Emergency medicine Flashcards
Define anaphylaxis
Severe, life-threatening systemic hypersensitivity reaction characterised by rapidly developing airway and/or breathing and/or circulation problems usually associated with skin and mucosal changes
Describe the pathophysiology of anaphylaxis
Severe type 1 hypersensitivity reaction
IgE mediated, usually triggered by allergen, stimulates mast cell degranulation with release of histamine and other pro-inflammatory chemicals
Causes rapid onset of symptoms
List the types of hypersensitivity reactions, their pathophysiologies and examples of each
Type I
IgE mediated
Acute-onset
Atopy, anaphylaxis, asthma, eosinophilic granulomatosis with polyangiitis
Type II
Antibody mediated - IgG, IgM, complement
Autoimmune haemolytic anaemia, rheumatic heart disease, Goodpasture’s, Grave’s, myasthenia gravis, pemiphigus vulgaris
Type III
Immune-complex - IgG, complement, neutrophils
RA, post-strep glomerulonephritis, membraneous nephropathy, SLE, lupus nephritis, reactive arthritis, hypersensitivity pneumonitis
Type IV
Cell mediated - T-cells (cytotoxic), antibody-independent
Contact dermatitis, chronic transplant rejection, MS, coeliac, Hashimoto’s
Describe the clinical presentation of anaphylaxis
History of exposure to allergen usually
Rapid onset of symptoms:
Urticaria
Itching
Angio-oedema – swelling around lips and eyes
Abdominal pain
Shortness of breath
Wheeze
Swelling of larynx – stridor, hoarse voice
Tachycardia
Pre-syncope
Collapse
Will feel and look unwell
List common triggers of anaphylaxis
In children most commonly food – nuts
Drugs most common in adults – anaesthetics, antibiotics (penicillin, cephalosporins), NSAIDs, aspirin
Describe the acute management of anaphylaxis
A-E approach
Airway – manoeuvres, adjuncts, consider securing airway with ET intubation/tracheostomy
Breathing – ABG, oxygen, nebulised bronchodilators (salbutamol, ipratropium bromide)
Circulation – IV cannulation, bloods, IV fluids
Disability – assess consciousness, blood glucose
MOST IMPORTANT INTERVENTION =
IM adrenaline
Adult dose (>12) = 500 micrograms (0.5ml 1 in 1,000)
Children’s doses
<6 months – 100-150 micrograms
6 months-6 years – 150 micrograms
6-12 years – 300 micrograms
Can repeat adrenaline every 5 minutes if necessary, best site is anterolateral aspect of middle third of thigh
For refractory anaphylaxis (doesn’t respond to 2 doses of IM adrenaline) – IV fluids, senior (ICU) help with consideration of IV adrenaline infusion
How should patients with anaphylaxis be managed after they have been stabilised?
Non-sedating oral antihistamines especially if persisting skin symptoms
Serum mast cell tryptase can be measured to confirm diagnosis of anaphylaxis (within 6 hours of event)
Monitor for biphasic reaction
Educations and follow-up – refer for allergy testing, adrenaline auto-injector training
Discharge:
Fast-track (2-hours after symptom resolution)
- Good response to single dose of adrenaline
- Complete resolution of symptoms
- Given adrenaline auto-injector and know how to use it
- Adequate supervision following discharge
Minimum 6 hours after symptom resolution
- 2 doses of IM adrenaline needed or previous biphasic reaction
Minimum 12 hours after symptom resolution
- Severe reaction requiring >2 doses of IM adrenaline
- Has severe asthma
- Possibility of ongoing reaction e.g. slow-release medication
- Present late at night
- Live in area where emergency case may be difficulty to access
List reversible causes of cardiac arrest
4 Hs and 4 Ts:
Hypoxia – airway obstruction, asthma, drowning, hanging, asphyxia
Hypovolaemia – external blood loss, internal blood loss, other causes of fluid loss (diarrhoea, vomiting, dehydration, renal disease)
Hypothermia – temp below 35
Hypo-/hyperkalaemia (electrolyte disturbance) – renal impairment, medications (ACE-inhibitors), DKA, trauma, burns
Tension pneumothorax
Cardiac tamponade
Toxins – overdose (tricyclic antidepressants, beta-blockers, opioids), illicit drug use, anaphylaxis
Thrombosis – PE, MI
List the shockable and non-shockable rhythms
Shockable – pulseless ventricular tachycardia or ventricular fibrillation
Non-shockable – pulseless electrical activity or asystole
Which airway adjuncts/manoeuvres should be potentially avoided in major trauma? Why?
Head-tilt chin-lift – can exacerbate a c-spine injury
Nasopharyngeal airway – avoid if basal skull fracture signs (CSF leak, panda eyes, battle’s sign)
Describe c-spine immobilisation
3-point immobilisation
Collar – semi-rigid (unless airway compromise, spinal deformity)
Blocks
Tape – wide Elastoplast tape anchored to trolley at ear level
List the potentially life-threatening chest injuries
TOM CAT
Tension pneumothorax
Open pneumothorax
Massive haemothorax
Cardiac tamponade
Airway injury
Tracheobronchial injury
Describe the immediate management of a tension pneumothorax, haemothorax, open pneumothorax and flail chest
Tension pneumothorax – immediate needle decompression with large-bore (14- or 16-gauge) needle into 2nd intercostal space, midclavicular line, chest drain insertion into ‘triangle of safety’ (anterior border of latissimus dorsi, lateral border of pectoralis major, between axilla and horizontal level of nipple)
Haemothorax – insertion of chest drain, if >1.5L considered massive haemothorax and may need surgical intervention
Open pneumothorax – cover wound with sterile dressing, taped on 3 sides (creates valve to allow air to exit but not enter chest cavity), once stable can insert chest tube, consider surgery
Flail chest – early intubation and ventilation, discussion with surgeon for repair
Define major haemorrhage
Loss of more than one blood volume within 24 hours
50% of total blood volume lost in less than 3 hours
Bleeding in excess of 150mL/minute
Or in the acute setting – bleeding (visible or presumed) which results in:
Blood pressure <90mmHg systolic
Heart rate >110bpm
Describe the management of major haemorrhage
Restore circulating volume
Wide bore peripheral cannulae
Give crystalloid fluids, warmed if possible, may tolerate permissive hypotension (maintain vasoconstriction, prevent coagulopathy and further bleeding)
Give oxygen
Summon help! – 2222, may need surgical, anaesthetics, ICU, obstetric support etc.
Stop bleeding – early surgical obstetric or interventional radiology involvement
Send blood samples – crossmatch, FBC, clotting screen, U&Es, bone profile
Give packed red cells and FFP in 1:1 ratio
May need to give platelets, cryoprecipitate later (haematology guided)
If on warfarin – give prothrombin complex concentrate, consider reversal (vitamin K)
On DOACs – discuss with haematologist for reversal agents
How is cardiac tamponade diagnosed and managed in an acute setting?
