arr ate " Ce General Toxicology Prof. /Mohammed Fathy NERAL TOXICOLOGY [Definitions: : _ Gerived from the Latin word {Toxieum =poison, ¥ Toxieology is the word Logy=science} and it mea living organism. 7 : 4 Clinical toxicology is the branch of medicine that deals with forms)and Toxic dose\Glinical pictur), diagnosis & treatment of poisoning. ¢ that produces harm to the body. ns the study the effects of poisonous substances on 4 A poison is any substanc 6 Sour | Classification of poison’ orgie comosives], FTF 7? ® Poison has local action + Poison has remote action: [Alkaloids and most Therapeutics) Syskew'e ° {Poison has double (local and remote) action: [Metals and Organic & 1, Heavy Mebods > corrosives). fylic_ acre Factors affecting toxin effects: (Important) a2 1) Factors related to poison: (4) 3) cenconbraki 1. Dose: Increase the dose increases effect o)- Ph 2, Route of administration: The quickest and most dangerous is IV route, followed by inhalation, IM, Subcutaneous, ingestion; absorption through the ‘mucous membranes and lastly the slowest route is absorption through ki 3, Form: Poison in gaseous form is the most rapidly @bsorbed) Liquid poisons are_more rapidly sbsorbed than solids. Tine powders are more rapidly absorbed than big lumps. 4, Cumulating: Drugs accumulate in the body upon repetition of the dose for AVC prolonged petiod, It is due to extensive tissue distribution of drug with its abd poor metabolism, Example: digitalis) — 2) Factors related to patient: (8) 1, Age: Extremes of ay si ible to the effect of poison. 2, Sex: Women hy ter bioavailability for ethanol 7 3. Stomach state: ‘¢ Empty stomach helps absorption and f toxicity. . ca the type of stomach content can change the rapidity of absorption as it helps the absorption of lipid soluble compounds as organophosphates, while fat delay absorption of arsenic.» J) co\\ le. A DG Webby athe, By| General Toxicology 4, Pre-existing pathological condition: ¢ Hepatic impairment will @ecrease the metabolism with subsequent increase of the toxicity of the poison. | © Renal impairment will Geerease the elimination With subsequent increase -— of the toxicity. SOON” 5, ‘Tolerance: it is the decrease the response to certain drug on repetition of the dose, so that larger doses are required to obtain the same effect of the original itement, It may be due to genetic abnormalities. Crier ) Hypersensitivity: It is an exaggerated response to drug. May be severe up to producing anaphylactic shock. It is dose non-related. 8. Drug interaction: Due to concomitant administration of more than one drug at the same time. It may be in the form of synergism: (1+1>2) barbiturates & alcohol, addition: (1+1=2) salicylates & paracetamol or antagonism:( 1+1= 0) lead & BAL. Diagnosis of poisoning: Han 4 cpt I. History: 'SATS" ar Be alpda +S: substance taken. + A: amount ingested. + T time of ingestion. $: symptoms appeared. (© ComPicston— IL. Physical examination. A. General findings. Perform a careful examination that may cover one of the common autonomic syndromes. Q. what are toxidromes (Fingerprints) in toxicology? ‘These_are_symptoms_and_signs, when appear in a patient, direct the 7 sisi to poisoning by a specific substance (s). meee. 1, Sympathomimetic toxidromes: Hypertension _is__accompanied _by y tachycardia, upils_are dilated but reactive. The skin. is sweaty. (Examples: cocaine and amphetamines). MH] 2. Cholinergic toxidrome: Because both nicotinic and muscarinic receptors are stimulated, mixed effects may be seen. The pupils are usually miotic (of Pinpoint size). The skin is sweaty, and peristaltic activity is inereded. Easciculations are a manifestation of nicotinic stimulation and may progress to muscle weakness or paralysis, (Examples: organophosphate and carbamate insecticides and physostigmine). 