It’s about - Semmelweis...
Transcript of It’s about - Semmelweis...
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It’s about
• Epidemiology, ways of poisoning• Aspecific symptoms, aspecific therapy• Toxidromes• Specific therapy• Some more frequent poisonings:
– alcohol– street drugs, opiates– paracetamol– tricyclic antidepressants– benzodiazepins– ethylen-glycol and methanol– carbon monoxide
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Poisons, decoctions and brews
Paracelsus: „Alle Ding' sind Gift, und nichts ohn' Gift; allein die Dosis macht, daß ein Ding kein
Gift ist.”
in other words:
Size do matter!
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Epidemiology: “the numbers” Nearly 90% of medicinal exposures occur at home
During pre-adolescence: slight male predominance
This reverses in ages 13-19 with females accounting for 55 %
Children, especially under age 6, are more likely to have unintentional poisonings
About half of all poisonings among teens are classified as suicide
Approximately 1/3 of ingestions of toxic medications occur with meds intended for someone else
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Contamination and poisoning
acute
chronic
unintentional intentional
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LD50, LD95
Volume of distribution (Vd)
The nominal volume where the agent can be distributed
If Vd>5 L/kg low plasma cc. tissue binding ↑
Protein binding
If >90% low free fraction
Clearance (Cl)
The amount of plasma that can get rid of the agent during a given periodof time
e.g. renal clearance =
Half life
T(½) = 0.693 x Vd / Cl
urine conc. x urine volume.serum conc.
Some necessary basic pharmacology
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Dose-response curve
NOAEL
LOAEL
NOAEL: No Observed Adverse Effect Level - safeLOAEL:Lowest Observed Adverse Effect Level – notrecommended
cum
ula
tive
resp
on
se(%
)
Dose (mg/kg)
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Examples (LD50)
*
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What happens inreality?
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Primaryinsult
• recognition, unknown circumstances, associated injuries, mass intoxication
Secondarydamage
• circulatoiry, respiratory arrest, organdamage (direct and indirect), trauma during transport
Definitivecare
• aspecific therapy
• specific therapy
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Scheme of care
SYMPTOMATIC, ASPECIFIC TREATMENT
DECONTAMINATION
ELIMINATION
ANTIDOTE
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Aspecific symptoms
• (D)ABCDE
• Applies to ANY episode of poisoning
• WHAT
• HOW MUCH (Ideally mg/kg)
• WHEN
• WHAT ELSE (Including alcohol)
• WHY
• Use paramedics, friends, relatives, anyone!!
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General Management -1
• A (Airway)
• B (Breathing)
• C (Circulation)
• D (Disability-AVPU/ Glasgow Coma Scale)
• DEFG ( Don’t Ever Forget the Glucose)
• G (Get a set of basic observations)
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General Management -2
• Use all your senses, search for the clues• LOOK
– Track Marks– Pupil Size
• Hear– Type Breathing (Kussmaul, Hyperventilation)
• FEEL– Temperature, Sweating
• SMELL– Alcohol– Fruity– I would NOT taste
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Airways in danger!
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Aspecific therapy
• Ventilation
– As long as it’s required
– special cases:
• CO poisoning
• aspiration
• inhalation of direct irritants
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Aspecific therapy
• Maintain circulation
– Ensure DO2, increase CaO2
– EGDT
– CPR
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Toxidromes
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ToxidromesSigns and symptoms
HR BP RR pupil size GIT sweating temp
ANTICHOLINERGIC ↑ ↑ ↓ ↓
CHOLINERGICSLUDGE (Salivation, Lacrimation, Urinary incontinence, Diarrhea/Diaphoresis, GI upset/hyperactive bowel, Emesis)
↓ ↑ ↑
OPIOID ↓ ↓ ↓ ↓ ↓ ↓ ↓
SYMPAThO-MIMETIC
↑ ↑ ↑ ↑ ↑ ↑ ↑
SEDATO-HIPNOTIC
↓ ↓ ↓ ↓ ↓ ↓
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Toxidromes, cont’dToxidrome Most frequent poison
ANTICHOLINERGIC atropin, scopolamin
CHOLINERGIC carbamates, mushrooms, organophosphates
OPIOID opiates
Toxidrome Most frequent poison
SYMPATHOMIMETIC salbutamol, amphetamins, cocain, ephedrine (Ma Huang), metamphetamine, phenylpropanolamin(PPA), pseudoephedrin.
