Tag Archives: trauma

The Thromboelastogram (TEG®): A Five-Minute Primer for the Emergency Physician

Author: Erica Simon, DO, MHA (@E_M_Simon, EM Chief Resident at SAUSHEC, USAF) // Edited by: Alex Koyfman, MD (@EMHighAK, EM Attending Physician, UTSW / Parkland Memorial Hospital) and Brit Long, MD (@long_brit, EM Attending Physician, SAUSHEC)

It’s three o’clock in the morning on your fourth night shift in a row.  While mustering the courage to rescue your energy drink from the dank, dark depths of the staff mini-fridge, you hear a familiar page: “trauma team to the trauma room.”  As you walk towards the ambulance bay, the trauma surgeon approaches with information regarding the incoming transfer:

  • 17 year-old male – MVC versus pedestrian
  • Seen at OSH where CTs demonstrated: epidural hematoma, grade III liver laceration, grade II splenic laceration, open book pelvic fracture, and extraperitoneal bladder rupture
  • Patient underwent external pelvic fixation and transfusion of blood products (8U PRBCs, 8U FFP and 4U Plts)
  • Most recent VS: BP 136/89, HR 92, RR (intubated/ventilated):14, SpO2 99% (FiO2 70%)

Drawing your attention to a piece of paper in his hand, detailing what appear to be labs from the outside facility, the surgeon points to a colorful figure: “I’m very concerned about this”:


Scanning your mind for intelligent thought, you realize that it’s been some time since you’ve ordered a thromboelastogram (TEG), let alone interpreted one.

If you’re like this physician, take a few minutes to scan the following review – the quick and dirty on TEGs is coming your way.

Thromboelastography – What is it?

Developed in 1948 by Dr. Hellmut Harter, thromboelastography is a mechanism of assessing coagulation based upon the viscoelastic properties of whole blood.2-8  In contrast to traditional, static measurements of hemostasis (PT, aPTT, INR, fibrinogen level, and fibrin degradation products), thromboelastography allows for an assessment of near real-time, in-vivo clotting capacity, providing the interpreter information regarding the dynamics of clot development, stabilization, and dissolution.7  When utilized as a point-of-care assay, graphic interpretation of thromboelastography (the TEG), offers the opportunity for an expedited assessment of coagulopathies (thrombocytopenia, factor deficiency, heparin effect, hypofibrinogenemia, and hyperfibrinolysis).7,9,12,13

How is a TEG performed?

In order to perform a TEG, a citrated-sample of whole blood is placed into a heated sample cup with calcium chloride (to overcome the effects of the citrate), kaolin (a negatively charged molecule known to initiate the intrinsic pathway10), and phospholipids (required for optimal functioning of the extrinsic pathway11) (Figure 2).  As the sample cup oscillates in a limited arc, formation of clot results in the generation of rotational forces on a pin suspended from a torsion wire.  Forces translated to the torsion wire are then, in turn, transmitted to an electrical transducer, creating a characteristic waveform (Figure 3).



I’ve heard of the Rapid TEG (r-TEG), is there a Difference?

When performed by a trained laboratory specialist, an r-TEG may be completed within 15 minutes as compared to the average 30-45 minutes processing time for a standard TEG.4,5,14  In contrast to a TEG, whole blood samples for an r-TEG may be performed with citrated or non-citrated samples.4 Samples utilized for an r-TEG are combined with tissue factor (activating the extrinsic pathway), and kaolin (activating the intrinsic pathway as above) +/- calcium chloride as applicable.4

I’ve also heard of ROTEM, what is it?

Although utilizing the technique developed by Dr. Harter, rotational thromboelastometry (ROTEM) differs from traditional thromboelastography in its mechanical application.  Unlike traditional thromboelastography, which utilizes a sample cup rotating in a limited arc, ROTEM employs a static sample cup with an oscillating pin/wire transduction system.  By comparison, ROTEM is also a more complex diagnostic test as it requires a number of differing reagents.  A complete discussion of ROTEM is outside the scope of this review.  If interested in further reading, see:

Tanaka K, Bolliger D. Practical aspects of rotational thromboelastometry (ROTEM). Available from: https://www.scahq.org/sca3/events/2009/annual/syllabus/workshops/subs/wkshp6pdfs/ROTEM%20-%20Tanaka.doc.pdf

Haemoview Diagnostics. ROTEM analysis: thromboelastometry. Available from http://www.haemoview.com.au/rotem-analysis.html

Haemoview. The 5 ROTEM tests. Available from http://www.haemoview.com.au/uploads/2/5/4/9/25498232/the_5_rotem_tests.pdf

How Do I Interpret TEG and r-TEG Results?

Drs. Semon and Cheatham of the Orlando Regional Medical Center Department of Surgical Education generated an excellent quick reference chart:


*Note: TEG-ACT (rapid) – reported for r-TEG only.

A TEG-Guided Transfusion Strategy

In addressing TEG and r-TEG abnormalities, experts recommend the following3:


The Quick and Dirty: Pattern Recognition

Perhaps most useful for the ED physician is knowledge of qualitative TEG representations:


Some clarification on DIC Stage 1 and 2:

  • Stage 1: Fibrinolysis results in the degradation of fibrin, increasing fibrin degradation products (FDPs). Excess FDPs result in clot de-stabilization.1
  • Stage 2: The cycle of clot formation and breakdown results in platelet and clotting factor consumption.1

Why Might an Emergency Medicine Physician Want to Know about this Test?

Coagulation abnormalities in trauma patients have demonstrated a significant association with infection, multi-organ failure, and death.15-18 Given its ability to quickly detect hematologic pathology, the TEG is becoming a tool for the evaluation of transfusion requirements/coagulopathy post transfusion in this patient population.3,12,13

What does the literature say?

Cotton, et al., 20114:

  • Pilot study to evaluate the timeliness of r-TEG results, their correlation to conventional coagulation testing (CCT – PT, aPTT, INR, platelet count, fibrinogen), and the ability of r-TEG to predict early blood transfusion.
    • 272 patients meeting requirements for major trauma activation
    • Outcomes:
      • All r-TEG values available within 15 minutes vs. 48 minutes for CCTs
      • ACT, r-value, k-time correlated with PT, INR, PTT (r >0.70; p<0.001)
      • MA and a-angle correlated with platelet count (p<0.001, p<0.001)
      • Controlling for demographics and ED vitals: ACT>128 predicted massive transfusion (>10 U) in the first 6 hours of presentation and treatment

Bottom line – r-TEG results were available within minutes, results correlated with conventional coagulation test results, and were predictive of the requirement for early massive transfusion.

Holocomb, et al., 201219:

  • Study to evaluate the reliability of r-TEGs versus CCTs in predicting blood product transfusion
    • 1974 major trauma patients, median ISS 17 (25% meeting criteria for shock; 28% transfused, 6% died within 24 hours)
    • Outcomes
      • When controlling for age, injury mechanism, weighted-Revised Trauma Score, base excess and hemoglobin, ACT predicted RBC transfusion and a-angle predicted massive transfusion better than PT/aPTT or INR (p<0.001).
      • a-angle was superior to fibrinogen for predicting plasma transfusion, and MA was superior to platelet count for predicting platelet transfusion (p<0.001)

Bottom line – r-TEG was more accurate in the prediction of requirements for RBC, plasma, and platelet transfusions as compared to traditional CCTs.

Wikkelso A, et al., 201612:

  • Cochrane Review including 17 current RCTs (n=1493 participants)
    • Per the authors:
      • Low quality studies: numerous biases
      • Limited generalizability: majority of studies center on cardiac patients undergoing surgical intervention

Bottom line – There is growing evidence to suggest that the utilization of TEG and ROTEM reduce transfusion requirements and improve morbidity in patients with bleeding, but additional studies are required.

Back to Our Case

Why was the trauma surgeon concerned? If we interpret our TEG values:

  • R time 20.0 => well above the upper limit of normal (10.0 minutes) = significantly prolonged time for clot formation
  • K time 13.2 => normal: up to 10.0 = prolonged fibrin cross-linking
  • a-angle 16.5 => normal >53.0 = limited clot formation
  • MA 38 => normal platelet function >50 = limited platelet function

More importantly, one quick glance at our TEG and through pattern recognition, we known that aside from his significant traumatic injuries, the patient is in trouble. This waveform is characteristic of DIC Stage 2.

Key Pearls

  • A TEG can be used as a rapid assessment of thrombosis and fibrinolysis.
  • Although additional RCTs are needed, TEGs utilized in trauma patients have been demonstrated to reduce transfusion requirements (important when we consider TACO/TRALI, risk of DIC, and blood-borne pathogens).
  • If nothing else, take a few minutes to review the characteristic TEG waveforms – depending on your laboratory processing time, knowledge of above tracings could allow early identification of coagulopathy and immediate treatment.


References / Further Reading

  1. Williams. Haemscope Basic Clinician Training: Fibrinolysis and Hyperfibrinolysis TEG Analysis. Available from: www.medicine.wisc.edu/~williams/TEG5_analysis.ppt
  2. Walsh M, Thomas S, Howard J, Evans E, Guyer K, et al. Blood component therapy in trauma guided with the utilization of the perfusionist and thromboelastography. J Extra Corpor Technol. 2001; 43(4):162-167.
  3. Semon G, Cheatham M. Thromboelastography in Trauma. Surgical Critical Care Evidence-Based Guidelines Committee. 2014. Available from: www.surgicalcriticalcare.net/Guidelines/TEG%202014.pdf
  4. Cotton B, Faz G, Hatch Q, Radwan Z, Podbielski J, et al. Rapid thromboelastography delivers real-time results that predict transfusion within 1 hour of admission. J Trauma. 2011; 71:407-417.
  5. Teodoro da Luz L, Nascimento B, Rizoli S. Thromboelastography (TEG): practical considerations on its clinical use in trauma resuscitation. Scand J Trauma Resusc Emerg Med. 2013; 21:29.
  6. Bollinger D, Seeberg M, Tanaka K. Principles and practice of thromboelastography in clinical coagulation management and transfusion practice. Transfus Med Rev. 2012: 26(1): 1-13.
  7. Thakur M, Ahmed A. A review of thromboelastography. Int J periop Ultrasound Apply Technol. 2012; 1(1):25-29.
  8. Nickson C. Critical Care Compendium: Thromboelastogram (TEG). 2014. Available from http://lifeinthefastlane.com/ccc/thromboelastogram-teg/
  9. Kashuk J, Moore E, Sawyer M, Wolhauer M, Pezold M, et al. Primary fibrinolysis is integral in the pathogenesis of acute coagulopathy of trauma. Ann Surg. 2010; 252: 434-444.
  10. Zhu S, Diamond S. Contact activation of blood coagulation on a defined kaolin/collagen surface in microfluidic assay. Thromb Res. 2014; 134(6): 1335-1343.
  11. Heemskerk J, Bevers E, Lindhout T. Platelet activation and blood coagulation. Throm Haemost. 2002; 88(2):186-193.
  12. Wikkelso A, Wetterslev J, Moller A, Afshari A. Thromboelastography (TEG) or thromboelastometry (ROTEM) to monitor haemostatic treatment versus usual care in adults or children with bleeding (Review). Cochrane Database of Systematic Reviews. 2016; 8:1-149.
  13. Luddington R. Thromboelastography/thromboelastometry. Clin Lab Haematol. 2005; 27(2):81-90.
  14. Jeger V, Zimmerman H, Exadaktylos A. Can rapid TEG accelerate the search for coagulopathies in the patient with multiple injuries? J Trauma. 2009; 66:1253-1257.
  15. Niles S, McLaughlin D, Perkins J et al. Increased mortality associated with the early coagulopathy of trauma in combat casualties. J Trauma. 2008; 64:1459-1463.
  16. Brohi K, Sing J, Heron M. Coats T. Acute traumatic coagulopathy. J Trauma. 2003; 54:1127-1130.
  17. Cotton B, Gunter O, Isbell J, et al. Damage control hematology: the impact of a trauma exsanguination protocol on survival and blood product utilization. J Trauma. 2008; 64;1177-1182.
  18. Cohen J, Call M, Nelson M, et al. Clinical and mechanistic drivers of cute traumatic coagulopathy. J Trauma Acute Care Surg. 2013; 75:S40-47.
  19. Holocomb J, Minei K, Scerbo M, Radwan Z, Wade C, et al. Admission rapid thromboelastography can replace conventional coagulation tests in the emergency department: experience with 1974 consecutive trauma patients. Ann Surg. 2012

The motorcycle accident patient: ED considerations + management / Pearls & Pitfalls

Author: Laryssa Patti, MD (Instructor, Department of Emergency Medicine, Rutgers Robert Wood Johnson Medical School) // Edited by: Alex Koyfman, MD (@EMHighAK, EM Attending Physician, UTSW Medical Center / Parkland Memorial Hospital) and Brit Long, MD (@long_brit, EM Attending Physician at SAUSHEC)

A 26-year-old male is brought to the emergency department after a being involved in a motorcycle collision. The patient was wearing a partial face helmet and was ejected approximately 30 feet. Upon presentation, the patient is awake, alert, and oriented, with abrasions over his exposed skin. What do you do next? 

Why do we care about motorcycle injuries?

