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BPs Decks > TRAUMA & RETRIEVAL - A (50) > Flashcards

TRAUMA & RETRIEVAL - A (50) Flashcards

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1
Q

CRUSH/TOURNIQUET REPERFUSION SYNDROME

A
  • Release of major muscle masses after prolonged compression (both legs to mid thigh for more than an hour) can result in sudden death if there is an intact return circulation to carry the accumulated CO2, acids and K+ back to the heart
  • MANAGEMENT
    • controlled release with tourniquets etc
    • cannulate and load with saline*, HCO3- and Ca++ prior
    • Intubate and blow down CO2 prior

* no K+

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2
Q

EARTHQUAKE SYNDROME

A
  • ~20% of buried earthquake victims will be alive if rescued within 24h, but nearly 1/2 will go on to develop EARTHQUAKE SYNDROME due to muscle crush
  • muscle crush causes immediate physical damage, and if continued, superadded ischaemic injury
  • injured muscle cells leak K+ and MYOGLOBIN out, and rapidly draw water in, producing hypovolaemic shock, hyperkalemia, compartment syndrome and myoglobinuric renal failure
  • MANAGEMENT
    • start large vol saline immediately: while still trapped (no K+)
    • alkalinise urine with HCO3- to incr Myoglobin solubility*
    • give MANNITOL & fluids to produce diuresis, but not if already anuric
    • avoid FASCIOTOMY: unlike other compartment syndromes the muscle is already dead & this only causes sepsis and bleeding without improving survival: use Mannitol instead to drag water out
    • monitor volume, acid base and elecs in ICU if possible
    • watch for hypocalcaemia

* no longer advocated in EMSB

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3
Q

CK LEVEL INDICATIVE OF SERIOUS RISK OF MYOGLOBINURIC RENAL FAILURE?

A
  • >50-75,000
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4
Q

KETAMINE DOSE FOR DISASTER ANAESTHESIA

A
  • KETAMINE is an induction agent: make it look like one, mix 200mg in 20mls
  • Induction dose = 1-2mg/kg IV, (same as Sux), or 5-10 IM
  • Maint = 1/4 of the induction dose 1/4 hourly, titrated to patient ‘assistance’, or 2-4mg/kg/h in the paralysed pt.
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5
Q

GLASGOW COMA SCALE

A
  • The Glasgow Coma Scale is a 15 point head injury scoring system with 4 points for Eyes Open, 5 for Voice and 6 for Motor response (EVM)
  • EYES OPEN:
    • spontaneously = 4
    • to voice = 3
    • to pain = 2
    • nil = 1*
  • VOICE:
    • lucid = 5
    • confused = 4
    • words = 3
    • sounds = 2
    • nil = 1
  • MOTOR RESPONSE:
    • obeys commands = 6
    • localises to pain = 5
    • withdraws = 4
    • flexes = 3
    • extends = 2
    • nil = 1

*Note, a sleeping person can have a GCS of 7-8 and you get 3 points just for turning up!

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6
Q

ASSESSING GCS IN INTUBATED PATIENTS

A
  • when intubated patients are lightened for neurological examination, the presence of the ETT prevents them scoring higher than 1/5 for ‘voice’
  • to reflect this, their GCS is annotated ‘T’, and an 11-T equates to a GCS of 15
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7
Q

5 MEDICAL CAUSES OF ALTERED MENTAL STATE IN MINOR MVAs

A
  1. Sugar
  2. Seizures
  3. Strokes
  4. Sick sinus (& other arrhythmias)
  5. Substances (including CO),
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8
Q

THE MONROE KELLY DOCTRINE

A
  • States that the skull is a rigid box containing 3 elements
  1. Brain
  2. Blood
  3. CSF
  • and that a rise in the volume of 1 of these components is initially compensated by displacement of the other 2, minimising ICP rise
  • but once this mechanism is exhausted, a rapid rise ensues
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9
Q

CPP vs ICP

A
  • CPP is defined as MAP - ICP
  • MAP is defined as Diastolic BP + 1/3 pulse pressure, and is N > 90mmHg (120/80)
  • ICP is N < 10 mmHg (with > 20 bad), so CPP is N > 80mmHg
  • but the normal brain auto regulates down to a CPP of 50mmHg (ie MAP = 60, or BP = 80/50)
  • The ideal CPP for injured brain is ? ~60mmHg
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10
Q

