trunk trauma Flashcards

1
Q

3 Mechanisms of chest injury

A

blunt, crush, penetrating

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2
Q

Blunt happens when? (acceleration/deceleration)

A

Commonly result from fall from height, or RTA at speed

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3
Q

Blunt consequences?

A

Sudden deceleration leads to intrathoracic organs taking on large apparent weights

Causes destruction of attached vasculature

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4
Q

crush happens when

A

elastic limits of the chest and its contents have been exceeded

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5
Q

crush presentation

A

flail chest with multiple rib fractures, pneumothorax or haemothorax,
pulmonary contusion

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6
Q

Penetrating happens when

A

Stabbing, shrapnel, missile or bullet

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7
Q

other mechanism of injury

A

blast, inhalation burns, foreign body aspiration

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8
Q

ATMIST: paramedic handover to trauma team stands for

A
Age
time of injury
mechanism of injury
injuries identified
symptoms and signs
treatment given
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9
Q

what is major trauma

A

Major injury affecting more than one body system

Injury severity score >15

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10
Q

what is “golden hour”

A
  • urgency of care required by major trauma patients to prevent ‘early deaths’
  • Some patients have overwhelming injuries and will die immediately, others have injuries that are
    salvageable if addressed in time, if this window is missed then they will die
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11
Q

what is seatbelt sign

A

Contusions and abrasions on abdomen of a restrained occupant in an MVA

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12
Q

what will seatbelt sign mandates?

A

Mandates close observation of abdominal CT

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13
Q

seatbelt syndrome?

A

small bowel, stomach and colon and vertebral injury

Chance fracture

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14
Q

primary survey airway includes?

A
  • maintenance with cervical spine protection(Jaw thrust/chin lift, suction)
  • Two aspects to a good airway :patent and protected
  • Endotracheal intubation with decreased LOC
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15
Q

Breathing includes?

A
  • Inspect thorax and neck for deviated trachea, open wounds, abnormal chest movement,
    crepitus-
    Auscultate for breath sounds
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16
Q

consequence of rib fracture?

A

Isolated = CXR to exclude associated injury
Multiple = beware pneumothorax
Flail segment = beware pneumothorax

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17
Q

Circulation and haemorrhage control

A

Assess blood volume–skin colour, cap refill, radial/femoral/carotid pulse,BP

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18
Q

Signs of haemorrhagic shock:

A
  • Tachycardia > reduced pulse pressure > hypotension > reduced perfusion to peripheries and brain
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19
Q

haemorrhage control includes?

A
  • Place 2 large bore peripheral IV catheter
  • Rapid infusion of warm crystalloid solution if needed
  • Direct pressure to sites of external bleeding
  • Consider central venous access if peripheral sites are unavailable
  • Consider pericardiocentesis for suspected pericardial tamponade Left lateral decubitus position for third trimester pregnancy
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20
Q

Disability includes assessment of?

A
Neurologic screening, MSE
Pupil size and reactivity
-Limb length and movement ,grip strength
- Orientation,GCS
- Measure glucose
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21
Q

exposure means?

A

Expose the patient–inspect for burns, toxic exposure

- Log roll maintaining neck stabilisation – inspect and palpate thoracic spine, flank, back and buttocks

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22
Q

what is DCR

A

Damage control resuscitation

  • Approach to trauma combining ABC rather than just ABC o Catastrophic bleeding > airway > breathing > circulation
  • Requires early recognition and pre-emptive management
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23
Q

6 killing conditions in primary survey: ATOM-FC

A
Airway obstruction or disruption
Tension pneumothorax
Open pneumothorax
Massive haemothorax
Flail chest
Cardiac tamponade
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24
Q

The bloody viscous cycle

A

Bleeding > acidosis > hypothermia > coagulopathy

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25
Q

What is secondary survey?

A

Top to toe examination for additional injuries or findings

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26
Q

what does secondary survey include?

A
Scalp wound bleeding – direct pressure, sutures o Facial instability, potential for airway instability
Identify haematotympanum
Identify epistaxis
Identify avulsed teeth, jaw instability
Abdominal distention and tenderness
Penetrating injuries
Pelvic stability
Inspect urethral meatus for blood
Peripheral pulses for vascular compromise
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27
Q

what is stress responses?

