Emergency medicine Flashcards
Target time for treatment 95% A+E pts?
4 hours
Factors increasing A+E strain?
warm, dry and sunny weather; local music festivals; national sports teams winning (mainly assault); major natural disasters; Mondays and Fridays/Saturdays (drinking)
How to deal with inappropriate A+E attendance and who?
triage by nurse; GPs working alongside ED Drs; patients prefer ED sometimes and can put strain on it rather than go to primary care where problem can be solved without a trip to the ED; may get some patients that turn up loads and are ‘crying wolf’
Major burn definition?
15% burn surface area (BSA) or 10% in child
When referred to burns specialist unit?
major then require resus and burns specialist treatment; also referred = inhaled, face, hands, feet, genitalia
First aid treatment for burns?
remove burnt clothing; irrigate for 10 mins (cool sterile saline); chemical burns = continuous irrigation; keep clean, cover with cling film, warm pt to stop shock
Assessing airways in burns?
assess from ICU; high flow O2; accurate hx vital (suspicion if injury in enclosed space); intubate if hypoxaemia/hypercapnia
S+Ss inhalational burns?
injury to face/neck, singed nasal hair, carbonaceous sputum, voice change, dyspnoea, soot area; systemic oedema can happen after fluid resus
Treatment for inhalational burns?
give continuous 100% O2 until carboxyhaemoglobin levels known, if raised continue until 10% for 6 hours; if high COHb levels then can be high cyanide from burning foam and suspect if also tissue poisoning; anaesthetist assessment needed, usually intubation with nasogastric before swelling needed (uncut endotracheal tube with >7.5mm diameter so bronchoscope passed)
C spine/chest injuries result in what?
can result in pneumothorax or flail chest (explosion)
Fluid resus in burns victims what and regime?
– extreme inflammatory response means lots of Hartmann’s needed to stop shock, using Parkland’s formula (vol in mils = 4 x body weight in kg x BSA % of burn); give 50% of this in first 8 hours then other half in next 16; may need other specific fluids; avoid colloid in first 24hrs due to colloid permeability; blood and clotting where needed and avoid IV in burnt skin; all products should be warmed and arterial and venous monitoring; minimum 0.5ml urine output for formula to work
How to measure BSA?
estimated by rule of nines (SEE BOOK FOR WALLACE RULE OF NINES) or palm of pt to estimate 1% BSA; Lund and Browder chart more accurate but longer to do; need to modify for burns in children
What S+Ss can be misleading and shouldn’t be taken into acc when assessing burn depth?
erythema, mild redness, blisters, oedema
What is a superficial burn?
red, painful with blistering but hair follicles intact
Deep dermal burn?
red, painful, peeling sheets rather than blistering, a few hair follicles intact
Full thickness burn?
pale and charred grey/black, no erythema, no hairs intact, skin is insensate, leathery and causes constriction if circumferential
Burn management?
• Analgesia should be given as painful; elevate to minimise risk of compartment syndrome and peripheral pulses monitored
Prognostic factors for burns?
BSA, pre-morbid conditions, inhalational injury and age
Most likely to drown?
usually in <5yrs and in adults can be associated with alcohol
Difference between distress and drowning?
- Distress = pending danger as shouting for help but still afloat but struggling
- Drowning = person already started to suffocate and usually silent
Initial management of drowning pt?
no CPR in water, immobilise C-spine, keep pt prone when out of water as water helps maintain venous return so don’t want venous collapse, hypoxaemia causes cardiac arrest so 100% oxygen and intubation with high PEEP (water dilutes surfactant so atelectasis more common)
Management of drowning pt after admission?
observe pt after drowning; can get pulmonary oedema; monitor = haemoptysis, basal crackles, CXR changes, hypoxia; asymptomatic after 4hrs discharge; 2wk CXR after to see if infected with anything
Other things to bear in mind with drowning pts?
hypothermia can mask clinical death so keep resussing until back at hospital aggressively (no pulse, breathing, muscle rigidity); hyperkalaemia = poor prognosis, ECG and end-tidal CO2 for diagnosing cardiac arrest
Causes of electric shock injuries?
utility working, poorly earthed appliances, appliances near water
Consequences from electric shocks?
