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GAP 2018 > Trauma CPGs > Flashcards

Trauma CPGs Flashcards

1
Q

Define shock

A

A condition where organs and tissues are not receiving adequate flow of blood, depriving the cells of oxygen and nutrients and allows the build up of waste products

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2
Q

Types of shock/fluid loss

A
  • hypovolaemia: intravascular volume has decreased
  • cardiogenic: failure of heart to pump effectively
  • neurogenic: sympathetic nervous system fails - vasodilation
  • septic: infection causes blood vessels to dilate - hypotension
  • anaphylactic: systemic allergic reaction - vasodilation - increased capillary permeability - hypotension
  • obstructive: blood flow is stopped (tamponade, PE)
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3
Q

Neurogenic shock patho

A
  • injury to spinal cord
  • loss of sympathetic vascular tone
  • vasodilation
  • decreased venous return
  • decreased stroke volume
  • decreased cardiac output
  • hpotension, bradycardia
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4
Q

Shock Process

A

Stage 1: injury

2: slow continuing haemorrhage - reduced VR and CO, detection by baroreceptors, via SNS to cardiovascular centre
3. Vasoconstriction - SNS/catecholamine mediated, reduced IHP, renin angiotensin
4. tachycardia - SNS/catecholamine mediated, optimal CO, renin angiotensin
5. decompensation - limit of compensation reached, collapse, brief increase in BP, poor perfusion - hypoxia/hypercarbia/wastes - vasodilation/inflammatory response and BP falls
6. Irreversible shock - leaky capillaries, clotting, profound organ damage, low BP

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5
Q

Modifying factors of fluid admin

A

Head injury - BP over 120 to maintain MAP and CPP
GI bleed - accept BP 80-100 as fluid may blow off clots
Uncontrolled haemorrhage - accept carotid, haemodilution, fluid may blow off clots
Spinal injury - up to 500ml bolus, hT caused by vasodilation
Chest injury - decompress, hT caused by increase ITP hence reduced VR
Diving - 1lt over 15-20 mins, then 1lt every 4 hours unless refuced perfusion: 20ml/kg

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6
Q

Life threatening chest injuries identified in primary survey

A

Airway obstruction - inadequate oxygenation in blood
Tension - one way valve, increase ITP and reduced VR
Open pneumothorax - if opening of wound greater than trachea, sucking chest wound: resp failure
Massive haemothorax - accumulation of blood in intrapleural space
I
Cardiac tamponade - accumulation of blood or fluid within the pericardial sac, impeding VR and CO

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7
Q

Chest injuries found on secondary survey

A

Flail chest - #2 or more adjacent ribs or sternum at 2 or more points causing moving segment
Aortic transection - mechanism involving high deceleration forces can cause transection usually to proximal descending section
Tracheal injury - reduced airway function
Pulmonary contusion - leakage of blood into alveoli and interstitium, culminating in consolidation and atelectasis (collapsed alveoli) causing hypoxia
Oesophageal rupture - ruptured oesophagus after blunt trauma is rare, but can be caused by valsalva
Diaphragm rupture - significant blunt force to abdo can force contents to rupture diaphragm causing resp compromise due to abdo content impeding lung expansion

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8
Q

Definition of a simple pneumothorax

A

presence of air in the pleural space caused by rupture of visceral or parietal pleura or chest wall

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9
Q

Patho of Simple Pneumothorax

A

-as air separates the 2 pleura, it destroys the negative pressure of pleural space and disrupts the equilibrium between elastic recoil forces of the lung and chest wall

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10
Q

Signs and symptoms of pneumothorax

A 
Chest trauma
Resp distress
Absent breath sounds to one side
Poor perfusion (hT)
Increased jugular vein distension
Subcutaneous emphysema
Tracheal shift away from injured side
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11
Q

Tension pneumothorax definition

A

creation of a one way valve causes lung to collapse as pleural pressure exceeds atmospheric pressure therefore high pressures push against the lung causing compression and displacement of mediastinum, increased ITP compresses major vessels reducing VR and CO

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12
Q

Patho of tension pneumothorax

A
  1. penetration of chest wall/lung tissue forms a one way valve
  2. air enters pleural space during inspiration (period of low ITP)
  3. air is trapped during expiration - hyperinflation
  4. ITP increases, exceeding atmospheric pressure and lung collapses
  5. slowly pressure increases to greater than SVC and IVC
  6. rapid decrease in VR, CO and conscious state
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13
Q

