Trauma and Pregnancy Summary Notes PDF

Trauma and pregnancy 1st trimester <12 weeks - Embryo/foetal rapid development Contained in pelvis 2nd trimester 12-27 weeks - Continued foetal development Uterus moves into abdominal cavity 3rd trimester 27 weeks to delivery - Foetus rapid weight gain Abdominal organs and diaphragms signifi...

Trauma and pregnancy 1st trimester <12 weeks - Embryo/foetal rapid development Contained in pelvis 2nd trimester 12-27 weeks - Continued foetal development Uterus moves into abdominal cavity 3rd trimester 27 weeks to delivery - Foetus rapid weight gain Abdominal organs and diaphragms significantly displaced Trauma considerations Cardiovascular - - Anatomical position of the heart increases as pregnancy progresses - 4th intercostal space by week 36 ECG changes - Lead III: T waves flattened/inverted, possible Q waves in III - Increase in ectopic beats Decreased PVR Increased HR 30% reduction in both systolic and diastolic BP Blood volume increases 40% Decrease in Hb concentration General increase in clotting factors - fibrinogen levels double by late pregnancy assists in combating haemorrhage LV ejection fraction increases from 70 ml to 80ml Systolic murmurs common - increased load Diastolic murmur - increased flow through tricuspid valve or mitral valve Clinical shock signs may not occur until 30-35% of volume loss Respiratory - As pregnancy progresses increased sensitivity to CO2 Inspiratory capacity increases by 300 ml Expiratory reserve volume decreases by 200ml TV increases 500 to 700ml O2 consumption increases by 15% Respiratory rate relatively unchanged By week 36 - lowers resistance in airway - greater inflow Confusion = hypoxia Genitourinary - Bladder capacity doubles Increased renal blood flow - increased excretion Ureters dilated and partially obstructed in 3rd Musculoskeletal - Relaxin release in 3rd trimester - increased risk of dislocations and subluxations Change in centre of gravity - increased risk of falling - - Endocrine Progesterone - Relaxes smooth muscle - Increased sensitivity to CO2 - Increased carbonic anhydrase in RBC - increased CO2 transfer Relaxin - Released late in pregnancy - Causes relaxation of ligaments Considerations - Past history: medical/obstetric - Current history: trauma/time/how was seat belt worn - Obs: hypotension = significant blood loss - Physical: abdo pain/cramping, uterine tenderness, premature labour, vaginal bleeding - Mother takes preference: look after mother = look after foetus Position: 15-30 degree tilt, lateral, head up Transport to obstetric unit Paediatric trauma Paediatrics compared to adults - More susceptible to multiple and more severe injuries given the same amount of force - Force more widely distributed throughout bodies: more significant internal organ damage, without significant external signs - Larger surface area to their weight - exposes them to significant heat loss - Capacity to maintain normal blood pressure despite loss of up to 25% to 30% of total blood volume - Changes in heart rate, respiratory rate and peripheral perfusion can indicate imminent cardiopulmonary collapse - Have a significantly higher metabolic demand when injured: oxygen extraction, consumption and glucose Primary survey Response Can the child speak? Are they crying if not yet verbal? Voice muffled? Foreign body or other obstruction? Floppy non-responsive child - very sick Airway Prominent occiput: place blanket under the shoulders Larger tongue falls against hypopharynx: OP airway, optimise head position and jaw thrust Larger adenoid tissues contribute to obstruction Floppy, U-shaped epiglottis: lift epiglottis with tip of laryngoscope blade Breathing Ventilate with small TV: only just make chest rise - decrease complications Lower fraction residual capacity: low intrapulmonary oxygen reserve - become hypoxic quicker Higher oxygen metabolism: avoid apnoea/low resp rate Respiratory fatigue quicker: lack chest wall musculature to aid in respiration Circulation BP late sign: compensate well, sudden drop as they increase HR and SV Causes of shock: external/internal blood loss, cardiac contusion/rupture, decreased return/SVR - spinal cord injury Secondary survey Head <2 years - More pliable skull - Sutures not completely fused - susceptible to skull fractures and haematomas - Accurate history not possible - Stranger anxiety 6 months to 2 years - physical assessment difficult - Intracranial injuries with no external signs - GCS of limited use - limited ability to comprehend and do what is asked <1 year - Palpate the anterior fontanelle - Evidence of anterior fontanelle fullness or bulging = suspicion of elevated ICP = haemorrhage Neck Children <8 more susceptible to cervical spine injury - Larger head size and weight compared to neck and trunk - Weaker C-spine musculature - Increased laxity of spinal ligaments - Immatured vertebral joints and ossification centres - Increased elasticity of the spinal column Chest - Children have more compliant chest wall - able to absorb and distribute forces therefore less rib fractures - Lack of external signs for underlying chest injury Mediastinum is more freely mobile: greater displacement with intrathoracic injury decreased venous return - decreased CO - hypotension Abdomina l Children have - Larger solid organs - Less-protective subcutaneous fat and abdominal muscles - More flexible rib cage - Smaller torso - Allows for wide transmission of significant force Solid organs such as liver and spleen most commonly injured in blunt trauma Handlebars to epigastric region/right upper quadrant results in duodenal/pancreatic injuries Limbs Greenstick fractures most common Paediatric drug calculations Drug Calculation NaCl 10/20ml/kg TXA 15mg/kg Morphine 200 microg/kg Fentanyl Methoxyflurane Ondansetron What is shock and types of shock Shock: A severe disturbance of haemodynamics in which the circulatory system fails to maintain adequate perfusion of vital organs. Perfusion: the ability of the cardiovascular system to provide tissues with an adequate blood supply to meet their functional demand and to effectively remove the associated metabolic waste products. Injury leading to shock Guide Blood volume Forearm - radius and the ulna Up to 400 mls Humerus Up to 800 mls Tibia Up to 1000 mls Femur Up to 2000 mls Pelvic Up to 5000 mls Abdominal blunt injury Up to 5000 mls Classification of shock Class I II III IV Blood volume (%) <15% 15-30% 30-40% >40% BV (mls) <750 750-1500 1500-2000 >2000 PSA Adequate Borderline Inadequate Assessment - Extremely poor/none Treatment By the time the patients blood pressure begins to drop the patient is already profoundly hypovolemic Respiratory rate, pulse pressure, cap refill, mental status and LOC are more sensitive indicators over blood pressure Hypovolemic shock secondary to uncontrolled haemorrhage is by far the most common shock scenario - Transport IV - don't waste time Permissive hypotension small fluid boluses - maintain BP around 90mmHg or a palpable radial pulse Extrication techniques Removing patient from car Capnography waveforms Capnography Capnometry The continuous analysis and recording of carbon dioxide concentrations in respiratory gases, i.e. waveforms and numbers. The analysis of the gases only, with no waveforms, giving number values only. Waveform capnography Adds continuous waveform display to the EtCO2 reading The waveform shape can provide clues about the airway and ventilation Semi-quantitative capnometry Also known as colorimetric Relies on pH change Paper changes colour: purple to brown to yellow Quantitative capnometry Absorption of infrared light Interpretation of EtCO2 - When CO is normal, the EtCO2 correlates with minute volume - A sudden spike in the waveform can indicate ROSC in cardiac arrest before a pulse is felt Use of EtCO2 with SpO2 Should be used together Pulse oximetry Capnography Oxygen saturation Reflects oxygenation SpO2 changes lag when patient condition changes Carbon dioxide Reflects ventilation Changes detected immediately Use of EtCO2 Non-intubated applications Intubated applications Bronchospasm Hypoventilation Shock and circulatory compromise Hyperventilation Verification of ETT placement ET surveillance during transport Contro, ventilations during HI management CPR: compression efficacy, early signs of ROSC, survival predictor Phase Characteristics I Beginning of exhalation Represents most of the anatomical dead space II Is where the alveolar gas begins to mix with the dead space gas and the CO2 begins to rapidly rise The anatomic dead space can be calculated using Phase I and II Significant increase in the alveolar dead space signifies V/Q mismatch III Corresponds to the elimination of CO2 from the alveoli usually has a slight increase in the slope as “slow” alveoli empty The “slow” alveoli have a lower V/Q ratio and therefore have higher CO2 concentrations In addition, diffusion of CO2 into the alveoli is greater during expiration. More pronounced in infants ETCO2is measured at the maximal point of Phase III IV Inspirational phase Abnormal waveforms - Increased