Pulmonary edema

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Classification according to ICD-10
I50.14 cardiac pulmonary edema
J81 Pulmonary edema
ICD-10 online (WHO version 2019)
Pulmonary edema in ARDS

Lung edema ( pulmonary edema , colloquially water lung ) is a non-specific term for an accumulation of fluid in the lungs caused by the leakage of blood fluid ( plasma ) from the capillary vessels into the intermediate tissue and into the alveoli . Because of the edema, chronic congestive lungs are damp and heavy. As a result of this impregnation of the lungs , the affected person can no longer absorb sufficient oxygen into the bloodstream . As symptoms a contact respiratory distress as a result of increased work of breathing , a breathing rattling or a foamy ejection on. Depending on the cause, pulmonary edema is divided into permeability edema (ARDS, toxic pulmonary edema) and hydrostatic pulmonary edema (cardiac edema and altitude edema). Formally, the permeability (the flow of water through the vessel wall) is described by the Starling equation ( Starling concept).

to form

Pulmonary congestion

A lesser degree of pulmonary edema is the subacute or chronic form, which is known as pulmonary congestion . The consumption of heroin and consumption coagulopathy can also lead to pulmonary congestion and even pulmonary edema. A congested lung can also be associated with congestive bronchitis.

Cardiac pulmonary edema

The cardiac pulmonary edema (also called cardiogenic pulmonary edema ), the most common form of pulmonary edema is not a lung disease. It arises in acute left heart failure in the low pressure system . The cause of the failure of the left half of the heart is usually an acute decompensation of chronic heart failure , in which the left half of the heart can no longer fully cope with the return of blood from the lungs due to a weak pump. This leads to a backlog of blood in the pulmonary vessels and - because of the resulting increased intravascular blood pressure in the small circulation - to a leakage of fluid into the lung tissue. This severely restricts the gas exchange. Often the patients breathe panting ( asthma cardiale ), they are restless and have fear of suffocation (in the 19th century both asthma, cardiale or bronchial, as well as pulmonary edema were called stick flow ). There is usually marked cyanosis .

Acute pulmonary edema in left heart failure is a medical emergency which, if left untreated, can lead to respiratory failure and thus to death of the patient within a few minutes . An early alert of the ambulance service and the emergency doctor is required.

therapy

Treatment is emergency with elevation of the upper body, which can already be done by first aiders , with artificial ventilation in the form of oxygen, with opiates to combat pain and sedation as well as as an antitussive , with catecholamines , with nitroglycerin and, above all, with diuretics for forced diuresis . Sometimes kidney dialysis or (especially with simultaneous polycythemia ) bloodletting may be indicated. In the past, only "bubbling pulmonary edema" was treated with a ventilator ; In the event of improper ventilation, this sometimes even triggered or worsened pulmonary edema.

Noncardiac pulmonary edema

Acute respiratory failure

The acute lung injury (engl. Acute Respiratory Distress Syndrome ARDS) arises as a consequence of increased vascular permeability, either due to inflammatory processes , or due to toxins (toxic pulmonary edema). Clinically, the ARDS is defined by typical shadows in the X-ray image, hypoxemia , the exclusion of cardiac edema (see above) and its acute onset.

Common causes of ARDS are sepsis , multiple trauma , aspiration of the stomach contents or severe burns . The SARS virus, which has only been described for a few years, also leads to the clinical picture of ARDS. ARDS often occurs in connection with the failure of other organs ( multi-organ failure ). The mortality rate in the presence of ARDS is still around 50 percent even if therapy is started early.

High elevation pulmonary edema

A high altitude pulmonary edema (short: Höhenödem ., English high altitude pulmonary edema , HAPE) may, at the altitude sickness occur. It is caused by increased pulmonary arterial pressure as a result of hypoxia due to the Euler-Liljestrand mechanism . It usually develops one to three days after a quick ascent above 2700m. It is hypertensive edema with increased microvascular permeability and with excessive vasoconstriction . Symptoms are increasing shortness of breath, dry cough with frothy or bloody sputum, cyanosis , weakness of the body and, in later stages, a coma . The causal therapy is the immediate descent or a return to deeper layers. Similar are the symptoms of sub-acute mountain sickness in children especially the Han Chinese of births at high altitude and in the chronic altitude sickness great for long-term residents heights ( Monge's disease after the first person to describe Carlos Monge Medrano, 1925) with polycythemia and complaints as the Pickwick disease . As with high-altitude edema, pulmonary edema can also develop with barotrauma and drowning .

