Swimming induced pulmonary edema

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swimming induced pulmonary edema

Swimming induced pulmonary edema

Swimming induced pulmonary edema also called “SIPE”, immersion pulmonary edema (IPE) or scuba divers pulmonary edema (SDPE) is pulmonary edema that occurs when competitive swimmers and divers develop lung injuries because their lung capillaries burst 1, 2, 3, 4, 5, 6, 4, 7, 8. Cases range from young, fit, military swimmers 5, 9, who have undergone careful medical screening, to older recreational athletes and divers with preexisting cardiopulmonary disease 10, 11. While the exact pathophysiology of swimming-induced pulmonary edema (SIPE) remains uncertain, it is believed to include a combination of intense physical exertion, immersion in cold water, and overhydration, resulting in central pooling of blood, increased pulmonary arterial pressure, capillary damage, and subsequent pulmonary edema 12, 13, 14, 15, 16. Cold water is believed to be a major contributing factor to the underlying pathophysiology. However, there have been numerous case reports and studies with individuals diving in tropical waters of 30 to 35 °C. The majority of the incidence of immersion pulmonary edema (IPE) in warm water was diving-related, but it has been seen with extreme exertion and overhydration in swimmers 17.

Swimming-induced pulmonary edema (SIPE) is characterized by acute onset of shortness of breath (dyspnea), cough, and occasionally coughing up blood (hemoptysis), and is associated with water immersion 2. The hallmark of SIPE has been described in the literature as a cough with a “frothy pink” sputum production 18. SIPE typically occurs in otherwise healthy individuals 4, 5, 19. A key feature in the majority of SIPE cases is a rapid resolution of symptoms within 24 to 48 hours after removal of the patient from water and rest, but SIPE occasionally may be life-threatening 20, 21, 2. Although fatal cases associated with SIPE have been reported regarding a snorkeler and a scuba diver 22.

Swimming-induced pulmonary edema (SIPE) risk factors include age older than 50, female sex, and presence of underlying cardiac disease, including left ventricular (LV) hypertrophy or hypertension 16. Situational risk factors include cold water immersion, high level of effort, tight wetsuits with full-length leg coverage, overhydration or fluid retention, and inadequate warm up 3.

Many athletes with SIPE have no underlying cardiopulmonary pathology; however, 1 study of older athletes (mean age 48 years) had up to 72% incidence of at least 1 risk factor such as hypertension, subclinical coronary artery disease, or left ventricle hypertrophy 10. A case series in divers found medical comorbidities in 68%, with 42% being cardiac, including valvular disease, Takotsubo cardiomyopathy and dysrhythmias 23. It is unknown why there is a female predominance 1.

A comprehensive review estimates the prevalence of swimming induced pulmonary edema of between 1.1% and 1.8% among triathletes and military combat swimmers 16. Another study that assessed risk prospectively in a large open water swimming event found a risk of 0.44% 24.

Adir et al 25 studied 70 naval trainees who developed SIPE during swimming time trials over 2.4 to 3.6 km in open seas. These trials took between 30 and 45 minutes with mean water temperatures during training of 19.6°C. All trainees developed shortness of breath (dyspnea), 67 developed cough, and 39 had coughing up blood (hemoptysis). On physical examination, 64 trainees had crackles, and 6 had wheezes. The mean oxygen saturation after exercise was 88.4%. Chest radiographs taken 12 to 18 hours after presentation were within normal limits. Sixteen trainees had recurrent episodes of SIPE 25.

Initial management requires safe water evacuation to prevent drowning and to perform a preliminary assessment 3, 26, 11. Symptoms usually begin to resolve after exiting the water and management may be supportive. Supplementary oxygen is important. The affected individual is often transferred to hospital for further investigations and management. The prognosis is generally excellent when treated, though fatal cases have been reported 27. Unfortunately, recurrent episodes are unpredictable and are common; thus, the biggest risk factor for SIPE is having a prior episode, with recurrence rate of 13% to 22%  2. Swimming-induced pulmonary edema (SIPE) has been proposed as a probable cause of unexplained death during swimming training in triathletes 28.

