2CaseYou’re on call on a Saturday in the ICU at VGH when the head nurse tells you that 2 traumas from an MVA had just come into the ER. Both the driver and the passenger were belted when their car lost control and hit a tree. The trauma team is currently assessing them and will let you know if they need any ICU services.
3CaseAfter speaking to the trauma senior, you find out that the driver is unstable. A FAST showed free fluid in the abdomen, and the patient is now being rushed to the OR for an exploratory laparotomy. She thinks that the patient will likely need to come to the ICU post-operatively.
4Question 1What are the most common organ injuries associated with a) blunt and b) penetrating abdominal trauma? What organ injuries are associated with deceleration injury? (Yoan)
5Liver and spleen : most frequently. What are the most common organ injuries associated with blunt abdominal trauma?Liver and spleen : most frequently.Small and large intestines : next most injured.Crush, Deceleration, trapped airPancreas (10-12%): in crush injury, direct blow, seat belt...Kidney, bladderSource: emedicine 2007, Salomone et al5
6What are the most common organ injuries associated with penetrating abdominal trauma ? Stabliver (40%)small bowel (30%)diaphragm (20%)colon (15%)pancreas, duodenum, vascular, gastric, rectum, porta hepatis, kidneys, uretersGunshot woundsmall bowel (50%)colon (40%)liver (30%)vascular (25%)Source: emedicine 2008, Testa et al6
13What organ injuries are associated with deceleration injury? Classic deceleration injuries include hepatic tear along the ligamentum teres and intimal injuries to the renal arteries. As bowel loops travel from their mesenteric attachments, thrombosis and mesenteric tears, with resultant splanchnic vessel injuries, can result.Source: emedicine 2007, Salomone et al13
16CaseThe senior then tells you that the passenger of the car is currently stable after aggressive resuscitation. He has a pelvic fracture and is complaining of chest pain. The CXR shows a widened mediastinum. The ECG is unremarkable. A CT chest is ordered and pending.
17Question 2Discuss the different types of pelvic fractures, their associated mechanism of injury, risk of bleeding, and initial management
18Biomechanics of pelvic fractures Lateral compression injuryMost commonAcute shortening of diameter across pelvisRarely destroy ligamentous integrityDo not typically cause large blood loss
19Anterior/Posterior Compression Force causes pelvic diameter to widenLigamentous disruptionManifest itself as a widened pubis symphysis and SI jointOften associated with substantial vascular damage: LS plexus and common/external iliac artery
20Vertical shear injury Fall from a height Severe ligamentous injury Vascular injury less severe than AP injuriesDisruption of all restraining ligament of the hemipelvis,
21Pelvic Fracture Classification Tile ClassificationConcentrate on rotational component of injury to address long-term reconstructive plansYoung and Burgess ClassificationSubdivide LC and AP compression injuries according to increasing level of energy
22The American Journal of Surgery 192 (2006) 211ﾐ223
23The American Journal of Surgery 192 (2006) 211ﾐ223
28The American Journal of Surgery 192 (2006) 211ﾐ223
29Indications for Angiography 4 U transfused for pelvic bleeding in <24 h>6 U transfused for pelvic bleeding in <48 hHemodynamic instability with a negative FAST or DPLLarge pelvic hematoma on CTPelvic pseudoaneurysm on helical CTLarge and/or expanded pelvic hematoma seen at the time of laparotomyTRAUMA - 6th Ed. (2008)
30External FixationUsed as definitive anterior fixation for open book fractureUsed if condition does not permit internal fixationUsed as a bridge to internal fixation“damage control” approach
31Question 3What associated injuries should you look for in patients with pelvic fractures?
32Which injuries may be associated with pelvic fractures? UKSo Cal
33The Pelvis Doesn’t Fracture Easily… Associated with high energy-transfer situations…FallsCrashesAssaultSports injuries(including, of course… falls and crashes)
34In UK Trauma Audit Research Network, associated with: Chest trauma (21%)Head trauma (17%)Hepatic/Splenic injury (8%)2 or more long bone fractures (8%)Urogenital (4%) (!?)
35But wait… there’s more!Longer mean hospital LOS (15 vs 8 days in trauma pts without pelvic fracture)More likely to be admitted to critical care setting (25% vs 12%)3 month mortality 14% vs 6%.Shorter period from injury to death in pelvic # patients (6 hrs vs 40 hrs)
36Trauma Registry at LA County/ USC Trauma Center 1993-2000
39CaseThe CT chest showed a descending thoracic aortic dissection with no contrast extravasation. The patient arrives in the unit and is hemodynamically stable.
40Question 4Discuss the diagnosis, the radiographic features as well as the management of blunt aortic injury.
