به نام او که به ما افتخار اموختن و طبابت داد

1. به نام او که به ما افتخار اموختن و طبابت داد

2. Body building drugs complications in anaesthesia and other side effects Supervised by: dr safari By:anispouyanfar

3. Case report: a bodybuilder 34 years old under rhinoplasty surgery in loghman hospital Sex:man W:92kg Height:165cm Duration of bodybuilding:10 y PMH:negative FH:DM in his mother c.c: negative Lab :HCT &Hg :NL BUN/Cr:NL HBSAg & HIV Ab: Negatie PH/E: NL: Airway examination Heart ausculation: systolic murmur at left 4nd intercostal space lung ausculation :NL

4. ANESTHESIA MANAGEMENT: • Premed: Hydrocortisone 100mg Midazolam3mg Fentanyl 200microg • INDUCTION Propofol 180mg Atracurium 50mg • Lidocain 100 mg 90 s before intubation • BP before induction :130/75 PR:60 • BP after induction:90/55 PR:85

5. THEN: Maintenance : propofol 150 µg/kg/min & remifentanyl0.5µg/kg/min 5 min later:!!! BP: 75/45 PR: 115spo2:99 eTCo2:25 propofol & remifentanyl dosage decrease to½ primary dose!!! And 500 cc N/S prescripted but heamodynamic state was unstable!!

6. THEN!!! AMP phenylephrine not available in OR ephedrine 5mg Ephedrine 10 mg BP: 70/40 PR:135

7. AND: so fluids prescription continued 100 mg hydrocortisone But without any response to our treatment 30 min later after 2.5 liter fluids intake& was held of all anesthesia drugs BP:75/45

8. It was decided that the patient awake: Reverse :neostigmine 5mg and atropine 2mg In 2 syrings separately Patient awaked and transfered to recovery In recovery:BP:80/50 &PR:130 Cardiology consult requested: Echocardiography: LVH &ventricular septalhyperthrophy&mildAS&mildMR&MS&mild diastolic dysfunction &normal systolic function EF:45%

9. Patient admitted at carsiovascular ward • Treatment in this ward: metoprolole & phenylephrine after 24 hours v/s was stable and patient transferred to ENT ward and discharged !without any surgery procedure next day Finally the patient was under rhinoplasty surgery with local anesthesia and discharged without any problem!!!

10. Other cases

11. Case2:a 43-year-old bodybuilder with a history of anabolic steroid abuse was admitted having been found unresponsive PMH:diarrhoea for 5 days DH:variety of anabolic streoid drugs PH/E erythematous rashes on anterior thorax and mild contusion in the frontal region&knees GCS:9-13 puppil:sluggish but reactive lung:nlheart:nl CT:nl Hb:7.7 others lab:NLToxicology:negative for barbiturat,paracetamol,salycylates LP:NL Patient intubated and addmited To ICU then Sedation was held with an intention to wean from the ventilator as the patient had a strong cough reflex and was moving all four limbs. Unfortunately he deteriorated, with increased ventilatory requirements, increasingly labile pulse rate and hypertension requiring glyceryltrinitrate (GTN) Infusion. He developed decerebrate posturing to pain with upgoing plantar responses. Peripheral reflexes were depressed but present. The pupils were unresponsive to light; there was no papilloedema evident. There were no vestibulo-ocularreflexes although the corneal reflex was preserved. Six days after admission, the patient was almost completely areflexic. Pupillary and peripheral reflexes were absent, although corneal responses and spontaneous breathing persisted

12. then Fourteen weeks after admission, the patient walked out of hospital to return home. Following discharge, he has been regularly reviewed by neurorehabilitation and psychology teams. Physically, the patient had slightly impaired balance . In the short term, there were some memorycognitive problems, including impaired short- He was ‘bodybuilding’ and at the time of admission using three different anabolic agents (Trembolone, Testolic and Boldenone) Prior to admission the patient was working full time, as well as working several night shifts as a doorman and was weight training. On the night of admission, he had consumed approximately 40 mL of vodka, and smoked a small amount of cannabis. No other drugs had been used. He recalls waking up and being unable to walk to the bathroom, tried to crawl on his hands and knees. However lacking the strength and coordination to do this he fell several times.

