Father and Son in Chamber. Photo by Kerri Rivera
Decompression Sickness (DCS) is often referred to as “the bends”, “divers’ disease” and “caisson disease”. DCS is, essentially, the condition caused by inert gases (usually dissolved in the bloodstream and body tissue) separating from the solution and forming micro-bubbles. Owing to the fact that the micro-bubbles can form anywhere in the body, as well as throughout the entire body, symptoms of DCS can take on a variety of manifestations: symptoms can affect the skin, musculoskeletal system, central nervous system, lymphatic system and the inner ear.
In effect, the mechanism through which micro-bubbles form can be summarised as follows: the gases that are absorbed into the blood and body tissue while the body is under pressure (when diving, for example) separate from the tissue and blood solution when the body depressurises. In a safe decompression process, the separating gas (termed “out-gassing”) will not form micro-bubbles and will instead be expelled from the body through the lungs. In a too rapid decompression, the body doesn’t have sufficient time to eject the gases absorbed under pressure through the lungs, and hence the micro-bubbles form.
As DCS is a relatively well-known phenomenon in the scuba and free diving fraternities, it is a somewhat rare occurrence: in the United States, for example, only 2.8 cases of DCS transpire per every 10 000 dives. This is, undoubtedly a favourable figure. The chance of experiencing decompression sickness is further reduced if the individual who recently experienced a form of significant decompression limits yet more depressurisation (usually through the avoidance of flying in an aeroplane for at least 24 hours after a dive). The reason for the avoidance of flight is that although airlines pressurise the cabin, it is pressurised to only 70% of sea-level air pressure and inert gases absorbed under pressure may still be present in the body.
There are various guides and ascent tables to ensure that a diver is as protected from DCS as is reasonably possible. As a rule of thumb, Navy divers are allowed to ascend at a rate of 20 metres per minute, whereas recreational divers should ascend at 10m/minute, and include decompression stops at regular intervals. It is also wise to include a safety stop at either 3 or 6 metres below the water surface to allow for a final decompression, especially if no stops have been included in a slow, even ascent. After the dive, and whereas no DCS symptoms may have been experienced, the body will continue to expel inert gases absorbed under pressure, but it will do so through the normal, natural channel. As stated, the fact that compressed gas is still present in the body is the primary reason why flying should be avoided after a dive.
If DCS is experienced, it might be worthwhile to bear the following in mind: the formation of bubbles in the skin tissue or in the joints (the bends), will result in the mildest DCS symptoms; but large quantities of micro-bubbles in the venous system may damage the lungs and bubbles in the arterial system might cause a heart-attack or stroke through the formation of an arterial gas embolism (AGE). Severe types of DCS interfere with the spinal-cord and can cause long-term damage, leading to paralysis, spinal-cord dysfunction and/or death.
Type I (termed “simple” DCS) is reserved for symptoms pertaining to the skin, musculoskeletal system and/or lymphatic system. Type II DCS (“serious”), involves the organs and central nervous system.
There are two main factors that are seen to define the risk of a diver suffering DCS:
- Henry’s Law: the rate and duration of gas absorption under pressure – that is, the deeper and longer the dive, the more gas (that will have to be out-gassed during decompression) is absorbed.
- As a corollary to point 1., the rate and duration allowed for out-gassing will determine the chances of DCS occurring. The faster a diver ascends to surface pressure and the shorter the interval between dives, the less time the pressured gasses are allowed to out-gas normally through the lungs.
Decompression sickness is treated through hyperbaric oxygen therapy (HBOT), or, in rare diving cases, by recompression through sending the diver back to an adequate depth in the water.
The decompression chamber (the progenitor of the contemporary hyperbaric chamber) was invented by Alberto Gianni in 1916. HBOT is the use of pressurised oxygen for medicinal purposes, and the equipment needed includes (in schematic form), an airtight pressure chamber and a means of delivering 100% pure oxygen into the chamber.
Although it was conceived of as a treatment for decompression sickness, HBOT has been proven to be effective treatment for the following conditions (as described by the South African Underwater and Hyperbaric Medical Association [SAUHMA]):
- Air or gas embolism
- Carbon monoxide poisoning (as well as CO poisoning complicated by cyanide poisoning)
- Gas gangrene
- Crush injury, compartment syndrome and other acute traumatic ischemia
- DCS
- The enhancing of healing in selected problem wounds
- Exceptional blood loss (anaemia)
- Intracranial abscesses
- Necrotising soft tissue infections
- Osteomyelitis
- Delayed radiation injury
- Skin grafts and flaps
- Thermal burns (as opposed to chemical burns)
Hyperbaric Chamber. Photo by James Heilman, MD
Prior to 1999, South Africa was without a hospital based, clinical hyperbaric unit. The initiative at St. Augustine’s Hospital in Durban was started by Daniel Gericke after he had served as a hyperbaric chamber specialist in the South African Navy. In Johannesburg, a clinical hyperbaric oxygen therapy unit was established at the Milpark Hospital in 2005, again owing to the initiative of Daniel Gericke and the Netcare group.
The traditional hyperbaric chamber is a hard shelled pressure vessel combined with various other components. Chambers can be run at pressures of up to 600 000Pa (6 bars). In terms of international practice, hyperbaric chambers can range in size from single person, portable units to large, room sized units that can accommodate upwards of eight patients. Soft shelled chambers can operate at up to 0.5 bars above atmospheric pressure. The components of a hard shelled chamber usually include: a pressure vessel made from aluminium and steel with transparent acrylic viewing portals; airtight entry hatches, and in larger units an airlock that allows for entry and exit with the chamber losing pressure; two way communication devices and video feeds; carbon-dioxide scrubbers that clean the air in the chamber of exhaled gases; and a control panel that regulates chamber valves, the compression unit, and the in- and out-flow of oxygen and air into the chamber. Fully translucent single person units are also available, and are made from high strength acrylic plastic.
In many cases, the chamber is pressurised with normal atmospheric air, while pure oxygen is supplied to individuals via oxygen masks. This is a norm for multi-person hyperbaric chambers. Atmospheric air consists of a mixture of about 21% oxygen and 78% nitrogen, and the intake of pure oxygen is broken up with intervals of breathing in atmosphere air that has been pressurised within the chamber; this practice avoids oxygen toxicity.
HBOT cures decompression sickness and arterial gas embolisms through increasing atmospheric pressure, decreasing the size of the micro-bubbles, and enhancing the transport of blood to tissue in the body. The high concentration of oxygen, resulting from breathing in pure oxygen under pressure, helps to keep tissue in the body alive: that is, the tissue is oxygen starved due to nitrogen micro-bubbles that have formed and escaped into the tissue. The oxygen further reduces the nitrogen in the micro-bubbles, replacing the nitrogen with oxygen that is readily absorbed back into the body.
After the micro-bubbles have been adequately dealt with, the pressure within the chamber is gradually reduced until it reaches a pressure that is equal with the atmospheric pressure in the room-at-large.