Athletes with a history of SIPE should be presumed to have a predisposition to recurrence. Although it is acknowledged that episodes of recurrence are unpredictable, these athletes should take care to swim in controlled environments to reduce the risk of drowning if a repeat episode was to occur. Spiteri et al 29 suggest that starting swimming at a slower pace may be appropriate to reduce the recurrence rate. A gradually progressive step-wise return to swimming is a sensible approach. SIPE prevention has been suggested. New developments have shown that a single oral dose of sildenafil 50 mg can lower pulmonary arterial pressure (PAP) and pulmonary arterial wedge pressure (PAWP) 30. In clinical practice, Martina et al 31 illustrated a case of a 46-year-old female ultra-triathlete with a history of at least five SIPE episodes who had no further recurrences during 20 subsequent triathlons while taking 50 mg of sildenafil before each swim.9 These findings require sufficiently powered controlled studies to support this prophylactic use. Sildenafil is currently not on the prohibited list of the World Anti-Doping Code (WADA).

Figure 1. Pulmonary edema

Pulmonary oedema

Table 1. Swimming induced pulmonary edema (SIPE) Key Points

Key questionsEvidence/commentAction/recommendations
Was it swimming induced pulmonary edema?• Clinical features are non-specific and a variety of features (e.g. cough, crackles, desaturation) are present in two thirds cases.
• Symptoms occur in close temporal association with water immersion.
• Rapid resolution (usually complete < 48 h) appears to be a universal feature and may be of use in differentiating SIPE from aspiration.
• Chest radiograph/ultrasound evidence of pulmonary edema is informative.		• Obtain a full and thorough collateral history, including assessment of timing of onset of symptoms.
• Evaluate any chest imaging and blood results.
• Utilize logical investigations to rule out other differential diagnoses (e.g. bronchoprovocation testing, continuous laryngoscopy during exercise) 32
Will swimming induced pulmonary edema recur?• Recurrence rates are variable (between 13 and 40%) but the condition can definitely recur.• Counsel the athlete that there is a reasonable chance of recurrence and provide safety advice for both athlete and medical teams.
• Stepwise return to swimming.
What can be done to avoid or treat swimming induced pulmonary edema?• Several risk factors are recognized.
• Detection of underlying cardiorespiratory disease is important		• Rule out underlying cardiac or respiratory disease process, e.g. by arranging echocardiogram, blood pressure monitor, lung function + more detailed investigations as indicated.
• Avoid over-hydration, tight fitting wetsuits, fish oil and aspirin.
• Consider the use of oral sildenafil prior to exercise in selected and well-characterized cases. This medication is not prohibited currently.
[Source 33 ]

Swimming induced pulmonary edema causes

Swimming induced pulmonary edema (SIPE) seems to occur mostly in apparently healthy individuals who have undergone careful medical screening 5, 9. Predisposing factors for swimming induced pulmonary edema (SIPE) include cardiopulmonary disease (especially hypertension) and pulmonary hypertension 34, 35. Other important factors during the event include ambient air temperature, exertion level, and anxiety 35, 36. Potential risk factors include cold water, wetsuit use, exercise, overhydration, elevated negative inspiratory pressure, older age (greater than 50 years of age), obesity, female sex, left ventricular hypertrophy, and emotional stress 37, 20, 4, 38, 39, 19. Cold water immersion causes an increase in central venous blood pooling and a subsequent increase in cardiac preload secondary to peripheral vasoconstriction; however, it should be noted that there have been reported swimming induced pulmonary edema cases in warm or tropical environments 40, 41. All of the military swimmers reported by Schupak et al. 5 had hydrated excessively prior to swimming to avoid dehydration during their long exposure. Over-hydration exacerbates central venous pooling due to an increase in circulating plasma volume 19. Tight-fitting wetsuits may also cause external compression of peripheral vessels and limb deep veins, leading to central venous pooling and a subsequent increase in cardiac preload 42. Nevertheless, there are several cases of SIPE where a wetsuit was not worn 5, 9, 19. Cases are commonly but not exclusively seen in open water swimming or immersion; however, there has been at least one reported case of SIPE in a scuba diver in a swimming pool 43. Postmortem studies have reported increased heart mass (9 of 20 available autopsies) and left ventricular free wall thickness (6 of 14 autopsies) in some triathletes 44.