In 2014, according to the National Highway Traffic Safety Administration, the number of deaths on motorcycles was over 27 times the numbers of cars. Over a decade’s worth retrospective data from Alberta, Canada, showed that motorcyclists are 3.5 times more likely to get injured or die in comparison to other drivers. According to 2014 from the U.S. Department of Transportation, the majority of motorcycle injuries and fatalities occur between the hours of 3pm and midnight, sometimes the busiest times in our emergency departments (“III: Motorcycle Crashes”, Aug 2016).

Why are motorcycles prone to crashing?

  1. They drive differently than cars

Not all motorcycles have antilock brakes. Braking a motorcycle is different than braking a car in that there are separate brakes for each wheel, and braking hard can lock the brakes, causing the motorcycle to roll over. Additionally, there rarely are airbags on motorcycles. The first motorcycle with airbags became available only in 2006 (“III: Motorcycle Crashes”, Aug 2016).

  1. Motorcycle passengers are at a higher risk

In a retrospective study from a trauma center in Singapore, passengers of motorcycles were more likely to have fatal injuries than the drivers after a crash (Leong et al., 2009). Fitzharris et al. (2009) found that pillion riders (i.e., those riding behind the motorcycle driver) were more likely to sustain lower extremity crush injuries.

  1. Motorcycles don’t have to drive on the road

A 2010 Australian study showed that even as on-road motorcycle accidents were decreasing, the overall number of motorcycle crash fatalities were increasing, likely due to off road accidents (Mikokca-Walus et al., 2010). Some of these off road accidents may occur because riders are frequently younger and unlicensed and are driving off-road because they are not legally permitted to operate motorcycles on roads (Pym et al., 2013).

  1. Riders aren’t restrained by the vehicle

It goes without saying that motorcycles don’t have seatbelts (and this is probably for the best), but the vehicle does also not contain a motorcycle driver after a collision, allowing for ejection of the driver. In a Chinese study, injury severity correlated with ejection velocity of motorcycle drivers (Chen et al., 2010). This compounds the number of injuries that a motorcycle driver can possibly sustain – for example, blunt trauma from a high fall if the rider is ejected; blunt trauma from a collision with a stationary object; and skidding across the ground.

  1. Motorcycles are missed by other vehicles

Motorcyclists are often taught to “slice and dice” (moving to leftmost lane of a multi-lane road in order to minimize hazards on their left side) and “split” lanes of traffic (moving between cars to avoid hazards), these practices can decrease visibility for drivers in cars (“How to ride in heavy traffic”). Additionally, motorcyclists may travel in groups, and slower riders can get separated, allowing them to be missed (“Group riding: safety in numbers”).

Motorcycle personal protective equipment (PPE) is not the same as in cars

  1. PPE is not required, but serious bikers will use it

The U.S. Armed Forces require motorcycle drivers to wear helmets, eye protection, above the ankle footwear, long sleeved shirts or jackets, pants that meet the top of the riding boot, full fingered riding gloves made from abrasion-resistant material, ideally in reflective or high visibility colors and materials (“Motorcycle PPE”). If a driver is not required to wear this gear by the military, there are very few requirements on PPE.

Many motorcycle interest groups and insurance forums recommend that motorcyclists wear protective gear, including specialized foam padded gear called “armor.” These jackets, pants, and gloves are covered in shred resident fabric to protect the rider should they skid on the ground. Additionally, specialized waterproof gear is recommended for inclement conditions, as motorcyclists are continually exposed to the elements. These garments are often thick and may be difficult to remove. Additionally, during short trips or hot weather, some cyclists often forgo this protective equipment, leading to increased rates of injury (“The 5 pieces of gear”, “Motorcycle safety gear”, “Personal protective gear”, de Rome et al., 2006).

  1. A comment on helmets in particular

In the 1960s and 1970s, mandatory helmet laws were required in order for states to receive federal highway and transportation funding, but by 1976, this requirement was repealed. Now, only19 states and the District of Columbia have universal helmet laws, requiring a motorcyclist to use a helmet at all times, and three states (Iowa, Illinois, and New Hampshire) have no helmet requirement (“Motorcycle helmet use”).

In 1997, after Arkansas repealed its mandatory motorcycle helmet law, epidemiologic studies showed an increase in fatalities in unhelmeted motorcycle accidents, longer ICU stays, and increased hospital financial burden (Bledsoe et al. 2002) and an increase in the number of alcohol related unhelmeted motorcycle fatalities (Bledsoe and Li, 2005).

A similar epidemiological study found that states with universal helmet laws, in comparison to those with laws only requiring helmets for riders under age 21, had decreased rates of traumatic brain injuries (TBI), less TBI associated disability, and lower rates of in-hospital death (Weiss et al., 2010). Several retrospective studies have shown that unhelmeted motorcycle drivers are more likely to sustain facial injuries (Crompton et al. 2012 and Christian et al. 2014). Motorcyclists wearing open face helmets were twice as likely to sustain injuries requiring operative intervention in comparison to those wearing full-face helmets in a retrospective Brazilian study (Cini et al., 2014). In a 2008 Cochrane review of 61 observational studies, motorcycle helmet use was associated with a reduction of risk of death by 42% and head injury by 69% in motorcycle accidents (Liu BC et al., 2008).

Where do motorcyclists get injured?

For motorcyclists in Maryland, the most common cause of accidents was a collision with another vehicle or fixed object (e.g., parked car, curb, guardrail, tree) (Dischinger et al., 2006).  Head and neck trauma is most common cause of fatal injury, followed by thoracic cage trauma (Ankarath et al., 2002), however, injuries to the extremities are more common (Doyle et al., 1995).

What’s road rash?

Road rash is a medical colloquialism for the wounds that result when a rider’s unprotected skin scrapes along a surface, usually asphalt, cement, or the ground. These wounds can manifest as abrasions, avulsions, or lacerations and are classified, like burns, by the depth of skin involvement. Although superficial injuries may only require good wound care including topical antibiotic ointment and pain control, deeper wounds may require excision and/or grafting, especially if abrasions cross joints. Additionally, asphalt particles may embed within the dermis and become re-epithelialized, causing skin tattooing (Fantus and Rivera, 2015).

What about high-risk groups?

Older riders present a particular risk during an accident. In 2014, riders over 40 accounted for over half of motorcyclist fatalities.  Older riders had a higher rate of upper trunk injuries and fractures, as well as internal organ injuries and brain injuries. This may be secondary to changes in bone strength, fat distribution, and chest wall elasticity with age, as well as a higher rate of co-morbid conditions (Jackson and Mello, 2013).  Motorcyclists operating large engine motorcycles (greater than 1L) were more likely to roll over, and had increased risk of head injury. Younger drivers (under age 40) were less likely to wear helmets and more likely to have head injuries. Riders over 40 were found to have significantly higher incidence of thoracic injuries and more likely to have multiple rib fractures (Dischinger et al., 2006).  Additionally, obese riders are also at risk for different injuries. In a four year review of the Trauma Registry System, riders with a body mass index (BMI) over 30 had an increased risk of humeral, pelvic, and rib fractures, and lower rates of maxillary and clavicle fractures (Liu et al., 2016).

Multiple studies have shown that intoxicated drivers have an increased risk of injury. In a retrospective study in Taiwan, where motorcycles are not allowed on highways, and most accidents occur in urban areas, intoxicated motorcyclists were more likely to not be wearing helmets but tended to have less severe injuries than sober motorcyclists. Authors attributed this difference to inattention being the most common cause of accident in intoxicated motorcyclists in comparison to sober motorcyclists.  However, unhelmeted intoxicated motorcyclists had a higher rate of severe head injury (e.g., cranial fracture, intracranial hemorrhage, cerebral contusion) (Liu et al., 2015). A review of the National Trauma Database found that alcohol and tobacco use were associated with decrease in helmet use (Lastfogel et al., 2016).

What else should I know about motorcyclists?

  1. Outlaw motorcycle gangs (OMGs) are a real thing in the U.S.

These criminally involved gangs take the name “one-percenter” motorcycle clubs, after a representative from the American Motorcycle Association stated that “there are 1% who are not [law-abiding]” after a motorcycle rally in Hollister, California, turned violent in 1947. There are multiple different types of these clubs, ranging from large clubs like Hells Angels and the Pagans, to less criminally active support clubs, like the Gray Ghosts. Gangs can be involved in alliances and feuds with other gangs in the area.

Patches and tattoos can give indication as to a gang member’s history. Jackets, referred to as “colors” made of leather or denim, will frequently have patches that show their wearer’s gang, chapter, and affiliates. Bikers have reacted hostilely when colors are damaged or treated without respect. Frequently, bikers have weapons on them; these may not be limited to guns and knives. For example, Hells Angels are known to carry hammers.

In addition, many of these gangs may be prone to respond aggressively to interpersonal violence between different OMGs. Although patients may be unwilling to go into detail about how injuries were sustained, it is important to ascertain whether the OMG member was injured in an altercation, involved in a motor vehicle collision with another member of an OMG, or involved in single person motor vehicle collision, in order to prevent violence with the emergency department (Bosmia et al., 2014 and Quinn and Forsyth, 2011).

  1. But most motorcyclists aren’t in gangs

According to a Media Audit survey, the majority of motorcycle owners are married, an average age of 41 years, and make higher than the average annual income (“Motorcycle Culture”).


  1. Motorcyclists are at high risk of injury because riding a motorcycle is inherently riskier than a car.
  2. Helmets decrease injuries.
  3. Older riders are more likely to have more severe thoracic injury.
  4. Be aware of the OMGs in your area, but don’t think that every motorcyclist is in one.


In the words of Hunter S. Thompson (which is likely applicable to most EM physicians):

“Life should not be a journey to the grave with the intention of arriving safely in a pretty and well preserved body, but rather to skid in broadside, in a cloud of smoke, thoroughly used up, totally worn out, and loudly proclaiming, ‘Wow! What a Ride!’”


References / Further Reading

  1. Bledsoe GH and Li G. Trends in Arkansas motorcycle trauma after helmet law repeal. Southern Medical Journal 2005; 98(4):436-440.
  2. Bledsoe GH, Schexnayder SM, Carey MJ, et al. The negative impact of the repeal of the Arkansas motorcycle helmet law. J Trauma. 2002 Dec;53(6):1078-86
  3. Bosmia AN, Quinn JF, Peterson TB, et al. Outlaw Motorcycle Gang: Aspects of the One-Percenter Culture for Emergency Department Personnel to Consider. Western J Emerg Med. 2014;15(4):523-528.
  4. Chen H-B, Hang J-J, Zhang B, et al. Establishment of the model of motorcyclist ejection injury. Chinese Journal of Traumatology 2010; 13(2):67-71
  5. Christian JM, Thomas RF, and Scarbecz M. The incidence and pattern of maxillofacial injuries in helmeted versus non helmeted motorcycle accident patients. J Oral Maxillofac Surg 2014, 72:2503-2506.
  6. Cini MA, Prado BG, et al. Influence of type of helmet on facial trauma in motorcycle accidents. British Journal of Oral and Maxillofacial Surgery 52 (2014) 789–792.
  7. Crompton JG, Oyetunji TA, Pollack KM et al. Association between helmets and facial injury after a motorcycle collision. Arch Surg. 2012;147(7):674-676.
  8. de Rome L Brandon T. (2007), A Survey of Motorcyclists in NSW, 2006: A report to the Motorcycle Council of NSW,Produced by LdeR Consulting for the Motorcycle Council of NSW, Inc., 15 Huddleston Street, Colyton
  9. Doyle D, Muir M, Chinn B. Motorcycle accidents in Strathclyde region, Scotland during 1992: a study of the injuries sustained. Health Bull. (Edinburgh), 53 (6) (1995), pp. 386–394.
  10. Fantus RJ and Rivera EA. Hit the road, jacked – road rash injures. Bulletin of the American College of Surgeons, 2015 June, 100(6):49-50
  11. Dischinger PC, Ryb GE, Ho SM, Braver ER. Injury Patterns and Severity Among Hospitalized Motorcyclists: A Comparison of Younger and Older Riders. Annual Proceedings: Association for the Advancement of Automotive Medicine (2006); 50:237-249.
  12. Fitzharris M, Dandona R, Kumar GA, Dandona L. Crash characteristics and patterns of injury among hospitalized motorised two-wheeled vehicle users in urban India. BMC Public Health 2009;9:11.
  13. “Group Riding: Safety in Numbers.” Motorcycle Safety. DMV.org. Web. “How to ride in heavy traffic.” Motorcycle Safety. DMV.org. Web. http://www.dmv.org/how-to-guides/motorcycle-traffic.php 22 Aug 2016.
  14. “How to ride in heavy traffic.” Motorcycle Safety. DMV.org. Web. http://www.dmv.org/how-to-guides/motorcycle-traffic.php 22 Aug 2016.
  15. Jackson TL and Mello MJ. Injury patterns and severity among motorcyclists treated in US emergency departments, 2001-2008: a comparison of younger and older riders. Inj Prev 2013;19:297-302 doi:10.1136/injuryprev-2012-040619
  16. Lastfogel J, Soleimani T, et al. Helmet Use and Injury Patters in Motorcycle-Related Trauma. JAMA Surg. 2016;151(1):88-90. doi:10.1097/SLA.
  17. Leong QM, Shyen KGT, et al. Young adults and riding position: factors that affect mortality among inpatient adult motorcycle casualties: a major trauma center experience. World J Surg (2009); 33:870-873
  18. Liu BC, Ivers R, Norton R, Boufous S, Blows S, Lo SK. Helmets for preventing injury in motorcycle riders. Cochrane Database of Systematic Reviews 2008, Issue 1. Art. No.: CD004333. DOI: 10.1002/14651858.CD004333.pub3.
  19. Liu H-T, Liang C-C, Rau C-S, et al. Alcohol-related hospitalizations of adult motorcycle riders. World Journal of Emergency Surgery 2015, 10(2): 1-8.
  20. Liu H-T, Rau C-S, Wu S-C, et al. Obese motorcycle riders have a different injury pattern and longer hospital length of stay than the normal-weight patients. Scandinavian Journal of Trauma, Resuscitation, and Emergency Medicine 2016, 24(50):1-9.
  21. Mikocka-Walus A, Gabbe B, Cameron P. Motorcycle-related major trauma: On-road versus off-road incidence and profile of cases. Emergency Medicine Australasia (2010); 22:470-476.
  22. “Military motorcycle PPE comparison chart.” org, Nov 2011. Web. http://www.motorcycleppe.com/ 22 Aug 2016.
  23. Monk JP, Buckley R, Dyer D. Motorcycle-related trauma in Alberta: A sad and expensive story. Can J Surg. 2009;52(6):235-240.
  24. Motorcycle Crashes.” III. Insurance Information Institute, Aug. 2016. Web. http://www.iihs.org/iihs/topics/t/motorcycles/fatalityfacts/motorcycles. 19 Aug. 2016.
  1. “Motorcycle Culture.” BScene Magazine. Sept 2012. Web. http://www.bscenemag.com/b-culture/motorcycle-culture. 22 Aug 2016.
  2. Motorcycle helmet use.” Insurance Institute for Highway Safety: Highway Loss Data Institute. Insurance Information Institute, Aug. 2016. Web. http://www.iihs.org/iihs/topics/laws/helmetuse/mapmotorcyclehelmets. 22 Aug. 2016.
  1. “Motorcycle Safety Gear: Safety Trumps Style.” Allstate Insurance, Web. https://www.allstate.com/tools-and-resources/motorcycle-insurance/tips-for-buying-motorcycle-safety-gear.aspx. 22 Aug 2016.
  2. National Highway Traffic Safety Administration. 2016. Traffic safety facts, 2014: motorcycles. Report no. DOT HS-812-292. Washington, DC: US Department of Transportation.
  3. “Personal Protective Gear for the Motorcyclist.” Cycle Safety Information. Motorcycle Safety Foundation, https://msf-usa.org/downloads/Protective_gear_REV.pdf. 22 Aug 2016.
  4. Pym AJ, Wallis BA, Franklin RC, Kimble RM. Unregulated and unsafe: the impact of motorcycle trauma on Queensland children. Journal of Paediatrics and Child Health (2013); 49:493–497.
  5. Quinn JF and Forsyth FJ. The Tools, Tactics, and Mentality of Outlaw Biker Wars. American Journal of Criminal Justice 2011; 36(3):216-230.
  6. “The 5 pieces of gear that you need to ride a motorcycle.” Best beginner motorcycles, March 2015. Web. http://www.bestbeginnermotorcycles.com/5-pieces-gear-you-need-ride-motorcycle 22 Aug 2016.
  7. Weiss H, Agimi Y, and Steiner C. Youth motorcycle-related brain injury by state helmet law type: United States 2005-2007. Pediatrics 2010 Dec;126(6):1149-55. doi: 10.1542/peds.2010-0902. Epub 2010 Nov 15.