Features – Beck’s triad
Hypotension
Raised JVP
Muffled heart sounds
Other features:
Dyspnoea
Tachycardia
Absent Y descent on JVP
Pulsus paradoxus – abnormal large drop in BP during inspiration
ECG – low QRS voltage, tachycardia, electrical alternans (consecutive, normally-conducted QRS complexes that alternate in height)
Can diagnose with FAST/bedside echo
Management
Pericardiocentesis – long 14/16G cannula, insert at angle of xiphisternum and left rib border, aim for ipsilateral scapula, aspirate while advancing (often US guided)
Define sepsis and septic shock
Sepsis – life-threatening organ dysfunction due to dysregulated host response to infection
Septic shock – circulatory, cellular, metabolic abnormalities, mainly persistent hypotension despite fluid correction and inotropes and hyperlactataemia with lactate >2
Results in organ hypoperfusion - hypoxia, oliguria, AKI, thrombocytopaenia, coagulation dysfunction, hypotension, hyperlactataemia >2
Describe the presentation of sepsis
Symptoms:
Localising symptoms of infection
Drowsiness
Confusion
Dizziness
Malaise
Oliguria
Signs:
Tachycardia
Hypotension
Tachypnoea
Cyanosis
Fever/hypothermia
Oliguria
Non-blanching rash
Mottled skin
Cyanosis
Arrhythmias – AF
List red and amber flags for sepsis
Red flags:
Responds to only voice or pain/unresponsive
Acute confusional state
SBP <=90 or drop >40 from normal
Heart rate >130
Respiratory rate >=25
Needs oxygen to keep SpO2 >=92%
Non-blanching rash, mottled/ashen/cyanotic
Not passed urine in last 18 hours, urine output <0.5ml/kg/hour
Lactate >=2mmol/l
Recent chemotherapy
Amber:
Concern about mental status
Acute deterioration in functional ability
Immunosuppressed
Trauma/surgery/procedure in last 6 weeks
Respiratory rate 21-24
SBP 91-100mmHg
Heart rate 91-130 or new dysrhythmia
Not passed urine in last 12-18 hours
Temperature <36
Clinical signs of wound, device or skin infection
Describe the components of the sepsis six
Give oxygen – aim to keep sats >94%
Take blood cultures
Give IV fluids – 500ml crystalloid over 15 minutes
Give IV antibiotics
Measure serum lactate
Measure accurate hourly urine output
List types of shock
Septic
Haemorrhagic
Neurogenic
Cardiogenic
Anaphylactic
Define status epilepticus
Single seizure lasting >5 minutes
Repetitive seizures without recovery in between
Define status epilepticus
Single seizure lasting >5 minutes
Repetitive seizures without recovery in between
Describe the WHO analgesic ladder
Originally to manage cancer-related pain, also often used for acute and chronic painful conditions:
Step 1 – non-opioid medications e.g. paracetamol and NSAIDs
Step 2 – weak opioids such as codeine and tramadol
Step 3 – strong opioids such as morphine, oxycodone, fentanyl and buprenorphine
Adjuvants for neuropathic pain:
Amitriptyline – tricyclic
Duloxetine – SNRI
Gapapentin – anticonvulsant
Pregabalin – anticonvulsant
Describe the prescribing for breakthrough pain
Immediate release morphine – 1/6th to 1/10th of regular 24 hour dose, as required up to a maximum of 6 doses in 24 hours
If 3 or more doses given within 4 hours review, if more than 6 doses in 24 hours review
Describe the conversion factor of a weak oral opioid (codeine, dihydrocodeine or buprenorphine) to oral morphine
Divide weak opioid dose by 10 to get morphine dose
Describe the conversion factor of oral morphine to subcutaneous morphine/diamorphine/oral oxycodone/SC hydromorphone
Oral morphine to SC morphine – divide by 2
Oral morphine to SC diamorphine – divide by 3
Oral morphine to oral oxycodone – divide by 4
Oral morphine to SC hydromorphone – divide by 10
Describe the triggers for and symptoms of opioid toxicity in palliative care patients
Triggers – rapid dose escalation, renal impairment, sepsis, electrolyte abnormalities, drug interactions
Symptoms:
Persistent sedation
Vivid dreams, hallucination, shadows at edge of visual field
Delirium
Muscle twitching/myoclonus/jerking
Abnormal skin sensitivity to touch
List the causes of acute kidney injury
Pre-renal:
Hypovolaemia – haemorrhage, over-diuresis, vomiting, diarrhoea
Renal artery stenosis
Low effective arterial blood volume – heart failure, cirrhosis, sepsis, third-spacing
Drug-induced – NSAIDs, ACE inhibitors, diuretics
Intra-renal:
Acute tubular necrosis – most common cause of AKI due to ischaemic or toxic injury to cells of PCT
Acute interstitial nephritis – drug-induced, infection, immune-mediated
Glomerular disease – primary renal disease, systemic disease with or without immune complex deposition
Intra-tubular obstruction – multiple myeloma with paraprotein, pigment
Other – scleroderma renal crisis, malignant hypertension
Post-renal (obstructive):
Ureters – nephrolithiasis, retroperitoneal fibrosis
Bladder – bladder cancer
Prostate – benign prostate hyperplasia, prostate cancer
Urethra – urethral stricture
External – retroperitoneal mass, ovarian tumours
List drugs which are potentially nephrotoxic and describe the mechanism of their nephrotoxicity
GFR alteration:
ACE inhibitors
ARBs
Cyclosporin
NSAIDs
Tacrolimus
Tubular cell toxicity:
Aminoglycosides
Amphotericin B
Cisplatin
Interstitial nephritis:
NSAIDs
Rifampicin
Crystal nephropathy:
Acyclovir
Ampicillin
How is an acute kidney injury defined? How is the severity graded?
AKI if any of the following present:
Urine output <0.5ml/kg/hour for 6 hours
Serum creatinine increased by 1.5x baseline over 7 days
Serum creatinine increase by 0.3mg/dL in 48 hours
AKI stages
I – rise in creatinine of 1.5-1.9x baseline, <0.5ml/kg/hour urine output for 6 hours
II – rise in creatinine of 2-2.9x baseline
<0.5mg/kg/hour urine output for 12 hours
III – rise in creatinine of >3x baseline
<0.3ml/kg/hour for 24 hours
List risk factors for developing acute kidney injury
Older age
Diabetes
Chronic kidney disease
Chronic liver disease
Congestive cardiac failure
Polypharmacy
Hypotension
Hypovolaemia
Drugs – ACEi, ARBs, NSAIDs, contrast
How is an acute kidney injury managed?
