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189 Cards in this Set
- Front
- Back
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Scene Assessment - S C E N E |
Safety Cause (Incl. MOI)Fall/assault etc. Environment - access/egress problems. No. Of Casualties Extra resources needed E.g. Fire, police, HEMS |
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Systematic Approach order - S P P S H H |
Scene Assessment Patient Assessment Triangle Primary Survey (CACBCDE) Secondary Survey History (Medical) Handover |
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Handover - A T M I S T |
Age Time MOI Injury Signs/sx. Treatments provided |
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Primary survey |
C - catastrophic hemorrhage A - airway C - c-spine B - breathing C - circulation D - disability E - expose/environment |
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3 Major incident categories |
Sudden Impact Rising Tide Cloud on the horizon |
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4 Major incident statuses |
Major incident standby Major incident declared Major incident cancelled Major incident stood down |
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METHANE |
M - major incident declared/standby E - exact location T - type of incident H - hazards present A - access - routes that are safe to use N - number, type & severity of casualties E - Emergency services present & required Update control when something changes or every 10-15 mins. |
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Catastrophic hemorrhage definition |
'Extreme bleeding likely to cause death within minutes’ (JRCALC, 2016) |
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Celox |
Locate source of wound. Remove excess blood. Completely pack the wound with Celox & additional regular gauze if a large cavity. Apply firm pressure for 3 minutes. If bleeding continues provide additional 3 minutes of firm pressure. Leave celox over wound & bandage. |
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Needle cricothyroidotomy indication/procedure - 10 steps |
Indication -CICV Procedure 1. Extend head slightly to stabilise trachea 2. Locate cricothyroid membrane & sterilise 3. Attach 10ml syringe w/ 5ml saline to cannula 4. Insert cannula into cricothyroid membrane at 45 deg angle. 5. Gently aspirate as inserting cannula, as you enter tracheal lumen bubbles should appear. 6. Advance further 1cm after bubbles are observed. 7. Railroad cannula over needle until hub flush with pts skin 8. Stabilise cannula and withdraw needle fully 9. Attach syringe to hub of cannula and aspirate to re-confirm placement. 10. apply 2 k-bandages either side of trachea for stabilisation and secure with tape. |
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Needle cricothyroidotomy ventilation |
1. Make a hole approx 40% of circumference of tube in o2 tubing and connect to back of cannula. 2. ventilate using a ratio of 1:4 - 1 second covered (inspiration), 4 seconds open (expiration). (Can modify to 1:8 or 1:10 if complete upper airway obstruction). 3. Observe chest rise & fall. 4. Auscultate. |
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Needle cricothyroidotomy complications - list 4 |
1. High failure rate – failure rate amongst anaesthetists of 60%. 2. Presence of large laryngeal tumours, neck pathology, obesity and coagulopathy. 3. After 30-45 mins this technique can provide high levels of PaCO2 and therefore a definitive airway must be established as soon as possible. 4. Overinflation of the lungs can result in barotrauma caused by pressure changes due to inadequate passive exhalation. |
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Respiratory assessment - TWELVE FLAPS |
Trachea Wounds/bleeding Emphysema (surgical) Larynx (crepitus/injury) Venous distention (jugular) Expose/examine Feel Look Auscultate Percuss Search (sides and back) |
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Blood on the floor + 4 more |
1. Catastrophic hemorrhage - obvious external 2. Thoracic cavity 3. Abdominal cavity 4. Pelvic cavity 5. Long bones |
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Fracture -BSLIPDUCT |
Bruising Swelling Loss of function Irregularities Pain Deformity Unnatural movement Crepitus Tenderness |
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Wound descriptors - BLAST DA PIC (Builds on DCAP BTLS) |
Burns Laceration Abrasion Swelling Tenderness Deformity Avulsion Puncture Incision Contusion |
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3 most common causes of spinal injury |
Falls RTC Sport/recreational |
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Highest spinal injury age range |
15-38 |
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How many spinal vertebrae in each section? Cervical Thoracic Lumbar Sacral Coccyx -Total |
7 12 5 5 4 -33 |
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Length & diameter of spinal cord |
42-45cm length 2cm diameter |
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How many pairs of spinal nerves are there? |
31 - 8 cervical, - 12 thoracic, - 5 lumbar, - 5 sacral, - 1 coccygeal |
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List the types of shock (5) - CASH-N |
Cardiogenic shock (due to heart problems) Anaphylactic shock (caused by allergic reaction) Septic shock (due to infections) Hypovolemic shock (caused by too little blood volume) Neurogenic shock (caused by damage to the nervous system) |
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What is the conus medullaris? |
Cone shaped end of the spinal cord - where cauda equina begins |
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Normal spinal range of extension / flexion |
55/45 |
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Normal rnge of L/R spinal rotation |
40 |
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Normal range of lateral extension |
70 |
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Which verterbrae does the hangmans fracture affect? |
Hangman fracture, also known as traumatic spondylolisthesis of the axis, is a fracture which involves the pars interarticularis of C2 on both sides, and is a result of hyperextension and distraction |
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What is the babinski reflex? |
Normal plantar response - toes curl downward positive babinski - toes upwards and splay + can indicate upper motor neuron lesion constituting damage to the corticospinal tract |
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Clinical indicators of spinal injury |
•Pain (midline) •Paraesthesia •Paresis •Paralysis •Priapism •Loss of sensation •Loss of bladder / bowel control |
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Verterbrae prominens - define |
Most prominent spinal process - c7 landmark |
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4 types of burns |
Superficial Partial thickness Deep partial thickness Full thickness |
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Organs within R Hypochondriac abdominal region - 3 |
Liver Gallbladder R kidney |
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Organs within L Hypochondriac abdominal region - 4 |
Liver (tip) Spleen Stomach L kidney |
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Organs within Epigastric abdominal region - 5 |
Stomach Liver Pancreas L & R kidneys |
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Organs within R lumbar abdominal region - 4 |
Liver (tip) Ascending colon Small intestine R kidney |
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Organs within umbilical abdominal region - 4 |
Small intestine Transverse colon Stomach Pancreas |
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Organs within L lumbar abdominal region - 3 |
Small intestine Descending colon L kidney |
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Organs within R Iliac abdominal region - 4 |
Small intestine Appendix Caecum Ascending colon |
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Organs within Hypogastric abdominal region - 3 |
Small intestine Bladder Sigmoid colon |
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Organs within L Iliac abdominal region - 3 |
Small intestine Descending colon Sigmoid colon |
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Name the three types of trauma |
Blunt Penetrating Crush |
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Kehr sign - define |
Acute pain in the tip of the left shoulder due to the presence of blood or other irritants in the peritoneal cavity when a person is lying down and the legs are elevated. Kehr's sign in the left shoulder is considered a classic symptom of a ruptured spleen. |
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Where are the sternoclavicular joints? |
Between the sternum and the clavicles |
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Where is the suprasternal notch? |
The top of the manubrium |
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Where is the costal arch? |
Lower edge of thorax |
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Impailed object treatment |
DO NOT remove (unless interfering with he airway) Cover with sterile dressing Pad the area and cover 3/4 of the height |
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3 potential complications of thoracic trauma |
ventilation oxygenation circulation |
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6 potentially fatal thoracic injuries ATOM FC |
Airway obstruction Tension pneumothorax Open pneumothorax Massive haemothorax Flail chest Cardiac contusion |
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Auscultation and percussion sites for OSCE - there are 6 (which lung field lies where?) |
2nd intercostal space, mid-clavicular line L & R - Superior lobes 4th intercostal space, mid-clavicular line - L superior lobe (lower), R middle lobe 6th intercostal space, mid-axillary line - L & R inferior lobes |
