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Post by blueeighty8 on Mar 12, 2005 23:17:01 GMT -5
Picture a rural community in anywhere ville USA. TherE is a large farm which your patient's granddad owns. In the barn where you know he keeps his "moonshine, or .........(insert whatever libation you'd like)" next to the farms chemicals and fertilizers ( He likes to drink occassionally on those HOT afternoons). So after a fun couple of hours of drinking "moonshine" and becoming inebriated. Your patient accidently grabs and drinks from an unidentified bottle near where the liquor is stored. The patients about 20 minutes later comes in to hte farmhouse bleeding from the mouth and screaming "it burns...it burns, I can't breathe!!!!" the family promptly calls 911 and said ems service responds. The EMS crew (we'll make it ALS for this scenario) respondes, and extricates the patient to the bus ( you were unable to recover the chemical, and the family only knows he had been drinking in the barn. your partner goes in and looks around and see alot of fertilizers, pesticides scattered around.). You initiate highflow O2 @15 lpm via NRB, establish 1 large bore IV, and draw labs, put the patient on the monitor and his ecg is Sinus-tach at 150, the patients spo2 initally 100%, is now 78%, the BP: 144/98, HR:150 RR, Resp Rate:34. ENroute to the hospital the patient detiorates, and declines into cardiac arrest. The patient gets sucessfully intubated (while entubating the patient you have a high volume of blood in the airway, bith upper and lower). You fluid bolus the patient, initate a second IV line and folow ACLS/local protocols. The patient is delivered to a level 1 facility ER and is pronounced dead after 20 minutes of being worked in the ER unsucessfully. The patient has an autopsy and it reveals......
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Post by karebear on Mar 13, 2005 20:11:02 GMT -5
A dairy farm uses a variety of chemicals, both acid and alkali-based for cleaning of the barns. The most dangerous are the alkali cleaners that are used to disinfect and clean residual milk out of pipelines.
The alkalis used in dairies are generally sodium hydroxide or potassium hydroxide-based . These products are way more caustic than a common household drain cleaner. These cleaners are so caustic that when they come into contact with skin or mucous membranes, they produce immediate chemical burns. People who have swallowed liquid pipeline cleaner have burns severe enough to perforate their esophagus, and some have died from large ingestions.
The alkali is stored in large containers and is poured into another small container, which is then carried to a point where it can be poured into the system. Some farmers use glasses, cups, squirt bottles, or other drinking containers for this transfer making the contents unknown to anyone not involved in the process.
So, possibly our inebriated patient grabbed a bottle containing pipeline cleaner. Which caused the severe burning in his mouth and esophagus and also caused a perforation of his gastrointestinal tract. He would have hematemesis, hence the blood in the airway seen upon intubation. Might this have possibly caused his early demise??
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Post by blueeighty8 on Mar 14, 2005 10:55:31 GMT -5
Paraquat poisoning- Paraquat is a poisonous dipyridilium compound whose dichloride and dimethylsulphate salts are used as a contact herbicide - the most common of which are "Weedol", "Pathclear", and "Gramoxone."
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Post by Medic13 on Mar 14, 2005 11:44:50 GMT -5
I cheated on this one and looked it up, which is why I didn't say anything. The key was that the patient declined after the 02 was administered. Paraquat poisoning is a contraindication for 02 therapy, believe it or not.
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Post by blueeighty8 on Mar 14, 2005 14:08:23 GMT -5
Paraquat is used to control broad-leaved weeds and grasses, being less effective on deep rooted plants such as dandelions. It does not harm mature bark, and is thus widely used for weed control in fruit orchards and plantation crops, including coffee, cocoa, coconut, oil palms, rubber, bananas, vines, olives and tea, ornamental trees and shrubs and in forestry. Other uses include weed control in alfalfa, onion, leeks, sugar beet, asparagus. It is used for weed control on non-crop land and can be used as a defoliant for cotton and hops before harvesting. Paraquat is used as a desiccant for pineapples, sugar cane, soya beans and sunflower(5). In pineapples, for example, paraquat is applied after harvest to accelerate the drying out process and enabling plants to be burnt after 3-5 weeks, compared to 13 weeks after the alternative cutting and natural drying. Paraquat is increasingly used to destroy weeds in preparing land for planting in combination with no-till agricultural practices which minimise ploughing and help prevent soil erosion. Although toxic to fish, it is used as an aquatic herbicide where it is absorbed by plant matter and silt. Toxic effects Acute toxicity Paraquat is highly toxic to animals and has serious and irreversible delayed effects if absorbed. As little as one teasthingyful of the active ingredient is fatal. Death occurs up to 30 days after ingestion. Absorbed paraquat is distributed via the bloodstream to practically all areas of the body. The lungs selectively accumulate paraquat, and therefore contain higher concentrations than other tissues. This develops into pulmonary oedema and other lung damage, leading to fibrosis. Liver damage occurs and renal failure may follow as the kidneys remove absorbed paraquat. At spray strength paraquat is of relatively low acute toxicity. It is classified as a solid and with an acute oral LD50 for rats of 157 mg/kg, which puts it into WHO as Class II 'moderately hazardous'(6). Paraquat is also toxic if absorbed through the skin, see 'health issues' below. The minimum lethal dose by oral ingestion in human beings is about 35 mg/kg body weight, although less could be lethal without treatment. In dogs the lethal dose is 25-50 mg/kg and in cows and sheep 50-75 mg/kg(7). There is no vapour toxicity, but it can cause nose bleeding if inhaled. No antidote for poisoning exists although it is