"Pneumothorax is a relatively common medical condition and exists when air enters the potential space between the lung and the chest wall"

Pneumothorax, Emphysema, A.G.E.

In the past two issues I discussed some of the lung problems divers can encounter (lung squeeze, shallow water blackout) and started to discuss the problems that can occur when the lungs are over-inflated with gas during ascent. In this column we will look at pneumothorax, mediastinal/subcutaneous emphysema, and arterial gas embolism.

Pneumothorax

Pneumothorax is a relatively common medical condition and exists when air enters the potential space between the lung and the chest wall. One of the most common causes is a penetrating chest wound, letting air in from the outside or allowing air to escape from the damaged lung. Divers work in a relatively dangerous environment and are quite susceptible to a pneumothorax from physical trauma.

Isolated pneumothorax from barotrauma is unlikely in normal lungs. The visceral pleura (the membrane that covers the outside of the lungs) is very tough and lung overpressure will almost always cause air to enter the capillaries or to track to the mediastinum long before the pleura ruptures. Therefore, pneumothorax in diving is usually accompanied by arterial gas embolism and/or mediastinal/subcutaneous emphysema and occurs in cases of massive overpressure such as "blow-up". In the blow-up situation, the gas in the lungs is expanding so rapidly that it cannot all escape into the mediastinum and the capillaries. This causes the pressure in the lungs to continue to climb until the visceral pleura finally ruptures, allowing gas into the pleural space.

In the abnormal lung the visceral pleura may be very thin and weak. This is the case with congenital cysts and blebs and these are the most common cause of spontaneous pneumothorax. Anyone with pulmonary cysts or blebs (history of spontaneous pneumothorax) is unfit diving. Any other anatomic abnormality of the lung which results in weakness of the visceral pleura (e.g. surgery) will also increase the likelihood of pneumothorax in an over-pressure situation.

The signs and symptoms of pneumothorax include the sudden onset of unilateral or pleuritic pain, dyspnea (difficulty breathing), and tachypnea (rapid breathing). There will be diminished chest wall movement (splinting), reduced breath sounds, and hyperresonance to percussion on the affected side. The apex beat (heart) and trachea may be shifted toward the good side and there may be cough with bloody sputum. The diagnosis is made with a chest X-ray at full expiration.

The treatment of a pneumothorax is routine. A chest tube must be inserted and connected to underwater drainage (a type of drainage system) or to a one-way valve if the pneumothorax is greater than about 10%. If the diver requires emergency recompression because of other injuries, the pneumothorax can be treated later because the gas in the pleural space will be compressed and the pneumothorax reduced as the pressure on the diver is increased. At depth however, any gas entering the pneumothorax will be at high pressure. Therefore, in a chamber, a chest tube may have to be inserted at depth before the diver can be brought up. A careful neurological exam to rule out A.G.E. is essential in all cases of diving related pneumothorax.

Mediastinal/Subcutaneous Emphysema

A more common occurrence in pulmonary overpressure is for the alveoli to rupture and for the air to track up along the vessels into the mediastinum and from there up to the neck under the skin. The gas may rarely enter the pericardium (sack around the heart ) or the peritoneum (abdominal cavity).

The signs and symptoms of mediastinal emphysema include substernal pain that is worse on inspiration, coughing, and swallowing. There may be X-ray evidence of mediastinal widening or frank (obvious) air but respiratory symptoms are present only in severe cases. It is usually accompanied by subcutaneous emphysema.

The signs and symptoms of subcutaneous emphysema include swelling of the neck, crepitus (air bubbles) under the skin of the neck, sore throat, brassy or monotone voice and dysphagia (painful swallowing). Syncope (fainting), shock or unconsciousness are possible but rarely encountered. The onset of symptoms will occasionally be delayed and brought on by coughing or straining after surfacing with damaged lungs. Air may be seen under the skin on soft tissue X-rays of the neck.

The treatment of both mediastinal and subcutaneous emphysema requires chest X-rays, the standard supportive measures of bed rest, oxygen, observation and careful neurological assessment to rule out A.G.E. It is vitally important to remember that mediastinal/subcutaneous emphysema can and often do co-exist with arterial gas embolism.

Arterial Gas Embolism

In 1932 it was first recognized at the USN Submarine Escape Tower at Groton, Connecticut that the students were not suffering from DCS but from arterial gas embolism. They were undergoing free ascents from 30, 60 and 100 feet and occasionally one of them would be unconscious on surfacing or lose consciousness within a few minutes. The etiology was pulmonary over pressure with gas going into the pulmonary capillaries to the pulmonary veins to the left heart. The pulmonary capillaries form a sheath around the alveoli and as the alveoli ruptures, large quantities of air can be forced into the vascular tree. From the left heart the gas would enter the aorta and then enters either the coronary arteries to give a classic heart attack (rare, only in horizontal divers) or the carotid arteries to result in cerebral embolization. The brain is most commonly affected because the diver is usually in the upright position during ascent. Almost any sign or symptom is possible because the shower of bubbles can affect any part of the brain. The signs and symptoms are very confusing and do not fit any of the single anatomical lesions that a neurologist would be looking for. Therefore, beware if a doctor makes a diagnosis of hysteria just because the symptom complex is unusual. The signs and symptoms of A.G.E. almost always start within five minutes of surfacing and if the delay has been more than 10 minutes, A.G.E. is unlikely.

