Tag Archives: trauma

Maximizing ED Management of Amputations

Authors: Cara Kanter, MD (EM Resident Physician, Temple EM) and Zachary Repanshek, MD (Assistant Professor of Emergency Medicine, Lewis Katz School of Medicine; Assistant Program Director, Temple EM) // Edited by: Alex Koyfman, MD (@EMHighAK, EM Attending Physician, UT Southwestern Medical Center / Parkland Memorial Hospital) and Brit Long, MD (@long_brit)

A Clinical Case

A 43-year-old male with a history of IV drug use presented to the Emergency Department after being struck by a train. EMS reported 10 minutes of extraction time. The patient reported copious alcohol use prior to the incident and complained primarily of right leg pain. Physical exam was notable for GCS 13 (E4V4M5), bilateral periorbital ecchymosis with tarsal sparing, and near total amputation of the right lower extremity below the knee.


Numbers Game (1)
  • Roughly 83,000 traumatic amputations in the U.S. yearly
  • Majority of victims are men age 15-40
  • Most common mechanisms: MVC (51%), industrial accidents (19%), agricultural accidents (10%)
  • Most common sites: partial hand amputation (1+ fingers), unilateral upper extremity
Definitions (1,2)
  • Partial Amputation: bone, muscle, or tissue keeps the amputated segment connected to the body
    • More common among civilians
    • Ideal treatment = revascularization
  • Complete Amputation: no connecting tissue
    • More common in military
    • Ideal treatment = reimplantation
  • Sharp/Guillotine Amputation: Well-defined edges, minimal damage to associated anatomy
    • Best prognosis for reimplantation
  • Crush Amputation: extensive soft tissue & arterial damage
    • Reimplantation less likely to be successful
  • Avulsion Amputation: forceful overstretching & tearing of nerves & vascular tissue at many different levels from the site of separation
    • Reimplantation unlikely


Pearl #1: ED management is the same for ALL types of traumatic amputation => ALL patients are candidates for reimplantation until a surgeon says otherwise!



  • Ischemia time (2)
    • Irreversible muscle necrosis begins at 6 hours of ischemia
    • Temperature & muscle amount in tissue predict tolerable ischemia time
      • Digits: less muscle mass, tolerate more ischemia time
        • Warm ischemia time: 8-12 hours
        • Cool ischemia time: up to 24 hours
      • Limbs: more muscle mass, tolerate less ischemia time
        • Warm ischemia time: 4-6 hours
        • Cold ischemia time: 10-12 hours
      • Mechanism of Injury
        • Guillotine amputations best chance of successful reimplantation
        • Crush/Avulsion amputations have worse prognosis for limb salvage
      • Co-morbidities
        • Young, healthy patients have better chance of successful limb salvage (shocking!)
        • Worse prognosis: smoking, diabetes, PVD, rheumatologic disease
      • Handedness
      • Occupation


PEARL #2: ISCHEMIA TIME predicts success for reimplantation!


Physical Exam  
  • Primary & Secondary Survey
    • Significant traumatic amputations portend significant internal injuries that may be more immediately life-threatening
    • Control hemorrhage & proceed with ATLS resuscitation as you would any trauma
  • Assess & document a complete exam of the injured extremity
    • Neuro exam
      • Test for sensation & 2-point discrimination in each nerve distribution
    • Vascular exam
      • Capillary refill
      • Pulses via palpation and Doppler, ABIs when appropriate
      • Ribbon sign: tortuous artery in amputated segment, indicates significant vascular compromise (3)
      • Use Allen test in hand injuries
    • Soft tissue & Bone (2)
      • Assess skin, muscle, bone, tendon and nail bed integrity
      • Identify fractures
        • Exposed bone, gross deformity, tenderness, crepitus


PEARL #3: Don’t forget ABCDE => look for other injuries that may kill the patient first!


ED Management

Care of the amputated segment (1,2,4)
  • Irrigate with saline or sterile water & remove gross contamination
  • Control any bleeding with a pressure dressing
  • Wrap in moistened sterile gauze & seal in water-tight container
  • Place container on ice, in ice water bath, or in refrigerator
  • Do NOT allow limb to freeze!
Care of the stump (2,5)
  • Elevate the limb
  • Irrigate with saline & cover with damp gauze
  • Splint obvious/unstable fractures, keep as near anatomic position as possible
  • Control hemorrhage!
Tourniquet Use
  • Indications for tourniquet use (5,6)
    • Uncontrollable bleeding from a site amenable to proximal placement of a tourniquet
    • Limb amputation or mangled extremity
    • Exsanguinating wound associated with shock
    • Life-threatening hemorrhage inadequately controlled with direct pressure, elevation and other hemostatic methods
  • Pearls of tourniquet application (5)
    • Place the tourniquet as distal as possible, at least 5 cm proximal to the injury
    • Spare joints as much as possible
    • Apply directly onto exposed skin
    • Time of application should be recorded
    • Any amputated limb should be transported with the patient to the hospital


PEARL #4: Life over limb!


Other Considerations
  • Tetanus prophylaxis
  • Prophylactic antibiotics (2,7)
    • Strep & staph coverage
    • Should be given within 6 hours of trauma
      • Cefuroxime 1.5g IV q8h or Cefazolin 0.5-1.5g IV or IM q6-8h
        • Peds: 25-100mg/kg/d divided q8hr (max 6g/d)
      • MRSA coverage: Vancomycin 15-20mg/kg IV q12h
      • Clostridia coverage: Piperacillin/Tazobactam 80mg/kg IV q8h
    • Immediate surgical consultation – orthopedics, plastics, vascular, trauma! Time is limb!


PEARL #5: Traumatic amputation is a surgical emergency! Get the patient to a surgeon ASAP!


Review of the Pearls

  1. ED management is the same for ALL types of traumatic amputation => ALL patients are candidates for reimplantation until a surgeon says otherwise!
  2. ISCHEMIA TIME predicts success for reimplantation!
  3. Don’t forget ATLS => look for other injuries that may kill the patient first!
  4. Life over limb!
  5. Traumatic amputation is a surgical emergency! Get the patient to a surgeon ASAP!


Case Resolution

The patient was intubated in the trauma bay for airway protection. A CT head obtained demonstrated multiple skull fractures and an epidural hematoma without mass effect. The patient was taken to the OR with trauma surgery for a right through-knee guillotine amputation. A repeat CT head obtained immediately post-op demonstrated an expanding epidural hematoma. The patient went immediately back to the OR with neurosurgery for a hematoma evacuation. The patient was taken back to the OR a few days later with trauma surgery for a formal above-knee-amputation.


