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 ................
................

In order to avoid copyright disputes, this page is only a partial summary.

Google Online Preview   Download