physiological changes, thermal tissue destruction, secondary damage from muscle spasm and falls
Poor prognostic factors and explanations for electric shocks?
type of current (AC more dangerous than DC as can cause muscle spasm so victim won’t let go of source, AC cause VF and DC causes systole); energy delivered (applied voltage x current; can cause extreme heating meaning internal/external burns, coagulation necrosis); current pathway (where it goes through body, head and chest is worse); resistance encountered (fluid and electrolyte tissues conduct well; bone is most resistant and skin thickness can limit amount of current into body, hearts and nerves do badly so check these as they conduct electricity the best); contact duration (briefer = better)
Treatment of electric shocks?
turn source off; paradoxical triage (treat apparent dead first; resus long and aggressively); more fluids needed if burnt than normal burns as can go deeper; check of rhabdomyolysis; treat arrhythmias; usually can cause compartment syndrome in legs
3 types of lightning strike injuries?
direct = strikes and enters ground through pt; side flash = lightning hits object first then jumps sideways; ground strike = strikes nearby and travels through ground to pt
Consequences of lightning strikes?
pt usually unaware what happened and confused with tympanic rupture; safe to touch pt; full trauma assessment; visual acuity assessed (can cause electrical cataracts)
Immediate S+Ss of lightning strikes?
asystole due to secondary hypoxic arrest; generalised muscle aches and neuro usually resolve in 24hrs
Associations with altitude problems?
• Usually from skiing, trekking or working; ascend faster than bodies can acclimatise
Patho of acclimatisation?
in ascent pO2 drops from barometric pressure drop, this means chemoreceptors respond to the hypobaric hypoxia by increasing resp rate and depth; kidneys prevent resp alkalosis by excreting bicarb and reabsorbing hydrogen ions; long-term increase in EPO increases RBCs and takes weeks
Rules for ascension to reduce risk of altitude sickness?
above 3000m = each night’s sleep should only be 300m higher with a rest of 2-3 days or 1000m ascended; >5500m will be physical and mental deterioration
Diagnosis and S+Ss acute mountain sickness (ACS)?
headache plus one of GI upset, fatigue/weakness, dizziness, difficulty sleeping couple of hours after ascent; common at >2500m, high cerebral blood flow, mild cerebral oedema, oxidative stress from oxygen free radicals
Moderate and severe management of ACS?
managed by rest, hydration, analgesia, antiemetics for mild; severe = acetazolamide (250mg/8h po) and/or dexamethasone (4mg/6h po) but can’t descend on dexamethasone
RFs for ACS?
rate of ascent, absolute altitude, blunted ventilatory response to hypoxia, level of exertion, home above >900m, previous AMS, concurrent URTI, neck irradiation/surgery
Patho and definition of high-altitude cerebral oedema?
potentially fatal encephalopathy, change in mental state and/or ataxia usually preceded by AMS; patho = vasogenic cerebral oedema from disruption of BBB with/out cytotoxic oedema; needs more descent than HAPE
Treatment high-altitude cerebral oedema?
acetazolamide, dexamethasone, consider O2, portable hyperbaric chamber, descent
S+Ss and patho high-altitude pulmonary oedema?
– more common than HACE; usually 2-4 days after ascending to >3000m; S+Ss = cough, dyspnoea at rest, haemoptysis, lethargy, tachycardia, tachypnoea, cyanosis, crackles; patho = patchy pulmonary vasoconstriction so stress failure of pulmonary caps and pulmonary oedema
RFs high-altitude pulmonary oedema?
strong hypoxic vasoconstrictor response, concurrent resp infection, congenital absence of pulmonary artery
Treatment high-altitude pulmonary oedema?
descent, portable hyperbaric chamber, O2, nifedipine, acetazolamide and dexamethasone, sildenafil PO, inhaled salmeterol
What is acetazolamide and what is it for?
carbonic anhydrase inhibitor causing more bicarb excretion from kidneys and aids acclimatisation; can use as prophylaxis 250mg/12h for those with previous AMS or rapid ascent; doesn’t hide AMS symptoms; helps sleeping; may have an allergy and give test dose prior to travel
Precautions to take if working at high altitudes?