General management:
Withdrawal of nephrotoxic medication
Adjustment of drug doses which are renally cleared to prevent toxicity
Fluid resuscitation
Urinary catheterisation – measure urine output, relieve urinary obstruction
Assess for evidence of sepsis and initiate sepsis six bundle if required
Targeted management dependent on cause
Renal replacement therapy – indications:
Metabolic acidosis pH less than 7.15 or worsening acidaemia
Refractory electrolyte abnormalities (hyperkalaemia over 6.5mmol)
Presence of dialysable toxins – toxic alcohols, aspirin, lithium
Refractory fluid overload – diuretics resistant fluid overload with AKI
End-organ uraemic complications e.g. pericarditis, encephalopathy, uraemic bleeding
List potential complications of acute kidney injuries
Fluid overload
Electrolytes derangement – hyperphosphataemia, hyperkalaemia
Acid-base disorder – metabolic acidosis
End-organ complications of uraemia
Chronic kidney disease
End-stage renal disease
Death
Describe the characteristics of human bites
Purposeful (e.g. fights – usually hands, sexual violence) or incidental (sports, occupational injury)
Most common bacterial agents – strep spp, staph aureus, haemophilus spp., eikenella corrodens, bacteroides spp., other anaerobes
Also small risk of transmission of viruses such as HIV and herpes simplex
Infections common, especially in clenched fist injuries (‘fight bites’)
Describe the characteristics of dog and cat bites
Dogs
Puncture and ripping/tearing/shearing wounds – make contact and hold on, powerful jaws which can cause significant tissue injury including crush wounds, devascularisation, bone damage, soft-tissue avulsion
Generally polymicrobial, most common bacterial agents – S aureus, pasteurella canis, P. multocida, capnocytophaga canimorsus (rare but serious)
Also risk of rabies (most commonly from dogs) – very low risk in the UK, more likely to be from bats
Cats
Fine sharp teeth – narrow, deep puncture wounds inoculated with saliva, able to penetrate bone, joints and tendons
2x as likely as dog bites to become infected due to deep inoculation, and deep infections such as abscesses and osteomyelitis more common as only small opening for drainage
Generally polymicrobial – pasteurella multocida common, can cause severe, rapidly-spreading infections
Describe the management and assessment of a bite wound
Immediate wound management:
Remove foreign bodies e.g. teeth
Encourage wound to bleed
Irrigate thoroughly with saline (1L)
Provide analgesia
Consider antibiotics if indicated – human bite which has broken skin and drawn blood, or high-risk area (hands, feet, face, genitals), risk factors for infection or clinical signs of infection (co-amoxiclav)
If visibly infected send pus or deep wound swab for culture (before cleaning wound)
Consider tetanus booster
Consider need for debridement – keep fasted
?Close wound
?Referral for assessment by plastics team
Assessment:
Document how bite occurred, whether skin was broken, and blood drawn
Examine bite – location, size and depth, type of wound, degree of crush injury, devitalised tissue, nerve/tendon damage, involvement of muscle/bone/joints/vessels
Check ROM if over a joint
Neurovascular function distal to bite – pulses and sensation
Signs of infection
Facial – intraoral examination to exclude cheek lacerations with intraoral communication
?X-ray – fractures or foreign bodies
Assess BBV risk
Consider possible child protection issues or safeguarding issues for vulnerable adult
Which bite wounds should be left to heal by secondary intention?
Over 24 hours old
Infected
Deep puncture wounds
Crush injuries
Heavy contamination
Uncertain adequacy of debridement
Bites to limbs, hands and feet
Describe the caused, presentation and management of Lyme disease
Cause - borrelia burgdorferi, spirochete bacteria spread by ticks
Early features (within 30 days)
Erythema migrans – ‘bulls-eye’ rash at site of tick bite
Typically develops 1-4 weeks after initial bite
Usually painless, >5cm in size and slowly increases
Systemic – headache, lethargy, fever, arthralgia
Late features (after 30 days)
Cardiovascular – heart block, peri/myocarditis
Neurological – facial nerve palsy, radicular pain, meningitis
Management
Early disease – doxycycline
Disseminated disease - ceftriaxone
Describe the differential diagnosis for acute rectal bleeding
Usually from source in rectum or colon, can also be due to upper GI bleed
Diverticular disease
Ischaemic or infective colitis
Haemorrhoids
Malignancy
Angiodysplasia
Crohn’s disease
Ulcerative colitis
Radiation proctitis
Describe the differential diagnosis for acute rectal bleeding
Usually from source in rectum or colon, can also be due to upper GI bleed
Diverticular disease
Ischaemic or infective colitis
Haemorrhoids
Malignancy
Angiodysplasia
Crohn’s disease
Ulcerative colitis
Radiation proctitis
Describe the management of acute lower GI bleeding
A-E assessment, resuscitation
Major haemorrhage protocol
Hb <70 (or <80 and cardiovascular disease) require transfusion
Reverse anti-coagulation
If unstable – CT angiogram to identify bleeding point, can then stop bleeding with IR (arterial embolisation) or endoscopic haemostasis (adrenaline injection, electrocoagulation, clips or bands)
May need surgical intervention
If stable – elective colonoscopy
Describe the differential diagnosis for an acute upper GI bleed and the features of each
Oesophageal causes
Varices – large volume fresh blood
Oesophagitis – small volume fresh blood, often streaking vomit, preceded by GORD symptoms
Cancer – small volume except as preterminal event with erosion of major vessels
Mallory-Weiss tear – small to moderate volume bright red blood following repeated vomiting
Gastric causes
Ulcer – small volume unless erosion into significant vessel, tends to present as IDA
Cancer – frank haematemesis or altered blood mixed with vomit, dyspepsia, constitutional symptoms
Dieulafoy lesion – developmental AV malformation, causes large haemorrhage
Diffuse erosive gastritis – haematemesis, epigastric pain
Duodenal causes
Ulcer – haematemesis, melena, epigastric discomfort
Aorto-enteric fistula – following previous abdominal aortic aneurysm surgery, major haemorrhage with high mortality
Describe the presentation of acute upper GI bleeding
Haematemesis – frank or ‘coffee ground’
Melaena – tar-like, black, offensive stools (altered blood)
Haematochezia – fresh blood PR if large volume upper GI bleed
Symptoms of underlying cause - abdominal pain (epigastric), jaundice, ascites
Haemodynamic instability – hypotension, tachycardia, pre-syncope, other signs of shock
Describe the management of acute upper GI bleeding
Risk assessment:
Glasgow-Blatchford score on first assessment
Rockall score after endoscopy
Resuscitation:
A to E assessment
IV access – ideally two wide bore cannulae
Bloods – FBC, U&Es (acute rise in urea with GI bleed), coagulation screen, LFTs (cirrhosis), crossmatch
IV fluid resuscitation, transfusion
Platelets given to those actively bleeding with platelet count <50
FFP if actively bleeding and PT or APTT >1.5x normal
Fibrinogen <1.5g/L despite FFP give cryoprecipitate
Prothrombin complex if taking warfarin and actively bleeding
Terlipressin – suspected variceal bleeding
Prophylactic antibiotic therapy – suspected or confirmed variceal bleeding (ciprofloxacin)
Endoscopy for all unstable patients with severe UGIB immediately after resuscitation (within 24 hours for all others)
Endoscopic haemostatic techniques:
Peptic ulcer - adrenaline injection, cauterisation
Varices – banding, Sengstaken-Blakemore tube if severe/uncontrollable bleeding
PPI can be used in variceal bleeding pre-endoscopy to reduced risk of re-bleed – NICE advise against PPI pre-endoscopy
Describe the risk assessment scoring systems for upper GI bleeding
Glasgow-Blatchford score
Pre-endoscopy, on initial assessment
Identifies low-risk patients who don’t need intervention
Components – urea, haemoglobin, SBP, pulse >100, melaena, syncope, hepatic disease, cardiac failure
Rockall score
Can be done pre- or post-endoscopy, post is more accurate
Identify risk of ongoing bleeding and death
Components – age, shock, comorbidities (cardiac failure, ischaemic heart disease, renal failure, liver failure, malignancy), diagnosis, major
Major stigmata of recent haemorrhage on endoscopy – dark spot, blood in upper GI tract, adherent clot, visible or spurting vessel
Describe the presentation and management of inhalation injury in the context of burns
Signs of airway compromise – stridor, hoarse voice, tachycardia, hypoxia, cyanosis
Singed nasal hairs
Facial burns
Soot deposits around nose
Requires early involvement of anaesthetics for potential intubation
Describe the classification of burns
By mechanism:
Thermal burns – scalds, flame injuries, contact burns
Electrical burns – low-voltage, high-voltage
Chemical burns – acids, alkalis
