Presentation on theme: "Case Based Presentation TRAUMA # 2. Case You ’ re on call on a Saturday in the ICU at VGH when the head nurse tells you that 2 traumas from an MVA had."— Presentation transcript:
Case Based Presentation TRAUMA # 2
Case You ’ 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.
Case After 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.
Question 1 What are the most common organ injuries associated with a) blunt and b) penetrating abdominal trauma? What organ injuries are associated with deceleration injury? (Yoan)
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 air Pancreas (10-12%): in crush injury, direct blow, seat belt... Kidney, bladder Source: emedicine 2007, Salomone et al
What are the most common organ injuries associated with penetrating abdominal trauma ? Stab –liver (40%) –small bowel (30%) –diaphragm (20%) –colon (15%) pancreas, duodenum, vascular, gastric, rectum, porta hepatis, kidneys, ureters Gunshot wound –small bowel (50%) –colon (40%) –liver (30%) –vascular (25%) Source: emedicine 2008, Testa et al
What 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 al
Case The 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.
Question 2 Discuss the different types of pelvic fractures, their associated mechanism of injury, risk of bleeding, and initial management
Biomechanics of pelvic fractures Lateral compression injury –Most common –Acute shortening of diameter across pelvis –Rarely destroy ligamentous integrity –Do not typically cause large blood loss
Anterior/Posterior Compression –Force causes pelvic diameter to widen –Ligamentous disruption –Manifest itself as a widened pubis symphysis and SI joint –Often associated with substantial vascular damage: LS plexus and common/external iliac artery
Vertical shear injury –Fall from a height –Severe ligamentous injury –Vascular injury less severe than AP injuries
Pelvic Fracture Classification Tile Classification –Concentrate on rotational component of injury to address long-term reconstructive plans Young and Burgess Classification –Subdivide LC and AP compression injuries according to increasing level of energy
The American Journal of Surgery 192 (2006) 211 ﾐ 223
Mechanism of injury
Blood loss in pelvic fractures
Initial Management ABC’s Xmatch and IV access Compressive device –Temporal control of hemorrhage –Design to reduce the volume of the pelvis –Less useful in LC injuries
Critical Care2007, 11:204
The American Journal of Surgery 192 (2006) 211 ﾐ 223
Indications for Angiography 4 U transfused for pelvic bleeding in <24 h >6 U transfused for pelvic bleeding in <48 h Hemodynamic instability with a negative FAST or DPL Large pelvic hematoma on CT Pelvic pseudoaneurysm on helical CT Large and/or expanded pelvic hematoma seen at the time of laparotomy TRAUMA - 6th Ed. (2008)
External Fixation Used as definitive anterior fixation for open book fracture Used if condition does not permit internal fixation Used as a bridge to internal fixation –“damage control” approach
Question 3 What associated injuries should you look for in patients with pelvic fractures?
Which injuries may be associated with pelvic fractures? UK So Cal
The Pelvis Doesn’t Fracture Easily… Associated with high energy-transfer situations… –Falls –Crashes –Assault –Sports injuries (including, of course… falls and crashes)
In 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%) (!?)
But 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)
Trauma Registry at LA County/ USC Trauma Center
Case The CT chest showed a descending thoracic aortic dissection with no contrast extravasation. The patient arrives in the unit and is hemodynamically stable.
Question 4 Discuss the diagnosis, the radiographic features as well as the management of blunt aortic injury.
Blunt 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 hospital Untreated, approximately 30% of surviving patients who are admitted to a hospital will die within the first 24 hours
Mechanism N Engl J Med 2008;359:
Diagnosis CXR findings –Wide mediastinum: >8cm on upright, mediastinal/chest width ratio of >0.38 –obscure or indistinct aortic knob –depression of the left mainstem bronchus –deviation of the nasogastric tube –opacification of the aortopulmonary window
CXR Also suggestive –widened paratracheal and paraspinous stripes –apical capping –1 st and 2 nd rib fractures have less an association –Between 7.3% and 44% of patients with blunt aortic injury may have a normal mediastinum on chest radiography
CT Scan Helical 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 angiography »Fabian TC, et a l. Ann Surg 1998;227:666-76
CT Scan 28% 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 drivers »Exadaktylos AK, et al. Cardiovasc J S Afr 2005;16:162-5.