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Clinical signs of tension pneumothorax |
••Pleuritic chest pain and dyspnoea ••Hypotension ••Tachycardia and tachypnoea ••Hyper-resonance on the affected side ••Absence of breath sounds on the affected side ••Jugular vein distension ••Tracheal deviation away from the affected side. |
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Needle thoracentesis sites |
Mid-clavicular line, 2nd intercostal space. If large pectoral muscle/unsuccessful can attempt 5th IC space mid-axillary line. Insert as minimally superior to rib as possible to avoid the azygos and hemiazygos veins which run in the center of the IC muscles. |
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Massive haemothorax definition |
Fast accumulation of > 1000ml of blood in pleural cavity (Lorna's notes) 1500ml according to other literature (doesn't specify need to be rapid accumulation) |
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Canadian C-spine rules - high-risk factors - 3 - if ANY present then immobilize Apply C-spine rules to: (PAD) -GCS 15 -trauma patients -stable vital signs -age > 16 -no acute paralysis -no known vertebral disease -no previous spinal injury |
1. Paraesthesia in extremeties 2. Age > 65 or 3. Dangerous mechanism* or * Fall from elevation > 3 feet/5 stairs * Axial load to head - diving * MVC high speed > 60mph (rollover, ejection) * Motorized rereational activities * bicycle struck/ collision |
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Myocardial contusion - clinical signs |
chest pain, pericardial rub, S3, muffled heart sounds, cardiac failure ECG: ST or T wave changes anteriorly, heart blocks, incomplete RBBB, inferior Q waves ECHO: contractility, RWMA TNT elevation |
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Canadian C-spine rules - low-risk factors - allows safe assessment of ROM - 5 (SSAAD) |
1. Simple read-end MVC* 2. Sitting position in ED 3. Ambulatory at any time 4. Absent mid-line tenderness on palpation 5. Delayed onset of neck pain *excludes pushed into oncoming traffic bus/large truck rollover hit by high speed vehicle |
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Burns - Zone of coagulation |
In this zone there is irreversible tissue loss due to coagulation of the constituent proteins |
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Burns - Zone of stasis |
The surrounding zone of stasis is characterised by decreased tissue perfusion |
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Burns - Zone of hyperaemia |
In this outermostzone tissue perfusion is increased. |
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Burns - 4 types |
Thermal Radiation Chemical Electric - Flash, contact, current |
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Adducted - definition |
Moved towards the centre |
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Abducted - definition |
Moved away from the centre |
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Name the key parts of the pelvis - 12 |
1. Ischium 2. pubis 3. illium 4. sacrum 5. sacroilliac joints 6. coccyx 7. acetabulum 8. pubic arch 9. pubic symphysis 10. inferior pubic ramus 11. superior pubic ramus 12. pelvic inlet |
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Photokeratitis - define |
Photokeratitis or ultraviolet keratitis is a painful eye condition caused by exposure of insufficiently protected eyes to the ultraviolet (UV) rays from either natural (e.g. intense sunlight) or artificial (e.g. the electric arc during welding) sources. |
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Types of pelvic fractures - 5 |
1. Rami 2. Straddle 3. Acetabular 4. Pelvic ring - lateral compression, anterior-posterior compression, vertical shear 5. Open pelvic |
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Pubic rami fracture |
Common in elderly patients and those with osteoporosis Usually a result of low-energy trauma (eg. Fall from standing) Isolated fractures are generally minor and don’t require surgery – can cause concurrent problems with posterior pelvis Not typically associated with major internal haemorrhage Many patients can weight bear – stable injury |
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Straddle fracture |
Bilateral fracture of inferior and superior pubic rami
Caused by ‘straddle’ injury – landing forcefully on the perineum Usually a result of low-energy trauma Typically stable and not associated with major internal haemorrhage Many patients can weight bear Don’t usually require surgery |
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Acetabular fracture |
Fracture of the ‘socket’ of the hip
Usually a result of high-energy trauma, often resulting in hip dislocation Femoral head is driven into the acetabulum 90% dislocations are posterior (leg flexed, adducted, shortened and internally rotated) Eg: Flexed knee hits dashboard Anterior dislocation (leg flexed, abducted and externally rotated) Eg: Skiing injury Potentially unstable fracture – surgery may be required Can result in significant internal haemorrhage |
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Acid burns |
Acids cause acoagulum (eschar) that may limit further damage – they appear ‘dry’ Mostacids produce a coagulation necrosis by denaturing proteins, forming a coagulum(eg,eschar) that limits the penetration of the acid |
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Alkaline burns |
Alkalis cause liquefactive necrosis allowing deeper penetration – appear ‘wet’ Alkalis typically produce a more severe injury known as liquefaction necrosis. This involves denaturing of proteins which prevents limitation of tissue penetration. Hydrofluoric acid is different from other acids in that it produces a liquefaction necrosis. symcb.com/gn.crt |
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Severity of burn factors |
Theseverity of the burn is related to a number of factors, including the pH of theagent, the concentration of the agent, the length of the contact time, thevolume of the offending agent, and the physical form of the agent. In addition,concentrated forms of some acids and alkalis generate significant heat whendiluted or neutralized, resulting in thermal and caustic injury. |
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Crush injury |
Large bore IV NaCl - 2l given prior to removal of object (caution in CHF), give after at a rate of 500ml/20 minutes. Consider tourniquet immediately before object removal if entrapment > 30 minutes. Cardiac monitoring - beware of Hyperkalemia (tall, 'peakd', symmetrical T waves, IVCD/BBB, diminished P waves) Consider AKI and rhabdomyolysis. |
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Burns treatment |
running tepid water (15 deg centigrade) [ Iced water should not be used as intense vasoconstriction can cause burn progression. Cooling large areas of skin can lead to hypothermia, especially in children. ] For up to 20 minutes - chemical burns can be longer •May reduce oedema by stabilising mast cells and histamine release. once cooled lay strips of sterile dressing over the burn, DO NOT wrap circumferially Be alert of cause of injury as there may be other pathology e.g. airway burns, c-spine injury |
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Burns - history taking |
Time sustained burning agent clothing worn first aid measures enclosed space identity of chemicals voltage of electricity inappropriate history |
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Burns - important signs to look for |
soot in nostrils carbonaceous sputum singeing of nasal hairs/eyebrows excessive coughing hoarseness/voice chage dyspnoea altered LOC |
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Carbon monoxide |
•0-10% - Minimal (normal in heavy smokers)•10-20% - Nausea, headache •20-30% - Drowsiness and lethargy •30-40% - Confusion and agitation •40-50% - Respiratory depression, coma •>50% - Death |
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Escharotomy - define |
a surgical procedure used to treat full-thickness (third-degree) circumferential burns. In full-thickness burns, both the epidermis and the dermis are destroyed along with sensory nerves in the dermis. The tough leathery tissue remaining after a full-thickness burn has been termed eschar. Complications - •Respiratory compromise•Abdominal compartment syndrome •Nerve injury•Muscle necrosis •Systemic complications –Myoglobinuria–Renalfailure–Hyperkalaemia–Metabolicacidosis |
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When do burns need fluid rescusitation? |
•10% TBSA in children •15-20% TBSA in adults ^^ Lorna's notes JRCALC says 1 litre initial dose (no repeat dose) if TBSA between 15 and 25 and TTH > 30 min or if TBSA >25% give regardless of TTH. if giving fluid for burns then the dose given is over 1 hour |
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Hypothermia in burns |
Impairs microcirculatory perfusion Induces shivering, which exacerbates hyper-metabolism seen in burnspatients Impairs neutrophil function, increasing the risk of infection Impairs platelet function, increasing the risk of bleeding Reduces cardiac output by up to 25% |
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Analgesia in burns |
multi modal |
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Trauma triad of death |
Hypothermia - anything below 35 degrees C. Tissue factor and PLT function are impaired. 100% mortality with temp < 32 degrees C. Acidosis - ph < 7.2 - hypoperfusion from hypothermia and blood loss leads to lactic acid from anaerobic energy production and decrease in pH. pH < 7.2 will decrease phothrombinase complex activity by at least 50%. Coagulopathy - INR > 1.5 - increased pre-hospital fluid levels associated with increased chance of coagulopathy. Hypothermia and pH also impair clotting cascade process. 50-90% mortality rate for patients with all three factors. We can counter by keeping patient warm, limiting fluids and maintaining adequate SBP and encouraging clotting on active bleeds, pressure, elevation, TXA etc. |
