ED - Study Points Flashcards
Outline a general approach to the poisoned patient (8)
General approach to the poisoned patient
1. Resuscitation
2. Risk Assessment
3. Supportive Care
4. Investigations
5. Decontamination
6. Enhanced elimination
7. Antidotes
8. Disposition
What is considered an Acute Single Ingestion Overdose of Paracetamol for:
- Adults and children over 6 years of age?
- Children (aged 0-6 years)?
Risk assessment for
paracetamol - Acute Single Ingestion
Adults and children over 6 years of age:
- >200mg/kg or 10g (whichever is lower) over a period of less than 8 hours
- >500mg/kg - is considered a massive ingestion. Note modification of NAC dose
Children (aged 0-6 years):
- >200mg/kg or more over a period
of less than 8 hours
Outline the metabolism of Paracetamol & the treatment given for overdose?
Paracetamol Toxicity - Case 1
C. Offer activated charcoal, check paracetamol level at 4hrs and plot on nomogram
Paracetamol Toxicity - Case 2
D. Check paracetamol level at 4hrs and plot on nomogram
Paracetamol Toxicity - Case 3
B. Start NAC, check LFTs and paracetamol level and plot on nomogram
Paracetamol Toxicity - Case 4
A. Start NAC, Check FBE, EUC, LFTs, coags, VBG, paracetamol level
Paracetamol Toxicity - Case 5
D. Start NAC, Check LFTs, paracetamol level, start NAC and plot on nomogram (12hrs)
Paracetamol Toxicity - Case 6
D. Intubate, give activated charcoal through NGT, check FBE, EUC, LFTs, coags, VBG, check paracetamol level at 4hrs and plot on nomogram, consider double dose of NAC in last bag
Paracetamol Toxicity - Case 7
- 2nd bag of NAC? Dosing timing?
- Anaphylactoid reaction?
C. Check FBP, U&Es, LFTs, paracetamol level, start NAC, stop only if ALT <50 and paracetamol <10
N-Acetylcysteine - 2 bag NAC
- 1st bag: 200mg/kg over 4 hours
- 2nd bag: 100mg/kg over 16 hours
- NAC (Parvolex) comes in 200mg/ml and they come in 10mL amps. When writing it to stop dosing errors - write number of mLs req (need multiple amps)
Paracetamol Toxicity - Case 8
D. Check paracetamol level at 4hrs and 8hrs, start NAC if either level above line or uptrending
Modified- Release paracetamol: Risk assessment for overdose?
- What are the pathophysiological mechanisms of TCA intoxication?
- Clinical features: 6 Minor? 4 Major?
- Risk of major toxicity dose?
- Anticholinergic effects
- Negative inotropy
- Vasodilatation
- Fast sodium channel blockade
Clinical features
- Minor: Tachycardia, dry mouth, dilated pupils, delirium, ileus, urinary retention
- Major: coma, hypotension, seizures, ventricular arrhythmias
- TCA ingestion > 10-20 mg/kg associated with potentially life-threatening complications
- Onset of severe toxicity usually occurs within 2-4 hours of ingestion (unusual to develop after 6 hours)
- Multiple ECG changes indicative of fast sodium channel blockade
TCA intoxication
- 4 Predictors of major toxicity?
- ECG Changes?
- Risk assessment?
- Management - Resuscitation? (7)
Predictors of major TCA toxicity
1. ECG parameters
2. Glasgow Coma Score
3. Plasma TCA levels
4. Combination of the above
ECG changes occur early
- QRS duration maximal at presentation in 80% of patients
- QRS duration maximal within 3 hours in the other 20% (range 1-9 hours)
- Terminal 40ms axis deviation (R wave aVR) maximal within 5 hours
- QT prolongation in TCA intoxication Torsades de Pointes is very rare in the setting of TCA intoxication
- Sinus tachycardia or QTc prolongation alone are not predictive of major complications or poor outcome in TCA intoxication
Calcium Channel Blockers Toxicology
Burns in the ED
- Aetiology?
- List 8 causes/types of burns.
- Factors determining the severity of the burn?
- Epidemiology: age distribution?
Types/Causes of Burn
2. Scald
2. Flame
3. Contact
4. Electrical
5. Chemical
6. Friction
7. Radiation
8. Frost burns
Factors Determining the Severity of the Burn
1. Mechanism
2. Immediate treatment given.
3. First aid
4. Total Body Surface Area
5. Resuscitation
6. Depth
7. Location of Burn
8. Agent
9. Age
10. Past Medical History
Pathophysiology of Thermal burns?
