Farming 1: Respiratory Illnesses Portal
Introduction/Etiology
Farming is a dangerous occupation, and farm injuries carry a high risk of infection and disability. When assessing a farm emergency patient, knowledge of the patient’s work environment may provide clues as to what caused the emergency. (For example, silage fermentation gases may have overcome a patient who has fallen from a silo.) Aggressive, immediate treatment may prevent further debilitating injury.
Airway/Breathing Illnesses
A myriad of gases and chemicals on a farm can cause respiratory compromise and should be considered as causes of difficult breathing. Silo Filler’s Disease, Toxic Organic Dust Syndrome (TODS), and Farmer’s Lung (Hypersensitivity Pneumonitis [HSP] or Extrinsic Allergic Alveolitis) are among the most common conditions. (Patients with TODS and Farmer’s Lung exhibit similar symptoms.)
Silo Filler’s Disease
Silo Filler’s Disease is caused by nitrogen dioxide gas exposure, which occurs during the fermentation of chopped corn, hay, or oats into silage. Incidence is usually higher during October and November—about 2 weeks after farmers fill their silos and open them to begin using silage. As fermentation commences, nitrogen oxides develop from nitrates in the silage. These form nitrites, which then combine with organic acids and begin to form nitrous acid. These break down into a mixture of nitrogen oxides (ie, nitrogen dioxide and nitrogen tetroxide) and are considered the primary cause of pulmonary injury. In a silo, the gases have a pungent, bleach-like odor and at times may appear reddish brown (nitrogen dioxide) and yellow (nitrogen tetroxide). In the lungs, these gases react with water and start forming nitrous and nitric acids, which can cause extensive damage to the bronchioles and alveoli. However, they don’t affect the upper airways.
Significant chemical pneumonitis develops. With higher gas
concentrations, pulmonary edema may also develop. (High concentration
of nitrogen oxide can
be fatal within minutes.) These gases
may render a farmer unconscious and in
respiratory arrest. If resuscitated, delayed symptoms often occur
later. Even with
small amounts of exposure, patients may develop bronchospasm. These
patientsare much more prone to viral and bacterial infections.1
Relapses can
occur up to 6 weeks after initial injury. Bronchiolitis obliterans
(characterized by cyanosis and
crackles) may occur 2 to 4 weeks after a mild exposure. The bronchioles
becomeobstructed with granulation tissue and fibrin
plugs. Air flow obstruction and
irreversible scarring occur. The National Institute for
Occupational Safety and Health (NIOSH)
2 has
established an immediately dangerous to life and health
value of 20 ppm for nitrogen dioxide and a short-term exposure limit
(15 minutes) of 1 ppm.
History
If the patient has a history of working in a freshly filled silo or of opening agricultural bags covering the silage pile, observe for signs and symptoms:
Silo Filler’s Disease: Signs and Symptoms
| Acute Phase | |
| Mild-to-Moderate Respiratory Distress:
|
Severe Respiratory Distress:
|
| Delayed
Phase (may occur from 2 to 4 weeks later) |
|
|
|
Testing
- Pulse oximetry to monitor severity.
- ABGs may show hypoxemia.
- CXR may show small, discrete nodules with or without confluence, perihilar infiltrates, and/or fulminant pulmonary edema.3
- Pulmonary function tests may show reduced vital capacity, increased airway resistance, and/or impaired gas transfer.
Treatment
- High-flow oxygen and intubation with PPV may be necessary.
- Use
bronchodilators if the patient is demonstrating
bronchospasm
and wheezing. Give nebulizer treatments using albuterol (Proventil)
0.5 mg and ipratropium (Atrovent) 0.25 mg. - Use high-dose corticosteroids for 8 weeks. Then, taper the dose to prevent relapse (prednisone—20 to120 mg/day).4
- Antibiotics may be required for secondary respiratory infection.4
Disposition/Follow-Up
- If hospital observation is recommended, observe for 6 hours if patient is asymptomatic and for 24 to 48 hours if patient is symptomatic but symptoms quickly resolve.
- Monitor all patients for 6 weeks following exposure for development of bronchiolitis obliterans.
Toxic Organic Dust Syndrome (TODS)
TODS is a nonallergic inflammatory response of the alveoli caused when significant amounts of bacterial and fungal spores and their byproducts (mycotoxins and endotoxins) are inhaled from grain dust, hay, or silage.
History
A patient may have been working in an area containing grain or house dust, or crust-covered silage, contaminated with a toxic-producing bacteria or fungus. As the farmer disturbs the contaminated material, the microorganisms and theirspores become airborne and inhaled by the farmer. 3 Onset of symptoms is 4 to 8 hours after exposure to spoiled plant material.3 Symptoms last from 2 to 10 days and may present as mild, flu-like symptoms or more severe respiratory distress. This does not appear to become a chronic disease.
Diagnostic Studies
- ABGs will be normal.
- CXR is usually clear.
- Immunology: Serum precipitins are usually negative.
- Pulmonary function tests will show mild to no restriction. (Useful in diagnosis, but not necessary.)
- Bronchoalveolar lavage may show polymorphonuclear neutrophils.
Treatment
-
Treat symptoms as needed. Illness is usually short-lived.
Farmer’s Lung (Hypersensitivity Pneumonitis)
Farmer’s Lung or HSP results from an allergic reaction when breathing in dusts from moldy farm byproducts such as hay or grains. Animal feeds have high moisture content and are a breeding ground for bacteria and fungi. These produce spores and byproducts that, when released into the air, may be inhaled, causing respiratory effects in the airways and alveoli.3 The last organism to grow is thermophilic actinomycetes. These spores often cause Farmer’s Lung. Onset can be acute and sudden or prolonged with worsening with each new exposure. The first time a person inhales a large amount of dust and spores from moldy hay or grain, the immune system often responds by producing specific antibodies against the antigens. Once the body has produced the antibodies, further exposure to moldy dust may generate a hypersensitive allergic reaction.5
Allergic alveolitis can become chronic and result in progressive irreversible damage to lungs, leading to permanent disability or death.3
History
Farmer’s Lung is most often caused by breaking open hay bales to feed livestock in barns or from working in a grain bin containing moldy grain. Onset of symptoms is 4 to 8 hours after exposure and lasts from 2 to 5 days.
