E-learning topics in Clinical ToxicologyGastric Lavage techniqueMaterials for gastric lavage Wide bore (36-42F) orogastric lavage tube, funnel, jugs, bucket, oropharyngeal airway, stethoscope, BP set. Materials for immediate intubation (Functioning laryngoscope, endotracheal tubes of different sizes, suction machine, suction catheters, Ambu bag with proper fittings, oxygen supply, syringes). Cardiac monitor (preferably supported with a defibrillator). In certain poisoning, lavage should not be attempted unless well monitored e.g. Digoxin, Organophosphates insecticides. Materials for sample collection.Gastric lavage technique1. Technique must be explained to the patient if conscious.2. An assistant (trained nurse to assist the physician).3. Remove dentures, mucous, vomitus from the patients mouth.4. Choose the gastric tubes proper size for age.5. Give the patient, if conscious, a glass of water.6. Place the patient on his left side and elevate his waist by a pillow and make his face out of the edge of the bed. This allows better washing of the fundus and greater curvature and decreases the risk of aspiration.7. Take the measure of length between the mouth and epigastrium; make a mark with adhesive plaster on the tube so as not to introduce the tube beyond this mark.8. Lubricate the end of the tube with paraffin oil, if the patient is conscious and cooperative, put the tube end on the back of his tongue and instructs him to swallow while you gently push it till it reaches the mark previously determined.9. If you find resistance, or the patient coughs, it means that the tube entered the trachea. Withdraw the tube and reintroduce.10. Check for proper tube position by compressing the epigastrium to see the regurgitated fluid contents of stomach or inject 50-100ml air in the tube to auscultate the bubbling air in the stomach11. Apply suction of the gastric contents by a syringe, for toxicological analysis.12. Introduce about 200-400 ml of a room-temperature saline lavage solution by a funnel then allow it to be removed by siphonage, and make sure that all the fluid introduced should come out so as to avoid gastric distension and reflex evacuation in the duodenum. This process should continue until fluid is clear from any particle.13. Give activated charcoal or oral antidotes at the end of lavage whenever indicated.
14. Gastric lavage tube is removed after clamping (to avoid dribbling of water in upper airways during removal). The patient is ordered to cough while the tube is pulled out. Button Batteries These are small disk-shaped batteries used in watches, calculators andcameras. They contain caustic metal salts such as mercuric chloride and corrosivealkalis such as sodium and potassium hydroxide. When swallowed or inhaled, theycan cause injury by corrosive effects resulting from leakage of the corrosive metalsalts or the alkali they contain.Clinical presentation- The case is always asymptomatic after ingestion. They cause serious injury only if they become impacted in the esophagus, leading to burns and subsequent strictures or perforation into the aorta or mediastinum. The clinical presentation may be in the form of abdominal pain, vomiting, fever or signs of bleeding due to perforation of the gut. If they reach the stomach without impaction in the esophagus, they nearly always pass via the stools within several days.- The case is usually symptomatic after inhalation. Symptoms are in the form of cough, dyspnea and stridor.Diagnosis 1- History of ingestion or inhalation. 2- X-rays of the chest and abdomen will reveal impacted button batteries (as shown in the x-ray. fig. 3). 3- Urine mercury levels have been reported to be elevated after button battery ingestion.Treatment 1- Airway assessment and initial stabilization. 2- If the battery is located in the respiratory tract it requires emergency removal by endoscopy. 3- If the battery is located in the esophagus it is removed by esophagoscopy. 4- If the battery is located in the stomach or intestine and the patient is asymptomatic, serial stool examination is done at home to check for battery passage and another x-ray will be done in 5-7 days. But if the patient is symptomatic, endoscopic or surgical removal should be done. 5- At any stage if the battery stops moving, it should be removed by endoscopy or surgery.
Fig. (3): Impacted button battery NaphthaleneILOs By the end of this chapter the student should be able to: K1: Describe the mechanism of action of naphthalene. K2: Describe the clinical picture of naphthalene toxicity. K3: Discuss the management of naphthalene toxicity. K4: Solve problems revolving around virtual cases presenting withnaphthalene toxicity. A1: Realize the importance of urgent appropriate treatment in cases ofacute intoxication. A2: Realize the importance of working in groups.Introduction• It is obtained from coal tar. Now, it contains paradichlorobenzene (tar camphor) which is less toxic. It is used as a moth repellent and used as toilet bowel deodorizer.• Poisoning occurs through accidental ingestion (in children), or inhalation of naphthalene vapor present in clothes and blankets.Mechanism of action• Its metabolite (alpha naphthoquinone) red cell hemolysis acts as an oxidative agent in cells with G6PD deficiency.Clinical picture 1. GIT: Nausea, vomiting and abdominal pain, diarrhea. 2. Neurologic: headache, restlessness, optic neuritis, lethargy, convulsions, and coma may occur. 3. Hematologic: hemolysis in G6PD deficiency individuals which occurs rapidly and with smaller dose, with hemolytic anemia hematuria…. 4. Hepatic: hepatocellular injury, 3-5 days post ingestion.
