Deep Diving Injuries

Deep Diving Injuries – 19 Interesting Facts

Most common DDIs (deep diving injuries) are related to barotrauma and DCS (decompression sickness) (ie, the bends or dysbarism)
DCI (decompression illness) is an umbrella term that includes both DCS and AGE (arterial gas embolism)
Barotrauma is the most common form of DDI and represents mechanical injury caused by inability to equalize pressure gradients between air-filled spaces and surrounding tissue
Usually occurs during descent if diver is unable to effectively equalize pressures between a confined air-filled space and adjacent structures; may occur on ascent, especially in the lungs, if diver holds breath
May result in conditions such as middle ear squeeze, pneumothorax, and alveolar rupture resulting in AGE
DCS may affect any organ system and occurs secondary to gas bubble formation in the circulatory system resulting in tissue ischemia, or bubble formation within tissues themselves causing direct tissue damage¹
Usually occurs during ascent, especially during uncontrolled overly rapid ascent or when other recommended diver decompression limits have been violated (eg, repeated deep diving, prolonged diving)
Most symptoms manifest after surfacing and frequently affected organs include the musculoskeletal system (especially joints), skin, vestibular apparatus, spinal cord, and brain. AGE can develop secondary to right-to-left shunting of air emboli
If critical diving injury is suspected, contact DAN 24 hours a day for diving emergencies at +1-919-684-9111
Diagnosis of DDI, including barotrauma and DCI, is largely clinical
Start 100% oxygen by nonrebreather face mask when DDI is suspected
Treat dehydration and manage hypothermia with goal of normothermia
Recompression therapy in hyperbaric (dive) chamber is the gold-standard treatment for DCI (ie, DCS and AGE) and contaminated air exposure
When indicated, initiate recompression therapy as soon as feasible and avoid delays in transfer to hyperbaric chamber for ancillary laboratory or imaging studies
Only contraindication to recompression therapy is pneumothorax without chest tube; therefore, chest radiography is advisable before recompression therapy to exclude previously undetected pneumothorax²
Prognosis for most patients with DCS (dysbarism, the bends) is favorable
Prognosis of most barotrauma depends largely on severity and type of barotrauma; most forms of barotrauma are self resolving or resolve with appropriate expedient management
Exception is inner ear barotrauma associated with cochleovestibular injury requiring procedural intervention in consultation with an otolaryngologist
Medical clearance to resume diving after significant DDI is largely individualized and based on shared decision-making in consultation with a dive medicine specialist

Alarm Signs and Symptoms

Loss of consciousness immediately after diving is highly concerning for AGE
Any neurologic changes or deficits that occur after diving are concerning for DCI involving the brain
Dyspnea with hemoptysis immediately after diving is concerning for pulmonary barotrauma
Persistent vertigo after a dive is concerning for inner ear barotrauma or DCS involving the inner ear (vestibular DCS)

Introduction

Most DDIs (deep diving injuries) are related to barotrauma and DCS (decompression sickness) (ie, the bends or dysbarism)
- Barotrauma
  - Mechanical injury caused by unequalized pressure gradients between air-filled spaces and surrounding tissue
  - May result in conditions such as middle ear squeeze, pneumothorax, and alveolar rupture resulting in AGE (arterial gas embolism)
  - Middle ear barotrauma usually occurs during descent if the diver is unable to effectively equalize pressures between a confined air-filled space and adjacent structures
  - Pulmonary barotrauma usually occurs on ascent, especially if the diver holds their breath
  - Barotrauma is the most common form of DDI
- DCS
  - Occurs secondary to gas bubble, and possibly particulate matter, formation in the circulatory system resulting in tissue ischemia or bubble formation within tissues themselves, causing direct tissue damage¹
  - May affect essentially any organ system
  - Most affected systems include musculoskeletal system (especially joints), skin, vestibular apparatus, spinal cord, and brain. AGE can occur via right-to-left shunt
  - Usually occurs during ascent, especially during uncontrolled, overly rapid ascent or when other recommended diver decompression limits have been violated (eg, repeated deep diving, prolonged diving)
- DCI (decompression illness)
  - Umbrella term that includes both DCS and AGE²
  - Both DCS and AGE can occur concomitantly, and treatment protocols are the same for both
Additional serious injuries may include immersion pulmonary edema and nonfatal drowning
Nitrogen narcosis, experienced at depths, is a leading factor in scuba-related injuries and physical trauma
Predominant factors related to most injuries include:
- Diver-specific factors: inexperience and preexisting comorbid conditions
- Dive-specific factors: rapid ascent and repeated deep diving
Adverse events may occur in a sequence beginning with trigger, then disabling agent, then disabling injury; most encountered adverse events include:³
- Triggers: insufficient gas, entrapment, equipment problems
- Disabling agents: emergency ascent, insufficient gas, buoyancy trouble
- Disabling injuries: asphyxia, AGE, cardiac incidents
Patients with injuries who survive to treatment generally recover

Epidemiology

Data indicate the following:
- An estimated 3 injuries per 100 dives⁴⁵
- Approximately 200 diving-related deaths per year worldwide⁴⁵
- Fatality rate of 1 per 200,000 dives⁴⁵
  - Drowning is the most common cause of death⁶
  - AGE is another common cause of death due to diving³
  - Cardiac incidents may be incidental and not directly dive related³