References/Further Reading

  1. Meenach, Dean. “How to manage traumatic amputations and uncontrolled bleeding.” EMS In Focus. EMS1.com, 30 Apr. 2014. Web. 24 Feb. 2017
  2. Schaider, J. (2015). Amputation Traumatic/Replantation. ROSEN & BARKIN’S 5-MINUTE EMERGENCY MEDICINE CONSULT. Retrieved February 24, 2017 from http://www.r2library.com.libproxy.temple.edu/Resource/Title/1451190670/ch0001s0822
  3. Van Beek AL, Kutz JE, Zook EG. (1978). Importance of the ribbon sign, indicating unsuitability of the vessel, in replanting a finger. Plastic and Reconstructive Surgery, 61(1):32-5.
  4. Stone, C. (2005). Traumatic Amputation. CURRENT ESSENTIALS OF EMERGENCY MEDICINE. Retrieved February 24, 2017 from http://www.r2library.com.libproxy.temple.edu/Resource/Title/0071440585/ch0022s2072
  5. Lee C, Porter KM, Hodgetts TJ. (2007). Tourniquet use in the civilian prehospital setting. Emergency Medicine Journal, 24, 584-7.
  6. Rush RM, Arrington ED, & Hsu JR. (2012). Management of complex extremity injuries: Tourniquets, compartment syndrome detection, fasciotomy, and amputation care. Surgical Clinics of North America, 92(4), 987-1007.
  7. Schmitt SK. Treatment and prevention of osteomyelitis following trauma in adults. In: UpToDate, Post TW (Ed), UpToDate, Waltham, MA. (Accessed on February 24, 2017).

Neurotrauma Resuscitation: Pearls & Pitfalls

Author: Brit Long, MD (@long_brit, EM Attending Physician at SAUSHEC, USAF) // Edited by: Alex Koyfman, MD (@EMHighAK, EM Attending Physician, UTSW / Parkland Memorial Hospital)

A 24-year-old male arrives by EMS with a GCS of 5 after a severe MVC. He was ejected from the vehicle, and EMS placed a C-collar, followed by positioning on a backboard for transport. Bilateral IV’s were placed, and 1 L NS was started. They did not intubate him in the field, as they were 4 minutes from your hospital. What are your priorities in evaluation and management of this patient? What are the pearls and pitfalls in resuscitating the sick neurotrauma patient?

Neurotrauma, particularly traumatic brain injury (TBI), is a significant cause of death around the world and the leading cause of death in patients age 1 to 45 years.1-5 Approximately 78% of patients are managed in the emergency department (ED), with males and young adults the two primary populations affected.1.2 Traumatic neurologic injury not only causes an initial primary injury, but it is associated with several secondary insults.1-6

Some pathophysiology…

Cerebral perfusion pressure (CPP) is defined by the mean arterial pressure (MAP) minus the intracranial pressure (ICP). ICP is a function of the brain parenchyma, blood, and cerebrospinal fluid.2,7-12 The key is that an increase in one requires a decrease in another.2,7-12 Once compensatory methods are exhausted, further volume leads to drastic increases in ICP. Cerebral perfusion pressure is related to ICP, and increase in ICP may decrease cerebral perfusion. The ultimate goal of resuscitation and management of the neurotrauma patient is to ensure normal ICP, while preserving cerebral blood flow and perfusion.2,8,11,12

Are there physiologic goals?

Hypotension is associated with increased morbidity and mortality. A CPP goal of 50 to 70 mm Hg should be used, with SBP of at least 100 mm Hg (ages 50-69) and 110 mm Hg for 15-49 years and > 70 years, per the Brain Trauma Foundation.2,8,11-13  Otherwise, a MAP of 70-80 mm Hg is advised.5 Avoiding cerebral hypotension is recommended, though aggressive CPP targeting is not associated with improved outcomes.13-15 Hypoxemia also results in a significant increase in mortality. Key targets of resuscitation are shown below.

Goal Physiologic Parameters5,11,12
-Pulse oximetry > 94%, less than 100% (avoid hypoxemia and hyperoxemia)

-PaCO2 35-45 mm Hg

-SBP > 100 mm Hg (ages 50-69), and > 110 mm Hg (ages 15-49, > 70 years)

-pH 7.35-7.45

-ICP < 20 mm Hg

-Glucose 80-180 mg/dL

-CPP > 60 mm Hg

-Serum Na 135-145, (Hypertonic saline goal is 145-160)

-INR < 1.4

-Platelets > 75 x 103/mm3

-Hgb > 8 mg/dL

What are several dangerous secondary injuries?

Neurotrauma begins a cascade that may cause further cell death.8,11,12 The following are significant secondary injuries, all which increase adverse outcomes. Awareness of these injuries is necessary for prevention.5,8,11-15

– Hypotension: 30% of patients, resulting in higher likelihood of poor outcome (OR 2.67).2,8,11-15

– Hypoxia: 50% of patients, resulting in higher likelihood of poor outcome (OR 2.14).2,8,11-15

– Hyperoxia: PaO2 levels above 300-470 mm Hg are associated with worse outcome.2,8,11-15

– Fever: Elevated temperature worsens morbidity by secondary brain injury aggravation.2,13

– Coagulopathy: Associated with the traumatic event and may cause worsening of the neurologic injury and death. Acute TBI may cause coagulopathy itself through tissue factor and phospholipid release.16

– Glucose: Hyper- and hypoglycemia are predictors of poor neurologic status.2,8,11-15

Pearls in Evaluation and Management

Focus on airway, breathing, circulation, disability, and exposure in the primary survey, with spinal precautions.2,11,17-20 Avoid secondary complications, and other markers of worse outcome include poor GCS motor score, pupillary dysfunction, and increased ICP. Abnormal pupillary response and altered motor function are markers for severe brain trauma, as is posturing. Decorticate posturing (arm flexion and leg extension) is due to injury above the midbrain, and decerebrate posturing (arm extension and internal rotation, wrist and finger flexion, leg internal rotation and extension) is a sign of more caudal injury involving the midbrain.11,12,17 Abnormal pupils, decreased mental status, abnormal GCS, penetrating injury, abnormal motor status, and severe injury require neuroimaging.  Severe neurotrauma requires consultation with neurosurgery.2,11,12,17  This post will focus on the hypotensive patient with neurologic injury.

ED Considerations
-Maintain spinal precautions

-Conduct primary and secondary surveys; address life-threatening injuries

-Advanced airway management may be needed for airway protection, hypoxia, and control of ventilation

-Obtain rapid IV access

-Optimize oxygenation, blood pressure, and ventilation

-Target oxygen saturation > 94%, with systolic blood pressure > 100-110 mm Hg

– Focused neuro exam: GCS, motor function, and pupillary function

-Obtain head CT noncontrast

-Any sign of worsening neurologic status warrants hyperosmolar therapy

Tiers of ICP management, per the Brain Trauma Foundation, are shown below.11,12,17 We will discuss pearls and subtleties for these therapies, but first, let’s discuss airway.