3. Anticholinergic toxidrome: Tachycardia with mild hy ertension is common. | The pupils are widely dilated and irreactive, The skin ig flushed, hot, and 2General Toxicology dry. Peristalsis_is ds creased, and urinary retention is common, Agitated sBivium is eommon, and hyperthermia may occur. (Examples: atropine, penztropine, antihistamines; and antidepressants). 4, Opioids toxidrome: Blood pressure ‘and pulse rate are both decreased. The Peristalsis is often decreased. pupils are_smal_often_of pia int size. nd opiates). (Examples: clonidine a ‘ure: hyperthermia can occur (in § Ficylate ‘and anticholenrgic gear B. Vital data: ( Temperat nt ‘ Barbiturates, narcotics, sedative poisons, while hypothermia may occur i hypnotics and alcohol. oe Pulse, bradyeardia is seen in opiate, digitalis cholinergic, beta blockers, and caloium changel blockers, while tachycardia occurs in amphetamine, cocaine & anticholenrgic. / i G Blood pressure: hypertension ip amphetamine and cocaine. | CC. SkinZ joss arene’ Flushing: in anticholinergic & alcohol. C2. 4, Diaphoresis: in OPI, salicylate & cocaine. —~ 3 Bullous lesion: in sedative hypnotics especial monoxide poisoning Eecymesd~ (-D: Breath; i's important to smell the patient's breath. Alcohol, cyanide, phenol, 2 phosphorous and H2S have characteristic odor. |, | ny Rkenstns > Plas Sedeath- Ihe los Pes swekey? barbiturate & carbon ea Pupily/ fs (71. Pinepointed: with opiates, OPI. phenothiazins and pontine lesions. 2. Reactive dilated: with sympathomaimetics (amphetamine, cocaine). 3, Non reactive dilated: occurs with anticholenrgics. + depth « hubs - F Respiratory system: @ wastagonts Teton Talsant, cthand* eau 4. Tachypnea: occur in aspiration pneumonia, toxic hypoxia & CNS stimulants (amphetamine, cocaine). 2. Bradypnea: occur in CNS depression as in(eikanol anf barbiturate) 3, Pulmonary edema: © Cardiac: in beta blockers and cyclic antide ressani dng - ‘© Non cardiac: in opiate, barbiturate, OPI & salic; h y on pi ¥ late, hy yx VD AL - ‘Wheezes: in organophosphorous, cholinergic medications ea mid . : Neurologleat; eareh neurological examination should be dove, grading of coma should be assessed in comatose patient. eerr a General Tasicolagy H, Abdomen: 1. Vomiting with 2, Diarrhea with arsenic hi of ernie Aho 3. Constipation: with chronic plumbism. — IIL, Investigations: D) Laboratory tests: 1. Routine investigations: Includes complete blood picture (CBC), renal function test (urea, creatinine), liver function test (SGPT, SGON), arterial blood gases (ABG), Glucose and electrolytes (Na, K) levels. 2. Specific investigations: Blood (serum levels of drugs, enzyme activity) or urinary detection of poisons. 2) Radiological tests: _—_Electrcardiologaphy (ECG), _ abdominal ultrasonography , chest X-rays, plain X-rays Q. Radio-opaque substances that may be visible on AXR? {COINS} ® Cocaine packets, calcium ‘© Opium packets # Iron, other heavy metals suchas lead, arsenic, mercury © Neuroleptic agents (phenothiazines) —p» O,'n Pati ¢ Sustained-release or enteric coated agents as ‘Treatment of Acutely Intoxicated Patient: eee ] T. Emergency and supportive measures. DE@ Ce 2. Specific Drugs and Antidotes.-¥'? ‘ Cae “we Decontamination P Enhanced elimination. Cig ae 1. Emergency and supportive measures. [Treat the patient not the poison}. IRWAY [keep airway patent]: “A. Position the patient and clear the airway. 1. Place the patient with head extended. 2, Remove any obstruction or secretions from oropharynx by suction, by a sweep with the finger, or with forceps. 