5. Renal: hemoglobinuria, oliguria, anuria. 6. Metabolic: fever, flushing, headache. 7. Pregnancy; hemolytic anemia of the newborn.Investigations 1. CBC 2. Liver functionsTreatment1. Emergency measures (ABCD)2. Elimination a. Remove to fresh air (in case of inhalation) and irrigate the eye with copious amounts of water in case of eye affected. b. Emesis by syrup ipecac. c. Gastric lavage. d. Activated charcoal 1 gm/kg.3. Supportive treatment Treatment of hemolysis by: • Urine alkalinization: • Blood transfusion • CorticosteroidsSummary Naphthalene is one of the household toxins. The clinical presentationand management were discussed in this chapter.Questions 1. Discuss the clinical picture and management of naphthalene toxicity. 2. Alkalinization of urine is used in the treatment of naphthalene toxicity for the following reason: a) To inhibit the precipitation of acid hematin in renal tubules. b) To inhibit reabsorption of naphthalene. c) To improve prognosis of rhabdomyolysis. d) To control arrhythmias.
Anticoagulants Coumarins (Warfarin)Pathophysiology • Coumarins depress the hepatic vitamin K dependent synthesis of substances essential to blood clotting: prothrombin (factor II) and factors VII, IX, and X. the antiprothormbin effect is the basis for detection and assessment of clinical poisoning. • Concurrently, the agents increase permeability of capillaries throughout the body, predisposing the animal to widespread internal hemorrhage. • Toxicity in humans follow regular consumption of coumarin contaminated food over several days, or ingestion of very large amounts of the rodenticide bait.Clinical picture Usually no apparent toxicity arise from a single modest dose of coumarins.If any, it will usually appear after a delay of 48 hours consequent to increasedprothrombin time in the form of: 1. Ecchymosis, nasal bleeding. 2. Spontaneous hemorrhage: gingival bleeding, hematemesis, hematuria and melena.Investigations 1. Prothrombin time: detectable reduction in prothormbin occurs within 24-48 hours of ingestion. It usually reaches a maximum in 36-72 hours and persists for 1-3 weeks.. 2. Complete blood count daily. Repeat hemoglobin and hematocrit 6 hours if prothrombin time is significantly prolonged to detect hidden bleeding. 3. Urine for hematuria, stool for occult blood.TreatmentA- Emergency treatment: ABCB- Elimination Emesis using syrup Ipecac or gastric lavage followed by activated charcoal.C- AntidoteVitamin K1 (phytonadione)a) If there is uncertainty about the amount of rodenticide ingested, phytonadione (vitamin K1) given orally protects against the anticoagulant effect of this rodenticide, with essentially no risk to the patient. Dosage is 15-25 mg for adults; and 5-10 mg for children under 12 years.b) Vitamin K 1 is given IM in a dose of 5-10 mg for adults or 1-5 mg for children under 12 years if large amounts are consumed or if prothormbin time is > 2 times normal (INR > 2).