Modern-Day Burn Resuscitation: Moving Beyond the Parkland Formula

Authors: Mary Ellen Billington, MD (EM Resident Physician, Parkland Memorial Hospital, Dallas, TX) and Brett D. Arnoldo, MD, FACS (Associate Professor, Department of Surgery, Parkland Memorial Hospital, Dallas, TX) // Edited by: Erica Simon, DO, MHA (@E_M_Simon) & Alex Koyfman, MD (@EMHighAK, EM Attending Physician, UTSW Medical Center / Parkland Memorial Hospital)

In the midst of a busy ED shift, a patient arrives by EMS. You immediately recognize the distinctive odor: a dry and unfortunately singed smell lingers in the air. As the catecholamines surge, you recognize your own tachycardia: it’s time to see a burn victim.

Thoughts race through your mind: What’s that  formula for fluid resuscitation? What rate do I use for the lactated ringers? What are the criteria that determine the need for burn center care? Where is my co-oximetry equipment?

Step away from your MDCalc – we’re going to calm that scorching stress-induced acid reflux with an update on the emergency department management of burns.

Mental Road Map

To adequately manage the burn victim, the emergency medicine physician must remember three key guidelines:

  1. The burn patient is a special type of trauma patient.
  2. The burn patient may be a toxicological patient.
  3. The burn patient requires comprehensive evaluation and management, and is best served by transferring to a burn center in accordance with ABA (American Burn Association) guidelines.

The Burn Patient is a Special Type of Trauma Patient

Begin with the ABCs: Is the airway intact? Is there concern that the airway may be lost? What is the patient’s projected course?

  • If the airway is not protected: intubate.
  • Signs of impending airway compromise include: stridor, wheezing, subjective dyspnea, and a hoarse voice.1
    • Severe burns to the lower face and neck may develop significant edema predisposing to airway obstruction.1
    • A history of the inhalation of superheated air, or steam in a confined space, is concerning for severe bronchial injury.1
    • Keep in mind that perioral burns and singed nasal hairs mandate an examination of the oropharynx for mucosal injury, however, these findings alone do not indicate airway involvement.2
    • Smoke inhalation victims may develop delayed respiratory failure: when in doubt, admit for observation and bronchoscopy.3
  • Projected Course: patients with burns involving >60% total body surface area (TBSA) tend to deteriorate rapidly: consider immediate intubation.1
  • Keep in mind that patients possessing burns involving a lower percentage of TBSA (e.g. < 40%), may require intubation if significant volume resuscitation is required.1
  • If the airway is intact, and the history and physical are not consistent with inhalational injury, it is prudent to administer oxygen by nasal cannula or face mask.1

Aside from airway concerns, complete your primary and secondary surveys and treat life-threatening emergencies as appropriate:

  • Consider a cervical collar if the mechanism is appropriate (blast injuries), or when doubt surrounds the circumstances of the injury.
  • Remember that full-thickness burns to the chest wall may lead to mechanical restriction of ventilation: consider escharotomy.1,3
    • Note: It is advised that escharotomies be performed in cooperation with a burn surgeon.4

In terms of fluid resuscitation:2

  • Burns <15% TBSA generaly require only PO fluid resuscitation.
  • Obtain large bore PIV access: two sites recommended for burns >40% TBSA.
  • Despite popular belief, IV access may be obtained through burned skin; ensure that lines are  well secured.
  • Obtain IO access if unable to obtain IV access.
  • Central lines equipped with invasive monitoring devices may provide useful volume-status metrics to guide resuscitation.

The What, When, and How Much of Fluids

  • In order to determine the volume of fluid resuscitation required for a burn patient, the Rule of Nines for adults and the Lund and Browder chart for children should be utilized (Figures 1 and 2 below).1,2
  • Remember: do not include first degree burns in the calculation of % TBSA.2
  • The over-estimation of % TBSA may result in hypervolemia, predisposing to a number of dangerous conditions:4
    • abdominal compartment syndrome
    • extremity compartment syndrome(s)
    • intraocular compartment syndrome
    • pleural effusions
Figure 1. Rule of Nines (Reference 5)
Figure 1. Rule of Nines (Reference 5)
Figure 2. Lund & Browder Chart (Reference 5)
Figure 2. Lund & Browder Chart (Reference 5)

Fluid Formulas:

  • The Parkland (or Baxter) Formula is possibly the most well-known and widely utilized formula:
    • 4 mL x weight in kg x % TBSA (up to 50%) = total volume of lactated ringers (LR) required for resuscitation
      • Half of the total volume is administered over the first 8 hrs post injury; the remaining, over the following 16 hours.
    • It is important to note that this formula is not universally accepted. Current trends in burn management literature emphasize a clinical assessment of volume status as essential in guiding fluid administration.1,2 Early consultation with a burn center is advised.1,2
  • The Advanced Burn Life Support (ABLS) handbook recommends the following for fluid resuscitation:
    • 2-4mL x kg body weight x % TBSA burn = volume of LR required for adult resuscitation (formula adjusted to 3-4mL x kg body weight x % TBSA burn for pediatric patients).6
      • Half of the total resuscitation volume is given over the first 8 hours, with administration of the remaining half titrated to patient response (urine output of 0.5mL/kg/hr for adults and 1mL/kg/hr for children).6
  • Inhalation injuries most commonly increase fluid resuscitation requirements.2
  • All resuscitation measures should be guided by perfusion pressure and urine output:4
    • Target a MAP of 60 mmHg, and urine output of 0.5-1.0ml/kg/hr for adults and 1-1.5mL/kg/h for pediatric patients.
    • The placement of a radial or femoral catheter is advised.4
    • Heart rate, pulse pressure, capillary refill, and mental status should also be assessed when determining resuscitation adequacy.
    • Additional markers, i.e. – lactate, base deficit, intestinal mucosal pH, and pulmonary arterial catheters are of limited use, and demonstrate varied mortality benefit.

We saw that the Parkland Formula and ABLS handbook recommend the use of LR, but are there recommendations regarding the use of other fluids for burn resuscitation?

  • Generally crystalloid solutions should be infused during the initial 18-24 hrs of resuscitation.1,4
  • It is recommended that 5% dextrose be added to maintenance fluids for pediatric patients weighing < 20kg.1
  • Hypertonic solutions tend to decrease initial resuscitation volumes, but are associated with increased renal failure and death, and therefore should be avoided.2,4,8
  • Colloid administration is a topic of debate.
    • Extensive heterogeneity exists regarding the recommendation for albumin utilization:
      1. Previous studies assessing albumin delivery in burn resuscitation (the most recent >15 years ago) demonstrated no statistically significantly improvement in patient outcomes.3  Today, however, a number of burn experts argue the value of albumin administration in the post capillary leak time frame (>18-24 hours post injury)given it’s ability to decrease third spacing.Further large scale, randomized control trials are needed.3
    • Blood transfusion is considered immunosuppressive, and is associated with increased mortality in burn patients. Blood products should be withheld unless there is an apparent physiologic need.2,4

The Burn Patient May be a Toxicological Patient

 In the evaluation of a burn patient, be sure to obtain a thorough history from EMS or from the patient. Victims of enclosed-space fires may be exposed to toxic levels of carbon monoxide and cyanide:

Your patient is the victim of an apartment fire. He has what appears to be red-tinged skin in areas absent burn; he is neurologically depressed, and suddenly decompensates into cardiac arrest. What toxic exposure do you suspect? How do you confirm your diagnosis? How will you treat your patient?

  • Carbon monoxide (CO) poisoning may manifest with persistent neurologic symptoms or even as cardiac arrest. Despite the board-style vignette stated above, cherry-red skin is a neither sensitive nor specific finding.3
  • If you suspect CO poisoning, order a carboxyhemoglobin level.1 In a patient with CO poisoning, pulse oximetry readings will be falsely normal, and the PaO2 and % hemoglobin saturation on ABG will be unaffected.1
  • How do you use a carboxyhemoglobin level? Subtract the carboxyhemoglobin level from the pulse oximetry level to determine true oxygen saturation.
    • Interpreting levels:3
      • Non-smokers: up to 1% normal
      • Smokers: 4-6% common
      • Any reading >10% = concern for significant exposure
    • To treat the toxic exposure administer 100% O2. Hyperbaric oxygen may be also be considered.2

Your burn patient, despite initial resuscitative efforts, maintains a persistent lactic acidosis and develops S-T elevation on EKG. What toxic exposure do you suspect? How do you treat your patient? 

  • The spectrum of the clinical presentation of cyanide poisoning varies from mydriasis,  to tachypnea and central apnea, to hypotension, to loss of consciousness and seizures.1
  • If concerned for cyanide toxicity, initiate 100% O2 therapy and administer hydroxocobalamin, with consideration for sodium thiosulfate (slower mechanism of action).1 Note: The commercially available cyanokit contains hydroxycobalamin.
  • Be sure to rule out other etiologies of lactic acidosis: under-resuscitation, CO poisoning, or missed traumatic injury.2

Additional Resuscitative Therapies and Considerations for Transfer

 What other resuscitative treatments may be indicated? When should you transfer a burn patient to a designated burn center?