Etiology

Injuries during descent (ie, transition from lower-pressure to higher-pressure environment)
- Barotrauma involving ears, sinuses, dentition (eg, tooth repair–related), and equipment-related (eg, mask, drysuit)
  - Any air volume trapped in spaces diminishes under pressure during descent and may result in barotrauma if pressures are not adequately equalized
- Middle ear barotrauma
  - Most common form of barotrauma on descent
  - As gas volume of the middle ear decreases during descent, the tympanic membrane bends or bows inward toward the middle ear. Middle ear squeeze (ie, barotitis) results if pressures are not equalized (air added to middle ear) through the eustachian tube
  - May progress to hemorrhage in the membrane itself or into the middle ear
  - Diver inexperience with equalization maneuvers, abnormal eustachian tube morphology, and inflammation of middle ear, nasopharynx, and eustachian tube (eg, upper respiratory tract infection, allergies, smoking) increase risk of development⁷
- Inner ear barotrauma
  - Often associated with excessive equalization maneuvers (eg, Valsalva maneuver) or overly rapid descent⁸
  - Often occurs concomitant to middle ear barotrauma but may occur in isolation⁸
- External ear canal barotrauma
  - May occur with external ear canal obstruction (eg, tight hood, cerumen, earplugs)
- Sinus barotrauma may occur secondary to lack of pressure equalization between the frontal, maxillary, and ethmoidal sinuses
  - Frontal sinus involvement is most common
- Equipment-related barotrauma is related to progressively increasing negative pressure inside the mask and drysuit during descent
Injuries at depth
- Nitrogen narcosis
  - Anesthetic effect as a result of breathing compressed air, specifically nitrogen component, at depths
  - Risk is increased with deeper dives, colder water dives, preexisting fatigue or alcohol intoxication, or anxiety⁹
- Oxygen toxicity
  - Risk is increased with higher PO₂ content in the tank along with increasingly prolonged exposure times¹⁰
- Contaminated air–related manifestation
  - Carbon monoxide– or carbon dioxide–related contamination is most common
- Immersion pulmonary edema
  - Noncardiogenic pulmonary edema is more common among freedivers (breath holding and lack of breathing compressed gas)
  - Most often develops at depth but may start to develop during descent
Injuries during ascent (ie, transition from higher-pressure to lower-pressure environment)
- Alternobaric vertigo
  - Experienced by up to 25% of divers⁵
  - Occurs due to the inability to fully equalize pressure within the middle ear on one side during ascent as air volume in middle ear space expands. Increased pressures transmitted to the vestibular system from the oval and round window result in brief, self-limited symptoms⁷
  - Vomiting secondary to vertigo while still underwater is a risk. May lead to aspiration (vomitus, salt water, fresh water) and panic¹¹
- Barotrauma involving pulmonary and gastrointestinal systems, ear, and dentition
  - Air volume expands with ascent as pressures diminish during ascent and can lead to barotrauma
  - Pulmonary barotrauma may result from rapid expansion of air in lungs during ascent and include pulmonary hemorrhage, thoracic air leaks (eg, pneumomediastinum, pneumothorax), and alveolar rupture
    - Holding breath during ascent and rapid ascent place the diver at significantly increased risk for serious pulmonary barotrauma
    - Rupture of alveoli can lead to AGE with release of gas bubbles directly into the systemic arterial circulation
  - Gastrointestinal barotrauma may develop when air in the gastrointestinal tract expands during ascent, leading to gastrointestinal manifestations
    - Can result in bowel perforation when severe (rare)
  - Ear barotrauma
    - Middle ear barotrauma (ie, reverse ear squeeze)¹²
      - Middle ear barotrauma during ascent occurs due to inability to equalize pressure secondary to eustachian tube obstruction that develops at depth
      - Often related to poor equalization on descent, upper respiratory tract infection, or decongestant use
    - Inner and external ear barotrauma may also occur on ascent
  - Dental barotrauma is caused by expanding trapped pockets of air during ascent and often involves previous dental repair, resulting in consequences such as ruptured filling
- DCI
  - Previously categorized into distinct entities of DCS types 1 and 2, DCI now encompasses all forms of DCS and includes AGE
    - DCI can develop during any dive, although adherence to formally accepted dive limit tables (eg, US Navy decompression tables, National Association of Underwater Instructors dive tables) and routine use of a dive computer can help reduce the chance of occurrence
  - DCS (ie, dysbarism, the bends)
    - May involve 1 or more systems (eg, musculoskeletal, pulmonary, cutaneous, vestibular, neurologic [central nervous system, spinal cord])
    - DCS pathophysiology
      - Breathing gas at increased partial pressures results in increased oxygen and nitrogen gas dissolved in tissues
      - Increased oxygen in tissue is used by normal metabolism and is not generally problematic
      - Nitrogen is physiologically inert and may cause problems as dissolved nitrogen in tissues is liberated to free nitrogen gas in the form of small bubbles during ascent
      - Insignificant amounts of venous gas emboli are common, effectively filtered by pulmonary capillaries, and asymptomatic²
      - If pulmonary filtration is overwhelmed or free gas bubbles enter arteriolar circulation through arteriovenous malformation, bubbles in arterial circulation may cause vascular occlusion with resultant ischemia²
      - Precipitation of nitrogen gas bubbles directly into tissue may cause mechanical injury and tissue hemorrhage²
      - Vasculature occlusion and mechanical tissue trauma result in activation of inflammatory and clotting cascades⁸
    - Airplane travel and driving over mountain passes at high elevations after diving may worsen the presentation or hasten symptom onset due to decreased atmospheric pressure at altitude
  - AGE
    - Much less common than DCS among divers²
      - AGE and neurologic DCS may be considered a continuum. DCS is less severe, slower in onset, and associated with lower mortality than AGE. No radiography findings differentiate. AGE usually appears more acutely and severely on ascent and is associated with higher mortality. Both are treated with oxygen and recompression therapy
    - Gas bubbles in the arterial circulation are thought to develop by 1 of 2 primary mechanisms:¹³
      - Paradoxical emboli secondary to precipitation of gas in venous circulation due to DCI with embolization through a right-to-left shunt (eg, pulmonary arteriovenous malformation, patent ductus arteriosus, atrial septal defect, PFO [patent foramen ovale])
      - Pulmonary barotrauma with alveolar rupture allowing gas bubbles to escape directly into arterial circulation
    - The result is systemic end organ tissue ischemia as air bubbles occlude vasculature. Ischemia may be significant, involving the brain, spinal cord, heart, lungs, retinas, skin, and kidneys
- Shallow water blackout among freedivers
  - Sudden loss of consciousness usually occurring just meters from the surface among freedivers when ascending from extreme depths
Other injuries outside the scope of this Clinical Overview include:
- Envenomation
- Motion sickness
- Sun exposure
- Hypothermia
- Physical trauma (eg, lacerations, musculoskeletal injury)

Risk Factors

General risk factors associated with DDI include:
- Diver inexperience
- Repeated dives
- Dives deeper than 21 meters²
- Rapid ascent (eg, loss of buoyancy control, panic, strong upward currents)
- Running out of gas
Additional risk factors specific to barotrauma include:
- Location near the surface of the water (surface to about 33 feet)¹⁴
- Diver inexperience
- Concomitant airway inflammation (eg, upper respiratory tract infection, allergic rhinitis)
Additional risk factors specific to risk of DCS include:²⁸¹⁵¹⁶¹⁷
- Cold water diving
- Higher degree of physical exertion during dive than typical (eg, currents)
- Inhaled air versus mixed gases (eg, nitrox)
  - Room air contains lower inhaled oxygen (about 21%) with relatively higher nitrogen concentrations compared with nitrox (typically 32%-36% oxygen) with overall lower nitrogen concentrations
- Previous history of DCS
- Dehydration
- Alcohol use during diving
- Air travel less than 18 to 24 hours after last dive
- Travel to altitude in vehicle after diving
- Comorbid medical conditions
- Presence of a right-to-left shunt (eg, pulmonary arteriovenous malformation, atrial septal defect, PFO, ventricular septal defect, patent ductus arteriosus)
- Elevated arterial carbon dioxide tension
- Poor physical fitness