Post-obstruction pulmonary edema

A rare form of pulmonary edema is post-obstruction pulmonary edema (negative pressure pulmonary edema , NPPE). This is caused by negative air pressure in the lungs, which can occur when the upper airways are blocked and the upper airways are simultaneously inhaled deeply. Causes for this can be, for example, laryngospasm , biting of the endotracheal tube or the laryngeal mask during anesthesia drainage or other obstructions of the airways. In addition, improper suctioning procedures are another possible cause. The NPPE is characterized by a rapid onset after a corresponding incident.

Cerebral pulmonary edema

Cerebral or neurogenic pulmonary edema occurs in brain lesions , i.e. as a result of acute cerebral processes. One also speaks of central pulmonary edema, for example as a result of traumatic brain injuries or meningoencephalitis . Also one can sunstroke or epilepsy lead to cerebral edema. After a subarachnoid hemorrhage there may be a neurogenic centralization of the blood with increase in lung volume come.

This must be differentiated from the cerebral consequences of pulmonary edema and other effects on the central nervous system .

Symptoms

The symptoms are present in cardiac as well as toxic or allergic pulmonary edema.

Patients with pulmonary edema suffer from restlessness, fear of suffocation, severe shortness of breath (even at rest) and even cyanosis. You usually sit by yourself with an upright upper body to enable the use of the auxiliary breathing muscles ( orthopnea ). When inhaling and exhaling, boiling and wet rattling noises can be heard, possibly accompanied by spastic breathing noises ( boiling on the chest ). Further signs are damp and cool skin (cold sweat) with pallor, a tachycardiac pulse , sometimes also arrhythmic , and different blood pressure behavior (e.g. high with simultaneous hypertensive crisis or low with heart failure with cardiogenic shock). Foamy or even bloody sputum can appear when coughing.

X-ray diagnostics

In pulmonary edema, the lungs show typical changes visible in the chest x-ray, such as Kerley lines in interstitial pulmonary edema. Typical signs of an increased water content (located outside the blood vessels) in the lungs are also a blurred border of central structures or (in the case of pronounced alveolar pulmonary edema) blotchy confluent shadows.

literature

  • Ulrike Bungeroth (Ed.): Basics Pneumology . 2nd Edition. Elsevier, Urban & Fischer, 2010, ISBN 978-3-437-42237-9 , pp. 72-73 .

