Syncope of Ascent

The so-called syncope of ascent is a cause of a transitory state of confusion, often described as either disorientation or lightheadedness and associated with a sensation of imminent loss of consciousness. It is caused by inadequate exhalation of the expanding lung gases during ascent, with resultant distension of the lungs and an increase in intrathoracic pressure causing an impairment of venous return. It is analogous to cough syncope.

Syncope of ascent most commonly occurs during rapid ascents, when the pressure gradients are magnified, and also when the diver attempts to retain the air in the lungs instead of exhaling it. In the past, free ascent training from 18 to 30 metres was carried out by divers and submariners, and this was a typical situation in which this disorder occurred – it caused considerable problems with differential diagnosis.

Because there is no actual lung disease, it is technically incorrect to describe this as PBT, but it could sometimes be a step in the progression to this disease.

Pulmonary Barotrauma: Prevention (Dive Training/Medical Selection)

Attempts to prevent PBT, or reduce its incidence, have centered on standards of fitness for divers and modification of training and diving techniques.

Dive training

Entry level recreational divers are taught that the most important rule in scuba diving is to breathe normally at all times and never hold your breath. Considerable effort goes into instilling this mantra. In addition, dangerous diving practices to be avoided include skip breathing, buddy breathing at depth and during ascent, ditch and recovery training, and emergency free ascent training when there are no experienced medical staff and full recompression facilities on site. In recent years major dive training agencies have abandoned free ascent training from bottom to surface, and instead simulate it in a horizontal orientation.

Medical selection

Predisposing disease includes previous spontaneous pneumothorax, asthma, sarcoidosis, cysts, tumors, pleural adhesions, intrapulmonary fibrosis, infection, previous penetrating chest wounds and inflammation. These disorders may result in local compliance changes or airway obstructions. Some (spontaneous pneumothorax and known gas trapping lesions in particular) merit automatic exclusion from diving, whereas others (e.g. ‘asthma’) imply an increase in the magnitude of risk that is very context sensitive, and determinations about diving are made for each case based on its own merits. Pleurodesis for spontaneous pneumothorax may protect from pneumothorax but does not mitigate the risk of other barotraumatic injuries arising from the same predisposing lesions that led to the pneumothorax.

Medical standards are dealt with in Chapters 53 and 54 and involve the exclusion of candidates with significant pulmonary disorders as described earlier. Diver evaluation may involve the performance of respiratory function tests and a pre-diving chest x-ray study. In most cases, a single full-plate chest x-ray film is acceptable. However, some groups insist upon inspiratory and expiratory x-ray studies to demonstrate air trapping in the latter view. If there is a high index of suspicion for gas trapping, more sophisticated lung function tests are indicated. High-resolution or spiral CT scans of the lungs are useful in demonstrating emphysematous cyst and pleural thickening but also frequently reveal lung changes whose significance is uncertain.

 

Diving After Pulmonary Barotrauma

It is widely considered that an incident of PBT is a contraindication for further scuba diving. The reasons are two-fold: first, the diver may have demonstrated a pulmonary abnormality or predisposition; and, second, pulmonary damage has been sustained and may produce local scarring on healing, thus predisposing to further problems by alteration of lung compliance.

It must be acknowledged that these considerations are largely based on first principles rather than hard outcome data, and some degree of uncertainty over the validity of considering prior PBT an automatic contraindication to further diving must be acknowledged. This becomes most problematic when there is doubt over the diagnosis of PBT itself, and the diver is highly motivated to continue diving. In the recreational diving setting this is often resolved by fully informing the diver of all the relevant issues and leaving the diver to make a decision about continued diving as an informed risk acceptor.

Pulmonary Barotrauma: Treatment

Aggravation of pulmonary barotrauma

As a general principle, at all stages of managing a diver with PBT it should be remembered that further decompression (e.g. ascent to altitude during air evacuation or decompression from hyperbaric treatment) can aggravate the problem. In particular, a diver with pneumothorax should always have a chest drain inserted before any air evacuation, or before recompression if there is another problem such as CAGE or DCS that justifies recompression in the presence of a pneumothorax. Failure to do this risks development of a tension pneumothorax during a reduction in ambient pressure.

Similarly, physical exertion, increased respiratory activity, breathing against a resistance, coughing, Valsalva’s maneuver and mechanical ventilation may also result in further pulmonary damage or in more extra-alveolar gas passing into the mediastinum or into the pulmonary veins. If a victim of PBT requires mechanical ventilation, a pressure-control mode should be used, employing the lowest inflation pressures required to achieve adequate tidal volumes. Higher rates may be appropriate to allow lower tidal volumes and minimal inflation pressures, although care must be taken not to cause ‘breath stacking’ or ‘auto-peeping’ with excessively high rates. Positive end-expiratory pressure should probably be avoided unless clinically indicated to treat hypoxia, and the diver should be kept well sedated and relaxed to minimize both inflation pressures and the possibility of coughing on the endotracheal tube.

