Trauma Flashcards
Triage
• Based on ABCDE
• Multiple casualties:
o Number of patients and severity do not exceed capability of facility
o Life threatening problems and multiple system injuries treated first
• Mass casualties:
o Number of patients and severity exceed capability of facility and staff
o Patients with greatest chance of survival are treated first
Colour coded.
-Red - life threatening injury which requires immediate intervention/operation.
- Yellow - injuries that may become life or limb threatening if care is delayed beyond several hours.
- Green - the walking wounded who have only suffered minor injuries.
- Black - dead patients
- Blue - ‘expectant’ patients - severely injured but given the number of casualties requiring immediate care, have been given palliative treatment while first caring for the red patients. (those who are severely injured who normally will be prioritised as red patients if only 2 or 3 casualties requiring immediate care)
Primary survery
• A
o Assess airway for patency
▪ Chin lift, jaw thrust
▪ Clear foreign bodies
▪ Oropharyngeal/nasopharyngeal airway – mouth to EAM
▪ Intubate/ cricothyroidotomy/ jet insufflation
o C-spine immobilisation
• B
o Sats, RR
o Trachea
o Percuss chest
o Auscultate chest
o Manage:
▪ Put on O2
▪ Ventilate if required
▪ Alleviate tension pneumothorax, seal open pnuemothroax
▪ Add CO2 monitoring + pulse oximeter
• C
o HR, BP, peripheries, level of consciousness
o Sources of bleeding
o Manage:
▪ Apply pressure / put on tourniquet
▪ IVC x 2, take bloods, warmed IVF as required
• D
o GCS, pupils, lateralising signs
o BSL
• E
o Expose patient
o Prevent hypothermia
• Adjuncts
o Abg
o Ecg
o Catheters – NGT, IDC
o XR chest, pelvis
o FAST
MIST
Mechanism and time of injury
Injuries found and suspected
Symptoms and signs
Treatment initiated
AMPLE history
Allergies
Medications
Past medical history
Last meal
Events
Primary vs secondary vs tertiary survey
Primary - assessment of life threatening injuries.
Secondary - assessment from head to toe to exclude any injuries once stabilised from potential life threatening injuries.
Tertiary - exclude any potential missed injuries following primary and secondary survey.
Trauma spiel
1) Concurrent assessment and resuscitation based on ATLS principles
2) Start haemostatic resuscitation and activate a massive transfusion protocol.
3) Actively prevent and treat coagulopathy, acidosis and hypothermia.
4) Make an early clinical decision regarding the need for damage control surgery
massive transfusion protocol
Definition
o Massive transfusion
▪ Replacement of >1 blood volume in 24h or >50% blood volume in 4h
o Activation criteria
▪ Actual or anticipated 4 units RBC in <4h + HD unstable +/- anticipated ongoing bleeding
▪ Severe abdominal, thoracic, pelvic, multiple long bone trauma
▪ Major obstetric, GI or surgical bleeding
• Goals
o Early recognition of blood loss
o Maintenance of perfusion and oxygenation by restoring blood volume and Hb
o Arrest of bleeding
o Judicious use of blood components to correct coagulopathy
• Once activated
o 4 units RBC, 2 units FFP (all coag factors) [some use ratio 1:1:1]
o Consider 1 unit platelets (1 pooled = 4 units), tranexamic acid (if trauma)
o Add cryoprecipitate (factors VIII, XIII, vWF, fibrinogen) if fibrinogen <1g/L (10 units)
• Monitor every 30-60 mins
o FBC, coags, ionized calcium, ABG
• Targets o Temp >35, pH >7.2, BE <-6, lactate <4, Ca _1.1, plt >50, PT <1.5x normal, INR <1.5, fibrinogen >1
TEG
Thromboelastography
Aims
Goal directed therapy
Rapid results - visual profile
