The Immersion-Induced Pulmonary Edema in Swimming and Diving
Das immersionsinduzierte Lungenödem beim Schwimmen und Tauchen
Summary
Staying in or underwater can lead to acute pulmonary complaints, which clinically present as an acute immersion-induced pulmonary edema (IPE), particular in strenuous swimming (SIPE) or diving (DIPE).
The IPE presents as a cardiac pulmonary edema and is induced by several pathophysiological processes during immersion, including fluid-shift, severe breathing, strenuous exercise, ambient cold, and aggravating cardiac pathologies.
This clinical review summarizes current evidence about the incidence of IPE in general, SIPE, and DIPE, the main aspects of its complex underlying pathophysiology, clinical symptoms, outcome and prognosis. It furthers provides recommendations for emergency treatment and indication of hospital admission.
Key Words: Acute Pulmonary Complaints, Strenuous Exercise, Ambient Cold
Background
Staying in or underwater can lead to acute pulmonary complaints in individual cases, which clinically present as an acute pulmonary edema (7, 13). The available literature shows that such a situation can happen in primarily obviously healthy people not only during strenuous swimming but also during Apnea or SCUBA diving (self-contained underwater breathing apparatus). With respect to the incidence of developing an acute pulmonary edema during immersion, estimates in e.g. triathletes show, that a swimming-induced pulmonary edema in this community is not a rare event, since the estimation calculated a prevalence of about 1.4%, matching to data around 1.1% in SCUBA divers (14). Women seem to be at higher risk to suffer from pulmonary edema (Odd’s ratio 2.1 in a civilian population) (24).
Because of the immersion situation in both conditions, this clinical picture has been called Immersion-induced pulmonary edema (IPE), subgroup-oriented “swimming-induced pulmonary edema” (SIPE) and Apnea- or SCUBA- “diving-induced pulmonary edema” (DIPE), respectively.
Whereas cases of SIPE have been reported particularly in endurance swimmers and triathletes for a longer time, literature points towards an increasing incidence of DIPE in recent years (7). This may be partly due to better awareness in medical professionals dealing with maritime incidents. Also, an increasing mean age within the diving population with often later beginning of a diving career at the age of 60+ years may introduce more cases with impaired left ventricular compliance due to age-related comorbidities, such as arterial hypertension.
IPE is seen nowadays as a common and potentially serious incident in or underwater that can have significant respiratory or cardiac consequences and, in some cases, be fatal (24). But, in contrast to decompression-sickness, barotrauma or inert gas-narcosis, IPE, and SIPE in particular, is not a typical “diving accident”. It is rather a pathologic medical condition, that develops during swimming and diving due to immersion, cardiac precondition, cold water temperature and other factors (22).
For the complex pathophysiology of both, SIPE and DIPE, several risk factors and comorbidities have been identified, which help to understand these diseases better and to improve prevention, therapy, and risk stratification for recurrence (24) (figure 1).
Pathophysiology of Swimming-Induced (SIPE) and SCUBA Diving-Induced Pulmonary Edema (DIPE)
Being in immersion and/or submersion causes a loss of hydrostatic pressure towards lower body parts because of buoyancy with a consecutive gain of about 500-700ml blood in the body center, similar to autotransfusion, with increases in mean arterial (MAP) as well as central venous pressure (CVP) (figure 2). This leads to an increased right atrial preload, stimulating the secretion of ANP and the activation of the Frank-Starling mechanism. At the same time, heart rate decreases, which may lead to bradyarrhythmias (i.e. loss of p-wave, ventricular bigeminy) (Supplemental video 1). The more powerful right ventricular contraction transports more blood into the pulmonary system, increasing peripheral capillary filling in the lung tissue (21). In addition, the general negative pressure inside the alveolar space during inspiration can be amplified by very powerful breathing during vigorous swimming, or while using a diving regulator. The resistance within the regulator can be higher than usual in particular at larger depths or, if the regulator is very cheap or not working very well for other reasons. Both, increased capillary filling and more pronounced negative-pressure breathing, may contribute to fluid transudation into the alveolar space (figure 2) (28).
