Can Running a Marathon Cause Pulmonary Edema?

A study presented at the European Respiratory Society's Annual Congress revealed that running a marathon has been linked to pulmonary edema. The researchers studied 26 people before and after a race. They found that 50 percent of the runners exhibited signs of pulmonary edema. Further research is planned to explain this connection.

Pulmonary Edema

Pulmonary edema "is an abnormal buildup of fluid" in the lungs and can lead to complete respiratory failure. Although it is often linked to congestive heart failure, this is not the only cause of the edema. Pulmonary edema can also occur because of trauma, infections, kidney failure and high altitudes. Some of the symptoms include coughing, problems breathing, paleness and sweating. If untreated, it can lead to cardiac arrest or death.

The Connection between Marathons and Pulmonary Edema

Researchers have debated the connection between marathons and pulmonary edema in the past and often disagreed about the link. However, the study presented at the European Respiratory Society's Annual Congress clearly showed a link between them. The 26 runners included in the research exhibited pulmonary edema on chest radiographs taken after the race. The study found 50 percent had the edema, and women were affected more than men. Additionally, they discovered that there was "no relation between marathon time" and the edema, so runners who were quicker were not more or less likely to be affected.

A Contradiction with Other Research

Recent research has recommended that older marathon runners can safely continue participating in the sport without increased risk. This study from the University of Manitoba in Canada seems to contrast with the findings at the European Respiratory Society's Annual Congress. Pulmonary edema is actually more common in older individuals, yet the Canadian study found that runners over the age of 50 can safely continue with marathons.

The connection between marathons and pulmonary edema must continue to be studied. The limited scope of previous research and small number of participants makes conclusions difficult. It has been an accepted fact that marathons place strain on the hearts of even the most experienced and young runners. However, pulmonary edema has been neglected in many studies.

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Lana has a B.S. degree in Biology and Chemistry. She is an avid athlete, youth coach and follows several sports. Follow @Lana_Bandoim on Twitter.

Sport Yahoo

Edema is a symptom that has many possible causes

August 2012

DEAR DOCTOR K: What can I do about my edema? The diuretics my doctor prescribed haven't helped.

DEAR READER: Edema is swelling caused by a buildup of extra fluid. Edema most often affects the feet and legs, but it can affect the hands and even the face. The skin becomes puffy and swollen.

The fluid in your body is in three places: inside each of the 13 trillion cells in your body; in the blood (which means inside all your blood vessels); and in the space between your cells and your blood vessels. Edema occurs when unusual amounts of fluid leak out of the blood vessels and into the space between your blood vessels and cells.

Diuretics, also known as water pills, are often used to treat edema. They help your kidneys eliminate excess fluid in your body.

Edema is a symptom that may be caused by many conditions. Your doctor will need to identify and treat the condition that is causing it. Possible causes include:

-- Prolonged standing or sitting. This can cause edema in your feet and lower legs. That's because gravity is pulling more blood into the blood vessels of your legs. When the blood vessels swell with fluid, some of the fluid leaks out of the vessels and into the tissues.

-- Venous insufficiency from varicose veins. Valves inside the veins of the legs weaken, making it more difficult for the veins to pump blood back to the heart. This leads to fluid buildup.

-- Severe chronic lung diseases. Emphysema and chronic bronchitis weaken the heart's ability to pump, particularly the right side of the heart.

-- Congestive heart failure. The left or right side of the heart can no longer pump efficiently.

-- Pregnancy. The enlarged uterus with the fetus inside can pinch off the veins carrying blood from the legs to the heart.

-- Pre-eclampsia. This serious condition can occur during pregnancy.

-- Low blood-protein levels. These can be caused by malnutrition, kidney and liver disease.

As for treatments, increasing the dose of your diuretic might solve the problem. A low-salt diet usually helps, since salt causes the body to retain fluid. You also should avoid drinking too much fluid.

If the edema is in your feet and legs, prop them up whenever you are sitting. This counters the effect of gravity and encourages more blood to move out of your legs. Compression stockings can help squeeze the edema fluid out of your tissues. Finally, if your edema is caused by varicose veins, traditional surgery or newer laser procedures can treat the condition.

It's important to protect feet and legs swollen by edema from pressure, injury and extreme temperatures. The skin over swollen legs becomes more fragile over time. Cuts, scrapes and burns in areas that have edema take much longer to heal and are more likely to get infected.