phase III slope: obstructive lung disease - Phase III dip: spontaneous respirations - Horizontal phase III with large Et-art CO2 change: PE, decreased CO, hypovolemia - Sudden decrease in EtCO2 to 0: dislodged tube, ventilation malfunction, ET obstruction - Sudden decrease in EtCO2: partial obstruction, air leak - Exponential decrease in EtCO2: Severe hyperventilation, cardiopulmonary event - Gradual decrease in EtCO2: hyperventilation, decreasing temp, gradual decrease in volume - Sudden increase in EtCO2: sodium bicarb administration, release of limb tourniquet, ROSC - Gradual increase in EtCO2: fever, hypoventilation - Increased baseline: rebreathing, exhausted CO2 absorber Waveforms Hypoxia, hypercapnia and hypocapnia ICP recognition and management TBI Ventilation strategies Head injury Brain injury Injury to the soft tissue, intracranial structures or skeletal structure of the head Head injury resulting in damage to the brain parenchyma, either as a result of the primary injury or secondary causes. Cerebral perfusion: a function of cerebral blood flow rather than cerebral blood pressure - pressure moving blood through the cranium Factors of cerebral blood flow 1. Blood pressure 2. Vascular resistance. If blood stops 1. Unconscious within 10 seconds 2. Dead within 4-6 minutes Normal systemic blood pressure is key to normal CPP - MAP must be at least 50mmHg - CPP = MAP - ICP - ICP normally <20mmHg Autoregulation Changes in ICP result in compensation: increased ICP = increased BP and vice versa Cerebral gas physiology High CO2 (from hypoventilation and hypertension) Low CO2 Cerebral vasodilation Encourages blood flow Contributes to increased ICP Cerebral vasconsitircion Results in cerebral anoxia Ventilation strategy: - 16-18 bpm - Avoid overinflation (6-7 ml/kg) - Avoid breath holding (1:4 I:E) - SpO2 >95% Skull fracture Types Linear Depressed Comminuted Basilar Impaled object Basal skull fracture signs Battles signs Raccoon eyes Behind the ear Associated with fracture of auditory canal and lower areas of skull Orbital fractures Primary brain injury Focal Diffuse Occur at a specific location in brain Contusions/laceration Concussion Moderate/severe diffuse axonal injury Diffuse axonal injury - Disruption of axonal fibres in white matter and brainstem - Usually as a result of widespread shearing forces - MVA common - Injury is immediate and essentially irreversible - Immediate rise in ICP, patients generally present unconscious Early signs of increased ICP - Drowsiness, confusion, dystaxia - Altered mental status, orientation, personality - Amnesia (retrograde, anterograde) - Blurred vision - Headache, neck pain/stiffness - Vomiting - Paresthesia/paraplegia Types of amnesia Retrograde Anterograde Loss of information that was acquired before the onset of amnesia Impaired capacity for new learning Secondary brain injury Hypoxia and hypotension double mortality Hypotension Decreased CPP will lead to increased cerebral ischemia, therefore increased ICP Must sustain MAP of 90mmHg with equates to SBP of 110-140mmHg Hypoxia Decreased PO2 will lead to increased cerebral blood flow (vasodilation) and localised hypoxia, increased swelling - increasing ICP Hypovolemia Cerebral ischemia, vasodilation and increased ICP Hypercapnia Vasodilation = increased ICP Hypocapnia Cerebral and carotid vasoconstriction, increasing ischemia and ICP Hyperthermia Initiates inflammation in cerebrum, increases metabolic demand, increased oxygen and glucose requirement, increased blood flow and increased ICP Hypoglycemia Neuronal dysfunction, increased blood flow and oxygen requirement, increasing ICP and accelerating cellular necrosis Seizures Neuronal dysfunction, increased blood flow and oxygen requirement, increasing ICP and accelerating cellular necrosis Haematomas Epidural haematoma Subdural haematoma Usually involves arterial bleeding Usually no underlying injury May quickly evolve into herniation All venous bleeds Indistinct on CT May not present with CF for hours or days Intracerebral haemorrhage: ruptured blood vessel within the brain. - Presentation similar to stroke - Clinical features worsen over time GCS and severity of head injury Minor 13-15 Moderate 9-12 Severe <9 Cushing's triad: indicative of upper brainstem compression - Hypertension - Reflex bradycardia - Adventitious respirations - Pupils become small and reactive - Decorticate posturing (flexion) - Decerbrate posturing: results from injury to midbrain and pons - usually indicative of graver injury GCS and what certain signs