3. The airway can be maintained with oropharyngeal airway. B, Perform endotracheal intubation, The tube is passed through the patient's ‘mouth into the trachea under direct vision. BREATHING : 1. Administer oxygen as indicated. Intubation may be required. When? 2, Assist breathing manually with a bag-valve-mask device 4General Toxicology 3, Program the ventilator and ventilate patient if respiratory failure occurred. CIRCULATION . no pulse 1.Perform cardiopulmonary resuscitation ey if there is no pulse. 2.Begin continuous ECG monitoring. 3,Seoure venous access. 44,Draw blood for routine studies. S.If the patient is hypotensive, begi (NS) or another ci sstalloid solution. oo. 6.In patients are Soretoee place 4 Foley catheter in the bladder, obtain urine for routine and toxicologic testing. 2—~~ ‘COMA (Important) A. Treatment 1. Maintain the airway ‘supplemental oxygen. 2. Give coma cocktail: dextrose, thiamine, and naloxone. Should be used as giiostic oF therapeutig ‘a. Dextrose, All patients with depressed consciousness should receive unless hypoglycemia is_ruled out with an it diate bedside glucose determination. Initial doses include the following: i, Adults: $0% dextrose, 50 mL IV. ii, Children: 25% dextrose, 2 mL/kg IV. b(Thiamine] Thiamine is given to prevent_abrupt_precipitation of Wenlelas anctome reuling fom Namie deficiency in{aleohoTo, patients. Give thiamine, 100 mg, in the IV bottle or intramuscularly. ¢. Naloxone. All patients with respiratory depression should receive naloxone, Caution: Naloxone may precipitate abrupt opiate withdrawal. i. Give naloxone, 2 mg IV. .If there is still no response and opiate overdose is highly suspected by history or clinical presentation (pinpoint pupils, (apnea) or liypotension), iv naloxone T0=20 mV, m d. Elumazenil (Anexate) if diazepines are the suspected cause of coma. B. Differential diagnosis: Causes of coma: yj = 1. Toxie (CNS see anticholinergics and toxin causing [cellular hypoxia e.g, CO) 2. Pathologie (hepatic failure, renal failure, metabolic e.g. hypoglycemia, 5 in infusion of intravenous normal_saline and assist ventilation if necessary. Administer |General Toxicology hypertensive encephalopathy, infections such as encephalitis or meningitis, ete.) 3, Traumatic (head injuries). C. Selected drugs and toxins causing coma, General CNS depressants Cellular hypoxia © Anticholinergi * CO © Antihistamines © Cyanide © Barbiturates © Hydrogen sulfide © Phenothiazines « Metlb-emia * Benzodiazepines “Othe * Carbamazepine © Hypoglycemic agents * Alcohols * Salicylate * Tricyclic antidepressants * Opiates Note: Coma sometimes represents a post-ictal phenomenon after a drug- or toxin-induced seizure, v Coma seales (grades): (Oral) Rapid evaluation of the level of consciousness AVPU system: it is a rapid mean of documenting the level of consciousness (A=alert, V=verbal response, P= response to pain and U = unresponsive). CONVULSIONS 1. Maintain open airway and assist ventilation, Administer oxygen. 2. Anticonvulsants: as diazepam (6-0mgly), short acting barbiturates. 3. Inrefractory cases, general anesthesia ee eee Il, Specific Drugs and Antidotes (very important) Antidotes (@ Loe: (W) Physiological A) Physico mechanical [systemic] B) Chemical E.g. Chelators:General Toxicology 1- Physicomechanical antidotes: These are agents that react with the ingested poison physically in the GIT without changing its nature, alse a. Demutcents: Protect the stomach mucosa by coating it eg. Milk & egg white for corrosives | b. Dissolving: Dissolve the poisons e.g. Ethanol 10% used to dissolve | phenol vearh aes |) ¢. Adsorbents: Adsorb the poisons e.g. Activated charcoal and cholestyramine. \Sxa d. Entanglers: Catch the solid objects e.g. cotton for pins 2- Chemical Antidotes: a. Oxidatior b. Reduction: Mercurie chi formaldhyde sulfoxylate (50 ml of 5% sok ‘Monovalent form (non toxic) ¢. Precipitation: © Ca precipitates Oxalic acid © Skimmed milk in mercury toxicity. d. Neutralization: Exothermic heat reaction increase destructive effect Weak alkalis used to neutralize acidic corrosives. (obser ¢ Weak_acids used to neutralize alkaline _corrosives. [Obsolete]. 