Signs and symptoms of tension pneumothorax

A 
Simple: unequal breath sounds, low spo2 RA, subcutaneous emphysema 
Tension: increase peak inspiratory pressure/stiff bag
-increased JVP
-reduced etco2
-reduced conscious state 
-poor perfusion
-tracheal shift
-low spo2 on supp o2
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14
Q

Primary head injury

A

initial injury sustained at time of traumatic event: lacerations, avulsions, compression, concussion, contusions, haemorrhage

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15
Q

Secondary head injury

A

after initial insult - swelling - reduced blood flow to brain - hypoxia - vasodilation - increased blood flow to brain - increased ICP - continuing process

  • hypoxia: vasodilation - increased ICP
  • hypercapnia: increase co2- cerebral vasodilation - increased blood flow - increase ICP
  • hT/hypovolaemia: reduced o2 - hypoxia - vasodilation - increased ICP
  • haemorrhage: increase ICP
  • Hypertension: increased ICP - ischaemia -necrosis
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16
Q

5HEDS

A 
5mins LOC 
Head injury (# skull, boggy mass, haematoma) 
Emesis greater than 1
Neuro deficit 
Seizure
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17
Q

Cushing’s Triad

A

reduced HR
increased BP
irregular breathing

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18
Q

Types of primary head injury

A

Concussion
Contusion
Compression

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19
Q

Concussion explained

A

mild-mod impact - the function of the brain stem (RAS) which is reponsible for regulating arousal and sleep wake transitions, or both cerebral cortices is temporarily disturbed - brief ACS - periods of drowsiness, restlessness, confusion

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20
Q

Contusion explained

A

Bruising to brain - structural change to brain tissue - neuro deficits - may cause LOC
May be injury to site of impact (coup) or opposite side (contrecoup)

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21
Q

Compression explained

A

Haemorrhage into brain or surrounding cavity with increased pressure in cranial vault
Reduced VR out of head and arterial blood squeezed out causing hypoxia and swelling
Intracellular ischaemia and loss of auto regulation causing altered permeability of cell membrane causing interstitial oedema which increases pressure on brain tissue

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22
Q

Types of Cerebral Haemorrhages

A

Extradural - hx between cranium and dura
Subdural - hx between dura and surface of brain
Subarachnoid - intracranial bleeding into CSF
Intracerebral - collection of blood within substance of the brain

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23
Q

Diffuse Axonal Injury

A

trauma from shearing or stretching of axonal fibers cause by acceleration or decceleration forces

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24
Q

Cushing’s triad explained

A

Bradycardia- effected CNX, vagal nerve. Trauma should have increased HR therefore low HR is suspicious
Hypertension - sympathetic response to bradycardia which increases pulse pressure or compensatory response to bleeding/swelling of brain
Altered resps - neural control for breathing compromised therefore respiration only in response to lower brain stem stimulus causing altered co2 levels with subsequent cheyne stokes resps
RAS = ACS, vasomotor centre = vasoconstriction = HT, cardioinhibitory centre = pressure on vagus nerve = bradycardia, resp centre = cheyne stokes/CNH resps

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25
Q

Early signs of increased ITP

A
  • headache
  • agitation
  • slow, deep resps
  • unequal pupils
  • nausea and vomiting
  • ACS
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26
Q

Late signs of increased ITP

A
  • decorticate, decerebrate posturing
  • paralysis
  • cushing’s triad
  • febrile - temp regulation failure
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27
Q

Spinal Cord anatomy

A 
7 cervical
12 thoracic
5 lumbar 
5 saccral 
4 coccyx
28
Q

Primary spinal cord injury:

A

happens at time of insult

29
Q

Secondary spinal cord injury:

A

after initial injury as a result of:

  • subsequent mishandling
  • hypoxia or hT
  • intrinsic metabolic changed, ischaemia, inflammation
30
Q

Patho of spinal injuries

A

c3,4,5: phrenic denervation of diaphragm
c6,7 to t4: impaired intercostals with reduced TV
t1 to t4: deinnervation of sympathetic outflow to heart therefore reduced SA and AV nodes innervation and intercostals innervation leads to unopposed vagal stimulation of the heart (bradycardia)
t12 - paraplegia and vasodilation of legs causes hT and tachycardia

31
Q

Types of spinal injuries

A

Hyperextension - spine arched backwards beyond limits, most common in upper cervical region
Hyperflexion - spine arches forward beyond normal limits
Compression - compressed following impact, injuries at c5-6 and t12-L1
Distraction - overstretching of spinal cord - hanging
Rotational - head and body rotate in opposite directions causes twisting of muscle, ligaments, vertebrae