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TXA - indications |
Patients with time critical injury, where significant internal/external haemorrhage is suspected age > 12 ? Injured patient fulfill step 1 or step 2 of major trauma triage protocol. Step one physiological Physiological signs, gcs <14 and bp <90 Step two mechanism of injury. Penetration to the head neck or torso, proximal to wrist or ankle Chest injury with altered physiology , e.g. haemo-pneumothorax Two proximal long bone fractures Crushed/degloved/mangled Amputation proximal to wrist or ankle i.e not digits Pelvic fracture Open or depressed skull fractures Sensory or motor deficit new onset. = activate major trauma alert and transfer to major trauma centre |
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TXA contraindications |
•Isolated head injury •Critical interventions required; leavinginsufficient time for tranexamic acid •Haemorrhage has stopped- |
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TXA how to administer (side effects) |
Slowly over 10 mins/ 10 aliquots with 1 minute interval between. Can cause hypotension if administered quickly, can also cause convulsions. |
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Haemorrhage control - NICE |
Restrictive fluid approach w/ active bleeding, once bleeding ceased then aim for palpable radial pulse or palpable carotid pulse in penetrating thoracic trauma. give fluids in 250ml boluses and re-assess. |
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Crush syndrome - complications (metabolic) |
Hyperkalemia > 5.0 mmol/l - hypocalcaemia < 2.2mmol/l - -Neuromuscular excitability -Carpopedal spasm -Tetany -Chvostek’s sign -Trousseau’s sign -Seizures -long qtc ecg > 450ms rhabdomyolysis DIC |
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Lateral compression fracture |
Most common pelvic ring fracture (60-70%)
Result of forceful impact to one side of the body Hit by car Falling from height onto one side Affected side rotates inwards around the sacrum Can result in a variety of fractures Pressure on bladder/incontinence Unstable injury – may require surgery Can result in internal haemorrhage – not usually severe Volume of pelvis is reduced due to internal rotation |
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Anterior-posterior compression fracture |
Accounts for around 15%-20% of pelvic ring fractures
Result of high-energy trauma, usually from the front Crush injury Hit by car Fall from height Variety of fractures can occur Pubic symphysis and supporting ligaments are torn apart Pelvis opens – ‘open book fracture’- increases pelvic volume Legs usually flexed and abducted Pressure on bladder/incontinence Potential for massive internal haemorrhage |
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Vertical shear fracture |
Lowest incidence (5-15%); highest mortality
High-energy trauma – major vertical force applied to pelvis Usually a result of landing on feet from significant height Results in one or both halves of the pelvis being detached and displaced upwards Multitude of possible fractures Posterior: usually fractures at sacroiliac joint or ilium Anterior: usually pubic rami or separation of pubic symphysis Risk of massive internal haemorrhage Nature of injury usually tears blood vessels |
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Open pelvic fracture |
Occur when the pelvic fracture is accompanied by the presence of a laceration:
In the pelvic region Vaginal laceration Rectal laceration Very uncommon High mortality rate Result of high-energy trauma Potential for massive internal and external haemorrhage |
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Pelvic fracture Assessment |
Assess Mechanism
Main mechanisms: RTCs, pedestrian vs vehicle, motorcycle accidents & falls from height ‘Read the wreckage’ - relate the mechanism to the patient’s anatomy & clinical presentation If mechanism of injury (and/or clinical assessment) suggests a fracture – treat for one Clinical Assessment Injured patients complaining of pain in the pelvis, lower back or hips should be considered as having an unstable pelvic injury Deformity, bruising and swelling around the pelvis, a shortened or rotated leg, wounds over pelvis and bleeding (PR, PU, PV) are all associated with pelvic fracture Vertical shear and open book fractures can often be identified by pelvic asymmetry. Do not stress the pelvis to assess it. |
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Pelvic fracture Tx. - Stable |
Stable, isolated pelvic fractures (pubic rami/straddle fractures):
Pain relief Comfortable positioning Do not require splinting Destination?Transport to nearest ED unless other major trauma indicators are present |
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Pelvic fracture tx. - unstable |
Unstable pelvic fractures (acetabular / pelvic ring fractures):
If active bleeding is suspected from a pelvic fracture following blunt high‑energy trauma: apply a purpose‑made pelvic binder Significant mechanism + haemodynamically unstable due to unknown cause = assume time critical pelvic injury If mechanism is suggestive and the patient presents with any of the following: Haemodynamically unstable Shock (pulse >100, systolic <90) GCS <13 Distracting injuries present Patient complaining of pelvic pain …apply pelvic binder |
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Pelvic fracture - overall tx. |
100% O2 Use IV TXA as soon as possible in patients with major trauma and active or suspected active bleeding Consider fluid resuscitation uIO/IV (wide bore cannula) For active bleeding, use restrictive approach to volume resuscitation until definitive early control of bleeding has been achieved– titrate to maintain a palpable central pulse (carotid or femoral) Consider pain relief (IV morphine) Entonox not contraindicated but caution is advised Treat necessary concurrent injuries and immobilise Transport decisions? Pre-alert and rapid transfer to MTC ,%`' |
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Long bones - 10 |
Humerus Radius Ulna Metacarpals Phalanges Femur Tibia Fibula Metatarsals Phalanges |
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Fracture types - 6 |
Simple Compound Comminuited Oblique Transverse Spiral |
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Traction splint indications |
Use only in mid-shaft femur fractures with no obviousknee, ankle or lower leg injuries |
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Referral criteria for burns units |
Burn > 5% inchildren or > 10 % in adult Full-thickness ordeep partial thickness > 5% Burns withinhalation injury Chemical burns and electrical burns Hands, feet, face, joints, perineum, genitalia Patient very old or very young Patients with pre-existing medical conditions Burns associated with other trauma |
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Nexus C spine rules (NSAID) |
Focal Neurologic Deficit Present Midline Spinal Tenderness Present Altered Level of Consciousness Present Intoxication Present Distracting Injury Present Unlike the Canadian C-spine Rule (CCR), NEXUS Criteria does not have age cut-offs and is theoretically applicable to all patients > 1 year of age. However, there is literature to suggest caution applying NEXUS to patients > 65 years of age, as the sensitivity may be as low as 66-84%. |
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The parkland formua (Burns) |
The Parkland formula for the total fluid requirement in 24 hours is as follows:
4ml x TBSA (%) x body weight (kg); 50% given in first eight hours; 50% given in next 16 hours. Children receive maintenance fluid in addition, at an hourly rate of: 4ml/kg for the first 10kg of body weight plus; 2ml/kg for the second 10kg of body weight plus; 1ml/kg for >20kg of body weight. End point Urine – adults: 0.5–1.0 ml/kg/hour; Urine – children: 1.0–1.5ml/kg/hour. |
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Stabwound/GSW - history |
What type of weapon Length of blade how far inserted distance from target Angle of insertion Where is entry & exit wound What structures might have been damaged? |
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Blast injury phases |
Primary - due to pressure wave - mainly effects gas containing organs causing spalling, implosion, inertia, and pressure differentials. Pulmonary contusion, TBI. Secondary - bomb casing projectiles collide with victim. Tertiary - blast wind propels victim or objects into victim |
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Electrical burns types - 3 |
1. Flash - From arcing of electricity arc High dry air temperature No internal injury Photokeratitis - damage to eye from UV rays 2. Contact - Low voltage (<1000v, household) High voltage (>1000v, industry) 3. Current - Alternating (mains) provokes tetanic contractures Direct (lightning) tends to throw the victim |
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Lightning strike - cause of arrest |
Lightning strike - cardiopulmonary arrest is typically the cause of death after a lightning strike. Immense electrical energy enters the body and acts like a massive defibrillation. As with a standard defibrillation, the electrical energy depolarises the myocardium and produces a period of asystole. However, due to the dysfunction of the autonomic nervous system and lack of a functioning medullary cardiac centre to provide stimulation to the myocardium, the heart remains in asystole. Thus, the initial presenting rhythm immediately following the event is asystole.