c) Vitamin K1 is given IV as infusion (10 mg for adults; 5 mg for children) if patient is bleeding. Repeat in 24 hours if bleeding continue.D) Symptomatic treatment Blood transfusion, fresh frozen plasma for severe bleeding. Nitrites and Nitrates − They may be inorganic or organic − They are used as fertilizers, food processing and in medicine. High levels of nitrates have now contaminated soil and water supplies especially shallow wells in ruler areas..Mechanism of toxicity: Nitrites and nitrates are potent smooth muscle relaxants that produce cardiovascular effects through coronary and peripheral vasodilatation. • They also oxidize hemoglobin to methemoglobin by oxidizing iron from ferrous (fe2+) to (fe3+) state. • Iron in the ferric state is incapable of binding oxygen. • Methemoglobin also causes shift of oxygen dissociation curve to the left and consequently impairs unloading of oxygen to tissues. • Methemoglobin is normally present as less than 1% of total hemoglobin under physiologic conditions. • Reduction of hemoglobin occurs through two enzymatic pathways in erythrocytes. The most active is the NADH-dependent methemoglobin reductase system. This accounts for 95% of methemoglobin reduction. • The second pathway is catalyzed by NADPH-dependent methemoglobin reductase. In this pathway NADPH combines with methemoglobin (MetHb) in the presence of the cofactor methylene blue. • NADPH pathway depends on functioning hexose monophosphate shunt, which requires in its first step G6PD. This account for less than 5% of MetHb reduction.Clinical Picture • The clinical effects are determined by the cardiopulmonary status and the total methemoglobin rather than just the methemoglobin percentage. • Vasodilatation may lead to a throbbing headache and flushed face up to rapid fall in blood pressure and cardiogenic shock. • The heart would compensate by increasing heart rate and force of contraction to elevate blood pressure. • In severe toxicity the heart may be unable to respond leading to hypotension, shock and cardiovascular collapse. • In addition to cardiovascular effects, the major toxic effect of nitrates and nitrites is methemoglobinemia:
• The initial manifestation of methemoglobinemia is cyanosis.The patient may appear deeply cyanosed and application of oxygen does not improve this cyanosis • At 50% to70%, arrhythmias, coma, seizures, respiratory distress, and lactic acidosis develop. • Levels more than 70% cause cardiovascular collapse and have a high degree of mortalityInvestigations 1. ABGs 2. Serum electrolytes. 3. ECG 4. Serum methemoglobin levelsTreatmentI- Emergency measures (ABCD)II- Elimination • Gastric lavage followed by activated charcoalIII- Toxin-specific measures 1- Methylene blue • Is the first-line antidotal therapy. It accelerates the enzymatic reduction of methemoglobin by NADPH-methemoglobin reductase • The initial dose is 1-2 mg/kg IV over 5 min. Its effects should be seen in approximately 20 min to 1h. • Patients may require repeated dosing, but the total dose should not exceed 7 mg/kg. • The methemoglobin level should be significantly improved within one hour of methylene blue infusion. • Methylene blue should be avoided in patients with G6PD deficiency, if possible, because this antidote may induce hemolysis in this patient population2- Exchange transfusion Should be used for: 1. Infants. 2. Patients who do not respond to methylene blue within 30 to 60 minutes. 3. Patients with G6PD deficiency. 4. Patients with metHb levels of more than 70%. LithiumUses
The salt of lithium carbonate is used as mood stabilizer in acute mania andmanic depressive psychosis.Pharmacokinetics• Rapid absorption from GIT• Delayed tissue distribution so serum levels after single acute overdose do not reflect the biologically active intracellular lithium.• Distribution in tissue follows water distribution, mainly excreted by the kidney..• It has a narrow therapeutic index and toxicity is enhanced by dehydration, thiazide diuretic and renal failure.Clinical picture of acute toxicityI- CNS • Mild toxicity: mental confusion, ataxia, tremors and exaggerated reflexes • Severe toxicity: convulsions and comaII- Renal • Polyuria, polydepsia, nephrogenic diabetes insipidus and renal failureIII- CVS • ArrhythmiasIV- GIT • Nausea, vomiting and diarrheaInvestigations 1. Serum lithium level (therapeutic level 0.4-1.3 meq/L) 2. Renal functions. 3. ECGTreatment I- Stabilization of the patient (ABCD) II- Elimination • Induction of emesis or G. lavage • Charcoal is not effective • Whole-bowel irrigation is effective especially in sustained-release preparations.III- In mild to moderate cases with serum level < 4 meq/L 1. Good hydration with IV infusion of normal saline.
2. Maintenance of electrolyte and fluid balance 3. ECG monitoring 4. Serial estimation of lithium levelIV- Hemodialysis 1. Severe toxicity (coma, convulsions or arrhythmias) 2. Serum lithium level > 4 meq/L N.B. slow distribution of lithium may account for delayed improvement ofpatients treated from lithium toxicity Ethylene Glycol Ethylene glycol is widely used as an engine coolant.Mode of ToxicityAccidental oral ingestion. Ethylene glycol has low volatility and does not causepoisoning by inhalation.Pathophysiology and kineticsOnce absorbed ethylene glycol is rapidly distributed to total-body water. Ethylene Glycol Alcohol dehydrogenase Glycoaldehyd e Glycolic acid Glyoxalic acid Formic acid Oxali Calcium oxalate• Ethylene glycol is partially eliminated unchanged through the kidney and expired air• Addition of thiamine and pyridoxine enhance formation of nontoxic metabolites.
