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Decompression Illness

Authors: Sarah Clayton, Claire Walklett / Editors: Claire Ashford, Doug Watts, Lauren Fraser / Code: CAP20, CAP28, CAP37, CAP5, CAP6, CAP7, CC1, CC2, CMP6, HAP11, HAP19, HAP26, HAP33, HAP5, HAP6, HAP8, HMP5 / Published: 03/09/2019 / Review Date: 03/09/2022

Diving-related problems are rarely covered during medical school and specialty training and the basic science underpinning diving is often not well understood. Diving-related problems can present in many ways and their appropriate and timely management is essential for good outcomes and patient safety.

The British Sub Aqua Club (BSAC) reported 215 diving incidents in 2018. There were up to 30-50 incidents per month between May September. In 2018, injury was the most common incident followed by Decompression Illness (DCI). This was incongruent with the previous four years where DCI was the most common. There were 19 fatal incidents in 2017, which was the highest number since 2004.1

Decompression Illness (The Bends) is a disease of compressed gas divers, aviators, astronauts and caisson workers where gas bubbles form in tissues and/or the blood during or after a decrease in environmental pressure.2 In the United Kingdom (UK) this is most commonly seen in divers.

There are two types of decompression illness: decompression sickness (DCS) and arterial gas embolism (AGE). These will be explained in more detail further in the module.

Learning Bite

Decompression illness is a disease caused by a reduction in pressure, where gas bubbles form in the tissues or circulation causing damage. It includes both decompression sickness and arterial gas embolism.

Pressure and Gas Laws

The most important concept to understand in diving medicine is pressure. Pressure can be measured in many different units- here we will focus on atmospheres absolute (ATA). At sea level, the pressure is 1 ATA. With every 10m of seawater, this pressure increases by 1 ATA.

0m: 1 ATA

10m: 2 ATA

20m: 3 ATA

30m: 4 ATA

Gas laws underpin most of basic diving physics and physiology:

  • Boyles law
  • Henrys Law
  • Daltons Law
  • Gay-Lussacs Law

The most important of these in diving and DCI are Boyles law and Henrys law.

BOYLES LAW: At a constant temperature, the absolute volume of a fixed mass of gas is inversely proportional to the absolute pressure.

P1V1 = P2V2

As pressure increases, volume decreases.

Why are pressure changes relevant in diving medicine?

BAROTRAUMA = trauma caused by pressure changes

  • Affects air spaces in the body- ears, sinuses, lungs
  • Divers can get pain in their ears and sinuses on ascent and descent

The most dangerous is pulmonary barotrauma.

  • Usually due to a very rapid ascent or divers holding their breath
  • Causes lung to burst
  • Can cause arterial gas embolism (a type of decompression illness)

HENRYS LAW: At a constant temperature, the amount of gas that will dissolve in a liquid is proportional to the partial pressure of the gas over that liquid.

Why are gases relevant in diving medicine?

Nitrogen is an inert gas. This means it is not metabolised by the body and so the content does not change in inhaled and exhaled gas. Nitrogen dissolves in the blood. More nitrogen dissolves at greater partial pressures. As the diver descends, more nitrogen dissolves in to the blood. This is called on-gassing. As the diver ascends, nitrogen comes out of solution. This is called off-gassing. The nitrogen coming out of solution can form bubbles, particularly if divers ascend too fast, or miss any stops on their ascent. These bubbles can lead to decompression sickness (a type of decompression illness).

At depth, i.e. at pressure, the partial pressure of nitrogen increases:

0msw: ppN2 = 0.8

10msw: ppN2 = 1.6

20msw: ppN2 = 2.4

30msw: ppN2= 3.2

Gas mixtures

Different divers breathe different gas mixtures depending on the type of diving they are doing. Therefore, varying their exposure to inert gases such as nitrogen. The most commonly used gas is air. However, many divers also use other gas mixes such as:

  • Enriched air nitrox (a higher content of oxygen than air, mixed with nitrogen)
  • Heliox (helium and oxygen)
  • Trimix (oxygen, helium and nitrogen),
  • Pure oxygen

Learning Bite

Boyles law and Henrys law are fundamental in understanding dive medicine. Boyles law helps to explain arterial gas embolism and Henrys law helps to explain decompression sickness.

Pathophysiology of Decompression Illness

Decompression illness (DCI) is the umbrella term used to encompass both decompression sickness (DCS) and arterial gas embolism (AGE).

