Polytrauma and Critical Care
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1 Polytrauma and Critical Care Dr Mike Brunner M.B.B.S., F.R.C.A. Consultant in Anaesthesia and Intensive Care Medicine Northwick Park and St Mark s s Hospital Harrow England
2 My Hospital
3 My Football Team
4 My Favourite Place
5 Trauma - Introduction
6 Introduction Trauma is the leading cause of death in the first 4 decades of life in most European countries. Third cause of death in all age groups (in 2020 may be second cause of death) 3.8 million deaths / year worldwide 312 million injured / year worldwide 3 patients permanently disabled / death
7 Lost life years Trauma Cancer Cardio vascular Claire Merrick et. al. Prehospital Trauma Life Support, Mosby, 2003
8 Introduction 1 in 3 deaths occurred in hospital as a result of an injury which could have been prevented (Royal College of Surgeons of England, 1988)
9 Motor vehicle accidents prevention PREEVENT EVENT POSTEVENT Host Vehicle Environment
10 Motor vehicle accidents prevention PREEVENT EVENT POSTEVENT Host Avoid alcohol consumption Vehicle Environment
11 Motor vehicle accidents prevention PREEVENT EVENT POSTEVENT Host Avoid alcohol consumption Use of safety belts Vehicle Environment
12 Motor vehicle accidents prevention PREEVENT EVENT POSTEVENT Host Avoid alcohol consumption Use of safety belts First aid by bystanders Vehicle Environment
13 Motor vehicle accidents prevention PREEVENT EVENT POSTEVENT Host Avoid alcohol consumption Use of safety belts First aid by bystanders Vehicle Antilock brakes Environment
14 Motor vehicle accidents prevention PREEVENT EVENT POSTEVENT Host Avoid alcohol consumption Use of safety belts First aid by bystanders Vehicle Antilock brakes Air bags deploys Environment
15 Motor vehicle accidents prevention PREEVENT EVENT POSTEVENT Host Avoid alcohol consumption Use of safety belts First aid by bystanders Vehicle Antilock brakes Air bags deploys Environment Speed limits
16 Motor vehicle accidents prevention PREEVENT EVENT POSTEVENT Host Avoid alcohol consumption Use of safety belts First aid by bystanders Vehicle Antilock brakes Air bags deploys Environment Speed limits Impact-absorbing absorbing barriers
17 Motor vehicle accidents prevention PREEVENT EVENT POSTEVENT Host Avoid alcohol consumption Use of safety belts First aid by bystanders Vehicle Antilock brakes Air bags deploys Environment Speed limits Impact-absorbing absorbing barriers Emergency medical service (access to trauma system)
18 Prevention Page last updated at 10:43 GMT, Thursday, 25 September :43 3 UK Road deaths fall to record lows Road deaths have fallen to their lowest level since records began in 1928, according to figures published by the Department for Transport. Last year a total of 2,946 people died - a 7% reduction on the previous year when 3,172 died.
19 Introduction 1 in 3 deaths occurred in hospital as a result of an injury which could have been prevented Deaths occur due to failure of simple management in the early stages ( GOLDEN( HOUR ), rather than a failure of complex definitive treatment (Royal College of surgeons of England, 1988)
20 Trimodal Death Distribution Number of Deaths Immediate Deaths Early Deaths Hours Time After Injury Late Deaths Weeks
21 Trimodal Death Distribution Number of Deaths Early Deaths Hours Time After Injury Weeks
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23 Plane crash in Nebraska,, killed, 4 injured
24 When I can provide better care in the field with limited resources than what my children and I received at the primary care facility there is something wrong with the system and the system has to be changed. ~ James Styner, MD, FACS ~ 1977
25 ATLS
26 These guidelines seek to set achievable standards for trauma treatment services which could realistically be made available to almost every injured person in the world. World Health Organization 2004