Swimming induced pulmonary edema pathophysiology

The pathophysiology of swimming induced pulmonary edema (SIPE) is poorly understood, it is believed to include a combination of intense physical exertion, immersion in cold water, and overhydration, resulting in central pooling of blood, increased pulmonary arterial pressure, capillary damage, and subsequent pulmonary edema 12, 13, 14, 15, 16. Cold water is believed to be a major contributing factor to the underlying pathophysiology 4. However, there have been numerous case reports and studies with individuals diving in tropical waters of 30 to 35 °C. The majority of the incidence of immersion pulmonary edema (IPE) in warm water was diving-related, but it has been seen with extreme exertion and overhydration in swimmers 17.

Cardiopulmonary disease could be a predisposing factor for developing pulmonary edema during swimming or diving 34. Ludwig et al. 45 performed acute and post recovery bronchoalveolar lavage (BAL) in a subject suffering from SIPE and found no evidence of an underlying infection. Immersion causes centralization of blood to the heart, leading to an increased central blood volume 46. Lange et al. 47 showed an increase in heart volume when immersing a standing subject. Exercise in cold water can augment this effect 48. Zarvorsky 49 reviewed literature and showed that pulmonary edema can also occur by exercise alone, especially during maximal effort exercise. In a few published cases, unilateral pulmonary edema occurred during swimming, suggesting an underlying hemodynamic mechanism 50, 51.

More recent studies suggest a right and left ventricular stroke volume mismatch and raised mean pulmonary arterial pressure (PAP) and pulmonary arterial wedge pressure (PAWP) 52, 53, 54.

Swimming induced pulmonary edema prevention

Swimming induced pulmonary edema (SIPE) is not correlated with level of experience or training 1. Barouch 1 recommends that athletes focus more on race day actions. Athletes should warm up by swimming for more than 15 minutes to allow the pulmonary vasculature to adapt before the race begins 16. Start the race at an easy pace and speed up gradually. Avoid races with very cold water, wetsuits, and excessive pre-race hydration or salt loading 16.

Pharmaceutical agents have been examined for their effectiveness in swimming induced pulmonary edema (SIPE) prevention. Moon et al. 53 observed a higher mean pulmonary arterial pressure and pulmonary arterial wedge pressure in individuals with a history of SIPE during submerged exercise in cold water and showed that these pressures can be reduced with sildenafil. Premedication with sildenafil 50 mg, 1 hour before racing 30. Nifedipine has also been used in select cases 55. For athletes with fluid retention, premedication with furosemide or other diuretic for 1 to 2 days before a race may be necessary. However, use of furosemide is not permitted in some sports at high levels of competition.

Swimming induced pulmonary edema symptoms

Sudden (acute) pulmonary edema symptoms may include:

  • Difficulty breathing (dyspnea) or extreme shortness of breath that worsens with activity or when lying down
  • A feeling of suffocating or drowning that worsens when lying down
  • A cough that produces frothy sputum that may have blood in it
  • A rapid, irregular heartbeat (palpitations)
  • Anxiety, restlessness or a feeling that something bad is about to happen
  • Cold, clammy skin
  • Wheezing or gasping for breath

Swimming induced pulmonary edema (SIPE) is characterized by sudden onset of breathing problems caused by accumulation of fluid in the lung extravascular space, induced by immersion, usually but not always in cold water, and intense physical activity 2. All cases (100%) developed their symptoms during physical activity (e.g., military fitness training, lake crossing, training or aqua jogging) and 16% during participation on races 2. Mean temperature was 19.6°C (ranging from 23° to 13°C) 2.