Pulmonary tissue damage

Treatment involves the maintenance of adequate oxygenation by administration of sufficient oxygen. The treatment is similar to that of near drowning or the acute respiratory distress syndrome. Positive-pressure respiration could increase the extent of lung damage and should be used only if necessary (see earlier). Cardiovascular support may be required.

Mediastinal emphysema

The need for therapy may not be urgent in mediastinal emphysema. However, exclusion of air embolism or pneumothorax is necessary, and, if in doubt, treatment for these disorders should take precedence. Management of mediastinal emphysema varies according to the clinical severity. If the patient is asymptomatic, observation and rest may be all that is necessary. With mild symptoms, 100 per cent oxygen administered by mask without positive pressure will increase the gradient for removal of nitrogen from the emphysematous areas. This may take 4 to 6 hours.

If symptoms are severe, cardiovascular support and therapeutic recompression using oxygen may be useful.

Pneumothorax

The treatment of a pneumothorax follows the standard principles used in treating a pneumothorax from any other cause.

Small pneumothoraces may resolve with the administration of 100 per cent oxygen. This will often appreciably reduce the size of the pneumothorax within a few hours. Larger pneumothoraces justify the insertion of an intercostal catheter.

The presence of a pneumothorax is not a contraindication to recompression if other sequelae of PBT such as CAGE are present. However, because the pneumothorax may re-expand during decompression, the placement of an intercostal catheter is mandatory before recompression. Staff managing a chest drain in a hyperbaric chamber must be experienced in this procedure; particularly in the management of underwater seal drains in the hyperbaric environment.

Pneumothorax must always be considered if a diver develops respiratory symptoms such as chest pain or dyspnea during decompression from a hyperbaric treatment (Case Report 6.4). The decompression should be halted and careful clinical examination undertaken, which is often difficult in the noisy confines of a recompression chamber. If a pneumothorax is found, then it must be vented before resumption of decompression. Ideally, this would be achieved with a standard intercostal drain, which could be connected to a Heimlich valve for expediency. If this is not possible, then insertion of a smaller catheter (e.g. a large intravenous angiocatheter) in the second interspace, mid-clavicular line, could be used as a temporizing measure.


CASE REPORT 6.4:This case was described by a diver/doctor, in his incident report.

On day 1 the diver, using a helium-oxygen system, carried out a bounce dive to 492 feet. The dive job was carried out successfully and was completed without incident in 13 minutes. During decompression upon reaching 90 feet, the diver reported tightness in his chest, some shortness of breath and discomfort while breathing.
The diver was recompressed to 100 feet, where he had complete relief and felt normal. The chamber atmosphere was at this point changed over to a saturation atmosphere, and the diver was decompressed at a saturation decompression rate.

The diving superintendent at this point informed Mr A (a senior diving supervisor). on shore that a treatment procedure was being carried out.
When the diver reached 85 feet, the symptoms redeveloped and other treatment procedures were instituted. The diver was recompressed to 185 feet and a treatment schedule was implemented.

Decompression was uneventful, with the diver feeling fine until day 2 at 02:53 hours, where, at 105 feet, the diver had recurrence of symptoms. The diver was recompressed according to the treatment schedules and then decompressed. He experienced a second recurrence of the symptoms at 85 feet during decompression, and he was once more recompressed to 185 feet for therapeutic decompression at 14:33 hours. At this point a special treatment was instituted at Mr A’s instructions. He had now diagnosed the case as a burst lung problem and discounted any kind of bend.

On day 3 at 13:00 hours, upon reaching 75 feet during his decompression, the diver complained of restriction to his breathing, whereupon he was recompressed to 125 feet, where he obtained complete relief. It was decided to attempt decompression once more to see whether the diver could be decompressed all the way or whether there would be a further recurrence of symptoms. At 23:25 hours while reaching 83 feet in the decompression, the diver again complained of breathing difficulties. Recompression to 135 feet relieved all symptoms.

At this point Mr A. decided that the problem could not be an ordinary decompression problem and was reasonably certain that the symptoms were the result of a pneumothorax. A doctor was called, and arrangements were made to go to the rig in the morning of day 4. The doctor was informed of the treatment to date and of the diagnosis and was asked to bring the necessary needles with him to vent a pneumothorax.

On day 4 at 10:49 hours Mr A. and the doctor arrived at the rig. At 13:49 hours while the diver was at 80 feet, the doctor made a cursory examination of the diver without taking his temperature and diagnosed the diver’s condition as ‘full blown pneumonia and pleurisy of the left lung’ and ruled out the possibility of a pneumothorax. The doctor was challenged on the fact that the diver obtained relief by recompression; however, the doctor stated that this would be the case with pneumonia and that he had previously treated a very similar case.