Replacement according to needs rather than coagulation profile
How is it performed
Collected whole blood placed in small cup
In the cup, a pin connected to a detector is suspended
The cup is oscillated
Fibrin strings form between cup and pin
Transmited onto detector via the pin and a trace is formed
Result time 3-10 mins
Results
R (time to taken to start clotting)
FFP
K and alpha Angle (time clot to reach fixed strength)
cryoprecipitate
Maximal amplitude (strength of clot)
platelets
Ly30 (excess fibrinolysis)
Tranexamic acid
Burns (definition and principles)
Definition
o Tissue damage sustained due to exposure to temperatures outside normal physiological range
o Principles
▪ Institution of adequate airway and breathing
▪ Prevention and treatment of burn shock
▪ Prevention and treatment of infection
▪ Provision of permanent and durable skin cover
▪ Correction of functional disabilities
▪ Correction of cosmetic concerns
▪ Rehabilitation and reintegration into society
o Aspects of management
▪ Fluid resuscitation
▪ Pain control
▪ Prevention of infection
▪ Pharmacomodulation of hypermetabolic state
▪ Nutrition
Pathophysiology of burns
1) Thermal injury causes coagulative necrosis of epidermis and variable depth of skin
NB chemical and electrical burns cause direct injury to cellular membranes + heat transfer
Depth of injury depends on temperature, type of heat, duration of exposure
2) Jackson’s model of burn wound
- Zone of coagulation (zone of necrosis) Irreversible damage with denaturing of cellular protein
- Zone of stasis (zone of ischaemia) Increased capillary permeability due to inflammatory cytokine response
Decreased tissue perfusion to vascular damage/leakage
- Zone of hyperaemia (zone of inflammation)
Expect complete recovery from injury in 7-10 days
3) Systemic response
Occurs due to cytokine release
Massive fluid shifts due to vascular permeability/inflammatory response
Classification of burns
• Superficial epidermal – 1st degree
▪ Epidermis only
▪ Dry, red, warm, blanches, no blisters
▪ Can be painful
▪ Normal or hypervascular
▪ some desquamation
▪ Heals in 7-10 days, no scar
• Partial thickness – 2nd degree
o Superficial dermal
▪ Epidermis and upper dermis
▪ Pale, pink, blisters, blanches with pressure
▪ Very painful
▪ Hyperrvascular
▪ Heals in 7-14 days, colour match defect, risk of hypertrophic scar
o Deep dermal
▪ Epidermis, significant part of dermis
▪ Blotchy, pale, blisters over pale deep dermis
▪ Decreased sensation
▪ Sluggish cap refill
▪ Heals in 21 days, high risk of hypertrophic scar
• Full thickness – 3rd degree
▪ Epidermis, dermis and adnexal structures all involved
▪ White, waxy, charred, no blisters, no cap refill
▪ No sensation
▪ No circulation
▪ Does not heal, wound contraction, heals by secondary intention
Primary survery for burns
Primary survey
o Airway:
look for history/signs impending airway obstruction
Face/neck burns, singed facial hair, carbon deposits oropharynx, hoarseness, carboxyhaemoglobin >10%
Immediate/early intubation if: stridor, circumferential neck burns, risk factors + prolonged transfer rqd to burn centre.
o Breathing:
assess for thermal/inhalation injury
carbon monoxide poisoning
CO higher affinity for haemoglobin, displaces O2. dissociates slowly.
Rx: 100% oxygen - CO dissociates ½ life 40min (rather than 4hr on RA)
torso burns restricting respiration – may need escharotomy
o Circulation:
crystalloid boluses to maintain UO 0.5-1ml/kg/hr
Parkland’s formula: 4ml CSL x wt in kg x % BSA 2nd/3rd degree burns over 24 hr (with ½ over first 8 hours, second ½ over 16hrs)
o Disability:
Assess GCS.