3- Physiological (Systemic) antidotes: A- Competitive antagonists: J- Naloxone (Narcan) and Naltrexone for opiates. 2- Flumazenil (Anexate): for benzodiazepines. 3- Atropine: used in ‘a+ Organophosphate and carbamate insecticides b- Correct bradycardia in digitalis, morphine & 8-blocker toxicity 4- Ethanol: used in methanol & ethylene glycol toxicity 5 d-methyle Pyrazole: used in methanol toxicity. B- Non-competitive antagonists: 1, Calcium gluconate: used in i, Oxalic aci ii, Lead (lead colie). Kmn041/5000 used for Cyanide [divalent, toxic] is_reduced by Na_ orally) to | | | aeGeneral Toxicology 2. Pralidoxime: in organophosphate toxicity 3. Physiostigmine: used in atropine overdose. C- Chelating agents: ' Definition: These are chelating agents which combine with metals forming non toxic compounds that are rapidly excreted in urine 'h anti-lewisite (BAL; dimercaprol): Chelates lead, arsentc, ‘mercury, gold and bisthmus 2. Cal (Na) 2 EDTA ( calcium disodium ethylene diamine tetracetic acid): Calcium disodium EDTA is used in Lead. The non calcium form of EDTA is used in digitalis toxicity. Disodium EDTA is used in digitalis poisoning, Dicobalt edta [Kelocyanor] is used in cyanide poisoning 3. Dimercapto succinic acid (DMSA): similar to BAL but it is orally . Chelates tead, arsenic and mercury, 4. Penicillamine: treat lead, mercury, zinc and copper 5. Deferoxamine [Desferal]: Used to treat iron toxicity. D- Increase detoxification: 1, N-acetyl cystiene (NAC, parvolex): for paracetamol 2, 100% oxygen: for CO and cyanide, E- Antibodies: J. Digoxin specific antibodies fragment (FAB fragment; digibind). 2, Antisera: used for snake, scorpion and botulism. F- Other antidotes 1. Vitamin B1: in alcoholic neuritis, alcohol. 2. Vitamin B2 (hydroxy-cobolamin): for cyanide. 3. Folic acid: used for methanol and ethylene glycols toxicity. 4, Sodium bicarbonate: Used in: a+ Correction of acidosis.b- Forced alkaline diuresis, c- TCA. 4-Telimination of Hb in hemoglobinurea ~S. Methylene blue: used for drugs causing met-Hb (e.g. Dapsone). Also used in cyanide toxicity. 6. Nitrites (Amyl nitrite and sodium nitrite): Used in cyanide ~Y¥. Vitamin C: used for drugs causing met-Hb. 8. Sodium thiosulphate: Used in toxicity of cyanide.General Toxicology I1l, Decontamination 1. Surface decontamination 1. Skin, 2. Eyes. 3. Inhalation, II. Gastrointestinal decontamination. 1. Emesis. 2. Gastric lavage, 3, Activated charcoal, 4. Catharties, 5, Whole bowel irrigation, 1, Surface decontamination: A. Skin: Corrosives rapidly injure skin, In addition, many toxins are absorbed through skin eg. OPI, and systemic absorption can be prevented only by rapid action, 1. Remove contaminated clothing and flush exposed areas with copious quantities of tap water or saline. Use soap for oily substances. 2. There is rarely a need for chemical neutralization of a substance spilled on the skin, Heat generated by chemical neutralization worsens injury. B. Eyes: The comes is sensitive to corrosives and hydrocarbons that may rapidly damage the cornea and lead to permanent scarring. 1, Flush exposed eyes with copious quantities of tap water or saline. 2. Do not instill any neutralizing solution. Why? C. Inhalation: (Irritating gases, CO, cyanide, or H2S), 1. Remove victim from exposure and give oxygen, Assist vei if necessary, : 2. Observe for upper respiratory tract edema (hoarse voice and stridor) which may progress to complete airway obstruction, Endotracheally intubate patients who show progressive airway compromise. ntilation 3. Observe for late-onset noncardiogenic pulmonary edema. 