By depth:
Superficial epidermal (previously 1st degree) – red, painful, dry, no blisters
Partial thickness (superficial dermal, previously 2nd degree) – pale pink, painful, blistered, slow CRT
Partial thickness (deep dermal, previously 2nd degree) – typically white, can have patches of non-blanching erythema, reduced sensation, painful to deep pressure
Full thickness (previously 3rd degree) – white/brown/black, no blisters, no pain
By percentage total body surface area (%TBSA) – various techniques for estimate, e.g. Wallace’s rule of nines, the ‘rule of palm’ (palm area is 1% of total body surface area, only accurate up to 15%) or Lund and Browder chart (most accurate, mainly paediatric)
Describe the classification of burns as complex or non-complex
Complex
All electrical and chemical burns
Any burn affecting a critical area – face, hands, feet, perineum or genitalia, crossing joints, circumferential
Any thermal burn covering >15% TBSA in adults, >10% in children (>5% in children under 1)
Non-complex
Partial thickness thermal burn covering up to 15% TBSA in adults, up to 10% in children (up to 5% in children under 1) that does not affect a critical area
Deep partial thickness burns covering up to 1% of the body
Describe the initial management of burns
Remove any source of burns and non-adherent clothing
A-E assessment:
Airway – signs of inhalation injury, consider intubation
Breathing – 100% oxygen via non-rebreather mask, evaluate need for escharotomy if circumferential burns, do ABG and check carboxyhaemoglobin levels for carbon monoxide poisoning
Circulation – two wide bore IV cannula, routine bloods, aggressive IVF, insert urinary catheter for fluid balance monitoring
Disability – evaluate neurological status, check temperature as risk of hypothermia
Exposure – fully expose patient to get accurate estimation of %TBSA burned and check for concomitant injuries
IV morphine for analgesia
Strict fluid balance chart
Clingfilm for initial wound dressing to minimise fluid loss
Reduce risk of hypothermia – warmed room, warmed fluids, reduce wound exposure time
Give tetanus booster if needed
How are minor burns managed?
First-aid
Remove source of burn and any non-adherent clothing
Wound under running water for 20 minutes as soon as possible
Clean with normal saline
Analgesia
Emollients
Leave blisters intact
Non-adherent dressing
Describe fluid resuscitation in burn management
Fluids calculated from time of burn
If clinically shocked on arrival, correct this before calculating burn fluid requirements
Modified Parkland formula most commonly used – describes the volume of crystalloid fluid to be administered in the first 24 hours post-burn:
Initial 24 hours (adult) = 4ml x weight (kg) x %TBSA
Initial 24 hours (children) = 3ml x weight (kg) x %TBSA
50% volume given in first 8 hours, remaining 50% in next 16 hours
Known to underestimate requirements in large full-thickness burns, inhalation injury and electrical burns
Maintain urine output >0.5ml/kg/hour
Which burn patients should be referred to a specialist burn service?
All 2% or more TBSA in children or 3% or more in adults
All deep partial or full-thickness burns
All circumferential
Any chemical, electrical or friction burns or cold injuries
Any burn not healed in two weeks
Suspicion of NAI
Burns over perineum, face, hands, feet, genitals, major joints
Pregnant or severe co-morbidities
Describe the definitive management and prognosis of burns
Superficial and superficial partial thickness usually heal naturally in three weeks, conservative management
Burn unit or burn centre care for more severe burns
Wound debridement – excision of necrotic tissue, may need amputation if unsalvageable limbs
Grafting – autograft (from patient’s body), allograft (from another human donor) or xenograft (from another species, typically pig)
Prognosis:
Superficial – heals without scarring
Superficial partial-thickness – heals without scarring
Deep partial thickness – heals in 3-8 weeks, likely to scar if taking >3 weeks to heal
Full thickness – heals by contracture, >8 weeks, will scar
Describe the pathophysiology of complications of burns
Typically in >25% TBSA, >65 years old or <2 years old, those with simultaneous major trauma or smoke inhalation
Systemic inflammatory response where exaggerated and dysregulated inflammatory response develops due to large burn injury, may progress to multiple organ dysfunction syndrome, where inflammatory response causes end-organ failure
Inflammatory response causes fluid third-spacing
Immunosuppression, bacterial translocation from gut lumen
List potential complications of burns
Early:
Respiratory distress from smoke inhalation (causes bronchospasm, pulmonary and laryngeal oedema) or circumferential chest burn
Poising from inhalation of noxious gases
Fluid loss, hypotension, hypovolaemic shock
Hypothermia
Wound infection and sepsis
Toxic shock syndrome – small burns in children, infected with staph aureus
Cardiac arrhythmias – electrical burns (ventricular fibrillation), electrolyte disturbance
Vascular insufficiency, distal ischaemia, compartment syndrome from circumferential burn of limb/digit
AKI – hypovolaemia, muscle breakdown (rhabdomyolysis), haemolysis
Limb loss
Curling’s ulcer – ischaemia of gastric mucosa, can cause GI bleeding or perforation
Death
Late:
Wound infection
AKI – sepsis, multi-organ failure, nephrotoxic drugs
Chronic neuropathic pain/itch
Contractures
Scarring
Psychosocial impact
Sleep disorders
Describe the differential diagnosis for acute chest pain
Cardiac causes:
Acute coronary syndrome – central crushing chest pain, radiates to left arm and/or jaw, lasting longer than 20 minutes, associated sweating, nausea, SOB
Stable angina – sudden onset chest pain radiating to left arm and/or jaw lasting for less than 20 minutes, triggered by exertion, complete resolution during rest
Pericarditis – gradual onset central chest pain worse lying flat, better leaning forwards
Thoracic aortic dissection – sudden onset central chest pain radiating to back, ‘tearing’ nature
Respiratory causes:
Pneumonia – gradual onset sharp chest pain, pleuritic, associated productive cough, SOB, fever
Spontaneous pneumothorax – sudden onset sharp pleuritic chest pain, SOB
Pulmonary embolism – sudden onset pleuritic chest pain, SOB, haemoptysis
GI causes:
GORD – central chest pain, burning, worse lying flat, associated nausea/vomiting
Oesophageal spasm – central chest pain, associated dysphagia, heartburn, regurgitation
Boerhaave’s syndrome – sudden onset severe chest pain after severe vomiting
MSK causes:
Costochondritis
Muscle strain
Chest wall trauma
Psychosocial/psychological causes:
Anxiety
Functional pain
Define hyperkalaemia and describe severity classification of hyperkalaemia
Plasma potassium 5.5mmol/L or more
Mild – 5.5-5.9
Moderate – 6.0-6.4
Severe >6.5
List causes of hyperkalaemia
Renal:
AKI
CKD
Hyperkalaemic renal tubular acidosis
Iatrogenic:
ACEi/ARBs
Potassium-sparing diuretics e.g. spironolactone
NSAIDs
Digoxin (toxicity)
Trimethoprim
Beta-blockers
Heparin
Ciclosporin
Tacrolimus
Other:
Trauma and burns
DKA – extracellular
Addison’s disease
Pseudohyperkalaemia – blood sample inaccurate
Describe the clinical features of hyperkalaemia
General weakness and fatigue
Palpitations, chest pain, SOB
Usually no clinical signs
Bradycardia – due to AV block
Depressed or absent tendon reflexes
Describe the ECG features of hyperkalaemia
Tall, tented T waves
Wide QRS
Prolonged PR
Flattened/absent P
AV block
Bradycardia
Describe the management of hyperkalaemia
If potassium less than 6, stable renal function, no ECG changes – no urgent treatment, stop precipitants
Potassium >6 with ECG changes or >6.5 – urgent treatment
Prevent further accumulation of potassium:
Stop IV fluids containing potassium
Suspend medications which could increase potassium
Suspend supplements containing potassium
Stabilise cardiac membrane:
IV calcium gluconate if ECG changes (reduces risk of fatal arrhythmia for 30-60 minutes), repeat if ECG changes not improving
Shift potassium intracellularly:
Insulin-glucose infusion
Salbutamol
Remove potassium from body:
Calcium resonium
Correct underlying cause
Haemodialysis if refractory hyperkalaemia
List the potential complications of hyperkalaemia
Potentially life-threatening cardiac arrhythmias
Muscle weakness
Paralysis
List causes of hypokalaemia
Hypokalaemia with alkalosis
Vomiting
Thiazide and loop diuretics
Cushing’s syndrome
Conn’s syndrome (primary hyperaldosteronism)
Hypokalaemia with acidosis
Diarrhoea
Renal tubular acidosis
Acetazolamide
Partially treated DKA
Magnesium deficiency – can be difficult to normalise until magnesium deficiency corrected
Describe the clinical features of hypokalaemia
Muscle weakness
Hypotonia
Muscle cramps
Severe – flaccid paralysis, hyporeflexia
What are the features of hypokalaemia on ECG?