Tier Options
0 -Head of bed elevation

-Control fever, pain, and agitation

-Optimize physiologic parameters such as blood pressure and oxygen

-Target PaCO2 to 35-38 mm Hg

1 -Osmotic therapy includes mannitol, hypertonic saline, or sodium bicarbonate

-External ventricular drainage system should be placed if acute obstruction is present

2 -Propofol drip titration

-Optimize other parameters

3 -Barbiturate coma

-Surgical decompression if ICP refractory to treatment

-Therapeutic hypothermia

-Moderate hyperventilation (only if active herniation)

How should the airway be managed?

Airway protection and blood pressure support for severe neurotrauma are priorities, and first pass success is vital. Rapid sequence intubation with in-line stabilization of the cervical spine may be necessary.2,11,18-20 Preoxygenation is important to avoid desaturation, so start your NO DESAT interventions early.21,22

Intubation Considerations
-Preparation: Proper positioning, preoxygenate, and use apneic oxygenation with nasal cannula, facemask, or noninvasive positive pressure ventilation

-Elevate head of bed to improve CPP and decrease aspiration

-Premedication regimens are controversial. Fentanyl at 2-5 micrograms/kg IV or esmolol 1.5mg/kg IV may decrease catecholamine surge and control the hemodynamic response to intubation

-Induction agent may include ketamine (does not adversely affect patients with neurotrauma) and etomidate – these agents have less hemodynamics effects

-Propofol has neuroprotective effects, but hypotension may occur

-Post intubation analgesia and sedation are essential – have your drips ready to go at the time of intubation


Up to 80% of patients may experience a hypertensive response to laryngoscopy or suctioning, and lidocaine was initially thought to blunt this. However, lidocaine has not demonstrated ability to reduce ICP or improve neurologic outcome.18-20,23 Fentanyl at doses of 2-5 micrograms/kg IV prior to intubation can reduce the hyperdynamic response to intubation, as can esmolol at 1.5 mg/kg IV. However, esmolol should be avoided in patients with hypotension, hemorrhagic shock, or signs of multiple trauma.18-20,24


Traditionally, ketamine was contraindicated for induction in intubation in TBI, but literature suggests that not only is it safe, but it may be beneficial. Ketamine improves cerebral blood flow, and evidence suggests it does not raise ICP.19,25  Propofol has high lipid solubility and rapid onset of action that can reduce ICP and oxidative stress. However, it may cause hypotension.19,20,26 Etomidate may result in less hypotension and cardiac dysfunction. It can reduce ICP and maintain CPP, but it also may lower the seizure threshold and increase the risk of vomiting and myoclonic movements.19,27 The key for an induction agent is utilizing lower doses in patients with hypotension, as any agent at full dose will worsen hypotension.


Paralysis is essential to improve first pass success including succinylcholine or rocuronium. Succinylcholine allows faster time to recovery and assessment of neurologic status, as rocuronium will last longer. Ultimately, the choice of paralytic rests on the physician, as both are safe and efficacious.19,20  However, defasciculating doses of paralytics such as succinylcholine or pancuronium are not beneficial and do not reduce ICP.19,20

Post Intubation

Post intubation sedation and analgesia are an absolute must.18-20 An intubated patient with inadequate analgesia and sedation may experience increased ICP due to sympathomimetic response.24 The key is to order your post intubation meds at the same time as your paralytic and induction agent.18-20 Analgesics including fentanyl and remifentanil are fast and predictable. Morphine and hydromorphone may accumulate with prolonged infusion, though they do have longer duration of action. Sedative medications include propofol, which possesses fast onset and offset, allowing for repeat neurologic assessment.  If used keep close tabs on blood pressure. Infusion, rather than bolus doses, will mitigate the risk of decreasing BP. Benzodiazepines can be used, though they can reduce BP and respiratory status. However, they do reduce cerebral blood flow and ICP.28 Unfortunately, tolerance may develop, and reassessment is difficult due to metabolite accumulation. The new kid on the block, dexmedetomidine, is a selective alpha-2 receptor agonist with anxiolytic and sedative effects.19,29 Hypotension and bradycardia are the most common side effects, most commonly seen with bolus dosing. It may reduce ICP, though further study is needed.

Avoid hypoxia post intubation, targeting O2 saturation 94%-98%. Hyperoxia with PaO2 greater than 300-470 mm Hg is discouraged due to worse outcomes.13,18-20  Unless actively herniating, hyperventilation is not recommended. PaCO2 levels of 35 to 45 mm Hg, or end-tidal CO2 30 to 40 mm Hg, are your goals.2,11,18

What about hypotension?

Hypotension increases mortality two-fold, specifically any SBP drop less than 90 mm Hg.2,11-15,19 The polytrauma patient with head trauma can be difficult.  These patients are often hypotensive, and permissive hypotension is not recommended. Target a SBP of at least greater than 100 mm Hg (for patients 50-69 years of age) or 110 mm Hg (for those 15-49 years and > 70 years).11 Keep in mind that ATLS states a MAP > 80 mm Hg in patients with severe TBI is reasonable.5 Start first with fluids, specifically normal saline or blood.2,11,18 Avoid hypo-osmotic fluids, which can increase cerebral edema and ICP.30  Albumin is associated with higher mortality, which was demonstrated in the SAFE trial in TBI patients.31 Literature suggests no difference between normal saline and HTS for patients with no signs of herniation.30

Wait, what’s this about neurogenic shock?

Neurogenic shock occurs with injury above T6 and is a form of distributive shock. It is caused by loss of sympathetic tone.32-35 Patients may show low HR and BP; however, hypovolemic shock must first be ruled out in the trauma patient. Spinal shock is different, with loss of sensation and motor function below the spinal cord injury. Reflexes are often depressed below the injury level.32-35

Are vasopressors needed?

A SBP of at least 100-110 mm Hg is recommended by the Brain Trauma Foundation, as hypotension increases morbidity and mortality.11 Specifically in neurogenic shock with hypotension and bradycardia, fluids and vasopressors will be needed.32,33 Loss of sympathetic tone is common within the first week of injury.6,32-35 A goal MAP of 85 mm Hg is recommended by the AANS and CNS in neurogenic shock.35  Dopamine, norepinephrine, or phenylephrine may be used.  Norepinephrine will increase afterload and inotropy, needed with the loss of sympathetic tone.  Phenylephrine will improve vascular tone and can be used in patients who are not bradycardic.6,33-35

What hyperosmolar therapies are available?

