Re: Re: Ammonia Hey Allan, Yeah, I've got some problems there. My doctor referred me to a neurologist a few years back cause of my hand tremors & he said I have "essential neuropathy" & it would just get worse - nothing can be

done. It has gotten worse, now it's jerky & I 'm dropping things a lot. I also went for a neuro-psych exam & the guy there said I was normal except for the lack of short term memory. I told him I've always scored in the upper 10% of the pop but he'd never seen me before so had no bench mark to reckon loss from. As far as day/night reversal, I've never heard of it but I worked the midnight shift (midnight to eight a m) for over twenty years. SuZieAllan W Anger Jr <allananger@...> wrote: Hiya SuZie, When I have a long day some times I will

sleep for the next 2 days. My record is 54 hours straight only getting up to pee. Do you have any problems with neuropathy? Muscle tremors? Day/Night reversal? Allan with 2 L's Next time I'm coming back as a cat

Next time I'm coming back as a cat

February 2, 2006

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Health Link to this site You are in: eMedicine Specialties > Emergency Medicine > Toxicology Toxicity, AmmoniaLast Updated: January 3, 2006 Rate this Article Email to a Colleague Get CME/CE for article Synonyms and related keywords: anhydrous ammonia, NH3, liquid ammonia, ammonia exposure, inhalation of ammonia, ingestion of ammonia, ammonia ingestion, ammonia inhalation, ammonium hydroxide, liquid anhydrous ammonia, toxic ammonia exposure, ammonia toxicity, ammonia poisoning, fertilizer AUTHOR INFORMATION Section 1 of 10 Author Information Introduction Clinical Differentials Workup Treatment Medication Follow-up Miscellaneous Bibliography Author: Issley, MD, CCFP, FRCPC, Emergency Physician, Faculty Lecturer, Emergency Department, McGill University Health Centre (Montreal General Hospital) Coauthor(s): Eddy Lang, MDCM, CCFP (EM), CSPQ, Assistant Professor, Department of Family Medicine, McGill University; Consulting Staff, Department of Emergency Medicine, The Sir Mortimer B -Jewish General Hospital Editor(s): Edmond Hooker, MD, Assistant Clinical Professor, Department of Emergency Medicine, University of Louisville, State University; T VanDeVoort, PharmD, Clinical Assistant Professor, College of Pharmacy, University of Minnesota; J Burns, MD, Instructor, Department of Emergency Medicine, Harvard University Medical School, Beth Israel Deaconess Medical Center; Halamka, MD, Chief Information

Officer, CareGroup Healthcare System, Assistant Professor of Medicine, Department of Emergency Medicine, Beth Israel Deaconess Medical Center; Assistant Professor of Medicine, Harvard Medical School; and J Roberge, MD, MPH, FAAEM, FACMT, Clinical Associate Professor of Emergency Medicine, University of Pittsburgh School of Medicine; Consulting Staff, Department of Emergency Medicine, Magee-Women's Hospital of the University of Pittsburgh Medical Center Disclosure INTRODUCTION Section 2 of 10 Author Information Introduction Clinical Differentials Workup Treatment Medication Follow-up Miscellaneous Bibliography Background: At room temperature, ammonia (NH3) is a highly water-soluble, colorless, irritant gas with a unique pungent odor. Ammonia has a boiling point of -33°C and an ignition temperature of 650°C. In 1993, anhydrous ammonia was the third most produced chemical by volume in the US. The farming industry uses approximately one third of the ammonia produced in the US as a component of fertilizer and animal feed. Industrial injury most often results from ammonia leaks in fertilizer tanks and hoses and toxic ammonia levels in animal buildings. Swine confinement buildings are particularly notorious

for containing toxic levels of ammonia that often exceed threshold limit values. Because ammonia is liberated during combustion of nylon, silk, wood, and melamine, firefighters also are at risk for exposure to this irritant gas. Before the 1970s, liquid ammonia stored under high pressure was widely used for refrigeration. Although Freon largely has replaced ammonia as a refrigerant, ammonia refrigeration is still used and numerous case reports exist of severe toxicity following accidental exposure. Ammonia also is used in the production of explosives, pharmaceuticals, pesticides, textiles, leather, flame-retardants, plastics, pulp and paper, rubber, petroleum products, and cyanide. Furthermore, ammonia is a major component of many common household cleaning and bleaching products (eg, glass cleaners, toilet bowel cleaners, metal polishes, floor strippers, wax removers, smelling salts). Permissible levels of exposure to toxic gases are defined by time-weighted

average (TWA), short-term exposure limit (STEL), and concentration at which toxic gasses are immediately dangerous to life or health (IDLH). The TWA is defined as the concentration for an 8-hour workday of a 40-hour workweek that nearly all workers can be exposed to without adverse effects. Similarly, the STEL is the concentration to which an exposure of longer than 15 minutes is potentially dangerous and may produce immediate or chronic compromise to health. Anhydrous ammonia has a TWA of 25 ppm, an STEL of 35 ppm, and an IDLH of 500 ppm. Although injury from ammonia most commonly is caused by inhalation, it also may follow ingestion or direct contact with eyes or skin. The clinical presentations of these injuries and their investigation and treatment are discussed in this article; chloramine gas inhalation injury also is discussed. Pathophysiology: The most common mechanism by which ammonia gas causes damage occurs when anhydrous ammonia

(liquid or gas) reacts with tissue water to form the strongly alkaline solution, ammonium hydroxide. NH3 + H2O ®NH4OH This reaction is exothermic and capable of causing significant thermal injury. Ammonium hydroxide also causes severe alkaline chemical burns to skin, eyes, and especially the respiratory system. Mild exposures primarily affect the upper respiratory tract, while more severe exposures tend to affect the entire respiratory system (see Clinical). The gastrointestinal tract also may be affected if ammonia is ingested. Tissue damage from alkali is caused by liquefaction necrosis and typically penetrates far deeper than that caused by an equipotent acid. In the case of ammonium

hydroxide, the tissue breakdown liberates water, thus perpetuating the conversion of ammonia to ammonium hydroxide. In the respiratory tract, this results in the destruction of cilia and the mucosal barrier to infection. Furthermore, secretions, sloughed epithelium, cellular debris, edema, and reactive smooth muscle contraction cause significant airway obstruction. Airway epithelium can regain barrier integrity within 6 hours following exposure if the basal cell layer remains intact. However, damaged epithelium often is replaced by granular tissue, which may be one of the etiologies leading to chronic lung disease following ammonia inhalation injury. Liquid anhydrous ammonia (-33°C) freezes tissue on contact. To put this in perspective, critical skin damage begins at -4°C and becomes irreversible at -20°C. The degree of tissue injury, however, is proportional to the duration and concentration of exposure. Similarly, damage to the respiratory system is

proportional to depth of inhalation, duration of exposure, concentration, and pH of the gas or liquid. Ammonia is a product of protein catabolism and is metabolized by the liver. Normal blood ammonia levels range from 80-110 mcg/dL. This increases 10% with exposure to 25 ppm but is not considered harmful. Theoretically, patients with liver dysfunction are at increased risk for ammonia toxicity; however, currently no sufficient clinical evidence can confirm this. Frequency: In the US: Similar to previous years, in 2002, US poison control centers reported nearly 6000 cases of toxic ammonia exposure. Of exposures, 93% were unintentional, and 11% resulted in moderate to severe outcomes. Of note, in cases of household exposure, only 5% were moderate to severe. Age: Of the 6000 toxic ammonia exposures reported in the American Association of Poison Control Centers' 2002 Annual Report,

70% occurred in adults and 20% occurred in children younger than 6 years. Ingestion of household solutions usually is accidental and occurs in young children; adult ingestions, however, most often are suicide attempts. Inhalation injury is almost always accidental. Because inhalation exposure generally occurs in an industrial setting, it usually is associated with working adults. CLINICAL Section 3 of 10 Author Information Introduction Clinical Differentials Workup Treatment Medication Follow-up Miscellaneous Bibliography History: The literature on ammonia toxicity in humans largely consists of case reports. In a 1996 literature review, de la Hoz et al found only 94 previously reported cases; of these cases, 20 resulted in fatality and only 35 had clinical follow-up of one year or more. Despite lack of data, most literature is consistent regarding clinical presentation and treatment of ammonia toxicity. Gaseous ammonia effects at various concentrations are as follows: 25 ppm or less - TWA 25-50 ppm - Detectable odor; unlikely to experience adverse effects 50-100 ppm - Mild eye, nose, and throat irritation; may develop tolerance in 1-2 weeks with no adverse effects thereafter 140 ppm - Moderate eye irritation; no long-term sequelae in exposures of less than 2 hours 400 ppm - Moderate throat irritation 500 ppm - IDLH 700 ppm - Immediate eye injury 1000 ppm - Directly caustic to airway 1700 ppm - Laryngospasm 2500 ppm - Fatality (after half-hour exposure) 2500-6500 ppm - Sloughing and necrosis of airway mucosa, chest pain, pulmonary edema, and bronchospasm 5000 ppm - Rapidly fatal exposure Inhalation injury Because of its high water solubility, ammonia has a tendency to be absorbed by the water-rich mucosa of the upper respiratory tract. However, unlike most highly water-soluble irritant gases that tend to affect exclusively the upper respiratory tract, ammonia can damage proximally and distally. In 1941, Caplin was the first to classify victims of accidental ammonia exposure; he described them as mild, moderate, and severe. Patients in the mild group presented with conjunctival and upper respiratory inflammation and pain but showed no signs

of respiratory distress. The moderate group presented similarly but with more exaggerated symptoms. The severe group presented in frank respiratory distress with productive cough, pulmonary edema, and dysphagia. Following a brief ammonia exposure, damage generally is limited to the upper airway mucosa. Brief exposures at very high concentrations, however, can be overwhelming and affect the entire respiratory system. People who are capable of escaping their environment usually are not subject to severe exposures, because they can flee upon detection of ammonia's pungent odor; furthermore, absence of symptoms following inhalational exposure to ammonia essentially rules out significant injury. Pain (oropharyngeal, retrosternal) Dyspnea, hemoptysis - As expected, individuals with reactive airway disease, such as asthmatics, are particularly sensitive to ammonia

inhalation. Hoarseness Dysphagia Loss of consciousness Farming industry In enclosed animal confinement buildings, ammonia is adsorbed by dust particles that transport it more directly to small airways. Because of this synergistic effect, symptoms have reportedly developed within minutes of entering animal confinement buildings. Symptoms include rhinorrhea, scratchy throat, chest tightness, cough, dyspnea, and eye irritation and usually subside within 24-48 hours. Contact - Burns and cold injury Gaseous ammonia combines with water of the skin, eyes, and airways to form ammonium hydroxide. This exothermic reaction results in both heat and chemical burns. Liquid ammonia freezes tissue on contact and may cause full-thickness tissue damage that

penetrates deeper than the more conspicuous superficial chemical burns. Concentrations greater than 10,000 ppm are required to cause skin damage. The eyes begin to feel irritated at concentrations of 50-100 ppm; at 700 ppm, immediate eye damage occurs. Ingestion Typical household ammonia products (3-10% ammonium hydroxide) have a pH less than 12.5, although the pH of industrial solutions (up to 30% ammonium hydroxide) is often greater than 13. Because caustic alkali burns generally are thought to occur when pH is greater than 12.5, ammonia ingestions in the home usually do not lead to significant damage. However, Klein et al reported 3 cases of oropharyngeal and esophageal injury following intentional ingestion of household solutions with a pH less than 12. Patients present with oropharyngeal, epigastric, and retrosternal pain.

Abdominal pain and other gastroenterologic symptoms may occur if ingestion causes viscus perforation (perforation may occur up to 24-72 hours postingestion). Respiratory symptoms may be present if aspiration pneumonia or pneumonitis complicates ingestion. Smelling salts are a less common source of household ammonia ingestion. Often in capsule form, smelling salts, which contain approximately 20% ammonia, release a pungent odor when broken. Smelling salts are found in many first-aid kits as a treatment for syncope; unfortunately, children sometimes bite into! them, r esulting in minor esophageal burns and mild respiratory symptoms. Physical: Inhalation injury Head, ears, eyes, nose, throat (HEENT) - Facial and oral burns and ulceration Respiration - Tachypnea, oxygen

desaturation, stridor, drooling, cough, wheezing, rhonchi, and decreased air entry Central nervous system (CNS) - Loss of consciousness (if exposure is massive) Contact - Burns and cold injury Skin - Alkali burns to the skin are yellow, soapy, and soft in texture. When burns are severe, skin turns black and leathery. HEENT - Burns to the eye penetrate particularly deeply and rapidly, leading to destruction of the inner structures within 2-3 minutes; this may progress to globe perforation. Ammonia typically causes more corneal epithelium and lens damage than other alkalis. Intraocular pressure and pH of the anterior chamber rise, resulting in a syndrome similar to acute narrow-angle glaucoma. Other symptoms include iritis, corneal edema, semi-dilated fixed pupil, and eventual cataract formation. Ingestion Cardiovascular - With intentional ingestion, hypovolemic shock may occur because of vomiting and third-spacing of intravascular fluid. HEENT - Symptoms include edema of the lips, oropharynx, and upper airway. GI - Patient may experience epigastric tenderness; mediastinitis and peritoneal signs may be present with viscus perforation, which can occur as late as 24-72 hours postingestion. Respiratory - Aspiration pneumonia and pulmonary edema may occur. DIFFERENTIALS

Section 4 of 10 Author Information Introduction Clinical Differentials Workup Treatment Medication Follow-up Miscellaneous Bibliography Acute Respiratory Distress Syndrome Anaphylaxis Burns, Chemical Burns, Ocular Burns, Thermal Esophagitis Hazmat Iritis and Uveitis Pediatrics, Anaphylaxis Pediatrics, Reactive Airway Disease Pediatrics, Respiratory Distress Syndrome Respiratory Distress Syndrome, Adult Toxicity, Chlorine Gas Toxicity, Hydrogen Sulfide Toxicity, Phosgene Other Problems to be Considered: Other toxic inhalations or ingestionsConcomitant traumaReactive airway dysfunction syndrome (RADS) Quick Find Author InformationIntroductionClinicalDifferentialsWorkupTreatmentMedicationFollow-upMiscellaneousBibliographyClick for related images. Related Articles Acute Respiratory Distress Syndrome Anaphylaxis Burns, Chemical Burns, Ocular Burns, Thermal Esophagitis Hazmat Iritis and Uveitis Pediatrics, Anaphylaxis Pediatrics, Reactive Airway Disease Pediatrics, Respiratory Distress Syndrome

Respiratory Distress Syndrome, Adult Toxicity, Chlorine Gas Toxicity, Hydrogen Sulfide Toxicity, Phosgene Continuing Education CME available for this topic. Click here to take this CME. Patient Education Burns CenterThermal Burns OverviewThermal Burns CausesThermal Burns SymptomsThermal Burns Treatment WORKUP Section 5 of 10 Author Information Introduction Clinical Differentials Workup Treatment Medication Follow-up Miscellaneous Bibliography Lab Studies:

