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Examples acrolein spasms shoulder purchase 30 pills rumalaya forte with amex, dalaphon spasms spasticity muscle cheap rumalaya forte 30 pills amex, paraquat gut spasms buy discount rumalaya forte 30 pills, diquat muscle relaxant otc usa discount 30 pills rumalaya forte overnight delivery, glyphosate, atrazine, propazine, simazine, nitrofen, trichloroacetic acid, and chlorophenoxy compounds. Hydrocarbons and Pesticides Paraquat and Diquat Paraquat and diquat are widely used herbicides which belong to the bipyridyl group. The granular form is available as colourless crystals (dichloride salt) or a yellow solid (bis(methyl sulfate) salt). Diquat is 1,1-ethylene-2,2-dipyridylium dibromide, and is less commonly used than paraquat. It has the same indications and mode of action as paraquat but produces much less severe pulmonary lesions. Section 8 Toxicokinetics Absorption through inhalation, skin contact, or eye contact is minimal, though prolonged contact can be hazardous. On ingestion, paraquat solution is much more rapidly absorbed than the granular form. More than 90% of an absorbed dose is excreted by the kidneys as the parent compound within 12 to 24 hours. Highest concentrations are found in kidney and lung; paraquat also accumulates in muscle tissue, which may represent a reservoir, explaining prolonged detection of plasma or urine paraquat weeks or months following ingestion. Examples, anticoagulants, thallium, vacor, phosphorus, zinc and aluminium phosphide, alpha-naphthyl-thiourea, cholecalciferol, arsenic, barium carbonate, bromethalin, Paraquat is a rapidly-acting herbicide. It kills the tissues of green plants by contact action with foliage and by some amount of translocation to the xylem. Corneal injury and protracted opacification of the cornea may result following eye exposure to paraquat. Extensive loss of superficial areas of the corneal and conjunctival * Other bipyridyl herbicides which are rarely encountered include chlormequat, difenzoquat and morfamquat. Irritation of the skin and mucous membranes may be severe following paraquat exposure. Irritation of the gut including abdominal pain, nausea, vomiting, and diarrhoea may occur immediately following ingestion. Tachycardia, hypotension, and cardiorespiratory arrest can occur with large ingestions. Pancreatitis may develop in some cases of acute paraquat poisoning, and can cause severe abdominal pain. Reaction with molecular oxygen yields the superoxide radical (O2-) and reforms the paraquat dication, ready to be reduced again. This process known as redox cycling is sustained by the extensive supply of electrons and oxygen in the lungs. This and the subsequent reactions explain why oxygen enhances the toxicity of paraquat, and paraquat enhances the toxicity of oxygen. Two superoxide species form hydrogen peroxide in a reaction catalysed by superoxide dismutase. The hydroxyl radical causes degradation of cell membranes through lipid peroxidation resulting in cellular death. Subacute Form: (ingestion of less than 30 mg/kg of paraquat) this is characterised only by gastrointestinal manifestations. Mortality in paraquat poisoning can be high and is related to two factors-concentration and quantity. Swallowing more than a mouthful can cause death in 72 hours because it corresponds to ingestion of more than 50 mg/kg. If it is less than a mouthful, death may be delayed upto 70 days and is usually due to pulmonary fibrosis. Pneumothorax, pneumopericardium and subcutaneous emphysema may develop in patients with paraquat induced lung injury. Survivors of severe paraquat poisoning often develop progressive pulmonary fibrosis within 5 to 10 days or longer after exposure. Occupational exposure to paraquat can cause a dry, cracking dermatitis and nail atrophy. X-ray of the chest may reveal patchy infiltration in the early stages, and opacification of one or both lung fields in later stages. However, if death is due to the hyperacute form of presentation, no abnormalities may be noted on the chest X-ray. Urine can be tested for gross amounts of paraquat by alkalising 3 to 5 ml with a few mg of sodium bicarbonate, then adding a few mg of sodium dithionite. Survival is usually associated with levels