SEDATO-HYPNOTIC anticonvulsants, barbiturates (?), BDs, GHB, metaqualon, ethanol
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Symptomorientated
differentiation
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Main groups of symptoms
• Mental state
• CNS symptomes
• Muscles
• Circulation
• Respiration
• Kidney
• Liver
• Heat balance
• Carbohydratemetabolism
• Ion balance
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MENTAL STATE
CONFUSION PREDOMINANT CONFUSIONDELIRIUM
PREDOMINANT AGITATIONPSYCHOSIS
AMANTADINANTICHOLINERG/HYCIMETIDINCOLITHIUM
AMPHETAMINCOCAINCOFFEINPCPMARIJUANATHEOPHYLLIN
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MENTAL STATE
COMA CNS DEPRESSION
CELLULAR HYPOXIA
SYMPATHOLYTICS
OTHERS
BARBITURATEALCOHOLTCADSEDATO-HYPNOTICS
COCIANIDE
OPIATEMETHYLDOPA
BROMINEDIQUATLITHIUMSALICYLATE
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CNS
SEIZURESADRENERGIC
ANTIDEPRESSANT
OTHER
AMPHETAMINCOFFEINTHEOPHYLLIN
TCADHALOPERIDOLPHENOTHIAZIN
ANTIHYSTAMINCARBAMAZEPINCHOLINERGICSORGANIC SOLVENTS
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CNS
MUSCLE TONEDYSTONIA
RIGIDITY
DYSKYNESIS
HALOPERIDOLMETOCLOPRAMIDPHENOTHIAZIN
LITHIUMMAO-INHIBITORPCPNMS / MHSPIDER – TOXIN (BLACK W.)
AMPHETAMINCOCAINTCADPCP
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CIRCULATION
ARRHYTHMIACONDUCTION DISTURBANCES
LONG QT
TORSADE DE POINTES
VT/VF
BETA-BLOCKERTCADDIGITALISQUINIDINE
ARSENICCITRATETCADORGANOPHOSPHAT
AMPHETAMINCOCAINDIGITALISFLUORIDETHEOPHYLLIN
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RESPIRATION
ACUTE RESP. FAILURE
MUSCULAR
CENTRAL
PULMONARY
HYPOXIAINHALATIONCARDIOGENICCELLULARPULMONARY
BOTULINUMORGANOPHOSPHATCARBAMAT
BARBITURATOPIATEALCOHOL
ORGANOPHOSPHATEBETA-BLOCKERCHLORINE
METHANETCADCYANIDEOPIATE
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LIVER
ACUTEHEPATICFAILURE
ACETAMINOPHENAMATOXINAROMATIC COMPOUNDSHALOGENIZED CARBOHYDRONSCOPPERETHANOLHALOTHANEIRONPHOSPHORUSVALPROATE
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MUSCLE
RHABDOMYO-LYSIS
CELLULAR
MUSCULAR
OTHER
AMATOXINCOCOLCHICINGLYCOL
AMPHETAMINECOCAINTCADLITHIUMMAO-INHIBITORPCPSTRYCHNINETETANUS
BARBITURATEETHANOLSEDATO-HYPNOTICS
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HEAT BALANCE
HYPERTHERMIA
MUSCULAR
METABOLIC
REGULATION
OTHER
AMPHETAMINECOCAINTCADLITHIUM LSDPCP
DINITROPHENOLSALICYLATE
ANTICHOLINERGICSANTIHYSTAMINTCADPHENOTHIAZIN
METALLIC VAPOURMNS / SS / MH
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CARBOHYDRATE BALANCE
BLLOD SUGARHYPO
HYPER
BETA-BLOCKERSETHANOLINSULINOADSALICYL
BETA-ADRENERGICSCOFFEINCORTICOSTEROIDSDIAZOXIDEEPINEPHRINEGLUCAGONTHEOPHYLLINTHIAZIDE
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ION BALANCE
POTASSIUM
HYPER
HYPO
ADRENERGIC AGENTSACEIDIGITALISFLUORIDELITHIUM
BARIUMCOFFEINDIURETICUSTHEOPHYLLINEPINEPHRINE
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Specifictherapy
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Specific care
• Starts with the aspecific therapy
• Sometimes they run parallel with frequentchecks
• „Semi-specific” therapy along with the toxi ABC– Oxygen!
