Locally anonymous license plates are better
Rainer Schmid Department of Anaesthesiology and Intensive Care Medicine at Wilhelminenspital, Vienna
1 Poisonings - Practical Case Studies Rainer Schmid Dept. of Anaesthesiology and Intensive Care Medicine Wilhelminenspital, Vienna
2 Poisonings - practical case studies EAPCCT - European Association of Poisoning Centers and Clinical Toxicologists Goldfrank: Toxicologic Emergencies Rätsch: Encyclopedia of Psychoactive Plants Albrecht: Intensive Therapy of Acute Poisonings K.Hruby, A.Schiel: Antidotarium
3 Case: about 20-year-old man, found lying on the floor in a devastated apartment (lying on his side, right); No relatives on site (anonymous phone calls, apartment door ajar.
4 case: GCS 3, pup. medium wide, isokor, LR numerous ESST at both WP, right. Arm swollen and hardened. RR 70syst., HR 110 / min. SpO2 82%, AF 12 / min.
5 poisonings with opiates / benzodiazepines: OPIATE: Substitol, Methadon, Compensan, Subutex, Heroin, Kapanol, Codidol, Tramal, BENZODIAZEPINE: Somnubene, Praxiten, Rohypnol, Xanor, Gewacalm, Psychopax, Zoldem,
6 Opioids: Key symptom # 1: Respiratory depression Bradypnea WITHOUT dyspnea
7 Opioids: Key symptom # 2: Sedation - somnolence - coma
8 Opioids: Key symptom # 3: Miosis
9 Opioids: other symptoms: analgesia, hypotension, bradycardia, urinary retention
10 opioids: Antidote therapy: NALOXON (Narcanti, Naloxon) according to respiratory rate and level of consciousness titration, 0.2mg (= 1/2 Amp.), Up to 1.2mg
11 Benzodiazepines: Key symptoms: clouding of consciousness - coma, shallow breathing, NO bradypnea
12 Benzodiazepines: Antidote therapy: FLUMAZENIL (Anexate, Flumazenil) according to the state of consciousness titration: 0.25mg (= 1/2 Amp.), Up to 1.0mg
13 Drug emergency: tension arc of outpatient observation subject to antidote ... emergency room or IMCU subject to ventilation subject to catecholamine requirement ... intensive care unit (Anexate, Flumazenil)
14 Drug emergency: hypoxic - organ damage caused by hypoperfusion: BRAIN
15 Drug emergency: hypoxic - organ damage caused by hypoperfusion: LUNGE toxic pulmonary edema (better: e vacuo edema)
16 Drug emergency: hypoxic - organ damage caused by hypoperfusion: COMPARTMENT SYNDROME damage to muscles (and nerves) due to box pressure CK, clinical examination,
17 Drug emergency: hypoxic - organ damage caused by hypoperfusion: KIDNEY acute kidney failure Crushing kidney hyperkalaemia!