climb high, sleep low; avoid undue exertion; avoid alcohol/sedating antihistamines/sedating hypnotics; feel unwell is from altitude unless proved otherwise; don’t ascend with AMS S+Ss; never leave AMS pt alone; descend if HAPE or HACE
Important points for wound management (6 points)?
o Irrigation with 0.9% saline asap
o Infiltrate with lidocaine (works by blocking voltage-gated Na+ channels to stop depolarisation) 3mg/kg or 7mg/kg adrenaline, lidocaine is vasodilator so clears itself systemically and adrenaline vasconstricts to help reduce bleeding is useful and lidocaine is needed over 3mg/kg – SEE PAGE 773 FOR SPECIFIC DOSE CALCULATION
o Can add some local anaesthesia 1% for suturing and put into devitalised tissue
o Remove debris, foreign objects and material and necrosis; trim ragged edges; avoid excessive resection of facial tissue as reconstruction tricky; abrasions scrubbed/debrided thoroughly immediately
o Avoid skin tension/wound inversion and use absorbable subcut sutures to bring skin together; use interrupted monofilament on the skin, 6’0 on the face and 5’0 or thicker elsewhere; brush suture knots away after 1 week
o Remove sutures: face = 5 days, upper limb/body = 7-10, lower limb = 14
Alternatives to sutures?
steri-strips = good for non-hairy strips and don’t get wet or rub, can be used with buried dermal absorbable sutures; glues (dermabond) = after haemostasis put on top of accurately apposed and dry skin edges, avoid thick layers as exothermic reaction can hurt, 30secs to dry then another layer, don’t get inside wound, don’t soak or scrub it
When to use abx in wound management?
animal bite, hand wound
Problems with pretibial lacerations?
poor blood supply and vulnerable to flap wounds (flap retracts back so can’t appose)
Treatment for pretibial lacerations?
iron out all flap, evacuate haematoma so no tension, skin closure with adhesive strips not sutures as can be loosened, wound glue, dress and give supportive bandage and elevation; review = infection, necrosis, wound tension
Wound healing limitations?
less easy with higher age, malnutrition, DM, steroids, smoking, peripheral vascular disease, irradiation
What is chloramphenicol for?
cosmetic on face when scarring due to infection
What is keloid and hypertrophic scarring?
keloid scarring = exaggerated as excess type 3 collagen production beyond wound and progressively; hypertrophic scarring = exaggerated scarring in the wound usually across a joint; both keloid and hypertrophic commoner in darker skin
Problem and treatment for a hammered finger?
subungual haematoma, relieve blood pressure by trephine hole in the nail with a 19G needle, no force needed
Problems with a swallowed fish bone and treat?
examine throat and tonsils, bone usually only grazed mucosa; if stuck remove with forceps; refer to ENT if fail
Problems with fish-hooked barbed finger and treatment?
infiltrate with plain lidocaine and push barb through finger unless important structures; cut barb off once through and remove hook
How to do a plaster cast for undisplaced forearm fxs?
remove anything stopping circ (rings); protect yourself and pt with apron; measure length for backslab (knuckles to below elbow); cut piece of plaster-impregnated bandage 5x longer and fold 5x; cut off corner for thumb hole and one on other side for the elbow; roll stockinette over forearm above elbow; wind roll of wool around this to protect from plaster; immerse hard plaster in water and apply to arm dorsum; reflect stockinette above and below over the hard plaster to protect at the edges; put bandage right around everything; takes 4mins to set; arm in sling for 1 day then encourage shoulder, elbow and finger movement
Cautions for plaster casts?
return to ED if fingers swell/blue/can’t move them; don’t get plaster wet; do not lift heavy objects with hand
How to remove a tight ring?
trauma and pregnancy; no.4 silk suture through ring distal to proximal, wind the suture at the distal end around the finger, then unwind from the proximal end distally; lubrication + compression + traction; can use a ring cutter
Caught penis in zip management?
lots of lubrication with mineral oil; cut bridge of zip with strong wire cutters so zip falls apart; can use Savile Row technique (lidocaine and gently unzip)
Mammal bites management in not risky?
clean well with soap and water/debride; avoid suturing unless deffo needed; give abx like co-amoxiclav
High risk for mammal bites?