However, there are additional factors, contributing to IPE. Pulmonary blood returning from the lung capillaries to the left atrium causes a peak of left atrial filling pressure. Increased filling pressure needs a well-working now left ventricular Frank-Starling mechanism to transport the blood volume into the general circulation. For proper function, the Frank-
Starling mechanism needs undisturbed left ventricular compliance to generate the necessary stroke volume after increased filling.
As a further but relevant factor contributing to this clinical picture, the left ventricular afterload must be discussed: particularly in case of physical stress in combination with cold environment (cold water) peripheral total resistance increases, and as a result left ventricular afterload (5, 22) (figure 2).
Additionally, hyperoxia during diving may contribute to the occurrence of DIPE, because high PO2 causes a decrease in heart rate of about 10-15%, due to an effect of hyperoxia on autonomic regulation towards sympatholytic/parasympathomimetic response (25).
Finally, one further possible factor to IPE needs to be addressed, which may contribute to the development of an IPE in some cases, although not have been published exactly with this focus so far: immersion/submersion, and particular exposure to cold water may trigger a so-called “autonomic conflict” between the primarily parasympathetic cold/wet face-reflex, and the sympathetic “cold shock-response” of the body coming into contact with cold water. This conflict-situation between both, sympathetic and parasympathetic stimulation, normally happens nearly immediately and may cause inadequate bradycardia and/or bradyarrhythmia and sometimes even more risky rhythm disturbances.
Pathophysiology of Swimming-Induced (SIPE) and SCUBA Diving-Induced Pulmonary Edema (DIPE)
In Patients with Cardiovascular Conditions
Hypertension and/or general advancing age often come along with decreased left ventricular compliance and higher resistance, and thus a fast equilibrium of increased blood volume return from the lungs is hampered, leading to increased left atrial filling pressure and consecutively elevated pulmonary arterial wedge pressure. This may cause a “classic” cardiac pulmonary edema (3, 9).
In cases of SIPE with reduced left ventricular compliance, at least in some cases, a Takotsubo-syndrome has been identified recently, with reduced left ventricular performance (7, 17) (figure 2). Cardiac malfunction (i.e. hypertension or Takotsubo-syndrome), carries an increased risk for IPE due to the combination of both, an increased pre- and afterload.
Furthermore, coexistence of an elevated pre- and afterload, together with a reduced heart rate, is complicating the transport of the necessary blood volume, particularly when compliance is reduced and thus stroke volume cannot increase adequately (figure 2).
Thus, IPE, SIPE and DIPE seem to be the result of a complex situation in swimming and/or diving, which finally leads to pulmonary transsudation and subsequently the clinical picture of lung edema, particularly in conditions with impaired left ventricular compliance.
Finally, in case of a prolonged arrhythmic situation, such as atrial fibrillation, arrhythmia may cause a significant reduction in cardiac output and thus trigger IPE-development (19, 22).
Case Report
A 50-year old, male, highly experienced diver (nearly 1,500 dives in 15 years) with a medical history of hyperlipoproteinemia and untreated arterial hypertension performed an otherwise uneventful wetsuit river dive (water temperature 10 °C, maximum depth 14.5 m). After about 15 minutes dive time, he suddenly experienced acute dyspnea, and the diver performed a controlled ascent over 2 minutes. Symptoms did not resolve after leaving the water, and the patient developed hemoptysis. Upon arrival in the emergency department, he presented with breathlessness, tachypnea and cyanosis (transcutaneous O2-saturation 88 %). An immediate arterial blood gas analysis while breathing room air showed moderate hypoxemia and hypocapnia (PaO2 52 mmHg, PaCO2 34 mmHg) with normal pH (7.42) and lactatemia (1.2 mmol/L). Additional laboratory findings comprised increased levels of ultrasensitive troponin (0.07 μg/L) and D-dimers (1.29 mg/L), all other clinical chemistry data was within the normal range. Neither ECG nor transthoracic echocardiography showed any pathological findings. Thoracic x-ray (figure 5) and high-resolution CT scan (figure 6) demonstrated bilateral basal ground glass opacities compatible with pulmonary edema-related diffuse pulmonary infiltration. Coronary angiography did not show any lesion either. Symptoms resolved within two days upon administration of supplemental O2 together with diuretic and antihypertensive treatment. This case shows a typical history of SCUBA diving-induced pulmonary edema, which must be considered as a relevant differential diagnosis for in water-accidents in addition to decompression injury and/or drowning, in particular in the context of risk factors, e.g. age, arterial hypertension, wetsuit utilization, and cold-water temperature.