– DEFG ( Don’t Ever Forget the Glucose)
– Thiamine (vitamin B1) 100 mg IV/IM
– Naloxone (Narcan) ADULT 0.2 mg IV/IM/ETT, CHILD: 0.01mg/kg IV/IO/ETT
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Further steps
SYMPTOMATIC TREATMENT
DECONTAMINATION
ELIMINATION
ANTIDOTE
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PLASMA COMPARTMENT
PROTEIN BOUNDFREE
LIVER
METABOLISM
KIDNEY
EXCRETION(MATERIAL / METABOL)
PHARMAC.ACTIVE
RECEPTOR
BOUNDFREE
TISSUE STOREBIO.INACTIVE
TISSUE
BOUNDFREEFREE FREE
FREE METAB/FREE
FREE
INGESTED AMOUNT
PATIENT COMPLIANCE
ABSORPTION
BIO. AVAILABILITY(NOT ABSORBED; FIRST PASS)
INDIVIDUALFACTORS
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PLASMA COMPARTMENT
PROTEIN BOUNDFREE
LIVER
METABOLISM
KIDNEY
EXCRETION(MATERIAL / METABOL)
PHARMAC.ACTIVE
RECEPTOR
BOUNDFREE
TISSUE STOREBIO.INACTIVE
TISSUE
BOUNDFREEFREE FREE
FREE METAB/FREE
FREE
INGESTED AMOUNT
PATIENT COMPLIANCE
ABSORPTION
BIO. AVAILABILITY(NOT ABSORBED; FIRST PASS)
DECONTAMINATION
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DecontaminationExternal
– clothes
– skin
– mucousmembranes
– oral cavity
Internal- induced emesis: NO!
- gastric lavage
Within 60 minutes, except drugs delaying gastricemptying: ANTICHOLINERGICS, TCA, BARBITURATES, OPIATES
- gut washoutPOLYETHYLENE GLYCOL 1500-2000 ml/h
- activated charcoal(1g = 1000-2000 m2 surface) 1 g / ttkg
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Further steps
SYMPTOMATIC TREATMENT
DECONTAMINATION
ELIMINATION
ANTIDOTE
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ELIMINATION – KIDNEYS
FORCED DIURESISNEUTRAL, ALKALINE, ACIDOTIC
Indication:
If the agent is filtrated by the kidneys(target: GFR ↑)
small molecular weight– small volume of distribution– low prot. binding
electrically charged molecules– ION TRAPPING
Method:
Monitor fluid balance, ion- and pH balance
Close observation
In: 300-500 mL/h Target urine output: 300 mL/h
(Furosemid, Etacrinic acid, Mannitol, Theophyllin /GFR↑/)
Alkalinization/acidification PRN
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ELIMINATION - GIT
If the poison is excreted by bile:
20 g of activated charcoal/ 4 h
Observation!! (ileus, bleeding, check INR !)
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ELIMINATION – EXTRACORPOREAL TECHNIQUES:
PERFUSION (HP),
ACT. CHARCOAL
ACETAMINOPHEN,AMMANITA TOX., AMOBARBITAL, ATENOLOL, CCl4, CHLORAMPHENICOL, CHOLHICIN, COFFEIN, DIGITOXIN, DYSOPYRAMID, DIPHEN.HYDANTOIN, GLUTETHIMID,INH,MEPBROMAT,NADOLOL, ORGANOPHOSPHAT,PARAQUAT, PHENYLBUTHAZON, PHENOBARBITAL, PHENYTOIN, QUININ, SALICYLAT , SOTALOL, THEOPHYLLIN, THYROXIN, CARBAMAZEPIN
If the agent binds to thematerial of the capsule(charcoal, resin)
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HEMODIALYSIS
• SMALL MOLECULAR WEIGHT(< 500 D)
» WATER SOLUBLE
» SMALL Vd; LOW PROT. BIND.
