Environmental Notes
Environmental Notes
HYPER/HYPOTHERMIA
Non-freezing Cold Injuries
Trench Foot
Pathology Direct injury to soft tissue from prolonged cooling; worse in wet
conditions; damages peripheral nerves most
Symptoms Tingling and numbness; pale, mottled, pulseless, immobile
Initially no change on rewarming
After hours: hyperaemic phase; severe burning pain; recovery of prox
sensation
After 2-3 days: oedema, bullae
Severe: tissue sloughing, gangrene
Treatment Supportive; oral PG’s may help circulation; clean, warm, dry, elevated
Chilblains / Pernio
Symptoms Mild inflamm lesion after longterm intermittent exposure to damp cold
Tingling, numbness, oedema, erythema, cyanosis, plaques, nodules,
ulcers, vesicles, bullae, burning paraesthesia
Rewarming causes tender blue nodules
Treatment Supportive as above; can use nifedipine / PG
Panniculitis
Mild necrosis of subC tissue after prolonged exposure to cold
Cold Urticaria
Hypersensitivity to cold air / water
ENVIRONMENTAL INGESTIONS
|Agent |Life Threat |Source |Pathophysiology |Symptoms |Treatment |
|Corrosives |Airway compromise |Batteries, bleach, |Acids ( coagulative necrosis |Airway: stridor, SOB, dysphonia, throat pain |Charcoal: no |
| | |dishwasher etc… |( eschar limits tissue |GI: stridor, drooling, vomiting |Rinse mouth with H20 |
| | | |penetration |Perf: chest pain, SOB, fever, subC emphysema,|Drink milk |
| | | |Alkali ( liquefactive |pleural rub |Avoid NG |
| | | |necrosis ( deep penetration | |ADT |
| | | | |Lack of oral burns doesn’t exclude GI injury |Endoscopy: if persistent |
| | | |Necrosis at 7-10/7 | |vomiting, oral burns, drooling,|
| | | |Stricture at 3/52 | |AP; do at 12-24hrs to determine|
| | | | | |extent of injury |
|Organo-phosphate|Coma |Chemical warfare |Inhibits AChesterase ( incr |Acute (muscarinic): rapid if inhaled, within |Personal protection |
|s + carbamate |Hypotension |Insecticides |ACh at muscarinic and |12hrs if ingested (may be life-threatening if|Decontamination |
| |Seizures | |nicotinic cholingeric |Sx on presentation; DUMBBELS, hyper(hypoT, |O2 |
| |Resp failure | |receptors |incr(decr HR, NCPO, arrhythmias, GI Sx if |Charcoal: yes (may help) |
| | | |Ageing occurs |ingested |Atropine: muscarinic |
| | | | |Intermediate (nicotinic): 24-96hrs; |Pralidoxime: nicotinic |
| | | | |fasciculations, muscular weakness ( resp |Diazepam for seizures |
| | | | |paralysis; unresponsive to atropine |FFP 2iu daily until atropine |
| | | | |Late: 2-3/52; rare; ascending sensorimotor |stopped |
| | | | |polyneuropathy |Avoid sux as will have |
| | | | | |prolonged effect |
| | | | | |May need vasopressors |
|Hydro-carbons |Coma |Petrol, turps, |Aspiration pneumonitis |RS: NCPO, aspiration pneumonitis |Decontamination |
| |Seizures |lighter fluid, glue|Surfactant depletion |Metabolic acidosis |Charcoal: no |
| |Arrhythmia | |Free radical formation |CNS: similar to ETOH, encephalopathy and |Gastric lavage if 3g, all die |Decontamination > resus |
| | | |death |Immediate: V+D |Give food / soil ASAP |
| | | |Transported into pneumocytes |Hrs: corrosive oral inj |Avoid O2 |
| | | |and renal tubular cells |10) |Charcoal - no |
|Met-Hb | |Nitrites, phenols, |Ferric rather than ferrous Fe|Onset: usually in 30mins |Methylene blue |
| | |recluse spider |in Hb ( Met-Hb ( poor O2 |25-40% level: chocolate blood, H, weakness, |HBO |