At this point the doctor took over the treatment and instructed the diver to be decompressed at the rate of 3 feet per hour and emphasized the fact that the diver would experience severe chest pains during decompression as a result of the pneumonia. By the afternoon of day 4 the diver was treated with penicillin injections, and, because of severe pain, the rig medic administered an injection of painkiller at 22:45 hours of day 4.

The doctor left the rig by evening of day 4. He stated that it was a routine case and that he would be available ashore for consultation. By the morning of day 5, the diver had been decompressed to a depth of 60 feet, and his condition had steadily deteriorated. Mr A. at this point requested the opinion of a second doctor regarding the diver’s treatment and condition. Attempts were unsuccessfully made to obtain another doctor to go to the rig.

The attending doctor was notified of these attempts and of the worsening of the diver’s condition. During day 5 the diver received injections of penicillin and painkiller, with little apparent effect. During the early hours of day 6, further drugs were administered, and the diver’s condition was worsening. The doctor had been summoned and examined the patient at 03:40 hours while the diver was at 39 feet.

The doctor stated that the diver’s condition had improved, that the pneumonia was disappearing and that the decompression rate was to be increased so that the diver could be transferred to a hospital as soon as possible.

At 09:00 hours the diver’s pulse had stopped, and by 09:15 he was pronounced dead by the doctor.

CAUSE OF DEATH

  1. Death resulted from a tension pneumothorax of the left lung (postmortem finding).

  2. The cause of the pneumothorax was unknown; however, it was learned that the diver had a slight chest cough on the day before the incident and complained to the rig medic of some pain on the left side of his chest and over the central area.


Cerebral arterial gas embolism

Treatment of CAGE is urgent. The effect of delay on treatment outcome is to increase mortality and morbidity.

POSITIONING

The ‘modified Trendelenburg’ position or the head-down left lateral position was recommended in the past. Some authorities even recommended a 45-degree angle, which is virtually impossible to maintain even in a conscious cooperative patient, let alone a seriously ill victim requiring resuscitation. This position was recommended to discourage bubbles passing into the aorta from entering the cerebral vessels. However, this is no longer recommended because of its impracticality and the possibility of compounding the embolic brain injury by increasing central venous pressure, reducing cerebral perfusion pressure and promoting cerebral oedema.

The current advice is that the patient should be nursed horizontally, on his or her back if conscious and/or the airway is not threatened, or lying on the side in the ‘coma’ position (preventing the tongue from causing airway obstruction, or if there is a possibility of aspiration of stomach contents or sea water).

A similar position should be maintained in transit to the chamber, while the chamber is being compressed and for an uncertain period of time (usually one to two oxygen periods) while breathing oxygen. This advice recognizes the potential for further gas to be trapped in places such as the heart chambers and pulmonary veins and that this gas could be released from those locations by postural change. The patient is initially allowed to sit or stand once recompressed to the initial treatment depth and after a period of oxygen breathing. A sudden deterioration in the clinical state may (rarely) follow the resumption of an erect position. This would suggest the continued existence of gas emboli.

OXYGEN

Oxygen (100 per cent), via a close-fitting mask, should be administered in transit to the chamber:

  • To improve oxygenation of hypoxic tissues.
  • To help dissolve bubbles.
  • To ensure that any subsequent bubbles introduced through injured lungs are composed of oxygen, instead of nitrogen.

RECOMPRESSION

Recompression should be instituted as soon as possible. The patient is kept horizontal for at least the first 30 minutes of 100 per cent oxygen breathing in the recompression chamber before being allowed to move and possibly redistribute emboli. Most treatment facilities use a conventional 2.8-ATA oxygen table such as the USN Table 6 (see Chapter 13). Compression reduces bubble size, and this may assist redistribution through the arterial and micro-circulation into the veins. The denitrogenated state of the blood assists in rapid bubble resolution. Oxygenation of damaged tissues and a reduction of cerebral oedema may be contributory to benefit. As discussed elsewhere, hyperbaric oxygen helps to suppress white blood cell activation and some of the related inflammatory consequences.

A variation in this technique is to expose the patient to an initial short 6-ATA compression during air breathing (e.g. USN Table 6A), to enhance the redistribution of obstructing arterial emboli before continuation with an oxygen table. This is becoming progressively less popular because it is logistically challenging, exposes chamber attendants to increased risk and seems unnecessary. The 4-ATA 50 per cent oxygen-nitrogen Comex tables may be an acceptable compromise between these opposing concepts. Repetitive hyperbaric oxygen treatment may be of value in those neurologically impaired patients who do not recover fully on the first compression. These treatments are continued until there is full recovery or no sustained improvement over two consecutive treatments (see Chapter 13).

ADJUVANT AND SUPPORTIVE THERAPY

Coronary artery gas embolism may cause cardiac arrest, and cardiopulmonary resuscitation may be necessary.