Complete blood count (CBC) Electrolytes, blood urea nitrogen (BUN), and creatinine Serial arterial blood gases (ABGs) in cases of significant respiratory distress Metabolic acidosis Respiratory alkalosis Increased alveolar-arterial gradient Note that serum ammonia levels are of little value because they do not correlate with clinical condition. However, patients with compromised hepatic function may show increased serum ammonia levels because of less efficient metabolism. Imaging Studies: Chest x-ray (CXR) Chest x-ray findings vary from normal to diffuse micronodular interstitial infiltrates. However, abnormal x-ray findings may take up to 48 hours to develop, even following severe exposure. Other findings to consider are noncardiogenic pulmonary edema, acute respiratory distress syndrome (ARDS), secondary bacterial bronchopneumonia, and pneumomediastinum. Abdominal series (to rule out perforation following ingestion) Other Tests: Cardiac monitor Oxygen saturation monitor Pulmonary capillary wedge pressure (PCWP) monitoring (in cases of severe pulmonary edema or ARDS) Pulmonary function tests (PFTs) - Once acute emergency is controlled; useful to gauge severity and monitor progress and recovery Obstructive lung disease (acute and chronic) Restrictive lung disease (chronic) Ventilation/perfusion (V/Q) scan - May be useful to gauge severity or progress of disease; unlikely to change acute management Ventilation deficits generally are more pronounced in the larger airways. The ventilation scan also may show abnormal air trapping in the setting of lower airway obstruction. Slit-lamp examination with fluorescein staining, tonometry and conjunctival pH (see Physical: HEENT) Procedures: Perform bronchoscopy to assess respiratory tract damage following acute inhalation injury (in severe cases). Airway edema, obstruction, and necrosis Epithelial sloughing Laryngitis and tracheitis Diffuse alveolar

damage Perform endoscopy for ingestion exposures. Indications are controversial; obtain a GI consultation. Perform endoscopy on symptomatic patients and patients with intentional ingestions within 48 hours following ingestion. The risk of perforation increases if endoscopy is performed more than 72 hours postingestion. Laryngeal and epiglottic edema Friable erythematous esophagus Corrosive injury TREATMENT Section 6 of 10 Author Information Introduction Clinical Differentials Workup Treatment Medication Follow-up Miscellaneous Bibliography Prehospital Care: Immediately remove patient from the contaminated environment. Remove all clothing. Support airway, breathing, and circulation (ABCs) as per advanced cardiac life support (ACLS) and advanced trauma life support (ATLS) guidelines. (ACLS and ATLS guidelines may vary by region, according to training and legal responsibilities of prehospital care providers.) If the patient is sufficiently stable, begin copious skin and eye irrigation immediately following exposure. Continue irrigation for at least 20 minutes. Patients then can be covered with a dry clean dressing and sheet. Provide a container for patients with ingestion exposure. Emergency Department Care: Decontaminate the patient (if not previously performed) and support ABCs as necessary. Provide warmed humidified oxygen. As with all burns, patients with facial

or oral lesions are at high risk for developing laryngeal edema. Airway intervention should be aggressive. Indications for intubation include severe respiratory distress (hypoxemia, hypercapnia), stridor, hoarseness, deep facial burns, burns identified by bronchoscopy or endoscopy, and depressed mental status. If intubation is necessary, use large size tube to prevent plugging by sloughed mucosa. Some consider procedural sedation preferable to rapid sequence intubation (RSI) because paralysis is risky with a difficult and edematous airway. Furthermore, ventilation cannot be predicted as successful if intubation fails in this context. Positive end respiratory pressure (PEEP) generally is useful (5 cm water minimum). Beware of fluid over-resuscitation. Patients may have or may be developing noncardiogenic pulmonary edema. Follow standard initial burn

management. (Discussion is beyond the scope of this article.) Once patient is adequately stable, irrigate skin with tepid water for at least 15 minutes. Continue frequent regular irrigation for the first 24 hours, in addition to conventional burn management. Debride wounds and dress with 1% silver sulfadiazine (avoid using on face). Administer tetanus prophylaxis. Irrigate eye injuries with copious amounts of tepid water for at least 30 minutes or until conjunctival pH is 6.8-7.4; use pH indicator paper to monitor. Examine eye with slit-lamp and fluorescein staining. Perform tonometry to determine if intraocular pressure is elevated. Consult ophthalmology promptly because of risk of perforation and/or permanent eye damage. Treat ingestions using the following steps: Rinse mouth and dilute ingestion

with approximately 250 cc of water or milk. Do not induce emesis, so as not to reproduce injury with a second pass of toxin. Consult gastroenterology promptly for subsequent endoscopic evaluation (not often performed before 12 hours postingestion). Consultations: When appropriate, immediately consult an intensivist, medical toxicologist, ophthalmologist (all eye injuries), gastroenterologist, and general and plastic surgeons. MEDICATION Section 7 of 10 Author Information Introduction Clinical Differentials Workup Treatment Medication Follow-up Miscellaneous Bibliography Management of toxic exposure to

ammonia is largely supportive, and medical therapy is directed at hypoxia, bronchospasm, pulmonary edema, hypovolemia, and burns of the skin and eyes. Antibiotics and corticosteroids are controversial therapies following ammonia inhalation and ingestion exposures. Although antibiotics and corticosteroids are often used in the acute treatment of patients with inhalation injury, neither has shown to improve outcome and many feel that corticosteroids may actually increase morbidity. Corticosteroids are recommended to treat bronchospasm in patients with underlying reactive airways disease and acute inhalation injury or for chronic respiratory complications that follow an acute inhalation injury. Most authorities, however, do recommend both IV corticosteroid and antibiotic administration to symptomatic patients following ammonia ingestion. Corticosteroids are administered to decrease the incidence and severity of esophageal strictures that occur during healing from

significant alkaline injuries. Antibiotics are given because of increased risk of mediastinitis associated with full-thickness esophageal alkaline corrosive burns. Although controlled animal studies do support the use of these therapies, no well-controlled human trials have been performed; thus, corticosteroids and antibiotics should be administered in consultation with a gastroenterologist. If steroids are administered, the recommended dose is 1-2 mg/kg/d of methylprednisolone for 3 wk followed by gradual tapering. If antibiotics are administered, a broad-spectrum antibiotic (second-generation cephalosporin) is appropriate. The decision to continue or stop corticosteroid and antibiotic therapy is based on endoscopic findings. Discontinue steroid and antibiotic therapies for patients with no injury or mild mucosal inflammation or ulceration, as they are not at risk for stricture formation. Furthermore, patients with severe transmural burns are at risk for stricture

formation, but steroid therapy will not alter their risk. Thus, antibiotic therapy alone is recommended for this group to diminish their risk of mediastinitis. Patients with extensive superficial ulceration or deep discrete or circumferential ulcerations are at risk for stricture formation and may benefit from steroid administration. Administer corticosteroid and antibiotics to this group of patients. Drug Category: Bronchodilators -- Bronchodilators selectively stimulate beta 2-adrenergic receptors of the bronchial tree and lungs. Bronchodilation results from relaxation of bronchial smooth muscle, which relieves bronchospasm and reduces airway resistance. Drug Name Albuterol, salbutamol (Proventil, Ventolin) -- Beta 2-agonist for bronchospasm refractory to epinephrine. Relaxes bronchial smooth muscle by action

on beta 2-receptors with little effect on cardiac muscle contractility. Adult Dose 5 mg/mL of solution for nebulization, mixed as 0.5-1 cc with 2.5 cc of water and nebulized prn Pediatric Dose 0.2 mg/kg/dose = 0.03 cc/kg/dose (standard solution), prepared as above Contraindications Documented hypersensitivity; tachydysrhythmias Interactions Beta-adrenergic blockers antagonize effects; inhaled ipratropium may increase duration of bronchodil! atation by albuterol; cardiovascular effects may increase with MAOIs, inhaled anesthetics, tricyclic antidepressants, and sympathomimetic agents; interactions are of relative importance when dealing with life-threatening toxicity Pregnancy C - Safety for use during pregnancy has not been established. Precautions Caution in hyperthyroidism, diabetes mellitus, and cardiovascular disordersDrug Category: Diuretics -- Are used to alleviate pulmonary edema. However, some believe that PEEP may be more useful than diuretics for optimizing oxygenation because pulmonary edema is secondary to alveolar capillary injury, not excess fluid. Nonetheless, a trial of diuretics poses little risk and may be used concomitantly with PEEP. Drug Name Furosemide (Lasix) -- Loop diuretic; inhibits sodium chloride reabsorption in the ascending loop of Henle. Administer IV because this allows for superior potency and a higher peak concentration, despite an increased incidence of

adverse effects, particularly ototoxicity (rare). Adult Dose 20 mg IV for patients not regularly using furosemide40-80 mg IV for patients regularly using furosemide80-120 mg IV for patients with symptoms refractory to the initial dose at up to 1 hHigher doses and more rapid redosing for patients in severe distressIf minimal or no response with initial dose, double next dose Pediatric Dose Not established Contraindications Documented hypersensitivity; hepatic coma; anuria; severe electrolyte depletion Interactions Metformin decreases furosemide concentrations; interferes with hypoglycemic effect of antidiabetic agents and antagonizes muscle relaxing effect of tubocurarine; coadministration with

aminoglycosides appears to increase auditory toxicity; hearing loss of varying degrees may occur; may enhance anticoagulant activity of warfarin when taken concurrently; increased plasma lithium levels and toxicity are possible when taken concurrently Pregnancy C - Safety for use during pregnancy has not been established. Precautions Perform frequent serum electrolyte, carbon dioxide, glucose, creatinine, uric acid, calcium, and BUN determinations during first few months of therapy and periodically thereafter; may induce prerenal failureDrug Category: Antibiotics -- Although expensive, topical Silvadene has antipseudomonal properties in addition to coverage for most gram-positive organisms.For eye exposures, antibiotic eye preparations will reduce risk of infection secondary to tissue injury. Drug Name Silver sulfadiazine 1% (Silvadene) -- Useful in prevention of infections from second- or third-degree burns. Has bactericidal activity against many gram-positive and gram-negative bacteria including yeast.Wash burn before application to remove previously applied agent.Not for ophthalmic use.Other products may be used instead of silver sulfadiazine for partial thickness burns; these include TransCyte, Acticoat, or Biobrane. Adult Dose Apply using sterile technique to affected areas qd/bid Pediatric Dose <2 years: Do not administer (risk of kernicterus)>2 years: Apply as in adults Contraindications Documented

hypersensitivity; late pregnancy (risk of kernicterus); facial burns (use Bacitracin instead) Interactions Effect of proteolytic enzymes is reduced when used concomitantly Pregnancy C - Safety for use during pregnancy has not been established. Precautions Caution in G-6-PD deficiency and renal insufficiency Drug Name Ciprofloxacin (Ciloxan) -- Fluoroquinolone with activity against pseudomonads, streptococci, MRSA, S epidermidis, and most gram-negative organisms, but no activity against anaerobes. Inhibits bacterial DNA synthesis and growth.Neomycin 5% is described in much of the literature on ammonia-related eye injury;

however, newer broad-spectrum antibiotics have fewer adverse effects Adult Dose 1 gtt qid (prophylaxis) Pediatric Dose <12 years: Not recommended>12 years: Administer as in adults Contraindications Documented hypersensitivity Interactions Antacids, iron salts, and zinc salts may reduce serum levels; administer antacids 2-4 h before or after taking fluoroquinolones; cimetidine may interfere with metabolism of fluoroquinolones; ciprofloxacin reduces therapeutic effects of phenytoin; probenecid may increase ciprofloxacin serum concentrations; may increase toxicity of theophylline, caffeine, cyclosporine, and digoxin (monitor digoxin levels); may increase effects of anticoagulants (monitor PT) Pregnancy C - Safety for use during pregnancy has not been established. Precautions Prolonged use may result in overgrowth of nonsusceptible organisms, including fungi Drug Name Erythromycin (E-Mycin) -- Indicated for infections caused by susceptible strains of microorganisms and for prevention of corneal and conjunctival infections Adult Dose Apply 1-cm ribbon 4-8 times/d depending on severity of infection Pediatric Dose Apply as in adults Contraindications Documented hypersensitivity; viral, mycobacterial, or fungal

infections of eye; patients using steroid combinations after uncomplicated removal of a foreign body from cornea also should avoid using this product Interactions None reported Pregnancy B - Usually safe but benefits must outweigh the risks. Precautions Do not use topical antibiotics to treat ocular infections that may become systemic; prolonged or repeated antibiotic therapy may result in bacterial or fungal overgrowth of nonsusceptible organisms and may lead to a secondary infection (take appropriate measures if superinfection occurs)Drug Category: Anticholinergic agents -- Induces cycloplegia by blocking the body's parasympathetic (cholinergic) effects in the eye. This is beneficial to prevent ciliary spasm. Drug Name Cyclopentolate (AK-Pentolate) -- Blocks muscle of ciliary body and sphincter muscle of iris from responding to cholinergic stimulation, thus causing mydriasis and cycloplegia.Induces mydriasis in 30-60 min and cycloplegia in 25-75 min; these effects last up to 24 hours Adult Dose 1 gtt into affected eye(s) once; may repeat in 24-48 h prn Pediatric Dose Administer as in adults Contraindications Documented hypersensitivity; narrow-angle glaucoma Interactions Decreases effects of carbachol and cholinesterase inhibitors Pregnancy C - Safety

for use during pregnancy has not been established. Precautions Caution in patients (eg, elderly patients) in whom increased intraocular pressure may be present; can cause toxic anticholinergic systemic adverse effects (common in children especially infants), but incidence is rare when used sparingly; compressing lacrimal sac by digital pressure for 1-3 min following application may minimize systemic absorption Drug Name Homatropine (Isopto Homatropine) -- Blocks responses of sphincter muscle of iris and muscle of ciliary body to cholinergic stimulation, producing pupillary dilation (mydriasis) and paralysis of accommodation (cycloplegia).Induces mydriasis in 10-30 min and cycloplegia in 30-90 min; these effects last up to 48 h. Adult Dose 1 gtt into affected eye(s) once; may repeat in 24-48 h prn Pediatric Dose 1 gtt into affected eye(s) once; may repeat in 24-48 h prn Contraindications Documented hypersensitivity; narrow-angle glaucoma Interactions None reported Pregnancy C - Safety for use during pregnancy has not been established. Precautions Caution in patients (eg, elderly patients) in whom increased intraocular pressure may be present; toxic anticholinergic systemic adverse effects can occur, but incidence is rare when used sparingly; adverse effects are more common in children, especially infants; compressing lacrimal sac by