Any serious sign or symptom immediately upon surfacing must be treated as A.G.E. This can include chest pain, cardiac arrest, any neurologic abnormality including loss of consciousness, confusion, aphasia (inability to speak), visual disturbances, paresthesia (numbness), vertigo, convulsions, hemiplegia (paralysis on one side of the body), focal weakness, focal hypesthesia (increased sensitivity), headache, etc. The EKG and EEG may also be abnormal.

A.G.E. is a serious and life threatening disorder. Any delay in treatment will increase the likelihood of permanent neurological damage or death. The initial response should be to lie the patient down, on either side if they are unconscious. If they are placed in the head down position it should be for only a very brief period as that position could cause problems with respiration and cerebral edema. Oxygen should be given in as high a concentration as possible. Use of an aviators mask or a scuba regulator will allow 100% O2. The patient must be transported to the nearest recompression chamber by the fastest means possible. It is very important not to expose the patient to reduced ambient pressure, and if air transport is used it should be pressurized, or if that is not possible, the pilot should fly as low as is safely possible.

The following discussion on treatment is for interest only. In 1965, Captain Charles Waite devised the Short Embolism Table for the USN. It involved a bounce to 165 feet followed by a USN 170 foot for 10 minute decompression schedule. In animals, most bubbles cleared between 60 and 80 feet on descent. The USN would only accept a 30 minute bounce to 165 feet added to a standard Treatment Table 6. The resultant table was called Treatment Table 6A (TT6A) and has been the standard treatment of A.G.E. for the past 25 years.

Hydration is important and IV normal saline (Ringer's Lactate) should be given until the patient voids. There is some evidence that sugar may increase the damage to the central nervous system and intravenous sugar should probably be avoided (most IV solutions contain sugar). Catheterization is required if the patient is unconscious. IV Diazepam may be given for seizures, agitation and vomiting. The role of steroids is controversial but current research suggests that they do more harm than good.

The definitive treatment for A.G.E. is recompression. There is currently a great deal of debate as to exactly which treatment table to use. The bounce to 165 ft for 30 min. on air (USN TT6A) results in a large increase in dissolved inert gas and in animals, results in worse outcome than TT6. TT6A using 50/50 HeO2 or Nitrox instead of air would give the same partial pressure of oxygen as TT6 and still retain the bubble reducing effect of 165 fsw pressure. Use of a short 5 minute bounce to 165 fsw followed by ascent to 60 fsw and a TT6 can also be supported. A strong correlation is seen between increased time to treatment and increased residual neurological damage. However, even if treatment is delayed for two or three days, some improvement is often seen. If the nearest chamber is only capable of TT6, delaying treatment to travel to a chamber capable of going to 165 fsw will result in a less favorable outcome than going to the closest chamber and conducting a TT6. In other words, take the quickest route to the closest chamber. Follow-up treatments with hyperbaric oxygen tables are often required for residual neurologic damage and are continued until no further improvement is seen on two consecutive treatments.

This has been a very heavy column with lots of medical terminology but I wanted to cover this complex, important, but relatively rare problem. For the recreational diver, the only things you really need to know is that if a diver loses consciousness within a few minutes of surfacing from a dive, especially if there was a rapid ascent or panic during the dive, the diver is most likely suffering from over-pressurized lungs and air in the circulation of the brain. The diver should be kept in a lying position on one side so that if they vomit, the vomitus will not end up in their lungs. If possible the diver should be given 100% oxygen and the nearest recompression chamber should be contacted so that transportation to the chamber can be arranged as quickly as possible. Many of these divers will die shortly after surfacing and there is little you can do.

It is therefore vital to ensure that this catastrophic problem does not occur. You should not dive if you have a cough or trouble breathing (asthma, bronchitis, etc.). You should also ensure that you have the required training and experience for the planned dive and that you are fully prepared for the dive so that the possibility of panic is reduced as much as possible. The diving medical you should have had before you started diving, if done correctly, will have identified all of those individuals with pre-existing problems with their lungs that would make them unfit for diving. However, any diver who develops a lung problem should seek the advice of a knowledgeable diving physician before they return to diving.

So you have had a pulmonary overpressure accident and you have survived. When can you return to diving or should you ever return to diving? In a future column I will look at all forms of decompression illness and discuss the return to diving problem. There is no right answer to the question but there are some guidelines and considerations I can give you.