A

Hormonal and metabolic changes following trauma/surgery

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28
Q

endocrine changes in stress response?

A

Increased secretion of pituitary hormones > increase in catabolism of food substrates (carb, protein, fat)
Increased activation of SNS
Insulin resistance in perioperative period

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29
Q

Sympathoadrenal changes in stress response?

A

Hypothalamic activation of ANS > increased secretion of catecholamines from adrenal medulla + release of NE from presynaptic nerve terminals = tachycardia, hypertension

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30
Q

what is local inflammatory response in stress response?

A

o Cytokines released – IL-1, TNF-a
o IL-6 (acute phase response): Production of acute phase proteins in the liver
- Increased CRP, fibrinogen, alpha 2 macroglobulin, copper
- Decrease in transferrin, albumin, zinc and iron
- Act as inflammatory mediators

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31
Q

what is type1 resp failure?

A

Hypoxemic - most common form
o Occurs because of damage to lung tissues, preventing oxygenation of blood (V/Q mismatch and
shunting, leading to widening of alveolar-arterial PaO2 gradient)
o Low arterial PaO2 + low/normal arterial PaCO2
o Almost all diseases of lung involving fluid filling or collapse of alveoli – cardiogenic and non-cardiogenic
pulmonary oedema, pneumonia, pulmonary haemorrhage

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32
Q

what is type 2 resp failure

A

Hypercapnic
o ‘Ventilatory failure’ – alveolar ventilation is insufficient to excrete CO2 produced o Low arterial PaO2 + high arterial PaCO2
o Drug overdose, neuromuscular disease, chest wall abnormalities and COPD

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33
Q

pattern of death in major traumas?

A
  1. immediate death(s-min)
    - unpreventable
    - high spinal or brain injury (apnoea)
    - great vessel disruption ( catastrophic haemorrhage)
  2. early death(min-hr)
    - haemorrhage related
  3. late deaths(hr-wk)
    - multiorgan failure or sepsis
34
Q

clinical presentation of airway obstruction?

A
o External neck deformity or haematoma
o Crepitus from laryngeal fracture
o Hoarse voice or gurgling
o Signs of complete airway obstruction – silent chest, paradoxical chest movements o Signs of partial airway obstruction – stridor, respiratory distress
o Cyanosis
35
Q

Rx of airway obstruction?

A

o High flow O2 via non-rebreather mask

o Achieve airway patency via airway maneuver or surgical airway

36
Q

what happens in tension pneumothorax

A

lung defect acts as a one-way valve, allowing ongoing air leaks into the pleural space without letting it leak back out

37
Q

how fatal is tension pneumothorax?

A

Can be rapidly fatal as intra-thoracic pressure rises causes decreased venous return and kinking of the great
vessels – obstructive shock

38
Q

presentation of tension pneumothorax?

A

o Tracheal deviation to the contralateral side
o Ipsilateral hyper expansion and decreased chest movement
o Ipsilateral hyper-resonance
o Anxiety and agitation
o Respiratory distress
o Tachycardia and hypotension
o Neck vein distention

39
Q

how to treat tension pneumothorax?

A

o High flow O2 to maintain saturation targets
o Immediate needle thoracocentesis – 14 gauge
o Intercostal catheter insertion after needle decompression

40
Q

what happens in open pneumothorax?

A

“Sucking” chest wound – communication between pleural space and surrounding atmospheric pressure

41
Q

presentation of open pneumothorax?

A
o trachea in the midline 
o Open wound on chest wall
o Anxiety and agitation
o Respiratory distress – due to lung collapse o Tachycardia
o Decreased chest movement ipsilaterally
o Hyper-resonance ipsilaterally
o Decreased breath sounds ipsilaterally
42
Q

how to treat open pneumothorax?

A

o three sided dressing
o High flow O2 to maintain saturation targets o Cover with ‘flutter valve’
o Catheter in separate intercostal space
o Formal exploration prior to closing

43
Q

when does Massive haemothorax happens?

A

blunt or penetrating trauma to the thoracic organs; massive haemothorax defined by volume on thoracotomy

44
Q

classification of massive harm-thorax?