• Glycolic , glyoxalic and oxalic acid metabolites are the cause of metabolic acidosis• Oxalic acid metabolite binds with calcium: 1- Forming Calcium oxalate crystals which precipitate in the renal tubules, leading to acute renal failure which may be caused also by direct toxic effect of ethylene glycol. 2- Causing hypocalcaemia and QTC prolongation with dysrhythmias and cranial nerve abnormalities.Clinical Pictures • Tingling and numbness • Twitches • Convulsions • Tetany • Arrhythmia • Acute renal failure • Other features are similar to ethyl alcohol toxicityInvestigations • Routine investigations: CBC, ABG, electrolytes (Ca, K). • ECG changes. • Urine analysis: calcium oxalate. • Renal profile: urea, creatinine.TreatmentI- Emergency MeasuresII- Antidotes • Ca gluconate IV slowly • Ethanol and 4 Methyl pyrazol (fomepizole) are used to prevent glycolate accumulation. • Thiamine and Pyridoxine enhance metabolism to less toxic productsIII- Symptomatic treatment. • Correct acidosis. • IV fluids: prevent calcium oxalate precipitation in the kidney. • Dialysis in case of renal failure MercuryForms and Sources 1. Elemental mercury vapor, dental amalgam, mercury of medical instruments as glass thermometer and sphygmomanometers. It causes toxicity after inhalation and has no toxic effects when swallowed as it is poorly absorbed. 2. Inorganic salts of mercury used as laxatives, teething powder, mercuric fulminate which is an explosive, mercuric Cl used as disinfectant.
3. Organic Mercury compounds: which have been incorporated and concentrated in the aquatic food as eating contaminated fish due to discharge of contaminated waste.Mercury absorption • After inhalation: 60-80% of mercury vapours are absorbed. • After dermal exposure 3-15% is absorbed. • After ingestion only <0.2 % of metallic mercury and about 15% of inorganic mercury are absorbed. However, more than 90% of organic mercury are absorbed via the GIT.Pathophysiology 1- Mercury has a high affinity for SH groups, which attributes to its effect on enzyme dysfunction. Choline acetyl transferase is one of the inhibited enzymes, which is involved in acetyl choline production. This inhibition may lead to acetyl choline deficiency, contributing to the signs and symptoms of motor dysfunction. 2- Glomerulonephritis is attributed to an immune mechanism. 3- Elemental mercury is pulmonary irritant and toxic to the CNS. 4- Inorganic mercury salts are corrosive to the skin and the GIT. Deposition of mercuric ions in the renal tubules causes acute tubular necrosis. 5- Organic mercury is especially toxic to the CNS and has teratogenic effects.Acute Mercury Toxicity A- Acute ingestion of liquid metallic mercury: • Since it is poorly absorbed in the GI, it causes no harm and needs no treatment. B- Acute inhalation of mercury vapors • Severe chemical pneumonitis, cough and dyspnea. • Acute respiratory distress syndrome. • Pulmonary fibrosis. • Mouth ulcers, metallic taste, nausea, vomiting, and diarrhea. • Metal fume fever: pyrexia, cough, malaise, flu-like symptoms • Kidney is final target organ where mercury accumulates as body tries to clear toxin • Erethism It is constellation of neurologic abnormalities collectively referred to as erethism and including mood alteration (emotional lability), shyness, anxiety, sleep disturbances, memory impairment, parasthesia, ataxia, muscle rigidity, visual and hearing impairment. C- Acute ingestion of inorganic mercurous salts Ingestion of single large dose of mercurous chloride does not usually cause symptoms, since it is poorly absorbed.