If altered, consider carbon monoxide poisoning, concurrent trauma or shock
o Exposure:
Stop the burning – remove clothes/chemicals/irrigate with water
Cool the burn: aim to achieve 20 minutes cool running water within 3 hours
Assess extent - body surface area: “rule of 9s”. Palm = 1% BSA or Lund-Browder chart
Assess depth of burns
Keep warm: Cover pt (warm blankets/bear hugger), warm room, warmed fluids
Escharotomy
Technique
o Minimal analgesia or anxiolytic usually required
o Electrocautery preferred
o Longitudinal incisions traversing depth of eschar until subcutaneous tissue spouts
o Extend to non-burned tissue proximally and distally
o Consider fasciotomy if improved perfusion and return of soft compartment is not confirmed
▪ Especially electrical burns
Electrical burns
• Normal overlying skin can coexist with deep muscle necrosis
• Types of injury
o Local thrombosis
o Nerve injury
o Muscle injury requiring fasciotomy
o Cardiac arrhythmia
o Rhabdomyolysis
• Management:
o Supportive
o IVF resuscitation
Criteria for burns transfer
• BSA >10%
• Burns to face, eyes, ears, hands, feet, genitalia, over joints
• Full thickness any age, any size
• Electrical or chemical burns
• Inhalational injury
• Burn in patient with comorbidities
• Concomitant trauma
• Children
• Suspected maltreatment or neglect
Cold injuries
• Types:
o Frost nip
▪ Pain, pallor, numbness
▪ Reversible with warming
o Frostbite
▪ Freezing of tissue with intracellular ice crystals
• Microvascular occlusion, anoxia
• Some damage on reperfusion also
▪ Severity:
• 1st degree – hyperaemia, oedema, no necrosis
• 2nd degree – large vesicles with hyperaemia, oedema, partial thickness necrosis
• 3rd degree – full thickness and subcutaneous necrosis, haemorrhagic vesicle
• 4th degree – full thickness skin necrosis with muscle and bone gangrene
o Non-freezing
▪ Microvascular endothelial damage, stasis, vascular occlusion
• Trench foot
o Arterial vasospasm/ vasodilation
o → oedema, blistering, redness, ulceration → infection, cellulitis, gangrene
Management of frost bite
o Rewarm
▪ Warm blankets
▪ Warm fluids orally
▪ 40 degree circulating water to reheat
o Supportive
▪ Analgesia
▪ Cardiac monitoring
o Limb preservation
▪ Thrombolysis can be considered if:
• <24h of injury
• Multiple digits/ proximal amputation
• No contraindication
▪ Preferably intraarterial TPA then intraarterial heparin
• Can use IV TPA + IV heparin
▪ Prostacyclin (iloprost) IV infusion
• Useful if <48h from injury
o Wound care
▪ Non-adherent gauze, sterile padding
▪ Pledges between toes
▪ Cradle/tent
▪ Prevent infection
o Tetanus Rx
o Definitive:
▪ Autoamputation or therapeutic amputation
Pathophysiology/classification of blast injury
Detonation results in a positive impulse.
Classification of injury
o Primary
▪ Direct effects of blast wave within body
▪ Affects parts of body with air-fluid interfaces
• Alveoli
• Tympanic membrane
• GI tract
o Secondary
▪ Penetrating injury from bomb-casing fragments, anti-personnel fragments (nails, nuts, bolts), environmental debris
▪ Manage as for penetrating trauma
o Tertiary
▪ Blast propels people onto a hard surface or causes objects to fall on victims
o Quaternary
▪ All other explosion related injuries
▪ Burns
▪ Asphyxia
▪ Radiation
▪ Toxins
▪ Psychological
Specific blast injuries
1) Tympanic membrane
▪ Commonest blast injury (lowest pressure threshold for injury)
▪ Symptoms
• Hearing loss, tinnitus, pain, dizziness
▪ Diagnosis confirmed on otoscopy
▪ Management
• Spontaneous healing in 75%
o 30% have permanent high frequency hearing loss
• Supportive treatment
o Keep ears dry
o Avoid loud noises
o No ear drops or antibiotics required
2) Pulmonary
▪ Injury occurs due to spalling and implosion at level of alveoli
- Symptoms
• Dyspnea, cough, haemoptysis, chest pain
▪ Management
• CXR – bat-wing bilateral fluffy infiltrates
• Chest drain not routinely required unless pneumothorax present
• Limited fluids – risk of APO