Signs and Symptoms
Following exposure to spoiled hay, grain, silage; breaking open bales of hay; removing top layer of silage from a silo; shoveling grain; or cleaning out grain storage structures3:
Delayed febrile illness
of variable severity with cough, dyspnea, myalgia,
fever and chills, and malaise
Exam
Fine, crepitant rales in the lower two-thirds of lungs may be heard on auscultation.3
Testing6
- ABGs—may have decreased PO2
- In acute cases, CXR may show fine nodular infiltrates in lower two-thirds of lung fields.
- In chronic cases, CXR may reveal pneumonitis, hyperexpansion, honeycombing of lungs or fibrosis.
- Immunoserology—Test for fungal precipitins. (serum precipitins test). Patient may test positive for thermophilic actin.
- Pulmonary function tests may reveal decreased lung volumes, small airway obstruction.
- Lung biopsy may be useful (but not necessary) for diagnosis. Lung biopsy will show a granulomatous interstitial pneumonitis (gross thickening of the alveolar-capillary membranes).
Treatment
Corticosteriods are thought to reverse the acute course and shorten the duration of the illness. Patients may need oxygen and rehydration in severe cases of acute Farmer’s Lung. Antibiotics, bronchodilators, and antihistamines are not effective.
A small concentration of antigen can provoke illness in highly sensitive individuals, and continued exposure can lead to permanent impairment. Avoidance of spoiled plant material as well as early diagnosis is imperative in preventing irreversible lung damage.3 Wearing a certified dust respirator may help to prevent sensitization. Monitor for further impairment by regularly obtaining pulmonary function tests and CXRs.3
Manure Pit Asphyxia
Manure pits are designed as open-air trenches or located in confinement facilities for animals. Hog confinement facilities are the most common. In addition to manure pit asphyxia, drowning in a manure lagoon is a potential hazard.
Issues with manure gases are worse during the winter when there may be less natural ventilation. Concentrations of gases are higher during hot, humid summer days. Disturbing the manure (by means of shoveling, moving, piling) may increase gas levels. As manure breaks down, it often separates into a layer of gases: methane, carbon dioxide, ammonia, and hydrogen sulfide. Methane gas may be flammable. Ammonia has a pungent, irritant odor, which may cause irritation to eyes, nose, throat, and chest.
Hydrogen sulfide gas is the most dangerous. Disturbance of manure can cause increases in hydrogen sulfide gas to 1500 ppm. It has a rotten egg smell at 0.13 ppm and can paralyze the olfactory nerve at rates above 150 ppm. Conjunctival irritation occurs at 20 to 50 ppm and irritation to the respiratory tract at 50 to 100 ppm. At 250 ppm, pulmonary edema may develop. At 500 ppm, hydrogen sulfide gas can cause unconsciousness, respiratory paralysis, and even death. Exposures for longer than 5 minutes to high levels can cause permanent neurologic effects. Hydrogen sulfide forms sodium sulfide when it reacts with water on skin or mucous membranes. Its primary effect is on the nervous system, causing paralysis of the respiratory center.
Symptoms
If patients recognize they are having symptoms and seek treatment early, they may display the following symptoms: conjunctival irritation, dyspnea, chest pain, cough, or pulmonary edema if the level of exposure has been high enough. Patients do not usually have long-term pulmonary damage if they are treated quickly. Chronic neurologic effects may be memory failure, lack of insight, disorientation, delirium, transient hearing loss, vision loss, ataxia, position/intention tremor, and muscle rigidity. These may progress to unconsciousness, respiratory paralysis, or death. Patients may develop subcortical white matter demyelination.
Treatment
- Remove patient immediately from contaminated area to fresh air.
- Remove clothing.
- Administer oxygen via non-rebreather mask at 15 L/min.
- Treat metabolic acidosis.
- Treat with hyperbaric oxygen, if available.
- Consider giving amyl nitrate or sodium nitrate to induce methemoglobin to scavenge for sulfide.
Prevention education is important. (Most patients die at the scene, along with 1/3 of rescue workers who try to save them.) Having odor testers or meters to recognize high gas situations and appropriate self-contained breathing apparatuses is an important teaching point for farm families.
References
- Haddad & Winchester, Clinical Management of Poisoning & Drug OD, W.B. Saunders Co. 1990, Philadelphia, PA, p. 1273-1275.
- National Institute for Occupational Safety and Health: Pocket Guide to Chemical Hazards (DHHS [NIOSH] Pub. No. 90-117). NIOSH, Cincinnati, OH (1994)
- http://www.inform.umd.edu/DUSTS_From_DECAYED_GRAIN_HAY_AND_SILAGE, May 10, 2000, p1-9. (article is now available at http://nasdonline.org/static_content/documents/1630/d001504.pdf accessed February 16, 2012)
- http://www.inform.umd.edu/EdRes/Topic/AgrEnv/ndd/o…/OXIDES_OF_NITROGEN.htm, 5/10/2000, p. 1-5.
- www.ccohs.ca/oshanswers/diseases/farmers_lung.html
- Agricultural exposures and respiratory illnesses/injuries, Steven Kirkhorn, MD, MPH, OHR-Mayo Health System, University of MN Rural Family Practice Residency.