Snap, Crackle, and Pop: Imaging and Management of Blunt Laryngeal Trauma

The Case

A 26 year-old male presents after a motorcycle accident. He was the helmeted, single-occupant of a motorcycle that crashed into the back of a stopped car. There are no external signs of injury, but he believes his neck may have hit the handlebars as he was thrown from the bike.  He denies loss of consciousness. His only complaint is that his voice sounds hoarse and he is having difficulty swallowing. He denies any intoxicants.

The patient has a normal primary traumatic survey. His secondary survey is notable for crepitus of the anterior neck. No chest wall crepitus is noted. No stridor or bruit is appreciated on anterior neck auscultation.  There is no cervical hematoma or ecchymosis. There is no midline C-spine tenderness. There is no blood in the oropharynx. His voice is raspy, but he is able to phonate and adequately handle his secretions. He has no other traumatic complaints or physical exam abnormalities on secondary survey.

A chest x-ray is without any evidence of pneumothorax.

You wonder what imaging should be performed next. Does he need a CT brain based on his history? Does crepitus count as a distracting injury? Should he have a CTA in the absence of any hard vascular signs? After discussion with the trauma team, CT imaging including a CTA neck is performed (Figure 1).

Figure 1: Non-contrast portion of the CTA neck.

Figure 1: Non-contrast portion of the CTA neck.

CT imaging reveals a left hyoid bone fracture, as well as a comminuted fracture of the right thyroid cartilage. His CTA is normal. He has no intracranial injuries, face or C-spine fractures. There is considerable soft tissue emphysema.

Background on blunt laryngeal trauma

Blunt laryngeal trauma is rare.  The reported incidence of laryngeal fractures is 1:30,000 patients presenting to the ER. The low incidence is secondary to the relative protection by adjacent bony structures (the mandible, manubrium, and vertebral bodies). Furthermore, humans are equipped with a protective reflex to flex their heads downward when startled, further shielding this vulnerable region from trauma.  

Laryngotracheal injury occurs when patients lose their ability to protect this area, and are most commonly associated with motor vehicle accidents, when a hyperextended neck strikes a fixed object (steering wheel, dash board).  Recreational vehicles are also increasingly implicated (motorcycles, four-wheelers striking branches). Other mechanisms of injury include strangulation, assault, or hanging.

The patterns of injury vary depending upon the age and gender of the patient. Women are at increased risk for subglottic and cervical tracheal injuries owing to their tendency towards longer necks.  The thyroid and cricoid cartilage also ossify as part of the normal aging process (typically beginning around age 18-20), and for this reason, elderly patients are at increased risk for comminuted fractures of these structures. Conversely, children have flexible cartilage and are much less likely to sustain laryngeal fractures.

Brief review of anatomy

The larynx consists of a cartilaginous skeleton, the intrinsic and extrinsic muscles, and a mucosal lining. The cartilaginous skeleton houses the vocal cords. It consists of the thyroid cartilage, the cricoid cartilage, and the paired arytenoid cartilages. The thyroid cartilage is connected superiorly to the hyoid bone. The extrinsic muscles connect the cartilage of the larynx to other structures of the head and neck (i.e. sternothyroid muscle, etc.). The intrinsic muscles alter the shape, tension and position of the vocal cords (Figure 2).

Figure 2: Anatomy of the laryngotracheal complex.

Figure 2: Anatomy of the laryngotracheal complex.

Injuries range from mucosal hematomas and lacerations to fractured cartilage. The most severe laryngeal injury is complete laryngotracheal separation (Figure 3). Classification of these injuries will be covered in the Classification and Definitive Management section.

Figure 3: Types of laryngotracheal injuries. trauma-070328.pdf

Figure 3: Types of laryngotracheal injuries. trauma-070328.pdf

Signs and Symptoms

The mechanism of injury is important. The provider should take careful consideration of any history which lends itself to the possibility of “clothesline” type injury, namely forced hyperextension and forward propulsion or direct trauma to the anterior neck (strangulation, hanging).

Patients will report dysphonia, odynophagia, dysphagia, neck pain, dyspnea or hemoptysis. Studies suggest that hoarseness is the most common presenting symptom of laryngeal trauma.  Juutilainen et al reviewed 33 cases of external laryngeal trauma, and 28 (85%) of those cases presented with hoarseness. Physical exam may reveal stridor, dyspnea, ecchymosis, subcutaneous emphysema, hemoptysis, loss of the thyroid prominence or drooling. However, it is important to note that no single symptom correlates with injury severity and the absence of these findings does not exclude the possibility of laryngeal injury.