digital pressure for 1-3 min following instillation minimizes systemic absorption Drug Name Tropicamide (Mydriacyl) -- Blocks sphincter muscle of iris and muscle of ciliary body from responding to cholinergic stimulation Adult Dose 1 gtt into affected eye(s) once Pediatric Dose Administer as in adults Contraindications Documented hypersensitivity Interactions None reported Pregnancy C - Safety for use during pregnancy has not been established. Precautions Caution in patients (eg, elderly patients) in whom increased intraocular pressure may be present; toxic anticholinergic systemic adverse effects can occur, but incidence is rare when used sparingly; adverse effects are more common in children, especially infants; compressing lacrimal sac by digital pressure for 1-3 min following instillation minimizes systemic absorptionDrug Category: Corticosteroids -- Decrease the formation of fibroblasts on the cornea and may limit intraocular inflammation. However, may potentiate infection. Drug Name Prednisolone (Pred Forte) -- Decreases inflammation by suppressing migration of polymorphonuclear leukocytes and reversing increased capillary permeability.Note that ophthalmologic steroids are controversial; discuss their use with

ophthalmology. Also, steroid-antibiotic combination may be useful. Adult Dose 1 gtt q1-6h based on severity of inflammation for 7-10 d Pediatric Dose Administer as in adults Contraindications Documented hypersensitivity; viral, fungal, or tubercular infections Interactions Effects may decrease in patients taking phenytoin, barbiturates, and rifampin Pregnancy C - Safety for use during pregnancy has not been established. Precautions Caution in hypertension; known to cause cataract formation with chronic use; in prolonged use, withdraw treatment by gradually decreasing frequency of applications to

avoid adrenal insufficiency; may increase corneal thinning and melting; risk of globe perforation; discontinue if acute rise in intraocular pressure or ocular infection Drug Name Fluorometholone (FML) -- Suppresses migration of polymorphonuclear leukocytes and reverses capillary permeability Adult Dose 1 gtt q1-6h based on severity of inflammation for 7-10 d Pediatric Dose <2 years: Not established>2 years: Administer as in adults Contraindications Documented hypersensitivity; herpes simplex; keratitis; viral and fungal diseases of the ocular structure Interactions None reported Pregnancy C - Safety for use during pregnancy has not been established. Precautions Prolonged use my result in elevated intraocular pressure or glaucoma Drug Name Rimexolone (Vexol) -- Decreases inflammation by suppressing migration of polymorphonuclear leukocytes and reversing increased capillary permeability. Adult Dose 1 gtt q1-6h based on severity of inflammation for 7-10 d Pediatric Dose Not established Contraindications Documented hypersensitivity; viral, fungal, bacterial

ocular infections Interactions None reported Pregnancy C - Safety for use during pregnancy has not been established. Precautions Caution in corneal or scleral perforation and posterior subcapsular cataractsDrug Category: Local anesthetics -- Used primarily for pain relief. Duration of action is relatively short-lived, limiting usefulness of local anesthetics outside of the hospital or clinic setting. Drug Name Proparacaine 0.5% (Alcaine) -- Has rapid onset of anesthesia that begins within 13-30 sec after instillation. However, has short duration of action of about 15-20 min.Least irritating of all

topical anesthetics. Prevents initiation and transmission of impulse at nerve cell membrane by stabilizing and decreasing ion permeability.Onset of action occurs within 20 s of application.Anesthetic effect may last up to 10-15 min Adult Dose Instill 1-2 gtt into affected eye; may repeat if desired Pediatric Dose Administer as in adults Contraindications Documented hypersensitivity; prolonged use Interactions Increases effects of phenylephrine and tropicamide Pregnancy C - Safety for use during pregnancy has not been established. Precautions Caution in cardiac disease or hyperthyroidism

and those with abnormal or reduced levels of plasma esterasesDo not use outside the ED because prolonged eye anesthesia can eliminate patient's awareness of mechanical damage to cornea; frequent use of anesthetics may retard healing FOLLOW-UP Section 8 of 10 Author Information Introduction Clinical Differentials Workup Treatment Medication Follow-up Miscellaneous Bibliography Further Inpatient Care: Admit patients to observation for at least 24 hours if they show significant and persistent signs, symptoms, or abnormalities in lab findings attributable to ammonia exposure. Admit unstable or potentially unstable patients to intensive

care. Following ingestion, patients may be discharged if endoscopy results are normal and oral intake is tolerated. Intentional ingestions require psychiatric evaluation. Complications: Patients often develop chronic respiratory sequelae, particularly with severe ammonia exposures. In a case series by Close et al, exposed patients experienced gradual deterioration of pulmonary function during the first 2-6 months following exposure. A period of slight improvement was then observed, followed by stabilization of symptoms. Long-term effects of ammonia inhalation injury include the following: Cough Hoarseness Obstructive and/or restrictive lung disease Hyper-reactive airway disease and reactive airway dysfunction syndrome

(RADS) Impaired gas exchange Residual parenchymal damage Bronchiectasis and bronchiolitis obliterans (following massive exposure) It is postulated that chronic obstructive disease is secondary to airway lesions more than hyper-reactivity and, therefore, often minimally improved by bronchodilators. Prognosis: Most individuals with ammonia inhalation who survive the first 24 hours will recover. Patients begin showing improvement within 48-72 hours and may recover fully during this time if exposure was mild. For patients with more significant respiratory symptoms, recovery can be expected within several weeks to months. Interestingly, Arwood et al found that initial chest x-ray and PaO2 poorly correlate with outcome and that

physical examination on arrival is a more sensitive prognosticating factor. Montague and MacNeil, however, note that patients who do not develop chest x-ray findings are less likely to have chronic respiratory sequelae. Patient Education: For excellent patient education resources, visit eMedicine's Burns Center. Also, see eMedicine's patient education article Thermal (Heat or Fire) Burns. MISCELLANEOUS

Section 9 of 10 Author Information Introduction Clinical Differentials Workup Treatment Medication Follow-up Miscellaneous Bibliography Special Concerns:

Chloramine gas Chloramines (NH2Cl, NHCl2) are highly water-soluble irritant gases formed when household bleach (5.25% sodium hypochlorite) is mixed with 5-10% ammonia solutions (usually cleaning products). Fumes contact moist mucous membranes, reacting with water to produce free ammonia gas (see Inhalation injury), hypochloric acid, and hypochlorous acid. The latter then reacts with water to form hydrochloric acid and nascent oxygen, a strong oxidizing agent with corrosive effects. At low concentration, symptoms include tearing, rhinorrhea, oropharyngeal burning, and cough. Although chloramine gases produce rapid onset of symptoms, these symptoms are mild enough

that patients often do not remove themselves promptly from the toxic environment; thus, patients often present after a prolonged exposure time. The physical examination following mild exposure reveals only mild wheezing and decreased air entry or may be entirely unremarkable. Patients with more significant exposure may present with dyspnea, pulmonary edema with secondary hypoxia, nausea, tracheobronchitis, toxic pneumonitis, intrapulmonary shunt and/or pneumomediastinum. Note that pulmonary edema may ensue within minutes or be delayed for up to 24 hours following exposure. Pulmonary function tests may reveal obstructive, restrictive, or combined patterns, and pulmonary artery occlusive pressure may be less than 17 mm Hg. Treat chloramine gas exposure as described under Emergency Department Care. Sodium bicarbonate has been suggested to be an adjunct to supportive treatment, but little clinical experience with this treatment exists. In and Storrow's case series of 22 patients with chloramine toxicity, treatment with sodium bicarbonate resulted in no clinical or statistical improveme! nt. BIBLIOGRAPHY

Section 10 of 10 Author Information Introduction Clinical Differentials Workup Treatment Medication Follow-up Miscellaneous Bibliography Am J Respir Crit Care Med: Respiratory health hazards in agriculture. Am J Respir Crit Care Med 1998 Nov; 158(5 Pt 2): S1-S76[Medline]. Arwood R, Hammond J, Ward GG:

Ammonia inhalation. J Trauma 1985 May; 25(5): 444-7[Medline]. Birken GA, Fabri PJ, Carey LC: Acute ammonia intoxication complicating multiple trauma. J Trauma 1981 Sep; 21(9): 820-2[Medline]. Burgess JL, Pappas GP, on WO: Hazardous materials incidents: the Washington Poison Center experience and approach to exposure assessment. J Occup Environ Med 1997 Aug; 39(8): 760-6[Medline]. Caplin M: Ammonia-gas poisoning: 47 cases in a London shelter. Lancet 1941; 2: 958-61. Close LG, Catlin FI, Cohn AM: Acute and chronic

effects of ammonia burns on the respiratory tract. Arch Otolaryngol 1980 Mar; 106(3): 151-8[Medline]. de la Hoz RE, Schlueter DP, Rom WN: Chronic lung disease secondary to ammonia inhalation injury: a report on three cases. Am J Ind Med 1996; 29(2): 209-14[Medline]. do Pico GA: Toxic fume inhalation. In: Bone RC, Dantzker DR, eds. Pulmonary and Critical Care Medicine. St Louis: Mosby-Year Book; 1998:N5-1- N5-16. do Pico GA: Hazardous exposure and lung disease among farm workers. Clin Chest Med 1992 Jun; 13(2): 311-28[Medline].

Ellenhorn MJ, Schonwald S, Ordog G, eds: Respiratory tract irritants. In: Ellenhorn's Medical Toxicology: Diagnosis and Treatment of Human Poisoning. 2nd ed. Baltimore: Lippincott, & Wilkins; 1996:1519-25. Flury KE, Dines DE, Rodarte JR, Rodgers R: Airway obstruction due to inhalation of ammonia. Mayo Clin Proc 1983 Jun; 58(6): 389-93[Medline]. Goldfrank LR: Toxicological imaging, ophthalmologic principle, occupational and environmental toxics. In: Goldfrank's Toxicologic Emergencies. 5th ed. Norwalk, Conn: Appleton & Lange; 1994:127, 368-9, 1183-1280. Haddad LM, Winchester JF, eds: Clinical Management of Poisoning and Drug Overdose. 2nd ed. Philadelphia: WB Saunders Co; 1990. Klein J, Olson KR, McKinney HE: Caustic injury from household ammonia. Am J Emerg Med 1985 Jul; 3(4):

320[Medline]. Klein JD, Olson KR: Caustic injury from household ammonia, too. J Pediatr 1986 Feb; 108(2): 328[Medline]. Leung CM, Foo CL: Mass ammonia inhalational burns--experience in the management of 12 patients. Ann Acad Med Singapore 1992 Sep; 21(5): 624-9[Medline]. O'Kane GJ: Inhalation of ammonia vapour. A report on the management of eight patients during the acute stages. Anaesthesia 1983 Dec; 38(12): 1208-13[Medline]. Pascuzzi TA, Storrow AB: Mass casualties from acute inhalation of chloramine gas. Military Medicine 1998 Feb; 163(2): 102-4[Medline]. GF Jr: Occupational medicine forum. J Occup Med 1994 Oct; 36(10): 1061-3[Medline]. Rakel RE, ed: Caustics and corrosives. In: Conn's Current Therapy 2000. 51st ed. Philadelphia: WB Saunders Co; 1999:1224-5. Reisz GR, Gammon RS: Toxic pneumonitis from mixing household cleaners. Chest 1986 Jan; 89(1): 49-52[Medline]. Rosenstock L: Acute inhalational injury. In: Textbook of Clinical Occupational and Environmental Medicine. Philadelphia: WB Saunders Co; 1994:236-7. Shenoi R: Chemical Warfare Agents. Clin Ped Emerg Med 2002; 3: 239-247. Sotiropoulos G, Kilaghbian T, Dougherty W, SO: Cold injury from pressurized liquid ammonia: a report of two cases. J Emerg Med 1998 May-Jun; 16(3): 409-12[Medline]. Swotinsky RB, Chase KH: Health effects of exposure to ammonia: scant information. Am J Ind Med 1990; 17(4): 515-21[Medline]. WA, Litovitz TL, Rodgers GC: 2002 annual report of the American Association of Poison Control Centers Toxic Exposure Surveillance System. Am J Emerg Med 2003 Sep; 21(5): 353-421[Medline]. Weiner AL, Bayer MC: Inhalation: Gases with Immediate Toxicity. Ford: Clinical Toxicology 2001; 679. NOTE: Medicine is a constantly changing science and not all therapies are clearly established. New research changes drug and treatment therapies daily. The authors, editors, and publisher of this journal have used their best efforts to provide information that is up-to-date and accurate and is generally accepted within medical

standards at the time of publication. However, as medical science is constantly changing and human error is always possible, the authors, editors, and publisher or any other party involved with the publication of this article do not warrant the information in this article is accurate or complete, nor are they responsible for omissions or errors in the article or for the results of using this information. The reader should confirm the information in this article from other sources prior to use. In particular, all drug doses, indications, and contraindications should be confirmed in the package insert. FULL DISCLAIMER Toxicity, Ammonia excerpt © Copyright 2006, eMedicine.com,

Subscribers We subscribe to the HONcode principles of the Health On the Net Foundation 1996-2005 eMedicine.com, Inc.. Kathy Brunow

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Toxicity, Ammonia Last Updated: January 3, 2006

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Synonyms and related keywords: anhydrous ammonia, NH3, liquid ammonia, ammonia exposure, inhalation of ammonia, ingestion of ammonia, ammonia ingestion, ammonia inhalation, ammonium hydroxide, liquid anhydrous ammonia, toxic ammonia exposure, ammonia toxicity, ammonia poisoning, fertilizer

AUTHOR INFORMATION

Section 1 of 10

Author Information Introduction Clinical Differentials Workup Treatment Medication Follow-up Miscellaneous Bibliography

Author: Issley, MD, CCFP, FRCPC, Emergency Physician, Faculty Lecturer, Emergency Department, McGill University Health Centre (Montreal General Hospital) Coauthor(s): Eddy Lang, MDCM, CCFP (EM), CSPQ, Assistant Professor, Department of Family Medicine, McGill University; Consulting Staff, Department of Emergency Medicine, The Sir Mortimer B -Jewish General Hospital

Editor(s): Edmond Hooker, MD, Assistant Clinical Professor, Department of Emergency Medicine, University of Louisville, State University; T VanDeVoort, PharmD, Clinical Assistant Professor, College of Pharmacy, University of Minnesota;

J Burns, MD, Instructor, Department of Emergency Medicine, Harvard University Medical School, Beth Israel Deaconess Medical Center;

Halamka, MD, Chief Information Officer, CareGroup Healthcare System, Assistant Professor of Medicine, Department of Emergency Medicine, Beth Israel Deaconess Medical Center; Assistant Professor of Medicine, Harvard Medical School;

and J Roberge, MD, MPH, FAAEM, FACMT, Clinical Associate Professor of Emergency Medicine, University of Pittsburgh School of Medicine; Consulting Staff, Department of Emergency Medicine, Magee-Women's Hospital of the University of Pittsburgh Medical Center

Disclosure

INTRODUCTION

Section 2 of 10

Author Information Introduction Clinical Differentials Workup Treatment Medication Follow-up Miscellaneous Bibliography

Background: At room temperature, ammonia (NH3) is a highly water-soluble, colorless, irritant gas with a unique pungent odor. Ammonia has a boiling point of -33°C and an ignition temperature of 650°C.