mean Assessing the conscious state GCS is a measure of conscious state, not focal deficit Patients best score is recorded on each occasion Sternal rub: extremely non-specific and causes trauma 1. Trap squeeze 2. Fingernail bed pressure - spinal arc reflex If eyes swollen and unable to open - C Verbal - Confused: can answer question e.g. wrong location - Inappropriate words: words that do not make a sentence - Incomprehensible sounds: groans or other noises Motor - Check bilateral response and not weakness e.g. L > R - If the upper limb is brought above the level of the clavicle in response to suborbital pressure = localises to pain - When the upper limb is flexed to suborbital pressure = withdrawal Tension pneumothorax identification and management Tension pneumothorax A buildup of air in the pleural space that cannot escape due to a one-way valve at the point of damage to the pleura Conscious person A normal breathing patient tensions over minutes to hours Widespread findings General findings Non-consistent findings Uncommon/rare findings Chest pain Tachycardia Low oxygen saturation Cyanosis Respiratory distress Decreased air entry on affected side Hypotension Decreasing LOC Tracheal deviation Unconscious ventilated person A ventilated patient tension within minutes Widespread findings General findings Non-consistent findings Uncommon/rare findings Rapid onset Immediate and progressive decrease in SpO2 Reduction in BP High ventilation pressures Affected side - Hyper-expansion - Hypomobility - Decreased air entry Surgical emphysema Venous distention In the setting of traumatic chest injury/asthma Indications for immediate chest decompression In the presence of traumatic chest injury - SpO2 <90% on O2 - Systolic BP <90mmHg - RR <10 - Decreased GCS on O2 - Cardiac arrest Select insertion site 1. Palpate clavicle to supra sternal notch 2. Down the sternum and locate the angle of Louis - this aligns with the 2nd rib to the midclavicular line 3. Palpate 2nd intercostal space Check insertion site - Eyeball check: normally halfway between the nipple and clavicle in men - Partner to double check Procedure SMART 1. Seconded intercostal space 2. Midclavicular line 3. Above the rib below 4. Right angle (90 degrees) 5. Towards the vertebrae Air or air and blood bubbles escape Leave cannula in situ and secure No air but copious blood Remove the cannula Cover insertion site with adhesive dressing Circle the insertion site No air Catheter not long enough? Not tension? Other pathology? Cannula size and chest wall thickness 14g: 4.5cm long 16g: 3 cm long Chest wall thickness about 4.8cm (3.1-9.4) Arms down by side, if arms up, chest wall thickness increases by up to 20% Spinal injuries Mechanisms 1. Hyperextension: head to back, central cord syndrome 2. Hyperflexion: head to front, central cord syndrome 3. Vertical compression: hitting bottom of pool 4. Flexion/rotation: MVAs: back seat passengers, lap seat belts, side impacts 5. Penetrating trauma: stabbings, gunshots, Brown-sequard syndrome Classification of SCI Quadriplegia/tetraplegia T1 and above Paraplegia T2 and below Complete No motor or sensory Incomplete Some preservation of motor or sensory Incomplete SCIs 1. Central Cord Syndrome: - Cervical cord damage - Lower limb function only (no upper function) - Altered trunk sensation - Varying loss of bladder and bowel function 2. Brown Sequard Syndrome - Hemiplegic type loss - Motor on one side with no sensory and vice versa 3. Anterior Artery Syndrome - Posterior column sparing - Damage due to infarction from the main anterior artery - Preservation of position, vibration and touch 4. Sacral Sparing 5. Cauda equina Spinal cord injury results in 1. Loss of movement 2. Loss of sensation 3. Decreased circulation 4. Altered respiratory function 5. Inability to control body temperature 6. Altered bladder and bowel control 7. Altered sexual function Types of injury 1. Transient concussion - Due to extreme acceleration/deceleration force - Temporary neurological dysfunction lasting less than 48 hours - No structural changes 2. Contusion - A bruising that includes bleeding, subsequent oedema, and necrosis from the oedematous compression - Fracture may not be present - Neurological involvement depends on the severity of contusion and tissue injuryLaceration 3. Compression of cord substance 4. Complete transection of the cord 5. Complete transection Pathophysiology 1. Initial injury causes haemorrhage into the cord and oedema formation - Oedema compromises blood flow - ischemia - Secondary