Rehydration may be crucial if there is hypotension or haemoconcentration. Intravenous fluid resuscitation with a non–glucose-containing balanced electrolyte crystalloid should be titrated to signs of vascular filling, urine output, haemodynamics and haematocrit.

There are no drugs with proven efficacy in the treatment of CAGE. There has been interest in the use of lignocaine (lidocaine) as a neuroprotective agent in this acute setting, and there are some supportive data from animal models of CAGE and human studies in cardiac surgery8. In an environment conducive to its safe administration, lignocaine could still be considered in cases strongly suggestive of CAGE. A loading dose in combination with an infusion regimen designed to produce a therapeutic antiarrhythmic level is appropriate. In a healthy adult male patient, this would usually be achieved with a 1 mg/kg loading dose given over 5 minutes, followed by 240 mg administered over 1 hour, 120 mg administered over the second hour, and 60 mg/hour administered thereafter for the duration of the infusion (usually 24 to 48 hours). Lignocaine is not, however, considered a standard of care in this setting.

Radiological investigations such as CT, magnetic resonance imaging and single photon emission CT may assist in the diagnosis and management of DCS and CAGE. These investigations are most helpful in post-recompression diagnosis and evaluation of treatment. These studies may show areas of infarction and oedema, and occasionally gas in acute cases, but they should take second place to recompression therapy in the acute phases.

Pulmonary Barotrauma: Clinical Features

Pulmonary barotrauma of ascent

Pulmonary tissue damage

At the point of surfacing in a panic ascent situation, an explosive exhalation of expanded gases may be accompanied by a characteristic sudden, high-pitched cry. Although lung damage resulting from barotrauma can produce respiratory symptoms in the absence of any of the other associated complications, this seems rare in practice. Nevertheless, symptoms that may be seen include dyspnoea, cough and haemoptysis. Clearly, these symptoms may occur in association with any of the complications of PBT discussed later, but the symptoms of pulmonary tissue damage are not invariably present, and their absence should never be used to rule out any of the following diagnoses.

Mediastinal emphysema

As previously described, after alveolar rupture gas may escape into the interstitial pulmonary tissues and track along the loose tissue planes surrounding the airways and blood vessels into the hilar regions and thence into the mediastinum and neck (subcutaneous emphysema). It may also extend into the abdomen as a pneumoperitoneum. When the pleura is stripped off the heart and mediastinum, a pneumoprecordium may be misdiagnosed as a pneumopericardium (Figure 6.2).

Pulmonary barotrauma of ascent
Figure 6.2 Pulmonary barotrauma of ascent: chest x-ray film showing mediastinal emphysema causing the ‘tram track’ sign, from air stripping the pleura from the edge of the cardiac shadow.

CASE REPORT 6.1:RJN, a 19-year-old, was having his second dive in scuba equipment at a depth of 5 metres when he noted a slight pain in his chest. He then noted a restriction in his air supply and thought he had exhausted his gas. He opened his reserve valve and ascended to the surface. He was asymptomatic after the dive, but later, during physical training, he noted that he was breathing heavily and felt weak. A few minutes later he noted slight retrosternal chest pain. During lunch, he developed a fullness in his neck (a ‘tightness’) and dysphagia.

An hour and a half after the dive, he decided to see the doctor because he was not feeling well. It was then noted that his voice was altered in quality and that he had subcutaneous emphysema in both supraclavicular fossae, bilateral generalized crepitus over the chest and positive Hamman’s sign. Chest x-ray study showed gas in the upper mediastinum and neck. An electrocardiogram showed ischaemic changes in leads II, III and aVF.

He was treated with 100 per cent oxygen and improved rapidly.

Chest x-ray study and electrocardiogram were normal 6 days later. Subsequent lung function studies showed that pulmonary compliance was reduced below predicted values.

Diagnosis: Pulmonary barotrauma with mediastinal emphysema and coronary artery embolism.


Symptoms may appear rapidly in severe cases, or they may be delayed for several hours in lesser cases (Case Report 6.1 and Case Report 6.2). Delay may reflect that the symptoms are often ‘mild’ or that it takes time for gas to migrate to the sites where it provokes symptoms. Symptoms may include a voice change including hoarseness or a brassy monotone, a feeling of fullness in the throat, dyspnoea, dysphagia and retrosternal discomfort. In very rare severe cases syncope and shock are possible. The voice changes are described as ‘tinny’ and have been attributed to ‘submucosal emphysema’ of the upper airways and/or recurrent laryngeal nerve damage, although it is difficult to see how bubbles external to the nerve in a relatively compliant tissue space would achieve nerve damage.


CASE REPORT 6.2:TC, an experienced Navy clearance diver, developed epigastric discomfort toward the end of a 90-minute, 11-metre scuba work dive. The dive was otherwise unremarkable, although he had at times worked hard, and he made four controlled ascents during the dive to change his tools.