D- Acute ingestion of inorganic mercuric salts Accidental or suicidal ingestion of mercuric ChlorideClinical picture1. GIT manifestations: irritation leading to nausea, vomiting, severe abdominal cramps, hematemesis, dehydration and collapse, burning sensation with metallic taste, dysentery (mercury is re-excreted in the caecum), also due to its re-excretion in the saliva leads to stomatitis, increased salivation and gingivitis (gingivostomatitis).2. Acute toxic renal tubular necrosis with hematuria and casts.3. Shock and death may occur.Causes of death • Within 24 hours: dehydration. • Later, in 1-2 weeks: uremia.TreatmentsI- Emergency measures (ABCD)II- Elimination • Induction of emesis or gastric lavage if ingestedIII- Antidote (chelators) • Immediate chelation therapy is the standard of care for a patient showing symptoms of severe mercury poisoning or the laboratory evidence of a large total mercury load (blood/urine mercury persistently > 100 – 150 mg/l). • Chelators of mercury include: Dimercaprol "BAL", D-penicillamine, Dimercapto succinic acid "DMSA" or 2, 3-Dimercapto-1- propanesulphonate "DMPS". • DMPS is the chelation therapy of choice for mercury for both acute and chronic mercury poisoning and for all forms of Hg (inorganic, metallic and organic).IV- Symptomatic treatment • IV fluids for dehydration, mouth hygiene, hemodialysis in renal failure.Chronic Mercury toxicity "Mercurialism"Mode of exposureIndustrial: chronic inhalation of mercury fumes.Clinical picture1. GIT irritation: recurrent stomatitis, ptyalism, gingivitis, grey line, recurrent vomiting and diarrhea and weight loss.2. Nervous affection: kinetic intention tremors, first appearing in the tongue leading to hesitant speech, then in the hands. There is also affection of the visual cortex leading to contraction of the visual field.
3. Psychiatric disturbances "erethism" in the form of shyness, fear, irritability, loss of self confidence, insomnia, mental deterioration.4. Renal affection: toxic tubular necrosis.5. Cutaneous affection in the form of dermatitis.Investigations • CBC, renal function tests, electrolytes.TreatmentA. Prophylactic • Prophylactic measures to decrease exposure as masks, gloves, ...etc • Periodic medical examination of workers.B. CurativeI- Stop further exposureII- Chelation therapy Chelation therapy using penicillamine, or DMSAIII- Symptomatic e.g. renal affection: hemodialysis. Cocaine• It is extracted from the leaves of erythroxylon coca, known for more than two centuries for the stimulant and anti fatigue properties.• Purified cocaine is now used by sniffing the powder, usually adulterated by other less expensive substances as salicylates, boric acid, quinine, talc powder, mannitol, sucrose, lactose or caffeine.• It is rarely smoked as freebase (crack) or taken intravenously (usually with heroin).Mechanism of action 1- Sympathomimetic action due to inhibition of reuptake of catecholamines. 2- Local anesthetic action of sensory nerves. 3- Vasoconstriction of blood vessels.Clinical picture of acute toxicityA. CNS stimulation followed by depression:• Euphoria, delayed fatigue and insomnia.• Irritability, talkativeness and hyperthermia.• Tremors up to convulsions.• Hallucinations.• Drowsiness, confusion up to coma.• Cyanosis and death from central respiratory depression.B. Peripheral sympathomimetic action:• Tachycardia, arrhythmia, tachypnea, dilated reactive pupil, hypertension which may be so severe to cause subarachnoid or intracranial hemorrhage and produces neurologic sequelae.
C. Vasoconstriction of the blood vessels:• Pallor, renal vasospasm (infarction and acute renal failure), cerebral VC (infarction), acute myocardial infarction and necrosis (occurs shortly after snuffing and is due to coronary vasospasm), and cardiac arrest which is a common incident in cocaine abusers.D. Irritation followed by paralysis of nerve endings leading to:• Numbness in the nose and throat on snuffing, then in the limbs.• Local anesthesia.Investigations 1. Urine screening to identify cocaine metabolites. 2. ECG.TreatmentI- Emergency measures (ABCD).II- Elimination: Gastric lavage and activated charcoal (if leaves are chewed).III- Symptomatic treatment: 1. Treatment of arrhythmia. 2. Treatment of hypertension using labetalol or IV Na nitropruside (vasodilator). Cocaine Dependence (Cocainism) Cocaine is euphoriant. It decreases physical and mental fatigue andincreases sexual activity. Tolerance and physical dependence to cocaine developrapidly.Picture of dependence 1- Mental change: • Decrease power of concentration with dementia (amnesia, decrease intelligence, decrease mental faculties). 2-Physical changes: • Anorexia and progressive weight loss (wasting). • Pallor of face due to vasoconstriction. • Dilated reactive pupils, irritability, tremors, insomnia and hypertension . • Loss of the sense of smell. • Perforated nasal septum due to: 1. Continuous vasoconstriction of nasal blood vessels by snuffed cocaine → devitalisation and sloughing. 2. Irritation by adultrants (Boric acid, quinine, salicylates). 3. Cocaine anesthesia: patient can not feel pain of necrosis →more snuffing →more necrosis.3-Moral changes • Patient becomes aggressive and dangerous.4-Psychological changes