recommended that the highly absorbent Fuller's Earth is administered. Hospital care must be sought without delay. Poisoning: suicides and accidents Accidental or deliberate ingestion of paraquat has been responsible for a large number of pesticide-related deaths. It is a major suicide agent in many developing countries. In Sri Lanka a 1989 study of 669 poison incidents indicated that agrochemicals were responsible for 59% and paraquat was the commonest poisoning agent with a fatality rate of 68%(22). Paraquat poisonings are still common in the UK, where a study of pesticide poisoning between 1990-1991 indicates 44 deaths with paraquat responsible for 75%(23). Many of these may be suicides. There is concern in developing countries that the easy availability of pesticides leads to suicides which might not otherwise occur. Most cases are self-poisoning, but not all intend to die(24). To prevent accidental deaths, Zeneca added three alerting agents in the formulations. A stenching agent, was added to some formulations in 1975, an emetic to induce vomiting in 1977, and a blue dye to prevent confusion with cola, black coffee or other beverages was added from 1977. These are included in most but not all formulations depending on cultural acceptance and product registration. What are the Clinical Manifestations of Paraquat Poisoning? The symptoms of poisoning from paraquat depend on the amount and the route of absorption into the body. Exposure to paraquat through brief dermal contact or inhalation of spray mist produces mild symptoms consisting of local skin irritation, reversible irregularities in nail morphology and ocassional epistaxis. Following exposure to the eye, corneal injury, lacrimation and protracted opacification may result. The major symptoms from paraquat ingestion are seen in the mouth and the oesophagus after ingestion of the concentrate and may include ulcers on the lips, burning and ulceration of the tongue and pharynx. In some massive ingestion cases, oesophageal ulceration may occur which can proceed to oesophageal perforation. Following ingestion of greater than 50 ml of the liquid concentrate, patient may develop pulmonary oedema, cardiac failure, renal failure (which may result within hours of ingestion), hepatic failure and also convulsions caused by central nervous system involvement. Under these circumstances, death may occur within several hours to a few days as a result of multiple organ failure. Ingestion of a smaller volume (10-20 ml) of the concentrate produces the same symptoms with the exception that the development of renal failure occurs within 2 to 6 days after ingestion. Renal failure may be manifested by proteinuria and oliguria which then progresses to acute tubular necrosis. The major effect of poisoning at this volume is the accumulation of high concentrations of paraquat in the lung. In the lung, the paraquat ion undergoes a continuous reduction-oxidation process to form free radicals capable of reacting with oxygen. This reaction leads to the production of a reactive oxygen also known as superoxide anion and the regeneration of the paraquat ions. The superoxide anion is then converted into hydrogen peroxide by the enzyme superoxide dismutase. The continuous generation of the superoxide anion under the depletion of precursor NADPH and hydrogen peroxide will then attack the polyunsaturated lipids present in the lung membranes to produce lipid hydroperoxides ( a form of lipid free radical) which in turn can react with further unsaturated lipids to form more lipid free radicals thereby perpetuating the system. The resulting cellular membrane damage reduces the functional integrity of the lung cells, affects efficient gas transport and exchange, and induces respiratory impairment. The development of pulmonary lesion as a result of cellular lipid peroxidation can be divided into two distinct phases. The first phase which occurs within 1-3 days after ingestion is shown by the destruction of the alveolar epitelial cells leading to alveolitis, characterised by the production of pulmonary oedema and infiltration of the air spaces of the lung and the interstitial tissue with neutrophil polymorphs. The second phase involves the development of extensive fibrosis as a response to the acute alveolitis occuring in the first phase. During this stage, the proliferation of the fibroblasts and deposition of collagen will further reduce the effectiveness of gaseous exchange. The consequence is death resulting from severe anoxia. In summary, as the lung function begins to deteriorate, the patient will suffer from breathlessness, tachypnoea, widespread crepitations and central cyanosis. This changes continue over a period of 5-7 days before the patient finally develops to respiratory failure. How is paraquat poisoning managed? There is NO specific antidote for paraquat poisoning. In such poisoning, treatment from confirmed ingestion of paraquat is largely supportive and aimed at interrupting the pathway for paraquat toxicity. Its management is primarily directed at removing paraquat from the site of absorption such as the gastrointestinal tract, increasing its excretion from blood and adopting measures aimed at preventing pulmonary damage. It should be noted that hospitalization is required in all cases of suspected paraquat poisoning. Prevention of Pulmonary Damage Oxygen therapy: Paraquat is known to accumulate selectively in lung tissues and destruction of the lung tissues is exacerbated by the adminstration of oxygen. Animal studies which correspond to the same biochemical changes in human showed that the administration of 100 percent oxygen resulted in a significantly higher mortality rate when compared to those breathing room air. Thus it is suggested that the supplemental oxygen concentration in the inspired air to be not greater than 21 percent so as to maintain an arterial oxygen tension between 40-50 mmHg. Drugs: Drugs such as steroids when given alone or in combination with immunosuppressants, colchicine, d-propranolol and superoxide dismutase have also been used to protect the lung through the reduction of fibrosis or displacing the paraquat from the lung. There is however no observed clear cut benefit unless they are given very early following paraquat ingestion.
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