less than 1mcg/ ml, while mortality is high when the level exceeds 10 mcg/ ml. When submitting samples for chemical analysis it must be ensured that only plastic containers are used, since paraquat binds to glass. Pesticides Usual Fatal Dose Estimated lethal dose is 10 to 15 ml of the concentrate. Prudence requires that all cases of paraquat ingestion be treated as potentially fatal poisonings. Initial Phase-pain in the mouth, oesophagus, and stomach due to corrosion, vomiting, diarrhoea, dysphagia, aphonia. Second Phase-begins after 2 to 5 days and is characterised by renal and hepatic toxicity, i. Although hepatic injury from exposure to paraquat may be quite severe, clinical outcome is generally not determined by hepatotoxic effects. Third Phase-begins after 5 days and is characterised by pulmonary fibrosis which leads to progressive respiratory failure.
Corrosive (Caustic) Poisons Uses Carbolic acid was introduced as a disinfectant in the 19th century by Lemaire spasms left rib cage order rumalaya forte 30 pills mastercard, and quickly became popular ever since Lord Lister (Fig 6 spasms 2012 cheap 30 pills rumalaya forte overnight delivery. Even today it is popular as a hospital and household disinfectant along with its related counterpart Lysol muscle relaxant uk cheap rumalaya forte 30pills on line,* even though several safer and more effective alternatives have been developed including cetrimide muscle relaxant drugs buy 30pills rumalaya forte visa, chlorhexidine (Savlon), chloroxylenol, parachlorometaxylenol (Dettol), terpineol, and xylenol. The various uses of carbolic acid are as follows Antiseptic and disinfectant: especially for sterilising floors, walls, furnishings, glassware, and instruments. Preservative: Phenol is a commonly used preservative in injectable medications. Y Neurolysis for spasticity (by injecting phenol solution into neuromuscular junctions). Mode of Action Carbolic acid is actually a very mild corrosive, but has profound systemic effects after absorption. Local: Skin or mucosal contact results in mild corrosion with hardening and whitish discolouration. However the white eschar (especially in the skin) drops off in a few days, leaving a brown stain. Locally there may be burning pain followed by tingling, numbness, and anaesthesia. Hepatorenal-Oliguria, with scanty urine which turns greenish or brownish on exposure to air because of phenolic metabolites (hydroquinone and pyrocatechol). Chronic Poisoning (Phenol Marasmus) this was common in earlier days among medical personnel when phenol was routinely used as a skin disinfectant. It is characterised by anorexia, weight loss, headache, vertigo, dark urine, and pigmentation of skin and sclerae (ochronosis). Urine collected and stored in a transparent container shows a gradual change in colour to brown or green (Table 6. A purple or blue colour which persists even on heating indicates phenol poisoning. Brownish-black Yellowish-brown Chapter 6 Yellow Organic Acids Yellowish-orange Greenish-blue Treatment 1. Distinct odour of phenol, especially around the mouth and in the stomach contents. Corroded areas are at first white, but if death has been delayed they turn brownish (Fig 6. Gastric mucosa is greyish white, swollen, and hardened (leathery), but Lysol poisoning is asociated with soapy and soft mucosa. Forensic Issues Most cases of poisoning are accidental in nature arising out of occupational exposure or therapeutic misuse. Poisoning with phenolic derivatives causes similar but usually less severe manifestations, and must be treated on the same lines as phenol. Oxalic Acid Corrosive (Caustic) Poisons Synonyms Ethanediolic acid; Dicarboxylic acid; Salt of sorrel. Physical Appearance/Derivatives Oxalic acid, the simplest dicarboxylic acid, is a potentially toxic chemical which is synthesised commercially and is also naturally present as a salt in many plants. Oxalic acid is a relatively strong acid, and forms a white, dihydrate precipitate. Alkali extraction of sawdust and the metabolism of many moulds will also produce oxalic acid. Oxalic acid is used in paint, stain and varnish removers, rust and ink stain removers, and ceramics. It is also used in general metal and equipment cleaning, wood cleaning, process