Diving Deep: Pulmonary Barotrauma in a Free Diver


A 24-year-old male presented to the Emergency Department with cough and hemoptysis. The patient had been spearfishing when his symptoms began. The patient had dove to a depth of 50 feet using 11 lbs of weights on his belt, holding his breath along the way. On the way to the surface, he developed chest pain. After getting onto the boat, the patient coughed up approximately 5 tablespoons of bright red blood. After feeling a bit better, he went down again to a depth of 30 feet in order to catch a large fish. After returning to his boat, the patient was still experiencing cough, pleuritic chest pain, and mild shortness of breath.

On arrival to the emergency department, the patient was breathing comfortably on room air. He did not complain of any headache, visual changes, ear pain, nausea, joint or muscle pain, or any other symptoms. On exam, he was comfortable and his lungs were clear to auscultation bilaterally. The patient had no further hemoptysis after arrival to the emergency department. Given the patient’s chest pain and subjective shortness of breath, a chest x-ray was performed.

 Chest X-ray notable for patchy, bilateral, midlung predominant airspace disease.

Chest X-ray notable for patchy, bilateral, midlung predominant airspace disease.

The patient was placed on supplemental oxygen and was admitted to the medical ICU for close monitoring overnight. Pulmonology was consulted who recommended supportive care and repeat chest x-ray the following day. A CT scan of the chest was preformed to evaluate for any underlying pulmonary parenchymal disorders.

 Single image from chest CT scan showing bilateral patchy airspace disease

Single image from chest CT scan showing bilateral patchy airspace disease

A chest x-ray was completed the following morning in the medical ICU.

 Chest X-ray notable for grossly stable, patchy bilateral airspace disease that is midlung predominant.

Chest X-ray notable for grossly stable, patchy bilateral airspace disease that is midlung predominant.

The patient remained hemodynamically stable and without respiratory distress throughout his hospitalization. He was discharged home on hospital day #2.


Spearfishing may be done while freediving, snorkeling or SCUBA diving. Our patient and his friends were freediving, or breath-hold diving.  Unlike SCUBA diving, breath-hold divers do not use supplemental air underwater.  Divers face a unique set of underwater hazards in addition to the general aquatic problems; such as drowning, hypothermia, water-borne infectious diseases, and interactions with hazardous marine life.  When diving deep, free divers are exposed to increased pressure, causing a spectrum of injuries to the body.

Pressure contributes either directly or indirectly to the majority of serious diving-related medical problems. As a diver descends underwater, absolute pressure increases much faster than in air. The pressure change with increasing depth is linear, although the greatest relative change in pressure per unit of depth change occurs nearest the surface, where it doubles in the first 33 feet of sea water. The body behaves as a liquid and follows Pascal’s law; pressure applied to any part of a fluid is transmitted equally throughout the fluid. When a diver submerges, the force of the tremendous weight of the water above is exerted over the entire body. The body is relatively unaware of this change in pressure.

 Pascal’s Law: pressure applied to any part of a fluid is transmitted equally throughout the fluid.  Source:

Pascal’s Law: pressure applied to any part of a fluid is transmitted equally throughout the fluid.


This is true of the body, however the spaces within the body that contain air, including the lungs, sinuses, intestines, and middle ear follow a different law. The gases in these spaces obey Boyle's law; the pressure of a given quantity of gas at constant temperature varies inversely with its volume. Therefore, as you dive deeper, the volume of air in the middle ear, sinuses, lungs, and gastrointestinal tract is reduced. Inability to maintain gas pressure in these body spaces equal to the surrounding water pressure leads to barotrauma.

 Boyle’s Law: the pressure of a given quantity of gas at constant temperature varies inversely with its volume.  Source:

Boyle’s Law: the pressure of a given quantity of gas at constant temperature varies inversely with its volume.