• Lung protective ventilation minimizing peak airway pressures
o GI
• Due to efficient propagation of blast through water
▪ Symptoms
• Can be subtle
• May have no external signs of injury
▪ Assessment
• XR / US / CT as appropriate
• Serial examination → peritonitis → surgery
• Delayed perforations can occur up to 14 days after injury
o Neuro
▪ Symptoms
• Headache, tinnitus, hypersensitivity to noise, amnesia, PTSD
▪ Mechanism
• Acceleration and deceleration of head as wave passes through
▪ Diagnosis
• Imaging with CT or MRI
▪ Management
• Supportive
o Cardiovascular
▪ Blast wave induces cardiogenic shock with myocardial compression without compensatory peripheral vasoconstriction
• Related to vagal overstimulation
▪ Management
• Guide fluid status using TOE or systemic pressure variation measurement
o Skeletal
▪ Management
• XRs
o Foreign bodies
o Articular involvement
• Tetanus
• IV ABX if open fracture
• Consider compartment syndrome/rhabdomyolysis (late presentation)
Monroe Kellie Doctrine
o Cranial cavity is a fixed volume containing parenchyma, CSF and blood
o An increase in 1 component implies an opposite and equal decrease in another
▪ If this does not occur, ICP rises
ICP
ICP
o CPP = MAP – ICP
o Aim to keep CPP >60, and ICP <20
• Cushing’s reflex
o Physiological response to raised ICP
o Hypertension (with widening pulse pressure), bradycardia, irregular respirations
o Mechanism
▪ Raised ICP → increased MAP to increase CPP
▪ Baroreceptors in aortic arch detect raised blood pressure and stimulate parasympathetic response via vagus nerve causing bradycardia
▪ Pressure rises to the point that there is compression of brainstem and respiratory centre → irregular respirations
Classification of head injuries
• By severity
o GCS 8 or less – severe
o GCS 9-12 – moderate
o GCS 13-15 – mild
• Skull fractures
o Cranial vault or skull base
▪ racoon eyes, battle’s sign, CSF rhinorrhoea, otorrhoea, 7-8 nerve dysfunction
o Linear or stellate
o Open or closed
• Intracranial lesions
o Diffuse
▪ Mild concussion
▪ Severe hypoxic ischaemic injury
▪ Diffuse axonal injury
o Focal
▪ Epidural haematoma
• Biconvex, lenticular
• Temporal/temporoparietal
• Lucid interval
• Middle meningeal artery
▪ Subdural haematoma
• Shearing of bridging veins
• Follow brain contours
• Cross suture lines
▪ Intracerebral haematomas/ contusions
• Frontal/temporal
• Evolve over a few days
• Need serial CT scanning
Management of head injuries
• Assessment:
o GCS
o Pupillary light reflex
o Focal neurological deficit
• CT scan:
o Indications for CT scan
▪ GCS <15 at 2 hours post injury
▪ Suspected open or depressed skull fracture
▪ Signs of basilar fracture
▪ Vomiting
▪ Older patients
o Relative indications
▪ LOC >5 minutes
▪ Amnesia >30 minutes
▪ Dangerous mechanism
• Mild injury
o Usually observation, discharge if patient will be appropriately supervised
• Moderate injury
o ICU admission for neurological observation
o Repeat CT in 24h or if deterioration
• Severe injury
o Neuroprotection
▪ Reduce ICP (ICP <20, CPP >70):
• Mannitol/hypertonic saline
• Hyperventilation
• Barbiturates
- nurse 30 degrees head up with head in neutral position
- sedation and paralysis
- EVD (CSF drainage)
- decompressive craniectomy
▪ Normoglycaemia
▪ Normothermia
▪ Normotension
▪ Normoxia
▪ Anticonvulsants
• Surgical management:
o Scalp wounds
▪ Clean and inspect wound thoroughly before suturing
▪ Haemostasis
▪ Clips/staples
▪ Inspect for CSF, foreign body
o Depressed skull fractures
▪ If degree of depression is greater than thickening of adjacent skull, open or grossly contaminated, needs operative intervention
o intracranial haemorrhage
- acute subdural haematoma -> indication for early evacuation -> 1cm subdural blood with midline shift
- epidural haematoma -> indications -> alteration of consciousness or change in neurologic function
▪ Craniotomy/burr holes by neurosurgeon
o Penetrating brain injuries
▪ Appropriate imaging
▪ Antibiotics
▪ ICP monitoring
Organs involved in zonal neck injuries.