13. The exact cause for this patient’s deterioration and comaremains unclear although it is highly likely that the heavyandrogenic agent usage in the preceding weeks and monthshave contributed. Although there was a degree of illicit drug use prior to admission The most significant deterioration was while in hospital following the decision to wake and wean from mechanical ventilation. This initially manifested as pulse and blood pressure lability, which has been reported in bodybuilders in response to anaesthetic induction Adverse cardiovascular effects often focus on acute myocardial infarction and a deleterious lipid profile Other adverse cardiovascular effects include left ventricular hypertrophy, altered diastolic function, and subclinically impaired left ventricular function. In addition, a number of other adverse cardiovascular effects have been reported including arterial thrombosis, pulmonary embolism and several cases of sudden cardiac death Other central phenomena described include a case of lethal cerebral oedema in a steroidabusing, previously healthy 21-year-old Withdrawal and dependency disorders are recognised,

14. Sudden cardiac death during anabolic steroid abuse: morphologic and toxicologic findings in two fatal cases of bodybuilders A 29-year-old bodybuilder suddenly collapsed after dinner in his apartment. He had a weight lifting workout at the gymnasium a few hours before. Cardiopulmonary resuscitation initiated by an emergency physician was unsuccessful. According to friends of the deceased, he had been taking anabolic steroids (testosterone, nandrolone, and stanozolol) parenterally for several years Microscopic examination revealed numerous foci of contraction band necrosis. There were two microfoci of fibrosis, one in the subendocardial anterior left ventricle and one in the interventricular septum. Segmentation of the myocardial cells and bundles of contracted myocardium alternating with bundles of distended myocardium with granular disruption of the myocytes were noted in all myocardial sections A 30-year-old male, first an amateur, and later a competitive bodybuilder, who worked out regularly at the gymnasium, suddenly collapsed at home and was pronounced dead by an emergency physician who does not start cardiopulmonary resuscitation. He had a weight lifting workout at the gymnasium a few hours before. In an ashtray near the body, a 2-ml vial of nandrolonedecanoate was found along with a used 2.5-ml syringe Coronary arteries showed scattered fatty streaks. Histopathologic examination of the heart revealed focal myocardial fibrosis; examination of the conduction system performed according to Sheppard and Davies was unremarkable. The liver showed cholestasis and vascular gaps compatible with the diagnosis of peliosishepatis

15. Discussion

16. Testosterone was first isolated in 1932. Evidence thatanabolic steroids (synthetic derivatives of testosterone thathave greater anabolic actions) enhanced physical strengthled to experiments conducted on soldiers by Nazi Germany during the Second World War : Testosterone is the main male hormone synthesised in the testis. The hormone is responsible for the secondary sexual characteristics that transform boys into men. In the adult male, testosterone regulates muscle protein metabolism, sexual and cognitive functions, erythropoiesis, plasma lipids, and bone metabolism. Testosterone has approximately equal anabolic and androgenic actions.

17. Mechanism of action of anabolic steroids Skeletal muscle is the primary target tissue of the anabolic steroids. The testosterone induced increase in muscle size is brought about by an increase in muscle protein synthesis leading to a dose-dependent hypertrophy associated with an increase in the cross-sectional area of both type 1and 2 fibres and increase in myonuclear number steroids enhance collagen synthesis and increase bone mineralisation (via a direct suppression on osteoclasts). Testosterone may enhance anabolism via a direct induction of growth hormone and insulin growth factor1

