Chemical Burns
Epidemiology
Pathophysiology
Account for 5-10% burn centre admissions
Cement (contains Ca oxide) most common chemical burn in Australia
Acids: coagulative necrosis  leathery eschar limiting penetration, immediate damage
Eg. Sulphuric acid (battery acid, drain cleaners), HCl ( NAGMA, severe GI inj, MOF), HFl (car wheel cleaner, rust remover, glass etching; see below),
HNO3, acetic acid
HFl acid: weak acid, penetrates tissues well causing liquefactive necrosis, very toxic; damage caused by direct H cellular damage and free Fl ions 
binds to intracellular proteins / Ca / Mg, interferes with cellular resp / Na,K,ATPase, incr K permeability  depolarisation of nerve endings, dec Ca,
efflux of K, severe metabolic acidosis; risk if high conc or >1% surface area (3-4% SA can cause systemic toxicity and death)
In eye: cause protein precipitates (limit further penetration)  ground glass cornea
In GI: oesophagus relatively resistant, most inj in stomach
Alkali: liquefactive necrosis, saponification of lipids  deeper tissue penetration, soft brown gelatinous eschar; incr systemic involvement; may have
delayed onset Sx
eg. Limes, ammonium, lithium, barium, caustic soda, airbag burns, NaOH (drain cleaner, dishwaster, over cleaner, button batteries), KOH (button
batteries), LiOH (batteries, photographic developers), CaOH (lime, cement), elemental Na, H2O2 (GI corrosion if >10% conc, cerebral gas embolism
if >30% conc)
In eye: rapid penetrating into anterior chamber (which can continue for days)  severe chemosis, corneal opacification, blanched conjunctiva,
venous damage ( glaucoma); need urgent eye review; major inj = >1/3 epithelial defect + hazy cornea
In GI: GI toxicity can occur in absence of oropharyngeal burns (up to 40% with normal exam); oral inj if crystals, oesophageal and gastric in liquids;
oedema max in 48hrs  necrosis in 7-10/7  strictures in 3/52
In RS: pul oedema
Specific agents
Severity of inj: Toxicity more likely if pH <2 / >12, but not only related to pH; dependent on: conc, quantity, duration of contact (continue to damage
tissue until removed), extent of penetration of skin, mechanism of toxicity, liquid vs solid, body site, integirty of skin
Grade 1: capillary dilation and hyperaemia
Grade 2: vesicles / bullae
Grade 3: skin necrosis
HFl acid: in stain remover, glass etching, computer chip making, electronics and chemical industries, rust removers; <10% conc commerical, >40%
industrial; causes acid reaction as above  but later 2Y necrosis due to fluoride ions with liquefactive necrosis, and complexes Ca and Mg  insoluble
salts causing cell destruction and severe pain
Little pain initially (unless >50% conc, in which case immediate pain and tissue destruction; even if weak solution, will get delayed onset destruction –
>20%  burn apparent in 7eral hrs, <20%  burn apparent after up to 24hrs)
 gradual onset delayed severe deep unremitting pain (out of proportion with external signs; delayed up to 24hrs <10% conc, 2-4hrs 20-40% conc,
within an hour >40% conc), erythema + blistering (may be mild despite severe toxicity)  blanching / vesicles / tissue necrosis / silver-grey
appearance; lasts 24-36hrs
>3-5% SA
Risk of systemic involvement if
hypoCa  coagulopathy, tetany, carpopedal spasm, hyperreflexia
hypoMg  QTc prolonged, arrhythmias
hyperK
metabolic acidosis
INH  immediate onset mucosal irritation  delayed onset SOB, cough, wheeze, NCPO, ARDS
PO  <20% minimally damaging; V, throat pain, dysphagia, AP; systemic fluorosis more common than with skin exposure, may occur in 30min-6hrs
Investigation: decr Ca / Mg, incr K (test Q2h; due to altered cell permeability); ABG (if head/neck exposure, severe, inhalational, >50% conc); CXR
(if head/neck exposure, inhalation); ECG (if electrolyte abnormality; long QTc, arrhythmias, do serials); endoscopy (if PO)
>15mm
Assessment
Mng
Button batteries: damage from direct p necrosis and alkali leak; <15mm rarely lodge;
may lodge in oesophagus  mucosal burns,
strictures, oesophageal perf (can occur <6hrs), T-O fistula, haem
Symptoms: usually delayed; dysphagia, pain, cough, irritability, resp distress
Investigations: AP CXR and AXR (double density sign on AP, stepped appearance on lateral)
Mng: in oesophagus: endoscopy within 6hrs
In stomach: if <15mm  discharge with advice Re: Sx
if >15mm  rpt XR in 48hrs  if not beyond pylorus, endoscopy
Symptoms: immedate airway difficulty: stridor, SOB, dysphonia, throat pain
GI inj: stridor, drooling, vomiting; Sx correlate poorly with extent of GI inj
Oesophageal perf / mediastinitis: CP, SOB, fever, subC emphysema, pleural rub
Investigation: indications for endoscopy: persistent vomiting, oral burns, drooling, AP
Skin exposure: Protection of medical personell
 brush away dry bits (check under nails, skin folds, hair)  remove clothing
 immediate dilution with water for at least 30mins (use pH paper to see when can stop; exception is carbolic acids where may incr penetration