| | |bite, sulphurs, |carrying capacity ( shifts |anxiety, syncope, incr HR, SOB, cyanosis |Exchange transfusion |
| | |antimalarials, |curve to L ( cellular hypoxia|45-55%: decr LOC |O2 may not help |
| | |LA’s, GTN | |55-70%: seizures, coma, arrhythmia | |
| | | | |Decr SaO2 but normal PaO2 | |
|CO | |Heating malfunction|CO has 240x affinity for O2 |Cherry pink skin ( cyanosis |High flow O2 |
| | |Car exhaust |than Hb ( shifts curve to L (|10-20% level: H, SOB, angina |HBO |
| | | |cellular hypoxia |20-30%: H, weakness, decr cognitive function | |
| | | |O2 free radicals ( inflamm |30-40%: N+V+H, weakness, visual disturbance, | |
| | | |cascade |incr HR, confusion, collapse | |
| | | |Disruption of cellular |40-50%: incr HR, SOB, syncope | |
| | | |oxidative processes |50-60%: coma, seizures, Cheyne-Stokes | |
| | | | |breathing, arrhythmia | |
| | | | |70-80%: CV and RS failure, death | |
|Iron | |Tablets |Direct corrosive GI effects (|Phase 1: 0-3hrs; GI symptoms ( may cause |Treat hypoV shock |
| | | |hypoV |hypoV shock |WBI if >60mg/kg until clear |
| | | |Mitochondrial dysfunction, |Phase 2: 3-12hrs; quiescent |rectal effluent |
| | | |venoD, 3rd spacing, direct |Phase 3: 12-48hrs; systemic (CV collapse, |Desferrioxamine |
| | | |myocardial damage, severe |AGMA, renal failure, DIC, CNS symptoms) | |
| | | |metabolic acidosis |Phase 4: 2-5/7; rare; hepatic failure | |
| | | | |Phase 5: 2/52; strictures | |
|Lithium | |Tablets |Renal excretion |Acute: GI Sx, may cause hypoV shock; CNS Sx |Charcoal – no |
| | | |HypoNa ( more reabsorption of|if delayed presentation or ARF |GI decontamination if acute OD |
| | | |Li with Na |Chronic: CNS Sx |of SR medication |
| | | |Decr GFR (NSAIDs, sepsis, |Grade 1: 3.5; seizures, coma, myoclonus, | |
| | | | |paralysis | |
|Arsenic | |Pesticides |Interferes with Embden |Acute: GI Sx; MOF; garlic odour; |WBI |
| | |Contaminated food /|Meyerhof pathway |hypersalivation; ARDS; CV collapse |Charcaol – no |
| | |water | |Chronic: Mee’s lines, desquamating rash, |Chelation therapy |
| | | | |mucosal irritation, RTA, peri neuropathy, CNS| |
| | | | |Sx | |
|Lead | |Petrol |Interferes with enzyme |Acute: GI Sx, CNS Sx (cerebral oedema, |Chelation therapy |
| | |Paint |systems, NT’s, haem |encephalopathy, seizures, coma), haemolytic |WBI |
| | |Metallic object |biosynthesis |anaemia, hepatitis, gout |Retrieval of FB’s |
| | |(eg. bullet) | |Chronic: vague multisystem disorder (GI, | |
| | | | |weakness, weight loss, personality and |If encephalopathy: mannitol and|
| | | | |attention change); peri neuropathy, |dexamethasone |
| | | | |nephropathy, decr fertility, constipation | |
|Mercury | |Elemental: | |Elemental: inhaled well; fever, chills, SOB, |Decontamination |
| | |barometers, dental | |metallic taste, stomatitis, confusion, |Gastric lavage and PEG WBI |
| | |amalgams | |lethargy, V+H ( interstitial pneumonitis |Charcoal – yes |
| | |Inorganic: | |Inorganic: GI (grey MM, metallic taste, |Chelation therapy |
| | |batteries, | |stomatitis, loose teeth, N+V+D+AP, | |
| | |industrial | |haematemesis), CV (incr HR, HTN), skin (hair | |
| | |Organic: food | |loss, red palms and soles, pruritis) | |
| | | | |Organic: GI; SOB; NS (may be delayed / | |
| | | | |permanent) | |
ENVIRONMENTAL DRUGS
ANTIDOTES
Cyprohepatadine Serotonin syndrome
MOA: competitive histamine and serotonin antagonist; anticholinergic properties
Indications: mild-mod SS (not useful in severe SS)