- Local effects?
- Systemic effects?
Pathophysiology of Non-thermal burns:
- Chemical?
- Electrical?
- Radiation?
Management of Burns
- Minor: Management of the burn area? Wound care? Pain management?
- First aid?
Primary Survey
A. Airway management with C spine control
B. Breathing and ventilation
C. Circulation with haemorrhage control
D. Disability / neurological status
E. Exposure + environmental control
F. Fluid resuscitation
Primary Survey for Burns: AIRWAY
- What are the priorities?
- Inhalation Injury - Classification? (3)
- When should you suspect an inhalation injury? (5)
- 9 Signs of Airway Injury in Burns?
- Management of Burns if Airway Compromised?
Signs of Airway Injury in Burns
1. Singed nasal hair.
2. Carbonaceous sputum or soot in oropharynx
3. Swelling of oropharynx
4. Change in voice – hoarseness.
5. Cough
6. Stridor
7. Dyspnoea
8. Tachypnoea
9. Reduced GCS
Primary Survey for Burns: BREATHING
- General principles of assessment & management?
- Carbon Monoxide Poisoning: presentation? Treatment?
- Cyanide Poisoning: presentation? Treatment?
Primary Survey for Burns: BREATHING
* Examine the chest
* Possible other injuries
* Provide high flow oxygen
* Measure respiratory rate
* Deep Circumferential chest burns
- Do they need an escharotomy?
Primary Survey for Burns: CIRCULATION
- General principles of assessment & management?
- What are Escharotomies?
Eschar = A skin lesion characterized by dried, necrotic skin tissue. Etiologies include burns, infection, gangrene, and pressure ulcers.
Escharotomy = Surgical procedure indicated for circumferential third-degree burns involving the limbs or the thorax with signs of impending vascular or respiratory compromise, respectively. Escharotomy is characterized by an incision of the burnt necrotic tissue to prevent constriction of the skin which may otherwise result in compartment syndrome and impaired movement of the thorax.
Management of Moderate/Severe Burns
- Airway?
- Breathing?
- Circulation?
- Disability?
- Management of the Burn area?
Primary Survey for Burns: DISABILITY
Assess Consciousness
- AVPU
- GCS
Altered consciousness can be sign of:
- Hypoxia
- Hypovolaemia
- CO intoxication
Look at Pupillary Response
Don’t forget Glucose (Paediatrics)
Management of Burns
- 4 Indications for treatment in a special burn unit?
- Wound care?
- Nutritional support?
- Pain management?
- Anxiety management?
- Prophylaxis?
Assessment of burn surface area involvement
- Rule of nines?
- Which chart?
- Palmar method?
- Rule of Nines for adults
- Lund and Browder chart
- Patients’ palm represents ~1% TBSA
What is the Wallace’s rule of nines?
Wallace’s rule of nines
The entire body surface of an adult can be divided into 11 regions that each comprise approximately 9% of total body surface. The external genitalia accounts for the remaining 1%. This rule of thumb is used to quickly estimate the surface area of burns in adult patients.
How does the rule of 9s for burns differ for:
- Infants?
- Toddlers?
- Adults?
Development of regions of the body in relation to total body surface area
Representation of development from infant to toddler to adulthood (according to Wallace rule of nines). The regions of the body that occupy the same percentage of the total body surface area throughout development are indicated in green, whereas regions of the body in which the relative proportion of the total body surface area varies with age are depicted in blue.
Burn Classification by Depth?
Burn classification - Burns are classified according to the depth of the burn.
- 1st-degree burns (superficial burns): only affect superficial layers of the epidermis. The skin is erythematous, dry, and may be swollen, but there is no blistering.
- 2nd-degree burns (partial-thickness burns) also affect the upper (2a; superficial partial-thickness burn) or lower (2b; deep partial-thickness burn) layers of the dermis. The skin blisters (vesicles and bullae) and in deep partial-thickness burns may appear mottled with red/white patches.
- 3rd-degree burns (full-thickness burns) also affect subcutaneous tissue. The skin is black, white, or grey in color and appears dry and leathery.
- 4th-degree burns (deeper-injury burns) also affect deeper structures (muscles, fat, fascia, and bones).