Main initial reported symptoms were shortness of breath or dyspnea (79%) and/or cough (71%), hemoptysis (56%), wheeze (9%) and chest tightness (9%) 2, 56. Three (8%) suffered from chest tightness or chest pain and two (5%) from confusion 2. Coughing up blood (hemoptysis) was also a main discovery reported in 26 cases (68%), approximately similar to the observations made by Adir et al. 56, where they observed hemoptysis in 55.7% subjects diagnosed with SIPE. Athletes can also develop hemoptysis during running 57, 58. Hopkins et al. 59 studied a group of elite cyclists and found higher red blood concentration in the bronchoalveolar lavage (BAL) after intense exercise compared to normal subjects without exercise. Interestingly, they found no difference between the two groups after submaximal exercise 60, suggesting that maximal stress to the blood gas barrier is necessary to produce hemoptysis. The fact that 68% of the SIPE cases developed hemoptysis might confirm the hypothesis that this level of stress is often reached by athletes during submaximal to maximal exercise in combination with immersion 2.

If considered individually, these symptoms are not very specific and could be caused by other conditions such as water aspiration, infections of the respiratory tract or an acute asthma attack 2. Nevertheless, if they occur in combination with the conditions mentioned above, swimming induced pulmonary edema (SIPE) is a possibility 2. Auscultation was reported in 19 of the 38 cases wherein all (100%) showed abnormalities, mostly crackles (47%) or wheezing (32%) suggesting an airway process 2.

The hallmark of swimming induced pulmonary edema (SIPE) is the rapid resolution of initial signs and symptoms within 48 hour 2. The symptoms usually resolve after normalization of the physiologic environment by removal from water to a warm environment and by supportive treatment, sometimes even without any examination. Thirty-one of the thirty-eight cases (82%) mentioned a rapid resolution of the initial signs and symptoms, at least within 48 hour. In 15 of these 31 cases with a rapid normalization (48%), restoration to original condition was confirmed with a normal follow up chest X-ray within 48 hour. In two cases (5%), a follow up chest X-ray 2 days after onset was not totally normal and in five cases (13%), it was not clear when the normalization exactly occurred 2.

Table 2. Characteristics of patients with swimming-induced pulmonary edema (SIPE) in published reports

AuthorsCasesGenderAge (years)ComorbiditiesWater temp. (°C)PresentationTime of resolution (hour)
Melau 613M = 230–40None14–17.5Dyspnea (3)<24
Chest tightness (1)
Hemoptysis (3)
SO2 < 92% (2)
Shah 621F60Repaired coarctation of aorta, bicuspid aortic valve10Dyspnea<48
Cough
Chest tightness
Smith 631F55None17Dyspnea<48
Cough
SO2 < 92%
Yamanashi 641M38None21.4Dyspnea<24
SO2 < 92%
Casey 652F = 155–60None13Dyspnea (2)<24
Chest tightness (1)
Hemoptysis (1)
SO2 < 92% (1)
Carter 663F = 343–58Asthma (1), seasonal allergies (2)15–22Dyspnea (3)<24 (2)
Hemoptysis (3)N/A (1)
Chest tightness (3)
SO2 < 92% (2)
Noti 671F23NoneN/ADyspnea<24
Hemoptysis
SO2 < 92%
Wenger 681M43None20Dyspnea<24
Hemoptysis
Chest pain
Beinart 691F54Hypertension22Dyspnea>48
SO2 < 92%
Deady 701F38None15Dyspnea<24
Hemoptysis
SO2 < 92%
Adir 2570M = 7018–19None16–22Dyspnea (70)<24
Cough (67)
Hemoptysis (63)
Mean SO2 88% ± 6.6
Biswas 711M36Diabetes mellitus22Dyspnea<24
Hemoptysis
Lund 723M = 321–27None19Dyspnea (3)<48
Cough (3)
Hemoptysis (1)
SO2 < 92% (1)
Shupak 7321M = 2118–19None16–18DyspneaN/A
Cough
Hemoptysis
SO2 91% ± 6.5
Weiler-Ravell 748M = 818–19N/A23Cough (7)<24
Hemoptysis (8)
SO2 < 92% (5)

Abbreviations: N/A = not available; SO2 = oxygen saturation.

[Source 75 ]

Swimming induced pulmonary edema diagnosis

Swimming induced pulmonary edema (SIPE) should be strongly considered in any athlete with cough, dyspnea, rales, or hemoptysis during or after open water swimming events. People who have breathing problems or swimming induced pulmonary edema (SIPE) should see a doctor. Be sure to tell him or her about the conditions you were in when you had the symptoms.

