ED - Burns And Poisoning Flashcards
Burns
Pathophysiology
Depths of a Burn
Assessing the Extent of a Burn
Complications
1.) Pathophysiology
- necrosis: thermal burn = coagulative, chemical = liquefactive (alkaline burns worse than acid)
- healing: damage to the epidermis is temporary whilst to the dermis is permanent so will heal with a scar
- scarring: epidermis healing around a damaged dermis, early scars are vascular and pink and become avascular after roughly a year
- loss of capillary membrane integrity can lead to extravasation of fluids from the burn site causing hypovolaemic shock (up to 48h after injury)
2.) Depths of a Burn
- superficial epidermal (1°): only damages the epidermis, appears red and painful, examples: flash burns, sunburns, should heal on its own
- superficial partial thickness (2°): damages up to the superficial dermis, appears pale pink, painful and blistered, will heal with a scar
- deep partial thickness (2°): damages up to the deep dermis, typically appears white but may have patches of non-blanching erythema, may have some reduced sensation, will need debridement
- full thickness (3°): affects all layers inc nerve endings, can be white/brown/black in colour, no blisters, no pain (there will be surrounding 1° and 2° burns that will be painful
4.) Assessing the Extent of a Burn - only worried about 2° and 3° burns
- estimate w/ palmar surface is ≈1% of total body surface area (TBSA)
- Rule of Nines: H+N = 9%, R+L arm = 9% each, anterior + posterior leg = 9% each, anterior + posterior chest = 9% each, anterior + posterior abdomen = 9% each
- Lund and Browder chart: the most accurate method
- a large burn is considered as >10% TBSA in kids, >15% in adults
4.) Complications
- circumferential burns causes functional difficulties as the skin cannot expand E.g. around the chest or wrist etc.
- contraction of burns (due to healing with fibroblasts): burns in flexures can prevent extension of the joint e.g. neck, eyelids, elbows - requires removal and fixation with a graft
- peripheral oedema secondary to hypoalbuminemia 2 weeks post-op
- mortality = Age + %surface area affected
Management of Burns
Immediate First-Aid/Management
Referral Criteria to Secondary Care
Management of Severe Burns
Eschar
1.) Immediate First-Aid/Management - first step is always ABC
- thermal burns: irrigate the burn with cool (not iced) water for 10-20 mins, cover the burn using layered (not wrapped) cling film
- electrical burn: switch off power supply, remove person from source
- chemical burn: brush any powder off then irrigate with water,
DO NOT attempt to neutralise the chemical
- review referral criteria to ensure can be managed in primary care
- superficial epidermal: symptomatic relief - analgesia, emollients etc
- superficial dermal: cleanse wound, leave blister intact, non-adherent dressing, avoid topical creams, review in 24hrs, will heal with a scar
2.) Referral Criteria to Secondary Care
- all deep dermal and full-thickness burns
- superficial dermal burns >3% TBSA in adults, or >2% TBSA in children
- superficial dermal burns involving the face, hands, feet, perineum, genitalia, flexure or circumferential burns of the limbs, torso, or neck
- any electrical or chemical burn, any inhalation injury
- suspicion of non-accidental injury
3.) Management of Severe Burns
- A: early intubation should be considered e.g. if deep burns to the face or neck, blisters or oedema of the oropharynx, stridor etc
- B: beware of eschar burns that can affect chest expansion
- C: IV fluids for large burns, volume over 24hrs= TBSA% x weight x 4, 50% given in first 8hrs, the rest given over the next 16hrs
- D&E: remove clothing (must keep pt warm), remove any jewellery
- complex burns may require excision and skin grafting (provide keratinocytes), AVOID primary closure due to high risk of infection
- blood transfusion: RBC haemolysis in large burns -> ↓Hb after 24hrs
- DO NOT need prophylactic antibiotics or topic abx
4.) Eschar - tough leathery tissue remaining after a full-thickness burn, there is reduced elasticity –> constriction –> impaired circulation
- can cause compartment syndrome in circumferential burns of a limb
- severe torso eschar burns can also impede respiration
- an escharotomy is a procedure used to divide eschar tissue in in circumferential burns of a limb and severe torso eschar burns
Assessment of Suspected Poisoning
History Taking
General Examination
Deliberate Self Poisoning
1.) History Taking
- what substance was taken, the amount, how it was taken (PO, INH, IV/IM), if any other medicines have been taken, and alcohol use
- when it was taken: exact timings of ingestion or contact
- why?: accidental, deliberate or a therapeutic error
- risk of repetition: require psychosocial assessment if self-harmed
- age, weight, sex, PMH, DH, SH
2.) General Examination - A-E obviously
- general signs: track marks (IVDU), alcohol or solvents on the breath, stigmata of liver disease (alcohol dependence), atypical bruising or fractures may raise safeguarding concerns
- neuro: assess pupils and eye movements, acute dystonic movements (antidopaminergics), hypertonia, hyperreflexia, and extensor plantar response (TCA poisoning)
- visual acuity and visual fields: may be affected with some drugs e.g. quinine poisoning
3.) Deliberate Self Poisoning - if in GP, immediately refer to A+E
- preliminary psychosocial assessment: mental capacity, insight, their level of distress and the possible presence of mental illness
- assess risk of further self-harm or suicide
- assess safeguarding concerns: consideration of risks to the person who has self-harmed, any children or adults in the person’s care and to other family members or significant others
General Management of Drug Poisoning
Sources of Information
Investigations
Types of Management
1.) Sources of Information
- TOXBASE: toxicology database, gives information about diagnosis, treatment and management of drugs, household products, and industrial and agricultural chemicals.
