Trauma Flashcards
What score predicts 6 month mortality following ACS
Grace score
Above which grace score would a glycoprotein 2b/3a inhibitor be indicated
above 3%
Above which grace score would clopidogrel be indicated
above 1.5%
What are the different types of burn
Thermal
chemical (acid/ alkali)
electrical
Different types of thermal burns
Flame
scald
contact
What is the difference b/w high and low voltage electrical burns
High= >1000volts
can burn internal tissue–> cause rhabdomyolysis
Low= <1000volts
burn at entry and exit points
What type of necrosis can acids and alkalis cause
Acids= coagulative
Alkalis= liquefactive
complication of hydrofluoric acid and mx
lethal hypocalcaemia hence needs calcium gluconate
Also hypomagnesaemia
Hyperkalaemia
What is the Jackson burn model and describe it
It describes the local burn response
There are 3 zones of a burn injury (closest-furthest):
-zone of necrosis= irreversible cell death due to coagulation of cellular proteins
-zone of stasis= area with compromised microvasculature hence reduced perfusion, can either develop into necrotic tissue if inadequate resuscitation OR improve w/ resus
-zone of hyperaemia= area with increased perfusion due to release of inflammatory mediators, usually completely recovers
Describe the different systemic responses to a burn injury
Cardiovas:
-peripheral and splanchnic vasoconstriction= hypotension, tachycardia, hypovolaemia
-vasodilation= increased capillary permeability= proteins escape= oedema
Renal:
-hypovolaemia= reduced renal perfusion= AKI
-reduced tissue perfusion= tissue damage/ death= myoglobin= renal injury
Resp:
-inhalation injury= oedema
-inhalation of toxic substances (CO/ cyanide)= acute lung injury
-release of inflammatory mediators= bronchoconstriction/ oedema= ARDS
-circumferential chest burns= unable to ventilate
GI:
-stress ulcers= curling’s ulcer
-impaired gut function= barrier breakdown= bacterial translocation
MSK:
-compartment syndrome
-reduced tissue perfusion= muscle breakdown
metabolic:
-burn= increased metabolic rate= catabolism
-hypothermia/ fluid losses/ electrolyte imbalance (hyperkal/ hypocal/ hypo/hypernat)
Immunological:
-depressed immune response= sepsis
-SIRS= multiorgan failure
Skin:
-fluid loss
-barrier lost= infection
2 ways to assess a burn
depth
% total body surface area
Methods to calculate %TBSA
-Wallaces rule of 9’s
-rule of palm
-lund & browder *paeds
What is parklands formula
amount of fluid resus needed in 24hrs
Adult= 4ml x weight x %TBSA
Paeds= 3ml x weight x %TBSA
*give first 50% in 8hours, rest in next 16hrs
What side does the O2 dissociation curve move to if there is an:
-increase
-decrease
in o2 affinity
increased affinity= left shift
decreased affinity= right shift
define a decreased affinity for oxygen on the dissociation curve
decreased O2 affinity= less o2 held at the same partial pressure/ oxygen released at a higher partial pressure
(holds less O2, hence less likely to let go)
What factors cause a right shift in the O2 dissociation curve/ decrease affinity
increased
-temp
-H+
-Co2
-2,3-diphosphoglycerate (DPG)
What factors cause a LEFT shift in the O2 dissociation curve/ INCREASE affinity
Decreased
-temp
-H+
-Co2
-2,3-diphosphoglycerate (DPG)
AND
-fHb
-myoglobin
signs of LA toxicity
-circumoral numbness
-tinnitis
-drop GCS
-coma
what are the safe doses for
-lidocaine
-bupivocaine
-prilocaine
-3mg/kg
-2mg/kg
-6mg/kg
what are the safe doses for
-lidocaine
-bupivocaine
-prilocaine
WITH ADRENALINE
-7mg/kg
-2mg/kg
-9mg/kg
Management of LA toxicity
-stop LA
-100% O2 mask
-cardiac monitoring
-give intralipid bolus over 1min (1.5ml/kg)
-give intralipid infusion
(if prilocaine= give mytheylene blue)
Complication of prilocaine toxicity
Causes methemoglobinaemia
Iron bound to Hb is in ferric (Fe3+) instead of ferrous (Fe2+) form hence doesn’t bind to O2 = causes cyanosis
causes of long QT interval
congenital: jervell-lange-neilson syndrome, romano-ward syndrome
drugs:
-antiarrhythmics (amiodarone, sotalol)
-TCA
-anti-psychotics
-erythromycin
-terfenadine
-chloroquine
-electrolyte: hypo Ca, K, Mg
-myocarditis
-hypothermia
-SAH
Mx of torsades de pointes
IV Mg sulphate
Describe the ECG changes associated with PE
-S1, Q3, T3
-P-Pulmonale (peaked P waves in inferior leads)
-atrial arrhythmias
-Tall R waves in V1
-right axis deviation
-RBBB
-right ventricular strain
-T wave inversion (V1-3)
(PARRRT)
Following trauma when would you carry out full spine immobilization
-GCS<15
-neck pain/ stiffness
-paraesthesia in limbs
-focal neurology
-suspected c-spine injury
1st line imaging for suspected c-spine injury
3 view c-spine xrays
Criteria for CT c-spine
-GCS <15
-intubated
-abnormalities on xr
-normal xr but ongoing c-spine concerns
-already having CT head
-focal neurology
indications for CT head within 1 hour for adults/ paeds
-GCS<13 on admission
-GCS<15 2hrs post admission
-suspected basal skull fracture
-suspected depressed/ open skull fracture
-focal neurology
-vomiting >1 episode
-post traumatic seizure
paeds:
-drowsy
-vomiting>3 episodes
-suspected NAI
indications for CT head within 8 hours for adults/ paeds
-age>65
-bleeding/ clotting disorders
-on anti-coag
-dangerous MOI
->30mins retrograde amnesia of events before head injury
causes of splenomegaly
infective:
-bacterial (typhoid, typhus, TB)
-viral (glandular fever)
-parasite (hydatid cyst)
-spirochete (syphilis, leptospirosis)
-malaria
neoplastic:
-lymphoma
-leukaemia
-polycythemia vera
-myelofibrosis
haemolytic:
-acquired haemolytic anaemia
-hereditary spherocytosis
-thrombocytopenic purpura
deficiency
-severe IDA
-pernicious anaemia
splenic vein HTN
-splenic vein thrombosis
-portal vein thrombosis
-cirrhosis/ portal HTN
inflammatory
-RA
-lupus
-sarcoid
-amyloid
Describe the management post splenectomy
2 weeks pre-op (splenectomy):
-pneumoccocal vaccine (PPV)
-Hib
-MenACWY
-influenza (annual)
(if emergency splenectomy)-give 2 weeks post-op
re-immunization needed every 5 yrs
prophylactic Abx (penicillin/ erythromycin) for atleast 2 yrs post-op
may need aspirin for thrombocytosis
AVOID malaria!!