18. Common anabolic stroids drugs in body buliding

19. Drugs commonly used in combination with steroids. Drug/supplement Reason for use Diuretics Masking agents; reduce oedema Tamoxifen Prevents gynaecomastia Thyroxine Increases basal metabolic rate. Human growth hormone Anabolic effects, increase muscle mass and strength Insulin Anabolic, increase muscle mass Insulin like growth factor Anabolic, increase muscle mass Beta blockers To reduce tremors Ephedrine Stimulant, fat loss Clenbutarol Stimulant, fat loss Amphetamine Stimulant, fat loss Opioids Analgesia CreatineErgogenic supplement

20. Cardiovascular adverse effects LVH Cardiomyopathy arythmia Diastolic dysfunction andCAD risk cronary vasospasm Acute vascular thrombosis increase platelet aggragation (thromboxaneincrease,prostacycline decrease) increase of factors VII,IX hyper homocysteinemia

21. Echo: LVH causes impaired isovolumetricrelaxation,diastolic dysfunction and fractional shortening Autopsy :focal areas of myocardial fibrosis caused by rapid myocardial fibre growth outstripping its blood supply,resulting in necrosis and fibrosis! And disturbance of ion fluxes and loss of membrane integrity lead to cell necrosis!!! this fibrotic areas Malignant arythmia,cardiomyopathy , MI,AND SUDDEN DEATH !!!

22. Other effects Hepatotoxity: increase SGOT ,SGPT,peliosishepatitis,HCC,adenoma,hematomas tendon injury Dermatological changes:acneastriae,repeated injections cause fibrosis Thyroid dysfunction ,renal failure Nephropathy IgA,rhabdomyolisis SO!!!!! Anaesthetists should be aware of the potential problems in managing steroid users in the peri-operative period. As part of this, an accurate history should be taken including drugs, doses and timing in their cycle in those who are suspected of taking steroids. The drug history should be taken in a systematic manner. The use of nutritional supplements and ‘accessory’ drugs (e.g. ephedra, insulin, growth hormone) should be excluded.

23. Abnormal laboratory tests in anabolic steroid abusers. Blood count Increased haemoglobin, haematocrit Liver function tests Increased ALT, AST. Plasma cholesterol decrease high-density lipoprotein cholesterol Electrocardiogram Left ventricular hypertrophy Echocardiogram Impaired diastolic function Hormone Decreased LH, FSH Increased testosterone (on anabolic steroid) Decreased testosterone (during withdrawal) Urine analysis Positive for anabolic steroids and its metabolites and other supplements Semen analysis Decreased sperm count and motility

24. ANAESTHESIC CONSIDERATIONS • Large muscle and high caloric intake can lead to high • Ventilatoryrequierments • Increase oxygen consumption & ETCO2 • A case report about a body builder who developed high ETCO2 following the fasciculation with succ needed higher than expected ventilatoryrequierment ! • risk of compartment syndrome increase! • Imbalance of fluids and electrolytes! • Mineralocorticoid effects!! • Diuretics are often combined with steroids mask these effects! • Serious problem: cardiovascular changes : arrythmia ,LVH…. • Prophylaxis aggainst deep vein thrombosis essential in the perioperative period because increase risk of thrombosis! • .

25. pharmacological changes!! • Resistance to NDMR drugs • Succ is not contraindicated • Oral anabolic steroids induce hepatic enzymes more than parentral ones higher doses of aneasthetics drugs needed • Increase sensivity to oral anticoagulants ! • There are also potentioal problems caused by other medications(thyroxine,diuretics,BB, sympathomimetics)used with anabolic steroids • consider dependancy and withdrawal problems!

26. نتیجه این همه بحث: • پس اگر یه فردی حتی جوان و با ظاهری ورزشکار و عضلانی کاندید عمل جراحی است به شما مراجعه کرد گرفتن یه هیستوری دقیق وشرح کامل ومصرف ودوز داروهای وی و معاینه کامل ضروری است!! • همچنین شناخت عوارض داروهای استروییدی و داروهای همراه الزامی است!! • به یاد داشته باشیم لزوما فردی با ظاهری ورزشکارو عضلانی سالم و نرمال نیست!!!!

27. مرسی از حوصلتون و تشکر از اساتید گرامی!!