Diagnosis

Approach to Diagnosis

If critical diving injury is suspected, immediately contact DAN (Divers Alert Network) 24 hours a day for diving emergencies at +1-919-684-9111 for diagnostic recommendations
Immediately start 100% oxygen while initiating diagnostic process for suspected DDI
- Oxygen is the mainstay for any DDI; early treatment with oxygen is safe and reduces morbidity and mortality
Focus on each portion of the dive (descent, depth, ascent) and clinical manifestations to tailor diagnostic process
Maintain awareness that non–dive-related conditions may manifest during a dive (eg, coronary artery ischemia, stroke, pulmonary embolism, asthma exacerbation)
Suspect DDI based on initial history and physical examination findings
- Document entire dive profile; dive computers may be used to corroborate historical information. Important aspects to confirm include:
  - Length of each dive and number of repeated dives
  - Type of gas used (eg, compressed air, enriched air nitrox, mixed gas, rebreather)
  - If decompression limits were exceeded (eg, uncontrolled rapid ascent)
  - Timing of symptoms (ie, during descent, ascent, or after exiting the water)
  - Recent past medical history (eg, sinus or ear infections) and other pertinent past medical history (eg, chronic obstructive pulmonary disease, asthma, coronary artery disease)
Barotrauma and DCS are clinical diagnoses²
- Timing of manifestations may help differentiate DCI from barotrauma
  - Barotrauma often develops acutely during ascent or descent, whereas decompression characteristically manifests with progressive symptoms after surfacing from dive
  - Manifestations that develop during descent or at depth are unlikely to be related to DCI and are overall more likely to represent other processes (eg, barotrauma, immersion cardiogenic pulmonary edema, coincidental medical problems unrelated to DDI)
- Severity of diagnosis is determined by careful history and physical examination
Laboratory and imaging studies are not necessarily indicated in the initial stages and do not often guide treatment decisions²
- Do not delay transfer to a facility capable of recompression therapy while completing ancillary testing
- Laboratory evaluation
  - No single laboratory test can rule in or rule out DCI or barotrauma
  - If laboratory studies are obtained, CBC, chemistry profile, liver enzyme levels, l-lactate dehydrogenase level, and creatinine phosphokinase level are appropriate
  - Obtain cardiac enzyme levels in patients with chest pain and shortness of breath
- Imaging considerations
  - Plain radiography
    - Important to detect pneumothorax or immersion pulmonary edema⁵¹⁸
    - Chest radiography is advisable before recompression therapy because pneumothorax is a contraindication to recompression therapy, provided there is no delay in therapy²
  - Head CT
    - Sensitive to detect bubbles related to nitrogen gas in the central nervous system⁵¹⁸
    - However, imaging does not correlate well to symptoms and negative scan findings do not rule out DCI (ie, DCS and AGE)⁵¹⁸
ECG
- Indicated when DCS is strongly suspected and in patients with symptoms concerning for cardiac ischemia (eg, chest pain, loss of consciousness)⁵
- Common finding related to DCS is right-sided heart strain⁵
Secondary postdiagnostic workup after AGE or significant clinical concern for AGE may be indicated and include studies such as:
- Brain MRI to assess for ischemic complications
- Cardiac echocardiography to assess for occult cardiac septal defect

Staging or Classification

Most DDIs can be divided into 3 categories based on when they are precipitated or develop during dive as listed in Table 1
DCI by severity
- Serious manifestations²
  - Cerebral symptoms
  - Spinal cord symptoms
  - Cardiopulmonary or cardiovascular symptoms
  - Inner ear symptoms
- Mild manifestations²
  - Mild to moderate musculoskeletal pain
  - Mild to moderate cutaneous symptoms
  - Constitutional symptoms
  - Lymphatic symptoms

Table 1. Deep diving injuries based on timing of development.

Timing of development	Deep diving injury
During descent	BarotraumaMiddle ear squeeze (barotitis)Inner or external ear canal squeezeSinus squeeze (barosinusitis)Tooth squeeze (eg, tooth repair–related)Equipment-related (eg, mask squeeze, drysuit squeeze)
At depth	Nitrogen narcosisOxygen toxicityContaminated airImmersion pulmonary edema
During ascent	Alternobaric vertigoBarotraumaPulmonary barotrauma (eg, pulmonary hemorrhage, pneumomediastinum, pneumothorax, alveolar rupture with AGE)Gastrointestinal barotrauma (eg, abdominal cramping, bloating, vomiting)Otologic barotrauma (ie, middle, inner, external ear canal)Dental barotrauma (ruptured filling)Decompression illnessDecompression sickness (ie, dysbarism)AGEShallow water blackout among freedivers

Caption: AGE, arterial gas embolism.