Approximately 15 minutes after leaving the water, he developed retrosternal chest pain, which increased in intensity over the next few hours. The pain extended from the epigastrium to the base of the throat. The pain was pleuritic in nature and aggravated by inspiration, coughing and movement. He was not dyspnoeic, and there was no associated cough or haemoptysis.

Examination was unremarkable; in particular there were no palpable subcutaneous emphysema and no positive neurological signs. He had no clinical evidence of pneumothorax.

Chest x-ray study revealed the presence of surgical emphysema in the neck and superior mediastinum. No pneumothorax was seen and the lung fields were clear. A computed tomography (CT) scan of the chest was reported as showing ‘air in the mediastinum. Inferiorly, this is seen around the oesophagus in the retrocardiac recess. Superiorly, it is seen surrounding the descending aorta at the level of the carina. It also extends along the major branches of the aortic arch adjacent to the trachea and oesophagus superiorly into the base of the neck on both sides. The spread of air appears to be mainly along the major vessels of the aortic arch into the base of the neck’.

He was treated with 100 per cent oxygen and bed rest, with complete resolution of his symptoms. He was considered permanently medically unfit to dive.

Diagnosis: Pulmonary barotrauma with mediastinal emphysema.


Clinical signs include subcutaneous emphysema of neck and upper chest wall, i.e. crepitus under the skin (described as the sensation of egg-shell crackling, by divers), decreased cardiac dullness to percussion, faint heart sounds, left recurrent laryngeal nerve paresis and in severe cases cyanosis, tachycardia and hypotension. Precordial emphysema may be palpable and produce Hamman’s sign – crepitus related to heart sounds that can sometimes be heard at a distance from the patient. An extension of the mediastinal gas into the tissues between the pleura and the pericardium, rather than gas in the pericardial sac, has occasionally produced cardiac tamponade with its classic clinical signs. There may be radiological evidence of an enlarged mediastinum with air tracking along the cardiac border or in the neck.

Pneumothorax

If the visceral pleura ruptures, air enters the pleural cavity and expands during any subsequent ascent. It may be accompanied by haemorrhage, forming a haemopneumothorax. The pneumothorax may be unilateral or bilateral, the latter being more common following dramatic emergency ascents.

Pneumothorax from diving has the same clinical features and management as pneu-mothorax from other causes.

Symptoms usually have a rapid onset and include sudden retrosternal or unilateral (sometimes pleuritic) pain, with dyspnoea and tachypnoea. Clinical signs may be absent, or they may include diminished chest wall movements, diminished breath sounds and hyper-resonance on the affected side, tracheal deviation toward the unaffected side with a tension pneumothorax, signs of shock and x-ray evidence of pneumothorax (Figure 6.3).


CASE REPORT 6.3:AI was a relatively inexperienced diver, 19 years old and in good health. He was performing a free ascent from 10 metres. On reaching the surface, he gave a gasp, his eyes rolled upward and then he floated motionless. While he was being rescued from the water it was noted that blood and mucus were coming from his mouth and that he was unconscious. Resuscitation was commenced immediately, using oxygen. He was noted to be groaning at this time but soon after appeared dead. Resuscitation was continued while he was rushed to the nearest recompression chamber. Thirty minutes after the dive he was compressed to 50 metres but with no response. Autopsy verified the presence of pulmonary barotrauma (PBT).

Diagnosis: air embolism resulting from PBT of ascent.


Arterial gas embolism

This dangerous condition is the result of gas passing from the ruptured alveoli into the pulmonary veins and thence into the systemic circulation, where it can cause vascular damage or obstruction, hypoxia, infarction and activation of an inflammatory cascade (see earlier).

Most of the clinical series refer to the brain (CAGE) as the dominant site of disease. Onset typically occurs immediately on surfacing or very soon afterward. In one large series5 of CAGE, the longest interval to onset of symptoms and signs was 8 minutes in a single case, with all other divers showing evidence of CAGE within 5 minutes of completing the dive. There were no cases occurring in excess of 10 minutes.

Serious neurological symptoms consistent with cerebral involvement, which develop immediately after ascent, must be regarded as air embolism and treated accordingly until a definitive diagnosis has been made.

MANIFESTATIONS

The manifestations of CAGE may include the following:

  • Loss of consciousness and other neurological abnormalities such as confusion, aphasia, visual disturbances, paraesthesiae or sensory abnormalities, vertigo, convulsions and varying degrees of paresis, which is usually lateralized (Case Report 6.3). Paraplegia with a sensory level is more likely to be caused by spinal decompression sickness (DCS) (see Chapter 10) than by CAGE.
  • Cardiac-type chest pain and/or abnormal electrocardiograms (ischaemic myocardium, dysrhythmias).

