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ORTEM > ED and trauma > Flashcards

ED and trauma Flashcards

1
Q

3 aims in a patient with major haemorrhage

A

1) Stop bleeding
2) Restore circulating volume
3) Restore/maintain tissue perfusion and oxygenation
- -> prevents hypovolaemic shock and the consequent multiorgan failure

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2
Q

What does major haemorrhage protocol involve?

A
  1. Establish IV access with 2x large-bore cannulas - can use any of the three main veins of the antecubital fossa (the cephalic, basilic, and median cubital)
  2. At the same time take bloods (G+S, clotting screen, FBC, LFTs, U+Es). LFTs are taken due to DIC.
  3. Transexamic acid 1g stat
  4. 1-2L fluids (Hartman’s)
  5. If stable can wait the hour for a full cross-match; if unstable MH pack 1 (6 units red cells, 4 FFP)
  6. Maintain normothermia and pass blood product through a blood warmer (hypothermia impairs platelet function, increasing DIC risk), removal of wet clothes, Bair hugger, bladder irrigation with warm fluids.
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3
Q

What is Cushing’s triad?

A

Hypertension, bradycardia, and irregular breathing.
Due to raised ICP - usually this response is seen in the terminal stages of acute head injury, and indicates imminent brain herniation.
Can also be seen after administering IV adrenaline.

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4
Q

Indications for urgent airway support?

A 
Respiratory distress
Hypoventilation
GCS 8 or less
Major trauma to skull/face/neck
Chest injuries
High SC injury
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5
Q

What should you be thinking if a patient tolerates a Guedel without gagging/coughing?

A

No protective reflexes so require ET intubation as soon as is practical to protect from aspiration
High GCS is an absolute contraindication to OPA.

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6
Q

What is PPV?

A

Positive pressure ventilation - mechanical ventilation either via bag valve mask (Ambu bag) or mechanical ventilator.

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7
Q

What is a supraglottic airway?

A

Includes the I-Gel and laryngeal mask airway (LMA).
Aim to maintain upper airway patency for ventilation and oxygenation + administration of inhaled anaesthetic e.g. propofol, without need for ET intubation.
Allows intermittent PPV (can’t use high airway pressures; also has a higher risk of gastric insufflation and so regurg)
Can be inserted with a comparatively low skill set compared to ET tubes, and lower risk of airway trauma.
Doesn’t fully protect from aspiration like ET does.
Can be a lifesaving tool in a ‘cannot intubate cannot ventilate’ (CICV) scenario. In addition, some supraglottic airways can be useful in difficult intubations as a conduit for an ET tube.

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8
Q

Purposes of airway management and specifically ET intubation?

A

a) Maintain patent airway, to b) allow ventilation and oxygenation to c) avoid cardiopulmonary arrest.

ET specifically: Protects from aspiration, and prevents gastric distension

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9
Q

Complications of bag-mask ventilation?

A 
Gastric inflation (can result in vomiting and so aspiration)
Lung injury (barotrauma) from over-stretching of lung tissue; can lead to ARDS
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10
Q

How do you assess breathing in critical care?

A

Look, feel and listen for signs of respiratory distress: measure RR and sats; check to see if the chest is rising and falling symmetrically; examine for peripheral/central cyanosis; percuss chest; feel for chest expansion and feel for tracheal deviation; listen for wheeze/stridor/secretions; auscultate for crackles, reduced air entry, bronchial breathing.

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11
Q

Causes of respiratory distress in ED/trauma?

A

Surgical: tension pneumothorax, simple pneumothorax, haemothorax, flail chest
Medical: asthma, COPD exacerbation, pulmonary oedema

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12
Q

Contraindications to a nasopharyngeal airway?

A

High GCS (though can be used in patients with a gag reflex intact)
Basal skull fracture
Mid-face fracture
Bleeding disorder

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13
Q

What is CPAP used for?

A

Acute pulmonary oedema

Sleep apnoea

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14
Q

What is BiPAP used for?

A

COPD exacerbations and ARDS

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15
Q

What % of oxygen can a non-rebreathe mask deliver? And what flow rate do you use with this mask?

A

15L flow rate and gives 85-90% oxygen

aim for sats of 94-98% with this, not 100%

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16
Q

Maximum FiO2 deliverable with Venturi mask?

A

60% (green mask), set flow to 12-15L/min

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17
Q

Flow rates and FiO2 deliverable by simple face mask?

A

5-10L/min

21-60% (depends on resp rate and depth)

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18
Q

Deadly triad of trauma?

A

Hypothermia
Acidosis
Coagulopathy (DIC)

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19
Q

3 drugs of RSI for intubation?