engraving, printing and dyeing, bleaching, textile finishing, leather tanning, and photography. Systemic absorption leads to hypocalcaemia, since it reacts with calcium in plasma, and insoluble calcium oxalate is precipitated which accumulates in the liver, kidneys, heart, lungs, and blood, and is excreted in the urine. Local: Whitish or yellowish corrosion (mucosa), or discolouration (skin), with underlying congestion. Later there may be metabolic acidosis, ventricular fibrillation, and renal failure. Calcium oxalate crystals can be deposited in the liver resulting in hepatic necrosis and failure in severe cases. Crystals of calcium oxalate may be demonstrated in scrapings of the mucosa, (examine with polarising micoscope). Accidental poisoning may also result from excessive ingestion of certain vegetables rich in oxalates (rhubarb leaves,* sorrel, etc. Chronic consumption of oxalic acid can lead to renal calculi with consequent renal colic. Alkalis and Other Caustics Physical Appearance Most of these occur as white powders or colourless solutions. Mode of Action Locally, alkalis produce liquefaction necrosis which results in extensive penetrating damage because of saponification of fats and solubilisation of proteins. Oesophagus is more severely affected than the stomach in contrast to acids (page no. Non-ulcerative oesophagitis-from ingestion of mild irritants, resulting in 1st degree burns. There is severe dysphagia with vomiting which may subside after 2 to 3 days only to reappear as slowly progressive dysphagia after 4 to 6 weeks due to stricture formation. Oesophagitis with complications-apart from oesophagitis, there are complications such as mediastinitis, perforation, pericarditis, pulmonary oedema, laryngeal obstruction, etc. It is important to perform oesophagoscopy and make accurate assessment as to the extent of local injury (Table 7.
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The differential diagnosis includes viral exanthems muscle relaxer 93 effective 30pills rumalaya forte, hypersensitivity vasculitis spasms in 7 month old cheap rumalaya forte 30pills without prescription, scarlet fever spasms under left rib cheap rumalaya forte amex, acute rheumatic fever infantile spasms 7 month old purchase generic rumalaya forte line, meningococcemia, disseminated gonococcemia, reactive arthritis, Lyme disease, Still disease, and Stevens-Johnson syndrome. These findings should prompt consideration for Stevens-Johnson syndrome, a potentially fatal hypersensitivity reaction. A Management and Disposition the diagnosis is clinical and based on history of exposure to a potential offending agent. Fever, joint pain, and erythematous plaques to face (A) and legs (B) 14 days after receiving amoxicillin in a 7-year-old girl. Serum sickness, as originally described, is typically in response to administration of a nonhuman species protein antigen. Present-day examples include sheep-derived Fab snake antivenom, heterologous immunomodulators containing murine components (rituximab and infliximab), streptokinase, and the human diploid cell rabies vaccine. Fever, joint pain, ankle swelling, and erythematous plaques seen here in an infant 11 days after taking ceclor, suggesting serum sickness. A strawberry hemangioma lies in the upper dermis and often originates as an erythematous macular patch, a pale macule, or a localized telangiectasia with a pale halo. The classic presentation is a bright red, slightly raised, noncompressible plaque. Hemangiomas can also affect the airway, eyes, and liver or cause high-output cardiac failure if sufficiently large. The most important local complication is ulceration which can be exquisitely painful. The differential diagnosis includes vascular malformations, malignant vascular neoplasms, pyogenic granulomas, and giant melanocytic birthmarks. Management and Disposition Most cases require no therapy because strawberry hemangiomas usually regress without residual problems. Treatment of hemangiomas in general is indicated when there is an obstruction of a vital orifice (ie, airway, mouth, or nares) or vision (eyelids) or if hematologic or cardiovascular complications are present. Education and parental reassurance are important because there is great pressure to treat for