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Emergency medicine ILAs Flashcards

1
Q

Status epileptic causes

A 
Drug withdrawal
Intercurrent illness
HYPOglycaemia
CVA - Haemorrhagic
Alcohol intoxication or withdrawal
Malignancy - Dex to reduce oedema
Febrile convulsions
Systemic infection - Lowers seizure threshold

Eclampsia - Give IV Magnesium Sulphate and CS
1. HTN
2. Proteinuria
3. Oedema
(After 20 weeks)

Electrolyte abnormality

  • HYPOnatraemia
  • HYPERkalaemia
  • HYPERcalcaemia

Neuro infection

  • Meningitis
  • Encephalitis
  • CNS abscess
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2
Q

Status epilepticus complications

A 
Metabolic acidosis - Lactate
Aspiration
Cerebral ischaemia - Neuro hypoperfusion
Hypoglycaemia
Hyperpyrexia

Cerebreal oedema
Pulmonary oedema

Rhabdomyolysis

  • HYPERkalaemia - Cardiac arrhythmias
  • Creatinine Kinase - Renal failure
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3
Q

ACS questionnaires

A

QRISK2 - Risk of heart attack/stroke in next 10 years

GRACE score - 6-month mortality for patients with ACS

TMAX - Rules out ACS

HEART - 6-week risk of major adverse cardiac event

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4
Q

PCI explained

A

“Wire passed into blood vessels around heart
Inject contrast - Lights up on XR - Shows narrowing
May need stenting, depending on how narrow
Insert a small wire tube to widen the passage and increase flow”

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5
Q

Fibrinolytics

A

Tissue plasminogen activator - Alteplase

Retaplase
Streptokinase
Urokinase

Ci if…

  • Acute bleeding
  • Recent haemorrhagic stroke
  • Bleeding disorders - VWD and haemophilia
  • Allergy to thrombolytic agent
  • Major trauma or brain surgery within 3 months
  • Aortic dissection is DDx
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6
Q

Consciousness and unconsciousness

A

Consciousness requires two key components of CNS

  1. Reticular Activating System - RAS
  2. At least one cerebral hemisphere

Unconsciousness requires…
- Failure of RAS
OR
- Failure of BOTH cerebral hemispheres

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7
Q

Causes of unconsciousness

A

RAS failure

  • Brain-stem stroke - Ischaemic or haemorrhagic
  • Pre-death event - Increased brain swelling pushes down on the brain stem

Failure of both hemispheres

  • Failure of adequate blood supply
  • Inadequate substrate for metabolism - Oxygen or glucose
  • Direct or indirect trauma to the cerebrum
  • Toxic insult - Infection, metabolites, poisons
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8
Q

Unconsciousness examination

A

Ensure patient is neither hypoxic nor hypotensive!

Look for evidence of injury

  • Obvious trauma
  • Bitten tongue - Seizure?

Assess temperature

  • Fever - Meningitis / Encephalitis
  • Hypothermia - Sepsis, cold exposure, hypothyroid
  • Brain injury - Pontine / Hypothalamic

Look for evidence of organ failure

  • Respiratory - Hypoxia / Hypercapnia
  • Cardiac - Hypotension
  • Pancreatic - Ketones
  • Renal - Uraemia
  • Liver - Fetor hepaticus
  • Organophosphate poisoning - Garlic smell

Evidence of toxin ingestion/inhalation

  • Needle marks
  • Bullae - Barbiturate overdose
  • Cherry red appearance - CO poisoning
  • Dry skin - Tricyclic / Anti-Ach overdose
  • Profuse sweating - Hypoglycaemia / Insecticide poisoning
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9
Q

GCS

A

EVM

Eyes

  1. No response
  2. To pain
  3. To voice
  4. open

Voice

  1. No response
  2. Moans / Unintelligible
  3. Nonsensical speech
  4. Disorientated
  5. Oriented and alert

Motor

  1. No response
  2. Decerebrate extension
  3. Decorticate flexion
  4. Withdraws to pain
  5. Localises pain
  6. Follows commands
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10
Q

Suitable methods for applying a painful stimulus

A 
Trapezius squeeze
Supraorbital pressure
Sternal rub
Pressure behind jaw
Pinch nailbed
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11
Q

Opioid overdose management

A

Naloxone - 400mcg IV
No response - Increase dose to 800mcg for 2 doses at 1 minute intervals
Still no response - Increase dose to 2mg for 1 dose
4mg may be used if severely poisoned