41Blunt aortic injury occurs in less than 1% of MVCs but is responsible for 16% of the deaths Up to 80% of patients die before their arrival at a hospitalUntreated, approximately 30% of surviving patients who are admitted to a hospital will die within the first 24 hours
43Diagnosis CXR findings Wide mediastinum: >8cm on upright, mediastinal/chest width ratio of >0.38obscure or indistinct aortic knobdepression of the left mainstem bronchusdeviation of the nasogastric tubeopacification of the aortopulmonary window
44CXR Also suggestive widened paratracheal and paraspinous stripes apical capping1st and 2nd rib fractures have less an associationBetween 7.3% and 44% of patients with blunt aortic injury may have a normal mediastinum on chest radiography
45CT ScanHelical CT of the thorax is more sensitive for blunt aortic injury than angiography and is estimated to have a sensitivity of 100%, as compared with 92% for angiographyFabian TC, et a l . Ann Surg 1998;227:666-76
46CT Scan28% rate of missed diagnoses and recommend that CT be performed in all patients with a hx of MVC at a speed of >15 km/h for unrestrained drivers and >50 km/h for restrained driversExadaktylos AK, et al. Cardiovasc J S Afr 2005;16:162-5.
48Other ModalitiesOther options for the diagnosis of BAI include transesophageal echocardiography, intravascular ultrasonography, and magnetic resonance imaging
49Management Immediate operative repair used to be the rule Several studies have demonstrated the relative safety of a delayed approach, particularly if there are substantial co-injuries, using a regimen of beta-blockers and antihypertensive agents to decrease the shear force on the aortic wallDemetriades et al J Trauma 2009, 66:
50Medical MgtFabian et al: a prospective study using beta-blockers with or without vasodilators to maintain a systolic blood pressure of 100 mm Hg (or 110 to 120 mm Hg in older patients) and a pulse rate of under 100 beats/minno patient had an aortic rupture while awaiting repair.Potential problem with severe HI and SCI
51Repair There are basically 3 option Open “clamp and sew” Open Bypass or shuntEndovascular repair
54ParaplegiaDemetriades et al J Trauma 2009, 66:Clamp and sew has an associated mortality of 16% and a striking 19% incidence of paraplegia
55Endovascular RepairMajority of the repairs currently done as seems much safer especially in multi-trauma patientsthe durability of endografts is unknown.There are questions about long-term device integrity as well as the natural history of the aorta itself after this type of injury and repair. These issues are particularly important considering the relatively young age of trauma patients
56CaseShortly after admitting these 2 patients, the head nurse tells you another trauma came into the ER, and was wondering if you were called about it. The patient is a 19 year-old man who was also involved in a MVA. On the scene, the patient was alert and oriented but unable to move or feel his extremities.
57Question 5Summarize the clinical findings and anatomical lesions of the related to the following clinical syndromes: (Neil)Central cord syndromeBrown-Sequard syndromeAnterior cord syndromeConus medullaris syndromeSpinal shock.
66Conus medullarisCauda Equina SyndromeLocation:L1-L2 vertebral levelInjury to sacral cord (S1-5)L2-Sacrum vert levelInjury to lumbosacral rootsCauses:L1 fractureTumors, gliomasVascular injurySpina bifida, tethering of cordL2 or below fracture/discSacral FracturesFracture of pelvic ringSpondylosisSigns and symptomsNormal motor function of lower extremeties,(unless motor S1-S2 involvement)Saddle anesthesiaNo painSymmetric abnormalitiesSevere bowel, bladder, sexual dysfunctionBCR may be presentFlacid paralysis of involved lumbar rootsAreflexic LE Sensory loss in root distributionPainAsymmetricHigh lesions spare bowel and bladderBCR often absentEMG NormalEMG root findings
67Spinal ShockConcussive injury to spinal cord that results in complete dysfunction below level of injuryUsually lasts <24 hours but can be daysBulbocavernosus reflex is not present during spinal shockImportant in prognosis
68CaseIn the trauma bay, the patient is hypotensive and bradycardic. He is on 10 mcg/min of dopamine. His c-spine films show a blowout fracture of his C5 vertebra.
69Question 6What are the cardiovascular complications of spinal cord injuries and how should you manage them? (Marios)
70Cardiovascular complications of SCI Occur in patients with cervical or high thoracic cord injury (T6 or higher).Degree of dysfunction is related to the location and severity of the injury, and is manifested by:Low resting blood pressure and orthostatic hypotensionHeart rate abnormalitiesAutonomic dysreflexiaNeurogenic shock typically lasts up to 5 weeks.
72Low blood pressure and orthostatic hypotension Hypotension occurs due to the reduced sympathetic outflow to the cardiovascular system.Mechanisms involved in orthostatic hypotension include:Loss of reflex vasoconstriction caudal to the injuryLack of muscular effects to counteract venous poolingReduced plasma volumes secondary to hyponatremiaCardiovascular deconditioning secondary to prolonged bedrest
75Heart rate abnormalities SCI alters cardiac electrophysiology and increase susceptibility to arrhythmias such as:Sinus bradycardiaRepolarization changesAV blocksSupraventricular tachycardiaVentricular tachycardiaCardiac arrestSecondary to a loss of sympathetic tone in the presence of intact parasympathetic tone.The most pronounced changes are seen during the acute phase post injury (weeks 2 to 6)
78Autonomic dysreflexia An increase in SBP of at least 20% associated with a change in heart rate and accompanied by one of the following signs or symptoms:SweatingPiloerectionFacial flushingHeadacheBlurred visionStuffy noseOften associated with a triggering factor such as bladder distension or bowel impaction.Relatively common in the chronic phase of SCI, but can also occur in the acute stage following SCI.