SUPERFICIAL BURNS
- Appearance?
- Capillary Refill?
- Sensation?
- Healing time?
- Scarring?
SUPERFICIAL DERMAL BURNS
- Appearance?
- Capillary Refill?
- Sensation?
- Healing time?
- Scarring?
MID DERMAL BURNS
- Appearance?
- Capillary Refill?
- Sensation?
- Healing time?
- Scarring?
DEEP DERMAL BURNS
- Appearance?
- Capillary Refill?
- Sensation?
- Healing time?
- Scarring?
FULL-THICKNESS BURNS
- Appearance?
- Capillary Refill?
- Sensation?
- Healing time?
- Scarring?
IV fluid resuscitation in burns:
- When to start IV fluid resuscitation in burns: In Adults? In Children 18 months and older? In Children less than 18 months?
- Calculation?
- Which solution & Why?
- Urinary output goals?
WHY HARTMANN’S? = Closest isotonically to the burn fluid that is
being lost.
▪ Sodium chloride 0.6%
▪ Sodium lactate 0.25%
▪ Potassium chloride 0.04%
▪ Calcium chloride 0.027%
- Ultimately any crystalloid fluid will do
- Don’t forget paediatrics need some glucose
OUTPUT
- Insert Urinary Catheter
- Monitor urinary output
▪Aim for 0.5-1ml/kg/hour
▪ADJUST fluids accordingly
▪Inhalation and electrical injury 2ml/kg/hour
Maintenance fluid requirements in burns?
- 82 kg man sustains 50% TBSA flame burn at 2am admitted today to your hospital 8am. How much fluid does he require?
Maintenance Fluid in Burns
Adults
- Approx 2000ml in 24 hours
- Preferably via NG feed to maintain GI function & nutritional demands
Children
- 1st 10kg – 100mls /kg /24hrs
- 2nd 20kg – 50mls /kg /24hrs
- Over 20kg – 20mls /kg /24hrs
- Add dextrose to paediatric maintenance
Burns
- Secondary Survey: History? Assessment?
- Monitoring of Patient?
- 7 Adjuncts?
MONITORING OF BURNS PATIENT
- Pulse
- Blood Pressure (+/- Arterial line)
- (CVP)
- Urine output – aiming for 0.5 ml / kg
- Specific Gravity - 1020
- Electrolytes
- Oxygen saturation if indicated
- Arterial blood gases if indicated
What is Acticoat?
ACTICOAT
- Nanocrystalline impregnated silver mesh, sustained released
- For ALL burns in first 48 hours
- Moisten Acticoat with water
- Can apply Flaminal or Intrasite under Secondary dressing
- wet gauze, jelonet, dry gauze OR Duoderm
Non-Accidental Burns in Children
- 7 Suspicious Features?
Suspicious Features
1. Delay in presentation
2. Incompatible history
3. Inconsistent history
4. Other signs of trauma
5. Pattern of injury
6. Demeanor
7. Interaction
10 Complications of Burns?
Inhalation Injury
- Definition?
- Aetiology?
- Diagnostics?
- Treatment?
- Complications?
- Prognosis?
Postburn Metabolism
- Definition?
- Pathophysiology?
- Clinical features?
- Management?
Management
1. Early excision and grafting
2. Analgesia
3. Nutritional support
4. Anabolic steroids
5. Glycemic control with insulin
6. Beta blockers (e.g., propranolol) to decrease resting metabolism
Toxic Shock Syndrome
- 2 Causes?
Streptococcus pyogenes and Staphylococcus aureus both cause TSS; however, streptococcal TSS and staphylococcal TSS often differ in their etiologies, clinical presentation, laboratory findings, and mortality rates.
Toxic Shock Syndrome
- Epidemiology: Age? Incidence?
- Aetiology?
Epidemiology of Toxic Shock Syndrome
- Incidence: ∼ 0.5–3/100,000
- Age: Invasive GAS infections and subsequent complications are more common in young children and adults > 65 years of age.
Aetiology
- TSS is most commonly caused by toxin-producing strains of Streptococcus pyogenes and Staphylococcus aureus.
Outline the Pathophysiology of Toxic Shock Syndrome.
Clinical Features of Toxic Shock Syndrome
- Onset?
- Prodrome?
- End organ dysfunction?
TSS typically manifests as a prodrome of nonspecific symptoms, followed by hypotension and rapid progression (8–12 hours) to end-organ involvement.