A

o Blood loss >1500ml or 1/3 blood volume

o Blood loss >200ml/hr for 2-4 hours

45
Q

aetiology of Massive haemothorax?

A

Injury to lung parenchyma, intercostal artery or internal mammillary branch

46
Q

why Massive haemothorax is life threatening?

A
  1. Acute hypovolemia doesn’t allow sufficient preload to sustain left ventricular function and CO
  2. Collapsed lung promotes hypoxia by creating alveolar hypoventilation, V/Q mismatch and anatomic shunting
  3. Hydrostatic pressure of haemothorax compresses vena cava and pulmonary parenchyma,
    further impairing preload
47
Q

presentation of massive hemothorax?

A

o Haemorrhagic shock – pallor, tachycardia, hypotension, cool peripheries
o Ipsilateral dullness
o Anxiety and agitation
o Evidence of external thoracic injury
o Decreased breath sounds ipsilaterally
o Persistent blood loss following intercostal catheter insertion

48
Q

how to treat massive hemothorax?

A

o High flow O2 to maintain saturation targets
o Treat with rapid restoration of blood volume
o Concurrent drainage of thorax
o Immediate intercostal catheter insertion
o Haemostatic resuscitation - transfusion

49
Q

what is flail chest?

A

Defined as fractures of 2 or more contiguous ribs in 2 or more locations; results in segment of the chest wall no longer being in continuity with the rest of the thoracic cage

50
Q

what will flail chest result in?

A

o Paradoxical movement results

  • Segment moves inwards on inspiration (when the rest of the chest expands)
  • Segment moves outwards on expiration( when the rest of the chest deflates)
51
Q

presentation of flail chest?

A

o Paradoxical chest wall movements of the affected segment
o Chest pain
o Respiratory distress
o Boney crepitus

52
Q

treatment for flail chest?

A

o High flow O2
o Analgesia
- Paracetamol, titrated opiates, ketamine infusion
- Consider adjunctive medications–pregabalin
- Early use of regional anaesthesia–intercostal nerve blocks, epidural anaesthesia
o Respiratory monitoring o Surgical intervention

53
Q

when will cardiac tamponade happen?

A

Accumulation of pericardial fluid under pressure
• As little as 75ml of blood accumulating in the pericardial space can impair cardiac filling, resulting in tamponade and obstructive shock
• Up to 80% of myocardial stab wounds may develop cardiac tamponade

54
Q

why cardiac tamponade result in death?

A

o Intrapericardial blood accumulation
o Elevated intrapericardial pressure
o Decreased right and left ventricular filling
o Myocardium shifts towards the left side, further reducing left ventricular function o Hypovolemic shock results in other organs from low CO and low venous return

55
Q

clinical presentation of cardiac tamponade?

A

o Obstructive shock – tachycardia, narrow pulse pressure, hypotension, cool peripheries
o Becks triad – muffled heart sounds, hypotension and distended neck veins
o Pulsus paradoxus
o Anxiety and agitation

56
Q

how to treat cardiac tamponade

A

o High flow O2

o Needle pericardiocentesis

57
Q

mechanism of blunt cardiac injury?

A

o Direct precordial impact
o Crush injury from compression between sternum and spine o Deceleration or torsion causing tear in heart
o Blast injury

58
Q

pathophysiology of blunt cardiac injury?

A

o Often right heart due to its anterior location
o Subendocardial haemorrhage > focal oedema > interstitial haemorrhage > myocytolysis with infiltration
of PMNs
o Lead to death from arrhythmias, cardiac free wall rupture or coronary artery laceration

59
Q

Commotio Cordis means?

A

“Disturbance of the heart” – sudden death because of blunt trauma to the chest wall; usually affecting young athletes with hypertrophic obstructive cardiomyopathy (HOCM), who are struck in the chest by hard projectiles

60
Q

pathogenesis of Commotio Cordis?

A

o Low velocity impacts with seemly innocent looking chest trauma
o However, in some people, especially young athletes with HOCM, this causes a primary electrical event
presentation
inducing V fib

61
Q

what causes pericardial inflammation syndrome?