In a series of 88 cases of CAGE7, mainly from free ascent practices, 34 per cent of the divers suffered loss of consciousness within seconds of surfacing, 23 per cent had become confused, disoriented or uncoordinated after emerging from the water, and 17 per cent had presented with paresis (6 cases with upper monoparesis and 6 with hemiparesis).

In another series presented by Pearson5 that included scuba divers without access to immediate recompression, 15 per cent had complete spontaneous remission within 4 hours, and 53 per cent had some spontaneous improvement before therapy; 77 per cent with coma improved to some degree before treatment. These spontaneous improvements were not always sustained, and 15 per cent of the divers died. It seems clear that divers who exhibit symptoms of CAGE may show partial or even complete recovery within minutes or hours of the incident. As discussed earlier, this may reflect redistribution of the embolus through the cerebral vasculature. Even those divers who become comatose may improve to a variable degree after the initial episode. Unfortunately, such recovery is unreliable. It may not occur or it may not be sustained. Recurrence of symptoms has an ominous prognostic significance.

DIFFERENTIAL DIAGNOSIS

Focal cerebral symptoms and signs (including unconsciousness) arising immediately after ascent from a compressed gas dive should always be considered most likely caused by PBT and CAGE, especially where the time and depth exposure would normally be considered ‘unprovocative’ for DCS (see Chapters 10 and 11). As previously mentioned, an absence of signs of the presumed barotraumatic injury to the lung (e.g. haemoptysis) is surprisingly common and should not influence the diagnosis.

The differential diagnosis for rapid-onset neurological symptoms after a dive that could be considered provocative for DCS is more problematic, but there are several relevant points. First, the principal competing diagnoses are CAGE and DCS, and distinguishing between them is unimportant from a management point of view. The management is virtually identical (see later). Second, it remains uncertain whether the venous bubbles formed from dissolved gas after decompression and ‘arterialized’ across a right-to-left shunt (see Chapter 10) are large enough to cause the stroke-like syndromes seen after PBT and CAGE. In addition, bubbles are unlikely to form from dissolved gas in the brain tissue itself (see Chapter 10). Third, for the purposes of diagnosis, emphasis should be placed on the putative organ involvement. Manifestations best explained by cerebral involvement (unconsciousness, lateralizing signs, loss of vision, aphasia) are most likely to result from PBT and CAGE (especially if there are concomitant symptoms of PBT), and manifestations best explained by spinal involvement (paraplegia, quadriplegia, loss of anal or bladder tone) are most likely caused by DCS. Confusingly, the two diagnoses may coexist and even interact. Thus, arterial bubbles from PBT may enter tissue micro-vessels and grow as a result of inward diffusion of supersaturated tissue inert gas (see Chapter 10). This mechanism has sometimes been referred to as type III DCS.

Another diagnosis that may cause confusion with CAGE is a haemorrhagic or thromboembolic cerebrovascular accident (CVA) occurring coincidentally with ascent from diving. Such events do occur but are extremely rare, and it is far more likely that cerebral symptoms occurring after a dive are the result of a diving disorder. Indeed, the principal reason for mentioning this differential diagnosis is the frequent inappropriate attribution of CAGE to a CVA when divers are taken to peripheral hospitals staffed by doctors unfamiliar with diving medicine. The same problem arises in cases of DCS.

Previously it was considered important to differentiate between CAGE and DCS because the recommended recompression regimen was different. DCS was treated with a 2.8-ATA oxygen table, e.g. US Navy (USN) Table 6, whereas CAGE was treated using USN Table 6A (which includes an initial deep excursion to 6 ATA). Several animal studies were not able to show an advantage in the initial deep excursion, and most centres now manage patients with CAGE and those with DCS identically (see Chapter 13). Consequently, recompression has become the priority rather than establishing the ‘correct’ diagnosis. It is still considered relevant subsequently to assess the likelihood of whether PBT occurred because this diagnosis has implications for future risk in diving.

Pulmonary Barotrauma: Predisposing Factors

Predisposing disorders include lesions that may result in local compliance changes, gas trapping or airway obstruction. These include sub-pleural blebs of the type associated with spontaneous pneumothorax, asthma, sarcoidosis, cysts and bullae, tumors, pleural adhesions, pulmonary fibrosis, infection and inflammation.

Precipitating factors include inadequate exhalation or outright breath-holding during ascent (often in association with panic), rapid ascent, faulty breathing apparatus or water inhalation.