> 50yrs, immunosuppressed, wound to hand/face/foot, delayed presentation, crush, reaches underlying structures
Treatment for monkey bites?
use valaciclovir to stop cercopithecine herpesvirus 1 leading to encephalitis
Dog bites treatment?
can give crush wounds so image, can transfer Pasteurella multocida streps and fusibacteria; check rabies and tetanus
S+Ss snake bites?
only adder in UK usually in summer in long grass; S+Ss = nausea, ptosis, reduced GCS, weakness, coagulopathy, muscle pain
Treatment for a snake bite?
immobilise limb and hospital (don’t do wound sucking, incisions, bandages and tourniquets), identify species asap; ABC = resp paralysis, hypotension, cardiac arrest, seizures
Investigations for snake bites?
check clotting time, renal function, CK, D-dimer, FBC, urine for myoglobinuria, venom detection kits
Specific treatments for snake bites?
UK use European viper venom antiserum, adrenaline to hand, if outside of UK antiserum in Liverpool/London, only admit if systemic symptoms under 2 hours for adders (advise rest, abx for secondary infection and antihistamine for swelling as can damage 4-5days after)
Specific treatments for lesser weaver fish stings?
5-20 min in water as hot as tolerated/>45degrees
S+Ss scorpion stings and treatment?
S+Ss = high/low bp, renal failure, LVF; treat = lidocaine, antidotes, prazosin/levocarnitine may help
What foreign objects swallowed that need romving?
; if ingested mainly children/drug smugglers and do X-ray, if below level of diaphragm then discharged and observed, button batteries can cause oesophageal necrosis and need urgent removal
S+Ss chronic oesophageal compaction?
poor feeding, FTT, stridor, PUO, repetitive aspiration pneumonia
Treatment for chronic oesophageal compaction?
most pass it, may need Foley catheter and bougienage if obstruction and endoscopy for impacted oesophagus
Treatment for bee stings?
scrape out with knife/credit card quickly; sting lasts longer if left in; pheromones released attracting more bees so run away; fatal >200 stings; treat = ice, calamine, antihistamines if severe itch, treat anaphylaxis
Definition of major trauma?
multiple, serious injuries that could cause serious disability/death; high global mortality cause; mostly in 17-45yrs male from sport
3 peaks of death from trauma?
trimodal distribution: first peak from major neurovasc disruption and not easy treat; second peak = head, thorax, limb, abdo haemorrhage; 3rd peak = sepsis and organ failure days later; mainly death in 1st two stages
Definition of hypotensive?
low if <90; low if >40 lower than normal, MAP <65
What does CABCDE stand for?
Control catastrophic haemorrhage, airway with C-spine protection, Breathing with ventilation, Circulation with haemorrhage control, Disability (Neuro status), Exposure/Environment (any limb injuries, pt warm, some bedside test, analgesia); THIS IS PRIMARY SURVEY IN TRAUMA
What to do if NEWS2 >7?
escalate to senior and immediate review, sepsis 6, hourly fluid monitoring, contact critical care, consultants
What to do if catastrophic injury?
clear any clots obscuring bleeding source; direct pressure; more direct pressure; indirect pressure; torniquet (2/3 inches above, not first line, less severe); haemostatic agents (ceelox)
How long to secure airway in catastrophic injury?
try and secure in 45 mins; rapid sequence induction = for even more severe and should happen quicker (for absolute indications for intubation)
Relative indications for intubation?
haemorrhagic shock when metabolic acidosis happening, agitated pt, multiple painful injuries, transfer to another hosp
Absolute indications for intubation?
Can’t maintain airway in any consciousness; can’t keep oxygenation with less invasive manoeuvres; can’t maintain normocapnia; deteriorating consciousness; significant facial injuries; seizures
Airway and c-spine management and main indications?
immobilise C-spine, provide O2, assess airway, go to RSI if indicated; 3 main indications for immobilisation = mechanism or injury, head/neck/facial injury and low GCS
Pathophysiology of clinical shock?
inadequate perfusion, cellular hypoxia, energy deficit, lactate build up (anaerobic resp), metabolic acidosis (vasoconstriction), cell membrane dysfunction, intracellular lysozyme release, cap endothelial damage, cell death
Causes of clinical shock?
distributive (neurogenic and endocrine [addison’s crisis]), endocrine, septic, cardiogenic (ischaemic, arrhythmia), spinal, obstructive (tension ptx, PE, tamponade), hypovolaemic, anaphylactic, haemorrhagic
Treatment pathway for clinical shock?