A

Rocuronium - antagonist of nicotinic AChR
Ketamine (anaesthesic dose - 2mg/kg)
Opioid (e.g. fentanyl)

20
Q

Why is RSI done?

A

To avoid laryngeal spasm (which results in totally obstructed airway)

21
Q

Why does hypothermia happen in trauma?

A 
Anaesthesia can cause hypothermia
Neuromuscular block (rocuronium) also stops shivering
Acidosis potentiates hypothermia and vice versa
22
Q

Why does acidosis happen in trauma?

A

Respiratory acidosis from hypoventilation (due to thoracic injury resulting in pain e.g. pneumothorax, broken ribs; or reduced respiratory drive due to head injury) –> Mx: if low GCS, intubation and ventilation will normalise CO2. If high GCS, give analgesia (10-20mg morphine IV, +/- analgesic dose of ketamine if needed)

Metabolic acidosis due to haemorrhage shock resulting in lactic acidosis; Mx is to control bleed, resuscitate, surgery for definitive management.

23
Q

pH down and CO2 up?

A

pH down = acidosis
CO2 up = hypercapnia

opposite so a respiratory acidosis.
ROME: respiratory opposite, metabolic

24
Q

Why does respiratory acidosis increase ICP?

A

Hypercapnia causes vasodilation of cerebral vessels

25
Q

What is the management of a tachyarrhythmia with adverse features in a peri-arrest scenario?

A

Remember this could be any rhythm - broad-complex, AF, atrial flutter, paroxysmal SVT.

  1. DC cardioversion under sedation (midazolam) and analgesia (fentanyl) - up to 3 shocks
  2. If unsuccessful, give amiodarone 300mg IV over 10-20 minutes, and then REPEAT SHOCK.
26
Q

Management of a regular broad-complex tachyarrhythmia with NO adverse features in a peri-arrest scenario?

A
  1. If VT or uncertain rhythm, give amiodarone 300mg IV over 20-60 mins, then 900mg over 24h. (i.e. no shocking)

Remember an SVT (AVNRT or AVRT) with known BBB can give a regular broad-complex tachycardia; if this is the case, treat as a regular narrow-complex tachycardia.

27
Q

What would you be thinking in a patient with an IRREGULAR broad-complex tachycardia with no adverse features?

A

This is either torsade de points (polymorphic VT), AF with WPW, or most likely AF with bundle branch block. In latter situation would treat as for narrow complex tachycardia.

28
Q

How would you manage an irregular, narrow-complex tachycardia in ED?

A

Likely to be acute AF.
Mx is either rate control (metoprolol, diltiazem, or if IHD then digoxin IV), chemical cardioversion (flecainide IV, or amiodarone IV), or DC cardioversion.
If symptoms >48h, cardioversion is contraindicated as risk of thrombosis; instead give rate control and LMWH.

29
Q

Uses of IV amiodarone in arrhythmias presenting to ED?

A

IV amiodarone is given in the peri-arrest scenario for:

  • Any tachycardia with unstable features if first-line DC cardioversion is unsuccessful after 3 shocks
  • A regular, broad-complex tachycardia with NO unstable features, as first-line (over 20-60 min, then a 900mg dose over next 24h)
  • For acute AF to chemically cardiovert (alternative is flecainide, however remember flec is CI in IHD)
30
Q

Management of a regular, narrow-complex tachycardia presenting to ED?

A

Likely to be a paroxysmal SVT, but could be atrial flutter with a physiological 2:1 AV block (150bpm). Consider if requires treatment.

  • Vagal manouvres
  • If unsuccessful, adenosine IV as a rapid bolus (requires cardiac monitoring)

If this is unsuccessful, suggests atrial flutter - seek expert help (tx is beta-blockers).

31
Q

Which veins are usually used in ED for central venous access? e.g. amiodarone

A

The internal jugular and subclavian.
IJV usually preferable due to risk of pneumothorax with the subclavian.
Right IJV is used where possible to reduce risk of damage to the thoracic duct.

32
Q

What is shock?

A

Failure to adequately perfuse and oxygenate vital organs.
Clinically, shock is recognised by:
- Hypotension (<90 mmHg), +/- associated tachycardia
- Altered consciousness and/or fainting (due to reduced cerebral perfusion)
- Poor peripheral perfusion (cool, clammy/sweaty skin, pallor, reduced cap refill) though note in the early phase of septic shock there may be vasodilation with warm peripheries
- Oliguria (urine output <50ml/hr)
- Tachypnoea

33
Q

Types of shock?