27 ATLS Concept ABCDE-approach to evaluation / treatment
28 ATLS Concept A B C D E Airway Breathing Circulation Disability Expose
29 ATLS Concept ABCDE-approach to evaluation / treatment Treat greatest threat to life first Definitive diagnosis not immediately important Time is of the essence Do no further harm
30 ATLS - Initial Assessment / Management Primary Survey Definitive Care Resuscitation Re-evaluation evaluation Detailed Secondary Survey Re-evaluation evaluation
31 Assessing the patient in 10 seconds Identify yourself Ask the patient his / her name Ask the patient what happened
32 Appropriate response confirms A B Patent airway Breathing C D Clear thinking
33 Beware Continue to observe and have a high index of suspicion Especially if patient has - Maxillofacial injury - Soft-tissue injury of neck - Facial or neck burns - Hoarse voice (Laryngeal injury / tracheal burn)
34 If no response, proceed with rapid primary survey
35 Primary Survey A B C D E Airway: C-spine protection Breathing: Oxygenation Circulation: Stop the Bleeding! Disability: Neuro Status Expose: Environment & Body Temp
36 A Airway Simple management manoeuvres Suction Chin lift Jaw thrust Use simple equipment to help
37 A Airway
38 A Airway LMA i-gel LMA
39 A Airway
40 A Airway Simple management manoeuvres Suction Chin lift Jaw thrust Definitive airway: Cuffed tube in trachea
41 A Airway (important message)
42 A Airway The reported incidence of cervical spine injury in the setting of major trauma is 1.5% 4%. Emerg Med J 2004;21: Anesth Analg 1991;73: Can J Anaesth 1990;37: Arch Surg 1994;129: Ann Emerg Med 1998;32:461 9.
43 Protecting the spine Immobilize entire patient on long spine board
44 Protecting the spine Apply semirigid cervical collar/head block
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47 Manual in-line stabilisation (MILS)
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53 Intubating Laryngeal Mask Airway (IMLA)
54 Combitube
55 Combitube 98% 2%
56 Combitube Inflation of the large pharyngeal cuff of the Combitube exerts pressure against the vertebral bodies of C2, C3 and/or C4, depending on placement.
57 Gold Standard airway management for patient with potential C-spine C injury requiring immediate and/or urgent airway control rapid sequence induction of anaesthesia orotracheal intubation with cricoid pressure manual in-line immobilization of the head and neck Precise cervical spine in-line immobilization should be maintained throughout the intubation manoeuvres. Criswell JC, Parr MJA, Nolan JP. Emergency airway management in patients with cervical spine injuries. Anaesthesia 1994; 49: 900-3
58 B Breathing Confirm ETT in the right place Look at chest movements Paradoxical Asymmetric Listen in the axillae
59 B Breathing Right main bronchus intubation
60 B Breathing Confirm ETT in the right place Look at chest movements Paradoxical Asymmetric Listen in the axillae End tidal CO 2 Assess oxygenation Pulse oximeter
61 End Tidal CO 2 Monitors/Pulse Oximeters The StatCO2 The Capnocheck II Hand-Held Held O2/SpO2 Monitor
62 B Breathing Think about Pneumothorax (tension) Haemothorax ETT in the wrong place (if in doubt.take it out!!)
63 B Breathing GIVE 100% O 2
64 B Breathing 100 % SaO PaO 2 (mm Hg/kPa)
65 Oxygen delivery (VO 2 ) VO 2
66 Oxygen delivery (VO 2 ) VO 2 = [Hb] x 1.34
67 Oxygen delivery (VO 2 ) VO 2 = [Hb] x 1.34 x SaO 2
68 Oxygen delivery (VO 2 ) VO 2 = [Hb] x 1.34 x SaO 2 x CO
69 Oxygen delivery (VO 2 ) VO 2 = [Hb] x 1.34 x SaO 2 x CO = 150 (g/dl) x 1.34 x 100% x 5 (l/min)
70 Oxygen delivery (VO 2 ) VO 2 = [Hb] x 1.34 x SaO 2 x CO = 150 (g/dl) x 1.34 x 100% x 5 (l/min) = 1000 ml/min