Still no response - Review diagnosis

Bag and mask ventilation

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12
Q

Naloxone risks

A

Short half-life
Ensure that it is not fully metabolised before opiate leaves their system

Norpropoxyphene has cardiotoxic effects
May require treatment with sodium bicarb or magnesium sulphate

Arrhythmias may occur for up to 12 hours

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13
Q

Intubation criteria

A

GCS < 8

Inability to maintain airway patency
Inability to protect airway against aspiration

Failure to ventilate
Failure to oxygenate

Anticipation of deteriorating course that will lead to respiratory failure

  1. Anaesthetist
  2. Laryngoscope
  3. Sedative with neuromuscular blocking agent - Etomidate, ketamine, propofol
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14
Q

Cervical collars

A

When to remove…

  • Patient has shown gross motor function in all 4 extremities
  • Patient has no paraesthesia or neuro symptoms
  • CT shows no cervical spine fracture or acute abnormality

Benefits - Reduces risk of cervical spine injury

Risks

  • Can cause mechanical asphyxiation and haemodynamic instability
  • Reduced venous return from the head - May lead to raised ICP
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15
Q

Major trauma - ATMIST

A 
Age
Timing
Mechanism of injury or medical complaint
Injuries / examination findings
Signs
Treatment given
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16
Q

Zero point survey

A

Optimises resuscitation effort - STEPUP

Self - Physical an cognitive readiness
Team - Leader identified, roles allocated, team briefed
Environment - Danger, space, light, noise, crowd control
Patient - Primary survey - ABCDE
Update - Share mental model of patient status
Priorities - Identify team goals and set mission trajectory

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17
Q

Tension pneumothorax clinical features

A 
Sweating
Pulsus paradoxus
Hypotension
Tachycardia
Raised JVP

Chest examination

  • Reduced movement on affected side
  • Tracheal deviation
  • Hyper-resonance on percussion
  • Reduced breath sounds
18
Q

Tension pneumothorax

Shock pathophysiology

Management

A

Collapsed lung on affected side + Compressed lung on contralateral side
= Compromised gas exchange = Hypoxia

Atrial wall compression = Decreased venous return

Hypoxia + Decreased venous return = Impaired cardiac function

Management - Urgent decompression - Needle aspiration / Chest drain

  • 2nd intercostal space MC line
  • 5th intercostal space axilla
19
Q

Life-threatening chest injuries

A

ATOM FC

Airway obstruction / Aortic dissection
Tension pneumothorax
Open pneumothorax - Three-sided dressing - One-way valve
Massive pneumothorax - Restore circulating blood volume + Chest drain

Flail chest
Cardiac tamponade - Aspiration and decompression

20
Q

Major haemorrhage protocol

A

Easy access to blood products in case of major haemorrhage

Red cells
FFP
Platelets
1:1:1

+ Cryoprecipitate

21
Q

Whole body CT indications

A 
High-speed MVC
Non-trivial motorcycle collision
Death at scene
Fall from height > 2 metres
Concerning mechanism of injury
Abnormal FAST or chest/pelvis XR
Abnormal vital signs

Non-contrast CT brain + face
Non-contrast CT cervical spine
CT thorax/abdomen in angiographic or delayed phase
CT abdo/pelvis in portal venous phase
Multiplanar reconstructions of the thoracic and lumbar spine

22
Q

Fracture splinting

A

Pain management
Prevents further displacement and neurovascular injury

Femoral nerve block
Morphine + O2
Gas and air

Afterwards

  • NV status
  • XR
23
Q

Rash associated with allergic reaction

A

Urticaria - Hives

Blanching
Raised palpable wheals

Linear
Anular - Circular
Arcuate - Serpiginous

24
Q

Clinical features of anaphylaxis

A

Airway - Pharyngeal/laryngeal oedema - Stridor
Breathing - SOB, wheeze, fatigue, hypoxic confusion, cyanosis, arrest
Circulation - Shock, tachycardia, hypotension, collapse, LOC, arrest