Barotrauma can potentially involve any area with entrapment of gas in a closed space. In addition to sinuses, lungs and the GI tract, the barotrauma can occur to the external auditory canal, includes teeth, the portion of the face under a face mask, and skin trapped under a wrinkle in a dry suit. The tissue damage resulting from such pressure imbalance is commonly referred to as a “squeeze”. 

Given that our patient’s only complains were respiratory in nature; hemoptysis, shortness of breath, cough with deep breathing, we will focus on pulmonary barotrauma. Pressure related injury to lung can occur on the way down or as a diver ascends to the surface.



Recall from physiology that if you were able to completely exhale, the absolute minimum lung volume remaining is called the residual volume (RV). Lung squeeze occurs when the when the diver descends to a depth at which the total lung volume is reduced to less than the residual volume. At this point, transpulmonic pressure exceeds intraalveolar pressure, causing transudation of fluid or blood from ruptured of pulmonary capillaries. (1) Patients exhibit signs of pulmonary edema and hypoxemia.

 Lung Volumes  Source:

Lung Volumes


Despite this presumed mechanism of barotrauma of descent, free divers are able to dive to depths beyond those that should cause mechanical damage to the lungs. Other physiologic mechanisms must play a role, although the exact pathophysiology of this condition remains unclear. When diving deep, the chest cavity itself gets smaller and there is central pooling of blood in the chest from the surrounding tissues. The central pooling of blood in the chest equalizes the pressure gradient when the RV is reached and thereby decreases the effective RV. This mechanism increases the pressure in the pulmonary vascular bed causing rupture of the pulmonary capillaries and intrapulmonary hemorrhage. This is the reason that many free divers cough up blood after deep dive. These mechanisms allow the lungs to be compressed down to about 5% of Total Lung Capacity in highly-trained breath-hold champions. (2) Although there are several  case reports of lung squeeze occurring with shallow diving, typically with repetitive dives with short surface intervals. (3) An individual’s anatomy, physiologic reserves, underlying pathology and the conditions of the day all play a role in the development of pulmonary barotrauma. (2)


As a diver ascends, the pressure within the alveoli of the lung increase as the pressure around the diver decreases. Remember Boyle’s law? If intrapulmonary gas is trapped behind a closed glottis, as the diver ascends and the surrounding pressure decreases, the volume of the intrapulmonary gas increases. Increased pressure within the lung causes an increase in transalveolar pressure leading to overexpansion injury and alveolar rupture. (4) A situation of rapid ascent to the surface, such as if a diver runs out of air, panics, or drops his weights, is often the cause of pulmonary barotrauma of ascent. Divers who hold a breath as they ascend and those with obstructive airway diseases, such as asthma or chronic obstructive pulmonary disease, are at increased risk. This was likely the case with our patient, he did not exhale and relieve the building pressure as he ascended, causing his pulmonary barotrauma.

Eventually, the intrapulmonary pressure rises so high that air is forced across the pulmonary capillary membrane. The specific clinical manifestations of pulmonary barotrauma depend on the amount of air that escapes the alveoli and location that it travels to. Air can rupture alveoli, causing localized pulmonary injury and alveolar hemorrhage. (4) Pulmonary interstitial air can dissect along bronchi to the mediastinum causing pneumomediastinum, the most common form of pulmonary barotrauma. This air can track superiorly to the neck, resulting in subcutaneous emphysema. Rarely, air may reach the visceral pleura, causing a pneumothorax.

If air enters the pulmonary vasculature, it can travel to the heart and embolize to other parts of the body, causing arterial gas embolism (AGE). Clinical manifestations of cerebral air embolism are sudden and can be life-threatening. Approximately 4% of divers who suffer an AGE die immediately from Total occlusion of the central vascular bed with air. (5,6) AGE patients who make it to the hospital usually present with hemoconcentration due to plasma extravasation from endothelial injury. (7)  The degree of hemoconcentration correlates with the neurologic outcome of the diver. (7) Creatinine kinase is elevated in cases of AGE and correlates with neurologic outcome of the diver. (8) All cases of AGE must be referred for hyperbaric oxygen treatment as rapidly as possible. (9) All suspected AGE patients should be referred for hyperbaric consultation, even if initial neurologic manifestations resolve prior to reaching an ED in order to prevent progression of subtle neurologic deficits that are not immediately detected.