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  2. ↑ Definition: Penetration of blood plasma into the alveoli . Quote: Gerhard Wahrig : German dictionary . Bertelsmann Lexikon-Verlag, Berlin, Munich, Vienna 1972, ISBN 3-570-06588-X , page 2325.
  3. ↑ Wolfgang Rotter : Textbook of Pathology , Volume II, 3rd edition, Schattauer Verlag , Stuttgart, New York 1985, ISBN 3-7945-1001-1 , page 162.
  4. ^ P. Hilpert and Richard Schaub: Lung . In: Pathophysiology , 2nd edition, Georg Thieme Verlag , Stuttgart, New York 1981, ISBN 3-13-602602-0 , page 351.
  5. ↑ Myron G. Sulyma: Sanol lexicon Angiology, Phlebology . Medikon-Verlag, Munich 1987, ISBN 3-923866-19-4 , page 196.
  6. ↑ Walter Siegenthaler et al. (Ed.): Textbook of internal medicine. 3. Edition. Georg Thieme Verlag, Stuttgart / New York 1992, ISBN 3-13-624303-X , p. 299.
  7. ↑ Consilium Cedip practicum 2006. 28th edition. Dortmund 2005, ISBN 3-9810440-1-0 , page 874.
  8. ↑ Joachim Frey : Diseases of the respiratory organs. In: Ludwig Heilmeyer (ed.): Textbook of internal medicine. Springer-Verlag, Berlin / Göttingen / Heidelberg 1955; 2nd edition ibid. 1961, pp. 599-746, here: pp. 717 f. ( Congestive bronchitis in congestive lung, lung hypostasis ).
  9. ↑ Otto Dornblüth : Dictionary of clinical art expressions , 1st edition, Verlag von Veit & Comp., Leipzig 1894, page 90: congestion phenomenon when the heart strength decreases , especially when the heart halves are unevenly active .
  10. ↑ Fluid in the alveoli in the case of congestion in the small circulation . Quote: Josef Hammerschmidt-Gollwitzer: Dictionary of medical terms . Rheingauer Verlagsgesellschaft, Munich 1981, ISBN 3-88102-061-6 , page 242.
  11. ↑ Hilmar Burchardi (editor): Acute emergencies . Thieme Verlag , Stuttgart and New York 1981, ISBN 3-13-589101-1 , page 90.
  12. ^ Max Höfler: German book of names of diseases. Piloty & Loehle, Munich 1899; Reprint Olms, Hildesheim / New York 1970 and 1979, ISBN 1-174-35859-9 , p. 162 f. ( Stick flow, Steck flow, Stöck flow ).
  13. ↑ Also Goethe's last illness, who died of heart failure with pulmonary edema after a heart attack, was called "Stickfluß". See Frank Nager: Goethe's terminal illness. In: Frank Nager: The healing poet. Goethe and medicine. Artemis, Zurich / Munich 1990; 4th edition ibid 1992, ISBN 3-7608-1043-8 , p. 38 f.
  14. ↑ Andreas Russ, Stefan Endres: Medicines pocket plus . 11th edition, Börm Bruckmeier Verlag, October 2014, ISBN 978-3-89862-763-4 , page 392.
  15. ↑ Carola Halhuber, Karl-Adolf Bungeroth, Bernd Landauer: Cardiological emergencies . Urban & Schwarzenberg, Munich, Vienna, Baltimore 1984, ISBN 3-541-00979-9 , page 179.
  16. ↑ Erich Lang: Cardiovascular emergencies . Perimed Fachbuch-Verlagsgesellschaft, Erlangen 1980, ISBN 3-88429-010-X , page 49.
  17. ^ Rudolf Gross , Klaus-Dieter Grosser , Heinz-Günter Sieberth: The internal emergency. Schattauer Verlag , Stuttgart / New York 1973, ISBN 3-7945-0339-2 , p. 310.
  18. ↑ The MSD Manual for Diagnostics and Therapy . 6th German edition, Urban & Fischer, Munich, Jena 2000, ISBN 3-437-21750-X , ISBN 3-437-21760-7 , p. 2965.
  19. ↑ Willibald Pschyrembel : Clinical Dictionary . 267th edition, de Gruyter , Berlin, Boston 2017, ISBN 978-3-11-049497-6 , page 1079.
  20. ↑ M. Alb, C. Tsagogiorgas, JP Meinhardt: Negative-pressure pulmonary edema. In: Anasthesiol Intensivmed Emergency Med Schmerzther. 2006 Feb; 41 (2), pp. 64-78.
  21. ^ Roche Lexicon Medicine . 5th edition, Urban & Fischer , Munich, Jena 2003, ISBN 3-437-15156-8 , page 1138.
  22. ^ Klaus-Dieter Grosser: Practice of general medicine . Volume 11, Cardiac Diseases . Urban & Schwarzenberg, Munich, Vienna, Baltimore 1985, ISBN 3-541-10861-4 , page 72.
  23. ↑ Gerd Herold : Internal Medicine . Edition 1981/82, page 172; no longer in the newer editions.
  24. ^ Carola Halhuber et alii: Cardiological emergencies . Urban & Schwarzenberg, Munich, Vienna, Baltimore 1984, ISBN 3-541-00979-9 , page 169.
  25. ↑ Hexal Taschen Lexicon Medicine . Urban & Fischer , 2nd edition, Munich and Jena 2000, ISBN 3-437-15010-3 , page 451.
  26. ↑ H. Jantsch, G. Lechner: Radiological monitoring of the ventilated patient. In: J. Kilian, H. Benzer, FW Ahnefeld (ed.): Basic principles of ventilation. Springer, Berlin a. a. 1991, ISBN 3-540-53078-9 , 2nd, unaltered edition, ibid 1994, ISBN 3-540-57904-4 , pp. 134-168; here: pp. 140–149.