(Dr. Komaroff is a physician and professor at Harvard Medical School. To send questions, go to AskDoctorK.com, or write: Ask Doctor K, 10 Shattuck St., Second Floor, Boston, Mass. 02115.)

Souix City Journal

Flash Pulmonary Edema in Multiple Sclerosis.

Sept 2012

Plummer C, Campagnaro R.

Source

Centre for Neuroscience and Neurological Research, St Vincent's Hospital, Fitzroy, Melbourne, Victoria, Australia.

Abstract

BACKGROUND:

Neurogenic pulmonary edema (NPE) occurs in the setting of an acute neurological insult and in the absence of a primary cardiopulmonary cause. No unifying theory on NPE pathogenesis exists. NPE triggered by a discrete neurological lesion is rare, but such cases offer valuable insight into NPE pathogenesis.

OBJECTIVE:

To describe an unusual and instructive case of NPE in multiple sclerosis.

CASE REPORT:

A young woman with multiple sclerosis presented to the Emergency Department in acute respiratory failure. She was cyanotic centrally, hypertensive, and tachycardic. The chest X-ray study suggested pulmonary edema. She required non-invasive mechanical ventilation for 12 h. Echocardiography revealed left ventricular hypokinesis. The asymmetrical pulmonary infiltrate raised the suspicion of pneumonia; she was given intravenous antibiotics. By 36 h, she had persistent dyspnea, paroxysmal tachycardia, nausea, and facial flushing; carcinoid syndrome was excluded. By 48 h, she had facial numbness and ataxia. Magnetic resonance imaging (MRI) revealed a demyelinating lesion at the rostromedial medulla. Her symptoms promptly resolved with intravenous steroids, as did the perilesional edema on follow-up MRI.

CONCLUSION:

Life-threatening pulmonary edema can complicate medullary demyelination. Lack of awareness of this diagnostic possibility and an asymmetrical pulmonary infiltrate culminated in diagnostic delay in this case. The case provides clinico-radiological evidence of the pathogenic link between medullary lesions and NPE. The pathogenesis is likely to rely on lesion involvement of the nucleus tractus solitarius or its immediate pathways. Non-uniform vasoconstriction of the pulmonary arterial bed might account for the other peculiarity of this case: the asymmetrical pulmonary infiltrate. Timely diagnosis of NPE is essential because the condition is best managed by nullifying the "neurogenic" trigger.

PubMed

Pathophysiology and treatment of edema following femoropopliteal bypass surgery.

Sept  2012

Te Slaa A, Dolmans DE, Ho GH, Moll FL, van der Laan L.

Source

Department of Surgery, Amphia Hospital, Breda.

Abstract

Substantial lower-limb edema affects the majority of patients who undergo peripheral bypass surgery. Edema has impairing effects on the microvascular and the macrovascular circulation, causes discomfort and might delay the rehabilitation process of the patient. However, the pathophysiology of this edema is not well understood. The Cochrane Library and Medline were used to retrieve literature on edema following peripheral bypass surgery. Factors other than local wound healing alone are suggested in the literature to play a role, given the severity and duration of this edema. Hyperemia, microvascular permeability, reperfusion-associated inflammation and lymphatic disruptions are likely to facilitate the development of edema. 

Preventive methods could be lymphatic-sparing surgery, intraoperative antioxidative therapy and postoperative elevation. Successful treatment strategies to reduce postoperative edema are based on lymph massage and external compression. 

In conclusion, the pathophysiology of edema following peripheral surgery is not fully understood, although reperfusion-associated inflammation and lymphatic disruptions are likely to play a crucial role. When future less-invasive techniques prove to be successful, postoperative edema might be minimized. Until then, a careful lymphatic-sparing dissection should be executed when performing a peripheral bypass reconstruction. Postoperatively, the use of compression stockings and leg elevation are currently the golden standards.

Vascular

High Altitude Pulmonary Edema and Augmented Vasoreactivity in Highlanders.

Interactions among Vascular-Tone Modulators Contribute to High Altitude Pulmonary Edema and Augmented Vasoreactivity in Highlanders.

2012

Ali Z, Mishra A, Kumar R, Alam P, Pandey P, Ram R, Thinlas T, Mohammad G, Pasha MA.