71 C Circulation & Heamorrhage Control Shock is a generalized state of hypoperfusion causing: Anaerobic metabolism Lactic acid production Cellular dysfunction Cell death MOF
72 Causes of shock Haemorrhagic vs Nonhaemorrhagic Blood loss Tension pneumothorax Cardiac tamponade Cardiogenic Neurogenic Septic
73 Treatment of shock Direct pressure STOP the bleeding! Operation Splint fractures
74 Treatment of shock Restore volume! CO = Stroke volume (SV) x Heart rate (HR)
75 Treatment of shock Starlings Law of the Heart Stroke volume (BP, CO, UO) Initial fibre length (CVP, PCWP, LVEDP)
76 Oxygen delivery (VO 2 ) VO 2 = [Hb] x 1.34 x SaO 2 x CO = 150 (g/dl) x 1.34 x 100% x 5 (l/min) = 1000 ml/min
77 The Rule of 2 s 2 s and 5 s5 Give 2 mls/kg fluid stat If CVP goes up by 5 stop giving fluid If CVP goes up by less than 5, give 2 mls/kg fluid again Keep giving 2 mls/kg fluid until CVP goes up by 5 and stays up
78 Monitoring the Response Identify Improved Organ Function CNS: Improved level of consciousness Renal: urinary output Skin: Warm, capillary refill Respirations: Improved rate and depth Vital signs: Return to normal
79 Treatment of shock Restore volume! Vascular access
80 Treatment of shock Restore volume! Warmed fluid
81 Which fluid?????? Crystalloid V Colloid
82
83 Oxygen delivery (VO 2 ) VO 2 = [Hb] x 1.34 x SaO 2 x CO = 150 (g/dl) x 1.34 x 100% x 5 (l/min) = 1000 ml/min
84 Treatment of shock Prevent hypothermia!
85 D Disability Baseline neurological examination GCS score Pupillary response OBSERVE FOR DETERIORATION!!!!
86 E Exposure / Environment Completely undress the patient PREVENT HYPOTHERMIA!!
87 The Golden Hour Multiple organ failure after trauma affects even long-term survival and functional status Critical Care 2007, 11:R95doi: /cc6111
88 The Golden Hour Multiple organ failure after trauma affects even long-term survival and functional status Critical Care 2007, 11:R95doi: /cc6111 MOF increased the overall risk of death 6.0 times.
89 The Golden Hour Multiple organ failure after trauma affects even long-term survival and functional status Critical Care 2007, 11:R95doi: /cc6111 MOF increased the overall risk of death 6.0 times. Patients with MOF were 3.9 times more likely to require personal assistance in activities of daily living.
90 The Golden Hour Multiple organ failure after trauma affects even long-term survival and functional status Critical Care 2007, 11:R95doi: /cc6111 MOF increased the overall risk of death 6.0 times. Patients with MOF were 3.9 times more likely to require personal assistance in activities of daily living. Conclusion - the presence of MOF greatly increased mortality and the risk of impaired functional status.
91
92 Secondary Survey Start only when ABCDE has been done and reassessed Vital functions are returning to normal
93 Secondary Survey - Components History
94 Secondary Survey - Components History AMPLE A M P L E Allergies Medications Past illnesses Last meal Events / Environment
95 Secondary Survey - HEAD GCS Score (again) Full neurological exam Motor and sensory and reflexes Full eye and ear exam
96 Intracranial Pressure (ICP) 10 mm Hg = Normal > 20 mm Hg = Abnormal > 40 mm Hg = Severe Sustained ICP leads to brain function and outcome
97 Monro-Kellie Doctrine ICP (mm Hg) Point of Decompensation Compensation Volume of Mass Herniation
98 Cerebral Perfusion Pressure MBP ICP = CPP
99 Cerebral Perfusion Pressure MBP ICP = CPP Normal
100 Cerebral Perfusion Pressure MBP ICP = CPP Normal Cushing s Response
101 Cerebral Perfusion Pressure MBP ICP = CPP Normal Cushing s Response
102 Cerebral Perfusion Pressure MBP ICP = CPP Normal Cushing s Response Hypotension
103 Cerebral Perfusion Pressure MBP ICP = CPP Normal Cushing s Response Hypotension
104 Treatment Minimize secondary brain injury - ABCDE - Maintain CPP - Maintain blood pressure (systolic > 90 mm Hg) - Reduce ICP