Other Modalities Other options for the diagnosis of BAI include transesophageal echocardiography, intravascular ultrasonography, and magnetic resonance imaging
Management 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 wall –Demetriades et al J Trauma 2009, 66:
Medical Mgt Fabian 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/min no patient had an aortic rupture while awaiting repair. Potential problem with severe HI and SCI
Repair There are basically 3 option –Open “clamp and sew” –Open Bypass or shunt –Endovascular repair
Paraplegia Clamp and sew has an associated mortality of 16% and a striking 19% incidence of paraplegia Demetriades et al J Trauma 2009, 66:
Endovascular Repair Majority of the repairs currently done as seems much safer especially in multi-trauma patients the 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
Case Shortly 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.
Question 5 Summarize the clinical findings and anatomical lesions of the related to the following clinical syndromes: (Neil) Central cord syndrome Brown-Sequard syndrome Anterior cord syndrome Conus medullaris syndrome Spinal shock.
Anterior cord Brown Sequrd Central Cord Pain/TempBilateralContralateralShawl distribution MotorBilateralIpsilateralArms>Legs Vibration/pos ition IntactIpsilateralIntact
Conus medullarisCauda Equina Syndrome Location: L1-L2 vertebral level Injury to sacral cord (S1-5) Location: L2-Sacrum vert level Injury to lumbosacral roots Causes: L1 fracture Tumors, gliomas Vascular injury Spina bifida, tethering of cord Causes: L2 or below fracture/disc Sacral Fractures Fracture of pelvic ring Spondylosis Signs and symptoms Normal motor function of lower extremeties,(unless motor S1-S2 involvement) Saddle anesthesia No pain Symmetric abnormalities Severe bowel, bladder, sexual dysfunction BCR may be present Signs and symptoms Flacid paralysis of involved lumbar roots Areflexic LE Sensory loss in root distribution Pain Asymmetric High lesions spare bowel and bladder BCR often absent EMG NormalEMG root findings
Spinal Shock Concussive injury to spinal cord that results in complete dysfunction below level of injury Usually lasts <24 hours but can be days Bulbocavernosus reflex is not present during spinal shock Important in prognosis
Case In 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.
Question 6 What are the cardiovascular complications of spinal cord injuries and how should you manage them? (Marios)
Cardiovascular 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: 1)Low resting blood pressure and orthostatic hypotension 2)Heart rate abnormalities 3)Autonomic dysreflexia Neurogenic shock typically lasts up to 5 weeks.
Degree of SCI and cardiovascular dysfunction
Low blood pressure and orthostatic hypotension Hypotension occurs due to the reduced sympathetic outflow to the cardiovascular system. Mechanisms involved in orthostatic hypotension include: 1)Loss of reflex vasoconstriction caudal to the injury 2)Lack of muscular effects to counteract venous pooling 3)Reduced plasma volumes secondary to hyponatremia 4)Cardiovascular deconditioning secondary to prolonged bedrest
SBP over time
DBP over time
Heart rate abnormalities SCI alters cardiac electrophysiology and increase susceptibility to arrhythmias such as: –Sinus bradycardia –Repolarization changes –AV blocks –Supraventricular tachycardia –Ventricular tachycardia –Cardiac arrest Secondary 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)
Heart rate over time
Autonomic 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: –Sweating –Piloerection –Facial flushing –Headache –Blurred vision –Stuffy nose Often 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.
Management 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.
Management 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.
Management Autonomic dysreflexia 1)If supine place in sitting position 2)Loosen constrictive clothing or devices 3)R/O bladder distention or bowel impaction 4)If SBP > 150, consider nitroprusside
Question 7 Is there any evidence for steroids in spinal cord trauma? (Naisan)
Question 7 - Is there any evidence for steroids in spinal cord trauma? NO… I think
Clinical 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.
The Studies MP 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 placebo and the third clinical trial evaluated the timing of initiation and duration of MP treatment following injury (8 vs 3 hours; 24 vs 48 hrs)
The 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)
The Results NASCIS III: Follow-up after 6 months revealed no signiﬁcant difference between the groups –At that point, patients were divided into treatment within 3 hours and after 3 hours but less than 8 hours after SCI –After 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
The Problems neither NASCIS II or NASCIS III addressed some of the potential confounding variables the 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
The Problems subsequent 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).
The Problems Only 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 confusing The 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
NASCIS III :Had no difference at one year in the Functional Independence Measure (FIM) developed by the American Spinal Injury Association So seems no clinically significant difference
Side effects All studies showed a significant increase in infection rates, ICU/Vent times, and GI bleeding
Venous 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 devices –Unfractionated heparin –Low molecular-weight heparin –IVC filters –Screening doppler U/S Which is best?
Chest Guidelines 2004 VTE 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.
Venous 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.
Low-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).