Therapy, Outcome, and Prognosis
Development of an IPE is a serious situation, that may have a fatal outcome in some cases, particularly in DIPE. Typical symptoms comprise shortness of breath and productive coughing as well as reduced transcutaneous oxygen saturation (figure 3). Diving may contribute to an aggravation of the situation, since the diver cannot ascent directly, despite having acute severe dyspnea and/or coughing, without a risk of suffering an additional diving accident.
However, if a swimmer and/or diver with IPE can be safely rescued, there is a surprisingly good chance of relatively fast clinical recovery after saving from water (4, 12, 13, 16), when several relevant factors for IPE, e.g. immersion, cold water, negative pressure breathing, are eliminated (figure 4). Typically, functional and clinical recovery happens within 24h to 2 days, either spontaneously or with the application of CPAP/NPPV (continuous positive airway pressure/non-invasive positive pressure ventilation), diuretics and a beta-adrenergic agonist (1, 11, 13, 18).
Recently, a specific algorithm has been recommended for diagnosis and therapy of IPE (20). Although most IPE victims are otherwise healthy (4, 6, 13, 23) there are some cases with identifiable cardiopulmonary risk factors (15). In particular, hypertension and reduced myocardial compliance (9, 10) have been identified as individual risk factors for DIPE, particularly in older SCUBA divers.
Conclusion
The complex aquatic environment causes several necessary physiological reactions primarily to cope with Immersion-induced increased central blood volume and cold-water environment, causing relevant increases in cardiac preload and afterload. Negative pressure breathing during strenuous swimming or regulator use in SCUBA diving may cause a fluid transfer into the alveolar space and, in some cases, disturbed myocardial function due to hypertension in DIPE or to a Takotsubo-syndrome in SIPE can even worsen the situation.
Thus, IPE may be relatively common in strenuous aquatic sports such as triathlon (4, 7) and also becomes more prevalent in SCUBA diving with the advancing age of divers particularly diving beginners (22).
Although the general prognosis for full recovery from IPE is good after saving, the acute clinical picture may be serious and can be fatal in rare cases. Individual risk factors for IPE should be identified after recovery from the acute situation to avoid the recurrence of IPE in future aquatic activities.
Conflict of Interest
The authors have no conflict of interest.
Funding
The authors received no funding related to this work. Funding and consulting fees received by SK as indicated in the ICMJE Uniform Disclosure Form for transparency reasons are not related to his work on this article.
Competing Interests
All authors have completed the ICMJE Uniform Disclosure Form at www.icmje.org/coi_disclosure.pdf and declare: The authors declare no support from any organization for the submitted work, no financial relationships with organizations that may have an interest in the submitted work in the past three years and no other relationships or activities that may have influenced the submitted work.
Summary Box
Immersion-induced pulmonary edema occurs during swimming and diving. Risk factors are higher age, vigorous exercise and cold environmental conditions. Increased cardiac pre- and afterload lead to
the clinical picture of acute left heart failure with acute respiratory distress, coughing and hypoxemia.
To prevent rare complications, such as Takotsubo-like syndrome, initial measures comprise a clinical examination, monitoring of vital signs and cutaneous oxygen saturation, the removal of risk faktors, nasal oxygen therapy and, in case of persistence of symptoms, emergency transport to a hospital.
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Section for Maritime Medicine
German Naval Medical Institute and
Kiel-University
Olshausenstrasse 74, 24098 Kiel, Germany
a.koch@iem.uni-kiel.de