DR ABC; hypovolaemic (fluids lots and some vasopressor), septic/anaphylactic (fluid, vasopressor and sometimes inotrope), cardiogenic (maybe fluid but lots of inotrope)
Basic life support for choking and not breathing?
• DRS ABC; CPR (100bpm, 5cm depth); for choking encourage coughing then 5 back blows then 5 abdo thrusts then alternate then CPR
ABCDE in advanced life support in trauma?
ABCDE; A = airway, jaw thrust to protect C-spine (sometimes chin lift), 100% O2; B = breathing and auscultate lungs and heart, percuss chest; C = circ and haemorrhage control (2 points of venous access, replace blood if over 1.5L, younger and symptomatic tends to be severe, cardiogenic/neurogenic shock, use hypotensive resuscitation); D = disability (GCS/AVPU, pupillary reflexes, lateralising injury, spinal cord, BM, head injury); E = exposure (rewarm body if hypothermia; secondary survey after all this)
What is ATMIST stand for and when is it applied?
age, time, mechanism, injuries, signs, treatments (how to handover in trauma)
What is SBAR stand for and when is it applied?
in normal handover; situation, background, assessment, recommendation
Reasons to send to a major trauma centre?
o Assessing vital signs and level of consciousness – GCS <14, sustained systolic <90, RR <10 or >29 or abnormal paeds value
o Assess anatomy of injury – chest injury with altered physiology, traumatic amputation, penetrating trauma (neck, chest, abdo, back, groin), suspected open/depressed skull fx, suspected pelvic fx, spinal trauma from abnormal neuro, trauma with facial/circumferential burns, time critical (>20% burns)
o Evaluate mechanism of injury – traumatic death in same passenger compartment, falls >20ft, person trapped under vehicle, bullseye window
o Others – trauma with: >55yrs, >20wks preggaz, bleeding disorder, morbidly obese
Main adjuncts to primary survey?
• CT scan within 30 mins rather than XRs and reported within 60; peripheral XRs in secondary survey also urinary catheters for outflow, NGT insertion if no facial injuries, ABG in cold pts for O2
What is a FAST and pros and cons of its use in major trauma?
focussed assessment sonography in trauma; don’t use if delays CT, low negative predictive value (good for ruling in not ruling out), good for triaging in major incident scenario
Portable CXR for in major trauma?
portable easily acquired; evaluate flail chest, massive pneumothorax, haemothorax, ET tube placement and widened mediastinum; lung contusion can look like atelectasis as blood fills lung from ruptured vessels; straight fluid line in lung is haemothorax and pneumothorax as air pushing against blood; flail chest just looks like a bit of rib cage floating
Airway management?
weigh C-spine injury against hypoxia etc; look at rib fxs; reasons to intubate = GCS <9, sustained seizures, facial/airway trauma, high aspiration risk, flail segments, resp failure
How to logroll a pt?
moving from bed to bed; keep spine secure and warn pt and person at head in charge; can disrupt: internal clots, induce spinal and pelvic movement, heighten distress; can move supine in a scoop too; try not to move if don’t have to
XR of spine features looking for?
look at bones, cartilage, soft tissues and alignment; soft tissue should be less than 1/3 width of vertebrae above C4 but then after less than its width on XR; can view C-spine through mouth as well (PEG view)
What is a jefferson’s fx?
C1/atlas fx; from load on top of head; usually a burst/4 part fx in posterior and anterior arches
What is a hangman fx?
C2; high force hyperextension; involved pedicles of C2 and anterior displacement of body and pedicle C2
Teardrop fx?
fx of anterior and inferior aspect of vertebra from traction of anterior longitudinal ligament connecting them both; from severe hyperextension; soft tissue swelling as well
Flexion teardrop fx?
opposite mechanism to above; bit lower; anterior cord compression
Burst fx?
squash vertically into vertebra and bursts out from vertical load
What is a normal facet alignment?