105 Treatment Maintain MAP Euvolaemic fluid resuscitation Isotonic fluids Inotropes
106 Treatment Reduce ICP Controlled ventilation Goal: PaCO 2 at 35 mm Hg Head up tilt Paralysis Mannitol Surgery
107 Treatment Mannitol Use with signs of tentorial herniation Dose: 1.0 g / kg IV bolus Consult with neurosurgeon first
108 Secondary Survey Cervical Spine Tenderness Complete motor and sensory exam Reflexes X-ray
109 Normal C-Spine C Xray
110 Secondary Survey Cervical Spine Only 6 vertebrae seen
111 Secondary Survey Cervical Spine Atlas fracture
112 Secondary Survey Cervical Spine C5/6 step fracture
113 Secondary Survey Cervical Spine Er!!!!!!!!
114 Secondary Survey Cervical Spine MRI of cervical fracture-dislocation with cord injury
115 Neurogenic shock Associated with cervical / high thoracic spine injury Neurological (not a heamodynamic) phenomenon Occurs shortly after cord injury Variable duration Flaccidity and loss of reflexes Hypotension and slow heart rate
116 Treat / prevent secondary injury Ensure adequate ventilation and oxygenation Properly immobilize entire patient Maintain blood pressure with fluid and inotropes Atropine as needed for bradycardia Avoid transfer delay! Methylprednisolone
117 IV Methylprednisolone Blunt injury only Start within 8 hours of injury 30 mg/kg over 15 minutes 5.4 mg/kg over next. 23 hours if started within 3 hours of injury 48 hours if started within 3 to 8 hours after injury
118 Secondary Survey - Neck Type of injury Blunt v Penetrating
119 Secondary Survey - Neck
120 Secondary Survey - Neck Type of injury Blunt v Penetrating Look for increasing airway obstruction, stridor or hoarseness KEEP KEEP LOOKING AND LISTENING!!
121 Secondary Survey - Chest Inspect Palpate Percuss Auscultate X-rays
122 Secondary Survey - Chest Haemothorax and flail
123 Secondary Survey - Chest Pneumothorax
124 Secondary Survey - Chest Pneumothorax deep sulcus sign
125 Chest Drain Insertion
126 Chest Drain Insertion
127 Chest Drain Insertion
128 Chest Drain Insertion
129 Chest Drain Insertion
130 Secondary Survey- Chest Tension pneumothorax This is a post mortem X-ray!!
131 Tension Pneumothorax Respiratory distress Distended neck veins Non-central trachea Hypotension and tachycardia Hyperresonance Absent breath sounds
132 Tension Pneumothorax - Treatment Immediate decompression
133 Secondary Survey - Chest Haemothorax
134 Haemothorax At least 1500 ml blood Flat (not distended) neck veins Hypotension and tachycardia Absent breath sounds Dullness to percussion (not hyperresonance) h
135 Haemothorax - Treatment Rapid volume resuscitation Operation
136 Haemothorax Multiple stab wounds Don t t forget the back
137 Secondary Survey Perineum Urethral blood Rectal tone, integrity, blood Vaginal blood, lacerations
138 Secondary Survey - Pelvis -Pain on palpation - Unequal leg length - Instability - SIGNIFICANT BLOOD LOSS!!
139 Secondary Survey Musculoskeletal:Extremities Contusion, deformity Pain Perfusion Peripheral nerve status Potential blood loss Compartment syndrome Fat embolus
140 Fat Embolism Syndrome (FES) Fat emboli were first noted by F.A. Zenker in 1861 in a railroad worker with a thoraco-lumbar crush injury Fat embolism develops in nearly all patients with fractured bones and is asymptomatic 1-3% chance of developing FES with single long bone fracture (increases with number of fractures) Mortality rate 10-20% Chest 2003;123:4
141 FES - pathophysiology 2 theories: Mechanical theory: Large fat droplets deposited in pulmonary capillary beds, and via a-v a v shunts to the brain. Causes local ischaemia and inflammation. Biochemical theory: Degradation of fat to free fatty acids cause vasculitis/ards in animals. Probably phospholipase A2 and CRP mediated.