tissue degeneration phase within hours of injury - release of membrane-destabilising enzymes and mediators of inflammation - These secondary events result in destruction of myelin and axons (the process is similar to secondary injury in TBI) Mechanisms Primary Secondary Initial crush, shear impingement of cord as a result of a trauma Vascular insults/insufficiency: Disautoregulation, hypotension, neurogenic shock Electrolytes: calcium release Oedema Cell toxicity: glutamate release, arachidonic acid metabolites, free radical generation Apoptosis: programmed cell death Spinal Cord Injury Without Radiological Abnormality (SCIWORA) - Tends to affect the elderly - Much more prevalent in cervical spine than thoracolumbar area as its related to degenerative changes in the c-spine Neurogenic vs spinal shock Spinal Neurogenic Loss of reflexes and sensorimotor function below the level of a spinal cord injury. Temporary - hours to days Hemodynamic instability that occurs in high spinal cord injury (T1-T4). 1. Hypotension: sympathetic denervation that causes loss of arteriolar tone and results in venous pooling 2. Bradycardia: occurs with interruption of cardiac sympathetic, allowing unopposed vagal stimulation 3. Hypothermia Spinal management Airway: jaw thrust only, be mindful of passive regurgitation, 15 degrees head up position Breathing: lesion above T12 may cause breathing compromise, increased likelihood of bronchospasm. Diaphragm innervated from C3-C5 Circulation: cardiac output affected by neurogenic shock. Hypotension with no tachycardia Neurological assessment 0 Total paralysis 1 Muscle contraction/movement on palpation ro visible 2 Active movement without gravity 3 Active movement with gravity 4 Active movement against some resistance 5 Active movement against full resistance Sensory testing Sensation compared to forehead due to being supplied by cranial nerves 0 Absent 1 Impaired 2 Normal NEXUS criteria 1. No posterior midline C spine tenderness 2. No evidence of intoxication 3. A normal level of alertness 4. No focal neurological deficit 5. No painful distracting injuries Cardiac contusions and Becks triad Blunt cardiac injury Usually from impact with steering wheel A tachycardia out of proportion to other injuries may be the only clue 3 injury patterns - Myocardial contusion - Electrical conduction system - Myocardial rupture Right ventricle usually injured due to its location behind the sternum 3 patterns - Myocardial contusion - Electrical conduction system - Myocardial rupture Cardiac (pericardial) tamponade Physiology - Collection of blood between heart and pericardium - Source of blood can be coronary arteries or myocardium - Pericardium may hold up to 200 ml of blood, CFs may develop after 20-30ml - 2% of penetrating injury, rare in blunt trauma - 10-20 ml of blood in pericardium can cause tamponade - ECG is usually non-specific unless there is an associated coronary artery injury Chest pain similar to MI Palpitations Dysrhythmias ECG changes: T wave and ST segment Tachycardia Paradoxical pulse Narrowing pulse pressures Muffled heart sounds Shock Beck's triad 1. Muffled heart sounds 2. Distended neck veins 3. Hypotension Basics Rule out PIC prior MVA Watch for ECG changes Basics Be aware of - Sudden hypotension - Bradycardia into PEA Fracture management and identification Causes Direct trauma Indirect trauma Pathologic conditions Blunt or penetrating force applied to an extremity For example, a vertical fall that produces a spinal fracture distant from the site of impact Malignancy Osteoporosis Fracture: a disruption in the continuity of a bone Fracture clinical features (PILSDUCT) 1. Pain 2. Irregularity 3. Loss of function/power 4. Swelling 5. Deformity 6. Unnatural movement/position 7. Crepitus (grating) 8. Tenderness Fracture issues - Fractures of the pelvis or femur have potential for significant blood loss. A single long bone fracture can result in the loss of 10-30% of total blood volume - Pelvic fractures may require greater than 6 units of blood in the first 72 hours Fracture/dislocation danger signs - Pallor - pale skin or poor cap refill - Paresthesia - pins and needles sensation - Pulses - diminished or absent - Paralysis - inability to move Fracture types Colles fracture Comminuted fracture Compound (open) fracture Greenstick Impacted fracture Oblique fracture Spiral fracture Transverse fracture Pathological fracture Prosthetic fracture Fractures Fractured humerus Issues - Force: chest wall injury/thorax cavity injury No IV in arm Fractured forearm