Although many cases of PBT may be caused by voluntary breath-holding during ascent or by the pathological lesions mentioned earlier, it is clear that these risk factors are not present in all cases. About half the submarine escape ascent trainees who develop PBT have been observed to carry out correct exhalation techniques. These divers were also passed as medically fit before the dive and exhibited none of the contributory pathological features afterward. A frequent finding with some of these subjects is a reduction of compliance at maximum inspiratory pressures, i.e. the lungs are less distensible (stiffer) and are exposed to more stress than normal diver’s lungs, when distended. Brooks and colleagues6 demonstrated that a lower than predicted forced vital capacity (FVC) was associated with PBT in submarine escape trainees, and this finding further supports the suggestion that reduced pulmonary compliance is a predisposing factor. Interestingly, many medical standards refer to the requirement for the ratio of forced expiratory volume in 1 second (FEV1) to FVC (FEV1/FVC ratio) to be greater than 75 to 80 per cent of predicted levels, yet this spirometric parameter has not been shown to be causally related to PBT in trainees who have no evidence of lung disease.

Pulmonary Barotrauma: Pathophysiology

Pulmonary barotrauma of ascent.

All gas-filled spaces within the body are potentially subject to volume change as ambient pressure changes. For highly compliant organs such as those of gastrointestinal tract, the contraction and expansion of gases with descent and ascent are accommodated with ease. The lungs are less compliant, however, and if gas breathed at depth is not adequately vented during ascent, transmural pressure gradients sufficient to cause injury may result. This disorder is known as PBT of ascent.

The pathophysiology of PBT is complex and poorly understood. Injury appears dependent to some extent on both volume distension of lung tissue and development of a harmful transmural pressure gradient. Thus, not surprisingly, there is evidence that the degree of overpressure required to cause lung tissue injury depends on the extent to which the lung is splinted by its surrounding structures2. Experimentally, cadaver lungs have been shown to rupture with a positive inflation pressure of 70 mm Hg, but if the thorax is prevented from expanding (e.g. by thoracic binding), pressures up to 110 mm Hg are tolerated before rupture occurs. It seems that a distended lung is damaged by a lower transmural pressure, whereas a higher transmural pressure is required to cause injury when the lung is prevented from distending2. It is notable that a transmural pressure of 70 mm Hg, shown to be harmful in cadaver studies, can be generated by an ascent from only 1 metre if the lungs are near total lung capacity (TLC) before ascent.

It is also possible that lung ‘injuries’ that are benign, unnoticed and possibly frequent at the surface may be unmasked and clinically relevant in diving. Denison3 reported cases of pulmonary rupture occurring with deep inspiration and suggested that this may be an asymptomatic yet frequent event. In addition, he postulated that when the lungs are close to TLC, sneezing or coughing generates enough pressure to exceed the elastic limits of the lung, thus possibly resulting in damage. Although this damage may remain asymptomatic and go unreported at 1 ATA, the leakage of gas from the lung into the mediastinum or chest cavity and its subsequent expansion with ascent in a diver may be symptomatic or even life-threatening. Novice divers, because of inexperience with their equipment and the environment, tend to swim with lung volumes close to TLC. Skip breathing, a procedure used by many divers in an attempt to conserve air, is a voluntary reduction in breathing rate, but it is usually associated with close to maximal lung volumes. Both these situations, in which the lungs are held close to TLC, may predispose the individual to PBT.

Scarring within the lung parenchyma has long been considered to increase risk of PBT. However, Calder4 reported that the site of injury was inconsistently related to the site of the scar. This finding may be explained by differing compliance in the scar and surrounding tissue. If gas begins to expand in both sites, the more compliant healthy tissue will expand more, creating a shear stress between the two zones. This shear stress may result in an injury to the adjacent healthy tissue.

When alveoli rupture, the escaping gas can either enter any blood vessels that are injured simultaneously or escape into the lung interstitium. The former process will cause alveolar gas to enter the arterial circulation, commonly referred to as ‘arterial gas embolism’. Escape into the interstitium allows gas to track along the outside of the pulmonary airways and blood vessels toward the hilum of the lung where the pleura is discontinuous. Its subsequent escape into the mediastinum gives rise to mediastinal emphysema. From there, gas can track upward along the trachea to lie subcutaneously at the base of the neck, thus giving rise to ‘subcutaneous emphysema’. Finally, if there is rupture of alveoli adjacent to the visceral pleura, then gas may enter the pleural cavity and produce a pneumothorax (Figure 6.1).

Pulmonary barotrauma of ascent.
Figure 6.1 Pulmonary barotrauma of ascent.

These events may occur singly or in combination. In a Royal Navy series5 of 109 non-fatal cases of PBT submarine escape training accidents, the disorder in the majority of the cases was cerebral arterial gas embolus (CAGE). However, 15 divers with arterial gas emboli also had mediastinal emphysema, 7 with arterial gas embolism also had pneumothorax (3 bilateral, 4 unilateral), 4 had only mediastinal and cervical subcutaneous emphysema, and 1 had only unilateral pneumothorax.