Functions of the spleen
-destroy:
old/ abnormal RBC
abnormal lymphocytes
normal/ abnormal plts
-immuno:
produce antibodies (T/ B/ plasma cells)
good at removing poorly opsinized/ encapsulated bacteria
Effects of hypersplenism
-pancytopenia (anaemia/ bruising/ bleeding/ infection)
-BM hyperplasia (compensatory)
Describe the internal structure of the spleen
Has red and white pulp
Red pulp contains sinusoids that traps the old/ defective RBC/ cells debris/ plts and destroys using macrophages
White pulp is made of a central artery surrounded by lymphoid nodules and lymphocytes
-T cells are in the immediate vicinity of the central arteries
-B cells in the nodules
-once activated the lymphocytes go the the edge of the white pulp, become plasma cells and circulate into the red pulp entering the sinusoids
What histological finding is present post-splenectomy
Howell-jolly bodies (RBC with cytoplasmic inclusions)
What is superior orbital fissure syndrome
-trauma to lateral orbital wall
-pressure on cranial nerves passing through SOF
Describe the signs/ sx of superior orbital fissure syndrome
-anaesthesia of forehead + upper eyelid
-lacrimal hyposecretion
-ptosis
-proptosis
-fixed dilated pupil
-opthalmoplegia
-loss of corneal reflex/ accomadation
which CN are affected in superior orbital fissure syndrome
3,4,5(opthalmic), 6
MOI of orbital blow out fracture
object slightly bigger than orbital rim hitting the incompressible eye ball
break in inferior orbital floor
herniation of periorbital fat- impinges the inferior rectus + inferior oblique muscles
prevents superior and lateral eye movements
signs/ sx of orbital blow out fracture
echymosis and bruising peri-orbitally
diplopia on upward gaze
mx of orbital blow out fracture
wait 5 days for swelling and bruising to settle
surgical fixation of inferior orbital wall
signs/ sx of retrobulbar haemorrhage
-red conjunctiva
-proptosis
-pain
-ophthlamoplegia
-loss of pupillary reflexes
-loss of visual acuity (colour vision first)
mx of retrobulbar haemorrhage
ocular emergency! [MAD]
-IV Mannitol (CI in HF/ pul oedema)
-IV Acetazolamide (reduced IOP)
-Dexamethasone (IV/PO)
Urgent lateral canthotomy + definitive surgery later (source of bleed)
Nasal fracture management
need to assess if old/ new
-if obvious deformity (<10 days old) manip
-if epixtaxis–> control bleed
-if csf rhinorrhea (cribriform plate breeched)–> Abx
-r/v in few days after bruising/ swelling settles
Describe orbital apex syndrome
Compression of the optic nerve (CN2) as it passes through the optic foramen in the orbit
Signs/ sx of orbital apex syndrome
-ipsilateral visual loss
-RAPD
same as superior orbital fissure syndrome
-anaesthesia of forehead + eyelid
-hyposecretion of tears
-ptosis
-fixed dilated pupil
-ophthalmoplegia
-loss of corneal reflexes
What are the grades of splenic injury
American association of surgery for trauma (AAST) splenic injury scale
Grade 1:
-capsular tear <1cm parenchymal depth
-subcapsular haematoma <10% surface area
Grade 2:
-capsular tear 1-3cm
-subcapsular haematoma 10-50% OR intraparenchymal <5cm
Grade 3:
-capsular tear >3cm
-subcapsular haematoma >50% OR intraparenchymal >5cm OR expanding/ ruptured haematoma
Grade 4:
-laceration involving hilar vessels (25% of splenic perfusion compromised)
Grade 5:
-shattered spleen
-hilar vascular injury (whole spleen devascularised)
How is a grade 3 splenic injury managed
conservative (if haemodynamically STABLE)
How is a grade 5 splenic injury managed
LAPAROTOMY
(POST-op- vaccines, prophylactic penicillin V, aspirin if plt>1000)
T/F patients with splenic injury with conservative treatment also need vaccinations
True
complications of conservative tx/ embolisation
continued bleeding
splenic necrosis
splenic abscess/ cyst
thrombosis (dvt/ portal vein)
why would you not want to suture/ resect during primary laparotomy for liver laceration
excessive bleeding
Indications for a bogota bag
abdo compartment syndrome
abdo wound dehiscence