  • In the evaluation of a burn patient, screening laboratory studies are appropriate.
    • Consider: ABG and CXR; cardiac enzymes, and a carboxyhemoglobin level.1,3
  • Administer a tetanus vaccination in the emergency department if indicated.
  • Control pain and administer anxiolytics as required.
  • Monitor resuscitation: bedside ultrasound is useful in the assessment of intravascular volume. Place a foley catheter or perform suprapubic cystotomy to monitor urine output and reduce the risk of abdominal compartment syndrome.3
  • Avoid hypothermia: warm the resuscitation room, administer warm inspired air, apply warm blankets, infuse warmed fluids, and cover wounds with clean dry sheets.2,4
  • Treat inhalation injury as indicated: intubate, order aggressive pulmonary toilet + bronchodilator (albuterol) +/- N-acetylcysteine, aerosolized heparin, aerosolized TPA, recombinant human antithrombin, surfactant, inhaled NO, or ECMO if required (the majority of this will be addressed in an ICU setting).2
  • Consider escharotomy or lateral canthotomy if concern for hypoventilation or compartment syndromes.4
  • After initial stabilization, follow the American Burn Association (ABA) Guidelines for the transfer of patients to designated burn centers. Suggested criteria for transfer can be found on the ABA webpage: http://www.ameriburn.org/BurnCenterReferralCriteria.pdf

A few words on steroids and antibiotics – Today there is no data to support steroid administration in the setting of inhalation injury.2 Prophylactic antibiotics are also withheld in the setting of burn injuries as several studies have demonstrated their administration as promoting systemic fungal infection.2

Morality – The Baux Score (% TBSA + Age) has historically been utilized as a predictor of mortality.2


In treating a burn patient:

  1. Follow ATLS guidelines in the initial evaluation and resuscitation of the burn patient, with special attention to unique airway considerations.
  2. Evaluate the patient for signs of toxic exposures, particularly carbon monoxide and cyanide.
  3. The burn patient requires comprehensive care. Follow ABA guidelines when considering transfer.


  1. DeKoning E. Thermal Burns. In: Tintinalli JE, Stapczynski J, Ma O, Yealy DM, Meckler GD, Cline DM. eds. Tintinalli’s Emergency Medicine: A Comprehensive Study Guide, 8e. New York, NY: McGraw-Hill; 2016. http://accessmedicine.mhmedical. com.foyer.swmed.edu/content.aspx?bookid=1658&Sectionid=109438787.
  2. Friedstat J, Endorf FW, Gibran NS. Burns. In: Brunicardi F, Andersen DK, Billiar TR, Dunn DL, Hunter JG, Matthews JB, Pollock RE. eds. Schwartz’s Principles of Surgery, 10e. New York, NY: McGraw-Hill; 2014. http://accessmedicine.mhmedical. com.foyer.swmed.edu/content.aspx?bookid=980&Sectionid=59610849.
  3. Drigalla D, Gemmill J. Chapter 45. Burns & Smoke Inhalation. In: Stone C, Humphries RL. eds. CURRENT Diagnosis & Treatment Emergency Medicine, 7e.New York, NY: McGraw-Hill; 2011.http://accessmedicine.mhmedical.com.foyer.swmed.edu/content.aspx?bookid=385&Sectionid=40357261.
  4. Latenser BA. Critical Care of the Burn Patient. In: Hall JB, Schmidt GA, Kress JP. eds. Principles of Critical Care, 4e. New York, NY: McGraw-Hill; 2015.http://accessmedicine.mhmedical.com. foyer.swmed.edu/content.aspxbookid=1340&Sectionid=80027724.
  5. Remote Primary Health Clinic Manuals. Burns. 2014. Available from: https://rphcm.allette.com.au/publication/cpm/Burns.html
  6. American Burn Association. Advanced Burn Life Support Course Provider Manual. American Burn Association 2007.
  7. Lawrence A1, Faraklas I, Watkins H, Allen A, Cochran A, Morris S, Saffle J. Colloid administration normalizes resuscitation ratio and ameliorates “fluid creep”. J Burn Care Res. 2010 Jan-Feb;31(1):40-7. doi: 10.1097/BCR.0b013e3181cb8c72. PMID 20061836.
  8. Saffle JI. The phenomenon of “fluid creep” in acute burn resuscitation. J Burn Care Res. 2007 May-Jun;28(3):382-95. PMID 17438489

Managing a Massive Hemothorax: A Guide to Stabilizing Your Patient

Author: Erica Simon, DO, MHA (@E_M_Simon, EM Chief Resident at SAUSHEC, USAF) // Edited by: Alex Koyfman, MD (@EMHighAK, EM Attending Physician, UTSW Medical Center / Parkland Memorial Hospital) and Brit Long, MD (@long_brit, EM Attending Physician at SAUSHEC)

A 16 year-old male status post MVC rolls into the trauma bay.  While EMS personnel bag the patient, they identify him as the front seat passenger in an auto vs. semi.  Per witness reports, the young male was ejected nearly 200 feet from his vehicle.  Attempts at endotracheal intubation in the field failed secondary to his severe facial trauma.  Remarkably, the patient has a pulse; a c-collar and pelvic binder encircle his small frame.  A nurse calls out a manual BP of 72/41, a HR of 147, and your team goes to work.

Within minutes the patient is intubated and ventilated.  A compression dressing has slowed the bleeding from his large galeal avulsion to an ooze.  The rapid infuser is pumping in a unit of O+ PRBCs, and your EFAST exam identifies a right-sided hemopneuomothorax.

Suddenly, the patient’s BP plummets.  The head of the bed reports left tracheal deviation and a right hemithorax absent breath sounds.  You quickly perform a needle decompression.  As you puncture the pleura to place a chest tube, blood pours onto the floor for what seems like hours.  You know immediately that this is a massive hemothorax.  What do you do next?  Let’s take a few minutes to review.

Epidemiology of Hemothoraces

A hemothorax,  or a collection of blood in the pleural space, most commonly occurs secondary to penetrating or blunt chest wall trauma.1-5  In the United States, 70-80%1 of hemothoraces are due to motor vehicle collisions causing injury to mediastinal structures (the heart, major vessels, thoracic spine, intercostal or mammary arteries), the diaphragm, or the lung parenchyma.1-5 

Diagnosing a Hemothorax

Patient presentations of hemothoraces range from shortness of breath (25% of hemothoraces are associated with concomitant pneumothoraces6), to hemodynamic instability secondary to hemorrhagic shock.4  In the hemodynamically stable patient, a hemothorax is most commonly identified on CXR.4-5  Ideally, the CXR should be performed in the upright position in order to detect blunting of the costophrenic angle (equating to 150-300 mL of blood in the pleural space).4-6  See image A below.

Note: An inadequate upright CXR, or CXR performed in the supine position is often misleading secondary to posterior diaphragmatic layering of blood.  It is no surprise then that the sensitivity of a supine CXR in the detection of a hemothorax is reportedly 40-60%. In fact, studies have demonstrated only vague opacification of the hemithorax as detectable on supine CXR despite >1,000 mL of intrathoracic blood collection.5,6  See image B below.


What does this mean for the trauma patient for whom a supine CXR is likely to be performed?

If patient vital signs (hypoxia, persistent hypotension), mechanism of injury (penetrating injury), or physical exam (multiple palpable rib fractures, flail segment, significant chest wall ecchymosis or tenderness to palpation) lead you to suspect a hemothorax à Do not let the supine CXR convince you otherwise.

In the hemodynamically unstable patient, the EFAST or Extended Focused Assessment with Sonography for Trauma is most commonly utilized to identify a hemothorax given its speed of employment.  Several studies have identified the sensitivity of ultrasound in the detection of hemothoraces as comparable to chest radiographs:

In their 1996-2007 MEDLINE search, utilizing the OVID interface, McEwan and Thompson7 cite the following:

Author Patient Population Study Design Outcomes Key Result Study Limitation
Rothlin et al., 1993, Switzerland8 Adults (15-88yrs) with blunt thoracic or abdominal injuries.  US performed by surgeons and compared to CXR & CT. Prospective Study Utility of US to detect hemothorax. Sn = 81% 5 of 11 False negative reports ultimately identified as operator error.
Ma et al., 1995, U.S.9 245 Adults (18+) presenting to the ED with blunt or penetrating torso trauma.  US compared to CT, supine CXR, formal echo or chest tube. Diagnostic Cohort Utility of US to detect hemothorax. Sn = 96%      Sp = 100% Composite gold standard.
Ma et al., 1997, U.S.10 240 Adults (18+) presenting to the ED with blunt or penetrating torso trauma.  US compared to CT, supine CXR, formal echo or chest tube. Retrospective Analysis of 1995 Study Clinical utility of ultrasound vs. plain supine CXR. Sn US = 96.2% vs. CXR = 96.2%;          Sp US = 99.6% vs. CXR = 99.6% Patient population from 1995 study utilized.
Sisley et al., 1998, U.S.11,12 360 trauma patients presenting to the ED with blunt or penetrating torso trauma. Prospective Study Clinical utility of US vs. supine CXR Sn US = 97.5% vs. CXR = 92.5%;          Sp US =  99.7% vs. CXR = 99.7% Results compared to supine CXR vs. independent gold standard (CT).
Abboud & Kendall, 2003. U.S.13 155 trauma patients who underwent CT scan during their evaluation. Prospective Study Clinical utility of US Sn = 92%, Sp = 100% Composite gold standard.

Table adapted from McEwan and Thompson’s Emergency Medicine Journal article, 2007.7 Sn = Sensitivity.  Sp = Specificity.

What about CT?

CT remains the gold standard in the diagnosis and evaluation of hemothoraces.  In their 2007 retrospective study of 141 blunt chest trauma patients presenting to a Level 1 trauma center, Traub et al. noted a hemothorax as detectable in 25% of patients, having been previously diagnosed with a negative supine CXR.14

Managing a Hemothorax

Volume resuscitation remains the #1 priority.  Transfusion should be initiated as appropriate.  Early consultation for penetrating chest trauma is recommended.4  As the majority of hemothoraces arise from injured lung parenchyma and are commonly self-limited, management with chest tube thoracostomy is frequently adequate.5  The placement of a chest tube is therapeutic in that expansion of the lung with apposition of the visceral and parietal pleural aids in hemostasis.4  Drainage of blood from the parietal cavity also prevents the common complication of empyema or fibrothorax.4,5

To perform tube thoracostomy, a large-bore tube (32F to 40F) should be placed in the 4th or 5th intercostal space at the anterior axillary line, and connected to water seal and suction (20-30 mL H20).5  Re-expansion of the lung parenchyma and resolution of the hemothorax should be monitored with serial CXRs.5


What is of major concern is the management of a massive hemothorax, defined as an immediate blood loss of >1,500 mL upon chest tube thoracostomy, or blood loss of >200 mL/hr (3mL/kg/h) over 2-4 hours post thoracostomy procedure.16,17  These, in addition to the conditions listed below, are recommended considerations for urgent thoracotomy:

  • Increasing hemothorax demonstrated on repeat CXRs.5
  • Hypotension despite adequate blood replacement (when other sites of blood loss have been ruled out).5
  • Patient decompensation after initial response to volume resuscitation.5

An urgent/emergent thoracotomy should be performed as follows:


After the parietal pleura has been accessed, clamping of the lung hilum (pulmonary vasculature) may allow for the attainment of hemostasis.5

 It is important to recognize that persistent hypotension, despite intervention to address bleeding from the lung parenchyma/hilum, points to additional injury.  Perform a thorough patient assessment.  Consider clamping the aorta if the patient remains hemodynamically unstable (the patient may later undergo trans-esophageal echocardiogram to assess aortic injury in the OR).5,6

Special Topics – Auto-Transfusion

To date, one French case study detailed the use of pre-hospital autologous blood transfusion in the setting of life-threatening hemothorax.19  In the study, 18 patients with life-threatening hemothoraces received autologous blood obtained from the thorax; 13 survived to the hospital setting.  Post transfusion laboratory studies and vital signs for the 13 patients revealed: Hct decrease from 24 +/- 3 to 19 +/- 3 and SBP increase from 78 +/- 11 to 88 +/- 12 mm Hg.  Platelet count was noted as 90,800 +/- 21,400/cu mm, prothrombin time 48 +/- 3%, partial thromboplastin time 197 +/- 18%, and serum potassium levels 3.6 +/- 0.5 mmol/L. According to the authors, no serious complications related to auto-transfusion were deemed crucial to the patients’ survival.19

This is an area that requires further study as researchers have now determined the following:

  • There is a statistically significant increase in pro-inflammatory cytokines (IL-6, IL-8, TNFα, GM-CSF) in shed pleural blood when compared with samples from healthy controls (P <0.05). Cytokine levels in unprocessed shed pleural blood are approximately 10- to 100-fold higher compared with healthy control venous samples.20 Thus, these pro-inflammatory cytokines may inhibit healing and stimulate transfusion reactions through systemic inflammatory cascades.
  • Unprocessed shed hemothorax blood (USHB) is significantly depleted of coagulation factors as compared to venous blood: In a study of 22 patients undergoing sampling of hemothorax blood and venous blood s/p traumatic injury: the INR of USHB was >9 as compared to a venous blood INR of 1.1 (p< .001), the aPTT of USHB was >180 in contrast to 28.5 seconds in the venous blood sample (p< .001), and the fibrinogen of USHB was <50 in comparison to 288 mg/dL in the venous blood sample (p< .001).21 Therefore, it would seem that little benefit in terms of hemostasis may be achieved in the transfusion of USHB.
  • Also of note, in the same study, the mean Hct of USHB was found to be 26.4 in contrast to 33.9 for venous blood (p = .003); Hgb was 9.3g/dL in comparison to a venous blood level of 11.8 g/dL (p = .004), and the platelet count of the USHB was 53 in contrast to 174 K/μL in the venous blood sample (p < .001). Ultimately, a hemothorax volume of 726 mL was calculated to be equivalent to 1 U of red blood cells.21


The emergency physician’s role in addressing a hemothorax is first to make the diagnosis utilizing CXR, US or CT.  Hemothoraces should be managed with the placement of a chest tube to avoid the later complications of empyemas and fibrothorax.  Massive hemothoraces warrant volume resuscitation, consultation with a trauma surgeon, and performance of a thoracotomy.  Early identification and intervention is the key to limiting the morbitidy and mortality associated with hemothoraces.4-6