Decompression Sickness

Decompression sickness is caused by nitrogen coming out of solution when a diver ascends from a dive. It is sometimes described as being caused by evolved gas. The inert gas that evolves from the tissues can then cause a mass effect and inflammatory response in that tissue. This can happen anywhere in the body but is commonly seen in the articular cartilage (joints) and nervous tissue especially the spinal cord.

The full mechanism and pathophysiology of DCS is poorly understood and still being researched. It is thought there are two main effects from evolved gas:

  1. Direct damage (PRIMARY). Direct damage to the tissue resulting from the gas bubbles is thought to be caused by artery occlusion, damage to vascular endothelium and venous outflow obstruction. The effects on the vessels results in a disturbance of vascular permeability and microvascular flow which can cause a breakdown in the blood brain barrier4
  2. Inflammatory response (SECONDARY). Gas bubbles cause secondary effects by activating the clotting cascade, platelets, complement and leucocytes resulting in an inflammatory response in the affected tissues3.

Due to these two mechanisms of tissue damage DCI can present anytime from 0-72 hours or more after a dive. The symptoms due to the direct effect of bubbles usually present quickly whereas inflammatory responses can cause a latent response. This also means that DCI can have an evolving course with inflammatory mediated symptoms worsening over time.

Arterial Gas Embolism

Arterial gas embolism occurs when nitrogen bubbles escape in to the arterial circulation. This can result from a few different mechanisms:

i. PULMONARY BAROTRAUMA. This is explained in more detail below.

ii. PATENT FORAMEN OVALE/ ARTERIOVENOUS MALFORMATION (right to left shunt). Any bubbles in the venous circulation which may not normally cause a problem shunt in the arterial circulation and become an AGE.

iii. OVERWHELMING THE PULMONARY FILTER. Most divers bubble after most dives these bubbles usually diffuse in to the alveoli where they are exhaled. If this filter is overwhelmed, for example due to exercise, the bubbles will pass through the lungs without being filtered out and will then pass in to the arterial circulation via the left heart.

The escaped gas (AGE) can then lodge anywhere in the arterial system, causing arterial occlusion and resulting ischemia. The most serious form is when a gas embolus lodges in the cerebral arterial circulation known as a cerebral arterial gas embolus (CAGE).

Due to the pathophysiology of AGE, symptoms usually have a quick onset and patients need swift recompression in order to reduce permanent irreversible damage caused by tissue ischaemia.

PULMONARY BAROTRAUMA

Pulmonary barotrauma is an important condition to remember when dealing with divers. As per Boyles law, gas expands in volume as pressure decreases. Therefore the air in a divers lungs expands as the diver makes their way to the surface. If a diver doesnt equalise the pressure (holds their breath on ascent) or has an underlying pulmonary disease (causing gas trapping in the lungs) an over inflation injury can occur. Air from the pneumothorax can then embolise in to the pulmonary circulation, and reach the left side of the heart, to then be pumped in to the systemic arteries. This causes an arterial gas embolism.

Learning Bite

Decompression illness can be caused by evolved gas (DCS) or escaped gas (AGE). There are two ways in which bubbles can cause damage to tissues: directly or by resulting inflammatory processes.

How does Decompression Illness present?

Bubbles can form in or move to most parts of the body and so decompression illness can present with almost any clinical picture. In 90% of cases symptoms present within 6 hours of a dive. The sooner, after ascent, that a diver notices a problem, the more likely it is to be DCI and usually the worse the prognosis.

These are some of the more common presentations:

  1. Limb or joint pain often a toothache type pain, usually not worse on movement or palpation
  2. Girdle pain pain coming from the back and spreading to the abdomen
  3. Neurological symptoms tingling, numbness, weakness, change in behaviour or personality, poor co-ordination, loss of bowel or bladder control, changes in hearing or vision, memory loss, unconsciousness
  4. Chest pain or breathing difficulties this could suggest a pneumothorax, gas within the coronary vessels or immersion pulmonary oedema.
  5. Rash often a mottled rash called cutis marmorata. This can precede a more severe neurological DCI. It is recommended to take a photograph of the rash as it can disappear quickly before the patient sees a dive physician.
  6. Audio vestibular hearing loss, balance and co-ordination problems, vertigo and vomiting. Audio-vestibular bends are difficult to differentiate from inner ear barotrauma.
  7. Not quite right(Constitutional symptoms) malaise, headache, lethargy, loss of appetite, apathy etc. This can also include cognitive symptoms with a reduced MMSE score.