cosmetic reasons. Oral corticosteroids, intralesional corticosteroids, pulsed dye laser, and recombinant interferon- are some of the therapeutic modalities available. In complex cases, consultation with a vascular malformation specialist or dermatologist is recommended. Kasabach-Merritt phenomena (hemolytic anemia, thrombocytopenia, and coagulopathy) is associated with Kaposiform hemangioendothelioma or tufted angiomas and not with common hemangiomas as was previously thought. In contrast to hemangiomas, vascular malformations, such as port-wine stains, do not proliferate or involute. Patients with hemangiomas of the face, and especially in the "beard" distribution, have a higher risk of also having an airway hemangioma. Hemangiomas over the midline lumbar spine should prompt an evaluation for spinal dysraphism. Raised umbilicated vascular lesion on the left upper chest consistent with strawberry hemangioma. In general, it is caused by Streptococcus pneumoniae, Haemophilus influenzae, Moraxella catarrhalis, and S aureus. If not treated promptly, it can lead to blindness, cavernous venous sinus thrombosis, meningitis, subdural empyema, or brain abscess. Preseptal (periorbital) cellulitis is much more common and usually presents with edema and circumferential erythema of the eyelids and periorbital skin, fever, and minimal pain. Proptosis and ophthalmoplegia are not characteristic as it does not involve the orbit or other ocular structures. Preseptal cellulitis usually results from sinusitis or contiguous infection due to local skin trauma, insect bite, or hordeolum. Adults and children greater than 1 year with mild cases (especially those with a history of trauma such as abrasion or insect bite or sting) can be treated with outpatient oral antibiotic therapy with close follow-up. Eye redness, swelling, purulent drainage, and mild entrapment are seen in this patient with painful orbital cellulitis. Right ethmoid sinusitis with subperiosteal abscess and extension into the orbital space in above patient. Left periorbital cellulitis with edema and erythema of the eyelids in a nontoxic cooperative toddler with a normal ocular exam. As the obliteration of the clefts occurs, a portion may remain, forming a cystic space. The anatomic location of a branchial cleft cyst depends upon the specific arch/cleft involved. Involvement of the first branchial cleft may result in a cyst in the region of the parotid gland, the preauricular or postauricular area, or inferior to the angle of the mandible. A second cleft anomaly represents 95% of these malformations, and may be found along the anterior border of the sternocleidomastoid muscle or deeper, in the vicinity of the carotid arteries. Cysts usually present clinically when they become infected and enlarge acutely usually in association with an upper respiratory infection. Branchial cleft anomalies are second only to thyroglossal duct cysts in frequency of congenital head and neck lesions in children. Management and Disposition the diagnosis is suggested by history and physical examination. Treatment includes antibiotics to decrease the inflammation if there is an associated infection. It usually presents as a painless, midline, anterior neck mass that moves with swallowing and protrusion of the tongue.
Ethanol has about 20 times the affinity for alcohol dehydrogenase compared Fig 14 spasms of the diaphragm generic 30 pills rumalaya forte visa. This competitive effect of ethanol gains more time for excretion of unchanged methanol from the body spasms mouth order 30pills rumalaya forte visa, and it also inhibits the formation of methanol metabolites that produce severe acidosis spasms with fever order rumalaya forte 30pills amex. Formic acid is metabolised to carbon dioxide and water via a folate dependant system muscle relaxant menstrual cramps purchase rumalaya forte 30pills mastercard. It is safer to maintain a blood ethanol concentration greater than 130 mg/100 ml than to have it fall below 100 mg/100 ml. A 10% (V/V) solution can be prepared by any of the following methods: Remove 50 ml from 1 litre of 5% ethanol solution and replace with 50 ml of absolute alcohol. Replace 100 ml of fluid from one litre of dextrose 5% in water with 100 ml of absolute ethanol. Adding 