U waves
Small or absent T waves
Prolonged PR
ST depression
What are the features of hypokalaemia on ECG?
U waves
Small or absent T waves
Prolonged PR
ST depression
How is hypokalaemia managed?
Mild, able to eat and drink – oral supplements (e.g. SandoK)
Moderate to severe, ongoing losses, unable to take oral – IV replacement
IV potassium given at maximum rate of 10mmol/hour on a ward
40mmol/1L 0.9% NaCl
Remember to check Mg and replace if deficient
Treat underlying cause
Define hyponatraemia
Serum sodium <135
List causes of hyponatraemia
Classified in terms of extracellular fluid status and urine sodium concentration
Urinary sodium >20mmol/L
Hypovolaemic – diuretics (thiazide, loop), Addison’s, diuretic renal failure
Euvolaemic – SIADH, hypothyroidism
Hypervolaemic – acute tubular necrosis
Urinary sodium <20mmol/L
Hypovolaemic – vomiting or diarrhoea, sweating, burns
Euvolaemic – acute fluid overload
Hypervolaemic – congestive cardiac failure, liver cirrhosis, nephrotic syndrome, psychogenic polydipsia
Describe the clinical features of hyponatraemia
Mostly asymptomatic
Usually related to volume status e.g. overloaded and oedematous or clinically dehydrated
Severe hyponatraemia – neurological signs including malaise, headache, confusion, progressing to reduced consciousness and seizures
How is hyponatraemia managed?
Need to know -
Is it acute or chronic?
Acute - less than 48 hours
Chronic - more than 48 hours
Severity of hyponatraemia
Mild – 130-134
Moderate – 120-129
Severe - <120
Symptoms – is the patient symptomatic?
Suspected aetiology
Hypovolaemic
Euvolaemic
Hypervolaemic
Management:
Consider precipitating medications and stop
Chronic hyponatraemia
Hypovolaemic cause – normal isotonic saline
Euvolaemic/hypervolaemic cause – fluid restrict
Acute hyponatraemia with severe symptoms
Close monitoring – HDU or above
Hypertonic saline (3% NaCl) to correct sodium more quickly
Why must chronic hyponatraemia be corrected slowly?
Rapid correction can cause central pontine myelinolysis – change in extracellular osmolality causes damage to myelin sheaths of brainstem neurons
Present with confusion and balance problems, develop pseudobulbar palsy and quadriplegia
List the potential complications of hyponatraemia
Complication of treatment – osmotic demyelination syndrome (central pontine myelinolysis)
Cellular swelling – cerebral oedema (raised ICP), impaired healing of tissues post-op
ECG changes – non-ischaemic ST elevation
Define hypernatraemia
Sodium >145
Symptoms usually only seen if >160
List causes of hypernatraemia
Hypovolaemic
Diuretics – loop mainly
Dehydration/fluid restriction – diarrhoea, vomiting, burns, febrile illness
Acute tubular necrosis
Hyperosmolar states – including HHS
Euvolaemic – diabetes insipidus
Hypervolaemic
Excessive hypertonic saline administration
Steroid excess – Conn’s syndrome or Cushing’s syndrome
Describe the clinical presentation of hypernatraemia
Generally asymptomatic
Excessive thirst
Severe – weakness, lethargy, irritability, confusion, seizures, coma
>180 – ataxia, tremor, coma, seizures
How should hypernatraemia be investigated?
Urine osmolality – hypernatraemia stimulates ADH release from hypothalamus, concentrates urine to reabsorb more water
If urine osmolality >600mOsmol/kg – hypothalamic and renal function intact, extra-renal cause
If urine osmolality <600mOsmol/kg with hypernatraemia, indicates ADH or renal-dependent mechanism, such as osmotic diuresis or diabetes insipidus
How is hypernatraemia managed?
Replace fluid deficit and correct serum sodium relatively slowly (risk of cerebral oedema)
Rate of no more than 0.5mmol/hour correction, or 10mmol/L/day in chronic hypernatraemia
Enteral fluid replacement preferred, including via NG if needed
If unable to tolerate enteral replacement use 5% dextrose (most preferred), 0.9% saline (if volume depleted) or Hartmann’s
List causes of hypercalcaemia
Malignant:
PTHrp production – squamous cell carcinoma
Bone primary tumours or metastases – osteolysis
Myeloma – increased osteoclastic bone resorption
Primary hyperparathyroidism - most common
Sarcoidosis
Thiazide diuretics
Acromegaly
Thyrotoxicosis
Dehydration
Addison’s disease
Paget’s disease of bone – prolonged immobilisation
List causes of hypercalcaemia
Malignant
PTHrp production – squamous cell carcinoma
Bone primary tumours or metastases – osteolysis
Myeloma – increased osteoclastic bone resorption
Primary hyperparathyroidism
Sarcoidosis
Thiazide diuretics
Acromegaly
Thyrotoxicosis
Dehydration
Addison’s disease
Paget’s disease of bone – prolonged immobilisation
Describe the management of hypercalcaemia
Rehydration with normal saline – 3-4L/day
May use bisphosphonates after rehydration
Other options – calcitonin (quicker than bisphosphonates), steroids in sarcoidosis
List the causes of hypocalcaemia
Vitamin D deficiency
Chronic kidney disease
Hypoparathyroidism e.g. post-thyroid/parathyroid surgery
Pseudohypoparathyroidism – target cells insensitive to PTH
Rhabdomyolysis
Magnesium deficiency – end-organ PTH resistance
Massive blood transfusion
Acute pancreatitis
Describe the clinical presentation of hypocalcaemia
Tetany – muscle twitching, cramping, spasm
Perioral paraesthesia
Chronic – depression, cataracts
ECG – prolonged QT
Trousseau’s sign – carpal spasm if brachial artery occluded with BP cuff
Chvostek’s sign – tapping over parotid causes facial muscles to twitch
How is hypercalcaemia managed?