18 drug tests: detection in urine: opiates, heroin, methadone: 2-3 days THC: 1-2 days THC - chronic consumption: up to 3 weeks cocaine: 2-4 days amphetamines: 1-3 days
19 hallucinogens: THC - tetrahydrocannabinol (cannabis) Leaves: Flowers: Resin: grass, marijuana, ganja, weed dope, hashish, shit, pot samples with a proportion of 0-40%,
20 hallucinogens: THC - Tetrahydrocannabinol (cannabis) spec. Cultivations 40-50% 1-3 plants for horticultural purposes tolerated without traces of harvest
21 hallucinogens: THC - tetrahydrocannabinol (cannabis) lifetime experience: up to 15 years: 14% up to 18 years: 35% up to 60 years:> 50%
22 Hallucinogens: GHB, GBL (liquid ecstacy) GHB (gammahydroxybutyric acid) GBL (gammabutyrolactone) very similar chem. Structure of GAB (gamaaminobutyrate) = neurotransmitter on the GABA receptor
23 hallucinogens: GHB, GBL (liquid ecstacy) Alkover, Somsanit GBL in the drug wholesaler GHB / GBL traded as a drug (Internet!) Approx. 340 products on the Austrian market with GBL as an ingredient: especially paints, varnishes, nail varnishes, rim cleaners
24 hallucinogens: GHB, GBL (liquid ecstacy) Symptoms: in low dosage: euphoric, relaxing, increasing libido; Intoxication is similar to an alcohol intoxication. Combination with alcohol in particular leads to
25 Aspiration when unconscious Hallucinogens: GHB, GBL (liquid ecstacy) Symptoms: mydriasis bradycardia cerebral cramps, unconsciousness
26 Hallucinogens: GHB, GBL (liquid ecstacy) Therapy: unspecific Legal situation: GBL is not listed in the Narcotics Act, but the distribution in Europe is largely monitored by the distributors. GHB has been in Austria since 2002 after the
27 Hallucinogens: LSD (lysergic acid diethylamide): Risks: unpredictability, horror trips paranoia, getting stuck (Psych sends its regards), flash backs, outbreak of latent psychoses
28 Hallucinogens: Psylocibin: active ingredient of the Nanacatl mushroom magic mushrooms = legal alternative to LSD (ethno shops!) Risks: similar. LSD, but with fewer side effects due to the lower dosage.
29 hallucinogens: mescaline rosewood seeds angel's trumpet etc. TIP: ask Mr. Dr. Rattle! Encyclopedia of Psychoactive Plants
30 the fast entactogens: Cocaine: effects well known ... (3% lifetime experience) alpha- and betamimetic
31 the fast entactogens: cocaine: problems: cardiovascular problems (ACS!) Hypertensive crises (cerebral hemorrhage!) Psychotic states (paranoia, fear)
32 the fast entactogens: cocaine: therapy: benzodiazepines! Urapidil, Nitro NO beta blockers if possible
33 the fast entactogens: synthetic drugs: amphetamine analogues (ecstasy, MDMA, PMA, ...) cathinones (mephedrone) ...
34 the fast entactogens: legal highs, new research chemicals: psychoactive substances that can be legally purchased in shops or on the Internet. since 2011: chemical compound classes are recorded (instead of individual substances as before).
35 the fast entactogens: amphetamine-like drugs: phenethylamine structure - thus related to the most important catecholamine transmitters in the CNS (where their main place of action is ...)
36 the fast entactogens: new research chemicals: e.g. new highs: Benzo-di-furane (flys): Bromo-Dragonfly, 3C-Bromo-Dragonfly,
37 the fast entactogens: new research chemicals: e.g. Cathinones: Mephedrone = MMC (4-methyl-meth-cathinone) chem. related to the active ingredient of the Kath (Quat) bush.
38 the fast entactogens: new research chemicals: e.g. Pyrrolidones: 4'-methyl-α-pyrrolidinopropiophenone, MPPP
39 the fast entactogens: new research chemicals: e.g. Piperazine
40 the fast entactogens: new research chemicals: side effects: stress component: tachycardia, hypertension, fever, convulsions Psychotic component: craving, confusion, anxiety, hallucinations, depression
41 the fast entactogens: new research chemicals: side effects: depressant components: apathy, coma
42 the fast entactogens: new research chemicals: non-pharmaceutical-industrial production uncontrolled distribution channels unclear composition unclear dose unclear effect unclear diagnosis / therapy / prognosis
43 the fast entactogens: neuroenhancing drugs (brain doping) e.g. Ritalin
44 the fast entactogens: neuroenhancing drugs (brain doping) Modafinil (Provigil, Modafenil, Modalert, Modiodal, ...) Donepezil (Alzheimer's therapy) Selegiline (Jumex; Parkinson's therapy)
45 the solution for all fast and hallucinogenic drugs: sedation!