Swimming induced pulmonary edema (SIPE) history may include:

  • Exercise in cold water
  • Absence of water aspiration
  • Absence of diseases concerning the cardiopulmonary system
  • Acute onset of symptoms during or immediately after swimming

Ludwig et al suggested the following criteria for swimming induced pulmonary edema (SIPE) 76:

  1. Acute onset of dyspnea or hemoptysis during or immediately after swimming;
  2. No history of water aspiration, laryngospasm, or preceding infectious process;
  3. Hypoxemia, defined by an oxygen saturation <92% by pulse oximetry or an alveolar-arterial gradient >30 mm Hg; and
  4. Radiographic opacities consistent with an alveolar filling process and/or interstitial pulmonary edema that resolve within 48 hours.
  5. Other potential cardiac causes of pulmonary edema need to be excluded 67.

Your doctor will do a physical exam to see if you have fluid in your lungs. Your doctor listen to your heart and lungs with a stethoscope. Your doctor be examining you for:

  • Increased or decreased heart rate or blood pressure.
  • Increased respiratory rate.
  • Abnormal heart sounds.
  • Crackling sounds or wheezing/whistling sounds in your lungs.
  • Swelling of your body.
  • Gray or bluish skin.

Based on the severity of your symptoms, he or she may order tests. Tests may include a chest X-ray, brain scan, or electrocardiogram (ECG). These help diagnose the type of illness and decide on a treatment plan.

Tests that can help diagnose pulmonary edema or determine the reason for fluid in your lungs include:

  • Chest X-ray. A chest X-ray can confirm the diagnosis of pulmonary edema and exclude other possible causes of shortness of breath. It’s usually the first test done when a health care provider suspects pulmonary edema.
  • Chest computerized tomography (CT) scan. A chest computed tomography (CT) scan gives more details about the condition of the lungs. It can help a provider diagnose or rule out pulmonary edema.
  • Pulse oximetry. A sensor is attached to a finger or ear. It uses light to determine how much oxygen is in the blood. A total of 73% of SIPE cases showed hypoxemia. Hypoxemia defined as pulse oximeter values <90% or arterial oxygen <60 mmHg
  • Arterial blood gas test. This test measures the amount of oxygen and carbon dioxide in the blood.
  • Brain-type natriuretic peptide (BNP) blood test. Increased levels of B-type natriuretic peptide (BNP) may signal a heart condition. Brain-type natriuretic peptide (BNP) is secreted by the heart muscle cells (cardiac myocytes) of the left ventricles in response to stretching caused by increased ventricular blood volume or increased intracardiac pressures. Elevated BNP levels correlate with left ventricular end-diastolic pressure as well as pulmonary occlusion pressure and can be seen in patients with congestive heart failure 77. BNP levels less than 100 pg/ml suggest heart failure is less likely, and levels greater than 500 pg/ml suggest a high likelihood of heart failure. Levels between 100 and 500 pg/ml do not help in the diagnosis of heart failure and are often seen in critically ill patients 77.
  • Troponin elevation is commonly noted in patients with damage to heart muscle cells (cardiac myocytes), such as acute coronary syndrome. They, however, are also noted to be elevated in patients with severe sepsis 77.
  • Other blood tests. Blood tests to diagnose pulmonary edema and its causes also usually include a complete blood count, metabolic panel to check kidney function and thyroid function test.
    • Hypoalbuminemia (≤3.4 g/dL) is an independent marker of increased in-hospital and post-discharge mortality for patients presenting in acute decompensated heart failure 78. Low albumin in isolation does not lead to pulmonary edema as there is a concurrent drop in pulmonary interstitial and plasma albumin levels preventing the creation of a transpulmonary oncotic pressure gradient 79.
    • Obtaining serum electrolyte levels, including renal function, serum osmolarity, toxicology screening, help in patients with pulmonary edema due to toxic ingestion. Obtaining lipase and amylase levels help diagnose acute pancreatitis.
  • Electrocardiogram (ECG or EKG). This painless test detects and records the timing and strength of the heart’s signals. It uses small sensors (electrodes) attached to the chest and sometimes to the arms or legs. Wires attach the sensors to a machine, which displays or prints results. An electrocardiogram (ECG) can show signs of heart wall thickening or previous heart attack. A portable device such as a Holter monitor may be used to continuously monitor the heartbeat at home.
  • Echocardiogram. An echocardiogram uses sound waves (ultrasound) to create pictures of the beating heart. It can identify areas of poor blood flow, heart valve issues and heart muscle that is not working properly. An echocardiogram can help diagnose fluid around the heart (pericardial effusion).
  • Cardiac catheterization and coronary angiogram. This test may be done if other tests don’t show the cause of pulmonary edema, or when there’s also chest pain. It helps health care providers see blockages in the heart arteries. A long, flexible tube (catheter) is inserted in a blood vessel, usually in the groin or wrist. It’s guided to the heart. Dye flows through the catheter to arteries in the heart. The dye helps the arteries show up more clearly on X-ray images and video.
  • Ultrasound of the lungs. This painless test uses sound waves to measure blood flow through the lungs. It can quickly reveal signs of fluid buildup and plural effusions.

