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ALCOHOL AND TOXIC ALCOHOLSETOHEpidemiologyMore harm to community from acute use than dependence; 20-30% ED attendances ETOH related; physicians identify <50% patients with ETOH-related problems (inadequate training, negative attitudes, scepticism about trt, belief not our prob, takes too long to screen); 6.5% Aussies have alcohol use disorder in past 1yr (9.4% men, 3.7% women); 7-20% unhealthy use (30-40% in ED patients, 10% have severe probs; 50% in patients with trauma, 30% driver + pedestrian deaths); 4th leading cause of disability world wide; >2/3 domestic violence cases; most morbidity due to 2Y injScreening toolsAUDIT: sens 50-97%, spec 78-96%CAGE: sens 43-94%, spec 70-97%Toxic doseStandard drinks contain 10g ETOH = 375ml can beer = 100ml wine = 30ml spirit0.5g/kg disinhibition + euphoria1g/kg slurred speech; significant CNS effects if non-tolerant2g/kg potential coma (ambulant if tolerant)>5g/kg coma, resp depression, hypotensionToxic MechanismAugmentation of GABAa receptors; others involved (eg. NMDA, 5-HT, adenosine) CNS depression / dose-dependent CV depression / decr gluconeogenesis / ADH secretion diuresis / incr lactate and free fa (mild-mod AGMA in 80%) / hypoMg / renal HCO3 loss (NAGMA in 20%) / incr uric acid / incr OG (2nd most potent cause, after meths; most common cause) / impaired thermoregulation / incr gastric acid secretionPharmacologyRapid PO, high BA; absorption quickest when stomach empty or carbonated drinks; no protein bindingMetabolismADH (main rate limiting step) acetaldehyde ALDH (inhibited by disulfiram and metronidazole; 40% Asians have decr activity) acetyl CoAProduction of NADH decr conversion lactate to pyruvate, decr gluconeogenesis, decr fa oxidation; >4mmol/L zero order kinetics + MEOS becomes more important; elimination rate 10g/hrHalf Life30minsPeak Level30-60minsSymptomsIncr HR, decr BP (ETOH is unlikely to be sole cause, seek other cause, adversely affects response to blood loss), decr T, ataxia, nystagmus, euphoria, coma etc…InvestigationsWhole blood ETOH used for legal driving limits; serum ETOH in hospital; whole blood concs usually 10% lower than serumTreatmentSupportive, thiamine 100mg PO/IV (give if evidence of malnutrition); IVF if dehydratedDecontaminationNoEliminationNoAntidoteNoMonitoringWhen readyDependenceAbuse: maladaptive pattern of substance use clinically significant impairment / distress with 1+ in 1yr period: failure to fulfil roles recurrent use on physically hazardous enviro continued use despite social probDependence: as above, with 3+ in 1yr period tolerance use of larger amounts over longer period than intended withdrawal persistent desire or rpted failed attempts to cut down time spent obtaining, using, recovering social activities reduced continued use despite knowledge of physical or psych probsHigh risk: middle aged males, adolescents, migrants, business execs, professionals, publicans, seamenIntervention: may decr consumption in up to 50% problem drinkersNaltrexone: blocks pleasurable effects and craving decr absolute rate of relapse to heavy drinking by 15% decr no. of drinking days doubles median time to relapse (40 vs 90/7)Acamprosate: enhances GABA transmission; may cause D+APDisulfiram: ALDH inhibitor; flushing/syncope/N+V+D with ETOH consumption; poor complianceWithdrawalEpidemiology: mortality rate 5%; likely if >20 units/dayPathophysiology: symptoms of GABA XS in withdrawal (due to downregulation of GABA receptors), withdrawal of inhibition of NMDA in withdrawal; withdrawal causes catecholamine overactivityOnset: 6-24hrs (ETOH may still be detectable in blood)Within hrs, peak 24-48hrs: tremor, agitation, sweating, incr HR, incr BP, N+V, hyperthermiaWithin 12-48hrs: hyperreflexia generalised TC seizures (in 5%; early, brief, multiple; 30% progress to DT’s if not treated) nightmares, hallucinationsDOA: 2-7/7Delirium tremens: Overall 1% incidence; mortality 8% (15% if untreated); occurs in 20% patients admitted to hospital with withdrawal; assoc with co-morbidities and delayed presentationOnset: rare before 3rd day of abstinence; peaks at 3-4/7DOA: up to 1/52Sx: above + T 40deg, mydriasis, delirium, resp and CV collapse (usually late and assoc with other illnesses) Mng Supportive; do as IP if severe, significant co-morbidities (psych or physical), poor social circumstances; carbamazepine and valproate are 2nd line drugs to benzos Mild = AWS 6-10: 5-10mg PO diazepam