In 1993, anhydrous ammonia was the third most produced chemical by volume in the US. The farming industry uses approximately one third of the ammonia produced in the US as a component of fertilizer and animal feed. Industrial injury most often results from ammonia leaks in fertilizer tanks and hoses and toxic ammonia levels in animal buildings. Swine confinement buildings are particularly notorious for containing toxic levels of ammonia that often exceed threshold limit values. Because ammonia is liberated during combustion of nylon, silk, wood, and melamine, firefighters also are at risk for exposure to this irritant gas.

Before the 1970s, liquid ammonia stored under high pressure was widely used for refrigeration. Although Freon largely has replaced ammonia as a refrigerant, ammonia refrigeration is still used and numerous case reports exist of severe toxicity following accidental exposure.

Ammonia also is used in the production of explosives, pharmaceuticals, pesticides, textiles, leather, flame-retardants, plastics, pulp and paper, rubber, petroleum products, and cyanide. Furthermore, ammonia is a major component of many common household cleaning and bleaching products (eg, glass cleaners, toilet bowel cleaners, metal polishes, floor strippers, wax removers, smelling salts).

Permissible levels of exposure to toxic gases are defined by time-weighted average (TWA), short-term exposure limit (STEL), and concentration at which toxic gasses are immediately dangerous to life or health (IDLH). The TWA is defined as the concentration for an 8-hour workday of a 40-hour workweek that nearly all workers can be exposed to without adverse effects. Similarly, the STEL is the concentration to which an exposure of longer than 15 minutes is potentially dangerous and may produce immediate or chronic compromise to health. Anhydrous ammonia has a TWA of 25 ppm, an STEL of 35 ppm, and an IDLH of 500 ppm.

Although injury from ammonia most commonly is caused by inhalation, it also may follow ingestion or direct contact with eyes or skin. The clinical presentations of these injuries and their investigation and treatment are discussed in this article; chloramine gas inhalation injury also is discussed.

Pathophysiology: The most common mechanism by which ammonia gas causes damage occurs when anhydrous ammonia (liquid or gas) reacts with tissue water to form the strongly alkaline solution, ammonium hydroxide.

NH3 + H2O ®NH4OH

This reaction is exothermic and capable of causing significant thermal injury.

Ammonium hydroxide also causes severe alkaline chemical burns to skin, eyes, and especially the respiratory system. Mild exposures primarily affect the upper respiratory tract, while more severe exposures tend to affect the entire respiratory system (see Clinical). The gastrointestinal tract also may be affected if ammonia is ingested.

Tissue damage from alkali is caused by liquefaction necrosis and typically penetrates far deeper than that caused by an equipotent acid. In the case of ammonium hydroxide, the tissue breakdown liberates water, thus perpetuating the conversion of ammonia to ammonium hydroxide. In the respiratory tract, this results in the destruction of cilia and the mucosal barrier to infection. Furthermore, secretions, sloughed epithelium, cellular debris, edema, and reactive smooth muscle contraction cause significant airway obstruction.

Airway epithelium can regain barrier integrity within 6 hours following exposure if the basal cell layer remains intact. However, damaged epithelium often is replaced by granular tissue, which may be one of the etiologies leading to chronic lung disease following ammonia inhalation injury.

Liquid anhydrous ammonia (-33°C) freezes tissue on contact. To put this in perspective, critical skin damage begins at -4°C and becomes irreversible at -20°C. The degree of tissue injury, however, is proportional to the duration and concentration of exposure.

Similarly, damage to the respiratory system is proportional to depth of inhalation, duration of exposure, concentration, and pH of the gas or liquid.

Ammonia is a product of protein catabolism and is metabolized by the liver. Normal blood ammonia levels range from 80-110 mcg/dL. This increases 10% with exposure to 25 ppm but is not considered harmful. Theoretically, patients with liver dysfunction are at increased risk for ammonia toxicity; however, currently no sufficient clinical evidence can confirm this.Frequency:

In the US: Similar to previous years, in 2002, US poison control centers reported nearly 6000 cases of toxic ammonia exposure. Of exposures, 93% were unintentional, and 11% resulted in moderate to severe outcomes. Of note, in cases of household exposure, only 5% were moderate to severe.

Age: Of the 6000 toxic ammonia exposures reported in the American Association of Poison Control Centers' 2002 Annual Report, 70% occurred in adults and 20% occurred in children younger than 6 years.

Ingestion of household solutions usually is accidental and occurs in young children; adult ingestions, however, most often are suicide attempts.

Inhalation injury is almost always accidental. Because inhalation exposure generally occurs in an industrial setting, it usually is associated with working adults.

CLINICAL

Section 3 of 10

Author Information Introduction Clinical Differentials Workup Treatment Medication Follow-up Miscellaneous Bibliography

History: The literature on ammonia toxicity in humans largely consists of case reports. In a 1996 literature review, de la Hoz et al found only 94 previously reported cases; of these cases, 20 resulted in fatality and only 35 had clinical follow-up of one year or more. Despite lack of data, most literature is consistent regarding clinical presentation and treatment of ammonia toxicity.Gaseous ammonia effects at various concentrations are as follows:

25 ppm or less - TWA

25-50 ppm - Detectable odor; unlikely to experience adverse effects

50-100 ppm - Mild eye, nose, and throat irritation; may develop tolerance in 1-2 weeks with no adverse effects thereafter

140 ppm - Moderate eye irritation; no long-term sequelae in exposures of less than 2 hours

400 ppm - Moderate throat irritation

500 ppm - IDLH

700 ppm - Immediate eye injury

1000 ppm - Directly caustic to airway

1700 ppm - Laryngospasm

2500 ppm - Fatality (after half-hour exposure)

2500-6500 ppm - Sloughing and necrosis of airway mucosa, chest pain, pulmonary edema, and bronchospasm

5000 ppm - Rapidly fatal exposureInhalation injuryBecause of its high water solubility, ammonia has a tendency to be absorbed by the water-rich mucosa of the upper respiratory tract. However, unlike most highly water-soluble irritant gases that tend to affect exclusively the upper respiratory tract, ammonia can damage proximally and distally.In 1941, Caplin was the first to classify victims of accidental ammonia exposure; he described them as mild, moderate, and severe. Patients in the mild group presented with conjunctival and upper respiratory inflammation and pain but showed no signs of respiratory distress. The moderate group presented similarly but with more exaggerated symptoms. The severe group presented in frank respiratory distress with productive cough, pulmonary edema, and dysphagia.Following a brief ammonia exposure, damage generally is limited to the upper airway mucosa. Brief exposures at very high concentrations, however, can be overwhelming and affect the entire respiratory system. People who are capable of escaping their environment usually are not subject to severe exposures, because they can flee upon detection of ammonia's pungent odor; furthermore, absence of symptoms following inhalational exposure to ammonia essentially rules out significant injury.Pain (oropharyngeal, retrosternal)Dyspnea, hemoptysis - As expected, individuals with reactive airway disease, such as asthmatics, are particularly sensitive to ammonia inhalation.HoarsenessDysphagiaLoss of consciousnessFarming industry

In enclosed animal confinement buildings, ammonia is adsorbed by dust particles that transport it more directly to small airways. Because of this synergistic effect, symptoms have reportedly developed within minutes of entering animal confinement buildings.

Symptoms include rhinorrhea, scratchy throat, chest tightness, cough, dyspnea, and eye irritation and usually subside within 24-48 hours.Contact - Burns and cold injuryGaseous ammonia combines with water of the skin, eyes, and airways to form ammonium hydroxide. This exothermic reaction results in both heat and chemical burns. Liquid ammonia freezes tissue on contact and may cause full-thickness tissue damage that penetrates deeper than the more conspicuous superficial chemical burns.Concentrations greater than 10,000 ppm are required to cause skin damage. The eyes begin to feel irritated at concentrations of 50-100 ppm; at 700 ppm, immediate eye damage occurs.IngestionTypical household ammonia products (3-10% ammonium hydroxide) have a pH less than 12.5, although the pH of industrial solutions (up to 30% ammonium hydroxide) is often greater than 13. Because caustic alkali burns generally are thought to occur when pH is greater than 12.5, ammonia ingestions in the home usually do not lead to significant damage. However, Klein et al reported 3 cases of oropharyngeal and esophageal injury following intentional ingestion of household solutions with a pH less than 12.Patients present with oropharyngeal, epigastric, and retrosternal pain.Abdominal pain and other gastroenterologic symptoms may occur if ingestion causes viscus perforation (perforation may occur up to 24-72 hours postingestion).Respiratory symptoms may be present if aspiration pneumonia or pneumonitis complicates ingestion.Smelling salts are a less common source of household ammonia ingestion. Often in capsule form, smelling salts, which contain approximately 20% ammonia, release a pungent odor when broken. Smelling salts are found in many first-aid kits as a treatment for syncope; unfortunately, children sometimes bite into!

them, r

esulting in minor esophageal burns and mild respiratory symptoms.Physical: Inhalation injuryHead, ears, eyes, nose, throat (HEENT) - Facial and oral burns and ulcerationRespiration - Tachypnea, oxygen desaturation, stridor, drooling, cough, wheezing, rhonchi, and decreased air entryCentral nervous system (CNS) - Loss of consciousness (if exposure is massive)Contact - Burns and cold injurySkin - Alkali burns to the skin are yellow, soapy, and soft in texture. When burns are severe, skin turns black and leathery.HEENT - Burns to the eye penetrate particularly deeply and rapidly, leading to destruction of the inner structures within 2-3 minutes; this may progress to globe perforation. Ammonia typically causes more corneal epithelium and lens damage than other alkalis. Intraocular pressure and pH of the anterior chamber rise, resulting in a syndrome similar to acute narrow-angle glaucoma. Other symptoms include iritis, corneal edema, semi-dilated fixed pupil, and eventual cataract formation.IngestionCardiovascular - With intentional ingestion, hypovolemic shock may occur because of vomiting and third-spacing of intravascular fluid.HEENT - Symptoms include edema of the lips, oropharynx, and upper airway.GI - Patient may experience epigastric tenderness; mediastinitis and peritoneal signs may be present with viscus perforation, which can occur as late as 24-72 hours postingestion.Respiratory - Aspiration pneumonia and pulmonary edema may occur.

DIFFERENTIALS

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Acute Respiratory Distress Syndrome Anaphylaxis Burns, Chemical Burns, Ocular Burns, Thermal Esophagitis Hazmat Iritis and Uveitis Pediatrics, Anaphylaxis

Pediatrics, Reactive Airway Disease Pediatrics, Respiratory Distress Syndrome Respiratory Distress Syndrome, Adult Toxicity, Chlorine Gas Toxicity, Hydrogen Sulfide Toxicity, Phosgene Other Problems to be Considered: Other toxic inhalations or ingestions

Concomitant trauma

Reactive airway dysfunction syndrome (RADS)

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Related ArticlesAcute Respiratory Distress Syndrome Anaphylaxis Burns, Chemical Burns, Ocular Burns, Thermal Esophagitis Hazmat Iritis and Uveitis Pediatrics, Anaphylaxis Pediatrics, Reactive Airway Disease Pediatrics, Respiratory Distress Syndrome Respiratory Distress Syndrome, Adult Toxicity, Chlorine Gas Toxicity, Hydrogen Sulfide Toxicity, Phosgene

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WORKUP

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Lab Studies:

Complete blood count (CBC)Electrolytes, blood urea nitrogen (BUN), and creatinineSerial arterial blood gases (ABGs) in cases of significant respiratory distressMetabolic acidosisRespiratory alkalosisIncreased alveolar-arterial gradientNote that serum ammonia levels are of little value because they do not correlate with clinical condition. However, patients with compromised hepatic function may show increased serum ammonia levels because of less efficient metabolism.Imaging Studies:

Chest x-ray (CXR)Chest x-ray findings vary from normal to diffuse micronodular interstitial infiltrates. However, abnormal x-ray findings may take up to 48 hours to develop, even following severe exposure.Other findings to consider are noncardiogenic pulmonary edema, acute respiratory distress syndrome (ARDS), secondary bacterial bronchopneumonia, and pneumomediastinum.Abdominal series (to rule out perforation following ingestion)Other Tests:

Cardiac monitorOxygen saturation monitorPulmonary capillary wedge pressure (PCWP) monitoring (in cases of severe pulmonary edema or ARDS)Pulmonary function tests (PFTs) - Once acute emergency is controlled; useful to gauge severity and monitor progress and recoveryObstructive lung disease (acute and chronic)Restrictive lung disease (chronic)Ventilation/perfusion (V/Q) scan - May be useful to gauge severity or progress of disease; unlikely to change acute managementVentilation deficits generally are more pronounced in the larger airways.The ventilation scan also may show abnormal air trapping in the setting of lower airway obstruction.Slit-lamp examination with fluorescein staining, tonometry and conjunctival pH (see Physical: HEENT)Procedures:

Perform bronchoscopy to assess respiratory tract damage following acute inhalation injury (in severe cases).Airway edema, obstruction, and necrosisEpithelial sloughingLaryngitis and tracheitisDiffuse alveolar damagePerform endoscopy for ingestion exposures. Indications are controversial; obtain a GI consultation. Perform endoscopy on symptomatic patients and patients with intentional ingestions within 48 hours following ingestion. The risk of perforation increases if endoscopy is performed more than 72 hours postingestion.Laryngeal and epiglottic edemaFriable erythematous esophagusCorrosive injury

TREATMENT

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Prehospital Care: Immediately remove patient from the contaminated environment.Remove all clothing.Support airway, breathing, and circulation (ABCs) as per advanced cardiac life support (ACLS) and advanced trauma life support (ATLS) guidelines. (ACLS and ATLS guidelines may vary by region, according to training and legal responsibilities of prehospital care providers.)If the patient is sufficiently stable, begin copious skin and eye irrigation immediately following exposure. Continue irrigation for at least 20 minutes. Patients then can be covered with a dry clean dressing and sheet.Provide a container for patients with ingestion exposure.Emergency Department Care: Decontaminate the patient (if not previously performed) and support ABCs as necessary. Provide warmed humidified oxygen.As with all burns, patients with facial or oral lesions are at high risk for developing laryngeal edema. Airway intervention should be aggressive.Indications for intubation include severe respiratory distress (hypoxemia, hypercapnia), stridor, hoarseness, deep facial burns, burns identified by bronchoscopy or endoscopy, and depressed mental status.If intubation is necessary, use large size tube to prevent plugging by sloughed mucosa.Some consider procedural sedation preferable to rapid sequence intubation (RSI) because paralysis is risky with a difficult and edematous airway. Furthermore, ventilation cannot be predicted as successful if intubation fails in this context. Positive end respiratory pressure (PEEP) generally is useful (5 cm water minimum).Beware of fluid over-resuscitation. Patients may have or may be developing noncardiogenic pulmonary edema.Follow standard initial burn management. (Discussion is beyond the scope of this article.)