32
Q

Neurogenic shock definition

A

characterised by hypotension, bradycardia and peripheral vasodilation, resulting from a loss of sympathetic vascular tone, due to an insult to the spinal cord

33
Q

Cause of hypotension and bradycardia in spinal injury

A

bradycardia: caused by unopposed vagal activity that disrupts sympathetic supply to heart
hypotension: caused by peripheral vasodilation distal to the lesion due to unopposed parasympathetic stimulation

34
Q

Burns definition

A

-tissue damage caused by excessive heat, electricity, radioactivity, corrosive chemicals that denature the proteins in the skin cells

35
Q

Degrees of burns

A

Superficial: damage to epidermis, dry, red, painful
Partial: damage to dermis, moist, red, blanching, blisters
Full: burn to fat, any colour, less painful

36
Q

Jackson’s Thermal Wound Injury Classification

A

zone 1: zone of coagulation, coagulation necrosis occurs here, tissue is non-viable

2: zone of stasis, potentially viable tissue, cells are ischaemic due to clotting and vasoconstriction
3: zone of hyperaemia, increased blood flow due to inflammatory response

37
Q

Patho of burns

A

acute burn injury - direct tissue injury - systemic inflammatory response - release of chemical mediators - increased capillary permeability - oedema/fluid shift from intravascular compartment to interstitial space - hypovolaemia and reduced tissue perfusion - decreased VR and CO - multi organ dysfunction

38
Q

Complications of burns

A
  • airway damage
  • hypercapnia
  • CO poisoning
  • hypoxia
  • shock
  • electrolyte disturbances
  • pain
  • arrhythmia
  • hypothermia
39
Q

Management of burns

A

-stop the burn: 20m cooling using running water or wet towels, no ice, continue until burn is cooled, do not allow shivering
-establish airway: MICA
-fluid resus: TBSA x weight = volume over 2 hours from time of burn
Children: 3 x TBSA x weight = volume given over 8 hours from time of burn
-analgesia
-protect the burn - cling wrap, do not impede blood flow
-transport - alfred, notify

40
Q

Why is fluid important for burns patients?

A

once integrity of skin is damaged, fluid loss through evaporation occurs.
perfusion of tissues is required to help minimise the extent of necrotic tissue so ensuring adequate fluid therapy helps maintain adequate perfusion and volume

41
Q

Airway burns signs and symptoms

A
  • smoke inhalation
  • cyanosis
  • nasal, oral, facial burns
  • resp distress
  • facial oedema
  • carbonaceous sputum
  • hoarseness, stridor, wheeze
42
Q

Crush injury definition

A

Damage to tissue as a direct result of a compressive force cell death through traumatic injuries not ischaemia.

43
Q

Compartment Syndrome definition

A

Result of crush injury, results from compressive force to muscle groups confined in tight fibrous sheaths with minimal ability to stretch - swelling of body tissues within the compartment

44
Q

Patho of Compartment syndrome

A

-Crush injury - haemorrhage and oedema - inreased pressure in closed fascial compartment - ischaemia - further cell swelling - increased inctracompartmental pressure - circulation compromised - irreversible tissue and nerve damage/necrosis due to lack of o2

45
Q

Signs and symptoms of crush syndrome

A
  • loss of distal pulses
  • colour changes
  • obvious swelling
  • ECG changes
  • loss of feeling and movement
46
Q

Management of crush syndrome

A
  • pain relief
  • IV access x2, pads on
  • lift slowly to avoid sudden reperfusion = hT
47
Q

Crush syndrome definition

A

Life-threatening complication of prolonged immobilisation or compression; pathological process that causes the destruction and alteration of muscle tissue; disruption of vascular integrity of the cell

48
Q

Clinical features of compartment syndrome

A
  • pain (on passive stretch)
  • pain disproportionate to injuries
  • parasthesia
  • pallor
  • pulseless limb
  • reduced sensation and movement
49
Q

Rhabdomyolysis definition

A

life threatening complication of severe muscle trauma with muscle cell loss. Myoglobinuria refers to the primary manifestation of the condition (excess myoglobin)

50
Q

Fracture definition

A

loss of continuity of bone structure

51
Q

Dislocation definition

A

soft tissue injury involving a 3rd degree (complete) tear of a ligament resulting in disruption of normal anatomical position