Source

Institute of Genomics and Integrative Biology, Delhi, India ; Department of Biotechnology, University of Pune, Pune, India.

Abstract

BACKGROUND: The interactions among various biomarkers remained unexplored under the stressful environment of high-altitude. Present study evaluated interactions among biomarkers to study susceptibility for high altitude pulmonary edema(HAPE) in HAPE-patients (HAPE-p) and adaptation in highland natives (HLs); both in comparison to HAPE-free sojourners (HAPE-f).

METHODOLOGY/PRINCIPAL FINDINGS:

All the subjects were recruited at 3500 m. We measured clinical parameters, biochemical levels in plasma and gene expression using RNA from blood; analyzed various correlations between and among the clinical parameters, especially arterial oxygen saturation (SaO(2)) and mean arterial pressure (MAP) and biochemical parameters like, asymmetric dimethylarginine (ADMA), serotonin (5-HT), 8-iso-prostaglandin F2α (8-isoPGF2α), endothelin-1 (ET-1), plasma renin activity (PRA), plasma aldosterone concentration (PAC), superoxide dismutase (SOD) and nitric oxide (NO) in HAPE-p, HAPE-f and HLs. ADMA, 5-HT, 8-isoPGF2α, ET-1 levels, and PAC were significantly higher and SOD activity non-significantly lower in HLs than HAPE-f. The expression of respective genes differed in the three groups. In the correlations, SaO(2) inversely correlated with ADMA, 5-HT and 8-isoPGF2α and positively with SOD in HAPE-MAP correlated positively with 5-HT and 8-isoPGF2α in HAPE-p and HLs (p≤0.004). A strong positive correlation was observed between ADMA and 5-HT, 5-HT and 8-isoPGF2α (p≤0.001), whereas inverse correlation of SOD with ET-1 in HAPE-p and HLs (p≤0.004), with 5-HT and 8-isoPGF2α in HAPE-p (p = 0.01) and with 5-HT in HLs (p = 0.05).

The expression of respective genes differed in the three groups. In the correlations, SaO(2) inversely correlated with ADMA, 5-HT and 8-isoPGF2α and positively with SOD in HAPE-p (p≤0.009). MAP correlated positively with 5-HT and 8-isoPGF2α in HAPE-p and HLs (p≤0.004). A strong positive correlation was observed between ADMA and 5-HT, 5-HT and 8-isoPGF2α (p≤0.001), whereas inverse correlation of SOD with ET-1 in HAPE-p and HLs (p≤0.004), with 5-HT and 8-isoPGF2α in HAPE-p (p = 0.01) and with 5-HT in HLs (p = 0.05).

CONCLUSIONS/SIGNIFICANCE:

The interactions among these markers confer enhanced vascular activity in HLs and HAPE in sojourners.

PLOSone

Several new treatment possibilities of hereditary angio-oedema.

August 2012

[Article in Danish]

Aabom AL, Palarasah Y, Bygum A.

Source

Hudafdeling I, Odense Universitetshospital, Sdr. Boulevard 29, 5000 Odense C. anne.aabom@ouh.regionsyddanmark.dk.

Abstract

Hereditary angio-oedema (HAE) is a rare genetic disease caused by deficiency of complement C1 inhibitor. It is characterised by recurrent episodes of subcutaneous or submucosal oedema typically involving the extremities, bowel, face or larynx. Within the latest years it has become evident that the active mediator of HAE attacks is an increased level of bradykinin and various new treatment modalities have been developed. The aim of this paper is to give an update from the Danish HAE Comprehensive Care Centre on current treatment possibilities and address some of the challenges when diagnosing HAE.

Ugeskrift for Laeger

Significant improvement in MRI-proven bone edema is associated with protection from structural damage in very early RA patients managed using the tight control approach.

Significant improvement in MRI-proven bone edema is associated with protection from structural damage in very early RA patients managed using the tight control approach.

June 2012



Kita J, Tamai M, Arima K, Kawashiri SY, Horai Y, Iwamoto N, Okada A, Koga T, Nakashima Y, Suzuki T, Yamasaki S, Nakamura H, Origuchi T, Ida H, Aoyagi K, Uetani M, Eguchi K, Kawakami A.