Dose: 8mg PO (child >7yrs: 4mg) TDS for 24hrs
End points: resolution of Sx
CI: acute asthma, closed angle glaucoma, GU obstruction (incr BPH)
Bromocriptine Neuroleptic malignant syndrome
Dose: 2.5-10mg PO TDS
Dantrolene Malignant hyperthermia
MOA: inhibits Ca release from SR
Dose: 1-2mg/kg IV ( rpt to max 10mg/kg/24hrs
Atropine Organophosphate poisoning
MOA: competitive muscarinic antagonist; SM relaxant; does not act at nicotinic receptors
Peak effect: 4 mins after IV injection
Metabolism: 50% hepatic
Excretion: 50% unchanged in urine
CI’s: closed angle glaucoma, GI/GU obstruction
SE’s: anti-cholinergic symptoms (delirium, incr HR, mydriasis, urinary retention)
Organophosphate Poisoning
Adult: 1.2mg IV ( double dose Q2-3minly ( continue until drying of secretions
Child: 0.05mg/kg IV
Very large doses will be required – need to procure sufficient stocks
Pralidoxime Organophosphate poisoning
MOA: reactivates AChesterase by binding OP; only effective if given before ageing so give early; reverses nictonic and muscarinic effects
Indications: severely symptomatic with definite/suspected poisoning that has not responded to atropine
Onset: 10-40mins (with improvement of muscle strength)
Dose: 1 – 2g in 100ml N saline IV over 15mins (child: 25-50mg/kg) ( 0.5-1g/hr (child: 10-20mg/kg/hr) infusion for 24-48hrs
End Point: plasma cholinesterase >10% (do levels before inf stopped and then repeat at 4-6hrs)
SE: mild: N+V+H, dizziness, blurred vision, drowsiness
Hydroxycobalamin Cyanide poisoning (first line)
MOA: forms stable compound with cyanide that is excreted in urine
Indication: known/suspected cyanide poisoning with serious clinical effects (altered LOC, seizures, hypoT, significant lactic acidosis); if failure to improve, consider alternative diagnosis
Dose: 2.5g in 100ml N saline IV over 15mins, repeated (child: 50-70mg/kg) ( repeat Q15mins if no improvement
End Point: improved LOC, haemodynamic stability, improved metabolic acidosis
SE’s: falsely elevates ABG COHb levels; falsely elevated bil; minor HTN, incr/decr HR; orange/red discolouration of skin, MM and urine for 12-48hrs
Pros: safe: less anaphylaxis; relatively benign if administered and not cyanide poisoned
Cons: expensive
Di Cobalt EDTA Cyanide poisoning
MOA: forms complexes with cyanide; higher affinity for cyanide than MetHb or cytochrome oxidase; compound formed is less toxic than MetHb
Indication: unequivocal cyanide poisoning
Dose: 300mg (child: 7.5mg/kg) in 20ml dextrose IV over 1-5mins ( repeat Q5min if no response
End point: improved LOC; haemodynamic stability; improved metabolic acidosis
CI: suspected cyanide poisoning
Cons: common and severe SE’s: hypoT, V, incr HR, anaphlyaxis, airway oedema, seizures, CP, SOB; toxic if no cyanide
Amyl Nitrite Cyanide poisoning
MOA: forms MetHb that can bind cyanide; clinical improvement in 5mins
Dose: inhalaed
Na nitrite: 300mg (child: 10mg/kg) over 2-3mins
CI: CO poisoning (ie. Smoke inhalation)
Sodium Thiosulphate Cyanide poisoning
MOA: speeds up metabolism of cyanide
Indication: reasonable suspicion of cyanide poisoning, after hydroxycobalamin given
Dose: 12.5g (child: 400mg/kg) IV over 10mins ( repeat Q30min if no response
End Point: improved LOC; haemodynamic stability; improved metabolic acidosis
Pros: few SE’s: hypoT, N+H+AP; useful in doubtful cases of cyanide poisoning with smoke exposure
Methylene Blue Meth-Hb
