COMPLIANCE INFO_2020 - Laserfiche WebLink

Home Browse Search

Chemwatch:4650.13 Page 4 of 18 Issue Date:11/12/2018 Version No:7.1.1.1 API Pond Ammonia Test Solution#1 Print Date:06/21/2019 metabolic acidosis due to"uncoupling of oxidative phosphorylation"which produces an increased metabolic rate,increased oxygen consumption, increased formation of carbon dioxide,increased heat production and increased utilisation of glucose.Direct stimulation of the respiratory centre leads to hyperventilation and respiratory alkalosis.This leads to compensatory increased renal excretion of bicarbonate which contributes to the metabolic acidosis which may coexist or develop subsequently.Hypoglycaemia may occur as a result of increased glucose demand,increased rates of tissue glycolysis, and impaired rate of glucose synthesis.NOTE:Tissue glucose levels may be lower than plasma levels.Hyperglycaemia may occur due to increased glycogenolysis.Potassium depletion occurs as a result of increased renal excretion as well as intracellular movement of potassium. Salicylates competitively inhibit vitamin K dependent synthesis of factors II,VII,IX,X and in addition,may produce a mild dose dependent hepatitis. Salicylates are bound to albumin.The extent of protein binding is concentration dependent(and falls with higher blood levels).This,and the effects of acidosis,decreasing ionisation,means that the volume of distribution increases markedly in overdose as does CNS penetration.The extent of protein binding(50-80%)and the rate of metabolism are concentration dependent.Hepatic clearance has zero order kinetics and thus the therapeutic half-life of 2-4.5 hours but the half-life in overdose is 18-36 hours.Renal excretion is the most important route in overdose.Thus when the salicylate concentrations are in the toxic range there is increased tissue distribution and impaired clearance of the drug. HyperTox 3.0 http://www.ozemaii.com.au/-ouad/SALI0001.HTA Treat symptomatically. For cyanide intoxication(and for certain nitriles which produce cyanide ion) Signs symptoms of acute cyanide poisoning reflect cellular hypoxia and are often non-specific. Cyanosis may be a late finding. A bradycardic,hypertensive and tachypneic patient suggests poisoning especially if CNS and cardiovascular depression subsequently occurs. Immediate attention should be directed towards assisted ventilation,administration of 100%oxygen,insertion of intravenous lines and institution of cardiac monitoring. Obtain an arterial blood gas immediately and correct any severe metabolic acidosis(pH below 7.15). Mildly symptomatic patients generally require supportive care alone.Nitrites should not be given indiscriminately-in all cases of moderate to severe poisoning,they should be given in conjunction with thiosulfate.As a temporizing measure supply amyl nitrite perles(0.2ml inhaled 30 seconds every minute)until intravenous lines for sodium nitrite are established.10 ml of a 3%solution is administered over 4 minutes to produce 20%methaemoglobin in adults.Follow directly with 50 ml of 25%sodium thiosulfate,at the same rate,IV.If symptoms reappear or persist within 1/2-1 hour,repeat nitrite and thiosulfate at 50%of initial dose.As the mode of action involves the metabolic conversion of the thiosulfate to thiocyanate,renal failure may enhance thiocyanate toxicity. Methylene blue is not an antidote.[Ellenhorn and Barceloux:Medical Toxicology] If amyl nitrite intervention is employed then Medical Treatment Kits should contain the following: One box containing one dozen amyl nitrite ampoules Two sterile ampoules of sodium nitrite solution(10 mL of a 3%solution in each) Two sterile ampoules of sodium thiosulfate solution(50 mL of a 25%solution in each) One 10 mL sterile syringe.One 50 mL sterile syringe.Two sterile intravenous needles.One tourniquet. One dozen gauze pads. Latex gloves A"Biohazard"bag for disposal of bloody/contaminated equipment. A set of cyanide instructions on first aid and medical treatment. Notes on the use of amyl nitrite:- AN is highly volatile and flammable-do not smoke or use around a source of ignition. If treating patient in a windy or draughty area provide some shelter or protection(shirt,wall,drum,cupped hand etc.)to prevent amyl nitrite vapour from being blown away.Keep ampoule upwind from the nose,the objective is to get amyl nitrite into the patients lungs. Rescuers should avoid AN inhalation to avoid becoming dizzy and losing competence. Lay the patient down.Since AN dilates blood vessels and lowers blood pressure,lying down will help keep patient conscious. DO NOT overuse-excessive use might put the patient into shock.Experience at DuPont plants has not shown any serious after-effects from treatment with amyl nitrite. ADDITIONAL NOTES: Major medical treatment procedures may vary e.g.US(FDA method as recommended by DuPont)uses amyl nitrite as a methaemoglobin generator, followed by treatment with sodium nitrite and then sodium thiosulfate. MODES OF ACTION:Amyl nitrite(AN)reacts with haemoglobin(HB)to form about 5%methaemoglobin(MHB).Sodium nitrite(NaNO2)reacts with haemoglobin to form approximately 20-30%methaemoglobin.Methaemoglobin attracts cyanide ions(CN)from tissue and binds with them to become cyanmethaemoglobin(CNMHB).Sodium thiosulfate(Na2S203)converts cyanmethaemoglobin to thiocyanate(HSCN)which is excreted by the kidneys. i.e.AN+HB=MHB NaNO2+HB=MHB CN+MHB=CNMHB Na2S203+CNMHB+02=HSCN The administration of the antidote salts is intravenous in normal saline,Ringers lactate or other available IV fluid. European practice may use 4-dimethylaminophenol(DMAP)as a methaemoglobin generator.Also hydroxycobalamin(Vitamin B12a)is used. Hydroxycobalamin works by reacting with cyanide to form cyanocobalamin(Vitamin B12)which is excreted in the urine. European and Australian NOHSC(ASCC)propose dicobalt edetate(Kelocyanor)as antidote.This acts by chelating cyanide to form stable cobalticyanide,which is excreted in the urine.In all cases hyperbaric therapy may increase the efficiency of a cyanide antidote kit. for non-steroidal anti-inflammatories(NSAIDs) Symptoms following acute NSAIDs overdoses are usually limited to lethargy,drowsiness,nausea,vomiting,and epigastric pain,which are generally reversible with supportive care.Gastrointestinal bleeding can occur.Hypertension,acute renal failure,respiratory depression,and coma may occur,but are rare.Anaphylactoid reactions have been reported with therapeutic ingestion of NSAIDs,and may occur following an overdose. Patients should be managed by symptomatic and supportive care following a NSAIDs overdose. There are no specific antidotes. Emesis and/or activated charcoal(60 to 100 grams in adults,1 to 2 g/kg in children),and/or osmotic cathartic may be indicated in patients seen within 4 hours of ingestion with symptoms or following a large overdose(5 to 10 times the usual dose). Forced diuresis,alkalinisation of urine,hemodialysis,or haemoperfusion may not be useful due to high protein binding. Continued...