Once patient is adequately stable, irrigate skin with tepid water for at least 15 minutes. Continue frequent regular irrigation for the first 24 hours, in addition to conventional burn management.

Debride wounds and dress with 1% silver sulfadiazine (avoid using on face).

Administer tetanus prophylaxis.Irrigate eye injuries with copious amounts of tepid water for at least 30 minutes or until conjunctival pH is 6.8-7.4; use pH indicator paper to monitor. Examine eye with slit-lamp and fluorescein staining.

Perform tonometry to determine if intraocular pressure is elevated.

Consult ophthalmology promptly because of risk of perforation and/or permanent eye damage.Treat ingestions using the following steps:Rinse mouth and dilute ingestion with approximately 250 cc of water or milk.

Do not induce emesis, so as not to reproduce injury with a second pass of toxin.

Consult gastroenterology promptly for subsequent endoscopic evaluation (not often performed before 12 hours postingestion).Consultations: When appropriate, immediately consult an intensivist, medical toxicologist, ophthalmologist (all eye injuries), gastroenterologist, and general and plastic surgeons.

MEDICATION

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Management of toxic exposure to ammonia is largely supportive, and medical therapy is directed at hypoxia, bronchospasm, pulmonary edema, hypovolemia, and burns of the skin and eyes.

Antibiotics and corticosteroids are controversial therapies following ammonia inhalation and ingestion exposures.

Although antibiotics and corticosteroids are often used in the acute treatment of patients with inhalation injury, neither has shown to improve outcome and many feel that corticosteroids may actually increase morbidity. Corticosteroids are recommended to treat bronchospasm in patients with underlying reactive airways disease and acute inhalation injury or for chronic respiratory complications that follow an acute inhalation injury.

Most authorities, however, do recommend both IV corticosteroid and antibiotic administration to symptomatic patients following ammonia ingestion. Corticosteroids are administered to decrease the incidence and severity of esophageal strictures that occur during healing from significant alkaline injuries. Antibiotics are given because of increased risk of mediastinitis associated with full-thickness esophageal alkaline corrosive burns. Although controlled animal studies do support the use of these therapies, no well-controlled human trials have been performed; thus, corticosteroids and antibiotics should be administered in consultation with a gastroenterologist.

If steroids are administered, the recommended dose is 1-2 mg/kg/d of methylprednisolone for 3 wk followed by gradual tapering. If antibiotics are administered, a broad-spectrum antibiotic (second-generation cephalosporin) is appropriate.

The decision to continue or stop corticosteroid and antibiotic therapy is based on endoscopic findings. Discontinue steroid and antibiotic therapies for patients with no injury or mild mucosal inflammation or ulceration, as they are not at risk for stricture formation. Furthermore, patients with severe transmural burns are at risk for stricture formation, but steroid therapy will not alter their risk. Thus, antibiotic therapy alone is recommended for this group to diminish their risk of mediastinitis. Patients with extensive superficial ulceration or deep discrete or circumferential ulcerations are at risk for stricture formation and may benefit from steroid administration. Administer corticosteroid and antibiotics to this group of patients.Drug Category: Bronchodilators -- Bronchodilators selectively stimulate beta 2-adrenergic receptors of the bronchial tree and lungs. Bronchodilation results from relaxation of bronchial smooth muscle, which relieves bronchospasm and reduces airway resistance.Drug NameAlbuterol, salbutamol (Proventil, Ventolin) -- Beta 2-agonist for bronchospasm refractory to epinephrine. Relaxes bronchial smooth muscle by action on beta 2-receptors with little effect on cardiac muscle contractility.Adult Dose5 mg/mL of solution for nebulization, mixed as 0.5-1 cc with 2.5 cc of water and nebulized prnPediatric Dose0.2 mg/kg/dose = 0.03 cc/kg/dose (standard solution), prepared as aboveContraindicationsDocumented hypersensitivity; tachydysrhythmiasInteractionsBeta-adrenergic blockers antagonize effects; inhaled ipratropium may increase duration of bronchodil!

atation by albuterol; cardiovascular effects may increase with MAOIs, inhaled anesthetics, tricyclic antidepressants, and sympathomimetic agents; interactions are of relative importance when dealing with life-threatening toxicityPregnancy

C - Safety for use during pregnancy has not been established.

PrecautionsCaution in hyperthyroidism, diabetes mellitus, and cardiovascular disordersDrug Category: Diuretics -- Are used to alleviate pulmonary edema. However, some believe that PEEP may be more useful than diuretics for optimizing oxygenation because pulmonary edema is secondary to alveolar capillary injury, not excess fluid. Nonetheless, a trial of diuretics poses little risk and may be used concomitantly with PEEP.Drug NameFurosemide (Lasix) -- Loop diuretic; inhibits sodium chloride reabsorption in the ascending loop of Henle. Administer IV because this allows for superior potency and a higher peak concentration, despite an increased incidence of adverse effects, particularly ototoxicity (rare).Adult Dose20 mg IV for patients not regularly using furosemide

40-80 mg IV for patients regularly using furosemide

80-120 mg IV for patients with symptoms refractory to the initial dose at up to 1 h

Higher doses and more rapid redosing for patients in severe distress

If minimal or no response with initial dose, double next dosePediatric DoseNot establishedContraindicationsDocumented hypersensitivity; hepatic coma; anuria; severe electrolyte depletionInteractionsMetformin decreases furosemide concentrations; interferes with hypoglycemic effect of antidiabetic agents and antagonizes muscle relaxing effect of tubocurarine; coadministration with aminoglycosides appears to increase auditory toxicity; hearing loss of varying degrees may occur; may enhance anticoagulant activity of warfarin when taken concurrently; increased plasma lithium levels and toxicity are possible when taken concurrentlyPregnancy

C - Safety for use during pregnancy has not been established.

PrecautionsPerform frequent serum electrolyte, carbon dioxide, glucose, creatinine, uric acid, calcium, and BUN determinations during first few months of therapy and periodically thereafter; may induce prerenal failureDrug Category: Antibiotics -- Although expensive, topical Silvadene has antipseudomonal properties in addition to coverage for most gram-positive organisms.

For eye exposures, antibiotic eye preparations will reduce risk of infection secondary to tissue injury.Drug NameSilver sulfadiazine 1% (Silvadene) -- Useful in prevention of infections from second- or third-degree burns. Has bactericidal activity against many gram-positive and gram-negative bacteria including yeast.

Wash burn before application to remove previously applied agent.

Not for ophthalmic use.

Other products may be used instead of silver sulfadiazine for partial thickness burns; these include TransCyte, Acticoat, or Biobrane.Adult DoseApply using sterile technique to affected areas qd/bidPediatric Dose%>Drug NameCiprofloxacin (Ciloxan) -- Fluoroquinolone with activity against pseudomonads, streptococci, MRSA, S epidermidis, and most gram-negative organisms, but no activity against anaerobes. Inhibits bacterial DNA synthesis and growth.

Neomycin 5% is described in much of the literature on ammonia-related eye injury; however, newer broad-spectrum antibiotics have fewer adverse effectsAdult Dose1 gtt qid (prophylaxis)Pediatric Dosenancy

C - Safety for use during pregnancy has not been established.

PrecautionsProlonged use may result in overgrowth of nonsusceptible organisms, including fungiDrug NameErythromycin (E-Mycin) -- Indicated for infections caused by susceptible strains of microorganisms and for prevention of corneal and conjunctival infectionsAdult DoseApply 1-cm ribbon 4-8 times/d depending on severity of infectionPediatric DoseApply as in adultsContraindicationsDocumented hypersensitivity; viral, mycobacterial, or fungal infections of eye; patients using steroid combinations after uncomplicated removal of a foreign body from cornea also should avoid using this productInteractionsNone reportedPregnancy

B - Usually safe but benefits must outweigh the risks.

PrecautionsDo not use topical antibiotics to treat ocular infections that may become systemic; prolonged or repeated antibiotic therapy may result in bacterial or fungal overgrowth of nonsusceptible organisms and may lead to a secondary infection (take appropriate measures if superinfection occurs)Drug Category: Anticholinergic agents -- Induces cycloplegia by blocking the body's parasympathetic (cholinergic) effects in the eye. This is beneficial to prevent ciliary spasm.Drug NameCyclopentolate (AK-Pentolate) -- Blocks muscle of ciliary body and sphincter muscle of iris from responding to cholinergic stimulation, thus causing mydriasis and cycloplegia. Induces mydriasis in 30-60 min and cycloplegia in 25-75 min; these effects last up to 24 hoursAdult Dose1 gtt into affected eye(s) once; may repeat in 24-48 h prnPediatric DoseAdminister as in adultsContraindicationsDocumented hypersensitivity; narrow-angle glaucomaInteractionsDecreases effects of carbachol and cholinesterase inhibitorsPregnancy

C - Safety for use during pregnancy has not been established.

PrecautionsCaution in patients (eg, elderly patients) in whom increased intraocular pressure may be present; can cause toxic anticholinergic systemic adverse effects (common in children especially infants), but incidence is rare when used sparingly; compressing lacrimal sac by digital pressure for 1-3 min following application may minimize systemic absorptionDrug NameHomatropine (Isopto Homatropine) -- Blocks responses of sphincter muscle of iris and muscle of ciliary body to cholinergic stimulation, producing pupillary dilation (mydriasis) and paralysis of accommodation (cycloplegia).

Induces mydriasis in 10-30 min and cycloplegia in 30-90 min; these effects last up to 48 h.Adult Dose1 gtt into affected eye(s) once; may repeat in 24-48 h prnPediatric Dose1 gtt into affected eye(s) once; may repeat in 24-48 h prnContraindicationsDocumented hypersensitivity; narrow-angle glaucomaInteractionsNone reportedPregnancy

C - Safety for use during pregnancy has not been established.

PrecautionsCaution in patients (eg, elderly patients) in whom increased intraocular pressure may be present; toxic anticholinergic systemic adverse effects can occur, but incidence is rare when used sparingly; adverse effects are more common in children, especially infants; compressing lacrimal sac by digital pressure for 1-3 min following instillation minimizes systemic absorptionDrug NameTropicamide (Mydriacyl) -- Blocks sphincter muscle of iris and muscle of ciliary body from responding to cholinergic stimulationAdult Dose1 gtt into affected eye(s) oncePediatric DoseAdminister as in adultsContraindicationsDocumented hypersensitivityInteractionsNone reportedPregnancy

C - Safety for use during pregnancy has not been established.

PrecautionsCaution in patients (eg, elderly patients) in whom increased intraocular pressure may be present; toxic anticholinergic systemic adverse effects can occur, but incidence is rare when used sparingly; adverse effects are more common in children, especially infants; compressing lacrimal sac by digital pressure for 1-3 min following instillation minimizes systemic absorptionDrug Category: Corticosteroids -- Decrease the formation of fibroblasts on the cornea and may limit intraocular inflammation. However, may potentiate infection.Drug NamePrednisolone (Pred Forte) -- Decreases inflammation by suppressing migration of polymorphonuclear leukocytes and reversing increased capillary permeability.

Note that ophthalmologic steroids are controversial; discuss their use with ophthalmology. Also, steroid-antibiotic combination may be useful.Adult Dose1 gtt q1-6h based on severity of inflammation for 7-10 dPediatric DoseAdminister as in adultsContraindicationsDocumented hypersensitivity; viral, fungal, or tubercular infectionsInteractionsEffects may decrease in patients taking phenytoin, barbiturates, and rifampinPregnancy

C - Safety for use during pregnancy has not been established.

PrecautionsCaution in hypertension; known to cause cataract formation with chronic use; in prolonged use, withdraw treatment by gradually decreasing frequency of applications to avoid adrenal insufficiency; may increase corneal thinning and melting; risk of globe perforation; discontinue if acute rise in intraocular pressure or ocular infectionDrug NameFluorometholone (FML) -- Suppresses migration of polymorphonuclear leukocytes and reverses capillary permeabilityAdult Dose1 gtt q1-6h based on severity of inflammation for 7-10 dPediatric Dosecolor="white" class="tblstyle">Rimexolone (Vexol) -- Decreases inflammation by suppressing migration of polymorphonuclear leukocytes and reversing increased capillary permeability.Adult Dose1 gtt q1-6h based on severity of inflammation for 7-10 dPediatric DoseNot establishedContraindicationsDocumented hypersensitivity; viral, fungal, bacterial ocular infectionsInteractionsNone reportedPregnancy

C - Safety for use during pregnancy has not been established.

PrecautionsCaution in corneal or scleral perforation and posterior subcapsular cataractsDrug Category: Local anesthetics -- Used primarily for pain relief. Duration of action is relatively short-lived, limiting usefulness of local anesthetics outside of the hospital or clinic setting.Drug NameProparacaine 0.5% (Alcaine) -- Has rapid onset of anesthesia that begins within 13-30 sec after instillation. However, has short duration of action of about 15-20 min.

Least irritating of all topical anesthetics. Prevents initiation and transmission of impulse at nerve cell membrane by stabilizing and decreasing ion permeability.

Onset of action occurs within 20 s of application.Anesthetic effect may last up to 10-15 minAdult DoseInstill 1-2 gtt into affected eye; may repeat if desiredPediatric DoseAdminister as in adultsContraindicationsDocumented hypersensitivity; prolonged useInteractionsIncreases effects of phenylephrine and tropicamidePregnancy

C - Safety for use during pregnancy has not been established.

PrecautionsCaution in cardiac disease or hyperthyroidism and those with abnormal or reduced levels of plasma esterases

Do not use outside the ED because prolonged eye anesthesia can eliminate patient's awareness of mechanical damage to cornea; frequent use of anesthetics may retard healing

FOLLOW-UP

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Further Inpatient Care:

Admit patients to observation for at least 24 hours if they show significant and persistent signs, symptoms, or abnormalities in lab findings attributable to ammonia exposure.Admit unstable or potentially unstable patients to intensive care.Following ingestion, patients may be discharged if endoscopy results are normal and oral intake is tolerated.Intentional ingestions require psychiatric evaluation.Complications:

Patients often develop chronic respiratory sequelae, particularly with severe ammonia exposures. In a case series by Close et al, exposed patients experienced gradual deterioration of pulmonary function during the first 2-6 months following exposure. A period of slight improvement was then observed, followed by stabilization of symptoms.Long-term effects of ammonia inhalation injury include the following:CoughHoarsenessObstructive and/or restrictive lung diseaseHyper-reactive airway disease and reactive airway dysfunction syndrome (RADS)Impaired gas exchangeResidual parenchymal damageBronchiectasis and bronchiolitis obliterans (following massive exposure)It is postulated that chronic obstructive disease is secondary to airway lesions more than hyper-reactivity and, therefore, often minimally improved by bronchodilators.Prognosis:

Most individuals with ammonia inhalation who survive the first 24 hours will recover.Patients begin showing improvement within 48-72 hours and may recover fully during this time if exposure was mild.For patients with more significant respiratory symptoms, recovery can be expected within several weeks to months.Interestingly, Arwood et al found that initial chest x-ray and PaO2 poorly correlate with outcome and that physical examination on arrival is a more sensitive prognosticating factor.Montague and MacNeil, however, note that patients who do not develop chest x-ray findings are less likely to have chronic respiratory sequelae.Patient Education:

For excellent patient education resources, visit eMedicine's Burns Center. Also, see eMedicine's patient education article Thermal (Heat or Fire) Burns.