11, Gastrointestinal decontamination (Removal of poison from GIT to Prevent further absorption)if General Toxicology A. Emesis: Syrup of ipecae (contains 2 alkaloids: emetine & cephaline induces vomiting by: * Local gastric irritation * Stimulation of CTZ. After syrup of ipecac administration, vomiting usually occurs within 20-39 minutes 1, Indications: Recent ingestion of toxins [within 3 hours post inge 2. Contraindications: a. Comatose or convulsing patient b. Ingestion of a substance likely to cause rapid onset of CNS depression oe eas (eo) ere peers, ene c. Ingestion of a corrosive agent 4. Ingestion of a simple aliphatic hydrocarbon. These are likely to cause pneumonitis if aspirated e. Under 6 months. Why? ni, 3. Complications a. Persistent vomiting delays administration of activated charcoal or oralantidotes (eg, acetyleysteine). = b. Forceful vomiting may result in hemorrhagic gastritis or a Mallory- Weiss tear. e. Repeated daily use _may result in cardiac arrhythmias and cardiomyopathy (accumulation of cardiotoxie alkaloids). 4. Technique. a. 30 mL of syrup of ipecac orally (15 mL for children under 5 years; 10 mL for children under 1 year; not used for children under 6 months). After 10-15 minutes, give 2-3 glasses of water. b. If emesis has not occurred after 20 minutes, a second dose of ipecac is given. : ©. If the second dose does not induce vomiting, use an alternative method of gut decontamination, 4d. There is no other acceptable alternative to syrup of ipecac. Manual digital stimulation, salt water, apomorphine, and other emetics are unsafe and should not be used. B. Gastric lavage (stomach wash): Lavage is effective if initiated within 60 minutes of ingestion, although it may still be useful several hours after ingestion of agents that slow gastric emptying (eg, salicylates or anticholinergics). Gastric 10General Toxicology lavage does not remove undissolved pills (especially sustained-release pr enteric- coated). 1. Indications: cuffed a, Semi or unconscious patient (must_be intubated first_with endotracheal tube). b. Loss of gog reflex after ETT. c. Emesis is not effective. 4. To administer activated charcoal and whole-bowel irrigation to patients unwilling or unable to swallow. 2. Contraindications: ‘a. Comatose or convulsing patients (must be intubated first endotracheal tube). b. Ingestion of sustained-release or enterie-coated tablets In suel sustained re c. Ingestion of aliphatic hydrocarbon except after ETT. d. Ingestion of a corrosive substance, WHY? with cuffed h cases, 3. Complications: a. Perforation of esophagus or stomach. b. Tracheal intubation. c. Vomiting with pulmonary aspiration. 4. Use of excessive volumes of plain tap water can result in hypothermia or tremia in small children. during administration of gastric tube (vagal stimulation), e. Bradycart 4, Technique: ‘a. If the patient is deeply comatose, endotracheal tube. b, Place the patient in left lateral decubitus position. This helps prevent ingested material from being pushed into the duodenum during lavage. ce Insert a large gastric tube through mouth to stomach. Cheek tube position with air insufflation while listening with a stethoscope positioned on the patient’s stomach. 4. Withdraw as much of the stomach contents as possible. fe. Administer activated charcoal, 1 g/kg, down the tube before starting lavage to begin adsorption of material that may enter the during lavage procedure. protect airway by a cuffedGeneral Toxicology f. Instill tepid water or'saline, 200- to 300-mL, and remove by gravity or active suction. Repeat instillation until the return is free of toxic ‘material, C. Activated charcoal. Activated charcoal is a highly adsorbent powdered ‘material made from a distillation of wood, Owing to its very large surface are, i is highly effective in adsorbing most toxins. Only a few toxins are poorly adsorbed to charcoal, What are they? 1. Indications: é 4. After any toxic ingestion even if the offending substance is not known to be well adsorbed to charcoal, in case other substances have been co- ingested. Eide it eeepc b. Repeated oral doses of activated charcoal may enhance elimination of some drugs from the bloodstream. 