Our patient dove to a depth of 50 feet and reported holding his breath while resurfacing, therefore it is likely that he experienced pulmonary barotrauma of ascent. However, cases of lung squeeze have occurred with free diving to more shallow depths. (3) Regardless, the emergency department management of the spectrum of pulmonary barotrauma is similar.



First of all, stop the dive! Ensure the safety of the injured diver and help them relax. Help the injured diver exit the water to prevent any strenuous physical activity. When available, have the diver breath 100% oxygen. Avoid exposure to pressures (such as flying or a repeat dive). On arrival to the ED, perform a complete history and physical. Evaluate for any signs of AGE, such as a transient episode of neurologic dysfunction immediately after surfacing.  

A diver with local pulmonary injury without any evidence of AGE does not require recompression and should be treated with supportive care, consisting of rest and supplemental oxygen in severe cases. Most diving-related pneumothoraces are small, therefore treatment may consist simply of supplemental oxygen and close observation. If the diver requires recompression, a chest tube must be placed in order to prevent a tension pneumothorax during depressurization from a hyperbaric chamber. Depending on where you practice, consider transferring the patient to a tertiary care facility if the clinical presentation is worsening, if there are further episodes of hemoptysis, or if the patient requires further testing, such as broncoscopy. To date, I have been unable to find any data that supports the use of steroids, diuretics, or other medications to treat this condition. Patients should rest for at least two weeks before resuming diving and preferably after being cleared fit to dive by a physician with knowledge of dive related injuries.


Divers Alert Network (DAN) is a not-for-profit diving safety medical organization. DAN's medical staff is on call 24 hours a day, 365 days a year, to handle diving emergencies. They can be reached via and through a medical hotline 1-919-684-9111.


  • Pressure contributes to the majority of diving-related medical problems.

  • The spaces within the body that contain air, including the lungs, sinuses, intestines, and middle ear obey Boyle's law; the pressure of a given quantity of gas at constant temperature varies inversely with its volume.

  • As you dive deeper, air in the middle ear, sinuses, lungs, and gastrointestinal tract is reduced in volume. As you resurface, the pressure of the gas decreases and the volume expands.

  • When breath-hold diving to deep depths, divers may experience “lung squeeze”, or transudation of fluid or blood from ruptured pulmonary capillaries causing non-cardiogenic pulmonary edema.

  • On ascent, over distension causes alveolar rupture and may cause air to escape into an extraalveolar locations.

    • Possible presentations are pneumomediastinum, subcutaneous emphysema, pneumothorax, or arterial gas embolization.

  • Treatment usually consists of supportive care, rest, avoiding further exposure to pressures (flying or repeat dives), and supplemental oxygen when needed.

  • Evaluate for any historical clues of physical exam findings suggestive of AGE as these patients require hyperbaric treatment.

  • When in doubt, call the 24-hour Divers Alert Network (DAN) emergency medical hotline at 1-919-684-9111.

Faculty Reviewers: Dr. Kristina McAteer and Dr. Victoria Leytin

Follow the discussion here on Figure 1


  1. Schaefer KE, Allison RD, Dougherty JH, Jr., et al. Pulmonary and circulatory adjustments determining the limits of depths in breathhold diving. Science 1968;162:1020-3.

  2. Lung Squeeze: Coughing your lungs out...or not! 2015. (Accessed July 15, 2018, at

  3. Raymond LW. Pulmonary barotrauma and related events in divers. Chest 1995;107:1648-52.

  4. Balk M, Goldman JM. Alveolar hemorrhage as a manifestation of pulmonary barotrauma after scuba diving. Ann Emerg Med 1990;19:930-4.