Eventually, the inherent automaticity of the cardiac conduction system produces electrical impulses and the heart begins to contract. However, the respiratory centre in the medulla remains shut off. Due to lack of adequate ventilation, the heart begins to become severely hypoxic and acidotic resulting in a secondary cardiac arrest from ventricular fibrillation. Contrary to the normal thinking in initial rhythms in cardiac arrest, the lightning strike victim may be more viable in the initial asystolic cardiac rhythm. The ventricular fibrillation rhythm may reflect a severely acidotic and hypoxic state associated with a secondary cardiac arrest that may be more difficult to resuscitate. |
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Healing process |
The inflammatory process is the first stage of healing during which the wound is subject to altered vascularity and altered coagulation. Initially, vasoconstriction produces hypoxia, tissue acidosis and lactate accumulation. Various cascades are activated - the coagulation cascade, the kinin cascade and the complement cascade. The coagulation cascade results in clot formation at the bleeding sites. The kinin cascade releases kinins and histamine whose actions produce vasodilation and increased capillary permeability, thus giving rise to oedema. The complement cascade produces molecules that lyse bacteria, cause histamine release and attract inflammatory cells such as polymorphonuclear leukocytes (PMNs) and monocytes to the injured area. PMNs help protect wounds from infection whilst monocytes result in phagocytosis of cell debris and bacteria |
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TXA Pharmacodynamics |
Tranexamic acid is an antifibrinolytic that competitively inhibits the activation of plasminogen to plasmin. Tranexamic acid is a competitive inhibitor of plasminogen activation, and at much higher concentrations, a noncompetitive inhibitor of plasmin, i.e., actions similar to aminocaproic acid. Tranexamic acid is about 10 times more potent in vitro than aminocaproic acid. Tranexamic acid binds more strongly than aminocaproic acid to both the strong and weak receptor sites of the plasminogen molecule in a ratio corresponding to the difference in potency between the compounds. Tranexamic acid in a concentration of 1 mg per mL does not aggregate platelets in vitro. In patients with hereditary angioedema, inhibition of the formation and activity of plasmin by tranexamic acid may prevent attacks of angioedema by decreasing plasmin-induced activation of the first complement protein (C1). |
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TXA Mechanism of action |
Tranexamic acid competitively inhibits activation of plasminogen (via binding to the kringle domain), thereby reducing conversion of plasminogen to plasmin (fibrinolysin), an enzyme that degrades fibrin clots, fibrinogen, and other plasma proteins, including the procoagulant factors V and VIII. Tranexamic acid also directly inhibits plasmin activity, but higher doses are required than are needed to reduce plasmin formation. |
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Immobilised C-spine Pt. vomits - Tx. |
Log roll if 4 people are available — one to hold the head, and three to perform the roll If insufficient numbers of people are available, tilt the bed head down so that vomit runs clear of the airway Suction away the vomitus with a Yankauer Administer antiemetics (e.g. ondansetron 4mg IV) Seek and treat underlying causes — patients often vomit due to pain or opioid analgesia, but it can also be a sign of worrying causes such as serious abdominal trauma, hypotension or raised intracranial pressure |
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How do patients with spinal injuries develop respiratory insufficiency? |
High cervical injuries may lead to airway obstruction due to local hematoma and swelling.
Lesions at the C5 level or higher lead to diaphragmatic paresis or paralysis, as the phrenic nerve arises from the C3-5 levels. Thoracic or higher lesions may lead to respiratory distress due to paralysis of intercostal muscles, as the intercostal nerves arise from the T1-12 levels. Other causes include: Coexistent thoracic injuries Coexistent traumatic brain injury (e.g. decreased respiratory drive from coma) Complications of spinal cord injury (e.g. aspiration, atelectasis, pulmonary embolus, metabolic acidosis from spinal shock) Complications of treatment (e.g. sedation, fluid overload, transfusion- associated acute lung injury, ventilator associated pneumonia). |
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Neurogenic vs spinal shock |
Neurogenic shock is classically characterised by hypotension, bradycardia and peripheral vasodilatation. Neurogenic shock is due to loss of sympathetic vascular tone and happens only after a significant proportion of the sympathetic nervous system has been damaged – as may occur with lesions at the T6 level or higher. Bradycardia caused by lack of sympathetic tone to the heart (key to neurogenic shock).
Tx. Atropine Fluids Vasopressors Spinal shock is not a true form of shock. It refers to the flaccid areflexia that may occur after spinal cord injury, and may last hours to weeks. It may be thought of as ‘concussion’ of the spinal cord and resolves as soft tissue swelling improves. Priapism may be present. |
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How are thoracic and lumbar spinal injuries assessed? |
There are no validated decisions rules for clearing the thoracic or lumbar spine. Imaging is generally required if there are the following:
Point tenderness Deformity or bony step Neurological findings consistent with a thoracic or lumbar injury High risk mechanism, especially in the presence of distracting injuries |
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What can be used to remove adhered tar from a wound? |
Butter Sunflower oil Baby oil |
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Severity of head injury |
•Minor GCS 15 •Mild – GCS 13-15 •Moderate – GCS 9-12 •Severe – GCS 3-8 |
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What is ICP and how and why is it maintained at a constant level? |
ICP is the pressure within the cranial vault. It is maintained at a constant level to ensure adequate CPP, if the ICP fluctuates then the brain may be over perfused or under perfused and autoregulation will have to alter the intracranial contents. |
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What is cerebral perfusion pressure? |
Blood flow to the brain.
MAP - ICP = CPP |
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What is mean arterial pressure (MAP) and why is this important? |
The average arterial pressure during a single cardiac cycle. It is important as it indicates the perfusion of organs and is used to calculate cerebral perfusion pressure, monitoring and correcting MAP can prevent hypoxia, acidosis and ischaemic cascade. |
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What is the mass effect? |
Mass effect is a phenomenon in which a focal lesion or contusion causes surrounding areas of brain tissue or brain structures to be compressed and injured due to the degree of space that leaking blood, cerebrospinal fluid, or edema takes up within the restricted skull space. Ischaemic cascade and inflammatory response cause breakdown of BBB and permeable capillaries which causes fluid and proteins to leak into ECF (vasogenic edema). Can lead to herniation (midline shift/foramen magnum).