C-spine injury without radiological abnormality (SCIWORA); dislocation can return back spontaneously or remain in dislocated position; do an MRI if suspect this
When to do intraosseus access and how?
no peripheral venous access; so go for this to deliver drugs if having difficulty finding a vein (trauma, DKA, severe burns); pushed into bone matrix to infuse through bone marrow into systemic circ; take sample of glucose, venous blood gas, electrolytes, haemoglobin first here before giving drugs
CIs for intraosseus access?
failed attempt, infections, trauma at site, surgery near site; can lead to compartment syndrome and fxs but this is rare; remove asap to prevent osteomyelitis
Initial fluid management for damage control resuscitation?
o Early haemostasis with surgery, splintage or angiography
o Treat the lethal triad
o Reduce crystalloid/colloid use if can (dilutes blood and doesn’t contain blood coagulants so can increase trauma based coagulopathy)
o Early RBC, plasma, platelets use 1:1:1
o Hypotensive resus
o May need damage control surgery
Hypovolaemic shock S+Ss?
tachypnoea, pallor, hypotension, anxiety, tachycardia, bradycardia, arrest
Causes of hypovolaemic shock?
blood on the (external haemorrhage) and 4 more (chest, abdo, pelvis and long bones = humerus, radius, femur, fibula, tibia, metacarpals)
Total blood volumes in adult, child and neonates?
70mls/kg in adults; 80 mls/kg in kids and 90 mls/kg in neonates
Osmolality definition?
osmoles per kg of solvent
Osmolarity definition?
osmoles per litre of solution
Tonicity definition?
ability of a solution to cause water movement
What electrolyte moves out of cells during burns and crush injuries?
K+
What is a crystalloid?
dissolved in water (Hartmann’s), more of this needed to give to pt than colloid
What is a colloid?
suspension and not mixed (gelloplasma etc); most fluid resus now with colloid
How to do a maintenance fluid calculation?
o For 0 - 10 kg = weight (kg) x 100 mL/kg/day; For 10-20 kg = 1000 mL + [weight (kg) x 50 ml/kg/day]; For > 20 kg = 1500 mL + [weight (kg) x 20 ml/kg/day]
o Replace deficit over 12/24 hours; 4mls/kg then 2 mls/kg then replace with 1mls/kg
o Need to do a U+Es everyday minimum if doing fluid resus
Treatment for internal haemorrhage?
– IV tranexamic acid (1g over 10min then 1g over 4h) in 3hrs of injury; avoid crystalloid (can contribute to hypothermia, haemodilution of clotting factors and Hb so worsens coagulopathy); can have permissive hypotension as higher bp hydrostatic forces can disrupt clotting; aim for bp: 70-80mmhg in penetrating trauma, 90mmhg in blunt and cerebration in awake pt; resus after haemostasis achieved
Best fluids to use?
see RBC, FFP and platelet ratio above (1:1:1); but the best is warm fresh whole blood but only really used by military due to difficulty storing; also fibrinogen for early clotting
What is trauma induced coagulopathy and how to assess and treat?
treat if clinical suspicion from the lethal triad; lab tests hard to determine; younger can compensate and mask the blood loss and hypoxia (cryptic shock); can assess lactate, base excess, central venous oxygenation for blood loss; starting to do point of care coagulation testing; give Orh-ve blood until blood type determined and beriplex if warfarin
When to fluid resus?
systolic below 90, HR >130mmHg, reduced consciousness, obvious massive ongoing blood loss
Causes of shock?
from hypovolaemia; haemothorax with chest drain, abdo = surgery, splint long bones and pelvis for haemorrhage control, other causes of shock = neurogenic (spinal), cardiac tamponade, drug effects and tension pneumothorax
What is FAST?
free fluid in pericardium/peritoneum (blood for trauma); 90% sensitivity and 200mLs+ detected; not for liver/spleen tears and hollow viscous injuries; extended FAST (eFAST) for haemo and pneumothoraces better than CXR, for hypotensive pt and no obvious bleeding; can be performed immediately after primary survey during secondary and non-invasive (don’t need diagnostic peritoneal lavage)
What is the lethal triad?