59 ml of 95% ethanol solution to one litre of 5% ethanol solution (if absolute alcohol is not available). Consider implementing the ethanol treatment regimen in these patients until a methanol level can be determined. Determine blood ethanol level before beginning ethanol therapy and modify the loading dose accordingly. The usual dose is 15 mg/kg, followed 12 hours later by 10 mg/kg 12th hourly for 4 doses, and then increased to 15 mg/kg 12th hourly for as long as necessary. For convulsions: Attempt initial control with a benzodiazepine (diazepam or lorazepam). Haemodialysis is very effective in removing methanol, formaldehyde, and formic acid. While ethanol treatment is also quite effective, it is extremely difficult to maintain therapeutic ethanol levels for long periods of time. Haemodialysis is strongly recommended in patients with acidosis or serum methanol levels of greater than 25 to 50 mg/100 ml. Lungs may reveal oedema, emphysematous changes, and desquammation of alveolar epithelium. Viscera must be preserved in saturated solution of sodium chloride and not rectified spirit, as in the case of all alcohols. In addition to the routine viscera, it is advisable to preserve one cerebral hemisphere. The latter are referred to quaintly as "liquor tragedies" and are reported in Indian newspapers at depressingly regular intervals from all parts of the country. Blood isopropanol concentrations of 128 to 200 mg/100 ml, measured within hours after ingestion, have been associated with deep coma and death. The absence of hyperglycaemia or glucosuria when acetone is present helps differentiate between alcohol intoxication or diabetic ketoacidosis versus isopropanol intoxication Isopropanol is metabolised to acetone. Acetone may be detectable in the urine by 3 hours after ingestion, and in the blood by one-half to one hour after isopropanol ingestion. A high serum or urinary acetone without metabolic acidosis is strongly suggestive of isopropanol intoxication. Treatment Usual Fatal Dose Toxicokinetics Isopropanol can be absorbed through all routes. Approximately 80% is converted to acetone and the remainder is excreted unchanged in the urine. Acetone is excreted in the urine and breath, and also metabolised to acetate, formate, and carbon dioxide. However, many investigators are of the opinion that activated charcoal does not adsorb isopropanol efficiently. Haemodialysis: Useful in patients demonstrating marked symptoms (persistent hypotension, coma) unresponsive to standard therapy. Supportive measures, including correction of hypotension, metabolic acidosis, etc. Forensic Issues Isopropanol may be generated spontaneously in a dead body, presumably due to bacterial or other putrefaction processes. Clinical Features Lethargy, vertigo, headache, confusion, ataxia, dysarthria, nystagmus, miosis, abdominal pain, gastritis, haemorrhagic tracheobronchitis, hypotension, and apnoea. Physical Appearance Colourless, syrupy, odourless, non-volatile liquid, with a bittersweet taste. More than 25% of the ethylene glycol produced is used in antifreeze and coolant mixtures for motor vehicles. It is also used widely for aircraft deicing, and used in condensers and heat exchangers. As a glycerine substitute in commercial products such as paints, lacquers, detergents, and cosmetics. High anion gap acidosis: Increased anion gap metabolic acidosis results from the metabolism of ethylene glycol to acidic metabolites, predominantly glycolic acid. The osmolal gap may be used to estimate the serum ethylene glycol level (in mg/100 ml) by simply multiplying the gap by 6. Ethylene glycol concentrations must be interpreted with regard to the time of ingestion and the acid/ base status of the patient. Shortly after ingestion ethylene glycol concentrations greater than 30 to 50 mg/100 ml (8. In severely acidotic or acidaemic patients lower ethylene glycol concentrations may be associated with severe toxicity. A fluorescent dye, sodium fluorescein, is present in many commercial antifreeze products. However, fluorescent urine is not a reliable indicator of ethylene glycol ingestion, due to variations in interpretation of urine fluorescence among observers and the fact that most normal urine specimens exhibit some degree of fluorescence.