» LOW CLEARANCE
ARSENIC, BORIC ACID, BROMINE, CHLORAT, DISOPYRAMID, ETHYLENGLYCOL, FLECAINID, INH, ISOPROPIL ALKOHOL, MAGNESIUM, OXALATE, SALICYLIC ACID, SOTALOL,
VALPROAT
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APHERESIS / PLASMAPHERESIS
If the agent’s protein binding > 90 % AMMANITA TOXIN, SNAKE POISONS, METHAEMOGLOBIN, NEUROLEPTICS, NIFEDIPIN, PARAQUAT, PHENYTOIN, SEDATO-HYPNOTICS, THYROXIN, TCA,VERAPAMIL
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Molecular Adsorbents Recirculation System (MARS)
• two separate dialysis circuits– first circuit consists of human serum albumin, is in
contact with the patient's blood through a semipermeable membrane and has two special filters to clean the albumin after it has absorbed toxins from the patient's blood
– second circuit consists of a hemodialysis machine -used to clean the albumin in the first circuit before it is recirculated to the semipermeable membrane in contact with the patient's blood
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„ANTI-TOXINS”
SYMPTOMATIC TREATMENT
DECONTAMINATION
ELIMINATION
ANTIDOTE
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ANTIDOTES
ACETAMINOPHEN NAC
ACEI ANGITENSINAMID
ANTICHOLINERG PHYSOSTIGMIN
NEOSTIGMIN
ARSEN BAL-MERCAPTOL
BENZODIAZEPIN FLUMANEZIL
ß-BLOCKER GLUCAGON
ISOPROTERENOL
BOTULINUS TOXIN ANTITOXIN
CARBAMATE ATROPIN
CA-CSATORNA BLOCK CALCIUM
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ANTIDOTES
COUMARINS VITAMIN K
DIGITALIS Fab
CYANIDE 4-DMA
DICOBALT EDTA
HEPARIN PROTAMINE-SULPHATE
FORMALDEHYDE FOLATE
ETHYLEN GLYCOL ETHYLALCOHOL
FOMEPIZOL
MERCURY BAL-DIMERCAPTOL
HYDROGEN-FLUORIDE CALCIUM
INSULIN GLUCAGON
GLUCOSE
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ANTIDOTES
OPIATES NALOXONE
METHGB METHYLENE BLUE
METHYL ALCOHOL ETHANOL
FOLIC ACID
PLUMB BAL-MERCAPTOL
ORGANOPHOSPHATE PAM
PARAQUAT FULLER EARTH
THEOPHYLLIN ADENOSIN
OXALATE CALCIUM
IRON DEFEROXAMIN
…
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Special
poisonings
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Alcohol
Level of alcohol (g/l) Level of alcohol (‰) Degree of drunkness
0,6-1,8 0,75-2,25 mild
1,8-3,0 2,25-3,75 medium
3,0-4,2 3,75-5,25 severe
>4,2 >5,25 life threatening
Therapy: supportive, frequent BM check, fluid administrationwith mechanical ventilation and circulatory support if requiredDisposition: depends merely on the initial state and theresponse to therapy but mainly home
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Ethylene glycol and methanol
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Ethylene glycol and methanol
• Treatment:– blocking alcohol dehydrogenase (with ethanol or fomepizol)
– PPI
– Bicarbonate (methanol)
– Hemodialysis, if• arterial pH < 7.10,
• pH decreases despite bicarb.infusion>
• pH < 7.3 despite bicarb.
• increase in serum creatinine
• if the initial plasma ethylenglycol/methanol level≥ 500 mg/l.
• Disposition: ITU
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Ethylene glycol and methanol
fomepizol
Mg, B6
folate
thiamine
NaHCO3
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Benzodiazepins
• The most frequent drug of choice in suicide• Symptoms: dizziness, confusion, somnolence, blurred
vision, loss of contact, anxiety, agitation• Treatment:
– Decontaminatiom: • gastric lavage within 60 seconds
– Aspec. and spec. therapy• single dose of 1 g/kg activated charcoal (aspiration!)• mechanival ventilation if required• flumazenil (0,3 + 0,1 mg), BUT REMEMBER: pts with BD abuse it might
trigger fits, in TCA overdose it may cause fits and arrhythmias!
– Differential diagnosis: other sedatives, controlled drugs
• Disposition: ED, ITU, psychiatry
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Tricyclic antidepressants
Main pharmacodynamic effects:– Alfa1-blockade– Na-channel blockade– Inhibition of reuptake of biogen
amines (NADR, SER)– Muscarinic receptor blockade
(anticholinergic)– Histamin receptor blockade
(antihistamin)– Inhibition of K-efflux– Indirect GABAA -blockade
• Effects on peripheral nervoussystem– Anticholinergic effects
• tachycardia,hyperthermia,midriasis, anhydrosis, skin flush, ileus, urinaryretention
– Alfa1-blockade• reflex tachycardia,myosis
• CNS effects– Excitative
• agitation, delirium, myoclonus, hyperreflexia, generalized fits, hyperthermia
– Inhibitory• sedation, coma
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Tricyclic antidepressantsPROBLEM/SYMPTOM TREATMENT
Hypertension Usually transient, no need to treat
Hypotension Crystalloid, NaHCO3, if QRS>100 ms, NADR, DA
Tachycardia Usually no need to treat
Monomorphic VT NaHCO3, syncDCCV, overdive pacing
Polymorphic VT (torsades) MgSO4
Bradydysrhythmia (late, usually notfrequent )
ACLS bradycardia protocol
QRS and QT prolongation If symptomatic: NaHCO3
Coma ETT, ventilatory support
Seizures diazepam, midazolam or propofol inf.