Hyperosmolar therapy is a foundation of management. These measures can reduce ICP and improve cerebral blood flow.2,12,17,18  Hyperosmolar agents should be used with signs of increased ICP, pupillary change, decrease in GCS > 2 points, or posturing.2,12,17,18   Agents include 20% mannitol 0.25-1 g/kg IV as a rapid infusion over 5 minutes or 3% NaCl 150 ml IV over 10 minutes (HTS 23.4% 30mL can be used through central line).2,11,17,18,30,36-38 We will discuss these agents further, but keep in mind that if hypotension is a concern, HTS may be a better resuscitation fluid.5,17,18  For ICP reduction, a 2015 meta-analysis finds no difference in neurologic outcome or mortality between mannitol and HTS.30

  1. Mannitol

Mannitol is administered as a 20% solution.2,30,36-38 This solution deforms RBCs and decreases blood viscosity, improving cerebral blood flow.36-38  A major consideration is autoregulation and the presence of intact Blood-Brain-Barrier, as if these are intact, ICP will decrease. If not intact, mannitol may worsen outcomes.11,18,30 Rebound increases in ICP can occur, and the solution may cause renal injury through excess diuresis. IV fluids are necessary when providing mannitol, along with Foley catheter.11,17,18

  1. HTS

HTS concentrations range from 2% to 23.4%, which also improves cerebral blood flow and reduces parenchymal water content.2,11,12,17 HTS can improve blood pressure as a volume expander. The risk of rebound ICP is less than that of mannitol.2,11,17,18,30 The most common side effect of HTS is hyperchloremic metabolic acidosis.2,18,30

What about ocular US for increased ICP?

Ultrasound can measure optic nerve sheath diameter (ONSD), which correlates closely with ICP.18,39,40 The normal optic nerve sheath is up to 5 mm in diameter, and ONSD will increase with elevated ICP. ONSD should be measured 3 mm posterior to the globe for both eyes, with an average between measurements. Values greater than 5 mm predict increased ICP, with sensitivity and specificity greater than 90%.39,40

When is surgery required?

Surgical management of TBI may be needed to repair depressed skull fracture or evacuate intracranial mass (such as blood).2,11,17,18 Decompressive craniectomy is indicated for refractory intracranial hypertension; however, decompressive craniectomy may not improve functional outcome while decreasing ICP, as shown in the DECRA trial.41-45 Ultimately, your neurosurgeon will make this decision, but they must be on board early in the patient’s management.11,45

Is hypothermia effective in neurotrauma?

Studies have not found an improvement in mortality or neurologic status with hypothermia in neurotrauma.2,11,18,46,47 However, hypothermia can reduce intracranial hypertension.46,47 Targeted management of temperature reduces cerebral metabolic rate and release of excitatory neurotransmitters, but more study is required.11,46,47

Should you reverse coagulopathy with traumatic intracerebral hemorrhage?

Coagulopathy is common, as close to 1/3 of patients with TBI display a coagulopathy, due to patient medication or release of tissue factor causing consumptive coagulopathy.11,16 Coagulation panel and TEG can be helpful, with reversal dependent on results and patient medication. Vitamin K, PCC/FFP, and novel antidotes can be utilized.11,48-50 We will not go into detail here on reversal. However, keep in mind that platelet transfusion in patients on antiplatelet medication with ICH may be harmful per the recent PATCH trial.51

What is the role of pharmacologically-induced coma?

Barbiturates can be used to reduce ICP, if refractory to other treatment, through suppression of cerebral metabolism, modification of vascular resistance, and decrease of neuronal excitotoxicity.2,18,52,53 However, barbiturates have significant side effects, as one in four experiences hypotension.2,11,53 A 2012 Cochrane Review found no change in outcomes for severe TBI with barbiturate coma.53

Corticosteroids used to be recommended, but what about today?

The CRASH trial suggests worse outcomes and increased mortality for patients with TBI given steroids.54-57 In the setting of spinal cord injury, the American Association of Neurologic Surgeons and Congress of Neurologic Surgeons do not recommend steroids.2,6,11

Should seizures be treated in neurotrauma?

Early posttraumatic seizures occur within 7 days of injury, with late seizures beyond 7 days.2,11,58,59 Seizures occur in up to 30% of TBI patients (50% of patients with penetrating injury).2,58,59 With seizures increasing ICP, any active seizure requires immediate treatment, with benzodiazepines first line. Prophylaxis on the other hand is more controversial. The presence of any risk factor including include GCS < 10, cortical contusion, any intracranial hematoma, depressed skull fracture, penetrating head injury, or seizure within 24 hours of injury requires prophuulaxis.11,58,59 Otherwise, prophylaxis is not recommended. Levetiracetam is equivalent to phenytoin for seizure reduction, and it is associated with less risk of side effect.58,59

Does tranexamic acid have a place in neurotrauma?

The CRASH-2 and MATTERs studies have suggested survival benefit within three hours of trauma for TXA.60,61 The CRASH-2 Intracranial Bleeding Study found a trend towards reduction in intracranial hemorrhage growth and lower mortality in patients with traumatic hemorrhage, with another study finding reduction in hemorrhage growth.60,62 CRASH-3 is underway, evaluating TXA in TBI specifically.63

Pitfalls in evaluation and management

Several medications have not demonstrated improvement in outcomes for TBI, including progesterone, magnesium, hyperbaric oxygen, and cyclosporine.2,11,64,65

Hyperventilation can reduce ICP for short periods.2,11,18,66,67 However, hyperventilation may result in secondary ischemia if used for prolonged periods and increases the risk of cerebral edema. Hyperventilation has demonstrated worse clinical outcomes in patients hyperventilated to PaCO2 less than 30 mm Hg for six hours up to five days.18,66,67 Mild hyperventilation can be used for acute worsening, but only for a short period, targeting PaCO2 30-35 mmHg.2,11,18

Key points

– Neurotrauma is common, as it is the leading cause of death in North America in those between ages 1 year to 45 years. Primary and secondary injuries result in severe morbidity and mortality.

– Neurotrauma includes head contusion, epidural hematoma, subdural hematoma, subarachnoid hemorrhage, diffuse axonal injury, skull fracture, and traumatic spinal cord injury.

– Cerebral perfusion pressure requires adequate cerebral blood flow.

–  Evaluation and management in the emergency department entails initial stabilization and resuscitation while assessing neurologic status.

– Targeting mean arterial pressure, oxygen levels, and neurologic status are key components. ICP management should follow a tiered approach.

Intubation of the patient with neurotrauma should be completed with several considerations.

– Hyperosmolar treatments include HTS and mannitol.