Source

Unit of Translational Medicine, Department of Immunology and Rheumatology, Nagasaki University Graduate School of Biomedical Sciences, 1-7-1 Sakamoto, Nagasaki, 852-8501, Japan.

Abstract

OBJECTIVE:

To identify the value of magnetic resonance imaging (MRI)-proven bone edema in patients with very early rheumatoid arthritis (RA).

METHODS:

All of the 13 patients included in the study were positive at entry for MRI-proven bone edema of the wrist and finger joints and anti-cyclic citrullinated peptide antibodies or IgM-rheumatoid factor. A tight control approach was applied for 12 months. Plain MRI and radiographs of both wrist and finger joints were examined every 6 months. MRI was scored by the RA MRI scoring (RAMRIS) technique and plain radiographs were scored using the Genant-modified Sharp score. Variables that were correlated with plain radiographic changes at 12 months were examined.

RESULTS:

Simplified disease activity index (SDAI) remission was achieved in 7 patients, and a significant reduction in the RAMRIS bone edema score, which declined to .... see article at link below. Program does not allow complete paragraph to be shown here.

CONCLUSIONS:

Improvement in  bone edema may be associated with protection against structural damage in very early RA patients managed using the tight control methods.

Singerlink

Modern approach in therapy of brain edema in cerebral ischemia.

August 2012

Anđelić S.

Source

City Institute for Emergency Medical Care, Belgrade, Serbia.

Abstract

Based on the national data register in Serbia, every 20 min a person develops acute stroke, and every 60 min one dies of the same disease. Studies have shown that during the first 24-40 hours patients develop cytotoxic brain edema and increased intracranial pressure. Up-to-date therapeutic concept must take into consideration possible pathophysiogical processes, so that antiedematous therapy becomes an unavoidable segment of this program. The paper presents a female patient who had cerebral ischemia outof- hospital to develop brain edema three years later. The diagnostic and therapeutic approach to this problem was in accordance with the National Guidelines for Brain Ischemic Disease.

PubMed

An unusual transudative pleural effusion succeeded by pulmonary and brain edema and death.

2012

Mortazavimoghaddam SG, Riasi HR.

Source

Pulmonary Ward, Vali-e-Asr Hospital, Birjand University of Medical Sciences, Birjand 9718766995, Iran.

Abstract

Here we report a 22-year old woman with massive and bilateral transudative effusion succeeded by pulmonary edema and brain edema and death. Investigations for systemic disorders were negative. Exacerbation of dyspnea after intravenous fluid infusion was a main problem. As effusion was refractory to medical treatment, the patient was referred for surgical pleurodesis and bilateral surgical pleurodesis were done separately. Postsurgically, dyspnea exacerbation occurred after each common cold infection. Vertigo and high intracranial pressure were also a problem postsurgically. CSF pressure was 225 mm/H(2)O. Therapeutic lumbar puncture was done in two sequential weeks, and the patient was on acetazolamide 250 mg/trivise a day. Despite the medical treatment, progressive dyspnea, headache, and high intracranial pressure followed by death nine months after pleurodesis. As there is a gradient of pressure between pleura and CSF, after pleurodesis brain edema must be a consequence of inversing this gradient. In conclusion, when there are any abnormalities about fluid volume or pressure in any of these cavities, we have to study other cavities.

PubMed

Capillary leak syndrome in trauma: what is it and what are the consequences?

2012

Stein DM, Scalea TM.

Source

University of Maryland School of Medicine, 22 South Greene Street, Baltimore, MD 21201, USA. dstein@umm.edu

Abstract

TICS is a complex disease that is clearly multifactorial in the traumatically injured patient (Fig. 2). Although systemic inflammation that occurs directly as a result of injury plays the most prominent role, the local tissue and organ injury effects of trauma not only cause local capillary leak and edema but also further amplify the SIRS response. High volume fluid administration and hypoproteinemic states further exacerbate the problem. All of this leads to organ dysfunction and failure, which is the third leading cause of death following injury. Strategies to treat TICS and attenuate its effects once it occurs by targeting inflammatory pathways have been wholly unsuccessful. The mainstay of therapy for TICS is prevention and minimization of its lethal effects. Newer resuscitation strategies such as hemostatic resuscitation and early goal-directed therapies are currently the best available strategies to combat TICS. Whether these result in better outcomes remains to be seen and the authors anxiously await the results of well-designed prospective trials.

PubMed