No IV Colles fracture Can involve shoulder and clavicle Hand injuries Look for wrist and lower forearm fractures Femur fracture Traction - Decrease muscle spasm - Decreases pain - Decreases pressure on bone ends - pain - Realignment of bones Issues - Blood loss - Force - other injuries? however Fractured NOF Issues - Foot on affected side: roasted and laterally shortened. May not be rotated if impacted fractures or marginally shorter - If fracture at end of prosthesis no rotation or shortening - Minimal pain when still - Splinting: tie both legs together, ankles figure 8 bandage around the knees Fractured lower leg No IO Foot and ankle fracture Pillow splint SAM splint Full eg vac splint Improvise Issues: circulation/sensation Dislocation Occurs when the normal articulating ends of two or more bones are displaced Subluxation Is a partial dislocation of the articulating surfaces of a joint. The surfaces are in contact but the alignment may be abnormal. Amputation Accidental severing of a body part Following management of other priorities - Do not wash parts - Retrieve parts and place in a plastic bag and seal - Place sealed bag in cold water - Seek advice regarding transport destination Partial amputation Partial loss of a body part with some soft tissue connection remaining Avulsion Forcible tearing away of a body part - Skin - Bone Place tissue back in normal location if possible - for degloving may be difficult General principles of splinting - The goal of splinting is to immobilise the injured body part - Immobilisation by splinting - Helps alleviate pain - Minimises further tissue injury, bleeding and contamination in an open wound - Simplifies and facilitates transport of the patient - Immobilise dislocations or fractures involving joints in position of comfort - Ensure good perfusion below the level of injury - Joint injuries are only realigned if there is no distal pulse - Elevate the extremity if possible - The joint above and below the injury is immobilised Basic fracture management - Open fracture: clean with NaCl prior to stabilisation - Open wound: irrigate if dirty/cover with moist dressing - Spliting appropriate for injury: neuro and circulatory check pre and post, joint above and below fracture Burns management and identification Burn types 1. Thermal: scalds, flames, hot object, cold, air 2. Chemical: acid/alkaline 3. Electrical: contact/flash 4. Radiation Burn zones 1. Coagulation (necrosis) - Occurs at point of maximum damage - Irreversible tissue loss due to coagulation of constituent proteins 2. Stasis (injury) - Decreased tissue perfusion - Tissue potentially salvageable - Aim of resus is to increase perfusion and prevent irreversible damage 3. Hyperaemia - Outermost zone - Tissue perfusion increased - Tissue will invariably recover unless infection or extended hypoperfusion Burns systemic response - Cytokines and other inflammatory mediators released from burn site - - - Capillary permeability increased - Loss of intravascular proteins and fluids into interstitial compartment - Peripheral and splanchnic vasoconstriction - Decrease in myocardial contractility - Fluid loss from burn Over result: systemic hypotension and organ hypoperfusion Respiratory - Bronchoconsctiron - ARDS Metabolic: basal metabolic rate 3 times that of normal Immune: down regulation of response - cell mediated and humoural pathways Burns assessment Depth Depth Pathology Appearance Sensation Superficial 1st degree Basal layer of epidermis Brisk cap refill. Dry and red Painful Partial thickness 2nd degree Damage into dermis - hair follicles and oil glands remain Moist, reddened with blisters, brisk cap refill Painful Full thickness 3rd degree Entire thickness of skin into fat White slough, reddened and mottles, sluggish or absent cap refill Painful 4th degree Burn into muscle, tendon, bone Dry, charred, whitish, absent cap refill Painless Adults: Wallace rule of 9’s - palm, including fingers is about 1% burn Paediatrics: Lund and Browder chart Specific issues Electrical burns Extent of injury may not be apparent Look for entry and exit points Damage occurs deep within tissues Damage frequently progresses Electricity contracts muscles - be mindful of associated injuries Cardiac arrhythmias may occur Should be monitored especially if pulse is irregular Myoglobinuria may be present - colour best indicator of severity Chemical burns Brush off powder Prolonged irrigation required Do not use antidote: delays treatment and may result in head production May require decontamination Chemical