Severe (tetany, seizures, prolonged QT) – IV calcium replacement, calcium gluconate, with ECG monitoring
Further management depending on underlying cause
List causes of hypomagnesaemia
Drugs – diuretics, PPIs
TPN
Diarrhoea
Alcohol
Hypokalaemia
Hypercalcaemia – secondary to hyperparathyroidism, compete for reabsorption in loop of Henle
Metabolic disorders – Gitleman’s and Bartter’s
Describe the clinical features of hypomagnesaemia
Paraesthesia
Tetany
Seizures
Arrhythmias
Decreased PTH secretion – hypocalcaemia
ECG similar to hypokalaemia
How is hypomagnesaemia managed?
Severe (tetany, arrhythmias, seizures) – IV magnesium replacement
Mild – oral magnesium salts (can cause diarrhoea)
List causes of hypermagnesemia
Haemolysis
CKD
Magnesium toxicity – pre-eclampsia management
Mild hypermagnesemia – DKA, adrenal insufficiency, hypothyroidism, hyperparathyroidism, lithium toxicity
Describe the clinical features of hypermagnesemia
Weakness
Confusion
Hyporeflexia
Arrhythmias
Hypotension
Respiratory depression
How is hypermagnesemia managed?
Mild and normal kidney function – no treatment except stopping drugs which may precipitate
Severe – calcium gluconate, calcium chloride
IV loop diuretics
Define traumatic brain injury and list types of traumatic brain injuries
Evidence of damage to the brain as a result of trauma to the head, represented by reduced GCS or focal neurological deficit
Mild traumatic brain injury – concussion, transient disturbance in the function of the brain caused by head injury
Focal e.g. contusion/haematoma
Extradural, subdural or intracranial haematoma
Contusions – coup or contre-coup
Diffuse e.g. diffuse axonal injury
Occurs due to mechanical shearing of axons following deceleration
Secondary brain injury due to physiological response to head injury – cerebral oedema, ischaemia, herniation
What is the Monro-Kellie doctrine?
Describes the relationship between the contents of the skull and intracranial pressure – skull is a closed rigid box with fixed capacity
Volume of brain is made up of – brain tissue, CSF, blood
If volume of one of these increases, to maintain a constant ICP, the volume of one of the others must decrease
Initially this can be achieved through compliance – mechanisms to keep intracranial pressure constant (e.g. decrease blood or CSF volume with space-occupying lesion)
Eventually compensatory mechanisms are exhausted and intracranial pressure begins to rise, eventually leading to herniation of brain tissue
Uncal herniation – displacement of medial part of temporal lobe (uncus) below tentorium cerebelli
Tonsillar herniation – cerebellar tonsils forced down through foramen magnum, causing compression on the brainstem
List the clinical features of raised intracranial pressure
Headache – worse in morning, worse with Valsalva manoeuvres, worse lying down
Nausea and vomiting
Visual disturbance
Reduced GCS
Slow, slurred speech
Papilloedema
Ipsilateral sluggish dilated pupil fixed dilated pupil
Cranial nerve palsy
Seizures
Abnormal respiration
Abnormal posturing – decorticate then decerebrate
Cushing’s triad – physiological response to raised ICP, aims to improve perfusion
Bradycardia
Hypertension
Irregular breathing
What formula describes cerebral perfusion pressure?
CPP = mean arterial pressure – intracranial pressure
(rise in ICP reduces CPP)
List the factors which can contribute to secondary brain injury and how they can be limited
Hypoxia and hypercapnia – maintain sats 94-98%, intubate to protect airway if poor respiratory effort
Hypovolaemia and hypotension – resuscitate with IV fluids or blood products, vasopressors
Cerebral oedema and raised ICP – position at 30 degrees to aid venous drainage, mannitol or hypertonic saline to reduce ICP, intubation and hyperventilation strategies
Expanding haematoma – reverse coagulation abnormalities, consider transexamic acid if <3 hours post-injury, neurosurgical intervention (craniectomy, Burr holes)
Hypoglycaemia or hyperglycaemia – maintain normal glucose with insulin/dextrose
Increased metabolic demand e.g. hyperthermia or seizures – maintain normothermia, anti-convulsants if seizure activity
Describe the initial management of head injuries
Cervical spine immobilisation if required
A-E assessment
A - GCS <8 cannot protect own airway, anaesthetic support required, avoid head-tilt chin-lift and nasopharyngeal airways
B – oxygen to prevent hypoxia
C – fluid resuscitation
D – GCS recorded and repeated every 30-60 minutes, pupil assessment, BM (avoid hypoglycaemia)
E – examine for lacerations, facial fractures, depressed skull fractures, basal skull fractures
List the indications for CT scanning of head injuries in adults
Within 1 hour:
GCS <13 on initial assessment
GCS <15 2 hours after injury
Suspected open or depressed skull fracture
Any sign of basal skull fracture – haemotympanum, panda eyes, CSF leakage, Battle’s sign
Post-traumatic seizure
Focal neurological deficit
More than 1 episode of vomiting
Within 8 hours:
Age >65
History of bleeding or clotting disorders, on anticoagulant therapy
Dangerous mechanism of injury – pedestrian or cyclist hit by car, fall from height greater than 1m or 5 steps
More than 30 minutes retrograde amnesia of events before injury
List the indications for CT scanning of head injuries in children
Within 1 hour, one of:
Suspicion of NAI
Traumatic seizure without history of epilepsy
At 2 hours after injury, GCS less than 15
Suspected open or depressed skull fracture or tense fontanelle
Sign of basal skull fracture
Focal neurological deficit
If under 1, bruising, swelling or laceration >5cm on head
Within 1 hour if more than one of:
Loss of consciousness >5 mins
Abnormal drowsiness
Three or more discrete episodes of vomiting
Dangerous mechanism of injury
Amnesia lasting more than 5 minutes
Describe the presentation, management, and prognosis of diffuse axonal injury
Loss of consciousness at time of injury then prolonged post-traumatic coma without expected neurological recovery
MRI best for detection (often missed on CT)
Limited options for treatment – prevent secondary brain injury, close monitoring including of ICP, rehabilitation
Spectrum of clinical consequences, most severe is long-term vegetative state
What is an extradural haematoma?
Describe the typical aetiology.
How does it present?