- National Poisons Information Service (NPIS): for severe/complex poisoning, significant comorbidities, uncertain after using TOXBASE, unknown poison
- UK Teratology Information Service (UKTIS) for advice if the person is pregnant
2.) Investigations
- toxicological investigations: blood and urine tests
- other bloods: FBC, U+Es, LFTs, clotting, glucose (exclude hypo for many presentations), ABG or VBG
- ECG and imaging investigations
- plasma or serum monitoring: used for specific drugs/poisons e.g. paracetamol, aspirin, alcohol, lithium, digoxin, methotrexate, carbamazepine, sodium valproate, iron, theophylline
3.) Types of Management
- antidotes (if available): e.g. acetylcysteine (paracetamol), flumazenil (benzos), naloxone (opiates), glucagon (insulin, CCBs, beta-blockers), protamine sulphate (heparin), atropine (organophosphates), fomepizole (ethylene glycol), sodium calcium edetate (lead)
- prevention of absorption: use of activated charcoal which can bind to the poison, the sooner given, the more effective, important for drugs toxic in small amounts
- active elimination (limited no of drugs): haemodialysis, repeated doses of activated charcoal, urine alkalinisation for salicylate poisoning
- removal from the GI tract: gastric lavage (rare, only if life-threatening), whole bowel irrigation may be used if there has been poisoning with certain sustained-release or enteric-coated medicines, or in severe poisoning with iron or lithium salts
Paracetamol Poisoning/Overdose
Clinical Features
Investigations
Management w/ Acetylcysteine
Management w/ Activated Charcoal
1.) Clinical Features - often asymptomatic, until 24-72 hours after when acute liver failure occurs, may have initial N+V that should settle within the first 24hrs
- hepatic necrosis: jaundice, RUQ pain, renal failure, oliguria, hypoglycaemia, metabolic acidosis, encephalopathy
- may present with ↓LOC, respiratory depression, or coma, if they have taken paracetamol with an opioid or alcohol
- dosage required for overdose: >70mg/kg OR 4-6g OR 12 tablets of paracetamol in <1 hour OR >150mg/kg OR ≈24 tablets within 2hrs
2.) Investigations
- plasma-paracetamol concentration: only accurate if >4 hours after ingestion
- LFT’s, U+E’s, glucose, clotting (inc PT and INR), ABG (metabolic acidosis)
3.) Management w/ Acetylcysteine - conjugation of circulating paracetamol
- use of N-acetylcysteine often depends on the time ingested, dose, treatment line on [paracetamol] graph, signs of hepatotoxicity
- N-acetylcysteine works best when given <12hrs of ingestion, it is often infused with 5% dextrose over 1 hour, usually continued for 24hrs
- Mx if <8hrs: usage depends on treatment line
- Mx if 8-24hrs: depends on the dose ingested: >150mg/kg OR >12g
- Mx if >24hrs: signs of hepatotoxicity: clearly jaundiced or have hepatic tenderness, ↑ALT, should also be seeking specialist advice
- give N-acetylcysteine in a staggered overdose (all tablets not taken within one hour) regardless of the treatment line on the graph
4.) Management w/ Activated Charcoal - only used if:
- >12g (>150mg/kg) ingested
- within 1 hour of ingestion
Opioid Overdose
Clinical Features
Investigations
Management w/ Naloxone
1.) Clinical Features
- classical clinical triad: reduced consciousness, respiratory depression, miosis
- other potential sx : N+V, constipation, pruritus, tiredness/drowsiness, confusion
- A-E: airway obstruction (↓consciousness), resp depression (RR<12, hypoxia), bradycardia, ‘pinpoint pupils’ ↓GCS, track marks, drug paraphernalia around them
- demographic: often heroin users who have previously gone ‘cold turkey’ and then return taking their usual dose which ends up being fatal
2.) Investigations
- bedside: vital signs, ABG, blood glucose (CBG)
- bloods: FBC, U+Es, LFTs, paracetamol levels (exclude mixed overdose)
- imaging: CT head if ↓consciousness doesn’t improve with Naloxone
3.) Management w/ Naloxone - competitive opioid receptor antagonist
- opioid reversal is almost instant but the effects can be short-lived due to a short half-life (60-90mins) therefore repeat boluses and close extended monitoring are required until the opiates in their system have been cleared.