Initial Management

Airway management is crucial. If a patient with a suspected laryngeal injury has no evidence of respiratory distress or airway compromise, proceed with a standard traumatic work-up.

If the airway is not patent (respiratory distress, airway obstruction, stridor, not handling secretions, hypoxic), establishing an airway becomes a priority.  In these cases, tracheotomy is preferred to endotracheal intubation, as intubation can exacerbate laryngeal trauma and precipitate complete obstruction. It can also be extremely challenging to intubate because of distorted anatomy and poor visualization, with a risk for passing the ET tube through a false lumen created by the trauma. Furthermore, adequate positioning can be challenging if there is associated maxillofacial injuries and/or the need for C-spine precautions. That being said, there is no absolute contraindication for endotracheal intubation and if the patient is crashing, the most experienced airway provider should attempt it. Again, most of the otolaryngology literature favors tracheotomy, but if palpation of the larynx reveals continuity of the thyroid cartilage and cricoid cartilage, cricothyroidotomy can be performed if it is the only available, expedient airway. 

Importantly, laryngeal trauma carries a high risk of concomitant injury. There is a 13-15% incidence of associated intracranial injuries; skull base and facial fractures are seen in approximately 21%; C-spine fractures are seen in 8%; and esophageal/pharyngeal injuries occur in approximately 3% of these cases. Thus, it is best to have a low threshold for additional imaging studies. CT is the imaging modality of choice, but should only be undertaken in those patients with a stable or secured airway. There is no definite literature on the utility of CTA in blunt laryngeal trauma, but if a patient has any hard signs of vascular injury (bruit/thrill, expanding hematoma, pulse deficit) or signs of an acute ischemic stroke, there should be significant concern for an associated vascular injury.

Classification and Definitive Management

The Schafer-Fuhrman Classification scheme has been created to characterize laryngeal injuries.

Grade I: Minor endolaryngeal hematomas or lacerations, no fracture

Grade II: Edema, hematoma, minor mucosal disruption without exposed cartilage, non-displaced fracture, varying degrees of airway compromise

Grade III: Massive edema, large mucosal lacerations, exposed cartilage, displaced fracture(s), vocal cord immobility

Grade IV: Group III with severe mucosal disruption, disruption of the anterior commissure, and unstable fracture, 2 or more fracture lines

Grade V: Complete laryngotracheal separation

This classification scheme relies on both CT imaging and direct visualization. As part of the work-up for laryngeal injury, flexible fiberoptic laryngoscopy should be performed, usually by otolaryngology. During laryngoscopy, care should be taken to observe for any deformities, edema, hematomas, lacerations, exposed cartilage and partial or complete vocal cord fixation (suggesting a recurrent laryngeal nerve injury).

There is no definite recommendation for the work-up of esophageal injury. In some instances, esophageal injury can be seen on CT imaging (paraesophageal stranding or gas, lumen communicating with gas/fluid).  If, however, the suspicion for esophageal injury is high, additional studies can be pursued, beginning with a gastrograffin swallow study, followed by a dilute barium swallow for more complete evaluation.

The definitive management of laryngeal injuries depends on the injury pattern. Group I and some Group II injuries can be conservatively managed. This generally consists of humidified air, voice rest, head of bed elevation, steroids, anti-reflux medications, and antibiotics. Patients will often be admitted to the ICU for the first 24-48 hours given the potential airway compromise. They may undergo serial laryngoscopy for daily injury surveillance.

Group III-Group V injuries require operative intervention. These are the injury patterns that usually undergo tracheotomy.  Group V patients always have tracheotomies and represent a significant surgical challenge. Notably, there are multiple operative approaches and interventions for laryngeal trauma that are beyond the scope of this post.

Case Outcome

The patient was seen and scoped by otolaryngology in the ED.  This showed a supraglottic hematoma, but no lacerations or exposed cartilage. His vocal folds were mobile.  He was admitted to the trauma ICU, where he underwent a negative barium swallow, and ultimately, did not require operative intervention.

Faculty Reviewer: Dr. Kristina McAteer


  1. Becker M, Leuchter I, Platon A, Becker CD, Dulguerov P, Varoquaux A. Imaging of laryngeal trauma. Europeal Journal of Radiology. Jan 2014: 83(1):142-154.  

  2. Eller RL, Dion G, Spadaro E. Management of Acute Laryngeal Trauma. Accessed on 12.05.07.  

  3. Font JP, Quinn FB, Rayan MW. Laryngeal Trauma. trauma-070328.pdf Accessed on 12.05.17.  

  4. Jalisi S, Zoccoli M. Management of laryngeal fractures—A 10-year experience. Journal of Voice. Jul 2011;25(4):473-479.