Toxic Shock Syndrome - Treatment
- Approach?
- Haemodynamic resuscitation?
- Management of source(s) of infection?
- Antibiotic therapy?
Treatment - Approach
- Hemodynamic resuscitation as needed
- Identify and manage the source of infection; obtain cultures of the suspected primary site(s) of infection.
- Within 1 hour of presentation; consider IVIG as adjunctive therapy in streptococcal TSS.
- TSS is a reportable disease in the US.
- TSS is a life-threatening emergency that requires early diagnosis and a multidisciplinary approach to management.
Burns
- 10 Referral Criteria for Immediate Transfer?
- Preparation for transfer?
- > 10% TBSA in adults
- > 5% TBSA in children
- Any full thickness burn
- Any circumferential burn
- Respiratory /inhalation burns
- Infected burns
- Electrical burns
- Chemical burns
- Special areas: hands, face, genitalia, feet
- Burns with concurrent injuries/co-morbidities
Envenomation: Snake Bites
- What are the 10 most lethal snakes (LD50) in the world?
- Epidemiology in Australia?
- Who gets bitten?
- 5 principle genera in Australia?
- LD50 = Lethal dose required to kill 50% of rats
- Australia = 1/year or 1/every other year
- Who gets bitten in Australia? = 5 Ts: Tattood, Entoxicated, Trucks, Toothless, etc.
- All venomous snakes in Australia are elapids (front fanged)
- 5 principle genera:
1. Brown
2. Tiger
3. Black
4. Taipan
5. Death Adder
Clinical Envenoming
- Presentation?
- 3 Local effects?
- 5 Systemic effects?
- 4 Major envenoming syndromes?
Clinical Envenoming
Sudden collapse
- Within 1 hour of the bite: Brown (most common), Taipan (uncommon), Tiger (rare)
- Hypotension & LOC
- Local effects: Pain, Swelling, Bruising
- Systemic effects: Nausea, Vomiting, Abdominal pain, headache, diaphoresis
Venom Induced Consumptive Coagulopathy (VICC)
- Which 3 snakes?
- Pathophysiology?
- Features: 3 Complete? 3 Partial?
- What syndrome is always associated with VICC? 4 Characteristic features?
Venom Induced Consumptive Coagulopathy
- Brown, Tiger, Taipan
- Most common major envenoming syndrome
- Australian snake venoms contain prothrombin activator toxins that mimic:
1. Factor Xa and Va prothrombinase complex
2. Activation of clotting pathways and consumption of clotting factors:
o Fibrinogen, factor V, factor VIII
* Rapid onset is typical
Clinical Envenomation Syndromes - Anticoagulant coagulopathy
- Which snakes?
- 4 Features?
- won’t bleed but you’ll start to see a rampant rise in their CK
Clinical Envenomation Syndromes - Myotoxicity
- Which 3 snakes?
- Which lab parameter rises?
Risk of rhabdo & AKI/failure
Clinical Envenomation Syndromes - Neurotoxicity
- Which 3 snakes?
- Clinical presentation?
- Do a regular PEEP flow to monitor for resp muscle failure
Brown Snakes
- Where?
- Clinical Presentation? (5)
Tiger Snakes
- Where?
- Clinical Presentation? (5)
Death Adders
- Where?
- Clinical Presentation? (3)
Black Snakes
- Where?
- Clinical Presentation? (5)
Taipans
- Where?
- Clinical Presentation? (4)
Black Snakes
- Most parts of Australia
- Clinical presentation
1. Large painful bite
2. Systemic symptoms
3. Anticoagulant coagulopathy
4. Myotoxicity
5. Acute haemolysis
Snake Envenomation
- 8 General Approach to Management?
- First Aid? (3 components)
General Approach to Management
1. Resuscitation
2. First Aid
3. Risk Assessment
4. Transport patient to a capable facility - Doctor, Laboratory, Adequate antivenom
5. Determine if there is objective evidence of envenoming - Don’t identify snake by vision!
6. Select appropriate antivenom & dose
7. Supportive care and adjuvant therapy
8. Disposition
General Approach to Management of Snakebite
- Risk Assessment?
- Seek evidence of envenoming?
General Approach to Management - Risk Asessment
- Any suggestion of snake bite mandates investigation and observation
- Ensure facility capable of assessment and management
1. Doctor
2. Laboratory
3. Adequate antivenom supply for relevant snakes
General Approach to Management of Snakebite
- Management of envenoming - 4 reasons to give antivenom?