Collection of blood between the dura and skull
Typical aetiology – traumatic injury, particularly to pterion (point of union of frontal, parietal, temporal, and sphenoid bones), which causes bleeding from middle meningeal artery (branch of maxillary from external carotid)
Can also occur with venous bleeding
Presentation:
Headache
Nausea and vomiting
Confusion
Loss of consciousness – immediately after head injury, followed by period of lucidity, then progressively decreasing level of consciousness several hours later
Signs – reduced GCS, focal neurological deficits, hyperreflexia, spasticity, Babinski’s sign, Cushing’s triad
Describe the appearance of an extradural haematoma on CT
‘Lemon-sign’ – dura attached to sutures, blood trapped and creates hyperdense biconvex bulge as cannot expand past sutures, can cause mid-line shift and herniation
How are extra-dural haematomas managed? What are the potential complications?
Correction of coagulation abnormalities – reverse anticoagulants
?Anticonvulsants
?Reduce ICP – mannitol, barbiturates
Definitive management
Conservative management if small with minimal midline shift
Burr hole craniotomy to allow evacuation of haematoma
Trauma craniotomy – acute EDH with significant mass effect
Generally good prognosis if early evacuation of haematoma
Complications:
Infection – skull fracture or post-op
Seizures
Cognitive impairment
Hemiparesis
Hydrocephalus
Brainstem injury – significantly raised ICP
How are extra-dural haematomas managed? What are the potential complications?
Correction of coagulation abnormalities – reverse anticoagulants
?Anticonvulsants
?Reduce ICP – mannitol, barbiturates
Definitive management
Conservative management if small with minimal midline shift
Burr hole craniotomy to allow evacuation of haematoma
Trauma craniotomy – acute EDH with significant mass effect
Generally good prognosis if early evacuation of haematoma
Complications:
Infection – skull fracture or post-op
Seizures
Cognitive impairment
Hemiparesis
Hydrocephalus
Brainstem injury – significantly raised ICP
What are subdural haematomas?
Describe their aetiology.
How do they present?
Collection of blood between dura and arachnoid mater
Acute – present <3 days following injury
Subacute – present 3-21 days after injury
Chronic – present >21 days after injury
Occur secondary to high or low energy trauma
Low-energy trauma more common in elderly, alcoholics – shrinkage of brain, fragile brains
Due to shearing of bridging veins – usually venous bleeding, often deceleration injury
Presentation:
Acute – loss of consciousness, headache, focal neurology, signs of raised ICP
Chronic – progressive worsening confusion, memory loss, ataxia
Describe the appearance of a subdural haematoma on CT
‘Banana sign’, crescent shaped, blood free to flow around brain between dura and arachnoid
Can cause midline shift, less than extra-dural
Acute – hyperdense as fresh blood
Chronic – hypodense altered blood
What is the gold-standard investigation for suspected intracranial bleeding?
Non-contrast CT head
How are sub-dural haematomas managed? What are the potential complications?
Correct coagulation abnormalities – reverse anticoagulation
?Anticonvulsants
Definitive
Conservative – small bleed with minimal mass effect
Trauma craniotomy – acute SDH with significant mass effect
Large bleed/lots of cerebral oedema – hemicraniectomy
Burr hole craniotomy – chronic SDH, allows evacuation of blood
Complications:
Permanent neurological deficits
Coma
Seizures
Infection
Recurrent subdural haematoma
How do patients with opioid overdose present?
Decreased level of consciousness
Nausea/vomiting
Constipation
Pruritus
Confusion
Respiratory depression
Miosis
Describe the immediate management of opioid overdose
A-E assessment
A/B – may need airway adjuncts/intubation due to decrease consciousness/respiratory depression
Remove source if possible – e.g. transdermal patch, syringe driver
Close monitoring – potential to deteriorate rapidly
Naloxone – competitive opioid receptor antagonist
IV, IM, SC, intranasal (most commonly IV acutely)
Almost instant response but short-lived (half-life 60-90 minutes), initial improvement with recurrence of opiate overdose features if further doses not given
Risk in IV drug users that they will abscond then relapse into coma when naloxone wears off
Chonic pain or palliative care patients – risk of causing distress/pain if fully reverse opioids, give small doses of naloxone and titrate to effect
High dose opioids – naloxone infusion better than intermittent boluses
Can precipitate acute withdrawal syndrome and nausea and vomiting
What are the potential complications of opioid overdose?
Respiratory depression –> death
Acute lung injury after heroin overdose is common – presents with symptoms acute respiratory distress syndrome
Describe the mechanism of action of tricyclic antidepressants
Re-uptake inhibition – increased action of serotonin (5-HT receptors) and noradrenaline
Post-synaptic receptor antagonism – decreased action of histamine (H1 receptors), A-1 adrenoreceptors, acetylcholine receptors
Also act on fast sodium channels in myocardial cells – sodium channel blockade
Describe the clinical presentation of tricyclic antidepressant overdose
Symptoms within six hours of ingestion
Anticholinergic toxicity – dry mouth, blurred vision, confusion, constipation, tachycardia, urinary retention
Noradrenaline – tachycardia, tremor
Sodium channel blockade – palpitations, arrhythmias
Serotonin - hyperthermia
Can presents with reduced consciousness, seizures
ECG – widened QRS, prolonged QTc
Predispose to ventricular tachycardia and ventricular fibrillation
ABG - mixed acidosis
Hypokalaemia
Describe management of tricyclic antidepressant overdose
No specific management – supportive
Oxygen
Continuous monitoring with ECG
Fluid bolus if hypotensive
Benzodiazepines for seizures
Activated charcoal if present within one hour of ingestion – prevents absorption
Sodium bicarbonate in arrhythmia and acidosis to prevent progression to ventricular arrhythmias
Cooling measures for hyperpyrexia
Catheterise if urinary retention
Describe the clinical features of salicylate overdose
Causes mixed respiratory alkalosis and metabolic acidosis – stimulation of respiratory centre causes hyperventilation and respiratory alkalosis, direct effects of salicylates combined with acute renal failure may lead to metabolic acidosis
Features:
Hyperventilation
Tinnitus - ototoxicity
Lethargy
Sweating, pyrexia
Nausea/vomiting
Hyper/hypoglycaemia
Confusion
Seizures
Coma
How should patients with salicylate overdose be assessed?
ECG – monitor for arrhythmias, QRS widening and QT prolongation
BM – hypoglycaemia/hyperglycaemia
ABG – monitor acid-base balance, initially respiratory alkalosis then metabolic acidosis
Plasma salicylate concentration – taken >2 hours after ingestion, repeat 2 hourly until peak
Mild less than 300mg/L
Moderate 300-700mg/L
Severe >700mg/L
U&Es – hypokalaemia common
Coagulation – INR and PT may be increased in hepatic dysfunction
Describe management of salicylate overdose
A-E assessment
Protect airway
Supportive care, consider ICU admission
Activated charcoal if within 1 hour of ingestion of >125mg/kg
IV fluid
Potassium replacement – must do before bicarbonate
Sodium bicarbonate – enhances urinary excretion, alkalinises urine
Ongoing management:
Cooling
Haemodialysis – if renal failure, severe metabolic acidosis, seizures, salicylate concentration >900mg/L or >700 with acidosis or coma
Benzodiazepines for seizures
List the potential complications of salicylate overdose
Seizures
Acute respiratory distress syndrome
Coma
Arrhythmia – cardiac arrest
Drug-induced hepatitis
Describe the clinical presentation of beta-blocker overdose
CV – hypotension, bradycardia, AV block, heart block
Respiratory – bronchospasm
Metabolic – hypoglycaemia, hyperkalaemia
Neurological – coma, seizures
How is beta-blocker overdose managed?