  5. Jewett BS, Shockley WW, Rutledge R. External laryngeal trauma analysis of 392 patients. Archives of Otolaryngology–Head & Neck Surgery. Aug 1999;125(8):877-880.

  6. Juutilainen M, Vintturi J, Robinson S, Bäck L, Lehtonen H, Mäkitie AA. Laryngeal fractures: clinical findings and considerations on suboptimal outcome. Acta Otolaryngol. Feb 2008: 128(2):213–218.

  7. Murr AH and Amin MR. "Laryngeal Trauma"In CURRENT Diagnosis & Treatment in Otolaryngology - Head & Neck Surgery, 2nd Edition Ed. by Anil K. Lalwani.

  8. Mendelsohn AH, Sidell DR, Berke GS, John MS. Optimal timing of surgical intervention following adult laryngeal trauma. Laryngoscope. Oct 2011;121(10):2122-2127.

  9. Schaefer SD. The acute management of external laryngeal trauma. A 27-year experience. Arch Otolaryngol Head Neck Surg. Jun 1992 :118(6):598–604

  10. Schaefer N, Griffin A, Gerhardy B, Gohchee P. Early Recognition and management of Laryngeal Fractures: A Case Report. Ochsner J. 2014: 14)10):264-265.

Orbital Floor Blowout Fracture


A 16-year-old male presents with head trauma. The patient was in gym class when another classmate ran into him, kneeing him in the left eye. There was no loss of consciousness. On presentation, the patient complains of headache, dizziness, nausea, visual disturbance, and photophobia. He has vomited several times. On review of systems, the patient also endorses double vision and numbness over the left cheek. The patient’s mother notes he is alert but is slow to respond to questions.  He has no prior history of facial fractures.

Physical Exam

BP 130/70, HR 58, RR 20, SpO2 99% on RA, Temp 98.6 F

The patient is alert and oriented.  He appears uncomfortable but is in no acute distress.

HEENT exam with left periorbital ecchymosis and edema, with tenderness to palpation. Diminished sensation to light touch over cheek and upper lip. Nasal bridge swelling and tenderness, with subtle nasal deviation to the right. No septal hematoma. Symmetric smile.

Pupils are equal, round, and reactive to light. No hyphema or subconjunctival hemorrhage. Left eye with decreased up-gaze as compared to the right. Extraocular movements of the left eye are painful.

The neck has normal range of motion. There is no cervical midline tenderness to palpation.

The patient’s history and examination are significant for trauma to the left eye and face. His examination reveals bony tenderness, with decreased sensation to light touch, and evidence of inferior rectus entrapment as evidenced by abnormal extraocular movements. These findings are concerning for orbital blow-out fracture. There is also concern for nasal bone fracture given nasal bridge swelling, tenderness, subtle deviation, and epistaxis. Given patient’s nausea, vomiting, dizziness, and slowed responses to questions (as per patient’s mother), intracranial injury was also considered.

The patient underwent a CT of the brain and face, with thin (1mm) cuts through the orbits (Figure 1).

Figure 1: Axial CT of the face (bone window) with fracture through the left orbital floor, with herniation of the orbital fat (“teardrop” sign) and inferiorly displaced inferior rectus muscle

Figure 1: Axial CT of the face (bone window) with fracture through the left orbital floor, with herniation of the orbital fat (“teardrop” sign) and inferiorly displaced inferior rectus muscle


Figure 2: Anatomy of the orbit (

Figure 2: Anatomy of the orbit (

The orbit is composed of six bones. The frontal bone forms the superior orbital rim and the roof of the orbit. The sphenoid bone and the zygomatic bone form the lateral wall of the orbit. The maxilla and the zygomatic bone form the infraorbital rim and floor of the orbit. Finally, the maxilla and ethmoid bones form the medial wall of the orbit (Figure 2).

Housed within, or within in close proximity to the bony orbit are the globe, six extra-ocular muscles, the infraorbital and supraorbital nerves, lacrimal duct system, medial and lateral canthal ligaments, and 4 pairs of sinuses (Neuman).

A blowout fracture is a fracture through any of the orbital walls, with an inferior fracture through the floor being the most common (Knipe). It is caused by direct force to the orbit. In children, nearly 50% of these injuries occur during sports, with the direct blow usually coming from a ball or another player (Hatton).

A trap door fracture is a sub-type of the orbital floor fracture. It is a linear fracture that inferiorly displaces and then recoils back to near-anatomic position. With this movement there is concern for entrapment of orbital fat and inferior rectus muscle, resulting in ischemia, restriction of ocular movement, and visual disturbance (Hacking). The trap door fracture is predominantly seen in the pediatric population, owing to increased elasticity of the orbital floor (Chung, Grant).