MOA: encourages metabolism of Met-Hb by NADPH metHb reductase by acting as cofactor
Indications: if O2 delivery compromised
Dose: 1 - 2mg/kg IV (child: 0.3-0.5mg/kg) over 5mins ( should show improvement over 30-60mins ( repeat 1mg/kg if still high Met-Hb at 1hr
SE: SOB, restlessness, N+V, trauma, apprehension, haemolytic anaemia; too high doses ( decreased effect
Cons: not as effective if G6PD def
Desferrioxamine Fe OD
MOA: binds free Fe (but cannot bind intracellular Fe) to form ferrioxamine ( excreted renally; cardiac monitoring mandatory
Indications: severe toxicity (severe GI Sx, shock, AGMA, altered LOC); serum Fe > TIBC (level >90mcmol/L at 4-6hrs); chronic Fe overload
Dose: 5-15mg/kg/hr IV up to 6g in 24hrs; reduce infusion rate if hypoT occurs; can got at max 40mg/kg/hr in life-threatening toxicity if BP allows
End Points: resolution of symptoms, serum Fe normal, normalization of AGMA
SE: incr infections with Fe dependent MO’s (eg. yersinia, PCP, staph aureus); hypoT (decr infusion rate); ARDS (do not continue >24hrs); toxic retinopathy
Succimer Lead OD (mild-mod)
MOA: chelator ( complexes excreted in urine
Indications: lead – symptomatic; asymptomatic but lead >60mcg/dL (>45 in paeds)
Mercury, arsenic, bismuth, copper
Dose: 10mg/kg PO TDS for 5/7 ( 10mg/kg BD for 14/7; further course if blood levels rebound
CI: ongoing heavy metal exposure
SE: few: GI upset, transient incr LFT’s, reversible neutropenia
Cons: may be difficult to obtain
Dimercaprol (BAL) Lead + inorganic mercury OD (severe)
MOA: chelator ( excreted in urine
Indications: severe lead and inorganic mercury poisoning
Dose: encephalopathy: 4mg/kg IM Q4hrly for 5/7
Severe Sx but not encephalopathy: 3mg/kg IM Q4hrly for 48hrs ( BD for 7-
10/7
SE: very high incidence of SE’s; nephrotoxicity (alkalinize urine before commencing); pain and abscess at injection site; fever, myalgia, CP, HTN, incr HR, H+N+V, peri paraesthesia, lacrimation, conjunctivitis, salivation
CI: peanut allergy; G6PD def; Fe supplementation therapy
Cons: difficult to obtain
Sodium Calcium Edetate (EDTA) Lead OD (severe)
MOA: chelator ( excreted in urine
Indications: lead encephalopathy; severely symptomatic lead poisoning; lead >70mcg/dL)
Dose: encephalopathy: 50-75mg/kg (max 2g; max 1g in children) in 500ml N saline
over 24hrs; start 4 hours after 1st dose of dimercaprol; continue for 5/7
severe Sx but not encephalopathy: 25-50mg/kg in 500ml N saline over 24hrs;
start 4 hours after 1st dose of dimercaprol; continue for 5/7
….then stop for 2-4/7 to allow redistribution of lead ( consider further 5/7
course. Continue until clinically stable, then switch to succimer.
SE: local pain and thrombophlebitis; malaise, fatigue, thirst, chills, fever, myalgia, dermatitis, H, anorexia, urinary f, lacrimation, hypoT, ECG changes, deranged LFT’s and INR; nephrotoxicity (proteinuria, microscopic haematuria; reversible; ensure hydration and UO 1-2ml/kg/hr); never given as sole therapy when levels >70 as can cause redistribution of lead to CNS; hyperCa
CI: anuria
ANTIVENOMS
Tick Antivenom
Dose: 1000iu slow IV infusion over 15-30mins; dilute 1:10 in crystalloid
Redback Antivenom
Indications: severe spreading / regional pain; systemic signs (eg. sweating, HTN, N); localized symptoms not improving with general measures
Dose: 2 ampoules (=1000iu) IM ( rpt @2hrs if ongoing symptoms
SE: allergy in ................
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