- Which antivenom?
- What guides management decisions?
- Role of VDK?
General Approach to Management of Snakebite - Management Decisions
- Visual identification is unrealiable
- VDK is unreliable
- Treat the patient based on:
1. Geographical location of bite
2. Clinical presentation & laboratory studies
VDK = Venom Detection Kit = not diagnostic of whether a patient has been envenomed or not. Being removed as not useful!
Management of Snakebite
- Current antivenom dose?
- Antivenom administration?
- 2 Antivenom Risks?
Antivenom Administration
- Always given IV - dilute 500mls NS over 20 mins
- Pre-treatment with adrenaline not recommended
- Children receive the same dose as adults
- Not contraindicated in pregnancy
- Highly effacacious but obviously no RCTs to demonstrate clinical benefit
Serum sickness: if giving antivenom warn of myalgias & flu-like illness in about 1 week – treat = give 50mg prednisolone (steroids).
- Quick A to E assess while pressure bandaging – firm but don’t cut off circulation
- Treatment – they have a doctor, antivenom and a lab – can be left in Karratha for now.
- What snakes in Karratha =
- Clinical signs - Systemic vs. VICC (coagulopathy – bleeding) vs. Neurotoxicity (ptosis, blurred vision) vs. Myopathy etc.
- Biochemical signs - Coags (INR, APT), CK, U&Es, LFTs, FBC
We know he has VICC so need to check for subsequent complications of renal failure and TMA.
- VICC Recovery - time? lab parameters?
- Role of blood products?
More Antivenom?
- 1 Ampoule (1000U) of antivenom is adequate to bind all free venom in most severe brown snake envenomings
- CSL - one vial of antivenom is sufficient to neutralise the maximum venom load from one snake
- ASP - Resolution of VICC is not affected by increasing the dose of antivenom
- Antivenom doesn’t resolve VICC – that takes about 16 hours for time for liver to produce new clotting factors.
- Give only if VICC + clinically bleeding, otherwise just leave
Snakebites - Case 2
* 44yo female
* Witnessed snakebite (ornamental garden pool)
* PBI placed by GP
* Patient is asymptomatic
* iStat INR 1.3 – Formal coagulation sample taken at the same time
* Patient and blood sample transferred to Albany hospital for further management
* Arrival at Albany
- Blurred vision and bilateral ptosis
- Repeat iStat INR 0.9 – Formal bloods taken
What is your clinical diagnosis?
Denmark (SW WA) + Neurotoxicity = Tiger Envenomation
Don’t rely on POC INR for VICC!!
Snakebite - Case 3
* 50yo female
* Bitten on right leg 6 hours ago, no PBI applied
* INR 1.4, aPTT 42, D-dimer >4.0
* No neurotoxicity, CK normal
* No antivenom given
* Admitted for serial bloods and clinical observation
* Pt feels well so discharges herself 4 hours later
Your assessment? What are the risks?
- Tasmania = Tiger snakes!
- Is she clinically envenomed? = No
- Is she biochemically envenomed? = Maybe
- Risks = Myopathy = type 2 respiratory failure
- Why we keep patients for 12 hours minimum – also just give antivenom regardless now
Snakebite - Case 4
Case 4 Issues
1. Snake identification - Green tree snake?
2. Whole blood clotting test - Incorrect technique & Unreliable
3. Antivenom administration - Indications & Dose
4. VICC after PBI release, despite antivenom pre-treatment - Efficacy of antivenom for coagulopathy
3 Venomous Spiders & 4 Venomous Marine animals in Australia?
Spiders
1. Red back
2. Funnel Web
3. White Tail
Marine
1. Jellyfish (Bluebottle, Box & Irukandji)
2. Stone Fish
3. Blue-Ringed Octopus
4. Sea Snake
Redback Spider Bite
- Epidemiology?
- Syndrome?
- Pathophysiology?
- Local Symptoms?
- Systemic Symptoms?
- Treatment?
Redback Spiders - Antivenom
- What is it?
- RAVE RCT?
- Current recommendation?
- Administration?
White Tailed Spiders
- Clinical presentation?
- Management?
Management
- Reassurance
- Simple analgesia
- Ulcers and skin lesions should be fully investigated for another underlying cause rather than being attributed to a spider bite
Funnel Web Spiders
- Toxin?