References/Further Reading

  1. Faul M, Xu L, Wald MM, et al. Traumatic brain injury in the United States: emergency department visits, hospitalizations and deaths 2002–2006. Atlanta (GA): Centers for Disease Control and Prevention, National Center for Injury Prevention and Control; 2010.
  2. Wan-Tsu WC, Badjatia N. Neurotrauma. Emerg Med Clin N Am 2014;32:889-905.
  3. Rutland-Brown W, Langlois JA, Thomas KE, Xi YL. Incidence of traumatic brain injury in the United States, 2003. J Head Trauma Rehabil 2006; 21:544.
  4. Stein DM, Roddy V, Mark J, Smith WS, Weingart SD. Emergency Neurological Life Support: Traumatic Spine Injury. Neurocrit Care 2012;17:S102-S111.
  5. ATLS Subcommittee; American College of Surgeons’ Committee on Trauma; International ATLS working group. Advanced trauma life support (ATLS®): the ninth edition. J Trauma Acute Care Surg. 2013 May;74(5):1363-6.
  6. Hadley MN, Walters BC, Aarabi B, et al. Guidelines for the management of acute cervical spine and spinal cord injuries. Neurosurgery 2013;72(Suppl 2): 1–259.
  7. Oddo M, Le Roux PD. What is the etiology, pathogenesis and pathophysiology of elevated intracranial pressure? In: Neligan P, Deutschman CS, editors. The evidenced based practice of critical care. Philadelphia: Elsevier Science; 2009.
  8. Swadron SP, LeRoux P, Smith WS, Weingart SD. Emergency Neurological Life Support: Traumatic Brain Injury. Neurocrit Care 2012;17:S112–S121.
  9. Bouma GJ, Muizelaar JP. Cerebral blood flow, cerebral blood volume, and cerebrovascular reactivity after severe head injury. J Neurotrauma 1992; 9 Suppl 1:S333.
  10. Bouma GJ, Muizelaar JP, Bandoh K, Marmarou A. Blood pressure and intracranial pressure-volume dynamics in severe head injury: relationship with cerebral blood flow. J Neurosurg 1992; 77:15.
  11. Carney N, Totten AM, O’Reilly C, Ullman JS, Hawryluk GWJ, bell MJ, et al. Guidelines for the Management of Severe Traumatic Brain Injury, Fourth Edition. Neurosurgery 2016;0(0):1-10.
  12. Stevens RD, Huff JS, Duckworth J, et al. Emergency neurological life support: intracranial hypertension and herniation. Neurocrit Care 2012;17(Suppl 1):S60–5.
  13. McHugh GS, Engel DC, Butcher I, et al. Prognostic value of secondary insults in traumatic brain injury: results from the IMPACT study. J Neurotrauma 2007; 24:287.
  14. Chestnut RM, Marshall LF, Klauber MR, et al. The role of secondary brain injury in determining outcome from severe head injury. J Trauma 1993;34(2):216-22.
  15. Marmarou A, Anderson RL, Ward JD, et al. Impact of ICP instability and hypotension on outcome in patients with severe head trauma. J Neurosurg 1991; 75(Suppl):S59–66.
  16. Harhangi BS, Kompanje EJ, Leebeek FW, Maas AI. Coagulation disorders after traumatic brain injury. Acta Neurochir (Wien) 2008; 150:165.]
  17. Emergency Neurological Life Support: Elevated ICP or Herniation. 2014. Available at http://enlsprotocols.org/files/ICP.pdf. Accessed 16 November 2016.
  18. Weingart S. EMCrit: Podcast 78 – Increased intra-cranial pressure (ICP) and herniation, aka brain code. Available at http://emcrit.org/podcasts/high-icp-herniation/. Accessed 16 November 2016.
  19. Bucher J, Koyfman A. Intubation of the Neurologically Injured Patient. JEM 2015;49(6):920-7.
  20. Seder DB, Riker RR, Jagoda A, Smith WS, Weingart SD. Emergency Neurological Life Support: Airway, Ventilation, and Sedation. Neurocrit Care 2010;17:S4-S20.
  21. Weingart SD, Levitan RM. Preoxygenation and prevention of desaturation during emergency airway management. Ann Emerg Med 2012;59:165–1751.
  22. Dixon BJ, Dixon JB, Carden JR, et al. Preoxygenation is more effective in the 25 degrees head-up position than in the supine position in severely obese patients: a randomized controlled study. Anesthesiology 2005;102:1110–5. discussion 1115A.
  23. Robinson N, Clancy M. In patients with head injury undergoing rapid sequence intubation, does pretreatment with intravenous lignocaine/lidocaine lead to an improved neurological outcome? A review of the literature. Emergency Medicine Journal : EMJ. 2001;18(6):453-457. doi:10.1136/emj.18.6.453
  24. Dahlgren N, Messeter K. Treatment of stress response to laryngoscopy and intubation with fentanyl. Anaesthesia 1981;36:1022–6.
  25. 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. Ann Emerg Med 2015;65:43–51.
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  29. Jakob SM, Ruokonen E, Grounds RM, et al. Dexmedetomidine vs. midazolam or propofol for sedation during prolonged mechanical ventilation: two randomized controlled trials. JAMA. 2012;307:1151–60.
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  36. Vialet R, Albanèse J, Thomachot L, et al. Isovolume hypertonic solutes (sodium chloride or mannitol) in the treatment of refractory posttraumatic intracranial hypertension: 2 mL/kg 7.5% saline is more effective than 2 mL/kg 20% mannitol. Crit Care Med 2003; 31:1683.
  37. Kassell N, Baumann K, Hitchon P, et al. The effects of high dose mannitol on cerebral blood flow in dogs with normal intracranial pressure. Stroke 1982;13(1): 59–61.
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  39. Sekhon MS, McBeth P, Zou J, et al. Association between optic nerve sheath diameter and mortality in patients with severe traumatic brain injury. Neurocrit Care. 2014;21(2):245-252.
  40. Hassen GW, Bruck I, Donahue J, et al. Accuracy of optic nerve sheath diameter measurement by emergency physicians using bedside ultrasound. J Emerg Med. 2015;48(4):450-457.