• Three parameters interacting in major trauma – cascade of inflammatory mediators with neuroendocrine compensatory mechanisms can lead to death from organ failure; hypothermia, coagulopathy and acidosis interaction can all be caused by and cause each other that makes pt condition worse
Definition of hypothermia?
<35degrees but <36 in trauma
RFs for hypothermia?
elderly, intoxicated, burnt and exposed
Patho for hypothermia?
dampens CVS compensation against hypovolaemic shock and worsens tissue hypoxia
Acidosis patho?
tissue hypoperfusion and lactic acid production with resp acidosis from hypoventilation (flail chest, COPD, opiates); temp and pH influence clotting and platelets so small changes = life-threatening coagulopathies which is exacerbated by haemorrhage
Coagulopathy patho?
¼ of severely injured and 4x mortality increase; can be from haemorrhage and haemodilution due to fluid resus, in minutes from tissue hypoperfusion, pre-existing medical conditions and anti-coagulating drugs
Lethal triad, what to do on scene?
early hypothermia and haemorrhage control (apply pressure to bleeds and pelvic binder for internal; use blankets [bear hugger] and warmed fluids)
Mnemonic for secondary survey?
Has My Critical Care Assessed Patient’s Priorities Or Next Management Decision? (Head/skull, Maxillofacial, C-spine, Chest, Abdo, Pelvis, Perineum, Orifices, Neuro, MSK, Diagnostic care)
Overview of RTA assessment?
• Some clinical signs may not appear til later due to compensation and catecholamines; assessing injuries before removing from scene is v helpful; need a good handover from first on scene to hospital; pictures useful
4 components leading to injury?
vehicle impacting with object; occupants hit in vehicle; organs jerked to a halt (rupture liver, aortic arch over 40mph); impact from unrestrained objects/people
4 points of occupant injury?
impact of vehicle with object; pelvic and femoral fxs from handlebars and fuel tank; impact of landing; organs jerked to halt
Questions to ask and general signs from RTA leading to injuries?
airbag deployed; state of car; other passengers; major injury visible; seatbelt worn and what type; relate vehicle damage to passenger injuries
• Bullseye on windscreen – facial fxs and internal head injuries
• Impact onto steering wheel – severe chest injuries/abdo compression (diaphragmatic rupture); seatbelt worn = clavicle, sternal, internal organ damage
• Intruding dashboard – compress femur and dislocate hip posteriorly; patellar injury
• Intruding engine compartment – tibia/fibular injuries/trapped feet
• Lateral impact – worse than frontal impacts; complications = aortic dissections, lateral chest/abdo/pelvic compression injuries
• Rear impact – lower back and whiplash
• Fall from height – onto heels = calcaneum fx, pilon ankle fx, tibial plateau fx, hip injury, spinal compression, base of skull fx
What is see saw movement of chest in resp mean?
obstruction as abdo sucked into chest during inspiration
Most serious feature of chest injury?
hypoxia (give 15L O2 in rebreather bag)
ATOM FC stands for what in primary survey?
Airway obstruction, tension pneumothorax, open pneumothorax, massive pneumothorax, flail chest, cardiac tamponade
Airway obstruction S+Ss and treatment?
trauma to neck/face/larynx (also posterior dislocations of clavicular head); S+Ss = noisy breathing, stridor, altered voice; suction available for vomit and stop aspiration; after recovery position and jaw thrust doesn’t work use guedel airway (don’t insert if resisting – nasal airway, intubate, gentle suction)
Tension pneumothorax S+Ss and treatment?
from penetrating injury making one way valve to thoracic cavity; can collapse lung and less venous return with other lung compression; S+Ss = diminished breath sounds, hyperresonance, distended neck veins, deviated trachea, hypoxia, tachycardia, hypotension (less venous return from increased intrathoracic pressure); treat = large-bore cannula into 2nd intercostal space in midclavicular line to decompress, chest tube if not work
Open pneumothorax S+Ss and treatment?
sucking chest wound (wound seals on expiration and more air in when inspire – turns to tension); immediate occlusion with sterile dressing taped on 3 sides so flutter-valve; complete seal with chest drain
Massive haemothorax S+Ss and treatment?