Key Pearls

  • Hemothorax presentation is variable
    • Step 1: Diagnose the hemothorax with CXR vs. US definitively with CT
    • If the mechanism suggests hemothorax = rule out hemothorax despite CXR findings (CT if patient hemodynamically stable)
  • Hemothorax Treatment = Chest tube
  • Massive Hemothorax Treatment = Transfuse, consult, thoracotomy PRN
    • If the patient is persistently hypotensive despite control of pulmonary bleeding => look for other etiologies
  • Auto-transfusion of unprocessed shed hemothorax blood => additional research needed


References / Further Reading

  1. Shorr R, Crittendenn M, Indeck M, Hartunian S, Rodriguez A. Bunt thoracic trauma. Analysis of 515 patients. Ann Surg. 1987;206(2):200-205.
  2. Meyer D. Hemothorax related to trauma. Thorac Surg Clin. 2007;17:47-55.
  3. Roodenburg B, Roodenburg O. Chest trauma. Anaesth Intensive Care. 2014; 15(9):411-414.
  4. Bernardin B, Troquet J. Initial management and resuscitation of severe chest trauma. Emerg Med Clin N Am. 2012;30:377-400.
  5. Eckstein M, Henderson S. Thoracic Trauma. Rosen’s Emergency Medicine. Ch 45, 431-458.e3.
  6. Meyer D. Hemothorax related to trauma. Thorac Surg Clin. 2007;47.
  7. McEwan K, Thompson P. Ultrasound to detect heamothorax after chest injury. Emerg Med J. 2007; 24(8):581-582.
  8. Rothlin M, Naf R, Arngwerd M, Candinas D, Frick T, Trentz O. Ultrasound in blunt abdominal and thoracic trauma. J Trauma. 1993; 34(4):488-495.
  9. Ma O, Mateer J, Ogata M, Kefer M, Witmann D, Aprahamian C. Prospective analysis of a rapid trauma ultrasound examination performed by emergency physicians. J Trauma. 1995; 38(6):879-885.
  10. Ma O, Mateer J. Trauma ultrasound examination versus chest radiography in the detection of hemothorax. Ann Emerg Med. 1997; 29(3):312-315.
  11. Sisley A, Rozycki G, Ballard R, Manias N, Salomone J, Feliciano D. Rapid detection of traumatic effusion using surgeon-performed ultrasonography. J Trauma. 1998; 44(2):291-297.
  12. Noble V, Nelson P. Manual of emergency and critical care ultrasound. (2011). Cambridge University Press, New York.
  13. Abboud P, Kendall J. Emergency department ultrasound for hemothorax after blunt traumatic injuy. J Emerg Med. 2003;25(3):181-184.
  14. Traub M, Stevenson M, McEvoy S, Briggs G, Lo S, Leibman S. Joseph T. The use of chest computed tomography versus chest x-ray in patients with major blunt trauma. Injury. 2007; 38(1):43-47.
  15. Kirsch T, Sax J. Tube Thoracostomy. Chapter 10. Roberts and Hedges’ Clinical Procedures in Emergency Medicine. p.189-211. Elsevier Saunders, Philadelphia, PA.
  16. Kortbeek J, Al Turki S, Ali J, Antoine J, Bouillon B, Brasel K, et al. Advanced trauma life supports, 8th editions, the evidence for change. J Trauma. 2008:64(6):1638-1650.
  17. Legome E, Shockley L. Trauma: A comprehensive emergency medicine approach. 2011. Cambridge University Press, New York.
  18. Jones R, Rivers E. Resuscitative Thoracotomy. Chapter 18. Roberts and Hedges’ Clinical Procedures in Emergency Medicine. p.325-339. Elsevier Saunders, Philadelphia, PA.
  19. Barriot P, Riou B, Vlars P. Prehospital autotransfusion in life-threatening hemothorax. Chest. 1988;93(3):522-526.
  20. Salhanick M, Sams V, Pidcoke H, Fedyk C, Scherer M, et al. Shed pleural blood from traumatic hemothorax contains elevated levels of pro-inflammatory cytokines. Shock. 2016;46(2):144-148.
  21. Salhanick M, Corneille M, Higgins R, Olson J, Michalek J, et al. Autotransfusion of hemothorax blood in trauma patients: is it the same as fresh whole blood? Am J Surg. 2011;202(6):817-821.

Pearls for the management of GSW associated traumatic injury

Author: Joshua Bucher, MD (Assistant Professor, Department of EM, Rutgers – RWJMS; Assistant EMS Medical Director, RWJ-MHS) // Edited by: Alex Koyfman, MD (@EMHighAK, EM Attending Physician, UTSW / Parkland Memorial Hospital) and Brit Long, MD (@long_brit, EM Attending Physician at SAUSHEC)


A 27-year-old male is brought in by EMS after sustaining several gunshot wounds. On arrival, the patient withdraws from painful stimuli, does not open his eyes and makes incomprehensible noises. His heart rate is 130 bpm, blood pressure 84/42, RR 26, and Sp02 88%. While preparing to begin resuscitation, what are the first and most important steps?


As with all critical patients, the first step is airway management. Care should be taken and best practices should be followed to allow for first pass success including preoxygenation if possible to avoid desaturation. Resuscitation before intubation if possible is important. The appropriate induction agent is of vital importance. Ketamine is associated with the most neutral hemodynamic properties, and it is also the ideal agent for head injured patients.1,2 By maintaining hemodynamic stability and its dissociative properties, it is useful to blunt the response to laryngoscopy. Fentanyl is another option as well at doses 3-5 mcg/kg IV.3

Gunshot wounds may directly involve airway structures. In that case, surgical airway may be preferred, compared to endotracheal intubation. Team preparation is key for this step, and verbalizing the need for potential surgical airway is essential.


Along with airway management, unless there is a focal neurologic injury, it is not necessary to perform cervical spine immobilization of patients suffering from gunshot wounds. This is based on a strong retrospective study as well as supported by the NAEMSP/ACS-COT position paper on spinal immobilization.4 Cervical spine immobilization can directly interfere with airway management, obscure the mouth opening, require increased laryngoscopic force and can lead to worse patient outcomes in the setting of a failed airway.5-7


Breathing can be significantly affected depending on where your patient has been shot. Any sign of a tension pneumothorax (decreased breath sounds on one side, tracheal deviation, or hemodynamic instability) needs to be immediately treated with needle decompression or finger thoracostomy followed by tube thoracostomy. A standard pneumothorax can be treated with tube thoracostomy, either during the primary survey or after. High flow NRB oxygen is indicated as well. A GSW to the abdomen may cause difficulty with ventilation due to pain or abdominal distention, and this needs to be monitored.

There have been some newer developments in the management of pneumo/hemothoraces. Inaba et al. described their experience using a smaller chest tube catheter for traumatic pneumo- or hemothoraces and found no difference in patient outcomes with 28-32 vs traditional 36-40 French chest tubes.8 Furthermore, Russo et al. studied a new method of using a pigtail catheter in a swine model vs traditional chest tube and found that both were able to drain the same amount of blood from a hemothorax.9 Although pigtail catheters have been used for pneumothoraces, this is a good step forward towards utilization of more patient oriented resources in the management of a hemothorax. The EAST guidelines currently recommend tube thoracostomy for all hemothoraces. They also suggest that occult pneumothoraces be treated with observation in a stable patient, even with positive pressure ventilation.10


The next step of the primary survey is circulation. At this point, fluid resuscitation should begin with blood products in the critically injured patient. Permissive hypotension should be considered to target a systolic of 90 mm Hg or a MAP or 45 – 50 mm Hg, although further prospective studies are required.11  In addition, blood products should be transfused in a 1:1:1 ratio of 6 units of PRBCs:6 units FFP:1 pack of platelets, based on the results of the PROPPR trial.12 Furthermore, crystalloid fluids should be limited unless absolutely necessary to maintain perfusion.13 Fluids can theoretically prohibit clotting and dilute hemoglobin carrying capacity, and this recommendation is supported by the EAST guidelines.14


Emergency department thoracotomy is a life-saving procedure for patients with a very low survival. The EAST guidelines define signs of life as pupillary response, ventilation, vital signs, cardiac electrical activity, or extremity movement. They released the following evidence-based recommendations.


Recently, there has been research looking at this issue. Inaba et al prospectively studied patients undergoing resuscitative thoracotomy in the ER and related it to the FAST exam. They found that if the FAST exam was negative for pericardial fluid or any cardiac activity, the sensitivity was 100% for predicting the patient would not survive.15  This can be added to the EAST guidelines to determine the efficacy and necessity of thoracotomy.


Resuscitative endovascular balloon occlusion of the aorta (REBOA) is a last-ditch procedure that can stop hemorrhagic shock in patients with bleeding below the diaphragm. The instrument is comprised of a sheath and balloon, which is inserted into the femoral artery and inflated at one of three areas in order to stop blood flow. This can be especially useful for pelvic fractures with hemorrhage or other intra-abdominal hemorrhagic processes. There currently is limited data since it is a novel device, but it appears to be promising for specific situations. You can read more about REBOA at http://lifeinthefastlane.com/ccc/resuscitative-endovascular-balloon-occlusion-aorta-reboa/.

Extremity Hemorrhage

I want to briefly mention two specific interventions that are geared towards pre-hospital providers. The first intervention is the use of tourniquets for extremity trauma. We now have a large body of literature that supports the use of tourniquets as a life-saving device for extremity trauma with minimal risk of side effects.16 Likewise, the use of clotting agents, such as the commercially named QuickClot agent, are safe and effective to stop bleeding and are recommended by the Tactical Combat Casualty Care guidelines for hemorrhage not amenable to tourniquet placement.16 These two options are highly efficacious and warrant our attention.

Case resolution:

The patient is intubated appropriately. Bilateral chest tubes are placed, with immediate return of 2L from the left chest and a large rush of air from the right. Massive transfusion protocol is activated, and the patient is immediately transfused blood and plasma products. An E-FAST is performed, showing no pericardial fluid but large intraabdominal fluid. The patient is taken to the operating room by the trauma team with successful repair of his thoracic and abdominal injuries and makes a full recovery.


Take Home Points

  1. Utilize ketamine for airway management as it is the most hemodynamically neutral agent.
  2. Use traditional large chest tubes for hemothoraces and large pneumothoraces.
  3. Aggressively resuscitate with blood products for the exsanguinating trauma patient.


References / Further Reading

  1. Bucher J, Koyfman A. Intubation of the Neurologically Injured Patient. The Journal of emergency medicine. 2015;49(6):920-927.
  2. Cohen L, Athaide V, Wickham ME, Doyle-Waters MM, Rose NG, Hohl CM. The Effect of Ketamine on Intracranial and Cerebral Perfusion Pressure and Health Outcomes: A Systematic Review. Annals of emergency medicine. 2014.
  3. Pouraghaei M, Moharamzadeh P, Soleimanpour H, et al. Comparison between the effects of alfentanil, fentanyl and sufentanil on hemodynamic indices during rapid sequence intubation in the emergency department. Anesthesiology and pain medicine. 2014;4(1):e14618.
  4. White Iv CC, Domeier RM, Millin MG, Standards, Clinical Practice Committee NAoEMSP. EMS Spinal Precautions and the Use of the Long Backboard -Resource Document to the Position Statement of the National Association of EMS Physicians and the American College of Surgeons Committee on Trauma. Prehospital emergency care : official journal of the National Association of EMS Physicians and the National Association of State EMS Directors. 2014;18(2):306-314.
  5. Gruen RL, Jurkovich GJ, McIntyre LK, Foy HM, Maier RV. Patterns of errors contributing to trauma mortality: lessons learned from 2,594 deaths. Annals of surgery. 2006;244(3):371-380.
  6. Santoni BG, Hindman BJ, Puttlitz CM, et al. Manual in-line stabilization increases pressures applied by the laryngoscope blade during direct laryngoscopy and orotracheal intubation. Anesthesiology. 2009;110(1):24-31.
  7. Goutcher CM, Lochhead V. Reduction in mouth opening with semi-rigid cervical collars. British journal of anaesthesia. 2005;95(3):344-348.
  8. Inaba K, Lustenberger T, Recinos G, et al. Does size matter? A prospective analysis of 28-32 versus 36-40 French chest tube size in trauma. The journal of trauma and acute care surgery. 2012;72(2):422-427.
  9. Russo RM, Zakaluzny SA, Neff LP, et al. A pilot study of chest tube versus pigtail catheter drainage of acute hemothorax in swine. The journal of trauma and acute care surgery. 2015;79(6):1038-1043; discussion 1043.
  10. Mowery NT, Gunter OL, Collier BR, et al. Practice management guidelines for management of hemothorax and occult pneumothorax. The Journal of trauma. 2011;70(2):510-518.
  11. Dunser MW, Takala J, Brunauer A, Bakker J. Re-thinking resuscitation: leaving blood pressure cosmetics behind and moving forward to permissive hypotension and a tissue perfusion-based approach. Critical care. 2013;17(5):326.
  12. Holcomb JB, Tilley BC, Baraniuk S, et al. Transfusion of plasma, platelets, and red blood cells in a 1:1:1 vs a 1:1:2 ratio and mortality in patients with severe trauma: the PROPPR randomized clinical trial. JAMA : the journal of the American Medical Association. 2015;313(5):471-482.
  13. Chatrath V, Khetarpal R, Ahuja J. Fluid management in patients with trauma: Restrictive versus liberal approach. Journal of anaesthesiology, clinical pharmacology. 2015;31(3):308-316.
  14. Cotton BA, Jerome R, Collier BR, et al. Guidelines for prehospital fluid resuscitation in the injured patient. The Journal of trauma. 2009;67(2):389-402.
  15. Inaba K, Chouliaras K, Zakaluzny S, et al. FAST ultrasound examination as a predictor of outcomes after resuscitative thoracotomy: a prospective evaluation. Annals of surgery. 2015;262(3):512-518; discussion 516-518.
  16. Defense Do. Tactical Combat Casualty Care Guidelines for Medical Personnel 2015.