  41. Bullock MR, Chestnut R, Ghajar J, et al. Guidelines for the surgical management of traumatic brain injury. Neurosurgery 2006;58(Suppl)S2-1-3.
  42. Cooper DJ, Rosenfeld JV, Murray L, et al. Decompressive craniectomy in diffuse traumatic brain injury. N Engl J Med 2011;364(16):1493–502.
  43. Honeybul S, Ho KM, Lind CR. What can be learned from the DECRA study. World Neurosurg 2013;79(1):159–61.
  44. Sahuquillo J, Martinez-Ricarte F, Poca MA. Decompressive craniectomy in traumatic brain injury after the DECRA trial. Where do we stand? Curr Opin Crit Care 2013;19(2):101–6.
  45. Hutchinson PJ, Kolias AG, Timofeev IS, Corteen EA, Czosnyka M, Timothy J, et al. Trial of Decompressive Craniectomy for Traumatic Intracranial Hypertension. N Engl J Med. 2016 Sep 7. [Epub ahead of print].
  46. Sydenham E, Roberts I, Alderson P. Hypothermia for traumatic head injury. Cochrane Database Syst Rev 2009;(2):CD00104.
  47. Clifton GL, Valadka A, Zygun D, et al. Very early hypothermia induction in patients with severe brain injury (the National Acute Brain Injury Study: Hypothermia II): a randomised trial. Lancet Neurol 2011;10(2):131–9.
  48. Morgenstern LB, Hemphill JC 3rd, Anderson C, et al. Guidelines for the management of spontaneous intracerebral hemorrhage: a guideline for healthcare professionals from the American Heart Association/American Stroke Association. Stroke 2010; 41:2108.
  49. Eller T, Busse J, Dittrich M, et al. Dabigatran, rivaroxaban, apixaban, argatroban and fondaparinux and their effects on coagulation POC and platelet function tests. Clin Chem Lab Med 2014; 52:835.
  50. Dickneite G, Hoffman M. Reversing the new oral anticoagulants with prothrombin complex concentrates (PCCs): what is the evidence? Thromb Haemost 2014; 111:189.
  51. Baharoglu MI, Cordonnier C, Al-Shahi Salman R, de Gans K, Koopman MM, Brand A, Majoie CB. Platelet transfusion versus standard care after acute stroke due to spontaneous cerebral haemorrhage associated with antiplatelet therapy (PATCH): a randomised, open-label, phase 3 trial. 2016 Jun 25;387(10038):2605-13.
  52. Eisenberg HM, Frankowski RF, Contant CF, et al. High-dose barbiturate control of elevated intracranial pressure in patients with severe head injury. J Neurosurg 1988;69(1):15–23.
  53. Roberts I, Sydenham E. Barbiturates for acute traumatic brain injury. Cochrane Database Syst Rev 2012;(12):CD000033.
  54. Roberts I, Yates D, Sandercock P, et al. Effect of intravenous corticosteroids on death within 14 days in 10008 adults with clinically significant head injury (MRC CRASH trial): randomised placebo-controlled trial. Lancet 2004;364(9442): 1321–8.
  55. Bracken M, Shepard M, Collins W, et al. A randomized, controlled trial of methylprednisolone or naloxone in the treatment of acute spinal-cord injury. Results of the Second National Acute Spinal Cord Injury Study. N Engl J Med 1990; 322(20):1405–11.
  56. Bracken MB, Shepard MJ, Holford TR, et al. Administration of methylprednisolone for 24 or 48 hours or tirilazad mesylate for 48 hours in the treatment of acute spinal cord injury. JAMA 1997;277(20):1597–604.
  57. Bracken M. Steroids for acute spinal cord injury. Cochrane Database Syst Rev 2012;(1):CD001046.
  58. Inaba K, Menaker J, Branco BC, et al. A prospective multicenter comparison of levetiracetam versus phenytoin for early posttraumatic seizure prophylaxis. J Trauma Acute Care Surg 2013;74(3):766-71 [discussion: 771-3].
  59. Torbic H, Forni A, Anger KE, et al. Use of antiepileptics for seizure prophylaxis after traumatic brain injury. Am J Heal Pharm 2013;70(9):759–66.
  60. Roberts I, Shakur H, Coats T, Hunt B, Balogun E, Barnetson L, Cook L, Kawahara T, et al. The CRASH-2 trial: a randomised controlled trial and economic evaluation of the effects of tranexamic acid on death, vascular occlusive events and transfusion requirement in bleeding trauma patients. Health Technol Assess. 2013 Mar;17(10):1-79.
  61. Morrison JJ, Dubose JJ, Rasmussen TE, Midwinter MJ. Military Application of Tranexamic Acid in Trauma Emergency Resuscitation (MATTERs) Study. 2012 Feb;147(2):113-9.
  62. Perel P, Al-Shahi Salman R, Kawahara T, Morris Z, Prieto-Merino D, Roberts I, Sandercock P, et al. CRASH-2 (Clinical Randomisation of an Antifibrinolytic in Significant Haemorrhage) intracranial bleeding study: the effect of tranexamic acid in traumatic brain injury–a nested randomised, placebo-controlled trial. Health Technol Assess. 2012;16(13):iii-xii, 1-54.
  63. Dewan Y, Komolafe EO, Mejía-Mantilla JH, Perel P, Roberts I, Shakur H. CRASH-3 – tranexamic acid for the treatment of significant traumatic brain injury: study protocol for an international randomized, double-blind, placebo-controlled trial. Trials. 2012;13:87.
  64. Wright DW, Yeatts SD, Silbergleit R, et al. Very Early Administration of Progesterone for Acute Traumatic Brain Injury. N Engl J Med 2014;371(26):2457-2466.
  65. Skolnick BE, Maas AI, Narayan RK, van der Hoop RG, et al; SYNAPSE Trial Investigators. A clinical trial of progesterone for severe traumatic brain injury. N Engl J Med 2014 Dec 25;371(26):2467-76.
  66. Coles JP, Minhas PS, Fryer TD, et al. Effect of hyperventilation on cerebral blood flow in traumatic head injury: clinical relevance and monitoring correlates. Crit Care Med 2002; 30:1950.
  67. Coles JP, Fryer TD, Coleman MR, et al. Hyperventilation following head injury: effect on ischemic burden and cerebral oxidative metabolism. Crit Care Med. 2007;35:568–78.