Hyperthermia GA, cooling
Disposition: depends on the initial state and the response to treatment
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Paracetamol• Abssorption:
– Rapidly from GIT– Peak conc. between
60-120 min. • Half life:
– 0.9 -3.25 hours• Metabolism:
– Indepenedent of age– Not influenced by renal
disease– May be up to 17 hrs in liver
disease!
• Factors influencingtoxicity
– total quantity ingested– time from ingestion to
treatment– age of the patient– alcohol– enzyme inducing
medications
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Paracetamol
Potential liver damage
– Adults: > 150 mg/kg in acute dose
– Adults: > 7.5 Grams in 24 hours (chronic)
– Children (<10 yrs): > 200 mg/k
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4 Stages of Acetaminophen Poisoning
• Phase I (30 minutes to 4 hours)
– Within a few hours after ingestion, patients experience anorexia, nausea, pallor, vomiting, and diaphoresis. Malaise may be present.
Patient may appear normal
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• Phase II (24 to 48 hours)
– Symptoms less severe. May seem like recovery. Right upper quadrant pain may be present due to hepatic damage.
– Liver enzymes become abnormal. Prothrombin time may be prolonged. Renal function may begin to deteriorate.
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• Phase III (3 to 5 days)
– Characterized by symptoms of hepatic necrosis. Coagulation defects, jaundice, and renal failure have been noted. Hepatic encephalopathy has been noted. Centrilobular necrosis. Nausea and vomiting . Death due to hepatic failure.
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• Phase IV (4 days to 2 weeks)
–Complete resolution or death
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Rumack-Matthew nomogram
Based on this:N-acetil-cisztein (NAC)Tretment with NAC should be started ASAP withan initial dose of 150 mg/ttkg, followed by 50 mg/ttkg maintenace dosebased on the nomogramIf levesl can not be measured: 72 hDisposition: ITU
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Treatment
– activated charcoal
– cathartics, bowel washout
– Haemodialysis
• Limited results due to rapid progression
– Haemoperfusion
• Ineffective
– Peritoneal dialyisis
• Ineffective
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Amphetamin, metamphetamin, mefedron
• Symptoms:– CNS: headache, agitation, anxiety– dsykinesis– stroke-like symptoms– chest pain– palpitation– dry mouth– nausea/vomiting– diarrhoea– urinary retention– sweating– mydriasis
Treatment:• Gastric lavage: general indications• Bowel washout (body packers)• Supportive treatment:
– BZDs, circulatory support– beta-blockers are contrainidcated –
unopposed alpha effects!!– cooling– haloperidol?
Disposition: depends on symptomsand response to treatment
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Opiates
• Versatile „usage”
• Quite severe dependency
• Conjugates in the liver–prolonged effects in liverdisease
• Quite often taken withsomething else
• Tipycal signs and symptoms:
– „skin popping, mainlining”
– nasal mucosa damage,
– poor general condition
– myosis (but mydrisasis insymp. tone!)
– RR: 4-6/min
– mild hypotension (if severelook for other causes!)
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Opiates
• Treatment:
– supportive
– airway safety! mechanical ventilation if required–respiratory depression is the main cause of death
– naloxone: • 0,1-0,4 mg /1-2 min.
• rapid and specific antagonist
• Disposition: depends on the very complexbackground (dependency, amount, etc)
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Carbon monoxide
• Might be a diagnosticchallenge
• Aspecific symptoms
• Quick poison
• Results from incompletecombustion
• Other sources
• Binds 230-270 timesbetter to Hb than oxygen
• 100 ppm causessymptoms
• Direct toxic effect on CIP-C and CIP 450
• Half-lives:– in room air: 3-4 h
– in 100 % oxygen: 30-90’
– in 100 % oxigénben AND at2,5 atm pressure:15-23’
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Carbon monoxide• Symptoms
– fatigue– weakness– palpitation– chest pain– nausea– vomiting– visual disturbances– incontinence– tachypnoe
• Diagnosis:– think of the possibility!– co-oxymetry: 5-10 % CoHb
is significant (smokers!)
• Treatment:– immediate rescue– fresh air– O2!!– hiperbaric oxygen
chamber: 100% oxygen at2.4-3 atm pressure for 90-120 minutes
Disposition: ITU/ED
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And at last:
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Situation.
Background.
Assessment.
Recommendation.
S
B
A
R