History

The important things to elicit from a history are:

  • What are their symptoms? DCI can present with almost any clinical picture
  • Dive profile: How deep? For how long? Any missed stops? What was their surface interval between dives? Decompression sickness is more likely with higher nitrogen loads. Nitrogen loads will be higher following long or deep dives.
  • Multiple dives: How many dives, over how many days and how may consecutive days diving? Multiple dives or multi-day diving increase risk as there is an accumulation of nitrogen.
  • Closed or open circuit and which gases used? This is explained below
  • Were there any problems during the dive e.g. Did the diver make a rapid ascent? Arterial gas embolism is more likely following rapid ascent (occurring with pulmonary barotrauma).
  • Has there been any improvement with oxygen? Symptoms tend to improve with oxygen, although this is not diagnostic
  • Timing of symptoms: Before the dive, during descent, at depth, during ascent, or after surfacing? Exactly how long after surfacing? Arterial gas embolism generally presents very quickly after surfacing, and decompression sickness usually presents within 6 hours of surfacing though can present late. It would be unusual for a patient to develop DCI before a dive (unless they have done a recent previous dive which may have caused DCI), on descent or while at depth. If a patient has carried on diving despite symptoms they may report an improvement in symptoms when returning to depth for subsequent dives.

Which circuit?

Divers use many different forms of equipment to deliver air/gas to them to breathe underwater. These are known as circuits and there are three main types:

  1. Open Circuit -The most common type of circuit used among recreational divers. Gas from the tank is supplied via the hose and regulator for a diver to breathe. When the diver exhales the gas in their lungs is lost to the environment (seen as bubbles). This means that depth time can be greatly limited by the amount of gas in the tank as most of it is wasted when the diver exhales.
  2. Closed Circuit Rebreather gas waste is limited in this system as a scrubber allows exhaled waste gases to be partially removed from the exhaled air. The air is then recycled through the loop and topped up by a small pony tank with a diluent gas (usually with oxygen but sometimes mixed gas). Therefore few or no gas bubbles are produced while diving. These systems are usually used by military or commercial divers but can be used by recreational divers with specialist training.
  3. Semi-closed Circuit Rebreather these are rarely used by recreational divers.

Closed or semi-closed circuits means a diver will inhale less inert gas throughout their dive meaning that their inert gas load will be less for a comparable diver on an open circuit.

Examination

As with any unwell patient, the patient should be assessed using an ABCDE approach.

Once the patient is stable, the most important aspects of a decompression illness examination are:

  • Chest examination: a thorough chest examination, pulse oximetry and a chest x-ray are helpful in looking for any pulmonary barotrauma, subcutaneous emphysema and subsequent tension pneumothorax. It can also help with assessing for immersion pulmonary oedema, another relatively common problem in divers caused by the fluid shifts which occur during immersion. Immersion pulmonary oedema is discussed in more detail later on.
  • Neurological examination: a full neurological examination including a thorough assessment of power, reflexes and sensation (sharp/ blunt, soft touch, vibration) as well as co-ordination, balance (gait, Rombergs, Unterbergers) and cranial nerves is very helpful for a diving physician to then be able to monitor progress after recompression treatment. It may not always be necessary to be quite so thorough in an emergency setting.
  • Joint examination: musculoskeletal DCI usually causes a deep unremitting joint pain which is unchanged on movement and palpation.
  • Skin examination: cutaneous DCI presents with cutis marmorata, a mottled appearance of the skin possibly associated with pruritis.

Risk factors for decompression illness

The following would be at an increased risk of developing DCI:

  • Deep dive, long dive, missed decompression stops, multiple dives
  • Age
  • Exercise during or after a dive
  • Flying/ ascending to altitude after diving
  • Obesity
  • Dehydration
  • Alcohol use prior to dive

Learning Bite

Decompression Illness can present with almost any symptoms. The majority (90%) of cases come on within six hours of a dive.

Decompression illness is primarily a clinical diagnosis and is assessed with a very thorough and detailed history and examination.

In the emergency department, it is vital to ensure there is no pulmonary barotrauma. This is crucial as it helps with the diagnosis and may need to be treated before a patient receives recompression therapy. A thorough examination and chest x-ray are important. If there is any uncertainty after this then a CT chest may be required to determine if there is any pulmonary barotrauma.

If there is any doubt as to the diagnosis, further investigations may be required to rule out other pathologies. For example, cerebral arterial gas embolism presents very similarly to a stroke a CT head would be useful in this case.

Learning Bite

A chest x-ray is often useful to assess for pulmonary barotrauma, although further investigations may be required.