Resuscitation – fluids
Hypoglycaemia – dextrose
Hyperkalaemia management
Activated charcoal if <1 since ingestion
Consider atropine if bradycardic
In resistant cases may use glucagon
How is a staggered paracetamol overdose defined?
Ingested total overdose in >1 hour
List risk factors for adverse outcomes in paracetamol overdose
Increased risk of hepatotoxicity:
Taking liver enzyme-inducing drugs – rifampicin, phenytoin, carbamazepine, chronic alcohol excess, St John’s wort
Malnourish e.g. anorexia, haven’t eaten in a few days
Acute alcohol intake is not associated with increased risk, may be protective
Describe the clinical presentation and potential complications of paracetamol overdose
Early symptoms:
Nausea and vomiting
Abdominal pain
If massive overdose can develop acidosis and coma early
Signs of hepatotoxicity (1-5 days post-ingestion):
RUQ pain
Jaundice
Renal failure
Transaminitis
Coagulation abnormalities
Hypoglycaemia
Hepatic encephalopathy
Multi-organ failure
Death
Describe the management of a paracetamol overdose
Need further assessment if – self-harm, symptomatic, taken 75mg/kg or more in within an hour, 75mg/kg or more in any 24-hour period and more than licensed dose in 24 hours, more than licensed dose in 24 hours and taken any paracetamol products in preceding 2 or more days
If non-staggered overdose presenting within 24 hours of ingestion
May benefit from activated charcoal if within 1 hour of overdose – rare
Take bloods at least 4 hours after ingestion (U&Es, HCO3, LFTs, FBC, INR, glucose, paracetamol level)
Ingested <150mg/kg – wait for results of bloods, plot on nomogram
Ingested over 150mg/kg –if won’t have blood results within 8 hours from ingestion then start NAC
If above treatment line on nomogram start NAC (if started and below treatment line can stop), give two NAC infusions
Can stop NAC when INR <1.3, ALT <100 and ALT <2x admission and paracetamol <20
If non-staggered after 24 hours
Take bloods
If features of hepatotoxicity start NAC, if none NAC not required
If staggered
Start NAC
Take bloods
Assess for hepatotoxicity - if none can stop NAC
What are the criteria for liver transplantation in the context of paracetamol overdose?
Arterial pH less than 7.3, 24 hours after ingestion
Or all of the following:
PT more than 100
Creatinine >300
Grade III/IV encephalopathy
Describe the clinical features of benzodiazepine overdose and the pathophysiology of this
Enhance GABA resulting in sedative, anxiolytic, anticonvulsant and muscle relaxant effects
Features:
Reduced consciousness
Respiratory depression
Hypotension
Bradycardia
Rhabdomyolysis
Hypothermia
Describe the management of benzodiazepine overdose
A-E assessment
Airway may be compromised by reduced consciousness – manoeuvre, adjuncts, anaesthetics involvement
Oxygen
Wide-bore IV cannulae, bloods (including CK)
ECG – may have arrhythmias
IV fluids – hypotension
Flumazenil – GABA receptor antagonist
Reverses CNS depression caused by benzodiazepines
Only used if requiring ventilation, only benzodiazepines (no possibility of mixed OD), patient is not benzodiazepine dependent
Risks of seizures if used incorrectly
List factors which may precipitate lithium toxicity
Dehydration
Hyponatraemia
Renal failure
Drugs – diuretics (thiazides), ACEi/ARB, NSAIDs, metronidazole
Describe the clinical presentation of lithium toxicity
Coarse tremor
Hyperreflexia
Acute confusion
Polyuria
Seizure
Coma
How is lithium toxicity managed?
Mild-moderate – IVF
?Sodium bicarb – urine alkalisation to promote excretion
Haemodialysis for severe toxicity
What is the therapeutic range for lithium? At what level does toxicity occur?
0.4-1.0mmol/L
>1.5 - usually toxicity
How is iron overdose managed?
Desferrioxamine – chelating agent
Describe the pathophysiology of carbon monoxide poisoning
Carbon monoxide binds readily to haemoglobin forming carboxyhaemoglobin – reduced oxygen-carrying capacity
Oxygen saturation of haemoglobin decreases – early plateau in oxygen dissociation curve
Describe the clinical features of carbon monoxide toxicity
Headache – most common
Nausea and vomiting
Vertigo
Confusion
Subjective weakness
Severe toxicity – pink skin, hyperpyrexia, arrhythmias, extrapyramidal features, coma
How should carbon monoxide poisoning by assessed and managed?
Pulse oximetry may be falsely high – similarity between oxyhaemoglobin and carboxyhaemoglobin
VBG/ABG should be done
Management:
100% high-flow oxygen, for minimum 6 hours
Hyperbaric oxygen?
Describe the assessment and management of lead poisoning
Measure serum lead level - >10 is significant
FBC – microcytic anaemia
Blood film – red cell abnormalities, basophilic stippling, clover-leaf morphology
Management:
Chelating agents –
Dimercaptosuccinic acid
D-penicillamine
EDTA
Dimercaprol
Describe the clinical presentation of lead poisoning
Abdominal pain
Peripheral neuropathy – mostly motor
Neuropsychiatric features
Fatigue
Constipation
Blue lines on gum margin
How is cyanide poisoning managed?
Hydroxycobalamin
List types of anti-emetics and their mechanisms of action
Anti-histamines e.g. cyclizine, promethazine
Dopamine antagonists, act by blocking the chemoreceptor trigger zone – prochlorperazine (used for chemotherapy-induced N+V), chlorpromazine hydrochloride, haloperidol (used in palliative care), domperidone (used in Parkinson’s, less likely to cause central effects)
5HT3-receptor antagonists – ondansetron (for N+V in those receiving cytotoxics)
Dexamethasone (for chemotherapy induced N+V), mechanism not fully understood
Metoclopramide – inhibit D2 and 5-HT3 receptors in chemoreceptor trigger zone
Describe the primary and secondary surveys in management of major trauma
Primary – purpose is to rapidly identify and manage impending or actual life threats to patient
C – catastrophic haemorrhage
A – airway with C-spine control
B – breathing
C – circulation
D – disability
E - exposure
Secondary – after primary survey completed, immediate life-threats identified and managed and patient is stable
Continue to monitor A-E
Examine head to toe for injuries, including log roll to look at back
Can include FAST scan – focused assessment with sonography for trauma
Look for intraperitoneal free fluid
How is GCS calculated?
Eyes
Open spontaneously – 4
Open to voice – 3
Open to pain – 2
No response – 1
Motor
Obeys commands – 6
Localises to pain – 5
Normal flexion/withdrawal to pain – 4
Abnormal flexion (decorticate posturing) – 3
Abnormal extension (decerebrate posturing) – 2
None – 1
Voice
Speech orientated to time, person, place – 5
Confused speech – 4
Inappropriate words – 3
Incomprehensible sounds – 2
None – 1
What is the ratio of compressions to breaths in adult and paediatric BLS?
Adult - 30 compressions, 2 breaths
Child - 15 compressions, 2 breaths