(with elemental metals need copious +++++)
 Debride and clean blisters (may contain contaminated fluid)
ADT
Consider systemic toxicity; review all digital exposures at 24hrs
Admit if: >15% superficial burn; all partial and full thickness burns
GI exposure: do NOT induce vomiting; analgesia; no NGT until after endoscopy; Abx if perf; ADT; observe at least 5 hrs  discharge if Sx free;
charcoal CI’ed; milk lavage (dissipates heat of neutralisation) or give 250ml water to drink; steroids if 2nd deg circumferential burns on
endoscopy; gastroscopy if symptomatic, at 12-24hrs to determine extent of injury
Eye exposure: LA eye drops; remove particulate matter; irrigate at least 30mins with N saline; test for neutrality with litmus paper and continue until
neutral (pH 7.4); cyclopentolate; chloramphenicol ointment; pad; top steroids may prevent further damage; 10% citrate + ascorbate drops Q2h and 1g
PO ascorbic acid OD prevents cornea melting and has improved prognosis
Indications for immediate referral: altered VA; corneal haziness; injection of limbal vessels
HFl acid: consider nail removal (SAQ said leave nails in place); cardiac monitor at least 12hrs if extensive / PO
Systemic poisoning: give Ca and Mg before decr levels seen: 60ml (0.1-0.6ml/kg in child) 10% Ca Glu IV  rpt Q5min until ROSC
MgSO4 10mmol IV
hyperK and arrhythmias will be resistant to standard trt
haemodialysis may be needed
IV 100mmol NaHCO3 if severe
Topical: Ca Glu 2.5% gel (mix 10ml 10% Ca Glu made up to 40ml with KY) Q15min for 1hr  6x per day for 3-4/7; not good if high
conc, only binds to superficial Fl
Oral: Ca Glu PO/NG if ingestion (1g Ca for every 1g fluoride solution ingested); GI decontamination, Ca/Mg containing antacids, drink milk
Local injection: 0.5-1ml/cm2 Ca Glu 10% SC - use only if small, localised exposure; may be v painful (due to incr osmolarity), only limited
amount can be given, more tissue damage possible if Ca not bound to Fl, vascular compromise if too much injected, can’t do in fingers, hands, feet
IV regional: 10ml 10% Ca Glu (+ 5000iu heparin IV) made up to 40ml in 5% dex  release tourniquet after 20mins or earlier if pain gone;
best for forearm and hand; less invasive, less SE, quick, easy, no IAL needed, 60% success rate, better for low conc
IA regional: gold standard; 10ml 10% Ca Glu made up to 40ml in 5% dex over 4hrs; radial artery if radial distribution, brachial artery if
ulnar; may need 2-3 infusions; may cause arterial spasm / thrombosis, haematoma, arterial dissection; requires IAL
Neb: 1.5ml 10% Ca Glu in N saline; use if inhalational exposure
Prognosis
Eye: LA eye drop, analgesia, water irrigation, 1% Ca Glu irrigation, consider chloramphenicol / mydriatics, ADT
Usually smaller than thermal burns, with lower mortality rate
Notes from: Dunn, Cameron, TinTin
Hydrogen Peroxide:
Ingestion: N+V, haematemesis, foaming at mouth, corrosive injury; incr HR, confusion, coma, seizures, sudden death with large
ingestions of >10% conc; gastric distension and belching; progressive neuro disturbance if cerebral O2 gas embolism
Inhalation: cough, SOB; high conc  shock, coma, seizures, pul oedema
Skin: inflamm, blistering, skin necrosis, subC emphysema
Eye: red eye, corneal and conjunctival bubbles, ulceration
May need CXR, AXR, CT head, endoscopy; hyperbaric O2 if gas embolism; NGT may help gastric distension; if >10% conc needs close
monitoring
Organophosphates
Acute intoxication:
Muscarinic
(paraS)
Nicotinic
CNS
RS
CV
Diarrhoea
+ decr HR, hypoT
Urination
Miosis (often occurs late)
Bronchorrhoea
Bronchospasm
Emesis
Lacrimation
Salivation
Fasciculation, tremor, weakness, resp muscle paralysis
Incr HR, HTN
Agitation, coma, seizures
Chemical pneumonitis; non-cardiogenic pul oedema
Long QT, STE, T wave inv, prolonged PR, arrhythmia
Carbolic acid (phenol): irrigate with polyethylene glycol + methylated spirits / isopropyl alcohol rinse; decreases extent of cutaneous
corrosion and decreases systemic toxicity; IV haemolysis, CV / pul / CNS toxicity, MetHb
Chromic acid: 10% burn can be fatal; systemic toxicity includes conjunctivitis, lacrimation, liver and renal failure, GI bleeding,
coagulopathy, CNS disturbance; excision may prevent systemic effects
Formic acid: systemic effects include decr RR, metabolic acidosis, hepatic necrosis, nephrotoxicity
HCl and sulphuric acids: found in toilet cleaner, bleach, fertilizer manufacturers, car battery fluid
Metals: water irrigation contraindicated if fragments embedded in skin as cause explosive exothermic reaction that can cause tissue injury;
cover with mineral oil then wipe away or excise
Phosphorus: hepatic necrosis, nephrotoxicity
Cresol: methaemoglobinaemia, massive haemolysis, MOF
Gasoline: severe pul, CV, neuro, renal and hepatic complications
Na/K nitrate: severe methaemoglobinaemia, refractory cyanosis