MISCELLANEOUS

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Special Concerns:

Chloramine gasChloramines (NH2Cl, NHCl2) are highly water-soluble irritant gases formed when household bleach (5.25% sodium hypochlorite) is mixed with 5-10% ammonia solutions (usually cleaning products). Fumes contact moist mucous membranes, reacting with water to produce free ammonia gas (see Inhalation injury), hypochloric acid, and hypochlorous acid. The latter then reacts with water to form hydrochloric acid and nascent oxygen, a strong oxidizing agent with corrosive effects.At low concentration, symptoms include tearing, rhinorrhea, oropharyngeal burning, and cough. Although chloramine gases produce rapid onset of symptoms, these symptoms are mild enough that patients often do not remove themselves promptly from the toxic environment; thus, patients often present after a prolonged exposure time.The physical examination following mild exposure reveals only mild wheezing and decreased air entry or may be entirely unremarkable.Patients with more significant exposure may present with dyspnea, pulmonary edema with secondary hypoxia, nausea, tracheobronchitis, toxic pneumonitis, intrapulmonary shunt and/or pneumomediastinum. Note that pulmonary edema may ensue within minutes or be delayed for up to 24 hours following exposure.Pulmonary function tests may reveal obstructive, restrictive, or combined patterns, and pulmonary artery occlusive pressure may be less than 17 mm Hg.Treat chloramine gas exposure as described under Emergency Department Care.Sodium bicarbonate has been suggested to be an adjunct to supportive treatment, but little clinical experience with this treatment exists.In and Storrow's case series of 22 patients with chloramine toxicity, treatment with sodium bicarbonate resulted in no clinical or statistical improveme!

nt.

BIBLIOGRAPHY

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Author Information Introduction Clinical Differentials Workup Treatment Medication Follow-up Miscellaneous Bibliography

Am J Respir Crit Care Med: Respiratory health hazards in agriculture. Am J Respir Crit Care Med 1998 Nov; 158(5 Pt 2): S1-S76[Medline].

Arwood R, Hammond J, Ward GG: Ammonia inhalation. J Trauma 1985 May; 25(5): 444-7[Medline].

Birken GA, Fabri PJ, Carey LC: Acute ammonia intoxication complicating multiple trauma. J Trauma 1981 Sep; 21(9): 820-2[Medline].

Burgess JL, Pappas GP, on WO: Hazardous materials incidents: the Washington Poison Center experience and approach to exposure assessment. J Occup Environ Med 1997 Aug; 39(8): 760-6[Medline].

Caplin M: Ammonia-gas poisoning: 47 cases in a London shelter. Lancet 1941; 2: 958-61.

Close LG, Catlin FI, Cohn AM: Acute and chronic effects of ammonia burns on the respiratory tract. Arch Otolaryngol 1980 Mar; 106(3): 151-8[Medline].

de la Hoz RE, Schlueter DP, Rom WN: Chronic lung disease secondary to ammonia inhalation injury: a report on three cases. Am J Ind Med 1996; 29(2): 209-14[Medline].

do Pico GA: Toxic fume inhalation. In: Bone RC, Dantzker DR, eds. Pulmonary and Critical Care Medicine. St Louis: Mosby-Year Book; 1998:N5-1- N5-16.

do Pico GA: Hazardous exposure and lung disease among farm workers. Clin Chest Med 1992 Jun; 13(2): 311-28[Medline].

Ellenhorn MJ, Schonwald S, Ordog G, eds: Respiratory tract irritants. In: Ellenhorn's Medical Toxicology: Diagnosis and Treatment of Human Poisoning. 2nd ed. Baltimore: Lippincott, Wilkins; 1996:1519-25.

Flury KE, Dines DE, Rodarte JR, Rodgers R: Airway obstruction due to inhalation of ammonia. Mayo Clin Proc 1983 Jun; 58(6): 389-93[Medline].

Goldfrank LR: Toxicological imaging, ophthalmologic principle, occupational and environmental toxics. In: Goldfrank's Toxicologic Emergencies. 5th ed. Norwalk, Conn: Appleton Lange; 1994:127, 368-9, 1183-1280.

Haddad LM, Winchester JF, eds: Clinical Management of Poisoning and Drug Overdose. 2nd ed. Philadelphia: WB Saunders Co; 1990.

Klein J, Olson KR, McKinney HE: Caustic injury from household ammonia. Am J Emerg Med 1985 Jul; 3(4): 320[Medline].

Klein JD, Olson KR: Caustic injury from household ammonia, too. J Pediatr 1986 Feb; 108(2): 328[Medline].

Leung CM, Foo CL: Mass ammonia inhalational burns--experience in the management of 12 patients. Ann Acad Med Singapore 1992 Sep; 21(5): 624-9[Medline].

O'Kane GJ: Inhalation of ammonia vapour. A report on the management of eight patients during the acute stages. Anaesthesia 1983 Dec; 38(12): 1208-13[Medline].

Pascuzzi TA, Storrow AB: Mass casualties from acute inhalation of chloramine gas. Military Medicine 1998 Feb; 163(2): 102-4[Medline].

GF Jr: Occupational medicine forum. J Occup Med 1994 Oct; 36(10): 1061-3[Medline].

Rakel RE, ed: Caustics and corrosives. In: Conn's Current Therapy 2000. 51st ed. Philadelphia: WB Saunders Co; 1999:1224-5.

Reisz GR, Gammon RS: Toxic pneumonitis from mixing household cleaners. Chest 1986 Jan; 89(1): 49-52[Medline].

Rosenstock L: Acute inhalational injury. In: Textbook of Clinical Occupational and Environmental Medicine. Philadelphia: WB Saunders Co; 1994:236-7.

Shenoi R: Chemical Warfare Agents. Clin Ped Emerg Med 2002; 3: 239-247.

Sotiropoulos G, Kilaghbian T, Dougherty W, SO: Cold injury from pressurized liquid ammonia: a report of two cases. J Emerg Med 1998 May-Jun; 16(3): 409-12[Medline].

Swotinsky RB, Chase KH: Health effects of exposure to ammonia: scant information. Am J Ind Med 1990; 17(4): 515-21[Medline].

WA, Litovitz TL, Rodgers GC: 2002 annual report of the American Association of Poison Control Centers Toxic Exposure Surveillance System. Am J Emerg Med 2003 Sep; 21(5): 353-421[Medline].

Weiner AL, Bayer MC: Inhalation: Gases with Immediate Toxicity. Ford: Clinical Toxicology 2001; 679.

NOTE:

Medicine is a constantly changing science and not all therapies are clearly established. New research changes drug and treatment therapies daily. The authors, editors, and publisher of this journal have used their best efforts to provide information that is up-to-date and accurate and is generally accepted within medical standards at the time of publication. However, as medical science is constantly changing and human error is always possible, the authors, editors, and publisher or any other party involved with the publication of this article do not warrant the information in this article is accurate or complete, nor are they responsible for omissions or errors in the article or for the results of using this information. The reader should confirm the information in this article from other sources prior to use. In particular, all drug doses, indications, and contraindications should be confirmed in the package insert. FULL DISCLAIMER

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February 2, 2006

Kathy Boo,

U DA BOMB!

Thank you, thank you, thank you. I learned a lot. Not only about ammonia but about some other meds I take AND 1 of the eye drops I had the other day.

Allan with 2 L's just having fun and more fun

Fwd: ammonia

Hi Allan so what are you doing for fun lately? Found this article on Ammonia..And there is a section on the liver and ammonia..Inhaleation, ingested etc..Kathy Boo

Kathy Brunow

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Synonyms and related keywords: anhydrous ammonia, NH3, liquid ammonia, ammonia exposure, inhalation of ammonia, ingestion of ammonia, ammonia ingestion, ammonia inhalation, ammonium hydroxide, liquid anhydrous ammonia, toxic ammonia exposure, ammonia toxicity, ammonia poisoning, fertilizer

AUTHOR INFORMATION

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Author: Issley, MD, CCFP, FRCPC, Emergency Physician, Faculty Lecturer, Emergency Department, McGill University Health Centre (Montreal General Hospital) Coauthor(s): Eddy Lang, MDCM, CCFP (EM), CSPQ, Assistant Professor, Department of Family Medicine, McGill University; Consulting Staff, Department of Emergency Medicine, The Sir Mortimer B -Jewish General Hospital

Editor(s): Edmond Hooker, MD, Assistant Clinical Professor, Department of Emergency Medicine, University of Louisville, State University; T VanDeVoort, PharmD, Clinical Assistant Professor, College of Pharmacy, University of Minnesota; J Burns, MD, Instructor, Department of Emergency Medicine, Harvard University Medical School, Beth Israel Deaconess Medical Center; Halamka, MD, Chief Information Officer, CareGroup Healthcare System, Assistant Professor of Medicine, Department of Emergency Medicine, Beth Israel Deaconess Medical Center; Assistant Professor of Medicine, Harvard Medical School; and J Roberge, MD, MPH, FAAEM, FACMT, Clinical Associate Professor of Emergency Medicine, University of Pittsburgh School of Medicine; Consulting Staff, Department of Emergency Medicine, Magee-Women's Hospital of the University of Pittsburgh Medical Center Disclosure

INTRODUCTION

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Background: At room temperature, ammonia (NH3) is a highly water-soluble, colorless, irritant gas with a unique pungent odor. Ammonia has a boiling point of -33°C and an ignition temperature of 650°C. In 1993, anhydrous ammonia was the third most produced chemical by volume in the US. The farming industry uses approximately one third of the ammonia produced in the US as a component of fertilizer and animal feed. Industrial injury most often results from ammonia leaks in fertilizer tanks and hoses and toxic ammonia levels in animal buildings. Swine confinement buildings are particularly notorious for containing toxic levels of ammonia that often exceed threshold limit values. Because ammonia is liberated during combustion of nylon, silk, wood, and melamine, firefighters also are at risk for exposure to this irritant gas. Before the 1970s, liquid ammonia stored under high pressure was widely used for refrigeration. Although Freon largely has replaced ammonia as a refrigerant, ammonia refrigeration is still used and numerous case reports exist of severe toxicity following accidental exposure. Ammonia also is used in the production of explosives, pharmaceuticals, pesticides, textiles, leather, flame-retardants, plastics, pulp and paper, rubber, petroleum products, and cyanide. Furthermore, ammonia is a major component of many common household cleaning and bleaching products (eg, glass cleaners, toilet bowel cleaners, metal polishes, floor strippers, wax removers, smelling salts). Permissible levels of exposure to toxic gases are defined by time-weighted average (TWA), short-term exposure limit (STEL), and concentration at which toxic gasses are immediately dangerous to life or health (IDLH). The TWA is defined as the concentration for an 8-hour workday of a 40-hour workweek that nearly all workers can be exposed to without adverse effects. Similarly, the STEL is the concentration to which an exposure of longer than 15 minutes is potentially dangerous and may produce immediate or chronic compromise to health. Anhydrous ammonia has a TWA of 25 ppm, an STEL of 35 ppm, and an IDLH of 500 ppm. Although injury from ammonia most commonly is caused by inhalation, it also may follow ingestion or direct contact with eyes or skin. The clinical presentations of these injuries and their investigation and treatment are discussed in this article; chloramine gas inhalation injury also is discussed.

Pathophysiology: The most common mechanism by which ammonia gas causes damage occurs when anhydrous ammonia (liquid or gas) reacts with tissue water to form the strongly alkaline solution, ammonium hydroxide. NH3 + H2O ®NH4OH This reaction is exothermic and capable of causing significant thermal injury. Ammonium hydroxide also causes severe alkaline chemical burns to skin, eyes, and especially the respiratory system. Mild exposures primarily affect the upper respiratory tract, while more severe exposures tend to affect the entire respiratory system (see Clinical). The gastrointestinal tract also may be affected if ammonia is ingested. Tissue damage from alkali is caused by liquefaction necrosis and typically penetrates far deeper than that caused by an equipotent acid. In the case of ammonium hydroxide, the tissue breakdown liberates water, thus perpetuating the conversion of ammonia to ammonium hydroxide. In the respiratory tract, this results in the destruction of cilia and the mucosal barrier to infection. Furthermore, secretions, sloughed epithelium, cellular debris, edema, and reactive smooth muscle contraction cause significant airway obstruction. Airway epithelium can regain barrier integrity within 6 hours following exposure if the basal cell layer remains intact. However, damaged epithelium often is replaced by granular tissue, which may be one of the etiologies leading to chronic lung disease following ammonia inhalation injury. Liquid anhydrous ammonia (-33°C) freezes tissue on contact. To put this in perspective, critical skin damage begins at -4°C and becomes irreversible at -20°C. The degree of tissue injury, however, is proportional to the duration and concentration of exposure. Similarly, damage to the respiratory system is proportional to depth of inhalation, duration of exposure, concentration, and pH of the gas or liquid. Ammonia is a product of protein catabolism and is metabolized by the liver. Normal blood ammonia levels range from 80-110 mcg/dL. This increases 10% with exposure to 25 ppm but is not considered harmful. Theoretically, patients with liver dysfunction are at increased risk for ammonia toxicity; however, currently no sufficient clinical evidence can confirm this.

Frequency:

In the US: Similar to previous years, in 2002, US poison control centers reported nearly 6000 cases of toxic ammonia exposure. Of exposures, 93% were unintentional, and 11% resulted in moderate to severe outcomes. Of note, in cases of household exposure, only 5% were moderate to severe.

Age: Of the 6000 toxic ammonia exposures reported in the American Association of Poison Control Centers' 2002 Annual Report, 70% occurred in adults and 20% occurred in children younger than 6 years.

Ingestion of household solutions usually is accidental and occurs in young children; adult ingestions, however, most often are suicide attempts.

Inhalation injury is almost always accidental. Because inhalation exposure generally occurs in an industrial setting, it usually is associated with working adults.

CLINICAL

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History: The literature on ammonia toxicity in humans largely consists of case reports. In a 1996 literature review, de la Hoz et al found only 94 previously reported cases; of these cases, 20 resulted in fatality and only 35 had clinical follow-up of one year or more. Despite lack of data, most literature is consistent regarding clinical presentation and treatment of ammonia toxicity.