Workup

History

Development during descent
- Barotrauma
  - Manifestations develop acutely during descent, particularly in about the first 33 feet¹⁴
  - Middle ear barotrauma (ie, middle ear squeeze, barotitis)
    - Ear fullness and ear pain that worsen with increasing depth during descent
    - Vertigo secondary to the caloric reflex after a rush of water into the middle ear may develop with tympanic membrane rupture
    - Facial baroparesis (ie, peripheral seventh nerve palsy) may complicate significant middle ear barotrauma because the seventh cranial nerve courses through the middle ear¹⁹
    - Often related to diver inexperience in equalizing middle ear pressure or upper respiratory tract infection limiting ability to equalize on descent
  - Inner ear barotrauma
    - Deafness, roaring tinnitus, and vertigo are common presenting symptoms
    - Symptoms are characteristically severe and persistent
    - May occur after overly vigorous equalization maneuvers (eg, Valsalva maneuver) or overly rapid descent⁸
  - Outer ear barotrauma presents with pressure and otalgia
    - Ear pain is the most common concern
    - Tightly fitting hood, use of earplugs, or anything obstructing the ear canal may be associated
  - Sinus barotrauma (ie, sinus squeeze)
    - Facial pain, especially over the frontal sinus, and epistaxis are the most common symptoms
    - Pain is usually self limited and resolves with successful equalization maneuvers
    - Presence of an upper respiratory tract infection or sinusitis may limit ability to equalize pressures between maxillary, frontal, and ethmoidal sinuses
  - Mask barotrauma (ie, mask squeeze)
    - Facial pain and soft tissue trauma (eg, bruising, petechiae) in distribution of mask are common symptoms
    - Subconjunctival hemorrhage may be associated
    - Often related to diver inexperience and ability to exhale into the mask itself to equalize the pressure
  - Other barotraumas related to pressure gradients include:
    - Tooth pain due to pressure changes in dental air collections (eg, dental fillings, root canals, false teeth)
    - Pain related to drysuit folds compressing skin due to uncompensated pressure changes
Development at depth
- Nitrogen narcosis
  - Euphoria, anxiety, lowering of inhibitions, and loss of higher executive functioning are experienced
  - Psychomotor coordination may be negatively affected
  - Symptoms take time to develop and often become apparent at around 30 meters (100 feet) and worsen with increasing depth
  - Symptoms characteristically worsen with increasing depth and improve with gradual ascent and during safety stops at shallow depths of 5 to 6 meters (15-20 feet)
  - Loss of consciousness may occur at depths greater than 90 meters (ie, 300 feet)
- Oxygen toxicity
  - Dizziness, headaches, paresthesia, tinnitus, and other central nervous system effects are described
  - Uncommon at recreational depths but may develop if the diver reaches depths greater than 60 meters (218 feet) or exceeds recommended exposure limits (ie, recommended cumulative daily dive time for concentration of oxygen used)
  - Recreational diver is most at risk while using nitrox (32%-36% oxygen concentration rather than 21%) for prolonged periods or at depths less than 130 feet²⁰
- Contaminated air
  - Central nervous system symptoms (eg, headaches, confusion, sleepiness) predominate with increased levels of carbon monoxide or carbon dioxide
- Immersion pulmonary edema
  - Onset of respiratory symptoms (eg, cough, shortness of breath) at depth may cause panic, resulting in rapid ascent
Development during ascent
- Alternobaric vertigo
  - Mild and brief (usually seconds) of dizziness, disorientation, and possibly nausea during ascent⁸
  - Self-limited and may resolve with further slow ascent
- Barotrauma
  - Manifestations often develop acutely during ascent, particularly with rapid ascent
  - Ear barotrauma
    - Reverse middle ear squeeze with ear pressure and otalgia can develop during ascent
    - Alternobaric vertigo and ruptured tympanic membrane are possible associations
    - Concomitant upper respiratory tract infection, allergic rhinitis, or use of decongestants may be reported
    - Inner and external ear canal barotrauma with ear pain can also develop during ascent
    - Inner ear barotrauma is associated with both cochlear (eg, tinnitus, hearing loss) and vestibular symptoms (eg, nausea, vomiting, vertigo)
  - Thoracic and pulmonary barotrauma
    - Pulmonary alveolar hemorrhage may present with hemoptysis, chest pain, and shortness of breath
    - Pneumomediastinum may be exhibited as subcutaneous emphysema, chest pain, and dyspnea
    - Pneumothorax may present with pleuritic chest pain, dyspnea, and tachypnea
    - AGE may accompany pulmonary barotrauma
  - Gastrointestinal barotrauma
    - Cramping, bloating, and occasional nausea and vomiting may be present
  - Barotrauma related to air trapped inside teeth
    - May cause self-limited pain
    - If the ascent is rapid, expanding trapped air may cause tooth fracture or dislodge a filling
- DCS (ie, dysbarism)
  - General
    - Timing of presentation⁵
      - Up to 40% of symptoms occur within 1 hour of surfacing
      - 98% manifest by 24 hours
    - Airplane travel after diving may worsen the presentation or hasten symptom onset due to decreased atmospheric pressure at altitude
    - Symptom progression is variable
      - Symptoms may evolve and progress over time, wax and wane, or be more static in nature
    - Constitutional symptoms (eg, headache, lightheadedness, fatigue, malaise, anorexia, nausea, vomiting) are common (in up to about 40% with DCI)²²¹
    - Patients may present with involvement of a single system or multiple systems at the same time
  - Musculoskeletal
    - Joint and muscle pain are most common symptoms (reported in up to about 65% of people with DCI) and typically the first concerns²
    - 1 or more joints may be involved
    - Shoulder, elbow, hip, and knee are the most common joints affected
    - Generalized back pain may indicate spinal cord involvement
    - May progress to involve other systems (eg, vestibular, cutaneous, neurologic): vertigo, rash, and mental status changes
  - Cutaneous
    - Numbness, tingling, and patchy paresthesia in nondermatomal distribution are the second most common concern (occurring in about 50% of people with DCI)²
    - Pruritis may occur with or without associated rash
    - Rash may be variable in morphology and is reported in up to 10% of people with DCI²
    - Cutis marmorata may be associated with increasingly severe DCI
    - Lymphedema with subcutaneous swelling rarely occurs
    - Underlying cause is unclear but is thought to be secondary to embolic phenomenon, either due to local bubble formation within skin vessels and tissues, or a manifestation of gas bubble embolization to the brainstem with consequent autonomic dysregulation resulting in skin blood vessel dilatation and constriction; most people with skin DCS are noted to have PFO at secondary evaluation²²²³
  - Neurologic
    - Spinal cord involvement may be associated with:¹⁸²¹
      - Numbness and dense paresthesia in up to 30%²
      - Girdle pain, back pain, chest pain, abdominal pain, and paresthesia without discrete localization may be reported and often herald more significant spinal cord involvement
      - Ascending paralysis beginning in the legs in up to 25%²
      - Bladder incontinence or urinary retention is possible
    - Central nervous system involvement
      - May be subtle or severe
      - Subtle symptoms often include memory loss, dysarthria, and personality and speech changes
      - Other symptoms may include headache, diplopia, blurry vision, tunnel vision, dizziness, hearing loss, tinnitus, vertigo, ataxia, poor coordination, and mental status changes
  - Vestibular (inner ear)
    - Vertigo, dizziness, and nausea are fairly common (reported in up to about 20%-35%)²²¹
    - Vertigo, tinnitus, disequilibrium, and hearing loss during ascent or after surfacing may occur¹⁸
  - AGE
    - Frequently related to an uncontrolled, panicky ascent from any depth with breath holding
    - Symptom onset is frequently quick and may be dramatic
    - Up to 92% of divers with AGE develop symptoms within 5 minutes of surfacing²
    - Obvious manifestations of pulmonary barotrauma (eg, chest pain, hemoptysis) are noted in about half²
    - Presenting symptoms are highly variable and may be subtle (eg, mild cognitive impairment)
    - Sudden loss of consciousness within 10 minutes of surfacing indicates AGE until proven otherwise
    - Most common symptoms include loss of consciousness (up to 39%), confusion (37%), dizziness and presyncope (30%), unilateral weakness (27%), visual changes (21%), headache (20%), dysphasia (11%), and seizures (11%)²
    - When severe, apnea and cardiac arrest can result in almost immediate death
  - Pulmonary DCI
    - Symptoms may include cough, chest pain, dyspnea, and hemoptysis
    - Rare and suggests parenchymal lung involvement
    - Characteristically worsens progressively after ascent, unlike direct pulmonary barotrauma (eg, pulmonary alveolar hemorrhage, pneumothorax) that occurs acutely after ascent
- Shallow water blackout among freedivers
  - Sudden loss of consciousness among freedivers when ascending from extreme depths
  - Characteristically occurs just meters from the surface and may require rescue diver cardiopulmonary resuscitation

Physical Examination

Head, eyes, ears, nose, and throat
- Conjunctival hemorrhage suggests ocular or facial barotrauma
- Nystagmus suggests inner ear DCS
- Petechiae and bruising around the face in distribution of the mask suggest facial and mask barotrauma
- Middle ear effusion, hemotympanum, or tympanic membrane rupture is suggestive of middle ear barotrauma
- Peripheral facial nerve palsy (weakness in seventh nerve distribution sparing the forehead) may be associated with significant middle ear barotrauma
- Oropharyngeal findings that mimic burns (eg, erythema, edema, erosions) may be noted in some with contaminated air exposure
Cardiopulmonary
- Crackles, rales, and wheezing may represent pulmonary edema or pulmonary hemorrhage
- Decreased or absent breath sounds may indicate pneumothorax
- Hamman sign (ie, crunching sound synchronous heartbeat) is pathognomonic for pneumomediastinum
Abdominal
- Diffuse nonspecific tenderness and abdominal distention may be consistent with gastrointestinal or spinal DCS²⁴
- Peritoneal signs (eg, significant tenderness, guarding, rigidity) suggest bowel perforation
Joints
- Mild joint swelling may be appreciated with musculoskeletal DCI
Skin
- Eruptions may be of variable morphology such as:
  - Nonspecific macular rash or scarlatiniform rash
  - More specific to DCS with mottling and marbling violaceous appearance of the skin (ie, cutis marmorata or livedo racemosa). May progress to irregular dark violet or purple patches
- Distribution of rash is variable (eg, truncal, single patchy, scattered)
- Lymphedema, especially of the upper body, is rarely evident
- Subcutaneous emphysema involving the chest wall and neck is suggestive of pneumomediastinum
Neurologic²⁵
- Almost any new subtle or pronounced neurologic finding may indicate central nervous system involvement (with DCI or AGE to the brain) and may include:
  - Cerebral findings
    - Subtle deficiencies such as inability to complete serial 7s, mild memory loss, and changes in affect
    - Visual field deficits
    - Localized or scattered weakness and abnormal reflexes that may not strictly adhere to anatomical neurologic distribution and may be subtle or pronounced
  - Cerebellar findings may include ataxia and abnormal heel-to-shin, Romberg, and finger-to-nose test findings
    - Ataxia may also be consistent with inner ear CDS
- Spinal cord involvement may not strictly adhere to dermatomal distributions or precise cord level
  - Deficits may be subtle or pronounced
  - Paraplegia or quadriplegia, abnormal sensory findings (especially fine touch and 2-point discrimination), and upper motor neuron signs²

