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IPE: When experience does not provide protection

  • Autorenbild: Michael Mutter
    Michael Mutter
  • 25. Jan.
  • 5 Min. Lesezeit

Case vignette: A 49-year-old, very experienced diver undertook a dive in a Swiss lake with his rebreather (JJ-CCR) in autumn. The water temperature was around 10 °C. After only about 10 minutes, he felt increasing shortness of breath, which rapidly worsened. After about 20 minutes, he had to abort the dive as an emergency.


The diver had remained within no-decompression limits (maximum depth 30 m, O₂ set point 1.3 bar). At the surface, he was no longer able to remove his equipment himself due to severe shortness of breath. His buddies helped him out of the water, administered oxygen and alerted the emergency services.


At the emergency department, a chest X-ray revealed severe pulmonary oedema. The patient was admitted to the intensive care unit, where his condition improved significantly within two days, allowing him to be discharged home.


Diving location ‘Street Lamp’, Walensee
Diving location ‘Street Lamp’, Walensee

The investigations carried out in the following weeks revealed:

  • Normal left and right ventricular function in echocardiography (heart ultrasound) without PFO

  • Normal performance in ergometry

  • Normal lung function


The patient had a history of well-controlled arterial hypertension (high blood pressure).


What had happened?

  • The clinical picture is typical of immersion pulmonary oedema:

  • acute respiratory distress underwater

  • rapid deterioration

  • radiologically confirmed pulmonary oedema

  • complete regression within a short period of time

  • no structural heart or lung disease

 

IPE

Pulmonary oedema occurs when fluid leaks from the pulmonary capillaries into the alveoli. In immersion-induced pulmonary oedema (IPE), this happens while the person is in the water.


Redistribution of blood in the chest cavity

The pathophysiology of IPE has not been conclusively clarified, but the following pathomechanism is assumed: When immersed in water, hydrostatic pressure causes blood to be redistributed from the extremities and abdominal cavity to the heart and lungs. Cold water further intensifies this effect through peripheral vasoconstriction (narrowing of the blood vessels). The pressure in the pulmonary vessels increases, causing fluid to leak into the alveoli. The resulting gas exchange defect leads to hypoxia (oxygen deficiency) and always represents a potentially life-threatening situation.


Although cold water is an important risk factor, IPE also occurs in warm waters. It is not uncommon in physically fit men, such as military divers or triathletes. Physical exertion also seems to increase the likelihood of its occurrence.


In addition to age and pre-existing cardiovascular disease, being female appears to be another risk factor for IPE.


IPE can affect even completely healthy and well-trained individuals without warning.

Specific risk factors in diving

A specific factor in diving is breathing against negative breathing pressure, where the water pressure on the chest is higher than the pressure of the inhaled gas.


In scuba diving, breathing mechanics depend largely on trim. A horizontal position in the water ensures that the hydrostatic pressure on the lungs corresponds to the pressure at which the breathing gas is delivered by the equipment. This means that there is no significant pressure gradient and inhalation takes place without additional negative pressure.


On the other hand, upright or semi-upright positions, in which the regulator is above the lungs, are unfavourable. In this situation, a relatively lower pressure than the regulator must be generated in the lungs to enable inhalation. This causes the pressure in the alveoli to fall below the pulmonary capillary pressure, causing fluid to be ‘sucked’ from the vessels into the alveoli. This effect is particularly pronounced in CCR diving with counterlungs mounted high on the back, as the hydrostatic pressure on the lungs is higher than the pressure in the breathing system. The resulting negative inhalation pressure also promotes the transfer of fluid from the pulmonary capillaries into the alveoli and thus the development of pulmonary oedema.


Such negative breathing pressure can also occur during snorkelling, malfunctions of the regulator, insufficient response of the ADV (Automatic Diluent Valve) and thus insufficient filling of the loop when diving with rebreathers, high breathing gas density at great depths, and tight diving suits or harnesses, further increasing the risk.


Underestimated occurrence and clinical signs

The occurrence of IPE is unclear and is probably underestimated. People with heart disease are particularly at risk, but healthy individuals can also be affected. IPE should always be considered in cases of shortness of breath, coughing, foamy sputum or coughing up blood during or shortly after swimming or diving. These symptoms are often misinterpreted as decompression sickness, barotrauma or (near) drowning.


Quick action is crucial

If IPE is suspected, the water must be left immediately. If symptoms occur underwater, surface immediately. As much weight as possible should be removed at the water's surface to reduce immersion. Once on land, the upper body should be elevated and high-dose oxygen administered (approx. 15 l/min via a mask with reservoir). The emergency services should be alerted without delay, and an emergency medical assessment is required in all cases, particularly to rule out acute heart disease.


What advice should the diver be given regarding his future fitness to dive?

The incident described is most likely a case of immersion pulmonary oedema (IPE). Unfortunately, the decisive factor here is not the unremarkable results of the subsequent cardiological and pneumological examinations, but the fact that IPE has already occurred. The occurrence of IPE in itself is associated with a significantly increased risk of recurrence, which is well documented in the literature. Recurrences can occur at any time, often earlier and sometimes more severely – even under seemingly more favourable conditions – and cannot be reliably predicted. Unfortunately, preventive measures cannot reliably eliminate this risk.


Anyone who has suffered an IPE once has a significantly increased risk of experiencing another episode in the future.

The Joint Position Statement of the South Pacific Underwater Medicine Society (SPUMS) and the UK Diving Medical Committee (UKDMC) therefore considers immersion pulmonary oedema to be so severe and the risk of recurrence so high that further diving is expressly discouraged after experiencing IPE. The reason given for this is that the risk of a recurrence underwater cannot be reduced to an acceptable level and such an event is potentially life-threatening.


At the same time, advice must always be based on a nuanced individual assessment that takes into account the specific circumstances of the event, such as high breathing gas density or CCR diving with back-mounted counterlungs.


These factors do not change the basic risk assessment, but they are important for transparent, technically sound and comprehensible decision-making.


This recommendation is often disappointing for those affected, but it is not a sanction, rather a preventive, safety-oriented medical decision. It is also crucial that divers are clearly and unambiguously informed about the high risk of recurrence.


Early recognition of IPE and clear differentiation from other diving incidents, in particular barotrauma or decompression sickness, with which it is often confused, are therefore of central importance for the safety of those affected.

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