CORE EM: Peri-Mortem C-Section

Originally published at CoreEM.net, who are dedicated to bringing Emergency Providers all things core content Emergency Medicine available to anyone, anywhere, anytime. Reposted with permission.

Follow Dr. Swaminathan and CORE EM on twitter at @EMSwami and @Core_EM

Written by: Allie Boyd, MD // Edited By:  Salil Bhandari, MD

Definition: A cesarean section preformed either during maternal cardiac arrest or during impending maternal cardiac arrest the primary goal of which is to increase the chance of successfully resuscitating the mother and, potentially, improving fetal survival.

Physiological Changes in Late Pregnancy

  • Blood volume and cardiac output increase by 30-40% above the nonpregnant state by 28 weeks
    • This hypervolemic state is protective for the mother, as fewer red cells are lost during hemorrhage
    • Clinical signs of maternal shock manifest only after 40% of maternal blood volume is lost
  • Late pregnancy is very susceptible to hypotension from compression of the inferior vena cava (IVC) in the supine position by the enlarged uterus
  • The enlarged uterus causes elevation of the diaphragm by about 4 cm, and results in a decrease in the functional residual capacity by about 20%

General approach to the pregnant trauma patient

  • Overall same general approach as in non-pregnant patients. Focus must always be on resuscitating the mother, not the fetus.
  • Special considerations in primary survey
    • Airway: There is physiologic narrowing of the upper airways in the third trimester
      • Use an endotracheal tube 1 size smaller.
      • Intubation medications are the same.
      • RSI is the preferred method of intubation for any indication in the third trimester due to the increased risk of aspiration.
    • Breathing: Pregnant patients are predisposed to rapid falls in Pa02 during apnea
      • Supplemental O2 should be provided for any pregnant patient being resuscitated regardless of saturation.
    • Circulation: Hypovolemia should be suspected before clinical signs of hypotension in trauma patients, as the state of hypervolemia and resulting hemodilution may mask underlying significant blood loss.
      • Aggressive volume resuscitation is encouraged regardless of blood pressure.
      • Resuscitation of the pregnant patient should include uterine displacement to relieve compression of the IVC and thus improve cardiac output and restore circulation.
        • Perform in any patient in whom the uterus could potentially cause compression regardless of gestational age or lack of knowledge of gestational age.
        • Traditional teaching: This can be done by tilting the backboard up a 30 degree angle to the left, but may be difficult to perform effective chest compressions while patient tilted
        • New model: It is more effective to manually move the uterus to the patient’s left with one or two hands during ongoing chest compressions, while patient remains flat on their back.

Decubitus Position - What-when-how.com

Purpose of Peri-Mortem C-Section (PCS):

  • Primary goal is improvement of maternal, not fetal, resuscitation
  • PCS decreases uterine compression on the IVC thus increasing venous return, resulting in improved maternal cardiac filling pressure.
  • PCS also allows for improved respiratory mechanics, as the diaphragm is lowered after the procedure

When to perform a PCS:

  • Traditional teaching: perform a PCS at 24 weeks in a peri-arrest or arresting mother, as a fetus is generally
    Size of Uterus in Pregnancy

    Size of Uterus in Pregnancy

    considered viable at 24 weeks gestational age.

    • At 24 weeks gestation, there is a 20-30% chance of extrauterine fetal survival if neonatal facilities are available.
  • New model: PCS is resuscitative hysterotomy for the mother
    • 24 week guideline is flawed
      • You will likely not have this information in this clinical setting.
      • Even the best ultrasound dating criteria is subject to 1-2 weeks of uncertainty.
      • PCS is primarily resuscitative for mother – best chance of saving the fetus is to save the mother.
    • Counter argument to new model: before 24 weeks gestation, the fetus is small and PCS will not have significant effect on maternal hemodynamics.
    • Alternate guide to perform PCS
      • There is a reported gestational age anywhere near viability
      • The abdomen is large, specifically if fundal height is above umbilicus
      • If baby looks big on ultrasound (may not have time to measure biparietal diameter, but can get a general sense of the size of the fetus)

How long after arrest do you have to perform a PCS?

  • Perform a PCS as soon as possible after maternal cardiac arrest.
  • After 4 minutes of maternal arrest there is a precipitous decline in fetal neurologic outcome and survival.
  • Despite decreased utility after 4 minutes for fetal survival, resuscitative hysterotomy will continue to hold benefits to the mother.

How to perform a PCS:

  • Make a vertical incision from xiphoid to the pubis using a scalpel (ideally #10 Blade)
  • Cut through subcutaneous tissue to get to peritoneal wall
  • Use fingers to bluntly dissect to the peritoneum
  • Cut through peritoneum vertically (ideally with scissors or use a scalpel to initiate an opening inferiorly)
  • Deliver the uterus, then cut into the lower half of the uterus vertically to avoid the placenta and then use scissors to extend the incision upwards until you reach the baby
  • Deliver the baby (neonate will likely need resuscitation)
  • Clamp and cut the umbilical cord
  • Place packing/towels in the opened uterus and abdomen

Below is a short blast talk on the Peri-Mortem C-Section from Core EM Faculty Salil Bhandari

Take home points:

  1. Think of PCS as a resuscitative hysterotomy primarily aimed at saving the life of the mother
  2. If you think PCS will improve maternal resuscitation, act quickly to start and complete the procedure
  3. The optimal surgical approach for a PCS is via a large vertical incision.


Ramanathan S, Porges RM. Anesthetic Care of the Injured Pregnant Patient. In Capan LM, Miller SM, Turndorf H Editors, Trauma Anesthesia and Intensive Care; J.B. Lippincott Company; 1991; 599-628.

Pimentel L. Mother and Child: Trauma in Pregnancy. Emerg Med Clin North Am. 1991 Aug;9(3):549-63. PMID: 2070767

Drost TF, Rosemurgy AS, Sherman HF, Scott LM, Williams JK. Major Trauma in Pregnant Women: Maternal/fetal Outcome. J Trauma. 1990 May;30(5):574-8. PMID: 2342141

Vanden Hoek TL, Morrison LJ, Shuster M, et al. Part 12: cardiac arrest in special situations: 2010 American Heart Association Guidelines for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care. Circulation. 2010;122(18 Suppl 3):S829. PMID20956228

O’Connor RL, Sevarino FB. Cardiopulmonary arrest in the pregnant patient: a report of a successful resuscitation. J Clin Anesth. 1994;6(1):66. PMID 8142104

Cordero DR, Toffle RC, McCauley CS. Cardiopulmonary arrest in pregnancy: the role of caesarean section in the resuscitative protocol. W V Med J. 1992;88(9):402. PMID: 1462532

Additional resources:

EMCrit: Peri-Mortem C-section

St. Emlyn’s: Peri-mortem C-section

JAMIT: Perimortem Caesarian Section

Geriatric Trauma and Medical Illness: Pearls and Pitfalls

Authors: Matthew R Levine, MD (Assistant Professor and Director of Trauma Services, Department of Emergency Medicine, Northwestern Memorial Hospital, Chicago, IL) and Lora Alkhawam, MD (Attending Physician, Duke Regional Hospital, Department of Emergency Medicine, Durham, NC) // Edited by: Erica Simon, DO, MHA (@E_M_Simon) and Alex Koyfman, MD (@EMHighAK, EM Attending Physician, UTSW / Parkland Memorial Hospital)

An 85 year-old male is brought in by EMS status post MVC. He is confused and unable to detail the events surrounding his accident. When questioned, he has no recollection of his PMHx, but repeatedly states that he is in pain secondary to his c-collar and backboard. Vitals: HR 70 and irregular, BP 110/65, RR 16, O2 sat 94% on room air. Primary and secondary surveys are remarkable only for scant wheezing upon pulmonary auscultation. GCS is 14 without focal neurologic deficits. As you contemplate the next steps in your patient evaluation, you scan your knowledge bank: What critical diagnoses should you be considering? Let’s discuss some pearls and pitfalls in addressing the geriatric trauma patient.



According to 2010 US Census data, adults > 65 years of age account for 14% of the current U.S. population.1,2 It is estimated that nearly one in five Americans will be elderly by the year 2050.1,2 Why is this relevant to the practice of emergency medicine? Approximately 1 million persons aged 65 and older are affected by trauma each year.3  In fact, trauma in the elderly accounts for $12 billion in annual personal and institutional medical expenditures, and $25 billion in total annual healthcare expenditures.4 While elderly patients comprise a small percentage of total major trauma patients (8-12%) presenting to emergency care centers, they represent a disproportionate percentage of trauma fatalities and costs (15-30%).4

To date, numerous studies have demonstrated mortality related to trauma as increasing with advancing patient age.5-7 In fact, the Major Trauma Outcome Study published in 1989 (n = 3,833 > age 65 and 42,944 < age 65) demonstrated mortality as rising sharply between the ages of 45-55 and doubling by age 75.5 This pattern occurred at all Injury Severity Scores (ISS), mechanisms, and body regions.5

Screen Shot 2016-08-20 at 1.43.38 PM

Representation of Trauma Mortality Data5

Today, we also know that advancing age is an independent risk factor for morbidity and mortality, despite lesser severity of injuries.1,2,5 However, while age has value in mortality projections for geriatric trauma patients presenting to the ED, literature suggests favorable functional outcomes for those who survive to hospital discharge.8 Therefore, age alone is not a criteria to deny or limit care in the elderly.9



 This review will highlight important differences in elderly trauma patients with respect to:

  • Triage
  • Pathophysiology in the Elderly
  • Mechanisms and Patterns of Injury
  • Trauma Bay Approach
  • Special Considerations

There will be many citations throughout, but please keep in mind the limitations of research in geriatric trauma:8

  • Few prospective randomized controlled trials
  • No widely accepted age cut-off (“elderly” used to characterize patients ages 45-80)6
  • Lack of a uniform definition of an elderly trauma patient
  • Limited current studies (majority based in the 1980s-1990s)


Triage of the Elderly Trauma Patient

In its statement regarding trauma in the elderly, the CDC notes: “under triage of the older adult population is a substantial problem.”10 Under triage is defined as a failure to transport a trauma patient to a state-designated trauma center.10 Why is this important? Current studies (Zafar et al. and Maxwell et. al, 2015) have identified a significant mortality benefit for elderly patients presenting to trauma centers having had repeat exposure to geriatric trauma.11,12 Zafar et al. reported elderly patients as 34% less likely to die in these trauma centers.11 While it is true that level 1 trauma centers traditionally have longer lengths of stay and higher total costs of care, a large percentage of elderly trauma patients survive discharge from these facilities.11,12 Elderly patients with multiple injuries benefit from trauma center care.11,12 The difficulty here is that standard adult EMS triage guidelines provide poor sensitivity for detecting older adults that require trauma center care.13 The under triage rate is reported as 50%14,15 in patients older than 65, versus 17.8% for those under 65.14 Given this data, several experts have concluded that an age threshold should be established which mandates triage to a trauma center (various age ranges (55-70) have been recommended).6,9,16,17,18

What difficulties are encountered in identifying trauma severity in the elderly population? Potential explanations for under triage of elderly trauma patients are: significant injury secondary to low energy mechanisms, and altered physiologic response to injury with aging.

  • The CDC recommends direct transport to a trauma center for any trauma patient age >65 with SBP <11010
    • What affect does this have on triage of the elderly population? One that is substantial:
      • Substituting SBP < 110 instead of SBP < 90 for patients older than 65 reduced under triage by 4.4%, while only increasing over triage by 4.3%.19

Once an elderly patient arrives at a trauma center, trauma team activation occurs significantly less often for elderly patients (14% vs 29%) despite a similar percentage of severe injuries (defined as ISS>15).l

  • The Eastern Association for the Surgery of Trauma (EAST) recommends a lower threshold for trauma team activation for patients 65 and older evaluated at trauma centers (level 3 evidence).20
    • Some trauma centers use age as mandatory criteria for trauma team activation. This is supported by data that 63% of elderly trauma patients with ISS > 15 had no standard physiologic activation criteria.20

Clinical implications: Have a low threshold for recommending EMS transport of elderly trauma patients to a designated trauma center, especially for patients with SBP < 110. Have a low threshold for activating the trauma team for elderly trauma patients.


Pathophysiology Concerns in the Elderly

No other population is more susceptible to serious injury secondary to low-energy mechanisms (particularly falls) than the elderly. The elderly are less able to compensate for physiologic stresses occurring during injury, and are more likely to suffer complications during treatment and recovery. Key reasons for this are:

  • Less physiologic reserve
  • Occult shock/misleading picture of stability
  • Comorbid illnesses (See Figure below)

Screen Shot 2016-08-20 at 1.49.35 PM

Comorbid Illnesses Contributing to Morbidity and Mortality in the Elderly

It is important to note that in elderly patients, profound shock may be present even in the setting of “normal” vital signs.  Pharmaceutical therapy in the elderly (beta blockers and calcium channel blockers) may prevent typical tachycardic responses in shock states.  Also significant, aging myocardium exhibits decreased sensitivity to endogenous catecholamines.