2 Coniraindications: a. Teus, b. Intestinal obstruction. 3. Complication a, Constipation or intestinal impaction or bezoar. b. Distension of the stomach anc ulmonary aspiration, ¢, Many commercially available charcoal Products contain charcoal and the cathartic sorbitol in a premixed suspension. Even single doses of Sorbitol often cause stomach cramps and vomit ting, and repeated doses may cause serious fluid shifts to the intestine, diarrhea, and dehydration, especially in children and elderly. d. May bind coadministered ipecae or acetyleysteine, 4. Technique: a. 1 g/kg PO or by gastric tube. ». Ifthe quantity of an ingested substance is known, give at least 10 times the ingested dose of toxin by weight to prevent desorption of the toxin in the lower gastrointestinal tract, 2General Toxicology Q. Poisons poorly adsorbed by Activated Charcoal: ‘C— Cyanide and Corrosives. H- Heavy metals (Iron, Lead, Arsenic, Lithium and Mercury). A= Alcohols. R- Rapid onset or absorption (Cyanide and Strychnine). C-Chlorine. O-Others insoluble in water (substances in tablet form). ‘A~ Aliphatic hydrocarbons. L-- Laxatives (magnesium and potassium) D. Cathar 5 1. Indications: a, To enhance gastrointestinal transit of the charcoal-toxin complex, decreasing desorption of toxin or development of a charcoal bezoar. b. To hasten passage of iron tablets and other ingestions not adsorbed by charcoal. 2. Contraindications: c. Ileus, d, Intestinal obstruction. 3. Complications: 4%. Severe_fluld loss and hypermatremia from repeated doses of cathartic. b, Abdominal cramping and vomiting. 4. Technique: Administer the cathartic of choice (70%-sorbital, 1-2 mL/kg) along with activated charcoal. E, Whole bowel irrigation. Irrigation of the entire GIT with nasogasttic tube until the bowel has been cleansed of the poison. This solution is given at high flow rates to force intestinal contents out by sheer volume. 1, In jons: ‘a. Large ingestions of iron, lithium, or other drugs poorly adsorbed to activated charcoal. b. Large ingestions of sustained-release or enteric-coated tablets (eg, ‘Theophylline, Salicylates). Ingestion of foreign bodies or drug-filled packets, Ingestion of foreign bodies or drug-filled packe 137 General Tas 2. Contraindications: a Ileus or intestinal obstruction, . Obtunded, comatose, or convulsing patient unless the ai protected, 3. Complications: a. Nausea and bloating. ». Regurgitation and pulnionary aspiration. 4. Technique: Administer PEG, 2 L/h by gastric tube (children, 500 mL Until rectal effluent is clear. Be prepared for large-volume stool within 1-7 hours. IV, Enhanced Elimination ie. Elimination of the poison from blood after absorption Methods available for enhanced elimination: J. Multiple dose activated charcoals (MDAC)(Gastrointestinal Dialysis) 2. Urinary manipulation: Diuresis and Alkalinization 3. Hemodialysis 4. Peritoneal dialysis. 5. Hemoperfusion 6. Plasma pheresis 1) Multiple dose activated charcoals (MDAC) (Gastrointestinal Dialysis Repeated doses of activated charcoal (0.5-1 g/kg every 3 hours) are given orally or via gastric tube. The presence of slurry of activated charcoal throughout Several meters of the intestinal lumen reduces blood concentrations by interrupting enterohepatic or enteroenteric recirculation of the toxin, MDAC facilitates the passage of toxin from plasma into intestine by creation of concentration gradient between blood and bowel fluid, this will enhance the efflux Gf toxin into intestinal lumen. So, it is referred to as Gat