A

delayed hypersensitivity reaction to presence of damaged myocardium

62
Q

presentation of pericardial inflammation syndrome?

A
o Fever
o Chest pain
o Pleural and pericardial effusions o Friction rub
o Arthralgia
o Pulmonary infiltrates
63
Q

presentation of cardiac rupture?

A
More common in thin walled atria
o Splashing mill wheel murmur (rare)
o ECG may show conduction defects
o Axis deviation – if herniation through pericardium has occurred o Cardiac thrill
o Hypotension
64
Q

aortic injury happens when?

A

Proximal ascending is most commonly injured in blunt trauma because of the fixation of vessels between left subclavian artery and ligamentum arteriosum
• Deceleration produces shearing forces that tear the aorta
• Diagnosis is rarely made because very few people survive it
o 15% of fatal MVC victims have aortic rupture (85% of which die instantly and 15% survive to hospital)

65
Q

oesophageal perforation présentation

A
o Chest/epigastric pain
o Dysphagia
o Hematemesis
o Neck or chest wound
o Pleural effusion
o Drainage of GI contents from an intercostal catheter o Shock
66
Q

how to treat oesophageal perforation?

A

o High flow O2
o Fluid resuscitation
o Nasogastric tube
o Broad spectrum antibiotics o Surgical repair

67
Q

when does tracheobronchial injury occur?

A

Usually occurs close to the carina, associated with severe blunt trauma

68
Q

presentation of tracheobronchial injury?

A

o Haemoptysis, cough and respiratory distress

o Subcutaneous emphysema

69
Q

how to treat tracheobronchial injury?

A

o High flow O2

o Multiple intercostal catheter o Urgent bronchoscopy

70
Q

when will blunt abdominal trauma happen?

A

Often insidious onset – can remain symptomatic with 50% volume loss

71
Q

3 mechanisms of blunt abdominal trauma?

A
  1. decelerations
    - Shearing forces causes organs to tear–distal aorta ,hepatic tear along ligamentum teres
  2. crushing
    - Abdominal contents crushed between anterior abdominal wall and posterior vertebral column
    - Kidneys and spleen especially vulnerable
  3. external decompression
    - Increases intra-abdominal pressure>rupture organ(usually liver and spleen)
72
Q

presentation of blunt abdominal injury?

A

o Lap belt marks – small intestine rupture
o Steering wheel contusions
o Ecchymosis indicating retroperitoneal haemorrhage – flanks (Grey-Turner sign), umbilicus (Cullen sign) o Abdominal distention
o Auscultation of bowel sounds in thorax – herniation through diaphragm injury
o Abdominal bruit – traumatic AV fistula
o Tenderness, guarding, rigidity, rebound tenderness – peritoneal injury
o Fullness on palpation – intra-abdominal haemorrhage
o Crepitus – instability of lower thoracic cage
o Look out for hip fractures (especially in elderly)

73
Q

how to dx blunt abdominal injury?

A

FAST scan

CT

74
Q

how common you will see chest trauma in paediatrics?

A

Children’s chest walls are quite compliant and may not show external signs of intrathoracic injury

75
Q

what is common mechanism of injure that cause chest trauma in paediatrics?

A

Blunt trauma is more common

76
Q

presentation of chest trauma in paediatrics?

A

§ Bony defects
§ Crepitus
§ Paradoxical chest movement
§ Unequal breath sounds

77
Q

presentation in paediatric abdominal trauma?

A
§ Abdominal tenderness ,distention, bruising 
§ Haematuria
§ Vomiting
§ Neurologicobtundation
§ Fallingorlowhaematocrit
§ Absent bowel sounds
78
Q

How common is paediatric splenic trauma?

A

Most commonly injured abdominal organ in children

79
Q

what is difference in paediatric in terms of splenic trauma?

A

Children with splenic injuries are more likely to be haemodynamically unstable than adults, but are more
likely to be managed non-operatively
- Thicker splenic capsule
- Larger amounts of elastin and smooth muscle § Lower velocity injuries

80
Q

how to treat paediatric splenic trauma?

A

Splenectomy required

- Pneumococcal vaccine required to prevent post-splenectomy sepsis