Penetrating neck injury = breach in platysma
Vascular injury 25%
Aero-digestive injury 30%
Neural injuries
o CN 7-12
o Sympathetic chain
o Cervical/brachial plexus
o Spinal cord
Zone I: sternal notch to cricoid
o Structures at risk: trachea, oesophagus, major vessels (aortic arch, brachiocephalic, subclavian, common carotid, IJV), thoracic duct (on left), lung apices, c-spine, cord, nerve roots
o Mx: imaging/endovascular approach where possible. Surgical approach – median sternotomy, extend along anterior SCM
Zone II: cricoid to angle of mandible
o Structures at risk: trachea, pharynx, larynx, oesophagus, thyroid, major vessels (carotid sheath, vertebral), c spine, cord
o Mx: surgical exploration – ant SCM approach. No obvious injury on exam/imaging – consider observation, panendoscopy/laryngoscopy/contrast swallow
Zone III: angle of mandible to base of skull
o Structures at risk: trachea, oesophagus, parotid/submandibular gland, major vessels (internal/external carotid, IJV, vertebral), spine, cord
o Mx: imaging/endovasc approach where possible. Surgical approach – extend ant SCM incision, divide omohyoid (avoid injury glossopharyngeal n).
Hard signs of penetrating neck injury
Definition
Injuries extends deep to platysma
o Shock
o Pulsatile bleeding or expanding haematoma
o Audible bruit or palpable thrill
o Airway compromise
o Wound bubbling
o Subcutaneous emphysema
o Stidor
o Neurological signs of evolving stroke
Specific neck injuries Mx
Venous
o Small vessels – ligate
o IJV injury <50% lumen - repair 6/0 prolene
o IJV >50% unilateral - ligate
Arterial
o Proximal & distal control
o Injury without contusion/vessel loss – primary repair
o Injury with contusion/vessel loss – resection + anastomosis or graft
o External carotid – can ligate
o Internal carotid – shunt if not repairable
o Vertebral – endovasc control or ligation
Tracheal
o Repair single layer absorbable suture
o Tracheostomy 2nd cartilaginous ring if significant injury
Oesophageal
o Debride, repair in 2 layers. Contrast swallow 1/52.
o Large volume tissue loss – distal ligation, proximal oesophagostomy, jejunostomy feeding tube.
Thoracic duct
o Rare, zone 1 or 2 injury on left. Ligation to prevent chylothorax.
o Delayed diagnosis with chylothorax – chest tube, low fat diet.
Le Forte fractures
o midface fracture patterns with separation of tooth bearing bone and cranium. Involves bilateral pterygoid plate fractures plus:
o Type 1: horizontal fracture through the maxilla superior to the maxillary dentition.
o Type 2: pyramidal fracture through the maxilla and orbit, outlining the nose.
o Type 3: fracture of the facial bones from the skull, a complete craniofacial separation
Goals: restoration of the continuity of the facial bones with the cranium and reduction of fractures with the goal of returning the patient to the preinjury occlusion.
Mx: ORIF/ MMF
Mandibular fracture
o 2nd commonets facial fracture
o Classified by location
▪ Angle and body > symphysis/parasymphysis
o Assessment
▪ Symptoms –trismus, malocclusion, numbness, loose or missing teeth
▪ Palpate mandible, inspect dental wear, test mental nerve
▪ CT facial bones
o Management
▪ CR if greenstick
▪ Maxillomandibular fixation
▪ ORIF depend on type and extent of fracture
Nasal fractures
o Commonest fractured facial bone
o Unilateral, bilateral, non-displaced, displaced
o Assessment
▪ Epistaxis, nasal airway obstruction, cosmetic deformity, change in smell
▪ Palpate bones, dorsum
▪ Intranasal examination for septal haematoma
▪ Look for halo sign with suspected CSF leak / can test beta 2 transferrin
o Management
▪ CR -> Within 10 days of injury
▪ OR with osteotomy -> Can revise poorly healed CR (3 months) or in some complex acute fractures
▪ External fixation with nasal splint
▪ Drain any septal haematoma to prevent cartilage necrosis, septal perforation