Laboratory Tests

CBC
- Hemoglobin and hematocrit levels may be increased in patients with third spacing or hemoconcentration secondary to endothelial leak associated with DCS¹⁸
Liver enzymes
- AST and ALT levels may be elevated secondary to presence of significant systemic nitrogen gas bubbles associated with AGE¹⁸
L-lactate dehydrogenase
- Elevations may be secondary to presence of significant systemic nitrogen gas bubbles associated with AGE¹⁸
Creatinine phosphokinase
- Measurement is indicated for patients with concern for rhabdomyolysis (eg, severe persistent musculoskeletal pain) secondary to musculoskeletal DCS
- Marked elevation may be consistent with rhabdomyolysis secondary to significant musculoskeletal involvement in DCS
- Slight elevations are possible with inflammatory cascade changes related to nitrogen gas bubbles in the bloodstream and tissues
Cardiac troponins
- Measurement is indicated for patients with chest pain, dyspnea, or other cardiac anginal equivalents to assess for cardiac injury¹⁸
- Levels may be increased due to bubbles related to nitrogen gas
  - If there is no prior history of occlusive coronary artery disease, troponin levels may be more likely related to bubble formation and not true cardiac disease; careful correlation with clinical picture (eg, ECG findings, coronary artery disease risk factors) is necessary
  - Height of troponin levels does not necessarily differentiate between occlusive coronary artery disease and DCS
Blood gas and carboxyhemoglobin concentration
- May be useful in the setting of altered mental status or level of consciousness changes that may be secondary to hypercapnia or increased carbon monoxide concentrations

Imaging Studies

Chest radiography
- Indicated in divers with chest pain, dyspnea, hemoptysis, or concern for pulmonary barotrauma
- Advisable to obtain before recompression therapy, time permitting, to exclude findings suggestive of previously undiagnosed pneumothorax²
- Useful to assess for pneumothorax related to barotrauma and immersion pulmonary edema
Head CT
- Non–contrast-enhanced CT of the head is indicated for patients with neurologic manifestations and suspected intracranial DCI including AGE
- May be helpful to assess for alternative diagnosis such as intracranial hemorrhage
- Negative imaging findings do not rule out AGE
- Imaging may show evidence of bubbles, but gas bubbles in the central nervous system are slowly reabsorbed and unlikely to be appreciable outside of the acute setting
- Findings suggestive of intracranial DCI (DCS and AGE involving the brain) may not initially be present but can include evidence of gas bubbles in the subarachnoid space, localized infarction, and pneumocephalus when severe
Spinal CT
- Noncontrast CT of thoracic and/or lumbar spine may be indicated for patients with neurologic manifestations suggestive of spinal cord insult and suspected AGE involving the spinal cord
- May be helpful to assess for alternative diagnosis such as vertebral artery dissection, transverse myelitis, and disk herniation
- Findings suggestive of spinal cord DCI involvement are not generally notable on CT scan imaging, and MRI or CT angiography is indicated if suspicion persists for alternative diagnosis (eg, dissection)
MRI of the brain or spinal cord
- May be indicated for persistent neurologic dysfunction to evaluate for complications (eg, ischemia) of central nervous system DCI and arterial air embolism
Ultrasonography using M mode
- May be used to visualize bubbles related to nitrogen gas in the bloodstream but cannot rule in or rule out the presence or severity of DCS because intravascular bubbles can be visualized in most divers who are asymptomatic⁵¹⁸²⁶

Diagnostic Procedures

ECG
- Indicated when DCS is strongly suspected and to assess for cardiac ischemia, arrhythmia, and heart strain in patients with acute-onset chest pain and unexplained dyspnea⁵
- Maintain low threshold in patients at risk for coronary artery syndrome and other cardiac conditions given potential of non–dive-related medical disease presenting during dive
Cardiac echocardiography
- No indication in the emergent or initial workup because diagnosis is largely clinical and not based on echocardiographic abnormalities
- May be indicated as part of secondary postdiagnosis workup in patients with concern for AGE to exclude occult cardiac septal defect
- Occult cardiac septal defect may result in paradoxical embolism from venous to arterial system through right-to-left shunt
- Most patients with cutaneous skin DCS are found to have PFO at secondary evaluation²²
- Testing requires use of agitated saline (ie, bubble study) to evaluate for PFO or other right-to-left shunt