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Average ICP level? |
7-10 mmhg in some sources others say 5-15. |
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Average intracranial volume and breakdown |
1700ml (adult) - total 1400ml brain 150ml csf 150ml blood |
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Monroe-kellie hypothesis |
A pressure-volume relationship that aims to keep a dynamic equilibrium among the essential non-compressible components inside the rigid compartment of the skull and aids to maintain the ICPlevel (7–10mmHg)
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How much can compensatory mechanisms accomodate for in ICP maintainence? |
100-120 mls, after this a 'critical volume' is met and rapid sustained increases in ICP will begin. |
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How is CSF tapped off with raised ICP? |
Cranial and spinal arachnoid villi have been considered for a long time to be the predominant sites of CSF absorption into the venous outflow system. Experimental data suggest that cranial and spinal nerve sheaths, the cribriform plate and the adventitia of cerebral arteries constitute substantial pathways of CSF drainage into the lymphatic outflow system. |
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Normal Cerebral perfusion pressure |
70-80 mmhg |
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Lowest permissible CPP? |
If itdrops below 60 mmHg the brain will be poorly perfused leading to ischaemicbrain damage and impaired brain function (PHTLS, 2016) |
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CPP calculation |
MAP - ICP = CPP ICP during a head injury can easily be over 20 mm Hg. Over 40 is almost certainly going to create significant symptoms and over 60 is fatal Normal ICP = 10 mmhg |
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MAP = |
The mean arterial pressure (MAP) is an average blood pressure in an individual. It is defined as the average arterial pressure during a single cardiac cycle Average MAP - 85-95 mmhg ((2 x diastolic) + systolic) / 3 = MAP |
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6 H's of secondary head injury |
hypoxia hypoxaemia hypo/hyper-carbia hypoperfusion hypotension hyperpyrexia |
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What is cerebral autoregulation? |
Cerebral autoregulation may be defined as the maintenance of locally controlled constant cerebral blood flow despite changes in cerebral perfusion pressure, where CPP is equivalent to MAP-ICP (or CVP, whichever is greater). This is in response to tissue pH and tssue CO2. |
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How is TXA given? |
1g in 10ml over 10 minutes in 10 aliquots to avoid hypotension. |
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Clinical indicators of TBI |
Agitation Reduced GCS Anisocoria 'cerebral' T wave inversion with long QT (ECG) seizures decorticate/decerebrate posturing irregular respirations - hyperventilation/cheyne stokes/biots/ataxic/stertorous etc. Vomiting fixed gaze - direction of eyes should signify the hemisphere of brain injured hemiparesis/plegia cranial nerve defecit Cushings triad |
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Management of pre-hospital TBI |
1.Optimising oxygenation (with added pulse oximetry) 2.Maintaining ETCO2 to 30-40 mmHg - Avoid hypo- and hyperventilation 3.Maintenance of MAP ≥ 80 mmHg - to maintain cerebral perfusion pressure (CPP) > 60 mmHg for a treatment threshold of ICP > 20 mmHg 4.Management of agitation Midazolam (AP only) 5. Major trauma centre conveyance |
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Systolic BP, ideal range with TBI |
120-140 mmhg seems to be the ideal systolic BP to minimise mortality with TBI |
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GCS - stepwise approach |
Check Observe Stimulate Rate Fingertip -> trapezius -> supraorbital notch Motor 6 - Obey 2-part request 5 - Brings hand above clavicle to stimulus on head 4 - Bends arm at elbow rapidly but features not predominantly abnormal 3 - Bends arm at elbow, features clearly predominantly abnormal 2 - Extends arm at elbow 1 - No movement in arms / legs, no interfering factor NT - Paralysed or other limiting factor Abnormal Flexion Slow Sterotyped Arm across chest Forearm rotates Thumb clenched Leg extends Normal flexion Rapid Variable Arm away from body |
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TBI - 90-90-9 rule |
•A single drop in SP02 to less than 90% doubles chance of death •A single drop in the patients systolic BP to less than 90 mm Hg doubles chance of death •A single drop in the patients GCS to less than 9 doubles chance of death |
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Primary survey Catastrophic haemorrhage |
Check for cat. haem use tourniquet on limb approx 5cm above bleed, can apply second tourniquet proximal if still actively bleeding. if site of bleed can be visualised then wound can be packed with haemostatic agent - remove excess blood and pack wound elevating limb if possible and applying pressure for three minutes, apply further pressure for another three minutes if bleeding still hasnt ceased. Consider pressure/blast dressing DO NOT pack penetrating thoracic wounds DO NOT proceed until bleed has slowed or stopped Note time of tourniquet application |
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Primary survey - airway/C spine
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Look inside airway - conider suction /postural drainage if blocked. Apply appropriate airway maneuver - HTCL/ jaw thrust (considering MOI) Apply airway adjunct Look listen and feel for breath sounds. Apply Collar if concerned for C-spine and keep manual stabilisation on afterwards. Consider CICV and needle cricothyroidotomy. |
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Primary survey - Breathing |
Tracheal deviation - place ring and index finger onto sternoclavicular joints and middle finger onto trachea - use ring and index fingers as a guide to assess deviation. Wounds - assess for DCAP BTLS to chest & dress appropriately e.g. chest seal Emphysema (subcutaneous) - palpate thorax and neck and listen/feel for this. Laryngeal damage/crepitus - inspect larynx for obvious external damage. displace larynx from L to R and feel/listen for crepitus. Venous distention (jugular) - look at external jugular veins to see if engorged, can ask pt.to rotate head 45 degrees to properly assess, pt. should be sat semi-recumbent to accurately assess. Can be a sign of cardiac tamponade, PE, RVF. Exclude tension pneumothorax - use previous findings to weigh the probability of a tension pneumo and findings on the FLAP. Feel - place hands on lower thorax and watch for several breath cycles. Feel chest excursion - depth and symmetry and assess the general rate of respirations. Also palpate sternum and check for stepping-off, palpate ribs for #'s and flail segment. Look - together with the feel - evaluating excursion etc. Auscultate - 2nd & 4th IC spaces L & R, 6th IC space mid-axillary line. Know the anatomy of which lung field you're auscultating (e.g. inferior, superior lobe etc.) Percuss - same sites as auscultation - listening for hyper/hypo-resonance. Evaluate findings and perform interventions - 100% o2, NRB/BVM, Needle decompression, chest seal. |
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How does TXA work |
anti-fibrinolytic fibrinolysis- Tissue plasminogen activator -> converts -> plasminogen into -> plasmin (this breaks down fibrin mesh) TXA interferes with the conversion of plasminogen into plasmin, thus inhibiting fibrinolysis |
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Spinal landmarks |
External Occipital Protuberance Verterbrae prominens ( At C7 ) Clavicle Spinous Process of Scapula ( At T3) Inferior Angle of Scapula (T7) Iliac crest ( At L4 ) |
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Dimples of Venus |
The dimples of Venus (also known as back dimples) are sagittally symmetrical indentations sometimes visible on the human lower back, just superior to the gluteal cleft. They are directly superficial to the two sacroiliac joints, the sites where the sacrum attaches to the ilium of the pelvis.corresponds to lowest part of sacral vertebral columnlocation of posterior superior iliac spine |
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Burns - systemic responses - 6 |
1. increased capillary permeability 2. decresed immune response 3. myocardial depressant factor - decreased myocardial contractility 4. peripheral and splanchnic vasoconstriction - exacerbates hypoperfusion 5. histamine - bronchoconstriction 6. BMR increased 3X |
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Burns thermal injuries - types - 3 |
Scalds Flame Contact |
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Burns - Electrical injuries - types - |