80Management Hypotension R/O other causes of hypotension, including adrenal insufficiency.Guidelines recommend the use of fluids +/- vasopressors to maintain a MAP of 85 mmHg or greater during the first 7 days following SCI.Based on Grade III evidence, this is thought to improve spinal cord perfusion and therefore possibly neurological outcome.High thoracic or cervical cord lesions, where hypotension is often accompanied by bradycardia should be treated with dopamine or norepinephrine.Lower thoracic cord lesions which are primarily affected by vasodilation can be treated with phenylephrine.
81Management Symptomatic bradycardia May occur with noxious stimuli such as suctioning.Can be treated with atropine or vasopressors that have both alpha- and beta-adrenergic actions such as dopamine, norepinephrine, and epinephrine.
82Management Autonomic dysreflexia If supine place in sitting position Loosen constrictive clothing or devicesR/O bladder distention or bowel impactionIf SBP > 150, consider nitroprusside
83Question 7Is there any evidence for steroids in spinal cord trauma? (Naisan)
84Question 7 - Is there any evidence for steroids in spinal cord trauma? NO…I think
85Clinical Practice Guideline SCI 2008 No clinical evidence exists to definitively recommend the use of any neuroprotective pharmacologic agent, including steroids, in the treatment of acute spinal cord injury to improve functional recovery.
86The StudiesMP has been investigated in three large-scale, multicenter clinical trials collectively referred to as NASCIS (National Acute Spinal Cord Injury Study; Bracken et al.1984, 1990, 1997)NASCIS 1 trial compared 2 doses of MP after traumatic SCI (100mg vs 1000mg for 10 days)second clinical trial compared the effects of a much higher dose of MP (30 mg/kg then infusion) with those of naloxone and a placeboand the third clinical trial evaluated the timing of initiation and duration of MP treatment following injury (8 vs 3 hours; 24 vs 48 hrs)
87The Outcomes NASCIS I: no difference found between groups NASCIS II: if <8hrs, improved motor function was statistically signiﬁcant at 6 months and even after 1 year in the MP group compared with the control group (17.2 and 12.0 points improvement, p=.030)
88The ResultsNASCIS III: Follow-up after 6 months revealed no signiﬁcant difference between the groupsAt that point, patients were divided into treatment within 3 hours and after 3 hours but less than 8 hours after SCIAfter this statistical maneuver, there was a signiﬁcant difference in motor score who received MP for 47 hours compared with 24hrs, in the groups treated between 3 and 8 hours
89The Problemsneither NASCIS II or NASCIS III addressed some of the potential confounding variablesthe NASCIS II trial did not include details about other interventions such as radiology , surgical manipulations, or the extent of rehabilitative therapies, which may have contributed to improvements or recovery
90The Problemssubsequent post hoc analysis failed to demonstrate improvement in outcome measures (motor scores, pinprick scores,and light-touch scores)meaning that improved recovery with MP may represent random events, thus weakening the overall study findings (Coleman et al., 2000; Hurlbert, 2000, 2006; Short et al., 2000).
91The ProblemsOnly right-sided motor scores were reported in NASCIS II, but bilateral sensory scores were reported. Lack of evidence describing left-sided motor scores and total body motor scores in NASCIS II is confusingThe data were presented as obtained from the whole study population; however, the fact is that in the groups that presented within 8 hours, only 62 patients of the placebo group and 65 of the MP group were analyzed
92NASCIS III :Had no difference at one year in the Functional Independence Measure (FIM) developed by the American Spinal Injury AssociationSo seems no clinically significant difference
93Side effectsAll studies showed a significant increase in infection rates, ICU/Vent times, and GI bleeding
94Question 8Discuss DVT prophylaxis in spinal cord injury. (Todd)
95Venous Thromboembolism Prophylaxis in Spinal Cord Injury Spine trauma, immobility and paralysis all conspire to place SCI pts at risk for VTE.Options include:Pneumatic calf compression devicesUnfractionated heparinLow molecular-weight heparinIVC filtersScreening doppler U/SWhich is best?
96Chest Guidelines 2004VTE prophylaxis is recommended for “…all trauma patients with at least one risk factor.” Grade 1A.Data on pneumatic compression devices is conflicting, but they may be useful in patients with a contraindication to anticoagulants.IVC filters not recommended as routine treatment unless absolute contraindication to anticoagulation.Not cost-effective to screen with U/S.Continue until discharge.
97Venous Thromboembolism Prophylaxis in Spinal Cord Injury Low Molecular-Weight Heparin (LMWH).Spine uses it; we use it…and it’s worked out pretty well so far.
98Low-dose UFH vs LMWH: Geerts, WH, Jay, RM, Code, KI, et al A comparison of low-dose heparin with low-molecular-weight heparin as prophylaxis against venous thromboembolism after major trauma. N ENGL J MED 1996;335,Contraindications:Intracranial hemorrhage.Active bleeding.Uncontrolled coagulopathy.Known or suspected perispinal hematoma (incomplete sci).