burn - Weak solutions (10%) may cause pain for hours hydrofluoric acid Penetrates tissues very quickly Interferes with body calcium metabolism Small amount can be fatal weeks later Smoke inhalation Confined dire CO poisoning Cyanide poisoning Rhabdomyolysis The breakdown of muscle fibres that leads to the release of muscle fibre contents (myoglobin) into the bloodstream Aetiology Clinical features Muscle is damaged, myoglobin (a protein) is released into the bloodstream Is then filtered out of the body by the kidneys Myoglobin breaks down into substances that can damage kidney cells May cause any condition that damages skeletal muscle especially injury Abnormal urine colour Decreased urine production General weakness Muscle stiffness or aching (myalgia) Muscle tenderness Weakness of the affected muscles Fatigue Joint pain Seizures Burns management - Cooling: tap water >20 minutes - maximum 60 minutes - Protect against hypothermia (cool the burn, warm the patient) - Remove burnt clothing - leave if stuck to skin - Remove conserve objects - rings, bracelets - If eyes affected remove contact lenses - O2 8L via face mask or 100% if confined fire/CO/cyanide poisoning - Assist ventilation if needed - Pain relief - Hydrogel dressing <10% BSa paeds and <20% BSA adults - Cling Wrap dressing only if skin back to normal temp - not circumferential burns - Frequent reassessment every 15 minutes at least - Transport to appropriate facility and position depending on pt burn and location Abdominal injuries, identification and management 6.0 Abdominal and Pelvic Trauma Mechanisms of injury Blunt Penetrating mechanisms Forces - Compression forces - Shearing force - Deceleration forces Courses - MVAs: seat belt injury, steering wheel injury - Falls - Assaults - Blast Low energy - Stabbing - Impaled objects High energy - GSW: transient shock waves, cavitation Risk factors for intra abdominal injuries - High speed vehicle collisions - Pedestrian struck by vehicle Hypotension (BP <100mmHg at any time) Presence of significant chest or pelvic injuries Significant injuries on physically opposing sides of the abdomen Causes of abdominal pain Haemorrhage Spleen, liver, kidney, retroperitoneal, mesentery Inflammation, infection Appendicitis, cholecystitis, pancreatitis, UC Perforation of abdominal organs Peptic ulcer, ectopic pregnancy, AAA Obstruction of hollow viscera Bowel obstruction, paralytic ileus, adhesions, malignancy, cholelithiasis Visceral vs parietal pain Visceral pain Parietal pain Referred pain Caused by stretching of fibres in walls/capsules of hollow/solid organs Pain ranges from steady ache or vague discomfort to excruciating or colicky pain Can present along midline May be referred (appendicitis) May have sweating, nausea, vomiting, tachycardia Irritation of nerves i the parietal peritoneum, usually anterior abdominal wall Aggravated by respiration, thoracic and abdominal movements Sharp, localised, constant pain Guarding, legs raised, decreased movements As localised as periodontitis develops, rigidity and tenderness occurs Pain presenting in an area away from the noxious stimuli Intense stimulation of the nerve irritates surrounding nerves at the common nerve root Kehr’s sign: occurrence of spain at the shoulder tip due to presence of blood or other irritants in the peritoneum irritating the diaphragm when a patient is supine Abdominal assessment Hx, general appearance, position (knee flexion, movement), VSS, OPQRST Bowel sound or absence of add little clinical information Abdominal inspection - Abrasions - Bruising Abdominal palpation - Pain - Tenderness - Rigidity - Guarding - Distension Vomiting - Type (normal/projectile) - Haematemesis (coffee grounds, frank, food matter, bile, smell (faecal smelling) - Frequency, amount Output - Urine (concentration, smell, blood) - Faeces (consistency, blood) Clinical features of abdominal injuries - Distended or irregularly shaped abdomen - Bruising of the abdomen flank or back - Tenderness (pain on palpation) - Pain, ranging from mild discomfort to intense and intolerable pain - Pain other than at the injury site Pain radiating to either shoulder Guarding: voluntary contraction of the abdominal muscles Foetal position or lying with legs drawn up toward the chest and abdomen Weak peripheral pulses Abdominal cramping Stiff ro hard abdomen on palpation Nausea/vomiting Open wounds and penetrations Organs protruding through open wounds Blood in the urine Signs of shock Any patient with significant blunt or penetrating injury anywhere in