Differential Diagnosis

Table 2. Differential Diagnosis: Presenting patterns among deep divers.*

Condition	Description	Differentiated by
Deep diving injury associated with vertigo
Middle ear barotrauma	Ear pain, usually with descentPossible tympanic membrane rupture with resultant vertigo due to caloric reflex (water rushing into middle ear)Examination may find hemotympanum, tympanic membrane trauma, or other evidence of traumaBell palsy (seventh nerve) may develop with significant middle ear traumaConcurrent upper respiratory tract infection, allergic rhinitis, and difficulty equalizing are common	CommonUsually transient and improves with equalization maneuversTypically evident by clinical presentation
Inner ear barotrauma†	Ear pain with vertigo, usually on descent; may occur on ascent or develop after surfacing¹Often associated with excessive or forced Valsalva maneuvers, inability to equalize, and overly rapid descent⁸Cochlear symptoms (eg, tinnitus, hearing loss) usually predominate presenting pattern¹Vestibular manifestations (eg, nausea, vomiting, nystagmus) are often less pronounced	Fairly uncommonSymptoms are typically severe and persistentChronic conditions (eg, labyrinthine fistula) may resultOften difficult to differentiate from vestibular (ie, inner ear) DCS; requires evaluation by an otolaryngologistNot expected to respond to recompression therapy
Alternobaric vertig	Self-limited episode of vertigo on ascent lasting secondsMild disorientation and nausea may be associatedMay resolve with gradual further ascent	CommonSymptoms are mild, transient, and self resolving and do not persist long after surfacingUnlikely the cause if vertigo persists after surfacing
Vestibular (ie, inner ear) DCS†	Usually occurs shortly after surfacingHigh-risk dive profile exceeding decompression limits (eg, rapid ascent, deeper depths, prolonged diving) may be associatedVestibular symptoms (eg, vertigo, nausea and vomiting, disequilibrium, ataxia, nystagmus) characteristically predominate¹Cochlear symptoms (eg, tinnitus, hearing loss) are often less pronounced	UncommonDCS involving other systems (eg, joints, skin) in addition to inner ear apparatus is suggestive of diagnosis; however, up to 75% of inner ear DCS presents in isolation without other system involvement¹²Manifestations persist after dive and often dissipate with time. May improve with recompression therapyOften difficult to differentiate from inner ear barotrauma; requires evaluation by an otolaryngologist
Neurologic (ie, brain) DCS†	Presentation including dizziness, vertigo, nausea, and vomiting with associated hearing loss is possible, but more typical presenting pattern is with mild cognitive impairment and other subtle (eg, personality changes, memory loss, impaired concentration) or frank neurologic changes (eg, numbness, paresthesia, visual field deficits, ataxia, motor weakness)Dive profile is often concerning for exceeding decompression limits (eg, rapid uncontrolled ascent)	Manifestations begin after ascent or after surfacingConcomitant neurologic manifestations (eg, paresthesia) are often evidentSymptoms improve with time and recompression therapy
Neurologic manifestations during deep diving
Nitrogen narcosis	Transient euphoria, disinhibition, and disorientation that develop at extreme depthsDyscoordination may developRisk is increased with concomitant fatigue, exertion, hypothermia, recent alcohol use, and hypercarbia	Common at extreme depthsSymptoms worsen with further descent and resolve with ascent to shallower depthsFocal neurologic findings are lackingUsually benign but physical injuries and drowning are possible results of diver disorientation and disinhibition
Oxygen toxicity	Extreme depths or excessive cumulative daily dive time (especially with higher concentration of oxygen blends such as nitrox) may result in headache, dizziness, and tinnitusSoft neurologic symptoms may be present (eg, paresthesia) and seizure can develop when extreme. Underwater seizure may be fatal, especially when not wearing a full-face mask (mask and regulator covering entire face rather than separate mask and regulator)²⁷
Uncommon among recreational diversPrimarily a clinical diagnosis differentiated by presenting featuresManifestations resolve with time breathing room air at normal PO₂
Contaminated air	CO₂-related narcosis and CO poisoning are the most common contaminated air exposuresBoth may present at depth with diminished level of consciousness, dizziness, confusion, and impaired concentrationConcomitant dyspnea may occur. Loss of consciousness and seizures may occur when extreme	Uncommon among recreational diversElevated end-tidal CO₂ level measured in the field may suggest CO₂-related toxicity²⁸High CO₂ levels present with hypercapnia on blood gas analysis and high CO levels are detectable with measurement of carboxyhemoglobin on co-oximetryManifestations resolve with time breathing noncontaminated room air at normal partial pressure
Neurologic (ie, brain) DCS†	Usually, manifestations begin to develop on ascent or soon after surfacing (within about an hour), particularly after an uncontrolled, rapid ascent⁵Dive profile is often concerning for exceeding decompression limits (eg, rapid uncontrolled ascent)Typical presenting pattern may include mild cognitive impairment and other subtle (eg, personality changes, memory loss, concentration problems) or frank neurologic changes (eg, numbness, paresthesia, visual field deficits, ataxia, motor weakness)Much more common (in up to 93%) than AGE among divers presenting with neurologic manifestations²Discrete focal findings are less common with DCS than with AGE²	Improvement of manifestations with time and recompression therapy are supportiveDifferentiation of AGE and DCS involving the brain may be difficult and both may occur concomitantly. Neurologic DCS and AGE may be considered a continuum. DCS is less severe, slower in onset, and associated with lower mortality than AGEBecause treatment protocols are essentially identical (eg, oxygen, recompression therapy), differentiation may be of minimal clinical significance
AGE	Symptom onset is rapid and can be dramatic (eg, hemiplegia) but may be subtle (eg, mild cognitive impairment). Neurologic manifestations are obvious within 5 minutes after surfacing in up to 92%²Dive profile is often concerning for exceeding decompression limits (eg, rapid uncontrolled ascent)Rapid, uncontrolled, panicky ascent with breath holding is noted in mostDistribution of emboli is often diffuse, affecting multiple cerebral territories, thereby resulting in manifestations that are multifocalMost common symptoms include loss of consciousness, confusion, dizziness and presyncope, unilateral weakness, vision changes, headache, dysphasia, and seizuresDiscrete focal findings are overall more common with AGE than DCS²Obvious pulmonary barotrauma (eg, chest pain, hemoptysis) is noted in about half²Rare diagnosis (about 7%) compared with neurologic DCS among divers presenting with neurologic manifestations²	Improvement of manifestations with time and recompression therapy are supportiveDifferentiation of AGE and DCS involving the brain may be difficult and both may occur concomitantly. AGE and neurologic DCS may be considered a continuum. AGE usually appears more acutely on ascent, often presents with more severe clinical manifestations, and is associated with higher mortality than neurologic DCSBecause treatment protocols are essentially identical (eg, oxygen, recompression therapy), differentiation may be of minimal clinical significance
Stroke	Sudden symptom onset can include neurologic changes (eg, hemiplegia, dysarthria, dysphagia, facial asymmetry)Symptoms may include headache, vomiting, blurred vision, gait instability, altered mental status, and decreased level of consciousnessSudden loss of consciousness is less likely and is more common with AGEIn general, these patients may be more chronically ill or at advanced age at baseline than the generic diver due to the comorbidities associated with acute stroke²⁹Common comorbidities include hypertension, diabetes, chronic kidney disease, hyperlipidemia, coronary artery disease, atherosclerosis, and obesity	Acute stroke is unrelated to diving, and neurologic DCS or AGE should be considered first if the symptoms begin directly after a divePotentially differentiate with CT scan if there is evidence of hemorrhagic involvement; ischemic strokes may appear similar to DCS or AGEMRI is the gold standard but should be initially delayed if presentation is more consistent with a diving injury
Near drowning	May manifest at any point of dive (eg, descent, depth, ascent, surface of water before exiting water)Dyspnea and hypoxia develop with aspiration of water. Panic with eventual loss of consciousness and seizure may ensue	Typically evident by history
Thoracic manifestations during deep diving
Immersion pulmonary edema	May present with dyspnea and chest pain that begin to develop at depth during dive and occasionally during descentMay be associated with hemoptysisMore common among freedivers than scuba diversRecurrence is common	Differentiate by clinical presentation and chest radiography findings consistent with noncardiogenic pulmonary edemaMay result in rapid diver ascent, contributing to concomitant deep diving injury (eg, barotrauma, DCS, AGE)
Cardiopulmonary DCI	Rare for DCS to present with cardiopulmonary manifestationsPresents with cough, chest pain, and dyspnea (referred to as “the chokes”). Cyanosis and syncope may be associated²Dive profile often shows risks for DCI (eg, rapid ascent, dives deeper than 25 meters)²	DCS involving other systems (eg, joints, skin) in addition to cardiopulmonary system is suggestive of diagnosisECG may show right-sided heart strain pattern. Chest radiography findings are typically unremarkableDissipates with time and may improve with recompression therapy
Pulmonary barotrauma	Pneumothorax, pneumomediastinum, and pulmonary hemorrhage may all present with chest pain and dyspnea on ascentSignificant barotrauma may occur in association with AGE	Unilateral decreased breath sounds suggest pneumothoraxCrepitance in the thoracic region and Hamman sign suggest pneumomediastinumSignificant hemoptysis suggests pulmonary hemorrhageChest radiography is usually diagnostic of thoracic barotrauma
Acute coronary syndrome	Characterized by decreased oxygenation and blood flow to myocardial tissueTypically a group of 3 syndromes: STEMI, NSTEMI, and unstable anginaTypical and atypical symptoms include chest pain, shortness of breath, lightheadedness, nausea, diaphoresis, pain in the left arm or left side of the jawRisk factors include hypertension, diabetes, hyperlipidemia, age > 35 years, obesity, male sex, tobacco use, family history of early myocardial infarction (age < 55 years)³⁰Physical examination findings are frequently unremarkable, although patients may be diaphoretic and/or have abnormal or new heart murmurs	ACS is typically described as chest pressure radiating to left jaw and left armMay be associated with anginal equivalents (eg, dyspnea, lightheadedness, nausea, diaphoresis)Can be triggered by stress, so maintain heightened awareness among patients with multiple risk factorsInitial diagnostic study findings, including ECG and troponin levels, are characteristically abnormal and usually differentiateChest radiography findings are generally unremarkable unless there is associated new-onset congestive heart failure, and pulmonary edema or pleural effusions may be presentECG may indicate ST segment elevations in contiguous leads with associated ST segment depression in opposing leads (STEMI); ECG may also be nondiagnostic (NSTEMI)Troponin levels tend to rise within the first 6 hours and remain elevated for up to 6 days³⁰
Pulmonary embolism	Caused by deep venous thrombi that embolize to the pulmonary circulatory systemAcute pulmonary embolism is associated with sudden-onset dyspnea at rest or with exertion, pleuritic chest pain, calf or thigh pain or swellingSome risk factors may include bed rest > 3 days, extended immobility such as air travel > 8 hours, surgical procedures, pregnancy, prior venous thrombus, hormone replacement therapy, oral contraceptive use, malignancy, spinal cord injuryPhysical examination may find tachypnea, tachycardia, unilateral limb tenderness, edema, hypoxia	ECG may be nondiagnostic, although tachycardia is the most common findingECG may also show right-sided heart strain pattern (ie, right axis deviation, ST segment depression in the inferior leads [II, III, and aVF], right bundle branch block, and T-wave inversions in anterior and inferior leads)³¹Chest radiography findings are most commonly normal, although Hampton hump (peripheral airspace opacity) and Westermark sign (regional oligemia) may be presentLaboratory values cannot reliably diagnose pulmonary embolism, although a negative D-dimer test result in patients who are low risk reliably excludes pulmonary embolismGold-standard diagnostics include CT pulmonary angiography, which indicates filling defects in the pulmonary vasculature