Gaseous ammonia effects at various concentrations are as follows:

25 ppm or less - TWA

25-50 ppm - Detectable odor; unlikely to experience adverse effects

50-100 ppm - Mild eye, nose, and throat irritation; may develop tolerance in 1-2 weeks with no adverse effects thereafter

140 ppm - Moderate eye irritation; no long-term sequelae in exposures of less than 2 hours

400 ppm - Moderate throat irritation

500 ppm - IDLH

700 ppm - Immediate eye injury

1000 ppm - Directly caustic to airway

1700 ppm - Laryngospasm

2500 ppm - Fatality (after half-hour exposure)

2500-6500 ppm - Sloughing and necrosis of airway mucosa, chest pain, pulmonary edema, and bronchospasm

5000 ppm - Rapidly fatal exposure

Inhalation injury

Because of its high water solubility, ammonia has a tendency to be absorbed by the water-rich mucosa of the upper respiratory tract. However, unlike most highly water-soluble irritant gases that tend to affect exclusively the upper respiratory tract, ammonia can damage proximally and distally.

In 1941, Caplin was the first to classify victims of accidental ammonia exposure; he described them as mild, moderate, and severe. Patients in the mild group presented with conjunctival and upper respiratory inflammation and pain but showed no signs of respiratory distress. The moderate group presented similarly but with more exaggerated symptoms. The severe group presented in frank respiratory distress with productive cough, pulmonary edema, and dysphagia.

Following a brief ammonia exposure, damage generally is limited to the upper airway mucosa. Brief exposures at very high concentrations, however, can be overwhelming and affect the entire respiratory system. People who are capable of escaping their environment usually are not subject to severe exposures, because they can flee upon detection of ammonia's pungent odor; furthermore, absence of symptoms following inhalational exposure to ammonia essentially rules out significant injury.

Pain (oropharyngeal, retrosternal)

Dyspnea, hemoptysis - As expected, individuals with reactive airway disease, such as asthmatics, are particularly sensitive to ammonia inhalation.

Hoarseness

Dysphagia

Loss of consciousness

Farming industry

In enclosed animal confinement buildings, ammonia is adsorbed by dust particles that transport it more directly to small airways. Because of this synergistic effect, symptoms have reportedly developed within minutes of entering animal confinement buildings.

Symptoms include rhinorrhea, scratchy throat, chest tightness, cough, dyspnea, and eye irritation and usually subside within 24-48 hours.

Contact - Burns and cold injury

Gaseous ammonia combines with water of the skin, eyes, and airways to form ammonium hydroxide. This exothermic reaction results in both heat and chemical burns. Liquid ammonia freezes tissue on contact and may cause full-thickness tissue damage that penetrates deeper than the more conspicuous superficial chemical burns.

Concentrations greater than 10,000 ppm are required to cause skin damage. The eyes begin to feel irritated at concentrations of 50-100 ppm; at 700 ppm, immediate eye damage occurs.

Ingestion

Typical household ammonia products (3-10% ammonium hydroxide) have a pH less than 12.5, although the pH of industrial solutions (up to 30% ammonium hydroxide) is often greater than 13. Because caustic alkali burns generally are thought to occur when pH is greater than 12.5, ammonia ingestions in the home usually do not lead to significant damage. However, Klein et al reported 3 cases of oropharyngeal and esophageal injury following intentional ingestion of household solutions with a pH less than 12.

Patients present with oropharyngeal, epigastric, and retrosternal pain.

Abdominal pain and other gastroenterologic symptoms may occur if ingestion causes viscus perforation (perforation may occur up to 24-72 hours postingestion).

Respiratory symptoms may be present if aspiration pneumonia or pneumonitis complicates ingestion.

Smelling salts are a less common source of household ammonia ingestion. Often in capsule form, smelling salts, which contain approximately 20% ammonia, release a pungent odor when broken. Smelling salts are found in many first-aid kits as a treatment for syncope; unfortunately, children sometimes bite into! them, r esulting in minor esophageal burns and mild respiratory symptoms.

Physical:

Inhalation injury

Head, ears, eyes, nose, throat (HEENT) - Facial and oral burns and ulceration

Respiration - Tachypnea, oxygen desaturation, stridor, drooling, cough, wheezing, rhonchi, and decreased air entry

Central nervous system (CNS) - Loss of consciousness (if exposure is massive)

Contact - Burns and cold injury

Skin - Alkali burns to the skin are yellow, soapy, and soft in texture. When burns are severe, skin turns black and leathery.

HEENT - Burns to the eye penetrate particularly deeply and rapidly, leading to destruction of the inner structures within 2-3 minutes; this may progress to globe perforation. Ammonia typically causes more corneal epithelium and lens damage than other alkalis. Intraocular pressure and pH of the anterior chamber rise, resulting in a syndrome similar to acute narrow-angle glaucoma. Other symptoms include iritis, corneal edema, semi-dilated fixed pupil, and eventual cataract formation.

Ingestion

Cardiovascular - With intentional ingestion, hypovolemic shock may occur because of vomiting and third-spacing of intravascular fluid.

HEENT - Symptoms include edema of the lips, oropharynx, and upper airway.

GI - Patient may experience epigastric tenderness; mediastinitis and peritoneal signs may be present with viscus perforation, which can occur as late as 24-72 hours postingestion.

Respiratory - Aspiration pneumonia and pulmonary edema may occur.

DIFFERENTIALS

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Acute Respiratory Distress Syndrome Anaphylaxis Burns, Chemical Burns, Ocular Burns, Thermal Esophagitis Hazmat Iritis and Uveitis Pediatrics, Anaphylaxis Pediatrics, Reactive Airway Disease Pediatrics, Respiratory Distress Syndrome Respiratory Distress Syndrome, Adult Toxicity, Chlorine Gas Toxicity, Hydrogen Sulfide Toxicity, Phosgene

Other Problems to be Considered:

Other toxic inhalations or ingestionsConcomitant traumaReactive airway dysfunction syndrome (RADS)

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Acute Respiratory Distress Syndrome Anaphylaxis Burns, Chemical Burns, Ocular Burns, Thermal Esophagitis Hazmat Iritis and Uveitis Pediatrics, Anaphylaxis Pediatrics, Reactive Airway Disease Pediatrics, Respiratory Distress Syndrome Respiratory Distress Syndrome, Adult Toxicity, Chlorine Gas Toxicity, Hydrogen Sulfide Toxicity, Phosgene

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WORKUP

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Lab Studies:

Complete blood count (CBC)

Electrolytes, blood urea nitrogen (BUN), and creatinine

Serial arterial blood gases (ABGs) in cases of significant respiratory distress

Metabolic acidosis

Respiratory alkalosis

Increased alveolar-arterial gradient

Note that serum ammonia levels are of little value because they do not correlate with clinical condition. However, patients with compromised hepatic function may show increased serum ammonia levels because of less efficient metabolism.

Imaging Studies:

Chest x-ray (CXR)

Chest x-ray findings vary from normal to diffuse micronodular interstitial infiltrates. However, abnormal x-ray findings may take up to 48 hours to develop, even following severe exposure.

Other findings to consider are noncardiogenic pulmonary edema, acute respiratory distress syndrome (ARDS), secondary bacterial bronchopneumonia, and pneumomediastinum.

Abdominal series (to rule out perforation following ingestion)

Other Tests:

Cardiac monitor

Oxygen saturation monitor

Pulmonary capillary wedge pressure (PCWP) monitoring (in cases of severe pulmonary edema or ARDS)

Pulmonary function tests (PFTs) - Once acute emergency is controlled; useful to gauge severity and monitor progress and recovery

Obstructive lung disease (acute and chronic)

Restrictive lung disease (chronic)

Ventilation/perfusion (V/Q) scan - May be useful to gauge severity or progress of disease; unlikely to change acute management

Ventilation deficits generally are more pronounced in the larger airways.

The ventilation scan also may show abnormal air trapping in the setting of lower airway obstruction.

Slit-lamp examination with fluorescein staining, tonometry and conjunctival pH (see Physical: HEENT)

Procedures:

Perform bronchoscopy to assess respiratory tract damage following acute inhalation injury (in severe cases).

Airway edema, obstruction, and necrosis

Epithelial sloughing

Laryngitis and tracheitis

Diffuse alveolar damage

Perform endoscopy for ingestion exposures. Indications are controversial; obtain a GI consultation. Perform endoscopy on symptomatic patients and patients with intentional ingestions within 48 hours following ingestion. The risk of perforation increases if endoscopy is performed more than 72 hours postingestion.

Laryngeal and epiglottic edema

Friable erythematous esophagus

Corrosive injury

TREATMENT

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Prehospital Care:

Immediately remove patient from the contaminated environment.

Remove all clothing.

Support airway, breathing, and circulation (ABCs) as per advanced cardiac life support (ACLS) and advanced trauma life support (ATLS) guidelines. (ACLS and ATLS guidelines may vary by region, according to training and legal responsibilities of prehospital care providers.)

If the patient is sufficiently stable, begin copious skin and eye irrigation immediately following exposure. Continue irrigation for at least 20 minutes. Patients then can be covered with a dry clean dressing and sheet.

Provide a container for patients with ingestion exposure.

Emergency Department Care:

Decontaminate the patient (if not previously performed) and support ABCs as necessary. Provide warmed humidified oxygen.

As with all burns, patients with facial or oral lesions are at high risk for developing laryngeal edema. Airway intervention should be aggressive.

Indications for intubation include severe respiratory distress (hypoxemia, hypercapnia), stridor, hoarseness, deep facial burns, burns identified by bronchoscopy or endoscopy, and depressed mental status.

If intubation is necessary, use large size tube to prevent plugging by sloughed mucosa.

Some consider procedural sedation preferable to rapid sequence intubation (RSI) because paralysis is risky with a difficult and edematous airway. Furthermore, ventilation cannot be predicted as successful if intubation fails in this context. Positive end respiratory pressure (PEEP) generally is useful (5 cm water minimum).

Beware of fluid over-resuscitation. Patients may have or may be developing noncardiogenic pulmonary edema.

Follow standard initial burn management. (Discussion is beyond the scope of this article.)

Once patient is adequately stable, irrigate skin with tepid water for at least 15 minutes. Continue frequent regular irrigation for the first 24 hours, in addition to conventional burn management.

Debride wounds and dress with 1% silver sulfadiazine (avoid using on face).

Administer tetanus prophylaxis.

Irrigate eye injuries with copious amounts of tepid water for at least 30 minutes or until conjunctival pH is 6.8-7.4; use pH indicator paper to monitor. Examine eye with slit-lamp and fluorescein staining.

Perform tonometry to determine if intraocular pressure is elevated.

Consult ophthalmology promptly because of risk of perforation and/or permanent eye damage.

Treat ingestions using the following steps:

Rinse mouth and dilute ingestion with approximately 250 cc of water or milk.

Do not induce emesis, so as not to reproduce injury with a second pass of toxin.

Consult gastroenterology promptly for subsequent endoscopic evaluation (not often performed before 12 hours postingestion).

Consultations: When appropriate, immediately consult an intensivist, medical toxicologist, ophthalmologist (all eye injuries), gastroenterologist, and general and plastic surgeons.

MEDICATION

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Management of toxic exposure to ammonia is largely supportive, and medical therapy is directed at hypoxia, bronchospasm, pulmonary edema, hypovolemia, and burns of the skin and eyes. Antibiotics and corticosteroids are controversial therapies following ammonia inhalation and ingestion exposures. Although antibiotics and corticosteroids are often used in the acute treatment of patients with inhalation injury, neither has shown to improve outcome and many feel that corticosteroids may actually increase morbidity. Corticosteroids are recommended to treat bronchospasm in patients with underlying reactive airways disease and acute inhalation injury or for chronic respiratory complications that follow an acute inhalation injury. Most authorities, however, do recommend both IV corticosteroid and antibiotic administration to symptomatic patients following ammonia ingestion. Corticosteroids are administered to decrease the incidence and severity of esophageal strictures that occur during healing from significant alkaline injuries. Antibiotics are given because of increased risk of mediastinitis associated with full-thickness esophageal alkaline corrosive burns. Although controlled animal studies do support the use of these therapies, no well-controlled human trials have been performed; thus, corticosteroids and antibiotics should be administered in consultation with a gastroenterologist. If steroids are administered, the recommended dose is 1-2 mg/kg/d of methylprednisolone for 3 wk followed by gradual tapering. If antibiotics are administered, a broad-spectrum antibiotic (second-generation cephalosporin) is appropriate. The decision to continue or stop corticosteroid and antibiotic therapy is based on endoscopic findings. Discontinue steroid and antibiotic therapies for patients with no injury or mild mucosal inflammation or ulceration, as they are not at risk for stricture formation. Furthermore, patients with severe transmural burns are at risk for stricture formation, but steroid therapy will not alter their risk. Thus, antibiotic therapy alone is recommended for this group to diminish their risk of mediastinitis. Patients with extensive superficial ulceration or deep discrete or circumferential ulcerations are at risk for stricture formation and may benefit from steroid administration. Administer corticosteroid and antibiotics to this group of patients.

Drug Category: Bronchodilators -- Bronchodilators selectively stimulate beta 2-adrenergic receptors of the bronchial tree and lungs. Bronchodilation results from relaxation of bronchial smooth muscle, which relieves bronchospasm and reduces airway resistance.

Drug Name

Albuterol, salbutamol (Proventil, Ventolin) -- Beta 2-agonist for bronchospasm refractory to epinephrine. Relaxes bronchial smooth muscle by action on beta 2-receptors with little effect on cardiac muscle contractility.

Adult Dose

5 mg/mL of solution for nebulization, mixed as 0.5-1 cc with 2.5 cc of water and nebulized prn

Pediatric Dose

0.2 mg/kg/dose = 0.03 cc/kg/dose (standard solution), prepared as above

Contraindications

Documented hypersensitivity; tachydysrhythmias

Interactions

Beta-adrenergic blockers antagonize effects; inhaled ipratropium may increase duration of bronchodil! atation by albuterol; cardiovascular effects may increase with MAOIs, inhaled anesthetics, tricyclic antidepressants, and sympathomimetic agents; interactions are of relative importance when dealing with life-threatening toxicity

Pregnancy

C - Safety for use during pregnancy has not been established.

Precautions

Caution in hyperthyroidism, diabetes mellitus, and cardiovascular disordersDrug Category: Diuretics -- Are used to alleviate pulmonary edema. However, some believe that PEEP may be more useful than diuretics for optimizing oxygenation because pulmonary edema is secondary to alveolar capillary injury, not excess fluid. Nonetheless, a trial of diuretics poses little risk and may be used concomitantly with PEEP.

Drug Name

Furosemide (Lasix) -- Loop diuretic; inhibits sodium chloride reabsorption in the ascending loop of Henle. Administer IV because this allows for superior potency and a higher peak concentration, despite an increased incidence of adverse effects, particularly ototoxicity (rare).