  5. Van Hoesen K., Lang, M. Diving Medicine.  Auerbach’s Wilderness Medicine. 7th ed: Elsevier, Inc.; 2017:1583-618.

  6. Neuman TS, Jacoby I, Bove AA. Fatal pulmonary barotrauma due to obstruction of the central circulation with air. J Emerg Med 1998;16:413-7.

  7. Smith RM, Van Hoesen KB, Neuman TS. Arterial gas embolism and hemoconcentration. J Emerg Med 1994;12:147-53.

  8. Smith RM, Neuman TS. Elevation of serum creatine kinase in divers with arterial gas embolization. N Engl J Med 1994;330:19-24.

  9. Cales RH, Humphreys N, Pilmanis AA, Heilig RW. Cardiac arrest from gas embolism in scuba diving. Ann Emerg Med 1981;10:589-92.

Do You 'See More' Fractures? Don’t Overlook 'Seymour' Fractures!

Co-Authors: Dr. Madalene Boyle and Dr. Andrew Beck

Case 1

A 10-year-old male presents to the ED with his parents after his finger was slammed in a car door. His parents are concerned that it’s bleeding and appears deformed. The incident occurred 30 minutes prior to presentation. His parents state that there was “a lot of bleeding.” His past medical history is notable for asthma, and there is no history of fragility fractures, connective tissue disorders, or bleeding diatheses. Physical exam reveals the injury as shown. Flexion of the digit is preserved and extension is limited due to pain and deformity. Neurovascular exam is intact. 

 Car door injury to 5th digit.

Car door injury to 5th digit.

Screen Shot 2018-08-24 at 11.41.07 AM.png

An x-ray was taken to assess for fracture and/or foreign body. The original film was unavailable, but an illustrative lateral view is shown(3). No foreign body was noted, but a characteristic injury pattern was observed.


Case 2

A 14-year old right-handed football player presents to the community Emergency Department with a right middle finger deformity. Patient was playing football when he went to make a tackle and his finger was crushed beneath another player.  

Screen Shot 2018-08-24 at 11.45.28 AM.png

On exam, his middle finger has dried blood at the base of the nail. The proximal nail appears partially avulsed. His finger appears flexed at the DIP although he is able to fire his extensors/flexors at the DIP.  He has no sensory deficits. 

 Image from Azburg, 2013.

Image from Azburg, 2013.


The Seymour Fracture

Definition & Epidemiology(1,2): Originally described in 1966 by Seymour, the eponymous Seymour fracture is defined as an open, displaced distal phalangeal fracture with associated nail bed injury. This injury can easily be overlooked as minor trauma to the nail which can have consequences for infection and growth arrest, leading to chronic deformity and loss of function.1 20-30% of phalangeal fractures in children involve the physis, and the long finger is most commonly affected. The mechanism is typically a crush injury in a door. These are Salter-Harris Type 1 or 2 fractures and the nailbed injury is commonly a laceration or plate avulsion. Often, interposition of soft tissue at the fracture site impedes bedside reduction. 

The Seymour fracture will often resemble a mallet finger. For this reason, any pediatric patient with an apparent mallet finger deformity and blood at the nail fold should be evaluated seriously for this fracture. The mallet finger appearance occurs because of an imbalance between the flexor and extensor tendons.  The extensor tendon inserts at the epiphysis of the distal phalanx. The flexor digitorum profundus inserts at the metaphysis.  There is no actual injury to the extensor tendon (as in Mallet finger). The imbalance is created through the physis or fracture site (see image). 