Caption: AGE, arterial gas embolism; CO, carbon monoxide; CO2, carbon dioxide; DCI, decompression illness; DCS, decompression sickness; DDI, deep diving injury; NSTEMI, non–ST-elevation myocardial infarction; STEMI, ST-elevation myocardial infarction.

*Maintain awareness that non–dive-related medical conditions (eg, stroke, acute coronary syndrome, pulmonary embolism, asthma exacerbation) may manifest during diving. It is important for treating physician to maintain a broad differential diagnosis and consider DDI along with non–dive-related conditions. In general, manifestations that develop during descent or at depth are unlikely to be related to DCI and are overall more likely to represent barotrauma, immersion cardiogenic pulmonary edema, nitrogen narcosis, air contamination, or coincidental medical problems unrelated to DDI. Barotrauma often develops acutely during ascent or descent, whereas decompression characteristically manifests with progressive symptoms after surfacing from dive.

†Important to differentiate ear-related barotrauma from DCS (neurologic, vestibular) because management strategies differ. DCS treatment is recompression therapy. Patients with inner ear barotrauma need otolaryngology consultation, bed rest, avoidance of Valsalva maneuvers, and potential surgical repair.

Treatment

Approach to Treatment

If critical diving injury is suspected, contact DAN 24 hours a day for diving emergencies at +1-919-684-9111
Start 100% oxygen by nonrebreather face mask when DDI is suspected
- First line treatment for all diving-related injuries is 100% oxygen via nonrebreather
- Avoid high flow and oxygen administration under pressure (ie, CPAP or BPAP and mechanical ventilation) because they can worsen certain injuries such as thoracic air leaks (eg, pneumothorax)
Provide supportive care and advanced cardiac life support as needed
- Tension pneumothorax requires immediate needle decompression followed by tube thoracotomy³²
  - Recommended needle placement for needle decompression is either second intercostal space mid clavicular line or fourth or fifth intercostal space anterior lateral line. Insert needle over the top of the rib to avoid neurovascular bundle
- Consider IV fluids because dehydration is common among divers with DDI²
  - Goal urine output is at least 0.5 mL/kg/hour
- Gently warm patient if hypothermic and maintain normothermia
- Maintain patients in horizontal supine position and avoid Trendelenburg position⁵¹⁸
- Consider IV lidocaine for neuroprotective effects in patients with serious neurologic manifestations³³
First step to determine appropriate definitive management strategy is to differentiate between diseases that require recompression (eg, DCI) and those that do not
Recompression therapy in hyperbaric oxygen chamber
- Definitive treatment for serious DCS, AGE, and contaminated air exposure
- Consult with hyperbaric medicine or dive medicine specialist
  - DAN maintains a list of active dive medicine specialists in various regions
- Do not delay treatment for additional diagnostic tests such as laboratory or imaging studies
  - Treatment response deteriorates with increasing time to treatment²
- Only contraindication to recompression is untreated pneumothorax
- Transfer to hyperbaric chambers using ground transportation if possible; air transport may worsen symptoms
  - If air transport is required, avoid unpressurized altitudes exceeding 300 meters²
- Treat symptoms in standard fashion (eg, benzodiazepines for seizures related to AGE)
Mild DCS manifestations may be managed conservatively with oxygen, oral or IV fluid rehydration, and consideration of NSAIDs without recompression therapy²
- May include mild to moderate musculoskeletal pain, cutaneous symptoms, and constitutional symptoms without abnormal neurologic examination findings
Specific management for barotrauma and other non-DCS DDI
- Middle ear barotrauma
  - Topical nasal phenylephrine and oxymetazoline to reduce the effusion¹⁸
  - Oral steroids may be indicated with associated seventh nerve palsy¹⁸
- Inner ear barotrauma
  - Manage in consultation with an otolaryngologist familiar with diving injuries given potential for cochleovestibular injury
  - Initial management often includes bed rest, head of bed elevation, and decongestants⁵
- Barosinusitis
  - Decongestants and antibiotics as needed¹⁸
  - Antibiotics are indicated when symptoms persist longer than 10 days or fever, purulent nasal discharge, facial pressure or tenderness, or nasal obstruction is present³⁴
  - Amoxicillin is first line treatment, followed by doxycycline or levofloxacin in patients allergic to penicillin³⁴
- Face squeeze, tooth squeeze, and drysuit squeeze
  - Symptomatic pain control as needed; manifestations are typically self limited and no specific treatment is indicated¹⁸
- Pneumothorax and pneumomediastinum
  - Inhaled oxygen at 100% with face mask is standard of care in effort to increase rate of gas absorption in patients with thoracic air leak syndromes
  - Manage in consultation with a thoracic surgeon
  - Tube thoracostomy as indicated based on established guidelines for management of primary spontaneous pneumothorax³⁵
  - Management of pneumomediastinum is largely supportive; manifestations are typically self limited
  - Avoid air travel for at least 1 to 3 weeks after thoracic air leaks resolve³⁶³⁷³⁸
- Pulmonary hemorrhage and noncardiogenic pulmonary edema
  - Management involves standard supportive care