EARLY TREATMENT OF HEAD INJURY

A
  1. optimize ABCs
  2. look for reversible causes of raised ICP
  3. consider Osmotherapy/hyperventilation
  4. aim for a CPP of 60
  5. minimise venous back pressure with 30deg headup, neutral position and attention to C collars and ties
  6. consider seizure prophylaxis with Phenytoin/Keppra
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11
Q

IMPACT APNOEA AND THE IMMEDIATE CATECHOL SURGE OF SEVERE HEAD INJURY

A
  • all serious blunt head impacts are followed by a period of IMPACT APNOEA ranging in duration from a momentary gasp to forever, and this is usually due to brainstem concussion, not structural brain damage.
  • Although rarely attended by EMS in this phase, isolated case reports suggest that up to 50% (!) of immediately lethal (blunt) head injuries could recover well if promptly ventilated on scene.
  • simultaneously, a CATECHOLAMINE SURGE occurs*, generating major increases in BP and afterload which can can cause ‘flash’ cerebral oedema, pulmonary oedema and myocardial strain
  • some believe that the severity of the initial apnoea and hypertension are the principle determinants of outcome, as they set the physiological scene for all subsequent events

* and indeed, an ongoing ‘sympathetic storm’ which may persist for days, and require beta blockade

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12
Q

4 MAJOR CAUSES OF SECONDARY BRAIN INJURY?

A
  1. HYPOXIA
  2. HYPOTENSION
  3. HYPERTHERMIA
  4. SEIZURES
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13
Q

ANTICONVULSANT DOSES FOR HEAD INJURY

A
  • PHENYTOIN
    • LD = 15mg/kg slow IV, THEN - 300mg/d
  • Increasingly KEPPRA
    • 20 mg/kg
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14
Q

UNDERSTANDING OSMOTHERAPY IN HEAD INJURY

A
  • the key to understanding OSMOTHERAPY in raised ICP is to understand that it is aimed at areas of NORMAL BRAIN TISSUE, not the injured parts
  • the brain is kept in a fixed volume box, and under normal circumstances, BRAIN VOLUME is controlled by regulating BRAIN WATER by having a BLOOD-BRAIN BARRIER controlling the entry of osmotically active molecules into the brain.
  • This is achieved by having TIGHT JUNCTIONS between the cells of the vascular endothelium of the brain, forcing even small electrolytes to transit the endothelial cell membranes (via protein channels etc) if they are to enter the brain*
  • the intent of OSMOTHERAPY in raised ICP is to increase the osmolarity of the plasma to pull water out of the brain. Because the total osmotic tension of the plasma is so high (>5000 mmHg!!), this is easily done with only minor increases in Na (or MANNITOL etc) concentration, BUT requires an intact BBB to prevent escape of these molecules into the brain.
  • This is why osmotherapy may be more beneficial in focally injured brains (with largely intact BBB) than in diffusely injured brains with widespread endothelial dysfunction.

* although lipid soluble molecules, like alcohol, cross these lipid barriers easily

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15
Q

MANNITOL DOSE FOR RAISED ICP?

A
  • 20% Mannitol, 2-5 ml/kg
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16
Q

HYPERTONIC SALINE DOSE FOR RAISED ICP?

A
  • = 7.5% Saline, 4ml/kg, or
  • 20% Saline, 10ml bolus (no longer carried)
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17
Q

NS V HARTMANS IN NEURO-ANAESTHESIA?

A
  • although evidence of benefit and magnitude of effect are probably weak, some neurosurgeons prefer NS over HARTMANS for its higher osmolarity: 308 v 274, which has a mild brain shrinking effect
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18
Q

HYPERVENTILATION FOR RAISED ICP

A
  • Normal arterial pCO2 = 35-40mmHg
  • In raised ICP, this may be be blown down to 28-30mmHg to produce vasoconstriction to reduce the volume of blood in MONRO-KELLY’S BOX
  • BUT: risks ischaemic damage from vasospasm
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19
Q