dialysis) Caution: Repeat-dose charcoal should not be used in patients with ileus or obstruction. wy #Q. This technique has been shown to shorten the half-life of: a. Drugs remain in GF 1. SR-prep: Theophylline 2. Coneretions: Salicylates 3, Slowing GIT motility: Anticholinergics b. EHC: Digoxin, TCA, phenobarbital c. Passive diffusion from blood to lower GI lumen: Theophylline 4General Toxicology 2) Urinary manipulation: Forced diuresis (producing urine volumes of up to 1 Lh) increases glomerular filtration rate, and_ion trapping by urinary pH manipulation enhances elimination of polar drugs. Alkalinization is commonly used for salicylate and phenobarbital, overdoses, but “forced” gerierally not used because of the risk of fluid overload. ‘a. Forced diuresis: Principle and method: Removal of the poison from the blood through increasing the glomerular filtration rate, Fluid diuresis is accomplished by dextrose 5-10% or a mixture of glucose & normal saline followed by a diuretic agent (mannitol or furosemide). . Alteration of the urine pH (ion trapping): Principle and method: Changing PH of urine makes the poison ionized “ion trapping” (i.e. poison can’t bbe reabsorbed through the cells of the renal tubule as ionized drugs are poorly a —— 7) this will lead to increase excretion. absorbable through cell membranes) this_will lead to increase excretion. fnizatiomf urine is used for acidic drugs e.g, salicylates and barbiturates by using NaHCO), 1-2 mEq/ kg to keep urine pH at 7.5-8.0, Note: Acidification is no longer used to enhance elimination owing to complications associated with urinary acidosis (myoglobinuric renal failure in patients with rhabdomyolysis) Fiicatiotof urine was used for removal of alkaline drugs e.g. Amphetamine 3) Hemodialysis: Blood is taken from a large vein (usually femoral vein) with a double-lumen catheter and is pumped through the hemodialysis system. The patient must be anticoagulated to prevent clotting of blood in the dialyzer. Drugs and toxins flow passively across the semipermeable membrane down a concentration gradient into a dialysate (electrolyte and buffer) solution. Characteristics of the drug or toxin that fit for hemodialysis include small size (molecular weight <500 daltons), water solubility, low lipid solubility and low protein binding. 4) Hemoperfusion: Using equipment and vascular access similar to hemodialysis, the blood is pumped directly through a column containing an_ adsorbent material (either charcoal or resin). Systemic anticoagulation is also required. 1, Because the drug or toxin is in direct contact with the adsorbent material, drug size, water solubility, and protein binding are less important limiting factors. 2. Hemoperfusion can achieve greater clearance rates than hemodialysis. Q. Substances fit for hemodialysis or hemperfusion: LET ME SAV P: (Lithium, Ethylene glycol, Theophylline, Methanol, Salicylates, Valproic acid and Potassium).General Toxicology 8) Peritoneat dialysis: Dialysate fluid is infused into the peritoneal cavity through a transcutaneous catheter and drained off, and the procedure is repeated with fresh dialysate. The gut wall and peritoneal lining serve as the semipermeable. membrane. 1. Peritoneal dialysis is easier to perform than hemodialysis or | hemoperfusion and does not require anticoagulation, but it is only about | 10-15% as effective owing to poor extraction ratios and slower flow rates. Peritoneal dialysis can be performed continuously, 24 hours a day; a 24- hour peritoneal dialysis with dialysate exchange every 1~2 hours is equal to 4 hours of hemodialysis. Plasma pharesis: A volume of blood is removed, and all blood components except plasma are returned to the circulation. The plasma is replaced with a crystalloid solution. Indicated for poorly dialyzed toxins, 16