The most feared (and probably the most common) of these events is arterial gas embolism. During overdistension of the lung, the capillaries and small vessels are stretched and may tear, along with other lung tissue. Because these vessels are small and often compressed by distended air sacs, air embolism may not result until overdistension is relieved by exhalation. Gas from ruptured alveoli is introduced to the pulmonary veins and carried back to the heart. Rarely, the volumes of gas are so great that the left ventricle can become air-locked and the diver will die instantly. More commonly, smaller and variable amounts of gas are entrained into the arterial circulation. The bubbles tend to distribute with flow; thus, those organs receiving a significant proportion of the cardiac output, particularly the brain, are likely to suffer the greatest exposure to bubbles. There is also some evidence that the distribution of bubbles in large blood vessels, particularly larger bubbles, can also be influenced by buoyancy. Therefore, in an upright diver (e.g. during ascent, when PBT is most likely to occur), larger bubbles tend to track around the roof of the aortic arch and are more likely to enter the vessels supplying the upper body and brain.

Presenting signs and symptoms in 114 Royal Navy submarine escape training accidents and 74 scuba diving accidents involving arterial gas embolism
Table 6.1 Presenting signs and symptoms in 114 Royal Navy submarine escape training accidents and 74 scuba diving accidents involving arterial gas embolism

Passage of these bubbles through the circulation is interrupted by the systemic capillary beds. Bubble behaviour and effects at this point are largely influenced by their size. Bubbles that are large enough that their leading end occupies several generations of branching arterioles may stick and cause obstruction to flow. Smaller bubbles can redistribute through the microcirculation and thus cause minimal obstruction. Even larger bubbles redistribute in this way as the gas inside them is absorbed and they shrink. Clearly, however, even transient obstruction to flow in a tissue sensitive to hypoxia (e.g. the brain) may result in damage before bubble redistribution occurs. Loss of oxygen supply impairs neuronal ability to regulate intracellular ionic homeostasis because of breakdown in the sodium-potassium pump. Uncorrected inward leak of sodium is followed by cellular oedema and depolarization, the latter resulting in release of excitotoxins (e.g. glutamate) and a cascade of injurious events that may lead to early neuronal death or delayed apoptosis. The resulting cerebral dysfunction manifests most commonly as sudden-onset unconsciousness and/or multifocal stroke-like events (see later).

Even the redistribution of bubbles is not a benign event. Bubbles may cause endothelial disruption as they pass through small arterioles and capillaries, and white blood cells adhere to the damaged vessel walls. Their activation leads to release of inflammatory cytokines which can also cause tissue oedema and other forms of secondary damage. There is clear evidence from animal studies that shows a secondary decline in blood flow and neuronal function in cerebral tissue following redistribution of small aliquots of gas; this decline is caused by these processes and does not take place if the animal is depleted of white blood cells before the bubble exposure. This sort of inflammatory sequel to arterial gas embolism is thought to explain the frequent observation of initial improvement in early symptoms (which may reflect bubble redistribution) followed by a secondary deterioration (caused by the inflammatory events).

Secondary deterioration may also be caused by re-embolization by further bubbles that have been trapped in the pulmonary veins and heart chambers. Although there is little proof that this process is materially affected by postural changes, this possibility underpins the frequent advice to keep an apparent victim of arterial gas embolism in a supine position, even in the presence of apparent recovery, until the diver is seen at a hyperbaric chamber.

The understandable focus on cerebral effects of arterial gas embolism should not be allowed to obscure the potential for effects on other organs. It has already been suggested that large amounts of gas can cause early cardiac arrest by air locking the heart. It is also possible for bubbles to enter the coronary arteries and cause myocardial ischaemia and arrhythmias. The heart may also be affected indirectly by disturbance in function of the brainstem cardiovascular centres by cerebral arterial emboli. It is likely that many other tissues are affected by arterial bubbles without necessarily producing symptoms. For example, creatinine kinase levels (skeletal muscle fraction) and some liver enzymes are commonly elevated after arterial gas embolism, a finding suggesting that subclinical injury has occurred in these organs.

Pulmonary Barotrauma

Pulmonary barotrauma (PBT) of ascent is the most serious of the barotraumas, and it causes concern in all types of diving operations. It is a clinical manifestation of Boyle’s Law because it affects the lungs and results from overdistension and rupture of the pulmonary tissue by expanding gases during ascent. It can occur in compressed air divers, submariners undertaking escape ascent training, hyperbaric patients during decompression and airline passengers during ascent to altitude (though the last two situations are rare and invariably associated with gas-trapping disease in the lung).

A 1988 review1 of submarine escape training from 11 nations showed that despite careful selection procedures and extremely high standards of training and supervision, hooded buoyant ascent (in which the trainees head is enclosed by a hood providing a breathable air space) had an incident rate for PBT between 0.1 and 0.6 per 1000 escapes and a fatality rate 10 to 50 times lower than that. In non-hooded ascents (in which the trainee must breathe out continually during the ascent), the incident range was 1 to 19 per 1000 escapes. The incidence in recreational diving is unknown.