46 ... and what is that ... ??? the central anticholinergic e.g .: Calmaben (diphenhydramine)
47 last but not least: ... a little social criticism ...
48 Case: 62-year-old patient, awake, depression known, according to the husband's information, 40 tablets of Saroten and 20 tablets about 30 minutes before the rescue service arrives. Xanor taken with suicidal intent
49 Case: when the ambulance arrives, the patient is awake, sitting in the armchair, motor is very restless (fiddling), speaks incomprehensibly (babbling); RR 140/95, HF 128 / min, rh. SpO2 95% in RL, AF 22 / min mydriasis, dry tongue; mute belly
50 poisonings with psychotropic drugs: CAVE: TCA (tricyclic antidepressants): Saroten, Tryptizol, Anafranil, Harmomed, Sinequan, Ludiomil, ...
51 Poisoning with psychotropic drugs: CAVE: TCA (tricyclic antidepressants): Mechanism of action: Reuptake inhibition of neurotransmitters (TCA mainly noradrenaline), others mainly serotonin, dopamine, (adrenaline), ...
52 Poisoning with psychotropic drugs: CAVE: TCA (tricyclic antidepressants): Symptoms: ANTICHOLINERG neurological: agitated / calm course (hallucination, restlessness, somnolence, coma) fidgeting and babbling
53 Poisoning with psychotropic drugs: CAVE: TCA (tricyclic antidepressants): Symptoms: ANTICHOLINERG neurological: Mydriasis
54 Poisoning with psychotropic drugs: CAVE: TCA (tricyclic antidepressants): Symptoms: ANTICHOLINERG peripheral: reddened, dry (mucous) membrane, reduced peristalsis, paralysis
55 Poisoning with psychotropic drugs: CAVE: TCA (tricyclic antidepressants): cardiovascular: arrhythmia (long-qt) App: QTc Calculator
56 Psychotropic drug poisoning: tricyclic AD tetracyclic AD SSRI atypical AD MAO inhibitors atypical antipsychotics neuroleptics ...
57 Poisoning with psychotropic drugs: CAVE: TCA (tricyclic antidepressants): Therapy: ANTICHOLIUM (monitoring!) SODIUM BICARBONATE ACTIVATED CHARCOAL
58 Poisoning with psychotropic drugs: CAVE: TCA (tricyclic antidepressants): Therapy: ANTICHOLIUM (= physostigmine salicylate) reversible cholinesterase inhibitor, administration: titrated iv. after effect (bypass up to 2mg / hour) monitor conditions required
59 Poisoning with psychotropic drugs: CAVE: TCA (tricyclic antidepressants): Therapy: SODIUM BICARBONATE alkalization causes increased serum protein binding of the TCA, therefore lower bioavailability. Sodium loading improves cardiac conduction and reduces ECG changes
60 Detoxification process: ACTIVATED CHARCOAL no evidence! initially 1 / 2-1g / kg body weight (= 30-50g), repetitively (every 4-6 hours) approx. 15g with enterohepatic circulation of drugs
61 Detoxification process: (STOMACH RINSE) EAPCCT: Indication only for organotoxic substances and up to max. 1 hour after ingestion
62 Detoxification process: (HEMOFILTRATION) Lithium (Quilonorm)
63 Detoxification procedure: (liver replacement procedure - MARS) ??? Severe paracetamol poisoning, death cap mushroom (if liver function is measurably severely impaired)
64 Detoxification process: Lipid rescue therapy 1996 (Weinberg): Lipids protect rats from local anesthetics 2006: first use in humans (for local anesthetic intoxication): immediate success 2008: first use in humans (for neuroleptic intoxication): immediate success
65 Detoxification procedure: Lipid rescue therapy Indications: Lipid solubility: Oil-water coefficient logp> 2 Severe poisoning with a life-threatening course. No established antidote available
66 Detoxification process: lipid rescue therapy 3 theories: lipid sink: fats envelop lipid-soluble substances Mitochondria: local anesthetics interfere with fatty acid metabolism Ca ++ metabolism: myocardial Ca channels are opened by lipids