Diagnosis (1,2,3): Physical exam demonstrates a flexed dorsal interphalangeal joint, ecchymosis, swelling, and mallet deformity. The nail plate lies superficial to the eponychial fold which will give the appearance of a longer-than-normal nail.1,2,3 Imaging reveals a fracture through the physis along with other potential fractures. The AP radiographic view may be normal since lateral deviation is not commonly seen. The lateral view is more sensitive and will show a widened physis, displacement, and angulation. It is important not to confuse the presentation for a mallet finger which is the key differential diagnosis. Mallet fractures involve the joint while the Seymour fracture is isolated to the growth plate without epiphyseal displacement. 

...any pediatric patient with an apparent mallet finger deformity and blood at the nail fold should be evaluated seriously for this fracture.

Risks: A Seymour fracture has many associated complications. Based on fracture location, the germinal matrix (responsible for nail production) can become entrapped in the fracture site (See image above). This prevents a simple reduction of the fracture. Additionally, damage to the germinal matrix can cause a permanent nail plate deformity.  If soft tissue becomes incarcerated in the physis, it can cause growth arrest and finger length discrepancy. Importantly, failure to treat Seymour fractures as open fractures can result in infection and even chronic osteomyelitis. 

Management: These are open fractures.  In the ER, it is appropriate to give a dose of parenteral antibiotics. A first generation cephalosporin such as Cefazolin is suitable. Patients should be treated with a short (5-7 day course) of oral antibiotics upon discharge. 
A hand specialist should manage Seymour fractures. Appropriate treatment of Seymour fracture consists of removal of the nail plate, exploration of the fracture site (to ensure no tissue entrapment), thorough irrigation and debridement, and reduction. For unstable fractures, a K-wire through the fracture and DIP is sometimes necessary to maintain this reduction.  The nail bed laceration should be repaired. The nail should be replaced or stented with suture packaging material. 
Younger patients may require anesthesia and an operating room for exploration and adequate treatment. Older patients may be able to have treatment within the department with adequate pain control and local nerve blocks. 
Appropriate management of Seymour Fractures is crucial. A recent review by Reyes (2017) evaluated management and associated complications of Seymour fractures.  There was a much higher rate of infection (both superficial and osteomyelitis) in those patients who do not receive proper treatment.  Emergency Medicine providers must be able to recognize this injury in order to initiate antibiotics and facilitate appropriate consultation with a hand specialist. 

Prognosis (3): As mentioned above, nonoperative management may be possible for minimally displaced Seymour fractures. However, by definition, Seymour fractures are open and displaced, and the majority of these injuries require open reduction and fixation. Functional and cosmetic outcomes at two years are equivalent between operative and nonoperative groups when selected for treatment based on degree of displacement. Major complications include reduced range of motion, nail dystrophy, and digit length discrepancy, all of which can have major functional consequences especially if involving the 2nd or 3rd digits on the dominant hand, or if the patient requires the use of multiple digits for a profession (pianist, artist, and typist). 

Case 1 Resolution

This patient received a bedside nail bed repair with avulsion and replacement of the nail plate, then reduction via hyperflexion followed by traction and extension. The patient was splinted and received operative repair within one week of the injury. 

Case 2 resolution

A hand team was not available at the community hospital. Patient was transferred to the Children’s Hospital where he was treated by the hand team.  He underwent I+D in the ER and reduction/repair. He has since had an uneventful follow-up appointment. 


1)    Nellans KW, Chung KC. Pediatric Hand Fractures. Hand Clin. 2013 Nov; 29(4): 569–578. doi:  10.1016/j.hcl.2013.08.009. 
2)    Watts E. Seymour Fracture. Accessed 11/27/2017.
3)    Krusche-Mandl I, Kottstorfer J, Thalhammer G et. Al. Seymour fractures: retrospective analysis and therapeutic considerations. J Hand Surg Am. 2013 Feb;38(2):258-64. doi: 10.1016/j.jhsa.2012.11.015.
4)    Abzug JM, Kozin SH. Seymour fractures. J Hand Surg Am. 2013;38:2267–2270. 
5)    Reyes BA, Ho CA.  The High Risk of Infection With Delayed Treatment of Open Seymour Fractures: Salter-Harris I/II or Juxta-epiphyseal Fractures of the Distal Phalanx With Associated Nailbed Laceration. J Pediatr Orthop. 2017: 37: 247-253. 
6)    Kattan AE, AlShomer F, Alhujayri AK, Alfowzan M, Murrad KA, Alsajjan H. A case series of pediatric seymour fractures related to hoverboards: Increasing trend with changing lifestyle. International Journal of Surgery Case Reports. 2017: 38: 57-60. 




