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.


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.


  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.


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 (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 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).


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.