67 Detoxification process: lipid rescue therapy Side effects: Fat embolism: what does it look like? dangerous? Immunosuppression? Protein allergy: Intralipid has chicken protein as an emulsifier, Lipofundin has soy protein
68 Detoxification methods: lipid rescue therapy Contraindications: the worse the clinical situation, the more relative the CI: Age <16a pregnancy (chickens) protein allergy Intracranial bleeding
69 Detoxification process: lipid rescue therapy Procedure according to checklist: Identification according to drug list. Brief status and blood sample BEFORE lipid administration. Lipid administration. Brief status and blood extraction (4-6 hours) AFTER lipid administration
70 Lipid administration: Intralipid 20% 100ml BOLUS 1.5ml / kg body weight over 2-3min. Re-evaluation if symptoms do not decrease after a few minutes: Infusion 15ml / kg / h up to 30min Bolus can be repeated, infusion can be increased to 30ml / kg / h LIMIT DOSE: 10ml / kg / h in 30min Detoxification procedure: Lipid rescue therapy
71 Detoxification process: Lipid rescue therapy Dose calculator - Example: Use Intralipid 20% infusion Body weight 50kg bolus (1.5mg / kgKG) Infusion (15ml / kgKG) Infusion (30ml / kgKG) 75ml 750ml / h Infusion rate 1500ml / h Infusion rate
72 Detoxification process: lipid rescue therapy With which drugs? all local anesthetics: lidocaine, ropivacaine, bupivacaine, levobupivacaine others: amiodarone, amlodipine, amitryptiline, carbamazepine, carvedilol, clozapine, clomipramine, doxepin, felodipine, haloperidol, maprotiline, ..., verapamiline, proprotiline, ...
73 Detoxification process: high-dose-insulin-therapy also: HIET (high-dose-insulin-euglycaemiatherapy) intoxication with calcium channel blockers case reports experimental?
74 Detoxification process: high-dose-insulin-therapy also: HIET (high-dose-insulin-euglycaemiatherapy) Inotropic effect of insulin Alteration of the myocardial lipid metabolism Insulin influences calcium channels
75 Detoxification process: high-dose-insulin-therapy also: HIET (high-dose-insulin-euglycaemia-therapy) Literature (excerpts): Life-threatening calcium channel blocker overdose and its treatment: Rizvi I et al Amlodipine poisoning complicated with acute non -cardiogenic pulmonary edema: Hasson R et al. High-dose insulin: A consecutive case series in toxin-induced cardiogenic shock: Joel SH et al all: BMJ Case Reports
76 Case: 55-year-old winegrower, rescue is called by the son because he finds the father lying unconscious in the wine cellar.
77 Case: Pre-clinical initial examination: patient in prone position, lying in vomit GCS 6 (1 = no answer to speech, 1 = no eyes open, 4 = untargeted defense against pain stimulus) pupils wide, isocorative, LR +, conspicuous hyporeflexia; Machine breathing (AF30 / min, SpO2 97%) RR 90syst., HR 100 / min
78 Poisoning with painkillers: PARACETAMOL (acetaminophen): active ingredient = acetaminophen breakdown in the liver (cytochrome P-dependent oxidases). If the breakdown path is overwhelmed, toxic metabolites bind to liver cells cell death
79 Poisoning with painkillers: PARACETAMOL (acetaminophen): Potentially hepatotoxic dose: 7-15 g in adults, mg / kg body weight in children
80 poisonings with painkillers: PARACETAMOL (acetaminophen): 1st phase (12-24 hours): nausea, vomiting, abdominal cramps 2nd phase (24-48 hours): latency phase (relative well-being) 3rd phase (after 48 hours): Pain right Upper abdomen, increased TA, collapse 4th phase (3rd-5th day): jaundice, hypoglycaemia,
81 Poisoning with painkillers: PARACETAMOL (acetaminophen): Therapy: activated charcoal (repetitive) gastric lavage ?? Serum level determinations (4-hour peak!)