Plain chest radiograph (chest X-ray)

The chest radiograph (chest X-ray) remains the most practical and useful method of radiologically assessing and quantifying pulmonary edema 80, 81. Mild pulmonary edema shows evidence of upper lobe diversion with constriction of lower lobe vessels and enlargement of upper lobe vessels, correspondent to a pulmonary capillary wedge pressure (PCWP) between 13 and 18 mmHg. Interstitial edema with loss of vascular definition, peribronchial cuffing, and Kerley lines occur with an elevation of pulmonary capillary wedge pressure (PCWP) to 19–25 mmHg. PCPW above 25 mmHg produces alveolar filling showing airspace opacities in the perihilar and lower lung zones 82, 83. Moon et al. 53 showed that pulmonary capillary wedge pressure (PCWP) values of 18 ± 3.9 mmHg can be reached in SIPE-susceptible individuals by rapid submersion into water of 20 °C, rising to 18.9 ± 5.5 mmHg with additional exercise.

Pleural effusion can also occur 84. 250–600 ml of fluid are required for it to be evident on an erect anteroposterior chest radiograph 85. Smaller amounts about 50 ml could be detected in a lateral radiograph by blunting of the sharp posterior costophrenic angle. Ultrasound has a sensitivity of 100% by detecting pleural fluid as little as 5–50 ml. Computed tomography (CT) of the chest is not routinely used, but is very sensitive in detecting pulmonary edema and pleural effusion 86. Signs of pulmonary edema are usually bilateral, but can be unilateral 50.

A mnemonic to remember the radiographic signs of pulmonary edema is ABCDE 87:

  • A: alveolar opacification
  • B: batwinging
  • C: cardiomegaly
  • D: diffuse interstitial thickening (septal lines) and diversion (vascular upper zone diversion, cephalisation)
  • E: effusions (pleural)

Features useful for broadly assessing pulmonary edema on a plain chest radiograph include 88:

  • upper lobe pulmonary venous diversion (stag’s antler sign)
  • increased cardiothoracic ratio/cardiac silhouette size: useful for assessing for an underlying cardiogenic cause or association
  • features of pulmonary interstitial edema:
    • peribronchial cuffing and perihilar haze
    • septal (Kerley) lines
    • thickening of interlobar fissures
  • features of pulmonary alveolar edema:
    • air space opacification classically in a batwing distribution
    • may have air bronchograms
  • pleural effusions and fluid in interlobar fissures (including ‘vanishing’ pulmonary pseudotumor)

There is a general progression of signs on a plain radiograph that occurs as the pulmonary capillary wedge pressure (PCWP) increases (see pulmonary edema grading below). Whether all or only some of these features can be appreciated on the plain chest radiograph, depend on the specific cause 89. Pulmonary edema is usually a bilateral process, but it may uncommonly appear to be unilateral in certain situations and pathologies (unilateral pulmonary edema).

