A 25 year old divemaster made one dive to 40 feet for 38 minutes and then spent 3 hours and 45 minutes on the surface. His second dive was to 55 feet for 27 minutes, at the end of which he struggled with a heavy anchor, swimming with it to the surface. At the surface he raised out of the water, yelled, became comatose and was pulled from the water. apparently convulsing. He was placed in the head low position, given O2 by mask and on arrival at a recompression chamber 50 minutes later, he was alert, oriented and really felt well. He complained of a slight numbness of both right extremities but otherwise had a normal exam. Is this DCS, epilepsy or pulmonary over-pressure? What is the one clue you need to make the diagnosis?
This diver obviously had a pulmonary overpressure accident with arterial gas embolism and was treated by placing him on Table 6A ( 165 feet for 30 minutes) and then on Table 6. The fact that it occurred immediately on surfacing indicates that it’s not DCS and surely a person with epilepsy should never have been certified as a divemaster.
This episode underlines the potential risk of pulmonary overpressure accidents on every compressed gas dive regardless of depth and time. Prevention of pulmonary overpressure accidents starts with a good diving physical exam to ensure no history of pulmonary pathology which would prevent free pressure equilibration of all parts of the lungs as well as psychological evaluation of propensity to panic. The scuba instructor has in his hands the final prevention by teaching the dangers of breath-holding.
Mechanisms of Action
The mechanisms that occur when a pulmonary overpressure accident occurs are directly related to Boyle’s Law, and the greatest danger is at shallow depths-with the greatest gas volume expansion near the surface. Boyle’s Law states that with the temperature constant, the volume of a gas is inversely proportional to the pressure. When pressure differential between gas in alveoli and water (or chamber gas pressure in a compression chamber) exceeds 50-100 mmHg (3 to 5 FSW),free gas can be forced across the fine alveolar membrane into pulmonary interstitial tissues, pulmonary capillaries or rarely through the path of greatest resistance, the visceral pleura.
The results of this air movement across these natural barriers are:
1). Arterial gas embolism
2). Mediastinal and subcutaneous emphysema
Arterial gas emboli
Arterial gas emboli arise in the gas bubbles in the pulmonary capillaries – pulmonary veins to the left side of the heart->possible coronary artery emboli or internal carotid and vertebro-basilar arteries to the brain-> cerebral artery embolism with the clinical picture of a stroke.
The clinical manifestations of cerebral gas embolism include a sudden onset of unconsciousness associated with a generalized or focal seizure. There is often confusion, vertigo and cardiopulmonary arrest. In a series of 24 USN cases in which the time was known, 9 occurred during ascent in the water, 11 within one minute at the surface and 4 occurred within 3-10 minutes at the surface.
Other clinical manifestations include the sudden onset of hemiplegia, focal weakness, focal hypesthesia, visual field defect, blindness, headache and cranial nerve defects. The operative word here is “sudden”-nearly all of these symptoms can also be caused by neurological decompression sickness. Less common manifestations are chest pain and bloody, frothy sputum.
Mediastinal and subcutaneous emphysema, due to bubbling in the tissues, cause substernal pain, subcutaneous crepitus (a crunching feeling ), a definite x-ray appearance and occasionally circulatory embarrassment (rare).
Pneumothorax occurs when the visceral pleura is ruptured by the air pressure and the lung collapses. When this occurs there is pain, decreased respiration on the affected side, changes to auscultation and percussion on physical exam with typical x-ray findings. If the opening is large-a tension pneumothorax can occur, requiring tube decompression of the chest before treatment with the compression chamber.
Read more about Spontaneous pneumothorax
All of these things can happen when two precipitating factors occur:
1). Breath-holding ascent
2). Local air trapping
A breath-holding ascent occurs in association with panic, buddy-breathing and acute laryngospasm (a breath of sea water). Local air trapping is the result of bronchospasm (asthma), mucous plugs (post-bronchitis), blebs (blisters on the surface of the lung), air-containing pulmonary cavities(as in scarring from TB), and very often no reason whatsoever.
Treatment of these three entities varies from the simple ( bedrest, O2, and observation for the emphysema) to immediate compression to 6 ATA and resuscitation while in transport for the arterial gas embolism. A chest tube is standard care for pneumothorax with a good neurological exam to rule out cerebral embolism.
Compression takes precedence over treatment of the pneumothorax and mediastinal emphysema and frequently attendants must also treat coexistent near-drowning, using endotracheal tube, 100% oxygen and IV fluids and dexamethasone.
Our young divemaster had a close encounter with the ghost of Sir Robert Boyle when he apparently held his breath while straining to swim to the surface with the anchor. The lessons of this episode should be readily apparent and can be acted upon by all of us, no matter how experienced we think we are.
Coxson HO, Rogers RM, Whittal KP, et al: A
Quantification of the Lung Surface Area in Emphysema Using
Computed Tomography. Am J Respir Crit Care Med