ABCDE and call the National Diving Accident Helpline 07831 151 523 (in England and Wales) or 0345 408 6008 (Scotland) or Divers Alert Network (Worldwide) +191968491111.

  1. OXYGEN this is the most effective management of decompression illness in the emergency department. It improves prognosis and is usually all patients need in terms of analgesia. ALL PATIENTS SHOULD BE STARTED ON HIGH FLOW OXYGEN AT 15L/MIN VIA A NON-REBREATHE MASK REGARDLESS OF THEIR OXYGEN SATURATIONS
  2. CHEST X-RAY A good chest examination and CXR are very important to identify a possible pneumothorax or pulmonary oedema. Pneumothorax is a particular concern in divers because gas expands in the lungs as divers ascend, possibly causing an overexpansion.
    • Insert a chest drain if there is evidence of a pneumothorax.
  3. FLUIDS oral if the patient is alert, not vomiting, and is passing urine. Have a very low threshold for giving IV fluids.
    • Insert a catheter if there is any suspicion the patient may be in retention

Things you shouldnt do:

  • Do not give Entonox under any circumstances to anyone who has recently dived as the nitrous oxide is highly soluble and will increase the inert gas load, making the symptoms of DCI worse. It can also expand within the air filled spaces of the body and cause barotrauma to the lungs, ears, sinuses or gut.
  • Do not give pain killers unless you have a very long transfer to a chamber, and only after discussion with a diving doctor. Oxygen is usually sufficient to control pain. NSAIDs are best avoided as they can exacerbate micro-haemorrhages caused by DCI (particularly in neurological DCI) which can lead to permanent sequelae. Opiates should also be avoided where possible as they can increase the risk of oxygen toxicity. Patients will be exposed to high partial pressures of oxygen during recompression therapy and so lowering their toxicity threshold can be dangerous and may increase their likelihood of a seizure.

Recompression Therapy

Recompression therapy is the definitive treatment of decompression illness and involves the patient being transferred to a dedicated facility. The patient is re-pressurised in a chamber breathing 100% oxygen at a high partial pressure.

There are 3 main effects of recompression therapy:

i. Bubble crushing: as per Boyles law, increasing pressure decreases the volume of bubbles

ii. Flushing out the nitrogen bubbles with oxygen

iii. Healing damaged tissue with hyperbaric oxygen

Learning Bite

The most important thing you can do for a diver in the emergency department is put them on high flow oxygen and call the National Diving Accident Helpline (or Divers Alert Network).

Immersion Pulmonary Oedema

Background

Immersion pulmonary oedema is being increasingly recognised as a fatal complication of SCUBA diving. It can occur with any type of immersion, so is also worth bearing in mind in swimmers, and is especially recognised in open water triathlon swimmers.

Basic Science and Pathophysiology

When a body is immersed in water, the increased hydrostatic pressure causes redistribution of blood to the chest. This increases cardiac filling pressures and stroke volume, and decreases total lung capacity. This increases pulmonary alveolar capillary pressure, increasing transudation of fluid from capillaries to alveolar spaces, and causing pulmonary oedema.

Risk Factors

Any condition that predisposes to a relatively high left ventricular filling pressures. Most commonly this is hypertension and heart failure.

Clinical presentation

  • Cough
  • Dyspnoea
  • Pink frothy sputum

Investigations

  • Chest x-ray

Management

  • Sit still, in an upright position
  • Keep warm to reduce vasoconstriction
  • High flow oxygen
  • Vasodilators e.g. nitrates
  • Diuretics
  • Mechanical ventilation in severe cases
  • These patients do not need recompression therapy

Ears

Background

Ears can be problematic in divers. Like swimmers, they are prone to otitis externa. They are also at risk of middle and inner ear barotrauma because of the pressure changes they are exposed to.

Basic Science and Pathophysiology

The middle ear is an enclosed gas-filled space. It is therefore exposed to Boyles law and so vulnerable to barotrauma if it is not equalised correctly. This can affect the round window and the oval window, causing subsequent inner ear barotrauma.

Clinical Presentation

Otitis externa: Infection presents with pain, discharge and sometimes fever.

Barotrauma:

  • Middle ear barotrauma presents with pain and loss of hearing. The tympanic membrane is usually injected and there may be fluid behind the tympanic membrane. The worst cases present with ruptured tympanic membrane. The TEED score can be helpful in classifying severity.
  • Inner ear barotrauma usually presents with vertigo, tinnitus, co-ordination and balance problems. It is often confused with audio-vestibular DCI.