One pulmonary edema grading based on chest radiograph appearances and pulmonary capillary wedge pressure (PCWP) is as follows 90:

  • Grade 0: normal chest radiograph, pulmonary capillary wedge pressure (PCWP) 8-12 mmHg
  • Grade 1: shows evidence of upper lobe diversion on a chest radiograph, pulmonary capillary wedge pressure (PCWP) 13-18 mmHg
  • Grade 2: shows interstitial edema on a chest radiograph, pulmonary capillary wedge pressure (PCWP) 19-25 mmHg
  • Grade 3: shows alveolar edema on a chest radiograph, pulmonary capillary wedge pressure (PCWP) greater than 25 mmHg

Figure 2. Pulmonary edema chest X-ray

Pulmonary edema chest x-ray

Footnote: Acute pulmonary edema showing alveolar edema (white arrows) and interstitial edema (black arrowheads). Alveolar edema manifests as ill-defined nodular opacities tending to confluence (white arrows). Interstitial edema can be seen as peripheral septal lines – Kerley B lines (black arrowheads).

[Source 91 ]

Pulmonary edema CT

Interstitial pulmonary edema is most commonly demonstrated by the following CT signs 92:

  • ground glass opacification
  • bronchovascular bundle thickening (due to increased vascular diameter and/or peribronchovascular thickening)
  • interlobular septal thickening

Alveolar edema is demonstrated by airspace consolidation in addition to the above findings.

Pleural effusions are a frequent accompanying finding in cardiogenic/hydrostatic pulmonary edema.

Figure 3. Pulmonary edema CT

Pulmonary edema CT

Footnotes: Bilateral airspace opacification in a central peribronchovascular distribution is seen, associated with smooth interlobular septal thickening (which indicates interstitial edema) and bilateral moderate pleural effusions with underlying segmental basal consolidation/collapse. Mild cardiac enlargement is noted. Reactive mediastinal and right epiphrenic lymphadenopathy and mild cirrhotic changes of the liver are also seen.

[Source 93 ]

Pulmonary edema ultrasound

Pulmonary edema ultrasound is a newer technique that is non-invasive and does not involve radiation exposure. It is most commonly used in intensive care units, emergency rooms, and operating rooms. It helps detect the accumulation of extravascular lung water (EVLW) ahead of the clinical manifestations 94.

The appearance of pulmonary edema is defined as a function of the perturbation of the air-fluid level in the lung, a spectrum of appearances coined the alveolar-interstitial syndromes.

As subpleural interlobular septa thicken among air-filled alveoli, they create a medium in which incident ultrasound waves will reverberate within, creating a short path reverberation artifact. Referred to as B-lines, these are pathological when more than three appear, garnering the title lung rockets, and consistent with thickened interlobular septa. When spaced 7 mm apart they correlate with radiographic interstitial edema and when 3 mm apart with ground glass opacification. When surrounding alveoli become fluid-filled, the resultant interface assumes a tissue-like pattern. The tissue-like sign and shred sign are pathognomonic 95.

Pulmonary artery catheterization

Often considered a gold standard in the determination of the cause of pulmonary edema, it is an invasive test that helps monitor systemic vascular resistance, cardiac output, and filling pressures. This test may be done if other tests don’t show the cause of pulmonary edema, or when there’s also chest pain. It helps health care providers see blockages in the heart arteries. A long, flexible tube (catheter) is inserted in a blood vessel, usually in the groin or wrist. It’s guided to the heart. Dye flows through the catheter to arteries in the heart. The dye helps the arteries show up more clearly on X-ray images and video. An elevated pulmonary artery occlusion pressure over 18 mm Hg is helpful in the determination of cardiogenic pulmonary edema 77.

Transpulmonary thermodilution

It is an invasive testing modality performed in patients typically undergoing major cardiac, vascular, or thoracic surgeries. They are also used in septic shock and monitors several hemodynamic indices such as cardiac index, mixed venous oxygen saturation, stroke volume index, and extravascular lung water (EVLW) 94.

