Diving Emergencies

This document contains general information on the assessment, management and disposition of patients presenting with suspected decompression sickness or other diving related emergencies


Fiona Stanley Hyperbaric Medicine Unit is the state referral centre for Western Australia. All diving emergencies requiring advice or treatment should be referred to the on-call hyperbaric physician contactable through the Unit in working hours (08 6152 5222) or Fiona Stanley Hospital switchboard (08 6152 2222) out of hours.

Decompression illness is caused by intravascular or extravascular bubbles that are formed as a result of reduction in environmental pressure (decompression). The term covers both arterial gas embolism, in which alveolar gas or venous gas emboli (via cardiac shunts or via pulmonary vessels) are introduced into the arterial circulation, and decompression sickness, which is caused by in-situ bubble formation from dissolved inert gas. Both syndromes can occur in divers, compressed air workers, aviators, and astronauts, but arterial gas embolism also arises from iatrogenic causes unrelated to decompression.


Decompression sickness starts with the formation and increase in size of extravascular and intravascular bubbles when the sum of the dissolved gas tensions (oxygen, carbon dioxide, nitrogen, helium) and water vapour exceeds the local absolute pressure. A state of supersaturation in the tissues is caused by the increase in tissue inert gas partial pressure that occurs when the gas (usually nitrogen, but occasionally helium) is respired at high pressure. If the rate of ambient pressure reduction exceeds the rate of inert gas washout from tissue bubbles form. Bubbles can have mechanical, embolic, and biochemical effects with manifestations ranging from trivial to fatal.

Clinical manifestations can be caused by direct effects from extravascular (autochthonous) bubbles such as mechanical distortion of tissues causing pain, or vascular obstruction causing downstream ischaemia. Secondary effects can cause delayed symptom onset up to 24 h after surfacing. Endothelial damage by intravascular bubbles can cause capillary leak, extravasation of plasma, and haemoconcentration. The majority of cases occur within 6 hours of diving but symptoms and signs may present up to 24 hours.


AGE results from sudden overinflation of the lungs resulting in alveolar rupture and passage of air into the arterial circulation (via pulmonary vein). It generally occurs after a rapid, uncontrolled ascent with breath holding after breathing gas under pressure. Divers usually ascend in the upright position so develop cerebral arterial gas embolism (CAGE).  Onset is sudden and symptoms will begin within five minutes of surfacing from the dive.

Presentation may be any symptoms of cerebral dysfunction and may range from localised paraesthesia, hemicortical deficits, bilateral asymetrical neurology to overwhelming collapse, convulsion, coma or cardiac arrest.

CAGE is a life threatening disease and requires urgent referral to the Hyperbaric Facility for recompression therapy. CAGE can also occur as a result of a PFO or other right to left shunt  from the venous circulation.


DCI has a wide range of presentations. There is no specific test to confirm a diagnosis of DCI. A thorough diving history is essential. Specific points include:

  1. Maximum depth of the dive
  2. Duration of the dive
  3. Diving equipment and gas mixture used
  4. Diving site and weather conditions
  5. Any difficulty whilst diving notably a RAPID ASCENT
  6. Use of a dive computer and warnings issued by the computer during the dive (if the diver has a dive computer and is referred to the Hyperbaric Facility, send the computer with them)
  7. Episodes of returning to the surface during the dive (referred to as bounce diving)
  8. Decompression stops, time and depth
  9. Other dives within the last 24 hour period
  10. Surface interval between dives if multiple dives within a 24 hour period
  11. Type of symptoms and latency after diving
  12. Exercise, alcohol or air travel pre or post dive
  13. Past history of DCI
  14. Past medical history and medications


Again no specific examination signs are specific to DCI but often serve as a baseline for treatment.

Important parts of routine examination include:

  • Respiratory examination for signs of pneumothorax or pneumomediastinum

Any symptom or sign occurring within 24 hours of diving that has no other plausible explanation consider DCI.



Urgently consider need for Hyperbaric opinion and recompression.


Give 100% Oxygen via non-rebreathing mask. Oxygen serves to washout the inert gas and establishes the largest possible gas gradient from tissue to alveolar gas.


Diving causes dehydration.

Encourage oral hydration otherwise use Isotonic Intravenous fluids.

Fluids given until adequate urine output > 0.5 ml /kg /hour.

Avoid fluid overload as this can worsen cerebral, spinal cord or pulmonary oedema.


Analgesia should be used for pain.

NSAIDs (except aspirin due to its antiplatelet activity) have been shown to reduce the number of hyperbaric treatments needed and are recommended unless there are contraindications.

Avoid Nitrous Oxide as this can worsen symptoms by increasing bubble size due to inward diffusion.

Suspected CAGE

Bed rest and keep supine (to prevent gas embolism becoming cerebral). DO NOT sit up even for CXR.  Possible pneumothorax is best assessed with bedside lung ultrasound.  Refer for urgent recompression.


Recompression treatment involves breathing 100% oxygen at an increased pressure. This serves to reduce bubble volume with pressure and wash out the inert gas with oxygen. The oxygen also serves to reduce the inflammatory response caused by the bubbles effect on the endothelium.

Different treatment tables are used but normally involve treatment to 2.8 Atmospheres absolute (18 metres of sea water equivalent depth) for up to 5 hours.


Middle ear barotrauma

This is the commonest problem occurring whilst diving. Due to Boyle’s law the volume of gas decreases with depth causing a negative pressure in the middle ear. This can lead to minor bleeding within the tympanic membrane to haemorrhage within the middle ear and tympanic membrane rupture.

Inner ear barotrauma

Rupture from forced valsalva of the (most commonly) round window leads to endolymph leakage. This can cause severe symptoms of vertigo and hearing loss. Differentiating between inner ear barotrauma and inner ear DCI can be difficult and discussion with an experienced diving physician is recommended.


Vann RD, Butler FK, Mitchell SJ, Moon RE. Decompression illness. Lancet. 2011 Jan 8;377(9760):153-64. doi: 10.1016/S0140-6736(10)61085-9. Review. PubMed PMID: 21215883

McMullin AM. Scuba diving: What you and your patients need to know. Cleve Clin J Med. 2006 Aug;73(8):711-2, 714, 716 passim. Review. PubMed PMID: 16913196.

Lynch JH, Bove AA. Diving medicine: a review of current evidence. J Spec Oper Med. 2009 Fall;9(4):72-9. PubMed PMID: 20112651.

Rosen’s Emergency Medicine – Concepts and Clinical Practice, 7th Edition

Date implemented – 09/2015
Review date – 09/2018
Author – Dr U Nic Ionmhain, Dr Ian Gawthrope

Dr James Wheeler
Dr James Wheeler

Emergency Physician, SCGH, WA, Australia

Articles: 498

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