the torso must be assumed to have abdominal trauma until proven otherwise Solid organs - May be due to blunt or penetrating mechanism - Death usually secondary to haemorrhage Spleen Frequently injured solid organ Usually due to blunt trauma Often secondary to trauma to ribs 9-11 on left side Bleeds easily: capsule around spleen tends to promote slow development of shock but when ruptures deteriorate fast May present with left shoulder pain Liver Largest organ in abdomen Frequently injured organ May be due to blunt or penetrating trauma Often secondary to ribs 8-12 on right side Bleeding is slow and contained under the capsule Pancreas Positioned transversely across lumbar spine Injury due to compression against vertebral column by steering wheel, handlebars etc Very little haemorrhage Irritation to peritoneum Kidney Direct blow to back, flank, upper abdomen Suspect in 10th-12th rib Acceleration/deceleration forces - shearing of renal artery/vein Rare in penetrating trauma Hypovolemia Costovertebral angle: the angle that outlines a space over the kidneys formed by the lateral and downward curve of the lowest rib and vertical column Hollow organ injuries - May result from penetrating or blunt trauma - Spilt contents create most problems Small bowel and colonic injuries Peritoneal contamination caused by spillage of contrast into peritoneal cavity Bacterial content causing peritonitis - inflammation may take 6-8 hours to develop Urinary bladder Either a blunt or penetrating injury can rupture the bladder Urine will spill into the surrounding tissues Suspect if you see blood at the urethral opening or physical signs of trauma on the lower abdomen, pelvis or perineum Abdominal vascular injuries - High mortality due to rapid blood loss: survival dependent upon the extent of injury and time to surgery - Abdominal aorta, inferior vena cava, mesenteric vessels: shearing, dissection Abdominal evisceration - Do not replace organs into abdomen - Cover exposed bowel with saline moistened multi trauma dressing - Cover first dressing with second dry dressing/plastic dressing Injuries to genitals Male Female Ensure pain relief Use sterile, moist compresses to cover areas of exposed tissue Apply direct pressure to control bleeding Never manipulate impaled objects Identify and bring avulsed parts to the hospital If part of the penis or scrotum is caught in a zipper, cut off the zipper fats need and separate the teeth Well protected and normally not inured Ensure pain relief Use sterile, moist compresses to cover areas of exposed tissue Apply direct pressure to control bleeding Never manipulate impaled objects Rectal bleeding - Common complaint - Blood may appear in undergarments or may be passed during a bowel movement - Can be caused by anal sex, sexual assault, hemorrhoids, colitis or ulcers of the digestive tract - Acute bleeding should never be passed off as something minor - Pack the crease between the buttocks with a dressing Abdominal compartment syndrome Direct external pressure on vascular structures, the diaphragm and abdominal wall Causes Intra-abdominal Ruptured AAA Bleed/trauma Retroperitoneal Pelvic bleeds Ruptured AAA Abdominal wall Burn eschar Types Primary Secondary A process within or involving the abdomen itself leading to intra-abdominal hypertension - Penetrating trauma - Haemorrhage Intra-abdominal hypertension - Without direct abdominal injury Strongly related to fluid resus - Infusion >3L Treatment Penetrating object - do not remove - support pad around Evisceration: cover with moistened dressing then dry dressing/plastic dressing Fluid resuscitation Reassessment at least every 15 minutes Pelvic injuries Complications - Bleeding (10-15% will have arterial bleeds) - Up to 4L of blood can be lost before vascular pressure is overcome and tamponade occurs - Urinary and gynaecological injuries - Rectal injuries - Verve root injuries - Chronic pain - Sexual dysfunction - Disability (only 60-70% of patients will return to previous occupation) Pelvis assessment - Think pelvis if multi-trauma - A patient can die form isolated pelvic fracture - Look at the mechanisms of the patients injuries - Pain as an indicator - Expose the area - Look at the skin and for symmetry of pelvis - Gentle pressure when examining - do not spring Pelvic splint - Can be placed on the stretched prior to patient or fitted later - Must never be removed once applied - We can immobilise it and stabilise it Traumatic cardiac arrest Envenomation Hypothermia and hyperthermia identification and management