Flash - current does not pass through body, radiation burns are experienced instead. True high tension injuries - There is extensive tissue damage and often limb loss. There is usually a large amount of soft and bony tissue necrosis. Muscle damage gives rise to rhabdomyolysis, and renal failure may occur with these injuries. This injury pattern needs more aggressive resuscitation and debridement than other burns. Contact with voltage greater than 70 000 V is invariably fatal. A particular concern after an electrical injury is the need for cardiac monitoring. There is good evidence that if the patient's electrocardiogram on admission is normal and there is no history of loss of consciousness, then cardiac monitoring is not required. If there are electrocardiographic abnormalities or a loss of consciousness, 24 hours of monitoring is advised. |
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Burns- history of non-accidental burns |
• Evasive or changing history• Delayed presentation• No explanation or an implausible mechanism given for the burn• Inconsistency between age of the burn and age given by the history• Inadequate supervision, such as child left in the care of inappropriate person (older sibling)• Lack of guilt about the incident• Lack of concern about treatment or prognosis |
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Burns - injury pattern of non-accidental burns |
• Obvious pattern from cigarettes, lighters, irons• Burns to soles, palms, genitalia, buttocks, perineum• Symmetrical burns of uniform depth• No splash marks in a scald injury. A child falling into a bath will splash; one that is placed into it may not• Restraint injuries on upper limbs• Is there sparing of flexion creases—that is, was child in fetal position (position of protection) when burnt? Does this correlate to a “tide line” of scald—that is, if child is put into a fetal position, do the burns line up?• “Doughnut sign,” an area of spared skin surrounded by scald. If a child is forcibly held down in a bath of hot water, the part in contact with the bottom of the bath will not burn, but the tissue around will• Other signs of physical abuse—bruises of varied age, poorly kempt, lack of compliance with health care (such as no immunisations) |
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Resp assessment |
Palpation is used both as a screening technique and as a means to confirm a specific diagnosis. Light palpation over the entire thorax posteriorly, laterally, and anteriorly will aid in the identification of cutaneous and subcutaneous nodules and the site of previously unsuspected tenderness. Nodules that are firm and freely moveable suggest a focal benign inflammatory or clinically insignificant problem. Those that are hard, fixed, and multiple suggest metastatic malignancy. Fleshy nodules may be indicative of a systemic disease such as neurofibromatosis. Vesicular sounds are thought to be produced by gas movement through the distalmost portions of lung units. They are low in pitch, predominantly inspiratory in timing, and have a breezy character. Bronchial or tracheal sounds are produced high in the upper airways and trachea. They are often loud and high pitched. The expiratory phase is longer than inspiration and follows a "silent gap." Bronchovesicular sounds are intermediate between the two. Under normal circumstances, air-filled lung units act as high-frequency filters so that the bronchial breath sounds generated in the upper airways are poorly transmitted through air-filled lung. On the other hand, when there is little air-filled lung between airways and the stethoscope, or when lung units are filled with liquid rather than gas, bronchial breath sounds are heard clearly. As a result, bronchial breath sounds are heard normally over the trachea, the upper sternum, and paraspinal areas of the upper thoracic vertebrae. As one moves peripherally and more air-filled lung is found between the airways and the stethoscope, breath sounds first become bronchovesicular in quality and eventually vesicular. Bronchial breath sounds may be either normal or abnormal. When they are heard on the periphery, where vesicular breath sounds are normally heard, one can imply that the airways to the lung units are open but that the lung units themselves are filled with liquid-like material. When this occurs without pleural fluid, the bronchial breath sounds are loud; when consolidation is associated with a pleural effusion, the bronchial breath sounds are present but often quite decreased in intensity. Confirmation of the presence of bronchial breath sounds can be obtained by listening for egophony ("E to A" sound). This sound is elicited by asking the patient to say the letter "E" as one listens over the suspicious area with the stethoscope. When consolidation is present, the spoken "E" sound is converted to an ausculted "A" sound, similar to that produced by a bleating goat.In addition to assessing the quality of breath sounds, it is also important to assess the duration of the expiratory phase. Timing the duration of expiratory sound while listening with the diaphragm over the trachea during a forced expiratory volume maneuver is used to identify airways obstruction. Expiratory sound should terminate within 6 seconds. If the sound is prolonged, airways obstruction manifested by an FEV1 of less than 1.5 liters can be assumed.Auscultatory wheezes imply the presence of slitlike openings through which a critical velocity of gas is passing. When wheezes are local, one must consider external compression of an airway. Enlarged lymph nodes and tumors do this. A lesion within the airway, such as an endobronchial malignancy or foreign body, also can produce a localized wheeze. Diffuse wheezing is present in inflammatory processes such as bronchitis (both acute or chronic), contraction of hypertrophied bronchial smooth muscle as seen in asthma, inspissated thick secretions of pneumonia, and airway collapse associated with the dynamic compression of pulmonary emphysema.Crackles imply the snapping open of airways or alveoli. Since larger airways open first as inhalation progresses from residual volume, early inspiratory crackles imply large airways disease while late inspiratory crackles either mean small airways problems (less than 2 mm) or poorly compliant alveoli walls such as seen in congestive heart failure, pulmonary fibrosis, or other interstitial pulmonary processes.Gurgles suggest fluid in the airways. This may be produced by excessive serous secretion in alveolar cell carcinoma, infected purulent secretion of acute or chronic bronchitis or bronchiectasis, or transudated fluid entering the airways from the alveoli as occurs in pulmonary edema |
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TBI mortality SBP on admission |
Case-mix adjusted odds of death were 1.5 times greater at <120 mmHg, doubled at<100 mmHg, tripled at <90 mmHg, and six times greater at SBP < 70 mmHg, p < 0.01. |
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Types of fractures - long bones |
1. Simple FractureAlso called closed fractures, they occur when your bone suffers breakage but does not pierce through the epidermis.
2. Compound FractureIt is opposite to simple fracture and is also known as an open fracture. There will be luxation of the bone and it will pierce through the epidermis. So it is more likely to develop an infection in this type of a fracture. 3. Oblique FractureIn this type of fracture, the fissure runs diagonal to the axis of your bone. They are basically slanted fractures caused by an intense force applied at an oblique angle. 4. Transverse FractureThis fracture is perpendicular to the axis of the bone. You get a transverse fracture when something applies serious force at a right angle to the bone. 5. Spiral FractureYou have a spiral fracture when the fracture line twists around the bone. You get this type of fracture because of severe twisting force applied to the bone. 6. Comminuted FractureAmong all different types of fractures, comminuted fracture is a serious one. The bone will be broken into several fragments. This is a highly complicated injury and usually heals quite slowly. 7. Liner FractureYou have this type of fracture when the break is parallel to the long axis of the bone. 8. Greenstick FractureMore common in children, it is partial fracture with one side of the bone unharmed. There will be torsion on the other side of the bone though. This type of fractureusually heals quickly. 9. Impacted FractureThis type of closed fracture occurs when there is too much pressure on two extremities of the bone. The bone splits into two fragments–the fragments will jam into each other. 10. Complete and Incomplete FracturesYou have a complete fracture if the bone is fragmented completely. It is an incomplete fracture when the two pieces of the bone partially avulse from each other–there will be some connection left between the both. 11. Compression FractureYou develop a compression fracture when at least two bones are forced against one another. You usually get it in the bones of the spine usually due to a collapse of the anterior portion of the vertebra or advanced osteoporosis. 12. Avulsion FractureThis closed fracture occurs when you break a bone due to a forceful contraction of a muscle. It is more common in athletes and people who start their workout without spending time in warm-ups. 13. Stress FractureIt is also called hairline fracture. You develop this type of fracture in joints that you use too often. It is an overuse injury and is more common in athletes, ballet dancers, runners, and basketball players. 14. Displaced FractureAmong the many different types of fractures, this type of fracture occurs when your bone breaks into two parts in a way that the bone loses its alignment. 15. Non-Displaced FractureIt is opposite to the displaced fracture. It means your bone snaps into two pieces but stays aligned. 16. Fatigue FractureYour bone becomes traumatized because of mundane stressors which cause weakness over a period of time. 17. Pathological FractureYou develop this fracture when you have an underlying health condition, such as osteoporosis. You can also get pathological fractures if cancer cells spread to the bones. |