Swimming induced pulmonary edema treatment

At present, there have been no randomized trials of swimming-induced pulmonary edema (SIPE) therapy and therefore the optimal strategy for treatment of swimming-induced pulmonary edema (SIPE) is unknown and mainly based on logic and anecdotal experience 96. The hallmark of swimming induced pulmonary edema (SIPE) is the rapid resolution of initial signs and symptoms within 24 to 48 hour after removal of the patient from water and rest, but SIPE occasionally may be life-threatening 20, 21, 2. The acute treatment of SIPE begins with immediate removal from the water, placing the individual in a warm environment, and removal of a constrictive wetsuit if present. Additional supportive care, including oxygen, diuretics and beta2 agonists may be considered on a case-by-case basis. While SIPE can be fatal, the majority of athletes recover and are completely symptom free within 48 hours.

The symptoms usually resolve after normalization of the physiologic environment by removal from water to a warm environment and by supportive treatment, sometimes even without any examination. Thirty-one of the thirty-eight cases (82%) mentioned a rapid resolution of the initial signs and symptoms, at least within 48 hour. In 15 of these 31 cases with a rapid normalization (48%), restoration to original condition was confirmed with a normal follow up chest X-ray within 48 hour. In two cases (5%), a follow up chest X-ray 2 days after onset was not totally normal and in five cases (13%), it was not clear when the normalization exactly occurred 2.

Administered therapies were reported in 35 of the 38 cases (92%) and consisted mostly of supplement oxygen therapy (27 cases, 77%): in 23% oxygen alone, in 37% in combination with beta2-agonist and in 11% in combination with diuretics 2. Other therapies included continuous positive airway pressure (CPAP), antibiotics, nitroglycerine and prednisolone 2. This study demonstrated that prehospital treatment of SIPE with continuous positive airway pressure (CPAP) or positive expiratory pressure (PEP) device is feasible on site during a large open-water swimming event 96. Most patients (91%) could be discharged safely from the on-site mobile medical unit after median of 10 to 20 minutes of treatment with CPAP or PEP device 96. Moreover, improvement after treatment was reflected by increased peripheral oxygen saturation (SpO2) and alleviation of patient-reported respiratory symptoms, whereas point-of-care lung ultrasound findings and lung auscultation remained unchanged. In a subgroup of individuals with peripheral oxygen saturation (SpO2) of ≥ 92% at admission, treatment with a PEP device seemed equally efficient to treatment with CPAP 96. Two cases resolved spontaneously without any intervention 2.

Swimming induced pulmonary edema prognosis

The hallmark of swimming induced pulmonary edema (SIPE) is rapid resolution of initial signs and symptoms, in most cases within 48 hours, but it can be fatal if the athlete continues to compete 2. Recurrent episodes of SIPE often occur. In five of the 38 summarized cases (13%), one or more recurrent episodes are reported 97, 19, 39. Recurrence of SIPE appears to be unpredictable and is not limited by age, sport, or environmental conditions 3. Adir et al. 56 reported a recurrence rate of 22.9 % (16 of the 70 military swimmers) SIPE. All cases took place at least 3 months after the first incident 9. Shupak et al. 98 found a significantly higher recurrence rate after severe events of swimming induced pulmonary edema (SIPE) 75% of these severe events occurred after a previous mild or severe episode, supporting a certain degree of susceptibility of subjects suffering from SIPE.

Furthermore, a fatal case of SIPE was described in a 51-year-old female recreational diver who logged 54 dives over the course of a year between episodes of SIPE 99. Carter and Koehle 39 highlighted that two of the three female triathletes in their group suffered with recurrence of SIPE. Among them, a 58-year-old female suffered at least four episodes over a 4-year period. On each occasion, symptoms started within 15 minutes of commencing swimming. However, not all of these episodes required hospitalization and in between the episodes she successfully completed two open water triathlons and multiple lake training sessions, further confirming the variable nature of this condition 39.

It is of paramount importance that athletes are warned about recurrent episodes and should be emphasized that it is essential that a thorough evaluation of their cardiac and pulmonary physiology has been performed to look for any underlying causes of SIPE 10. Authors from this study described a case of a 55-year-old female recreational triathlete who suffered with recurrent episodes of SIPE 100. The risk of potential recurrence was not highlighted to her during her hospital admission and she subsequently suffered a life-threatening episode when she returned to open water swimming 100.

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