- Clinical findings?
- Management: Pre-hospital? Hospital? Antivenom?
Clinical Findings
* Severe local pain
* Often visible fang marks
* Systemic envenoming:
- Autonomic excitation (both sympathetic and parasympathetic)
- Generalised diaphoresis, hypersalivation, lacrimation, piloerection, hypertension, brady-tachycardia
- Paraesthesia, muscle fasciculation and spasms
- May progress to CVS collapse and pulmonary oedema
Marine Envenomation: Bluebottles
- Where?
- Syndrome?
- Management?
Marine Envenomation: Bluebottles
- Australia wide
- Syndrome: Local pain
- “String of beads”
Marine Envenomation: Stonefish
- Where?
- Syndrome?
- Management?
Marine Envenomation: Stonefish
- Northern waters
- Dorsal spines with potent venom
- Syndrome: Immediate severe pain
- Systemic envenomation rare: Hypotension & Pulmonary oedema
Marine Envenomation: Irukandji
- Where?
- Symptoms?
- Progress?
- Management?
Marine Envenomation: Irukandji Syndrome - Progress
- Symptoms usually settle within 12 hours
- Severe envenoming is heralded by ongoing opiate requirement
- These patients are at risk of:
1. Cardiomyopathy
2. Shock
3. Pulmonary oedema
Marine Envenomation: Box Jellyfish
- Where?
- Prognosis?
- Symptoms?
- Antivenom: Indications?
Marine Envenomation
- Blue ringed octopus?
- Cone shell?
- Sea snakes?
Cone Shell
- Deaths very rare
- Syndrome: Local pain, Paralysis (ascending, potent neurotoxin)
- Management: No antivenom, supportive care
Toxicology: The General Approach
- Risk-assessment-based approach to management of poisoning?
- Resuscitation?
- 6 Emergency antidotes?
- Risk assessment – 5 components?
Risk assessment – 5 components
1. Agent
2. Dose
3. Time since ingestion
4. Clinical features and course
5. Patient factors
Toxicology: Investigations
- 3 Screening?
- 6 Specific?
- Reading the Tox ECG? (6)
Toxicology - Investigations
Screening
1. BGL
2. 12-Lead ECG
3. Serum Paracetamol level
Specific
1. Paracetamol
2. Carbamazepine
3. Digoxin
4. Iron
5. Lithium
6. Valproic acid
Reading the Tox ECG
1. Rate
2. Rhythm
3. PR interval
4. QRS interval
5. QT interval & plot on Nomogram
6. Dominant R wave in aVR
Reading the Tox ECG: Rate & Rhythm
- 4 Causes of Bradycardia?
- 3 Causes of Tachycardia?
- Enhanced automaticity?
Reading the Tox ECG: QRS Interval
- Normal QRS Interval?
- Slowing of phase 0 of the action potential leads to what 3 things?
- May progress to what? (2)
Rate & Rhythm
Bradycardia
1. CCB, BB, digoxin
2. Opioids/ethanol
3. Organophosphates
4. Lithium
Tachycardia
1. Sympathomimetic
2. Anticholinergics
3. Group Ia and Ic antiarrhythmic, TCAs
Enhanced automaticity - Digoxin, sympathomimetic
Fast Na Channel Blockade
- 3 Features on ECG?
- So the QRS is wide – so what? (3)
ECG predicts clinical deterioration
1. QRS >100 ms associated with seizures
2. R wave >3 mm in lead aVR associated with seizures
3. QRS >160 ms associated with
ventricular dysrhythmias
ECG changes correlate with response to
treatment
ECG – Fast Na Channel Blockers
- Which medication groups?
GI Decontamination in Toxicology: Methods
- Activated charcoal?
- Whole bowel irrigation?
Single-dose activated charcoal
- Large surface area absorbs toxins
- Reduces further absorption from GIT 50g or 1g/kg
- Mix ice-cream/juice
- Not everyone gets charcoal
- Repeated AC
Risk-assessment-based approach to management of poisoning
- 3 Options for Enhanced elimination?
- Which 8 Meds might you consider dialysis for?
Enhanced elimination - Dialysis
1. Toxic alcohols
2. Salicylate
3. Theophylline
4. Valproic acid
5. Carbamazepine
6. Metformin-induced lactic acidosis
7. Potassium
8. Lithium