Penetrating Wounds in the Emergency Department: Considerations for Management

Authors: Darren Cuthbert, MD, MPH (EM Resident Physician at Rutgers Robert Wood Johnson University Hospital) and Joshua Bucher, MD (EM Attending Physician, Rutgers Robert Wood Johnson University Hospital) // Edited by: Erica Simon, DO, MHA (@E_M_Simon) and Alex Koyfman, MD (@EMHighAK, EM Attending Physician, UTSW / Parkland Memorial Hospital)

Emergency physicians encounter penetrating trauma on a regular basis. Beyond Advanced Trauma Life Support protocols, the assessment of a patient presenting with a penetrating wound requires careful thought and thorough examination. If it’s been a while since you’ve reviewed the basics, let’s take a minute to work through a few cases and discuss the pearls and pitfalls for the management of penetrating injuries.

Case I: A 69-year-old intoxicated male presents via EMS with what appears to be a penetrating wound to the neck. The patient is in no obvious distress. Speaking clearly to the room, he reports robbery by an unknown assailant, and a singular knife wound to his neck. Upon examination the patient has clear breath sounds bilaterally. His pulses are equal and bounding, and his initial vital signs are within normal limits. Secondary survey is remarkable for a 3 cm superficial laceration to the lateral aspect of the left neck, localized to zone II. There is no evidence of a rapidly expanding hematoma or pulsatile bleeding. There is no violation of the platysma.

Case II: A 20-year-old female presents to the trauma bay intubated, ventilated, and sedated. EMS details arriving on scene to find the young women diaphoretic, in respiratory distress, and covered in blood. While holding her chest, she reported her fiancé as having inflicted a knife wound to her upper abdomen. Given the patient’s appearance, EMS performed intubation on scene. Emergency room evaluation revealed diminished breath sounds on the left. Tube thoracostomy was performed and resuscitation initiated (2U PRBCs), however, the patient remained tachycardic and hypotensive.

Case III: During an early morning shift, you receive a phone call regarding a patient en route from scene: 32-year-old male involved in an altercation with a machete; intubated on scene secondary to altered mental status, wounds localized to the head and left upper extremity. Upon arrival, primary and secondary survey reveal a hemodynamically stable male with a 7 cm gaping wound localized to the posterior occiput (hemostatic), and a 3 cm gaping wound localized to the left forearm (hemostatic).

Case IV: A 21-year-old male presents to emergency triage with the chief complaint of injury to the neck and armpit. The patient, in no acute distress, speaks in clear sentences while detailing his recent fall over a nail gun, with subsequent gun discharge and trauma to his neck and chest. As he was “feeling fine,” the patient reports having removed two nails prior to seeking treatment. Emergency department primary and secondary surveys are significant for puncture wounds to the anterior midline neck (zone III), and left midaxillary line at the level of T4. Crepitus is noted on palpation of the left anterior chest wall.

Let’s move on to a review of the fundamentals before we address our cases:

 The Head

The initial approach to penetrating head wounds centers on attaining hemostasis. After addressing airway and breathing in a patient with head trauma, direct pressure should be applied to any actively bleeding wound as these injuries (specifically injuries to the highly vascular scalp) may result in hemodynamic instability.1 If hemostasis is not attained following the application of direct pressure, experts advise local wound infiltration with lidocaine with epinephrine, or the ligation, suture, or clamping of visibly damaged vessels.1

The majority of patients with head trauma will required advanced imaging to rule out intracranial pathology and foreign bodies.1-3  If no evidence of foreign body or underlying depressed skull fracture, irrigate wounds thoroughly, explore to the base, and remove any organic material.1,2 If the galea is involved, consideration should be made for repair as failure to do so may lead to frontalis muscle (facial expression) deficit.1


The Face

In patients with penetrating facial trauma, management of the airway if paramount. During assessment pay close attention to voice changes and tachypnea, and evaluate for cyanosis as these are precursors of airway compromise and respiratory demise.1 Facial fractures and active bleeding into the oropharynx increase the level of difficulty when performing endotracheal intubation, therefore equipment preparation is advised (bougie or surgical airway kit). CT scans of the head, facial bones, and neck may be required to evaluate for underlying injuries to the face and surrounding structures of the head and neck.1 For impaled objects, admission is often required for surgical intervention, monitoring, and administration of broad spectrum antibiotics.1


The Neck

Patients with trauma to the neck who present with signs of respiratory compromise, such stridor, expanding hematoma, pulsatile arterial bleeding, bruit/thrill, or altered mental status should be emergently intubated.1,2 After attaining a definitive airway, be prepared to address circulation: exsanguination is the most common cause of death in this patient population.1 Consider placing the patient with a penetrating neck injury in Trendelenburg position to prevent air embolism, while addressing all actively bleeding wounds with direct pressure (caution as excessive force may occlude the carotid arteries).1 Although randomized controlled trials in the setting of penetrating neck trauma are lacking, hemostatic dressings including QuikClot, Combat Gauze, and HemCon are commonly utilized in the emergency department and have demonstrated affectivity in the attainment of hemostasis in the setting of life threatening hemorrhage.1 Clamping vessels of the neck is not recommended in the emergency department, as anatomic structures are not easily identified upon visual inspection, and probing of a neck wound is not advised.1,3 If active bleeding continues despite direct pressure and the use of a hemostatic dressing, consider mechanical tamponade with a Foley catheter: insert the catheter into the tract of the wound and inflate until bleeding ceases.1,2 If these attempts are unsuccessful, emergent surgical intervention is required.

Definitive management of wounds to the neck historically centers upon patient presentation and zone classification (see Figure 1). Patients experiencing hemorrhagic shock, airway obstruction, air discharge from their wound, active pulsatile blood flow, massive hemoptysis, and uncontrolled bleeding (the hard signs of neck trauma), regardless of zone classification, require surgical evaluation and treatment.1 Hemodynamically unstable patients with Zone I injury may require ED thoracotomy.1

  • Zone I => sternal notch to cricoid cartilage
    • CT angiography, endoscopy, and bronchoscopy are indicated for evaluation.1,2,5
      • Note: suspect hemothorax or pneumothorax in patients presenting with dyspnea or absent breath sounds (20% of patients with penetrating neck trauma have a pneumothorax or hemothorax on further examination1).
    • Zone II => cricoid cartilage to angle of the mandible
      • Violation of the platysma mandates surgical exploration.1
    • Zone III => angle of the mandible and above
      • CT angiography and endoscopy indicated for evaluation.1,2,5

Note: Importantly, esophageal injuries occur in up to 9% of patients with penetrating neck trauma. As the sensitivity of CT in the detection of early esophageal injury is reported as 53%,6 patients with esophageal perforation most commonly present with sepsis secondary to mediastinitis.1 If concern for esophageal perforation exists: initiate antibiotic therapy, obtain surgical consultation, and perform esophagograpy with a water-soluble contrast material.1

Figure 1. Zones of the Neck

A cervical collar may prevent adequate examination and stabilization of the patient with a penetrating neck injury. As vertebral and spinal cord injuries are rare in the setting of isolated penetrating neck trauma, current guidelines recommend against c-spine immobilization.1,5


The Thorax

Thoracic trauma is the third leading cause of traumatic death in the United States.2 Injury to the heart or major vessels should be assumed in all patients presenting with injury localized to the “cardiac box” – i.e. the area bordered by the sternal notch, bilateral nipples, and xiphoid process. Patients experiencing penetrating trauma at this anatomic locale may suffer right ventricular injury (most anterior mediastinal structure) and subsequent tamponade or exsanguination.1-3 On examination, the most reliable sign of developing tamponade physiology is a narrowed pulse pressure (Beck’s Triad is present in < 10% of cases).1