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Crush/entrapment pathophysiology |
Caused bycrushing injury to large muscle masses – usually thigh or calf Crush syndromecan occur with: Prolonged entrapment (4-6 hours) – don’t discountelderly falls! Traumatic injury to muscle mass Compromised circulation to the injured area Damaged muscle - cells rupture - membrane and phospholipid bi-layer break - release of intracellular contents: myoglobin, phosphorous, creatine kinase andpotassium Once extricated, toxins flow into blood stream causing: -Acute tubular necrosis and Renal failure (myoglobin can block the cortical collecting ducts) -Hyperkalaemia -hypocalcaemia -Cardiac arrest Can develop compartment syndrome: -Early signs: --Pain (disproportionate to injury) --Paraesthesia - Classic/latesigns: --Pulselessness --Pallor --Paralysis |
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Head injury pathophysiology |
•Primary head injury (direct insult) – safety campaigns, vehicle technology etc. can prevent. •Secondary head injury – Ongoing injury processes set in motion by the primary injury •Intracranial mechanisms of secondary injury can be related to the increase in ICP, mass effect, ischaemic cascade, vasogenic edema due to breakdown of BBB. •6H’s: Hypoxia, Hyper/hypo-carbia,Hypo-perfusion, Hyperpyrexia, Hypotension and Hypoxaemia •Loss or reduced LOC may lead to poor airway or inadequate ventilation leading to poor oxygenation, carbon dioxide retention and acidosis |
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Cushings triad - what is it? |
A physiological nervous system response to increased intracranial pressure (ICP). Systolic HTN Bradycardia Irregular respirations First described in detail by American neurosurgeon Harvey Cushing in 1901. |
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Cushings triad - pathophysiology |
•1. sympathetic stimulation to increase cerebral flow (tachycardia andhypertension) •2. parasympathetic response attempting to rectify the hypertension, by stimulating the Vagus nerve (reduced heart rate) and mechanical distortion of Vagus nerve •3. mid-brain involvement causing respiratory malfunction |
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Airway - NPA -indication -procedure -limitations/complications |
Indication -Provide an airway adjunct in patients with an intact gag reflex - trismus with difficult airway Procedure -Size: Average height females - 6 NPA and average height males - 7 NPA, length from the tip of nose to tragus of ear. -Apply lubricant then insert tube with concave side facing away from the nasal septum -advance along the septum horizontally and rotated 90 degrees to lie in the nasopharynx -place a safety pin over the end just behind the flange to prevent it advancing too far -The tip should be seen behind the uvula COMPLICATIONS/limitations -Epistaxis and aspiration -ulceration -insertion through the cribriform plate into the brain -not a protected definitive airway |
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Airway - OPA -indication -procedure -limitations/complications |
... |
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Airway - iGel/LMA
-indication -procedure -limitations/complications |
... |
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Airway - ETT -indication -procedure -limitations/complications |
Indication -GCS 3 |
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Haemothorax -pathophysiology -signs -management -complications/limitations of management |
Blood leaking into pleural cavity between visceral and parietal pleural layers. Can be due to torn parenchyma, rib #'s S/Sx -chest pain -clinical signs of haemorragic shock -hyporesonance on pn -diminished/absent breath sounds management -chest drain -thoracotomy complications of mangement -empyema -retained haemothorax |
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Tension/open pneumothorax -pathophysiology -signs -management -complications/limitations of management |
Abnormal colection of air between the visceral and parietal plaural layers w/ one way valve due to damaged tissue causing mediastinal shift. Can be due to penetrating/blunt injury, rupture of a bleb/bullae, spontaneous, barotrauma. Can cause pressure upon the heart, reducing preload and overall CO. Signs - Severe, and rapidly deteriorating respiratorydistress (tachypnoea, significantly increased work of breathing, cyanosis) -Pleuritic chest pain - Hyper-expansion of the affected chest side withpoor movement -Absence of breath sounds on the affected side- Surgical emphysema in chest/neck - JVD - Hyper-resonant percussion note - Tracheal deviation away from the midline inpre-terminal situations - May show clinical signs of shock Management -needle thoracentesis -thoracotomy w/chest drain -o2 -chest seal (open) Complications -failure to evacuate PTX (kinking, air leak> escape, Clots) -68-75% success rate -COPD (hyperinflation) -haemothorax -subclavian tear -pericardial effusion/tamponade -cannula occlusion -pneumonia/empyema -mimicing conditions (diaphragmatic herniation) |
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Flail segment -pathophysiology -signs -management -complications/limitations of management |
When an area of rib breaks and becomes detached from the chest wall. Variance in literature on the # of ribs required to be fractured, some say 2 some say 3. signs -paradoxical breathing -dyspnoea -chest pain -crepitus and contusion over the affected area management -encourage deep respirations -multi-modal analgesia -tripod position -RSI w/ mechanical ventilation -PPV causes -falls -RTC complications/limitations of management -Paramedics cannot RSI -can encourage correct respiration but pt. may not be compliant. -opiods can reduce respiratory voume and rate, eventually causing secondary t2 respiratory failure. -Cannot currently provide PPV |
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Cardiac tamponade -pathophysiology -signs -management -complications/limitations of management |
When fluid in the pericardium builds up and causes compression upon the heart. The pericardial sack can expand to hold upto 2L of fluid, however a rapid onset can cause tamponade after as little as 150-200ml build up of fluid. Not just blood can cause tamponade, pericardial fluid and pus can also be culprits. Causes -chest trauma (both blunt and penetrating) -myocardial rupture -cancer -uremia -pericarditis -cardiac surgery S/Sx. -JVD -muffled heart sounds -pericardial rub -electrical alternans and low voltage (ECG) -dyspnoea -hypotension -weakness -lightheadedness -cough -pulsus paradoxus Management -pericardiocentesis -pericardial window -fluids -dobutamine (sympathomimetic, primarily used for CHF) Complications/limitations -need urgent hospital intervention, nothing can resolve the tamponade pre-hopsital, (?HEMS) |
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Shock - Pathophysiology |
a life-threatening medical condition of low blood perfusion to tissues resulting in cellular injury and inadequate tissue function. The typical signs of shock are low blood pressure, rapid heart rate, signs of poor end-organ perfusion (i.e.: low urine output, confusion, or loss of consciousness), and weak pulses. peripheral vasoconstriction causing hypoperfusion and hypoxia - lactic acid byproduct from anaerobic metabolism - hyperventilation begins to blow off CO2 and correct acid balance - baroreceptors detect the falling BP and release catecholamines RAS activated to increase ADH and preserve sodium - results in oliguria. Progression of shock- Initial Compensatory Progressive Refractory |
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Burns - superficial classification |
-epidermis -dry -red -painful -brisk capillary refill |
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Burns - partial thickness classification |
-1/2 dermis -red/pink -wet surface (+ or - blisters) -very painful -brisk capillary refill |
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Burns - Deep partial thickness classification |
-full dermis -dark pink/mottled red -sluggish/absent capillary refill -+ or - pain |
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Burns - Full thickness classification |
-subcutaneous -white/waxy -charred brown -leather like -thrombosed vessels -absent capillary refill -?painless |
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Burns - treatment approach/indications |
... |
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Spinal verterbrae - anatomy |
Posterior vertebral arch -spinous process -(upper) articular process -transverse process -lamina -facet -pedicle vertebral foramen vertebral body -cancellous -cortical rim |
