Trauma

Front 1

Class 1 haemorrhage

Back 1

-15% of blood volume
-vital signs unchanged or postural hypotension
Rx: rapidly infuse 1-2L of crystalloid

Front 2

Class 2 haemorrhage

Back 2

-15-30% blood volume
- vital signs: mildly tachycardic, normotension or postural hypotension
-Rx rapidly infuse 2L of crystalloid

Front 3

Class 3 haemorrhage

Back 3

-30-40% blood volume
- vital signs: tachycardia, tachyopnoea, hypotension, delayed capillary refill, oliguria
Rx: rapidly infuse crystalloid 2L, check Hb and give blood

Front 4

Class 4 haemorrhage

Back 4

->40% blood volume
vital signs: severe tachycardia, profound hypotension, tachyopnoea, delayed capillary refill, oliguria and altered mental state
Rx: transfuse blood to maintain O2 transport

Front 5

3 types of inhalational injury

Back 5

1/ thermal burns
- smoke will cause supraglottic injury
- steam can cause injury all the way to bronchioles
- may present as stridor, hoarseness, swollen uvula, and evidence of singed facial hair and burns

2/ chemical pneumonitis
- inhaled smoke and debris caused chemical pneumonitis
- can cause an ARDS response
- presents as dyspnoea, laryngospasm, wheeze, hypoxaemia, cough

3/ systemic effects
- CO and cyanide poisoning

Front 6

carbon monoxide poisoning

Back 6

- 200x affinity for Hb, displaces O2
- lethal if HbCO is >60%, mild if 5-20%
- treatment via administration of O2, decreases the half life of HbCO from 4/24 to 30/60
- pulse oximtery will be unaffected due to same infrared absorption of HbO and HbCO

Front 7

cyanide

Back 7

- results in inhibition of oxidative phosporylation causing a metabolic acidosis with raised lactate and tissue hypoxia
- treatment with O2, nitrates, hydroxycobalamin and thiocyanate

Front 8

anaesthetic considerations in burns patients

Back 8

airway
- control is crucial, if intubated secure airway, use dental bars if needed
- if not have smaller ETT available in case of subglottic stenosis
- can use suxamethonium up to 24/24 post burn and then 12/12 afterwards

breathing
- can get restrictive defect from burn, leading o increased risk of barotrauma and PTx
- risk of ARDs, use ARDS ventilation strategy

circulation
- hyperdynamic circulation
- maybe on inotropes
- IV access maybe difficult
- prone to large fluid losses through unprotected skin

Disability
- likely on antibiotics, ensure up to date
- risk of hypothermia from fluid loss through damaged skin
- hypermetabolic state, minimise fasting time with NG feed and continue NJ feed

Front 9

fat embolism syndrome

Back 9

- associated with trauma or surgery of long bones or pelvis
- embolism of fat occurs frequently, but FES only about 1%
- incidence increases with multiple long bone fractures
- mechanism not well understood, may be mechanical effect on R heart or biochemical theory where embolised fat is degraded to free fatty acids and cause secondary lung injury
- occurs 24-72/24 after injury
- classic triad of neurological, respiratory and dermatological changes
- respiratory often 1st to develop with dyspnoea, tachyopnoea and hypoxaemia
- neurological changes include confusion, seizures, focal neurological signs
- dermatological changes with development of petechial rash. seen in conjunctiva, oral mucous membranes and upper body
- Gerd criteria helps with diagnosis (major and minor criteria)

Front 10

treatment of FES

Back 10

- supportive treatment is mainstay
A and B
- O2 and mechanical ventilation if needed
C: stable haemodynamics, inotropes if needed

preventative strategy if early immobilisation and operative intervention, limit intraosseous pressure during orthopaedic procedures

small reduction in risk if use methylprednisolone. Other treatment strategies include heparin and aspirin but scant evidence

Front 11

massive transfusion

Back 11

-replacement of entire blood volume in 24/24 or 10units in 24/24 period

Front 12

recombinant factor VII

Back 12

- designed for use with haemophiliacs with antibodies against factors 8 and 9
- works by increasing levels of factor X through both intrinsic and extrinsic pathways
- give if Ph >7.2, plts >50, fibrinogen >0.5, temp >35

Pros:
- easy to store and use
- limits blood and products and their disadvantages
- may be acceptable for JW

Cons:
- expensive
- potential increased hypercoagulable state and thrombotic events
- no mortality benefit
- no agreed best practice guideline

Front 13

coagulation changes in trauma

Back 13

- tissue damage leads to initiation of coagulation via exposure of tissue factor which activates factor 7 which activates factor 10 which forms fibrin from prothrombin
- results in consumptive coagulopathy (incl platelets and factors)
- can lead to hyperfibrinolysis at localised area of injury to prevent thrombus propagation, however if widespread injury can get widespread hyperfibrinolysis leading to generalised coagulopathy

Front 14

Cardiac investigations in trauma

Back 14

ECG
- clinically significant cardiac injury highly unlikely if normal 12 lead ECG
- changes highly variable if present eg tachycardia, non-specific ST changes, SVT, VT, conduction blocks

troponin
- sensitive marker for myocardial injury
high specificity (ie if normal very unlikely to have injury)

echocardiography
- TTE non-invasive and sensitive for assessment of cardiac function and presence of tamponade, valve dysfunction, septal injury, wall motion abnormalities
-TOE especially good for looking at RV (most likely to be injured)

CXR
- should be done as part of primary survey, not sensitive for injury

Front 15

Nexus cervical spine criteria

Back 15

- NSAID
- neurology absent
- spinal tenderness (midline)
- altered consciousness
- intoxication
- distracting injury

Front 16

massive transfusion pack

Back 16

initial pack has
- 4 blood
-1 ffp
-1 platelet

subsequent packs have
-4 blood
-2 FFP
- 1 Platelet