Otoscopy

To determine the difference between infection, DCI or barotrauma it is imperative that an ear examination is undertaken.

Management

Otitis externa: Most cases will resolve within a few weeks without treatment. However antibiotic ear drops can be useful in resolving the condition quickly. Oral antibiotics are not more effective due to limited absorption. Pain can be an issue so simple analgesia advice should be given. If there is a cartilage involvement an ENT review is advised as these patients may require admission for IV antibiotics. It is important that the ear is kept dry until treatment is complete.

Barotrauma:

  • Middle ear barotrauma mild cases will usually heal with conservative management in a few days to weeks. Perforations may require antibiotic drops and surgery if not healing. ENT opinion is advised in cases of perforation.
  • Inner ear barotrauma ENT review in ED is advised

Carbon Monoxide Poisoning

Background

Every year there are at least 25 accidental deaths from Carbon Monoxide (CO) poisoning in England and Wales and over 200 non-fatal poisonings which require hospital admission.

Basic Science and Pathophysiology

Carbon monoxide has a high affinity to bind to haemoglobin. If there are significant amounts of carbon monoxide present, oxygen carriage to the tissues is seriously compromised, with the heart and the central nervous system being especially susceptible to the abnormally low levels of oxygen. Where carbon monoxide binds with haemoglobin it forms carboxyhaemoglobin (COHB), which does not carry oxygen to the body tissues.

Carbon Monoxide also causes damage to the mitochondria interfering with respiration by affecting production of reactive oxygen species.

Clinical Presentation

CO poisoning can cause sudden collapse and loss of consciousness within minutes but symptoms may also take time to develop over hours or even days. Sometimes a whole household may be affected.

According to the Department of Health, the commonest symptoms and signs and an indication of their approximate frequency in CO poisoning are shown below4:

  • Headache 90%
  • Nausea and vomiting 50%
  • Vertigo 50%
  • Alteration in consciousness 30%
  • Weakness 20%

Investigations

Levels of carboxyhaemoglobin in the body are detected by a blood gas which is taken as soon after CO exposure is suspected. The levels found in this blood test will reduce over time so it is important to note when a person with suspected Carbon Monoxide poisoning was removed from the CO source.

Management with Hyperbaric Oxygen Therapy

In the acute instance it may help increase oxygen delivery to areas in the body where insufficient oxygen is being delivered due to the effects of the CO poisoning.

Hyperbaric oxygen therapy speeds up elimination of the carbon monoxide from the body and helps reduce the damage that it causes within the cells.

Recommendation from the Royal College of Emergency Medicine amongst other sources of expert opinion is that HBO may be useful if a person has suffered any of the following

  • new neurological deficit or mental status change
  • carboxyhaemoglobin of greater than 25% at any time
  • pregnancy
  • evidence of damage to the heart
  • loss of consciousness, even if subsequently recovered

Current recommendation is that three HBO sessions are undertaken in the first 24 hours after insult.

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The two biggest pitfalls with decompression illness are:

  • Not putting the patient on high flow oxygen, even if their oxygen saturations are high
  • Not calling for help soon enough. The National Diving Accident Helpline can be contacted 24 hours a day, 365 days a year, on 07831 151 523

All patients who may have decompression illness, should be started on high flow oxygen immediately regardless of their oxygen saturations. Oxygen is one of the only treatments, other than recompression therapy, which has strong evidence for its benefit.5

It is imperative to call a diving physician for help as soon as possible. Patients with DCI need recompression therapy, and this should not be delayed.

Decompression illness can present with a myriad of symptoms.

Pain and other symptoms in divers are not always due to DCI.

Urinary retention is relatively common with decompression illness so it is always worth having a low threshold for catheterising patients.

  1. BSAC. Annual Diving Incident Report. 2018. [Accessed July 2019].
  2. Diving and Subaquatic medicine 4th ed. Edmonds. P111. Chapter 10: Decompression sickness: history and physiology.
  3. Kindwall E and Whelan H, Hyperbaric Medicine Practice, 3rd Edition (2008), Chapter 4 page 71-89
  4. NHS Commissioning Board. April 2013. Clinical Commissioning Policy: Hyperbaric Oxygen Therapy. [Accessed July 2019].
  5. Stephenson JC. Pathophysiology, treatment and aeromedical retrieval of SCUBA-related DCI. Journal of Military and Veterans Health. 2009 Jun;17(3):10.

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