THE UNILATERAL BLOWN PUPIL

A
  • (unless a traumatic mydriasis), is caused by loss of CN3 PNS constrictor tone to the pupil, usually due to compression of the brainstem against the Tentorium
  • NOTE: the eye signs may occur IPSILATERAL, BILATERAL, or even CONTRA-LATERAL to the side of the lesion!
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20
Q

EFFECT OF NARCOTICS ON ‘FIXED DILATED PUPILS’

A
  • the PINPOINT PUPILS of Narcotic OD are caused by increased PNS constrictor tone carried in CN 3, whereas the FIXED DILATED pupils of severe head injury are caused by interruption of PNS constrictor tone in CN3, eg by compression against the tentorium
  • hence Narcotics do not prevent ‘fixed dilated pupils’ in head injury
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21
Q

ANTE vs RETROGRADE AMNESIA

A
  • RETRO GRADE = going backwards, ie before injury
22
Q

REPATRIATION OF BRAIN DEAD PATIENTS (US)

A
  • The US values repatriation for family re-union and donor discussions, but there are often cascading medical problems, including:
    • Hypotension despite inotropes
    • Metabolic Acidosis despite adequate filling
    • DI
    • Neurogenic Pulmonary Oedema
    • DIC
  • In many patients, these settle significantly with the institution of the T4 PROTOCOL:
    • THYROXINE
    • INSULIN* + 50% D
    • SOLU-MEDROL
    • VASOPRESSIN

* may need aggressive K+ replacement once begun

23
Q

WHAT IS NEUROGENIC PULMONARY OEDEMA

A
  • Neurogenic Pumonary Oedema = pulmonary oedema due to cardiac failure due to massive increases in afterload due to catecholamine surges in support of a dying brain
24
Q

NATURE OF PAEDIATRIC BLUNT CHEST INJURIES?

A
  • Children have elastic chests, so:
    • pulmonary contusions are common
    • rib # are uncommon
    • aortic injuries are rare
25
Q

4 PHYSIOLOGICAL CONSIDERATIONS IN PAEDIATRIC TRAUMA?

A
  • higher blood volume: 80-90 ml/kg, so ‘cope then crash’
  • higher BSA to volume ratios, so get cold faster
  • less urine concentrating ability: normal U/O, 1-2 ml/kg/h not 0.5
  • have lower glucose stores: consider giving IV
26
Q

SURGICAL AIRWAY IN CHILDREN

A
  • The CTM is said to be small and hard to find in children aged <12y, so use the needle not the knife ……hmmmmmmm
27
Q

CHEST TUBES IN CHILDREN

A
  • indications and sites are the same as in adults, but with size appropriate devices
  • due to their thin chest walls, may seal better if start one space lower and tunnel over the rib above
28
Q

HOW TO CLEAR THE C-SPINE

A
  1. assume C-Spine injured and protect
  2. Clear CLINICALLY if able: ie not concussed, drunk, drugged or distracted, and no Hx of ANY neurological loss
    • no pain in neck
    • then no tenderness
    • then N head control and neurological function
  3. Otherwise, IMAGE:
    • XR to ‘rule in’ (finds 95%)
    • CT to ‘rule out’
    • and MRI if still concerned
29
Q

WHO NEEDS ‘T’ and ‘L’ SPINE PRECAUTIONS?

A
  • Any patient who needs ‘C’ Spine precautions, also needs ‘T & L’ Spine precautions, ie Long board/Log rolls until cleared
30
Q

HOW TO CLEAR THE ‘T’ & ‘L’ SPINE?

A

Follows a similar plan to the C Spine, ie

  • assume injured and protect with a long board and log rolls
  • clear clinically if able
  • otherwise, IMAGE
31
Q

THE 4 person log roll

A
  • 1 to take the head and call
  • 2 at the side to do the roll
  • 1 at the back to remove long board, examine the back and do PR
32
Q

WHAT IS A JEFFERSON FRACTURE?

A
  • = a BURST # of C1 due to axial loading*
  • it is usually unstable, but the cord is often spared by the large canal size at C1/2 (if not, you die)
  • it’s diagnosed on the PEG view, with displacement of the lateral masses

* mental hook: picture Jeff getting patted on the head

33
Q

WHAT IS A HANGMANS FRACTURE?

A
  • = fracture of the posterior elements of C2, usually due to extension
34
Q

WHAT IS A CHANCE FRACTURE.