A

Hypovolaemic

  • Blood loss - trauma, GI bleed, ruptured AAA
  • Fluid loss/redistribution i.e. third spacing - burns, vomiting/diarrhoea, pancreatitis, sepsis, anaphylactic)

Cardiogenic

  • Primary: MI, arrhythmias, valve dysfunction
  • Secondary: cardiac tamponade, massive PE, tension pneumothorax

Septic shock
Anaphylactic shock
Neurogenic shock

34
Q

Bloods in shock?

A

FBC, U+E, glucose, LFTs, lactate, coagulation screen, (blood cultures)

35
Q

Areas that a FAST scan looks at for presence of free fluid?

A

Hepatorenal recess (Morrison’s pouch)
Splenorenal recess
Pelvis (Pouch of Douglas)
Pericardium

36
Q

Causes of metabolic acidosis?

A

Increased acid load (lactic acidosis, ketoacidosis, ingestion of salicylates/methanol/ethylene glycol/metformin)
Reduced removal of H+ (renal failure or RTA types 1 and 4, K+-sparing diuretics as Na+ gets exchanged for K+ rather than H+)
Any process that causes bicarbonate loss (diarrhoea, pancreatic/intestinal fistulas, acetazolamide, RTA type 2)

Raised AG MA:
Diabetic ketoacidosis, ethylene glycol poisoning, salicylate overdose, lactic acidosis from shock (note that this is kind of competing against the contraction alkalosis you’re getting b/c of hypovolaemia)

Normal AG MA = ABCD: Addison’s, Bicarbonate loss (diarrhoea, fistula, acetazolamide), Chloride excess (e.g. saline infusion), potassium-sparing Diuretics (spironolactone, amiloride).
A note: normal AG metabolic acidosis is hyperchloraemic, as kidney compensates for the reduced/consumed bicarbonate by retaining Cl-.

37
Q

Causes of metabolic alkalosis?

A
  • Hypochloremia e.g. due to vomiting
  • Hypokalemia e.g. aggressive diuretic therapy, GI loss (vomiting, diarrhoea, NG tube), hyperaldosteronism (Cushing’s / Conn’s)
  • Contraction alkalosis i.e. dehydration (due to stimulation of RAAS by low BP)
  • Bicarbonate GAIN – antacids, sodium bicarb infusion
38
Q

Causes of hypokalemia

A
  • Renal loss: diuretic therapy, diuretic phase following AKI, Conn’s/Cushing’s
  • Dietary
  • Cutaneous (sweating)
  • Transcellular shift due to insulin overdose, beta receptor agonists e.g. salbutamol, alkalosis.
39
Q

Causes of hyperkalemia?

A
  • Spurious
  • Renal failure (acute or chronic)
  • Parenteral infusion i.e. TPN
  • Adrenal insufficiency (Addison’s)
  • AID:
    • Metabolic Acidosis
    • Insulin deficiency
    • Drugs: digoxin overdose, non-selective β blockers, succinylcholine
40
Q

Biochemical features of DKA?

A

Ketosis, hyperglycaemia (>11), acidaemia.

Serum K+ can be normal or raised (hyperkalemia) but there is actually a whole-body K+ deficit because of K+ shifting out of cells and being lost in the urine, as a result of hyperglycaemiac hyperosmolarity

41
Q

Tx of DKA?

A

Fluid resuscitation
IV insulin
IV potassium

Do capillary and lab glucose, VBG, U+E, FBC, blood cultures.
ECG, CXR, MSU
Hourly monitoring of cap BG and ketones

42
Q

Tx of acute asthma?

A
  • High flow O2
  • High-dose nebulised salbutamol, or 10 puffs salbutamol via spacer
  • Corticosteroid (prednisolone PO, or hydrocortisone IV)
  • If acute severe/ life-threatening, add nebulised ipratropium bromide
  • Can add IV magnesium sulphate if not responding

If patient can’t talk, get senior ED and ICU help in case intubation is required.

43
Q

Why does coagulopathy occur in trauma?

A

Major haemorrhage uses up clotting factors/platelets

Hypothermia causes platelet dysfunction

44
Q

Mx of DIC/coagulopathy?

A

FFP, platelet transfusion, minimise movement

45
Q

What happens in a tension pneumothorax?

A

There is a valve mechanism where air enters the pleural space from a channel with the lung but can’t leave, causing mediastinal shift; increased intrathoracic pressure results in kinking of the IVC, preventing blood from returning to the heart so effectively causing cardiogenic shock as blood can’t enter the heart during diastole.

46
Q

What does a spirometer measure?

A

FEV1 (volume of air exhaled in 1s)

FVC (total volume of air expelled in a full exhalation)

ORTEM (1 decks)

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