- commonly administered in repeat IV boluses (other routes inc IM/SC/PO/INH)
- can give simultaneous IM naloxone in IVDUs due to high risk of recurrence
- may use a naloxone infusion in those with high opioid load (e.g. large overdose)
- naloxone can be used as a diagnostic tool in the unconscious patient where the cause of loss of consciousness is unclear
Salicylate Overdose
Pathophysiology
Clinical Features
Investigations
Management
1.) Pathophysiology - directly irritate the gastric lining
- types: ASPIRIN, NSAIDs, selected antacids and antidiarrheal medications, oil of wintergreen (mint smelling fragrance used in many products)
- ototoxicity: vasoconstriction causing reduced cochlear blood flow
- mixed respiratory alkalosis (stimulate medulla to cause hyperventilation) followed by metabolic acidosis (↑anaerobic respiration –> lactic acidosis)
2.) Clinical Features
- mild (<300mg/kg): N+V, epigastric pain, lethargy, dizziness, tinnitus
- mod: (300-700500mg/kg): fever, sweating, SOB, dehydration, confusion, deafness
- severe (>700mg/kg): pulmonary oedema, convulsions, metabolic acidosis
- signs in mod-severe toxicity: hyperventilation and ↑RR, pulmonary oedema, warm peripheries and bounding pulse, cardiac arrhythmia
3.) Investigations
- plasma-salicylate concentration: should be measured, but does not indicate the severity of poisoning, most accurate >4hrs after ingestion, repeated 2hrly
- severity is assessed using urine pH and blood pH (ABG), this is checked hourly:
stage 1: b-pH >7.4 + u-pH >6, stage 2: b-pH >7.4 + u-pH <6, 3: b-pH <7.4 + u-pH <6
- bloods: U+Es (hypokalaemia is common), FBCs, CRP, LFTs, clotting
- other: CBG (hyper/hypoglycaemia), paracetamol conc (exclude mixed overdose)
- ECG: monitor QRS duration and QT interval for evidence of prolongation
4.) Management - admit to ITU in moderate to severe toxicity
- aggressive IV rehydration (consider adding glucose because intracellular glucose is often depleted even if blood glucose remains normal, treat hypokalaemia)
- activated charcoal (if >125mg/Kg ingested <1hr ag) OR
OR gastric lavage (if >500mg/Kg ingested <1hr ago)
- urine alkalinisation (increases excretion of aspirin): give IV sodium bicarbonate (if >500mg/Kg ingested) to maintain urine pH between 7-5-8.5
- haemodialysis can be considered in severe cases: plasma salicylate >700mg/Kg, renal failure, heart failure, coma, convulsions, pH <7.2, non-resolution of CNS symptoms, despite correction of acidosis
- complications: ARDs, seizures, drug-induced hepatitis, cardiac arrest
Other Types of Overdose
Benzodiazepines
Tricyclic Antidepressants
Other (Beta-Blockers, Sympathomimetics, Carbon Monoxide)
1.) Benzodiazepines
- sx: agitation, euphoria, blurred vision, slurred speech, ataxia, slate-grey cyanosis
- signs: dilated pupils, reduced consciousness, hypothermia (cold)
- Ix: U+Es, CK (benzo OD can cause rhabdomyolysis), VBG (lactate), FBC, CRP, clotting, toxicology screen (?mixed overdose), ECG
- Mx: IV flumazenil (GABA antagonist) only used in severe CNS depression (needing ventilation) WITHOUT mixed overdose or benzo dependence (avoid withdrawal) to reverse sedative effects only, short half-life so may need multiple doses
2.) Tricyclic Antidepressants - amitriptyline, clomipramine, doxepin
- clinical manifestations of overdose become apparent within six hours of ingestion
- key clinical features include signs of anticholinergic toxicity and NaC blockade
- sx: SLUDGE sx, confusion and hallucinations, palpitations,
- signs:, resp depression, ↓BP, arrhythmias, ↓GCS, convulsions, hyperthermia
- Ix: ECG (wide QRS, prolonged QTc, VT/VF), CBG, ABG (mixed acidosis), OD bloods inc Mg and bone profile to correct any electrolyte disturbances
- Mx: activated charcoal (if w/in 1hr of ingestion), sodium bicarbonate in arrhythmia and acidosis to prevent progression to ventricular arrhythmias
3.) Other
- beta-blockers: treat w/ glucagon (tx hypocalcaemia if present)
- sympathomimetics e.g. cocaine, amphetamines: sx inc ↑HR, dilated pupils, euphoria, formication (crawling insects), tremor arrhythmias, convulsions. Tx w/ benzos
- ethylene glycol (anti-freeze) sx: ↓GCS, confusion, ataxia, slurring speech, Ix: metabolic acidosis w/ ↑anion gap and ↑osmolar gap, AKI, Tx: fomepizole
- carbon monoxide: sx inc headache, ↑HR, pulmonary oedema, drunkenness, shock , ↓reflexes, met acidosis, flushed cherry pink skin. Tx w/ hyperbaric oxygen