A
  • = a flexion injury of the lumbar spine, combining a wedge fracture of the vertebral body with posterior element disruption
  • first described by the Surgeon Trevor Chance in 1948 in lap-belted crash victims, and frequently associated with abdominal injury
35
Q

NORMAL SOFT TISSUE WIDTH ON LAT CSpineXR?

A
  • C1-4 = 50% of vertebral body width
  • C5+ = 100% of vertebral body width
36
Q

CERVICAL CANAL DIAMETER BY LEVEL

A
  • relatively spacious at C1/2, so # often spare the cord (or you are dead)
  • much tighter lower, so cord injury more likely (but more survivable)
37
Q

RISK OF NEUROLOGICAL INVOLVEMENT WITH T SPINE #

A
  • T Spine # are usually stable wedge fractures, but if displaced, usually transect the cord as canal diameter is small
38
Q

SIGNIFICANCE OF THORACO-LUMBAR JUNCTION #

A
  • fractures here occur where the rigid thorax meets the flexible lumbar spine
  • they are often unstable, but the cord ends at L1, so may produce an incomplete ‘CAUDA EQUINA’ lesion
39
Q

WHAT IS SACRAL SPARING?

A
  • = preservation of peri-anal sensation or VOLUNTARY anal wink after cord injury
  • It may be the only early sign that a cord lesion is incomplete
40
Q

SPINAL INJURY IN CHILDREN

A
  1. children are flexible, so SCIWORA is common
  2. C2/3 and C3/4 ‘subluxations’ are common normal findings
  3. Peg and spinous process growth plates may be mistaken for #
41
Q

PATHOPHYSIOLOGY OF HANGING

A
  • JUDICIAL Hangings aim to kill instantly by disrupting the vertebral column and severing the upper cord
  • SUICIDAL hangings often have insufficient drop height to disrupt the vertebral column, so the initial effect is vascular occlusion, which often obstructs venous but not arterial flow, resulting in LOC from cerebral oedema. Subjects found early often recover surprisingly well, even if pulseless and blue.
  • remember to investigate survivors for carotid or vertebral artery injury, as these can cause delayed CVA if missed
42
Q

MUSCLE POWER GRADING

A
  1. 0/5 = no contraction
  2. 1/5 = visible flicker
  3. 2/5 = full ROM if gravity elim
  4. 3/5 = full ROM against gravity
  5. 4/5 = full ROM but reduced power
  6. 5/5 = normal power
43
Q

EMERGENCY TREATMENT OF FROSTBITE

A
  • Dunk in 40C water for 1/2 hour!
44
Q

LEFT vs RIGHT DIAPHRAGMATIC HERNIA

A
  • Its harder to Dx on the R, as the liver prevents bowel herniation
45
Q

TRAUMATIC CAUSES OF PEA

A
  • Hypovolaemia
  • Tension PT
  • Cardiac injury: tamponade/contusion/rupture
46
Q

BECKS TRIAD

A
  1. shock +
  2. muffled HS +
  3. raised JVP

= CARDIAC TAMPONADE

47
Q

DIAGNOSIS OF CARDIAC INJURY IN TRAUMA?

A

Hx of chest trauma and:

  1. arrhythmias or ST changes on ECG (the best sign*)
  2. signs of Cardiac dysfunction clinically or on echo
  3. enzyme changes (Troponin or CK rise - least useful)

* but remember, the catechol surge of severe head injury can cause myocardial strain

48
Q

EFFECT OF MATERNAL SHOCK ON THE FOETUS

A
  • is disproportionately large, for the placental circulation is very sensitive to catechols, so foetal compromise occurs early in maternal shock
49
Q

PERIMORTEM LSCS

A
  • Usually futile in TRAUMA, as placental sensitivity to catechols generally means the FOETUS is in worse shape than the mother
  • may successfully rescue the baby if performed within 15* minutes of a ‘medical arrest’ in the mother
  • MUST be performed immediately for effective maternal CPR, with maternal survival reported with section up to 30m* later

* this has recently increased from 5m

50
Q

POSITION FOR CPR IN THE PREGNANT PATIENT

A
  • this is done supine, as in any other patient, but with a wedge placed under the R hip to relieve caval compression

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