Les Midfoot Fractures: A Franc Review


A healthy 33-year-old female presents after a mechanical fall while jogging. She stumbled while stepping from the curb and fell forward into the street. She has severe right ankle and foot pain and is unable ambulate. On examination, there is diffuse swelling of her right foot and ankle with tenderness throughout, especially at the dorsal aspect of the foot. There is a small amount of plantar ecchymosis. X-rays of the foot are obtained.

Case AP XR.jpg

What is your next move?

Do you provide the patient with and ace wrap and crutches and discharge her home? What else should be considered? Are the details of her mechanism helpful?  Are there radiographic findings suggestive of occult fracture? What examination findings are suggestive of an occult pathology?


Originally described during the Napoleonic wars without the aid of multidetector computed tomography scanners, Lisfranc injuries remain an important consideration in foot trauma but are fraught with diagnostic challenges. Often describing a fracture/dislocation to any portion of the tarsometatarsal joint complex, Lisfranc injuries can lead to significant morbidity and functional impairment if missed (which occurs in up to 20% of cases). The stability of the complex is primarily conferred by the articulation of the second metatarsal with the middle cuneiform and the Lisfranc ligament (oblique interosseous ligament) which connects the base of the second metatarsal with the medial cuneiform.

Mechanism of Injury 

The key to making a correct diagnosis begins with a high index of suspicion based on history (e.g. mechanism) and exam because radiographic findings may be subtle. Direct injury is usually from blunt trauma to the dorsal foot or from crush injury. Indirect injuries are often associated with extreme hyperplantarflexion or rotation of a fixed midfoot. Other common mechanisms include motor vehicle collisions and sports that require stirrups, bindings, or foot straps. Interestingly, one third of Lisfranc injuries are associated with seemingly minor mechanisms.

Radiograph Review 

Lisfranc injuries range from subtle, sometimes undetectable subluxations to obvious fracture-dislocations. A methodical review of x-rays is essential to assessing for a Lisfranc injury. Special attention should be paid to alignment and focuses on two key relationships. First, the medial borders of the second metatarsal and the middle (second) cuneiform should be well-aligned on the AP view, as should the lateral borders of the first metatarsal and the medial (first) cuneiform. Second, the distance between the first two metatarsals should be examined, as this distance is commonly increased with Lisfranc injuries. Widening between the metatarsals and/or cuneiforms may be more apparent with oblique views.

Suggestive Exam Findings

  • Inability to ambulate or stand on toes
  • Significant pain/swelling of the midfoot
  • Plantar ecchymosis
  • Positive pronation-abduction test (pain with forefoot abduction and pronation with fixed hindfoot)

Suggestive Radiographic Findings

  • Widening between the first and second metatarsals and/or medial and middle cuneiforms – Image 3
  • Malalignment of the first and second metatarsals with the medial and middle cuneiforms, respectively, on the AP view (as described above) – Image 4
  • Malalignment of the medial and lateral borders of the third metatarsal and lateral cuneiform on the oblique view
  • Malalignment of the medial borders of the fourth metatarsal and cuboid on the oblique view
  • Fleck sign (avulsion fracture of second metatarsal base) – Image 5
  • Step-off sign (dorsal metatarsal displacement) on lateral view
  • Cuboid or cuneiform fractures

Image 3: Radiograph demonstrating widening between the first and second metatarsals (Click to expand)