52
Q

Complications of fractures

A
  • blood loss
  • nerve damage
  • vascular compromise
  • soft tissue damage
  • damage to underlying organs
  • infection
  • fat embolism
53
Q

signs and symptoms of fractures

A 
Pain
Irregularity 
Loss of function
Swelling
Deformity 
Unnatural position
Crepitus
Tenderness
54
Q

Management of fractures

A
  • fix on site before moving pt
  • restful position and reassure
  • afford 3 areas of support
  • cover any wounds (sterile dressing)
  • treat as # if unsure
  • unnecessary movement should be avoided
  • relief of pain
  • elevation of affected limb
55
Q

Splinting principles

A
  • analgesia (pain can antagonise morphine therefore more susceptible to side effects once # is splinted)
  • splint
  • assess circulation and sensation before and after
  • immobilise joint above and below #
  • dress wounds and haemorrhage control before splinting
56
Q

Decompression sickness definition

A

As a diver descends the body tissues absorb nitrogen. On ascent the pressure within the body decrease and nitrogen should be exhaled via the lungs
If surfaces too quickly, nitrogen bubbles form within the body tissues and expand as pressure further reduces: bubbles in joint - joint pain, bubbles compressing nerves - numbness/tingling, bubbles in spinal cord - paralysis

57
Q

Cerebral Arterial Gas Embolism

A

occurs when a diver experiences barotrauma, causing air to enter the bloodstream where it follows the venous pathway to the heart and rest of the body. CAGE occurs when a gas embolism is pumped into the brain where it impedes blood flow/o2 supply causing tissue damage and iscahemia

58
Q

management of decompression sickness

A 
supine/lateral to keep bubbles from brain 
100% o2 
avoid increase temp
mx nausea
tx to hyperbaric service
59
Q

Barotrauma definition

A

-physical damage to body tissues caused by a difference in pressure between an air space inside or beside the body and the surrounding fluid

60
Q

Mx of mild pain in adults

A
  • Paracetamol 1000mg oral if not already admin in 4 hours OR
  • 500mg for under 60kg, elderly, frail, malnourished, liver disease
61
Q

Mx of moderate pain in adults

A

-Morphine IV or Fentanyl if IV available
-IV delayed/unsuccessful: Fentanyl 100mcg IN (under 60kg, elderly, frail) repeat up to 50mcg every 5 mins titrated to pain and side effects. Max 200mcg
OR- Fentanyl 200mcg repeat up to 50mcg every 5 mins max 400mcg
-Unable to give Fentanyl: Methoxy 3ml repeat if required

62
Q

Mx of severe pain in adults

A
  • Morphine up to 5mg IV, repeat up to 5 every 5 mins. Max 20mg
  • OR Fentanyl up to 50mcg IV, repeat up to 50mcg every 5 mins. Max 200mcg
  • titrate to pain and side effects
  • IM Morphine as last resort: 0.1mg/kg IM for elderly/frail once only
  • 10mg IM reapt 5mg after 15 mins once only
63
Q

Mx of headache

A

-paracetamol 1000mg oral if not admin in 4 hours
OR 500mg for elderly, frail, under 60kg, malnourished, liver disease
-Stemitil 12.5mg IM if pt over 21
-if after 15 mins pt headache remains severe and hospital remains over 15 mins away, treat as severe with IV or IN Fentanyl aiming to reduce pain to under 7

64
Q

Patho of Crush Syndrome

A

release from entrapment: 1. o2 rich blood returns to ischemic extremity - produces pooling of intravascular volume into crushed tissue - reduces total circulating volume due to disruption of vascular integrity

  1. release of various toxic substances and waste products of anaerobic metabolism - metabolic acidosis
  2. myoglobin is release from damaged muscle cells or injured extremity - filtered through kidney - renal failure
65
Q

Rhabdo patho

A
  1. primary injury
  2. normal function disrupted in muscle cells, energy for normal cellular function fails - muscle cells leaking potassium and phosphates and permitting entry of calcium, sodium and water
  3. muscle cells swell - further functional impairment - cell death
  4. muscle cell death and systemic complication may lead to renal dysfunction
66
Q

Specific diving hx

A
  • number of dives
  • surface intervals between dives
  • max depths and bottom times
  • type of ascent
  • decompression or safety stops
  • breathing gas mixture used
  • level of exertion during and after dive
  • which symptoms presented and what first aid was provided

GAP 2018 (13 decks)

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