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Spinal cord - anatomy |
C1-8 - T1-12 - L1-5 - S1-5 - C1 - 31 total spinal nerves 33 total spinal verterbrae |
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Forces/mechanisms involved in spinal injuries |
Compression Hyper-extension/hyper-flexion Axial impact Lateral flexion Rotation and flexion Rotation and extension Penetration Distraction Ones given in slides ... –Compression –Flexion/extension –Rotation –Combination |
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JRCALC immobilisation tool - 7 steps |
Adult w/ potential spinal injury - e.g. of potential MOI's (blunt trauma, axial loading, fall from height, RTC). -Decreased LOC or unable to fully cooperate? - yes- immobilize -pt. is under the influence of alcohol or illicit/prescribed drugs (including analgesia) - yes - immobilize -pt/ has complaint of spinal pain? - yes - immobilize -pt. has vertebral tenderness/deformity on palpation - yes - immobilize - pt. has neurological deficit - yes - immobilize - pt. has painful/distracting injuries (medical/traumatic) - yes - immobilize If no to all of above - do not immobilize. |
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Spinal immobilisation problems |
Increased ICP w/ collar Pressure sores Time to immobilise Discomfort Respiratory compromise Radiation from CT/xRAY Aspiration |
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Spinal examination - process |
examine: •dermatomes •myotomes •reflexes •In an alert, sober, neurologically intact patient younger than 65 (&Over 16) years with a low-risk mechanism, ask "Do you have any neck pain?" •(If the answer is "no," apply axial load and ask, "Do you have neck pain when I do this?") •If the answer is still no, assess for pain on palpation of the posterior midline neck from the nuchal ridge to the prominence of the first thoracic vertebra, or if the patient describes pain with direct palpation of any cervical spinous process. •If there is no midline tenderness, ask the patient to rotate the head 45o left and right, stopping immediately if there is any pain. •(If there is no pain, ask the patient to lift the head (i.e. flex the neck) - stopping immediately if there is any pain). •(If there is no pain, ask the patient to look up -stopping immediately if there is any pain). |
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Haemorragic shock - 4 stages |
Average blood volume approx. 5 litres. 1. blood loss <15 %(0.75 l). Normal BP, maintained by vasoconstriction. Pallor. 2. blood loss 15–30% (750–1500mL). BP - postural hypotension. Slight tachycardia. RR > 20. Skin pallor, cool, clammy. Mental status - slight anx, restlessness. U/O - 20-30ml/h. CBR increased. 3. blood loss 30–40% (1500–2000mL). Systolic BP < 100, tachycardia > 120, tachypnoeic > 30, confusion, increased diaphoresis, U/O - 20ml/h. CBR increased. 4.blood loss over 40% (over 2000mL). systolic < 70, extreme tachycardia > 140, extreme tachypnoea, lethargy, coma, extreme diaphoresis, possible mottling, CBR absent, anuria. |
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Hyper-pyrexia with TBI |
Correlation with temp and raised ICP. Hyperpyrexia has correlations with hypermetabolic state increased mortality, increased contusion volume, increased ICU stays, decreased GCS. Whether hyperpyrexia is caused by hypothalamic damage or there is a febrile response due to inflammatory mediators (PGE2) is unclear. if associated with fever then increased production ofglucocorticoids and anorexia also occur as part of the febrilestate and may negatively influence the metabolic expenditureand caloric intake Increased CA3 neuronal damage, increased bloodbrain barrier permeability and hemorrhage in the externalcapsule, increased numbers of swollen axons PGE2 - raises anterior hypothalamic regulatory temperature set-point. signifigant accumulation of neutrophils. increased cytokine activity, increased whiteblood cell accumulation, increased vascular permeability,and increased axonal damage Glutamate is released from injured cells in response toTBI and can result in excitotoxicity, calcium influx intoneurons via NMDA channels, and subsequent cell damageor death increased BBB permeability vasogenic edema ischemic cascade Management -anti-pyretics/NSAIDS can be of use, may be limited. -physical cooling may cause a drop in MAP, can cause shivering, which may exacerbate the hypermetabolic state. |
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Orthopaedic injuries |
Protect Rest Ice Compression Elevation |
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MSS - injuries |
1. History - MOI & PMH 2. Look - DCAP BTLS 3. Feel - bony tenderness 4. Move - Active & pssive 5. X-ray - transport |
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MSS - 5 P's |
Pain Pulses Pallor Paralysis Paraesthesia |
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Brachial Plexus injury |
Thebrachial plexus is the network of nerves that sends signals from the spine tothe shoulder, arm and hand. A brachial plexus injury occurs when these nervesare stretched, compressed, or in the most serious cases, ripped apart or tornaway from the spinal cord. |
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Axillary nerve |
•Motor functions–Paralysisof the deltoid and teresminor muscles. Patient unable to abduct the affected limb. •Sensory functions–Lossof sensation over the regimental badge area. |
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Musculocutaneous nerve |
•Motor functions: Flexion at the shoulder and elbow isweakened. •Sensory functions: Loss of sensation over the lateral sideof the forearm. |
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Radial nerve |
Sensory: Innervates most of the skin of theposterior side of forearm, and the dorsal surface of the lateral side of thepalm, and lateral three and a half digits. Motor: Innervates the triceps brachii,responsible for extension at the elbow. Innervates the majority of the extensormuscles in the forearm, responsible for extension of wrist and fingers andsupination of the forearm |
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Ulnar nerve |
•Motor functionsCertain muscles in the forearm and handaffected •Sensory functionAffects sensation in part of the hand |
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Median nerve |
•Motor functionAffects pronation of the forearm, flexion of the wrist andflexion of the fingers Sensory functionAffects sensation in parts of the hand |
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Shoulder dislocation |
Anterior Shoulder DislocationAn anterior dislocation accounts for 97%of recurrent or first time dislocations. It is the most common dislocation andis caused by the arm being positioned in an excessive amount of abduction andexternal rotation.Whenan anterior dislocation results from a traumatic event, the anteroinferiorly displaced humeral head stretches andtypically tears resulting in a loss of integrity of the anterior ligamentouscapsule, often resulting in a detachment of the anterior inferior labrum. Insevere cases, concurrent rotator cuff injuries may occur. Posterior Shoulder DislocationPosterior dislocation is less common asit accounts for 3% of shoulder dislocations. It is caused by an external blowto the front of the shoulder. There is an indirect force applied to the humerusthat combines flexion, adduction, and internal rotation. This is usually theresult of one falling on an out stretched hand (FOOSH injury), RTC, orseizures. Due to the traumatic mechanism of injury, posterior dislocations mayalso have concurrent labral or rotator cuff pathology. |
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# Management/assessment |
Look - DCAP BTLS Feel - Bony/muscular tenderness, sensation, pulses, anatomical landmarks Move - active & passive Immobilise - sling, splint etc. Elevate (if appropriate) Analgesia |
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Wound assessment/management |
•Assess –Typeof wound –Size(measurement) –Depth(underlying structures exposed?) –Underlyingstructures (nerves, vessels) –Haemostasis –Contamination •Manage –Firstaid (pressure, elevation, haemostats) –Don’tworry about decontamination –Generallyclean (saline or tap water), apply non-traumatic dressing |
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Stages of wound healing - HIPM |
Haemostasis - adrenaline release, vasocostriction, coagulation cascade Inflamation - kinin and complement cascade start and are responsible for errythma, odema etc. Profileration - granulation, contraction, epithelialisation - rebuilding and sealing the wounded site, scar tissue. Maturation - reorganisation of scar tissue and improvement in tensile strength. |
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Carpal bones - 8 TTCH TPSL |
Trapezium Trapezoid Capitate Hamate Triquetrum Pisiform Scaphoid Lunate |
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Tarsal bones - 7 CTN CCCC |
Calcaneous Talus Navicular Cuneform - medial, intermediate, lateral Cuboid |
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Traumatic cardiac arrest - statistics |
Hypovolaemia - poor outcome penetrating thoracic injury with pre-hospital thoracotomy - 11.8% of survivors hypoxia - 17% of survivors blunt trauma - 3.3% of survivors |