Adult Dose

20 mg IV for patients not regularly using furosemide40-80 mg IV for patients regularly using furosemide80-120 mg IV for patients with symptoms refractory to the initial dose at up to 1 hHigher doses and more rapid redosing for patients in severe distressIf minimal or no response with initial dose, double next dose

Pediatric Dose

Not established

Contraindications

Documented hypersensitivity; hepatic coma; anuria; severe electrolyte depletion

Interactions

Metformin decreases furosemide concentrations; interferes with hypoglycemic effect of antidiabetic agents and antagonizes muscle relaxing effect of tubocurarine; coadministration with aminoglycosides appears to increase auditory toxicity; hearing loss of varying degrees may occur; may enhance anticoagulant activity of warfarin when taken concurrently; increased plasma lithium levels and toxicity are possible when taken concurrently

Pregnancy

C - Safety for use during pregnancy has not been established.

Precautions

Perform frequent serum electrolyte, carbon dioxide, glucose, creatinine, uric acid, calcium, and BUN determinations during first few months of therapy and periodically thereafter; may induce prerenal failureDrug Category: Antibiotics -- Although expensive, topical Silvadene has antipseudomonal properties in addition to coverage for most gram-positive organisms.For eye exposures, antibiotic eye preparations will reduce risk of infection secondary to tissue injury.

Drug Name

Silver sulfadiazine 1% (Silvadene) -- Useful in prevention of infections from second- or third-degree burns. Has bactericidal activity against many gram-positive and gram-negative bacteria including yeast.Wash burn before application to remove previously applied agent.Not for ophthalmic use.Other products may be used instead of silver sulfadiazine for partial thickness burns; these include TransCyte, Acticoat, or Biobrane.

Adult Dose

Apply using sterile technique to affected areas qd/bid

Pediatric Dose

<2 years: Do not administer (risk of kernicterus)>2 years: Apply as in adults

Contraindications

Documented hypersensitivity; late pregnancy (risk of kernicterus); facial burns (use Bacitracin instead)

Interactions

Effect of proteolytic enzymes is reduced when used concomitantly

Pregnancy

C - Safety for use during pregnancy has not been established.

Precautions

Caution in G-6-PD deficiency and renal insufficiency

Drug Name

Ciprofloxacin (Ciloxan) -- Fluoroquinolone with activity against pseudomonads, streptococci, MRSA, S epidermidis, and most gram-negative organisms, but no activity against anaerobes. Inhibits bacterial DNA synthesis and growth.Neomycin 5% is described in much of the literature on ammonia-related eye injury; however, newer broad-spectrum antibiotics have fewer adverse effects

Adult Dose

1 gtt qid (prophylaxis)

Pediatric Dose

<12 years: Not recommended>12 years: Administer as in adults

Contraindications

Documented hypersensitivity

Interactions

Antacids, iron salts, and zinc salts may reduce serum levels; administer antacids 2-4 h before or after taking fluoroquinolones; cimetidine may interfere with metabolism of fluoroquinolones; ciprofloxacin reduces therapeutic effects of phenytoin; probenecid may increase ciprofloxacin serum concentrations; may increase toxicity of theophylline, caffeine, cyclosporine, and digoxin (monitor digoxin levels); may increase effects of anticoagulants (monitor PT)

Pregnancy

C - Safety for use during pregnancy has not been established.

Precautions

Prolonged use may result in overgrowth of nonsusceptible organisms, including fungi

Drug Name

Erythromycin (E-Mycin) -- Indicated for infections caused by susceptible strains of microorganisms and for prevention of corneal and conjunctival infections

Adult Dose

Apply 1-cm ribbon 4-8 times/d depending on severity of infection

Pediatric Dose

Apply as in adults

Contraindications

Documented hypersensitivity; viral, mycobacterial, or fungal infections of eye; patients using steroid combinations after uncomplicated removal of a foreign body from cornea also should avoid using this product

Interactions

None reported

Pregnancy

B - Usually safe but benefits must outweigh the risks.

Precautions

Do not use topical antibiotics to treat ocular infections that may become systemic; prolonged or repeated antibiotic therapy may result in bacterial or fungal overgrowth of nonsusceptible organisms and may lead to a secondary infection (take appropriate measures if superinfection occurs)Drug Category: Anticholinergic agents -- Induces cycloplegia by blocking the body's parasympathetic (cholinergic) effects in the eye. This is beneficial to prevent ciliary spasm.

Drug Name

Cyclopentolate (AK-Pentolate) -- Blocks muscle of ciliary body and sphincter muscle of iris from responding to cholinergic stimulation, thus causing mydriasis and cycloplegia.Induces mydriasis in 30-60 min and cycloplegia in 25-75 min; these effects last up to 24 hours

Adult Dose

1 gtt into affected eye(s) once; may repeat in 24-48 h prn

Pediatric Dose

Administer as in adults

Contraindications

Documented hypersensitivity; narrow-angle glaucoma

Interactions

Decreases effects of carbachol and cholinesterase inhibitors

Pregnancy

C - Safety for use during pregnancy has not been established.

Precautions

Caution in patients (eg, elderly patients) in whom increased intraocular pressure may be present; can cause toxic anticholinergic systemic adverse effects (common in children especially infants), but incidence is rare when used sparingly; compressing lacrimal sac by digital pressure for 1-3 min following application may minimize systemic absorption

Drug Name

Homatropine (Isopto Homatropine) -- Blocks responses of sphincter muscle of iris and muscle of ciliary body to cholinergic stimulation, producing pupillary dilation (mydriasis) and paralysis of accommodation (cycloplegia).Induces mydriasis in 10-30 min and cycloplegia in 30-90 min; these effects last up to 48 h.

Adult Dose

1 gtt into affected eye(s) once; may repeat in 24-48 h prn

Pediatric Dose

1 gtt into affected eye(s) once; may repeat in 24-48 h prn

Contraindications

Documented hypersensitivity; narrow-angle glaucoma

Interactions

None reported

Pregnancy

C - Safety for use during pregnancy has not been established.

Precautions

Caution in patients (eg, elderly patients) in whom increased intraocular pressure may be present; toxic anticholinergic systemic adverse effects can occur, but incidence is rare when used sparingly; adverse effects are more common in children, especially infants; compressing lacrimal sac by digital pressure for 1-3 min following instillation minimizes systemic absorption

Drug Name

Tropicamide (Mydriacyl) -- Blocks sphincter muscle of iris and muscle of ciliary body from responding to cholinergic stimulation

Adult Dose

1 gtt into affected eye(s) once

Pediatric Dose

Administer as in adults

Contraindications

Documented hypersensitivity

Interactions

None reported

Pregnancy

C - Safety for use during pregnancy has not been established.

Precautions

Caution in patients (eg, elderly patients) in whom increased intraocular pressure may be present; toxic anticholinergic systemic adverse effects can occur, but incidence is rare when used sparingly; adverse effects are more common in children, especially infants; compressing lacrimal sac by digital pressure for 1-3 min following instillation minimizes systemic absorptionDrug Category: Corticosteroids -- Decrease the formation of fibroblasts on the cornea and may limit intraocular inflammation. However, may potentiate infection.

Drug Name

Prednisolone (Pred Forte) -- Decreases inflammation by suppressing migration of polymorphonuclear leukocytes and reversing increased capillary permeability.Note that ophthalmologic steroids are controversial; discuss their use with ophthalmology. Also, steroid-antibiotic combination may be useful.

Adult Dose

1 gtt q1-6h based on severity of inflammation for 7-10 d

Pediatric Dose

Administer as in adults

Contraindications

Documented hypersensitivity; viral, fungal, or tubercular infections

Interactions

Effects may decrease in patients taking phenytoin, barbiturates, and rifampin

Pregnancy

C - Safety for use during pregnancy has not been established.

Precautions

Caution in hypertension; known to cause cataract formation with chronic use; in prolonged use, withdraw treatment by gradually decreasing frequency of applications to avoid adrenal insufficiency; may increase corneal thinning and melting; risk of globe perforation; discontinue if acute rise in intraocular pressure or ocular infection

Drug Name

Fluorometholone (FML) -- Suppresses migration of polymorphonuclear leukocytes and reverses capillary permeability

Adult Dose

1 gtt q1-6h based on severity of inflammation for 7-10 d

Pediatric Dose

<2 years: Not established>2 years: Administer as in adults

Contraindications

Documented hypersensitivity; herpes simplex; keratitis; viral and fungal diseases of the ocular structure

Interactions

None reported

Pregnancy

C - Safety for use during pregnancy has not been established.

Precautions

Prolonged use my result in elevated intraocular pressure or glaucoma

Drug Name

Rimexolone (Vexol) -- Decreases inflammation by suppressing migration of polymorphonuclear leukocytes and reversing increased capillary permeability.

Adult Dose

1 gtt q1-6h based on severity of inflammation for 7-10 d

Pediatric Dose

Not established

Contraindications

Documented hypersensitivity; viral, fungal, bacterial ocular infections

Interactions

None reported

Pregnancy

C - Safety for use during pregnancy has not been established.

Precautions

Caution in corneal or scleral perforation and posterior subcapsular cataractsDrug Category: Local anesthetics -- Used primarily for pain relief. Duration of action is relatively short-lived, limiting usefulness of local anesthetics outside of the hospital or clinic setting.

Drug Name

Proparacaine 0.5% (Alcaine) -- Has rapid onset of anesthesia that begins within 13-30 sec after instillation. However, has short duration of action of about 15-20 min.Least irritating of all topical anesthetics. Prevents initiation and transmission of impulse at nerve cell membrane by stabilizing and decreasing ion permeability.Onset of action occurs within 20 s of application.Anesthetic effect may last up to 10-15 min

Adult Dose

Instill 1-2 gtt into affected eye; may repeat if desired

Pediatric Dose

Administer as in adults

Contraindications

Documented hypersensitivity; prolonged use

Interactions

Increases effects of phenylephrine and tropicamide

Pregnancy

C - Safety for use during pregnancy has not been established.

Precautions

Caution in cardiac disease or hyperthyroidism and those with abnormal or reduced levels of plasma esterasesDo not use outside the ED because prolonged eye anesthesia can eliminate patient's awareness of mechanical damage to cornea; frequent use of anesthetics may retard healing

FOLLOW-UP

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Further Inpatient Care:

Admit patients to observation for at least 24 hours if they show significant and persistent signs, symptoms, or abnormalities in lab findings attributable to ammonia exposure.

Admit unstable or potentially unstable patients to intensive care.

Following ingestion, patients may be discharged if endoscopy results are normal and oral intake is tolerated.

Intentional ingestions require psychiatric evaluation.

Complications:

Patients often develop chronic respiratory sequelae, particularly with severe ammonia exposures. In a case series by Close et al, exposed patients experienced gradual deterioration of pulmonary function during the first 2-6 months following exposure. A period of slight improvement was then observed, followed by stabilization of symptoms.

Long-term effects of ammonia inhalation injury include the following:

Cough

Hoarseness

Obstructive and/or restrictive lung disease

Hyper-reactive airway disease and reactive airway dysfunction syndrome (RADS)

Impaired gas exchange

Residual parenchymal damage

Bronchiectasis and bronchiolitis obliterans (following massive exposure)

It is postulated that chronic obstructive disease is secondary to airway lesions more than hyper-reactivity and, therefore, often minimally improved by bronchodilators.

Prognosis:

Most individuals with ammonia inhalation who survive the first 24 hours will recover.

Patients begin showing improvement within 48-72 hours and may recover fully during this time if exposure was mild.

For patients with more significant respiratory symptoms, recovery can be expected within several weeks to months.

Interestingly, Arwood et al found that initial chest x-ray and PaO2 poorly correlate with outcome and that physical examination on arrival is a more sensitive prognosticating factor.

Montague and MacNeil, however, note that patients who do not develop chest x-ray findings are less likely to have chronic respiratory sequelae.

Patient Education:

For excellent patient education resources, visit eMedicine's Burns Center. Also, see eMedicine's patient education article Thermal (Heat or Fire) Burns.

MISCELLANEOUS

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Special Concerns:

Chloramine gas

Chloramines (NH2Cl, NHCl2) are highly water-soluble irritant gases formed when household bleach (5.25% sodium hypochlorite) is mixed with 5-10% ammonia solutions (usually cleaning products). Fumes contact moist mucous membranes, reacting with water to produce free ammonia gas (see Inhalation injury), hypochloric acid, and hypochlorous acid. The latter then reacts with water to form hydrochloric acid and nascent oxygen, a strong oxidizing agent with corrosive effects.

At low concentration, symptoms include tearing, rhinorrhea, oropharyngeal burning, and cough. Although chloramine gases produce rapid onset of symptoms, these symptoms are mild enough that patients often do not remove themselves promptly from the toxic environment; thus, patients often present after a prolonged exposure time.

The physical examination following mild exposure reveals only mild wheezing and decreased air entry or may be entirely unremarkable.

Patients with more significant exposure may present with dyspnea, pulmonary edema with secondary hypoxia, nausea, tracheobronchitis, toxic pneumonitis, intrapulmonary shunt and/or pneumomediastinum. Note that pulmonary edema may ensue within minutes or be delayed for up to 24 hours following exposure.

Pulmonary function tests may reveal obstructive, restrictive, or combined patterns, and pulmonary artery occlusive pressure may be less than 17 mm Hg.

Treat chloramine gas exposure as described under Emergency Department Care.

Sodium bicarbonate has been suggested to be an adjunct to supportive treatment, but little clinical experience with this treatment exists.

In and Storrow's case series of 22 patients with chloramine toxicity, treatment with sodium bicarbonate resulted in no clinical or statistical improveme! nt.

BIBLIOGRAPHY

Section 10 of 10

Author Information Introduction Clinical Differentials Workup Treatment Medication Follow-up Miscellaneous Bibliography

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NOTE:

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Toxicity, AmmoniaLast Updated: January 3, 2006

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Synonyms and related keywords: anhydrous ammonia, NH3, liquid ammonia, ammonia exposure, inhalation of ammonia, ingestion of ammonia, ammonia ingestion, ammonia inhalation, ammonium hydroxide, liquid anhydrous ammonia, toxic ammonia exposure, ammonia toxicity, ammonia poisoning, fertilizer

AUTHOR INFORMATION

Section 1 of 10

Author Information Introduction Clinical Differentials Workup Treatment Medication Follow-up Miscellaneous Bibliography

Author: Issley, MD, CCFP, FRCPC, Emergency Physician, Faculty Lecturer, Emergency Department, McGill University Health Centre (Montreal General Hospital)

Coauthor(s): Eddy Lang, MDCM, CCFP (EM), CSPQ, Assistant Professor, Department of Family Medicine, McGill University; Consulting Staff, Department of Emergency Medicine, The Sir Mortimer B -Jewish General Hospital