Q6-8hrly for 48hrs; quiet surroundings Mod = AWS 11-25: 10-20mg PO diazepam Q1-2hrly until AWS <10 (max 120mg/day) as above Severe = AWS 25: medical emergency; ABC, 5mg IV diazepam up to 4x in 30mins until seizures / agitation controlled 5mg IV up to Q30minly after 24hrs, transition to PO regular 10-20mg PO diazepam Q6hrly, and reduce dose over 3-5/7, trt hypoG, 100mg IV thiamineBenefitsMod consumption in middle aged and elderly decr mortality, decr CAD, decr CVA, improved lipid profiles, antioxidant effectsWernicke’s encephalopathyEpidemiology: medical emergency; mortality 10-20% untreated; also seen in other malnourished patientsPathology: due to thiamine deficitSymptoms: horizontal / vertical nystagmus + disorder of conjugate gaze (paresis of lateral gaze, bilaterally) + ataxia dyskinesia, incr tone, polyneuropathy in 80% + confusion, decr LOC change in behaviour, hallucinations, seizures Other: decr/incr T, CV instability, incr pyruvate; triad above only seen in 1/3Trt: thiamine 500mg IV over 30mins TDSPrognosis: eye probs usually fully recover; ataxia and confusion have poorer prognosisKorsakoff’s psychosisSymptoms: loss of short term memory + confabulation + progressive dementia; does not fully resolveOther neuroGeneralised mild myelin degeneration: earliest pathological change; in periV white matterCerebral atrophy: frontal lobes mostly; poor planning and organisationCerebellar degeneration: lower limb mostlyNeuropathy: peri ascending symmetrical sensorimotorMarchiafava Bignami disease: massive neuro changes, decr LOC, often fatalCentral pontine myelinolysis: profound coma, quadraparesis, pseudobulbar palsy, locked in syndromeGILiver: cirrhosis; AST:ALT >2 highly suggestive of alcoholic hepatitis; isolated incr GGT 75% spec for heavy ETOH intakeGIT: gastritis, PUD, varices, Mallory-Weiss tear, pancreatitis, Ca of oesophagus and pancreasEndoDM, gynaecomastia, testicular atrophyHaemDecr WBC motility, macrocytosis, prolonged INR, decr pltMetAlcoholic ketoacidosis, hyperuricaemia, hypoMg, hypoPhos, OPOtherProx myopathy, rhabdo, cardiomyopathyETHYLENE GLYCOL Charcoal resistantSourceIN CAR STUFF: Antifreeze, radiator additives, brake fluidLethal dose100ml (1ml/kg) 100%; unintentional ingestions of <mouthful is usually benign Toxic MechanismToxic metabolites (eg. Glycolic acid, lactate)Glycolic acid inhibits oxidative phosphorylation and protein synthesis AGMAOxalate precipitates with Ca crystals widespread tissue damage in renal tubules, myocardium, muscles, brain ARF within 12-24hrs, hypoCa; hepatic toxicity rarePharmacologyRapid CNS penetration; water soluble; rapid absorptionMetabolismBy ADH and ALDH glycoaldehyde and glycolic acid glyoxylic acid and oxalic acid (both toxic); zero order kineticsEliminationRenal (20% unchanged)Half Life3 hours (8x longer if ETOH on board)Peak Level1-4 hoursSymptomsDelayed onset of Sx if co-ingestion of ETOHPhase 1: 1-12hrs; CNS Sx similar to ETOH absent reflexes, nystagmus, myoclonic jerks, seizures, coma, cerebral oedema; maybe AP+N+VPhase 2: 12-24hrs; cardioresp Sx (due to resp, vasc, CV deposition of crystals) SOB, incr HR, HTN, CCF, APO, decr LOC, shock, coma, seizures, hypoCa prolonged QTc, arrhythmias; most deaths herePhase 3: 24-72hrs; renal Sx AP, ATN, oliguric ARF (most common major complication of serious poisoning) recovery of renal function nearly always completePhase 4: 5-20d – cranial neuropathiesInvestigationsBloods: Incr osmolar gap (can get significant toxicity without elevation of this; OG may normalise as metabolism of ethylene glycol occurs, but then AGMA develops due to metabolites) AGMA (with resp compensation; co-ingestion of ETOH may delay metabolism incr OG but normal AG) Only ethylene glycol, meths and alcoholic ketoacidosis cause incr OG AND AG incr lactate decr Ca Incr Cr / ketone levels Ethylene glycol level (rarely immediately available); do ABG’s Q4-12hrly after stopping haemodialysisECG: long QTcUrine: Ca oxalate crystals in urine (usually present within 6hrs; significant toxicity unlikely if absent at 6hrs; persist for days), renal epiT cells, protein, microscopic haematuria; urinary fluorescence (lasts 4hrs)TreatmentMaintain hyperV; benzos for seizures; trt hypoG / hyperK / hypoMgPyridoxine: 100mg (1mg/kg) IV OD until AGMA resolved; helps convert toxic metabolites to non-toxicThiamine: 100mg IV OD until AGMA resolved; as aboveHCO3: if pH <7.3; NaHCO3 1-2mmol/kg; correction of acidosis encourages metabolism by non-toxic pathwaysCa: if symptomatic of low Ca (eg. Seizures, prolonged QTc)Mg: helps conversionDecontaminationNoEliminationHaemodialysis Indications: OG >10 / pH <7.25 / ARF / level >4-8mmol/L / visual changes / deteriorating vital signs despite aggressive supportive care / electrolyte abnormalities resistant to other trt; may get rebound when stop haemodialysis Endpoint: level <1.5-3mmol/L, correction of acidosis, OG <10AntidoteUse until haemodialysisETOH: competitively inhibits metabolism by alcohol dehydrogenase, delaying toxic metabolite production; has 20x affinity for ADH than meths or ethylene Indications: unexplained AGMA / OG, positive Sx, level >3mmol/L; may be used as temporising measure while awaiting haemodialysis Dose: 1g/kg (8ml/kg) 10% ETOH IV in 5% dex 150mg/kg/hr (1-2ml/kg/hr) 10% ETOH (need to incr to 300mg/kg/hr during dialysis); aim ETOH conc 22-33mmol/L or 100-150mg/dL SE: thrombophlebitis, hypoG in childrenFomepizole: alcohol dehydrogenase inhibitor; experimental in Aussie, as alternative to ETOHMonitoringChild: well, bic >20, no OG, >4hrs homeAdult: well, bic >20, no OG, no ETOH, >4hrs homeAdult: symptoms admit; ensure FU to make sure no CN probs developMETHANOL Charcoal resistantSourcePetrol, home heating, industrial solvent, windscreen washer, antifreeze; not in methylated spirits in AussieToxic dose>25ml 40%; lethal dose >1g/kg or >0.5-1ml/kg; 30ml pure methanol can be fatal; <mouthful = benignToxic MechanismFormic acid impairs cellular respiration / oxidative phosphorylation anaerobic metabolism and lactic acidosis, severe AGMA and direct cellular toxicity; toxic metabolites are cause of toxicityPharmacologyDermal and inh can occur; rapid absorptionMetabolismLiver (ADH) formaldehyde ALDH formic acid; 0 order kinetics >15mmol/LEliminationRenal (2-5% unchanged)Half Life24 hours (4x longer if ETOH on board)Peak Level30-90minsSymptoms1hr – like ETOH but N+V+AP12-24hr (delayed even longer if ETOH co-ingested) – headache, dizzy, SOB; blurred vision, decr VA, photophobia, fixed dilated pupils, retinal oedema (visual Sx must be present to be life threatening; permanent visual impairment in 20-33% survivors); coma and seizures; severe gastritis and pancreatitis, AP+N+V; oliguric ARF; CCF; pul oedema. Death assoc with insp apnoea, opisthotonus, seizuresInvestigationsBloods: Incr OG (most potent of all alcohols at increasing OG) AGMA (with resp compensation) incr lactate (late) Meths level; do ABG’s Q4-12hrly after stopping haemodialysisCT head: >90% putamen hypodensity, 25% putamen haem, subcortical white matter haemTreatmentMaintain hyperV; benzos for seizures; trt hypoGNaHCO3: 1-2mmol/kg for urinary alkalinisation Indications: pH <7.3; improvement of pH will decr crossing of BBB and incr renal eliminationFolate: 50mg IV QID for 48hrsThiamine and pyridoxine and Mg: as aboveDecontaminationNoEliminationHaemodialysis: Indications: pH <7.3 / OG >10 / visual symptoms (regardless of methanol level) / ARF / worsening vitals or electrolytes despite trt / meth >15mmol/L Endpoints: correction of acidosis / OG <10 / meth level <6AntidoteETOH or fomepizole: as above; continue until methanol level <6mmol/LFolinic acid 2mg/kg IV Q6hrly helpsDispositionChild: well, bic >20, >8hrs homeAdult: well, bic >20, no ETOH, >8hrs homeAdult: symptoms admitISOPROPANOLSourceCLEANING: IV swabs, window cleaners, toiletries, paint removerToxic doseLikely if >1-2.5ml/kg of 70%; 4ml/kg can cause coma; taste / lick unlikely to cause probs, but 3 swallows can cause toxicity in children; twice as potent as ETOH in causing CNS depressionToxic MechanismAugments GABAa receptor CNS depression; causes ketonaemia; GI irritant; CV depressionMetabolism80% by liver (ADH) acetoneElimination20% unchanged by kidneys and lungs; the rest changed by kidneys and lungsHalf Life6-7hrs (16-27hrs if ETOH on board); DOA 2-4x longer than ETOHPeak Level30-120minsSymptomsAs per ETOH but longer and more potent; onset in 30-60mins, peak in few hrs; smell ketosis; AP+N+V, haematemesis, haemorrhagic tracheobronchitis, ATN, haemolytic anaemia, myopathy, resp depression, decr BP; hypoGInvestigationsMild incr osmolality and OG; ketosis; minimal metabolic acidosis despite ketosisKetones in urineTreatmentSupportive; thiamineDecontaminationNoEliminationHaemodialysis: if profound coma / decr BP refractory to IVF / >65mmol/LAntidoteNoMonitoringWhen readyNotes from: ToxBook, Dunn, TinTin, Cameron ................
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