• Hallucinations; the chronic effect on the sensory nerve endings gives rise to Magnans symptom, which is the feelings of sand under the skin or to Cocaine bugs, with sensation as if insects creep under the skin with severe itching.5-Withdrawal symptoms • Physical dependence occurs to cocaine but withdrawal symptoms are not serious as that with opiates. It includes irritability, neurologic pain in arms and legs, tendency to violence, depression and fatigue.Treatment1. Abrupt withdrawal in an institute.2. Good diet, vitamins and health care.3. Psychological care, tranquilizers and analgesics.4. Symptomatic treatment for hypertension and arrhythmia. Performance Enhancing Drugs Doping in SportsDefinition Doping is defined as administration of or use by a competing athleteof any substance foreign to the body with the sole intention of increasingperformance in competition. • The use of the performance enhancing drugs is linked to an epidemic number of deaths among competitors. Also, these drugs have shown unhealthy side effects in athletes. • The International Olympic Committee (IOC) and other sport organizations agreed to ban certain substances which could be used in the attempt to enhance performance, some commonly used and potentially harmful performance enhancers are: anabolic steroids, creatine, sympathomimetics, human growth hormones, amino acids, and erythropoietin. We shall focus on a commonly used performance enhancer i.e. anabolic steroids.Anabolic steroids Anabolic steroids (ASs) are a class of synthetic molecules structurallyrelated to testosterone. They exert anabolic i.e. muscle building properties. Unfortunately, these steroids are not purely anabolic. In fact, they possessandrogenic properties as well. These androgenic properties affect different organsystems. In 1991, the anabolic steroids were classified as controlled dangeroussubstance and were put in schedule ΙΙΙ of the Controlled substance Act. The similarities of anabolic steroid abuse to the classic substance abuse aresuggested through the facts that (ASs) are used over long periods than desired,failure of the attempts to stop taking the drug, continuing use despite theknowledge of health problems caused by ASs, and the occurrence of characteristic
withdrawal symptoms that lead to the use of the hormone to relieve thesesymptoms.Anabolic effectsASs adds to the building up of body tissues and assimilation of proteins and hence,promotes increasing muscle mass. When they are taken in combination with aspecific diet and a programme of intensive training, they accelerate muscle growthand increase body mass thus enhancing performance or appearance of anindividual. ASs are available as tablets, capsules for oral use, also preparations forintramuscular injections are available.Adverse and toxic effects of ASs 1. Reproductive effects: ASs suppress gonadotrophin secretion, Male athletes may suffer of testicular atrophy; decreased sperm count and increase in morphologically abnormal sperm, prostate enlargement, loss of libido and impotence. Female athlete may suffer of irregular menses or amenorrhea, miscarriage or stillbirth. 2. Feminization in male athletes Male athletes, who administered parenteral ASs, can develop gynecomastia and increased fat deposition. 3. Virilizing effect ASs possess some androgen effects. Women and children using ASs suffer from deepening of voice, hirsutism and decreased body fat. In addition, female may suffer of acne, male balding pattern and change in breast size. 4. Cardiovascular effects ASs cause numerous cardiovascular effects as: hypertension, decline in high density lipoprotein (HDL) and increased low density lipoproteins (LDL).also biventricular and interventricular septum hypertrophy are reported. Vasospasm, thromboemboli and increased platelet aggregation may also occur. Risk of congestive heart failure may be increased due to fluid retention. Case reports described myocardial infarction and sudden cardiac death in young bodybuilders taking ASs. 5. Hepatotoxicity: ASs use may be associated with elevated liver enzymes, cholestatic jaundice, and hepatic neoplasms (benign adenomas and malignant carcinomas). 6. Erythropoiesis: Ass stimulate erythropoiesis, can cause polycythemia, increased hematocrit value and increased leukocyte and platelet count. 7. Muscular effects: Rupture of tendons and ligaments of muscle size. 8. Infections: Through contaminated shared needles which may result in abscess formation, hepatitis, HIV and infected joints.
9. Psychological effects: Such as: aggression, irritability, memory effects, mood-swings, criminal acts and manic behavior.10. Withdrawal effects: Include depression, insomnia, anorexia, fatigue, decreased libido and loss of physical and muscular power. The dramatic change in body image and performance often drive the athlete to resume use of ASs.