Blood pressures considered normal in young patients may represent hypotension when compared to baseline BPs in an elderly patient. A landmark article by Scalea et al. assessing early invasive (PA catheter) monitoring in elderly trauma patients demonstrated that the majority of trauma patients experienced profound perfusion deficits despite “normal” vital signs.19 In fact, a HR>90 and SBP<110 have been correlated with increased mortality in the elderly trauma population.19,21 What does this mean for the EM provider? The window to intervene may be narrow; delayed recognition of shock may postpone life-sustaining resuscitation.

What about additional markers of perfusion?

Multiple studies have demonstrated that elevated lactate levels (>2) or abnormal base deficit (<-6) are associated with major injury and mortality in trauma patients.23-25 One such study, performed in 1987, identified a venous lactate > 2.5 as a marker of occult hypoperfusion in 20% of the included geriatric patients.26 Lactate levels or ABG base deficit should be used as an adjunct to vital signs for early identification of perfusion deficits in elderly trauma patients.

Clinical implications: Avoid being falsely reassured by normal vital signs in elderly trauma patients. Use lactate levels or ABG with base deficit as adjuncts to vital signs to detect occult shock and guide resuscitation in unclear cases. Also use ECGs as an adjunct to detect silent ischemia as a response to the physiologic stress of trauma. Have a low threshold for admitting elderly trauma patients to an ICU.


Mechanisms and Patterns of Injury

Which mechanisms and patterns of injury are more concerning in the elderly? They all are.

More specifically, falls from ground level, head trauma, chest wall injuries, pedestrian struck by vehicle, and cervical spine injuries have a disproportionate burden on elderly patients.

Screen Shot 2016-08-20 at 1.51.54 PM

Falls are the most frequent cause of injury in patients > 65 years of age, and are the most common fatal accident in patients > 80 years of age.27 More than one third of elderly patients presenting to the ED post fall return to the ED, or die within one year of initial evaluation.28 Same level falls must not be minimized – they are ten times more likely to cause death in an elderly vs. non-elderly patient (25% vs 2.5%).29 Even falls that seem purely mechanical can be a sign of occult illness. It is imperative that emergency physicians perform a complete H&P for all elderly patients having experienced a fall for:

  • Sudden disturbances in cardiovascular/neurologic function
  • New/progression of underlying conditions or emerging infection
  • Intoxicants/medication effects
  • Environmental safety
  • Impact of injury on functional status/ability to care for self

Why are falls so devastating in the elderly population?

Age-related atrophy of the brain leads to increased potential space and shearing forces on the intracranial bridging veins when exposed to trauma. The risk of intracranial bleeding is also markedly increased with medications commonly prescribed to the elderly (anticoagulants and anti-platelets).30,31 Keep in mind that older patients are excluded from studies that attempt to identify populations in which imaging is low yield = IMAGE the elderly.

 Outside of head trauma, are there any other areas for EM docs to be on the lookout?

Even “minor” chest injuries impair the elderly. Thoracic cage trauma is poorly tolerated secondary to decreased compliance, loss of alveolar surface area, impaired lung defenses, and increased pulmonary bacterial colonization with aging. A rigid C-collar and backboard can further impair chest wall expansion. Elderly patients with rib fractures are at increased risk for pneumonia (31% vs. 17% with 16% increase per rib fractured), pulmonary contusion, and delayed hemothorax.32 Mortality also increases 19% per rib fractured.32

 The elderly spine is vulnerable to fracture from minor mechanisms due to conditions such as cervical stenosis, osteoporosis, and degenerative, rheumatoid, and osteoarthritis.33 High cervical fractures (type 2 odontoid being the most common), and central cord syndromes are also more frequent in the elderly.34

Pedestrian struck by a vehicle is perhaps the most devastating mechanism of injury to disproportionately affect this population. Patients age > 65 account for 22% of pedestrian vs. MVC deaths.33 Current statistics report 46% of these accidents as occurring in crosswalks.33 Factors that predispose the elderly to increased severity of injury include decreased ability to raise or turn the head due to cervical arthropathy, and reduced speed and agility (crosswalk timers often allow for a pedestrian speed of 4 ft/sec).33

Clinical implications: Maintain a heightened suspicion for significant injury (especially intracranial and C-spine pathology) even from ground level falls. Assess elderly patients for medical impairments that may have precipitated the fall. Be liberal with CT scanning for elderly head and neck trauma, and always inquire regarding the use of anticoagulant and antiplatelet medications. Ensure adequate analgesia and oxygenation for chest wall injuries. Remove the collar and backboard as early as safely possible. Maintain a low threshold for admitting elderly patients with rib fractures.


Special Considerations

 ABCs in the Elderly

  • A – Early airway control. Edentulous patients may be difficult to bag; remove dentures for intubation.
  • B – Avoid respiratory decompensation by use of O2; analgesia for chest injuries; suction/pulmonary toilet; clear the C-spine, and remove the backboard as early as possible to prevent respiratory impairment.
  • C – Early transfusion to minimize fluid overload from crystalloids. Recognizing that “normal” BP may be relative hypotension for an elderly patient. Question patients regarding anticoagulant use and consider reversal early in the course.
  • D – Liberal use of head and C-spine CT; GCS is not a sensitive indicator in the elderly trauma patient.
  • E – Assess for signs of comorbidities that may not have been reported (i.e. surgical scars, pacemakers, medications or med lists in patient belongings, medical alert tags, bruising from anticoagulants).

Elder Abuse

No report on elderly trauma is complete without mention of elder abuse. Elder abuse can be very difficult to detect for several reasons:

  • Patient reluctance to identify a loved one
  • Patient dependence on the abuser
  • Perceived frailty limiting the patient from feeling empowered in seeking help
  • Patient mental or memory impairment limits the history
  • Abuse in the form of neglect can mimic cachexia from comorbidities

Clinical implications: When the scenario has stabilized, assess the patient’s social situation. Be wary of wounds or injuries that are suspicious for abuse or do not match the reported mechanism of injury. And of course, ask the patient, preferably in private!

A Quick Word on Anticoagulants

Anticoagulant use is far more prevalent in the elderly population. An increasing portion of the elderly population are being prescribed novel oral anticoagulants, which are not as readily reversible as warfarin. An elderly trauma patient should be questioned regarding anticoagulants ASAP. An irregular heartbeat may be a clue to chronic atrial fibrillation and anticoagulant use. Know your institution’s reversal protocol for the novel anticoagulants. If your institution does not have a protocol, then have a plan in mind. Know which prothrombin complex concentrates are available to you. Know if Praxbind is stored by your pharmacy.

Back to the Case

The patient in the initial case presentation may have been exhibiting his normal baseline mental status or could have been confused secondary to the emotional distress pertaining to the accident, but the provider must assume the confusion secondary to intracranial bleeding until proven otherwise. The patient’s irregular heart rate should alert the clinician to the possibility of aspirin or anticoagulant use, necessitating a plan for reversal should it be needed. In terms of the rest of the vital signs: the patient’s “normal” blood pressure may actually represent relative hypotension. The borderline hypoxia (and wheezing discovered on exam) is likely related to lung injury, aspiration, or an underlying comorbidity (i.e. COPD or CHF). This should serve as a warning – the patient is high risk for respiratory decompensation from chest injury and impaired chest wall motion from the C-collar and backboard. The backboard should be removed as soon as possible, pain from the chest injury treated as applicable, and supplemental oxygen employed. Suction may be considered as an adjunct. If and when the C-spine is cleared, the patient should be placed in an upright position to facilitate gas exchange and decrease work of breathing. The patient may have critical injuries and blood loss despite minimal symptoms so a lactate or ABG for base deficit should be sent. Imaging to rule out internal injuries is a must. Initial diagnostic work-up and resuscitation should be aggressive until the patient’s prognosis and wishes are clear. Volume resuscitation should be minimized, with blood products being the fluid of choice. The clinician should have a low threshold for trauma team activation vs. consultation and admission.



  • Resuscitation of the elderly trauma patient must be thoughtful but aggressive:
    • Heighten awareness that with age, signs and symptoms may be minimal, and that the outcome is often initially unclear, and commonly, but not necessarily poor.
    • Up to 85% of elderly trauma survivors return to baseline or independent function.9
      • This justifies initial aggressive approach which can be reassessed later when patient/family wishes and prognosis becomes increasingly clear.9
    • Less physiologic reserve leaves little time for delays in diagnosis and under- or over- resuscitation.
    • Blood is the fluid of choice.
    • The principles of diagnosis and management in trauma are the same regardless of age, but the incidence of physiologic changes and disease states mandates a different overall approach.
    • You may be the only one in the room who knows how sick the patient really is.


References / Further Reading

  1. Hashmi A, Ibrahim-Zada I, Rhee P et al. Predictors of mortality in geriatric trauma patients: A systematic review and meta-analysis. J Trauma Acute Care Surg. 2014;76:894-901.
  2. Vincent GK, Velkoff VA, U.S. Census Bureau. The next four decades the older population in the United States: 2010 to 2050. Population estimates and projections P25-1138. Washington, DC: U.S. Dept. of Commerce, Economics and Statistics Administration, U.S. Census Bureau; 2010. Available from http://purl.access.gpo.gov/GPO/LPS126596.
  3. CDC National Center for Health Statistics (NCHS), National Vital Statistics System. http://www.cdc.gov/nchs/nvss.htm.
  4. CDC Data and Statistics (WISQARSTM): Cost of Injury Reports Data Source: NCHS Vital Statistics System for Numbers of Deaths. http://wisqars.cdc.gov/8080/costT/.
  5. Champion HR, Copes WS, Buyer D et al. Major trauma in geriatric patients. Am J Public Health. 1989;79:1278-1282.
  6. Bonne S, Schuerer D. Trauma in the Older Adult – Epidemiology and evolving geriatric trauma principles. Clin Geriatr Med. 2013;29:137-150.
  7. Goodmanson NW, Rosengart MR, Barnato AE et al. Defining geriatric trauma: When does age make a difference? Surgery. 2012;152:668-675.
  8. Grossman MD, Ofurum U, Stehly CD et al. Long-term survival after major trauma in geriatric trauma patients: The glass is half full. J Trauma. 2012;72:1181-1185.
  9. Jacobs DG, Plaisier BR, Barie PS et al. Practice Management Guidelines for Geriatric Trauma. The EAST Practice Management Guidelines Work Group. J Trauma. 2003;54:391-416.
  10. Sasser SM, Hunt RC, Faul M et al. Guidelines for field triage of injured patients: recommendations of the National Expert Panel on Field Triage, 2011. MMWR Recomm Rep. 2012 Jan 13;61(RR-1):1-20.
  11. Zafar SN, Obirieze A, Schneider EB et al. Outcomes of trauma care at centers treating a higher proportion of older patients: The case for geriatric trauma centers. Acute Care Surg. 2015;78:852-859.
  12. Maxwell CA, Miller RS, Dietrich MS et al. The aging of America: a comprehensive look at over 25,000 geriatric trauma admissions to United States hospitals. Am Surg. 2015;81(6): 630-636.
  13. Ichwan B, Subrahmanyam D, Shah MN et al. Geriatric-specific triage criteria are more sensitive than standard adult criteria in identifying need for trauma center care in injured older adults. Ann Emerg Med. 2015;65:92-100.
  14. Chang DC, Bass RR, Cornwell EE et al. Undertriage of elderly trauma patients to state-designated trauma centers. Arch Surg. 2008;143:776-781.
  15. Kodadek LM, Selvarajah S, Velopulos CG et al. Undertriage of older trauma patients: is this a national phenomenon? J Surg Research. 2015;199:220-229.
  16. Caterino JM, Valasek T, Werman HA. Identification of an age cutoff for increased mortality in patients with elderly trauma. Am J Emerg Med. 2010;28:151-158.
  17. Lehmann R. The impact of advanced age on trauma triage decisions and outcomes: a statewide analysis. Am J Surg. 2009 May; 197(5):571-4.
  18. American College of Surgeon Committee on Trauma. Geriatric Trauma. In: ATLS: student course manual. 8th Chicago. 2008:247-257.
  19. Scalea TM, Simon HM, Duncan AO et al. Geriatric blunt multiple trauma: improved survival with early invasive monitoring. J Trauma. 1990; 30: 129–136.
  20. Brown JB, Gestring ML, Forsythe RM et al. Systolic blood pressure criteria in the National Trauma Triage Protocol for geriatric trauma: 110 is the new 90. J Trauma Acute Care Surg. 2015;78:352-359.
  21. Calland JF, Ingraham AM, Martin N et al. Evaluation and management of geriatric trauma: An Eastern Association for the Surgery of Trauma practice management guideline. J Trauma Acute Care Surg. 2012;73:S345-S350.
  22. Heffernan DS,Thakkar RK, Monaghan SF, et al. Normal presenting vital signs are unreliable in geriatric blunt trauma victims. J Trauma. 2010;69(4):813-820.
  23. Zehtabchi S, Baron BJ. Utility of base deficit for identifying major injury in elder trauma patients. Acad Emerg Med. 2007;14:829-831.
  24. Callaway DW, Shapiro NI, Donnino MW et al. Serum lactate and base deficit as predictors of mortality in normotensive elderly blunt trauma patients. J Trauma. 2009;66:1040-1044.
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Penetrating Trauma: What We Miss and How We Can Improve

Authors: Elliott Chinn, DO (EM Resident Physician at Jacobi Medical Center) and Steve McGuire, DO (EM Chief Resident at Jacobi Medical Center) // Edited by: Alex Koyfman, MD (@EMHighAK, EM Attending Physician, UTSW / Parkland Memorial Hospital) and Brit Long, MD (@long_brit, EM staff physician at SAUSHEC, USAF)


During your next shift you hear “Level 1 Trauma in 5 minutes”. The patient arrives. He is a 28 year-old male, stabbed in the chest, with the following vitals: T 98.6 HR 95 BP 105/70 RR 20 PO2 98% RA. He’s talking, you see a 2 cm stab wound to the left subcostal region, his breath sounds are even bilaterally, and his repeat blood pressure is 115/80. He’s moving all of his extremities so you log roll him and see no other injuries. A supine chest x-ray is done which is negative, and a quick FAST is unrevealing. You step away for a brief moment to put in orders when you’re notified that the patient is lethargic and his heart rate jumped to 160. You put on your stethoscope, suspecting to hear decreased breath sounds and when you do, you place a 14g angiocath into his chest and “wwhheeww”, you and your patient release some tension.