142 Pathogenesis of ARDS in FES Fat emboli obstructs lung vessel (20microns) platelets and fibrin adhere Lipase creates FFA Inflammatory changes->endothelial damage->ards
143 FES clinical signs Cardiopulmonary (12-72 hrs after insult) Early persistent tachycardia Tachypnoea, dyspnoea, and hypoxia due to V-Q V mismatch ½ of pts with FES require mechanical ventilation (Bulger, Archives of Surgery 1997; 132: 435-9) High temperature spikes
144 FES clinical signs Dermatological (24-36 hrs after insult) Reddish-brown nonpalpable petechiae over upper body, especially axillae Occur in 20-50% of patients and resolve quickly
145 FES clinical signs Subconjunctival & oral hemorrhages/petechiae
146 FES clinical signs Neurologic (80% of patients with FES) Agitated delirium Stupor, seizures, or coma Retinal haemorrhages with intra-arterial arterial fat globules visible on fundoscopy
147 FES - investigations Blood (non-specific) Thrombocytopenia Anaemia Hypofibrinogenaemia hypocalcaemia Fat globules seen in urine, blood & sputum stained with Sudan or oil red N.B. fat in urine common in all trauma patients Imaging CXR-diffuse bilateral pulmonary infiltrates
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149 FES - investigations Imaging Head CT-nil or diffuse white matter petechial haemorrhages BAL-staining of alveolar macrophages for fat (controversial benefit)
150 FES - treatment Medical care Supportive in nature Maintain oxygenation and ventilation Stabilize haemodynamics Blood products as needed Surgical care Early stabilization of fractures to minimize bone marrow embolization Arch Surg 1997; 132:
151 FES - steroids Steroid prophylaxis is controversial to prevent FES Theorized blunting of inflammatory response and complement activation Prospective studies suggests prophylactic steroids benefit high risk patients Few studies and small study size, so remains controversial Once FES established, steroids have not shown improved outcomes
152 FES alcohol!!!!!!! ABSTRACT: In an analysis of the cases of 100 consecutive patients with diaphyseal fractures in the major bones of the lower limb, the incidence of fat embolism syndrome was 17%. The blood alcohol level was determined at the time of admission. A raised level of alcohol in the blood was associated with a lower incidence of fat embolism. Bone Joint Surg Am. 1977;59: R Myers and JJ Taljaard
153 Marmara earthquake Turkey 1999
154 Crush Injury Crush syndrome first recorded in bombing of London during WWII: 5 people who were crushed presented in shock with swollen extremities, dark urine. Later died from renal failure.
155 Rhabdomyolysis - incidence Occurs in up to 85% of patients with traumatic injuries. Those with severe injury who develop rhabdomyolysis-induced induced renal failure have a 20% mortality rate Crush injury to any part of the body (e.g. hand) Laying on limb for long period of time
156 Rhabdomyolysis - pathophysiology Not usually directly due to ischaemia Muscle sarcolemma stretch and permeability increases Influx of sodium, water, & extracellular calcium into the sarcoplasm Cells swell reduced function myocytic death Leak of intracellular metabolites into circulation Free radicals then cause further membrane injury
157 Rhabdomyolysis symptoms and signs Clinical: Muscle pain & weakness dark urine (myoglobin) Hypovolaemic shock (fluid moves into damaged tissue) Electrolyte abnormalities: K + (leakage) Ca 2+ (sequestered in injured tissues) Metabolic acidosis phosphate Myoglobinaemia/uria
158 Rhabdomyolisis - ARF Myoglobin precipitates (particularly in hypovolemia) and obstructs renal tubules
159 Rhabdomyolisis - ARF Myoglobin directly toxic to the renal tubular cells especially in acid urine At ph < 5.6, myoglobin dissociates into its 2 components Globin (nontoxic) Ferrihaemate (probably toxic)
160 Lab tests Serum Creatinine Kinase Correlates with severity of rhabdomyolisis Levels peak within 24h Normally U/L >5000 U/L - high correlation with renal failure Serum myoglobin t(1/2) h Excreted in bile Urine sample Myoglobinuria dipstick will be (+) for haemoglobin, RBC s s and myoglobin Microscopy: no RBC s,, brown casts, uric acid crystals
161 Early Treatment Begin early (on the field) Ideally ½ NS with 100mmol/L bicarb corrects acidosis prevents tubular precipitation of myglobin reduces risk of hyperkalaemia 10ml/h 15% mannitol renal vasodilator free radical scavenger Forced diuresis w/in 6 hrs of admission
162 Late Treatment
163 In Summary
164 Successful management of the trauma patient requires. Teamwork Speed Efficiency Keeping it simple Using your skills Effective JUST LIKE
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