Nondrug and Supportive Care

Urinary catheterization
- May be necessary for select patients with neurologic DCI and impaired bladder emptying or urinary retention
- Inflate catheter balloons with saline instead of air to prevent pressure changes during recompression therapy
Deep vein thrombosis prophylaxis
- Pneumatic compression devices and fractionated heparin for prevention of deep vein thrombosis in patients at increased risk (eg, those who are nonambulatory, those with spinal cord manifestations)²
Endotracheal intubation for respiratory failure
- Inflate endotracheal cuffs with saline instead of air to prevent pressure changes during recompression therapy

Treatment Procedures

Recompression in hyperbaric chamber (ie, dive chamber)³⁹
- General
  - Gold-standard treatment for serious DCS, AGE, and contaminated air exposure²
  - Treat patients under consideration for recompression therapy in consultation with hyperbaric medicine or dive medicine specialist
  - Patients can undergo monotherapy or group therapy, depending on the protocol, and may lie on stretchers designed for the chamber or in chairs
  - Recompression therapy is typically conducted for several hours, although sessions can last up to several days with periods of regular pressures²⁵
  - Accepted treatment dive tables (eg, US Navy treatment tables) dictate protocol²⁵
  - Protocol selection depends largely on DCI severity and patient response to therapy, as well as facility and staff protocol familiarity⁴⁰⁴¹
  - Treatment is initiated based on presence of symptoms rather than time since symptoms developed; therefore, delay in reaching hyperbaric chamber does not preclude necessity for treatment⁴⁰⁴¹
  - Experts regard early recompression therapy as better than delayed therapy and delayed therapy as better than no therapy when clinically indicated
  - Database of hyperbaric chambers equipped for treating dive injuries is maintained by DAN⁴²
  - Chest radiography is advisable before recompression therapy to exclude previously undetected pneumothorax, provided there is no delay in therapy²
  - Contraindications to recompression therapy
    - Pneumothorax without chest tube is the only absolute contraindication
  - Indications include:⁴³
    - Definitive indications include life-threatening DCI manifestations²
      - DCS I and II
      - AGE
      - Contaminated air (eg, carbon monoxide poisoning)
      - Spinal cord involvement
      - Cerebral symptoms
      - Cardiopulmonary symptoms
      - Inner ear symptoms
    - May be appropriate for other moderate to severe DCI manifestations including:²
      - Moderate to severe musculoskeletal pain
      - Moderate to severe cutaneous symptoms
  - Complications of recompression therapy
    - Middle ear barotrauma
    - Oxygen toxicity
    - Pulmonary barotrauma
    - Symptoms may recur when flying, and patients who are recompressed should avoid flying for at least 72 hours after recompression therapy
  - Discontinuation of recompression therapy
    - Recompression therapy should be managed per US Navy dive tables (version 6)
    - The most common therapy is approximately 4 hours and 45 minutes long, but consultation with DAN specialists and hyperbaric specialists is encouraged to manage therapy duration⁴⁴
  - Return to diving
    - Avoid diving or descent to depth for 7 days after requiring recompression therapy for mild to moderate DCS and up to 4 weeks after severe DCS
    - Clearance for diving after moderate to severe DCI (including AGE) is typically determined by individualized, shared decision-making process involving dive medicine specialist and patient

Follow-Up

Monitoring

Divers after barotrauma
- Follow-up is tailored to specific injury (eg, otolaryngologist for monitoring of inner ear barotrauma, thoracic surgeon for thoracic air leaks)
- Recommendations for return to diving are individualized
  - Shared decision-making in consultation with a dive medicine specialist is recommended to determine future risks with diving after severe and pulmonary barotrauma (eg, pulmonary hemorrhage, pneumothorax)
Divers after DCI
- No specific follow-up is required for DCS
- Recommendations for return to diving are individualized
  - After recompression therapy⁵
    - Moderate DCS: avoid diving or descending to depth for at least 7 days
    - Severe DCS: avoid diving or descending to depth for at least 4 weeks
  - Discuss medical clearance for diving after moderate to severe DCI (including AGE) on an individualized basis with a dive medicine specialist
- Consider secondary postdiagnostic studies after AGE
  - Evaluate for PFO and presence of any left-to-right shunt, or other preexisting conditions that may have contributed to injury⁴⁵
  - Follow-up brain MRI for persistent neurologic deficits and abnormalities to assess for complications
Divers with epilepsy
- Medical clearance to dive may be permitted in consultation with the managing neurologist in patients with the following:⁴⁶
  - Seizure-free interval of 4 years off sedative-antiepileptic medications
  - Ability to fully consent to the risks of diving with history of seizure disorder
  - Consider a dive buddy who is certified in rescue dives and in agreement and aware of risk of seizures

Prognosis

DCI
- Prognosis for most patients with DCS (dysbarism, the bends) is favorable
  - Up to 80% of patients experience complete symptom resolution²¹
- Overall, patients presenting with more severe neurologic manifestations tend to be more likely to experience residual manifestations²¹
- Spontaneous neurologic recovery is reported in about half of patients with AGE²
- Neurologic response rates are optimized with shorter times to recompression therapy²
Barotrauma
- Prognosis of most barotrauma depends largely on severity and type
- Most forms of barotrauma are self resolving or resolve with appropriate expedient management (eg, pneumothorax)
- Exception may be inner ear barotrauma associated with cochleovestibular injury requiring procedural intervention in consultation with an otolaryngologist
Recurrence of DCI
- Treatment of DCI with hyperbaric oxygen therapy is generally well tolerated and most divers are left with minimal to no residual effects from their initial illness
- The risk of recurrent symptoms after returning to diving is higher in patients with the presence of a large left-to-right shunt (eg, PFO) and divers who do not modify to a more conservative dive profile after an episode⁴⁷
  - Decision for closure of PFO is not always clear cut and rests on individualized shared decision-making between patient and expert physicians in dive medicine; many experts recommend PFO closure in divers who have experienced serious symptoms attributable to PFO (eg, neurologic DCS, inner ear DCS, cutaneous DCS) before return to unrestricted recreational diving⁴⁸⁴⁹
  - Some experts recommend against routine closure of incidentally noted PFO without previous episode of DCS in divers who continue diving; conservative diving is prudent for divers with incidental asymptomatic PFO⁵⁰
- Divers with inner ear and eustachian tube injuries are recommended to consult an otolaryngologist to determine risk, given paucity of available information⁵¹
- No data are published on whether a diver can return to diving after severe DCS or AGE
- Divers should discuss their individual risk factors with a clinician experienced in dive medicine
- Divers who recover from COVID-19, whether severe or mild, are recommended to undergo pulmonary imaging before return to diving to assess for fibrosis and other potentially occult pulmonary conditions that could affect the dive profile⁵²

Screening and Prevention

Prevention

DCI
- Proper training and adherence to the dive tables and decompression limits lowers and manages but does not eliminate risk of DCS
Middle ear barotrauma
- Avoid diving with upper respiratory symptoms and for up to 2 weeks after resolution⁵
- Cancel dives when unable to equalize pressure on land⁵

Author Affiliations

Patrick Meloy, MD
Associate Professor
Department of Emergency Medicine
Emory University School of Medicine

References

1.Lindfors OH et al. Inner ear barotrauma and inner ear decompression sickness: a systematic review on differential diagnostics. Diving Hyperb Med. 2021;51(4):328-337.