Image 4: Radiograph demonstrating malalignment of the medial and lateral borders of the third metatarsal and lateral cuneiform (Click to expand)

Image 5: Radiograph demonstrating the "fleck sign." Indicative of an avulsion fracture of the base of the second metatarsal (Click to expand)

Role of CT  

Interpretation of radiographs may be limited secondary to suboptimal positioning and the inherent overlapping bony articulations of the midfoot. Classically, weight-bearing views are suggested; however, adequate weight-bearing views are often limited by pain. Advanced imaging is advantageous in these cases and allows for visualization of subtle findings in multiple planes. A CT should be obtained if the diagnosis remains in question despite normal-appearing radiographs if there are suggestive exam findings or the patient is unable to bear weight.


When improperly managed, Lisfranc injuries can lead to pes planus deformity and functional limitations secondary to arthritis and pain with weight bearing. Stable ligamentous injuries (with displacement <2mm) may be managed conservatively with short leg casting and non-weight bearing for 6 weeks. Stability can be reassessed with weight bearing radiographs at two weeks. Prior to proceeding with non-operative management, advanced imaging should be considered to better evaluate the extent of injury. Unstable or displaced injuries are typically managed with open reduction and internal fixation. In the emergency department, orthopedic consultation is recommended in all suspected or confirmed cases of Lisfranc injury.

Key Points

  • A high index of suspicion must be maintained to identify subtle Lisfranc injuries. Foot pain and swelling after trauma, especially when associated with inability to bear weight, should be suspected of having a Lisfranc injury.
  • The second metatarsal base should always be carefully assessed for displacement, avulsion, and fracture. The alignment of the second metatarsal with the middle cuneiform and spacing between the first and second metatarsals are the most consistent and easily assessed relationships on AP radiographs.
  • CT scan should be obtained in cases of normal-appearing radiographs when there is remaining clinical suspicion.
  • Missed Lisfranc injuries can result in long-term disability.

Faculty Reviewer: Jefferey Feden, MD

Image Credits

  1. Courtesy Dr. Henry Knipe,
  2. Courtesy Dr. Henry Knipe,
  3. Courtesy RMH Core Conditions,


Desmond, E. A., & Chou, L. B. (2006). Current concepts review: Lisfranc injuries. Foot Ankle Int, 27(8), 653-660.

Englanoff, G., Anglin, D., & Hutson, H. R. (1995). Lisfranc fracture-dislocation: a frequently missed diagnosis in the emergency department. Ann Emerg Med, 26(2), 229-233.

Foster, S. C., & Foster, R. R. (1976). Lisfranc's tarsometatarsal fracture-dislocation. Radiology, 120(1), 79-83.

Gupta, R. T., Wadhwa, R. P., Learch, T. J., & Herwick, S. M. (2008). Lisfranc injury: imaging findings for this important but often-missed diagnosis. Curr Probl Diagn Radiol, 37(3), 115-126.

Hunt, S. A., Ropiak, C., & Tejwani, N. C. (2006). Lisfranc joint injuries: diagnosis and treatment. Am J Orthop (Belle Mead NJ), 35(8), 376-385.

Lau, S., Bozin, M., & Thillainadesan, T. (2017). Lisfranc fracture dislocation: a review of a commonly missed injury of the midfoot. Emerg Med J, 34(1), 52-56.

Perron, A. D., Brady, W. J., & Keats, T. E. (2001). Orthopedic pitfalls in the ED: Lisfranc fracture-dislocation. Am J Emerg Med, 19(1), 71-75.

Ross, G., Cronin, R., Hauzenblas, J., & Juliano, P. (1996). Plantar ecchymosis sign: a clinical aid to diagnosis of occult Lisfranc tarsometatarsal injuries. J Orthop Trauma, 10(2), 119-122.

Watson, T. S., Shurnas, P. S., & Denker, J. (2010). Treatment of Lisfranc joint injury: current concepts. J Am Acad Orthop Surg, 18(12), 718-728.