82 Poisoning with painkillers: PARACETAMOL (acetaminophen): Antidote: N-acetylcysteine (Fluimicil) according to the scheme (Fluimicil = precursor for glutathione synthesis), forced diuresis (sodium bicarbonate) transplant contact!
83 Poisoning with painkillers: NSAIDs Different groups of substances: Profene, acetic acid derivatives, anthranilic acid derivatives, pyrazolones Common mechanism of action: inhibition of prostaglandin synthesis
84 Poisoning with painkillers: NSAIDs Neurological symptoms of poisoning: clouding of consciousness, coma, cerebral seizures (due to the storage of analgesic acids in cellular membranes of the CNS)
85 Poisoning with painkillers: NSAIDs Cardiovascular symptoms: hypotension, sinus brady, tachycardia
86 Poisoning with painkillers: NSAIDs Gastrointestinal symptoms: nausea, vomiting, severe abdominal pain (PGE2, therefore cytoprotective effect)
87 Poisoning with painkillers: NSAIDs kidney: metabolic acidosis, acute NV (decreased renal vasodilation due to PGE2)
88 Poisoning with painkillers: NSAID therapy: symptomatic activated charcoal, possibly urine alkalization
89 poisonings with painkillers: NSAIDs - Parkemed (mefenamic acid)
90 poisonings with painkillers: NSAID - Parkemed (mefenamic acid) 10g (= 20Tbl.)
91 CO poisoning (carbon monoxide): Combustion when there is insufficient oxygen: instantaneous water heaters, high-pressure weather, car exhaust fumes in closed rooms, barbecues in the garage, ...
92 CO poisoning (carbon monoxide): Effect: 240x higher affinity to Hb than oxygen (complex bond with Fe of hemoglobin) Toxicity depending on: CO concentration in the room air Duration of exposure to physical activity
93 CO poisoning (carbon monoxide): CO content of 0.3% in the room air means approx. 50% CO-Hb CO content of 1% in the room air means death in 5 minutes
94 CO poisoning (carbon monoxide): CO-Hb ~ 20%: cardiotoxic effects CO-Hb ~ 40%: unconsciousness CO-Hb ~ 50%: incipient respiratory paralysis
95 CO poisoning (carbon monoxide): Symptoms: tiredness, nausea, headache, drowsiness, somnolence, coma, convulsions, hypotension, AP, MCI dyspnea, Lö, ARDS acidosis encephalopathy, cortical blindness, basal ganglia damage.
96 CO poisoning (carbon monoxide): Therapy: fresh air (open window etc.) oxygen PEEP symptomatic therapy HBO ???
97 CO poisoning (carbon monoxide): CAVE: rosy skin false positive pulse oximetry saturation values!
98 CO2 poisoning (carbon dioxide): fermentation gas in wine cellars, silos, ... heavier than air!
99 CO2 poisoning (carbon dioxide): Symptoms and effects: Tachycardia RR Respiratory depression due to hypercapnia Suffocation due to displaced air
100 CO2 poisoning (carbon dioxide): Therapy: symptomatic
101 Smoke and fire gases: Smoke gas poisoning = smoke inhalation + thermal damage
102 Smoke and fire gases: thermal damage to the alveolar epithelium! Fire gas constituents: nitrogen, carbon dioxide, carbon monoxide, sulfur dioxide; Cyanide (hydrocyanic acid), phosgene ash, soot
103 Smoke and fire gases: Therapy: anti-obstructive therapy (sprays!) Early intubation ventilation with FIO2 1.0, PEEP corticoids (inhalation and systemic) no longer relevant!
104 Smoke and fire gases: Therapy: Hydroxocobolamine (Cyanokit)
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