Clinically, a patient will present with periorbital edema and ecchymosis. Altered sensation or numbness over the cheek, upper lip, and upper gingiva is suggestive of infraorbital nerve injury. Proptosis of the eye is suggestive of orbital hematoma. A posteriorly displaced globe (enophthalmos) is suggestive of increased orbital volume secondary to fracture. An inferiorly displaced globe (orbital dystopia) is a result of muscle and fat prolapse into the maxillary sinus. Restricted and/or painful extraocular movements are suggestive of muscle entrapment (Neuman).

In children, a phenomenon called the oculocardiac reflex can occur. Stimulation of the ophthalmic division of the trigeminal nerve due to traction or pressure on the extraocular muscles or globe results in excitation of the vagus nerve, leading to bradycardia, nausea, and syncope. In severe cases, asystole can occur (Sires).

CT of the face, with thin (1mm) cuts through the orbit is the primary modality used for identification of orbital blowout fractures. Plain radiographs of the face and orbits are no longer the gold standard as they have poor sensitivity and specificity.  Trap door fractures may be occult, but any evidence of soft tissue herniation into the maxillary sinus (also known as the “teardrop” sign) should raise suspicion for a clinically significant fracture.

These injuries can be severe, and are often more significant in the pediatric population than the adult population, owing to associated soft tissue and muscular injuries. Almost half of children with this injury will require surgery, most frequently due to entrapment. Nearly half of pediatric patients will have ocular injuries (globe rupture, hyphema, retinal tear) and nearly one third of patients will have a second facial fracture (Hatton). 

Urgent ophthalmology and facial surgery consultations are indicated for orbital floor fractures with concern for entrapment (Chung).

Symptomatic treatment includes:

  • Head of bed elevation

  • Ice

  • Sinus precautions: no nose blowing, sneeze with the mouth open, no straw use or sniffing

  • Analgesia and anti-emetics as needed


For orbital fractures with extension into a sinus, the use of prophylactic antibiotics has limited data and often varies by institution (Neuman).

Corticosteroids are recommended for patients with diminished extraocular movements to reduce swelling and expedite improvement in diplopia (Neuman).

For orbital blowout fractures with evidence of entrapment and/or oculocardiac reflex, repair should be performed within 24-48 hours. Delayed repair (more than 2 weeks after injury) can be considered if mild-moderate diplopia is not spontaneously improving, or patient has worsening of enopthalmos > 2mm after initial edema and inflammation has resolved.  Other indications for surgical repair include large fracture (involvement of greater than 50% of the orbital floor) or multiple fractures (Chung).



The patient was admitted for observation overnight in the setting of persistent nausea, vomiting, borderline bradycardia, and diplopia. He was placed on oral prednisone, as well as anti-inflammatory medication. Overnight his symptoms and heart rate improved, although he had persistent diplopia, with diminished upward gaze of the left eye. He was discharged home on hospital day 1, with plan for ophthalmology and facial surgery follow-up for operative planning.

Faculty Reviewer: Dr. Jane Preotle



  1. Chung, Stella Y., and Paul D. Langer. “Pediatric Orbital Blowout Fractures.” Current Opinion in Ophthalmology, vol. 28, no. 5, 2017, pp. 470–476., doi:10.1097/icu.0000000000000407.

  2. Grant, John H., et al. “Trapdoor Fracture of the Orbit in a Pediatric Population.” Plastic and Reconstructive Surgery, vol. 109, no. 2, 2002, pp. 490–495., doi:10.1097/00006534-200202000-00012.

  3. Hacking, Craig. “Trapdoor Fracture.”,

  4.  Hatton, Mark P., et al. “Orbital Fractures in Children.” Ophthalmic Plastic and Reconstructive Surgery, vol. 17, no. 3, 2001, pp. 174–179., doi:10.1097/00002341-200105000-00005. 

  5. Knipe, Henry, and Frank Gaillard.  “Orbital Blowout Fracture.”,

  6. Neuman, Mark, and Richard G Bachur. “Orbital Fractures.” UpToDate,

  7. Sires, Bryan S. “Orbital Trapdoor Fracture and Oculocardiac Reflex.” Ophthalmic Plastic & Reconstructive Surgery, vol. 15, no. 4, 1999, p. 301., doi:10.1097/00002341-199907000-00014.

  8. Soll, D. B., and B. J. Poley. “Trapdoor Variety of Blowout Fracture of the Orbital Floor.” Plastic and Reconstructive Surgery, vol. 36, no. 6, 1965, p. 637., doi:10.1097/00006534-196512000-00017. 

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


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  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.