Skin/mucosal changes - Urticaria

GI symptoms - N/D/V, cramps, bloating, distension

CNS symptoms - Confusion, dizziness, headache, agitation, anxiety

Absorption of allergen may be delayed

25
Anaphylaxis mechanism
Antigen binds to IgE antibodies Degranulation of basophils and mast cells Release of pro-inflammatory and vasoactive mediators ``` Increased vascular permeability Vasodilation Myocardial dysfunction Hypotension CV collapse Altered smooth muscle tone - Bronchospasm, asthma, uterine cramps ANS activation - Tachycardia, anxiety, mucus secretion Increased platelet aggregation ```
26
Anaphylactic vs anaphylactoid reaction
Anaphylaxis - Type 1 immune mediated - Allergen reacts with IgE - Degranulation of basophils and mast cells Anaphylactoid - Non-immune mediated reaction - Allergen causes direct release of mediators from basophils and mast cells Management is the same
27
Other useful drugs in anaphylaxis
Bronchodilators - Salbutamol - Ipatropium - Aminophylline - Magnesium - Nebulised adrenaline Cardiac drugs - Noradrenaline - Vasopressin - Metaraminol - Atropine Patient taking a BB - Glucagon to reverse
28
IV adrenaline
Indication - Cardiac arrest - Profound hypotension - Not responding to fluids and IM adrenaline Risks - Tachycardia - Hypertension - Arrhythmias - Myocardial ischaemia Only to be given by a specialist - Anaesthetist or ED consultant
29
Anaphylaxis safe discharge
Patients observed for 6-24 hours in case of second phase reaction (20%) - Young patients - Extreme primary reaction - Long delay in treatment Antihistamines and oral steroids for up to 3 days - Prevent further reaction Consider adrenaline auto-injector - Epi-pen Clear instructions to return to hospital if symptoms return Education on recognising early symptoms of anaphylaxis Carry epi-pen at all times Referral to allergy clinic
30
Anaphylaxis diagnosis
Serum tryptase | Immediately after treatment Second sample within 1-2 hours of symptoms onset No more than 4 hours
31
Which condition mimics anaphylaxis
C1-esterase inhibitor deficiency - Often diagnosed as not responding to anaphylaxis treatment Management - C1-esterase inhibitor concentrate - FFP - Supportive measures
32
Most common anaphylactic reactions
Hospital - Drug induced - Penicillins and NSAIDs - Anaesthesia - NM blocking agents, IV/local anaesthetics, opioids - Colloids - Latex Community - Food - Peanuts, shellfish, eggs, milk, fish - Insect bites - Exercise induced - 3-4 hours after food ingestion - NSAIDs
33
Pre-test probability
Probability of patient having the target disorder before a diagnostic result Decides whether to test or not If pre-test probability is very high or very low, a contradictory result will only lead to confusion and would be disregarded as false Testing may be useless if it will not change the management plan
34
D-dimer
Fibrin degradation product Small protein fragment in the blood after a clot is degraded by fibrinolysis
35
PE in pregnant ladies
V/Q scan USS doppler to look for DVT D-dimer + YEARS criteria PE can be ruled out if... - YEARS criteria not met and D-dimer < 1000 - YEARS criteria > 1 and D-dimer < 500 Start anticoagulation if... - YEARS criteria not met and D-dimer > 1000 - YEARS criteria > 1 and D-dimer > 500
36
Thrombophilia
Imbalance in natural blood-clotting factors Increased risk of developing blood clots Factor V Leiden Prothrombin 20210 Protein C, protein S, antithrombin deficiency - Natural anticoagulants Antiphospholipid syndrome
37
Paracetamol overdose history
How much was taken (Max is 4g over 24 hours) Over what time? - Acute < 1 hour - Staggered > 1 hour - Therapeutic excess - Taken with intention to treat pain How long since the last dose
38
Paracetamol toxicity pathophysiology
Liver - Cytochrome P450 saturated Toxic metabolite - N-acetyl-B-benzoquine imine Conjugated by glutathione to form mercapturic acid Glutathione saturated - Toxin forms covalent bonds with cell proteins Cell death - Hepatocytes and renal tubules N-acetyl cysteine increases glutathione production Renal - Tubular necrosis Peak concentration at 1-2 hours post-ingestion
39
Paracetamol overdose bloods
Serum paracetamol concentration LFTs Prothrombin time and INR Blood glucose - Hypoglycaemia in acute liver injury FBC U&E VBG/ABG - Lactic acidosis
40
NAC
Plot paracetamol level at 4 hours on graph Give NAC if this falls on or above the treatment line Starting NAC prior to seeing paracetamol level... Patient presents 8-24 hours after ingesting > 150ml/kg within 1 hour Patient presents > 24 hours after ingesting with... - Jaundice - Hepatic tenderness - ALT ^ - INR > 1.3
41
Important questions after overdose
Intentions? How do they feel now? Relieved or frustrated? Has this happened before? Was it an impulse decision? Did they make any plans/arrangements? What effort did they make to not be found?

3B (23 decks)

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