What happened? What did you miss and why?

Your next patient is a 50 year-old male with abdominal pain. He doesn’t look so great and doesn’t offer much for medical problems. You notice an old, vertical scar on his chest. “Oh yeah doc, I was stabbed a long time ago”. His labs come back, and he has an elevated WBC and lactate. Hours later, he is in the OR for a strangulated hernia that was in his thorax, a complication of an undiagnosed diaphragmatic injury.

What happened? What did you and the previous doctor miss and why?

Hours later you see another stabbing victim, only this time the wound is just underneath his umbilicus. The puncture doesn’t look that deep, and the patient’s vital signs are stable. While he is complaining of pain, his abdomen doesn’t feel like a surgical abdomen. A CT scan is ordered and when it comes back it is negative. You scratch your head and think to yourself, “Can I send this patient home?”

What are you worried about missing and what can be done to reassure you?

Your next patient is here for left-sided back pain. He was just discharged four days ago after being shot in the stomach. He is febrile, tachycardic, and has no other medical or surgical history aside from his previous trauma. Hours later, your CT scan shows a perinephric abscess, and he’s admitted for IV antibiotics.

What happened? What did the surgeons miss and why?

Our role as ED physicians is to stabilize the patient while determining their disposition. Inevitably, we are going to miss things, as it isn’t our job to diagnose every injury. This post will discuss injuries we can miss related to penetrating trauma in the acute and post-discharge setting.

Case #1: Tension Pneumothorax

Tension pneumothorax (TPTX) is one of the deadliest, cannot miss diagnoses we are responsible for. We are trained to think of pneumothorax when we see respiratory distress, chest pain, and decreased lung sounds, and when paired with hypotension, tachycardia, and dropping PO2, we should reflexively think of tension pneumothorax. Primarily a clinical diagnosis, it should not be diagnosed radiographically.

In the real world, diagnosing a tension pneumothorax, let alone before x-ray, is not as easy as we are led to believe. A review of 18 case reports in awake, non-ventilated patients showed that “classic” signs such as low Sp02, tracheal deviation, and hypotension are found in less than 25% of cases (1). Furthermore, a case series of 115 consecutive tension pneumothoraces in South Africa showed that 25% were missed on initial assessment, with 40% of those patients dying (2). Even more concerning, that series took place in a region that gets 30 cases of tension pneumothorax a year, which is more than most U.S. hospitals see.

That study did not look into why the diagnosis was missed. Perhaps they stopped their diagnosis at pneumothorax because they didn’t see textbook signs that as it turns out, may not be so textbook. So, what can we do to make sure we do not miss this diagnosis?

First, always have a high index of suspicion for tension pneumothorax, taking into account many of the classic signs we are taught to look for are often not present. Second, confirm your clinical exclusion of the diagnosis with ultrasound, as it has been shown to have a higher sensitivity than upright or supine chest radiography and has a negative predictive value approaching 100% (3). Finally, avoid supine CXR at all cost. A recent article showed it has a significantly lower sensitivity than upright, only catching 21% patients with a pneumothorax (4).

Case #2: Diaphragmatic Injury

Missing a diaphragmatic injury will not immediately harm your patient; however, months to decades later it can have devastating consequences if not recognized.

The range of diaphragmatic injuries missed on CT scan ranges anywhere from 12-63%, but more disturbingly, the mortality rate for subsequent complications can be as high as 60% (5,6). One study found complications like herniated stomach, large gut, spleen, liver, and gangrenous gut if there is a delay in presentation, even “fecopneumothorax” if that herniated organ is mistaken for a pleural effusion on chest x-ray and a chest tube is placed (6).

The gold standard for diagnosing diaphragmatic injury is surgery, but in an era of increased nonsurgical management, some of these injures are missed. CT scan lacks the sensitivity and specificity of surgery, so we cannot rule it out with imaging alone. There is a wide range of sensitivity for picking it up on CT. One review article cited a range of 61-87%, while showing that sensitivity is worse when the injury is on the right due to the homogeneity between the liver and diaphragm (5). In one small but well conducted study, patients with penetrating trauma to the left thoracoabdominal area who went to the OR 48 hours after CT scan showed a sensitivity of 82%, with a negative predictive value of 93%.

What can we do as ED physicians to improve?  First, be specific in your indication for why you are getting a CT scan. Traumas can be chaotic environments, and we might overlook the importance of identifying entry points and mechanism when we order imaging which can be valuable clues to radiologists. One might be so bold as to say “rule out diaphragmatic injury” to further clue them in, as there are several direct and indirect signs of diaphragmatic injury on CT, some of which are more common in penetrating trauma.

While a missed diaphragmatic injury isn’t usually at the top of our differential for most chief complaints, it should at least be considered in a patient with a history of thoracoabdominal trauma. It is definitely one with serious morbidity/mortality if left undiagnosed and unfortunately, could present days to years down the line and seem completely unrelated to their past medical history.

Case #3: Hollow Viscus Injury

In penetrating abdominal trauma there are hard signs for going to the OR: hemodynamic instability, evisceration, or peritonitis. What should be done when there are no hard signs has been a matter of debate since the 1960s. In 2009 the Western Trauma Association put out a guideline which was again tested in 2011 that advocates for local wound exploration in stable patients who have anterior abdominal stab wounds (8). Their goal was to bring everyone to the OR who needed to be there while minimizing unnecessary surgery, procedures, and imaging.

Their guidelines were simple: if the patient is stable, perform local wound exploration and if it is positive, admit for serial clinical assessments with a CBC every 8 hours. If the patient deteriorates clinically, they go to the OR. If they were stable for a day then they could be discharged.

If wound exploration was negative then the patient could be discharged, without relying on a negative CT scan or labs.

It should be noted that they had a strict protocol for wound exploration, which required anesthetizing the wound and probing the entire depth. If posterior fascia or peritoneum were violated, it was considered positive.

How did it all pan out? Patients in the protocol group were significantly less likely to get an unnecessary laparotomy, and they were not at increased risk for complications. They were just as likely to be discharged from the ED, and none of them had a CT scan. Patients whose surgeons did not follow the protocol and used imaging or labs to guide their decision had more unnecessary procedures, with increased length of stay in the hospital and more complications. Most patients who went to the OR after being admitted for serial exams went within four hours, with the last patient going at 15 hours, and their rate of complications was not any higher than those who went straight to the OR.

In the past, local wound exploration has gotten a bad reputation. If you are still not a fan of it, you can still skip the reflex to go straight to the CT scanner as long as your patient is stable and your surgical service can observe them. One study found that no injuries were missed when a patient was observed for 24 hours, and those who waited to go to the OR did not have a higher rate of complications than those who went immediately (9). This is important because some clinicians think they can discharge patients home if their CT scans are normal when in fact it could be a false negative.  Additionally, there are cases of false positives on CT that lead to wasteful trips to the OR (8).

The point here has more to do with empowering us to not instinctively take our patients to the CT scan or push our surgeons, unnecessarily, to take our patients to the OR. This is an opportunity to not miss an injury by not doing something, which harms our patients in a way we cannot yet quantify.

To summarize, hollow viscous injury is a diagnosis we can miss if we don’t watch a patient for long enough, and research shows that 24 hours is the longest it will take your patient to deteriorate (9). Local wound exploration could be a tool to let us exclude the diagnosis without having to admit every single patient with penetrating abdominal trauma. We should allow our clinical exam to guide our management, not imaging or lab values.

Case #4: Ureteral Injuries

Surrounded by some significant real estate, the ureters are very well protected. If those organs are involved, a ureteral injury may be missed, so it must be on the differential in any patient who presents shortly after being discharged from a hospitalization related to penetrating injuries.

A well conducted review of ureteral injuries showed they mostly affect men who were victims of penetrating trauma, involved the proximal ureter (defined as from the ureteropelvic junction down to the sacroiliac joint), and actually lacked hematuria, regarded as some to be the hallmark of ureteral injury (10). 90% of the time there will be an associated injury, almost always (96%) bowel injuries.

As with other rare injuries, they require a high index of suspicion. Close to 38% of ureteral injuries can cause complications such as retroperitoneal abscess, infected urinoma, and fistula, but in rare circumstances they can lead to renal failure and sepsis. CT scan by itself isn’t the best way to diagnose it, and even when patients go to the OR it is missed about 40% of the time.

So what can we do to avoid this? In any penetrating trauma patient with hematuria, consider getting GU involved, especially if your patient is going to have to sit in your department . Specially timed CT scans (“delayed excretory phase images”) might be necessary to make the diagnosis in the acute setting. Understand that the absence of hematuria is actually more common in ureteral injuries, so its absence cannot exclude it. If the patient was recently discharged after sustaining penetrating trauma, have a high index of suspicion for this injury, as it could have been missed on initial presentation.


As ED doctors we play a critical role in trauma. Many of our patients who suffer injuries from penetrating trauma get admitted, ultimately receiving a “trauma tertiary survey” prior to discharge. This is a critical step in their care, and research shows that it transforms many “missed injures” into “delays in diagnosis”, meaning they are caught before they cause a problem (11).

In the acute setting the most important thing we can miss is a tension pneumothorax. Thankfully, ultrasound is accessible and with ultrasound education being integral in most residency training programs, it is only a matter of time until most ED doctors can rule it out nearly 100% of the time.

In the patient with a history of penetrating trauma we need to be aware of two injures that could have been missed: diaphragmatic tears and ureteral injuries. While CT scans can miss asymptomatic tears, they are quite good at diagnosing organs that have herniated through the diaphragm so if you are suspicious of it, order that CT scan. In any patient with abdominal or flank pain, fever, or urinary symptoms who has a history of penetrating trauma, consider ureteral injuries because you may need special imaging to diagnose it.

Finally, despite advances in imaging, hollow viscus injuries continue to be a diagnosis that can be missed in the absence of observation and serial abdominal exams. The utility of local wound exploration will likely be debated for some time, but there is growing evidence that it can be used to exclude hollow viscus injury if done appropriately while saving patients from unnecessary radiation and trips to the OR.

References / Further Reading:

  1. Leigh-Smith SS. Tension pneumothorax – time for a re-think? Emergency medicine journal: EMJ. 2005-01;22:8-16.
  2. Kong VV. Traumatic tension pneumothorax: experience from 115 consecutive patients in a trauma service in South Africa. European journal of trauma and emergency surgery (Munich: 2007). 2016-02;42:55-59.
  3. Nandipati KK. Extended focused assessment with sonography for trauma (EFAST) in the diagnosis of pneumothorax: experience at a community based level I trauma center. Injury. 2011-05;42:511-514.
  4. Ball CC. Occult pneumothoraces in patients with penetrating trauma: Does mechanism matter? Canadian journal of surgery. 2010-08;53:251-255.
  5. Panda AA. Traumatic diaphragmatic injury: a review of CT signs and the difference between blunt and penetrating injury. Diagnostic and interventional radiology (Ankara, Turkey). 2014-03;20:121-128.
  6. Ganie FF. Delayed presentation of traumatic diaphragmatic hernia: a diagnosis of suspicion with increased morbidity and mortality. Trauma monthly. 2013;18:12-16.
  7. Yucel MM. Evaluation of diaphragm in penetrating left thoracoabdominal stab injuries: The role of multislice computed tomography. Injury. 2015-09;46:1734-1737.
  8. Biffl WW. Validating the Western Trauma Association algorithm for managing patients with anterior abdominal stab wounds: a Western Trauma Association multicenter trial. The journal of trauma. 2011-12;71:1494-1502.
  9. Inaba KK. Selective nonoperative management of torso gunshot wounds: when is it safe to discharge? The journal of trauma. 2010-06;68:1301-1304.
  10. Pereira BB. A review of ureteral injuries after external trauma. Scandinavian journal of trauma, resuscitation and emergency medicine. 2010;18:6.
  11. Pfeifer R, Pape H-C. Missed injuries in trauma patients: A literature review. Patient Safety in Surgery. 2008;2:20. doi:10.1186/1754-9493-2-20.

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