The FAST is a useful tool for evaluating cardiac injury and tamponade. Patients with tamponade secondary to cardiac trauma may require emergent pericardiocentesis prior to operative repair.1 Individuals who are hemodynamically unstable or become pulseless upon ED evaluation frequently undergo emergent thoracotomy.1

 Penetrating chest trauma that violates the pleura may also result in a pneumothorax or hemothorax.1,2,4 Pneumothorax should be presumed in patients with significant subcutaneous emphysema on examination.1,2,7 An EFAST may quickly identify the presence of a pneumothorax or hemothorax.1 All patients with evidence of tension physiology (hypotension, hypoxia, absent breath sounds, and tracheal deviation) should undergo needle decompression and subsequent thoracostomy.1 All patients with an identified hemothorax require thoracostomy to avoid the sequelae of fibrosis and empyema.1 An immediate indication for surgical intervention (versus ED thoracotomy) in the setting of a hemothorax is the release of greater than 1,500 mL of blood upon initial placement of a chest tube, or persistent drainage of at least 150-200 mL of blood for greater than 2 hours after chest tube placement.1,7


The Abdomen

Hemodynamically unstable patients with penetrating trauma to the abdomen, or those who present with frank evisceration, require exploratory laparotomy.1 Hemodynamically stable patients with a positive FAST are appropriate for advanced imaging (CT). If there is question regarding fascial penetration, bedside wound exploration should only be undertaken by a specialist (general/trauma surgeon).1,2


The Extremities

Similar to bleeding at other anatomic locations, initial management of extremity trauma concentrates on hemostasis through the application of direct pressure or pressure dressings.1 Tourniquet application should be considered in the setting of life threatening hemorrhage.1 In this patient population, the secondary survey should focus on the evaluation of injury to vascular, neurologic, and musculoskeletal structures.1 Similar to neck injuries, penetrating trauma localized to the extremities require attention to hard and soft signs (Figure 2).1 Hard signs which require surgical management are absent or diminished pulses, obvious arterial bleeding, expanding hematoma or pulsatile bleeding, audible bruit, palpable thrill, or distal ischemia.1 Soft signs requiring additional diagnostic evaluation include small hematomas, nerve injury, unexplained hypotension, history of hemorrhage, proximal vascular damage without hypotension, and complex fracture.1 As with neck injuries, avoid clamping vessels in the extremities as this intervention carries high risk of arterial or nerve damage.1

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Final Words

It is important to perform a thorough secondary examination of all patients presenting with a penetrating injury. Wounds hidden in skin folds, the axilla, or nape of the neck are easily missed. All impaled objects that remain in place upon arrival to the ED should not be removed, but rather stabilized.1,4

How should our patients in the cases be managed?

Case I: The patient is stable and does not require emergent surgical intervention as his wound is localized to zone II and does not violate the platysma. He is likely to undergo advanced imaging given his intoxication.

Case II: The patient should be taken to the operating room for diagnostic laparotomy given her persistent hypotension despite resuscitation.

 Case III: The patient is hemodynamically stable with gaping, hemostatic wounds to the skull and forearm. Given his altered mental status and absence of vital sign abnormalities, increased ICP should be assumed: head of bed elevated 30°, hyperventilated to a pCO2 of 35, and 3% NS delivered (+/- mannitol administered per institutional policy or in consultation with trauma surgery/neurosurgery). CT imaging subsequently revealed a large epidural hematoma with 3 mm of midline shift.

Case IV: The patient’s chest X-ray was notable for subcutaneous emphysema, and CT of the chest revealed significant subcutaneous emphysema with a large apical pneumothorax. A left sided chest tube was placed and the patient was admitted for further evaluation with bronchoscopy and EGD.



  • ED management of a patient with a penetrating injury begins with addressing the ABCs.
  • The first step in addressing active bleeding is the application of direct pressure.
  • Patients with head wounds commonly undergo advanced imaging to rule out foreign body and underlying trauma.
  • Hemorrhagic shock, airway obstruction, air discharge from a wound, active pulsatile blood flow, massive hemoptysis, and uncontrolled bleeding in patients with neck injuries mandate immediate surgical intervention.
  • Assume cardiac and great vessel injury in all patients with trauma to the cardiac box.
  • Hemodynamically unstable patients with abdominal trauma require operative intervention.
  • Patients with penetrating injuries to the extremities with absent or diminished pulses, obvious arterial bleeding, expanding hematoma or pulsatile bleeding, audible bruit, palpable thrill, or distal ischemia require operative intervention.


References / Further Reading

  1. Tintinalli, J.E., Stapczynski, O.J., Ma, D.M., Meckler, G.D., Cline, D.M. Tintinalli’s Emergency Medicine: A Comprehensive Study Guide, 8th www.accessmedicine.com. 2015.
  2. LoCicero, J., Mattox, K.L. Epidemiology of Chest Trauma. Surgical Clinics of North America. 69(1): 15-9. 1989. PMID: 2911786.
  3. Sormann, P., Wutzler, S., Sommer, K., Marzi, I., Lustenberger, T., Walcher, F. Gunshot and Stab Wounds: Diagnosis and Treatment in the Emergency Room. Emergency and Rescue Medicine. 2(1-9). 2016. DOI: 10.1007/s10049-016-0162-9
  4. Daya, N.P., Liversage, H.L. Penetrating Stab Wound Injuries to the Face. Europe PMC. 2004. 59(2):55-59. PMID: 15181702.
  5. White, C.C., Domeier, R.M., Millin, M.G. National Association of EMS Physicians and American College of Surgeons Committee on Trauma. EMS Spinal Precautions and the Use of the Long Backboard. Available from: http://www.naemsp.org/Documents/Position%20Papers/EMS%20Spinal%20Precautions%20and%20the%20Use%20of%20the%20Long%20Backboard_Resource%20Document.pdf
  6. Bothwell N. Acute Management of Pharyngoesophageal Trauma. Ch 30. Department of Defense. Otolaryngology/Head and Neck Surgery Combat Casualty Care in Operation Iraqi freedom and Operation Enduring Freedom. Army Borden Institute.
  7. Mowery, N.T., Gunter O.L., Collier, B.R., Diaz, J.J. Hemothorax and Occult Pneumothorax; Management of. Journal of Trauma. 2011. Feb; 70 (2): 510-8. Available from: https://www.east.org/education/practice-management-guidelines/hemothorax-and-occult-pneumothorax,-management-of

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.