> 1500mL blood in hemithorax; causes = wounds to intercostal vessels, great vessels, heart; S+Ss = hyporesonant; treat = large-bore chest drain (32G) with IV fluid/blood and maybe auto-transfusion of blood; may need thoracotomy; can cause haemopneumothorax
Flail chest S+Ss and treatment?
section of fractured ribs with no bony continuity with rest of chest wall; can cause = serious hypoxia from bad chest wall movement and pulmonary contusions; S+Ss = looks abnormal on respiration; treat = high flow O2, may need to intubate/ventilate depending on resp distress; can get pulmonary contusions in blunt trauma too
Cardiac tamponade S+Ss and treatment?
clinical diagnosis with Beck’s triad (rising JVP, falling BP and muffled HS) but easier with potable US; treat = pericardial aspiration before thoracotomy if needed; pericardial aspiration = 18G needle left to xiphisternum, aim at left shoulder with needle down, elevate legs for venous return; this is only temporary (can fail if clotted blood) and definitive treatment is pericardiotomy; afterwards = need cardiothoracic input, frequent ECHOs, invasive monitoring in ITU
Injuries of chest identified in secondary survey?
simple pneumothorax, simple haemothorax, tracheobronchial tree/aortic dissection, blunt cardiac injury, oesophageal rupture
Problems with simple pneumothorax?
can develop to tension
Management simple haemothorax and problems?
<1500ml, if lung/blood vessel lacerations no surgery needed, large-calibre chest tube if big enough to be visualised on CXR, if left can clot leading to lung entrapment and infection
Problems and management tracheobronchial tree/aortic disruption?
usually death at scene and urgent treatment, CXR and clinical diagnosis, if left can cause resp distress/bowel strangulation
Problems with blunt cardiac injury?
most die on-scene, ECG and US monitoring (serious arrhythmias), if troponin rise can be cardiac contusion
Problems with oesophageal rupture?
= if v unwell compared to injury, with left pleural effusions and/or pneumomediastinum
Definition and causes of ventilation perfusion mismatch?
when blood volume circulating the lungs doesn’t get a high perfusion of O2 even when 100% O2 (low O2); usually due to shunts in lung and alveoli not ventilated (causes: alveolar collapse (atelectasis)/bronchoconstriction – pneumonia, post-op, lying down; oedema)
Definitions of the different stages of CKD?
stage 1 = 1.5x, <0.5ml/kg/hr for >6 hours; stage 2 = 2x creatinine, <0.5ml/kg/hr for >12 hours; stage 3 = 3x creatinine, <0.3/kg/hr for 24 hours or anuria >12 hours or RRT
Patho of electrolytes in renal failure?
when renal failure K+ and H+ stay in capillaries and Na+ stays in tubules as pumps for these stop working (hyperkalaemia and acidaemia)
STOP causes of renal impairment?
sepsis/shock, toxins, obstruction, pressure optimisation
Pre-renal causes of renal failure?
S and P (S = hypovolaemic, septic [cap walls become leaky and less fluid, less O2 to proximal convoluted tubules so die and get acute tubular necrosis], cardiogenic [less blood pumped round]; P = )
Renal causes of renal failure?
T (acute interstitial nephritis = renal lesion meaning decline in kidney function and means inflammatory infiltrate in kidney interstitium [from NSAIDs]; T = tubular toxicity, contrast from scans, gentamicin esp with furosemide)
Post-renal causes of renal failure?
O (can be stones and calculi or cancer)
o For all forms acute kidney injury - CVVH machine or haemodialysis
Types and definitions of resp failure?
pO2 <8kpa; type 1 = low O2, low/normal CO2; type 2 = low O2, high CO2 (stop being able to hyperventilate to get rid of O2), respiratory acidosis
Types of O2 flow for different resp failure types?
- EPAP – expiratory positive air pressure; for low O2 problem; same as CPAP (continuous positive air pressure)
- IPAP – inspiratory for high CO2
- NIV – non-invasive ventilation
- BiPAP – biphasic positive air pressures; includes inspiratory and expiratory for type 2
- Treatment – PEEP (positive end expiratory pressure) for oedema to push fluid back into capillaries
What does a high base excess mean?
Metabolic acidosis
What does a high pCO2 mean?
Resp acidosis
