Given the prevalence of pulmonary oedema in the ICU, the intensivists' obsession with fluid balance, the daily Xrays ("it's more wet than yesterday" etc), the constant battle against lung water should probably be better represented in the final exam. One might surmise that the college examiners view this as a simple problem with solutions so puerile that even a shaved ape should be able to implement them. Question 29.1 from the second paper of 2008 is the only queston which has ever directly discussed pulmonary oedema, and it was in the context of distinguishing cardiac from non-cardiac causes.

This chapter addresses the topic of pulmonary oedema with greater respect than would be expected from its historical exam appearances. Of the many digital sources, LITFL offers the most concise review of acute pulmonary oedema, written by Mike Cadogan.  The time-poor candidate may limit their reading to the most exam-relevant reference for answering Question 29.1 from the second paper of 2008, which  would have to be the NEJM article by Ware et al (2005). For the complete nutter, Gluecker et al (1999) have published a classic article detailing the clinical and radiological features of pulmonary oedema, with numerous pictures and long digressions on physiology.

Causes of pulmonary oedema

These are numerous. Generally, people divide them into cardiogenic causes and non-cardiogenic causes.

Causes of Acute Pulmonary Oedema
Cardiogenic Non-cardiogenic

Excessive LV afterload

  • Severe hypertension
  • Aortic stenosis
  • HOCM (LVOTO)

Excessive LV preload

  • Fluid overload
  • Rapid fluid bolus

Excessive left atrial afterload

  • Mitral stenosis
  • Mitral thrombosis
  • Mitral prolapse
  • Atrial myxoma

Poor contractility

  • Cardiomyopathy
  • Drug effect (eg. beta blockers)
  • Metabolic disease (eg. hypothyroidism)
  • Infectious causes (eg. myocarditis)

Ineffective contractility

  • Mitral regurgitation
  • Takotsubo cariomyopathy

Increased capillary permeability

  • ARDS; systemic inflammatory state
  • Reperfusion (eg. following relief of an embolic occlusion)
  • Reperfusion of transplant lung
  • Near drowning (surfactant loss)

Neurogenic pulmonary oedema

  • Intracranial haemorrhage
  • Seizures
  • Electroconvulsive therapy

Drug-induced pulmonary oedema

  • Opiate induced (eg. heroin overdose)
  • Salicylate overdose

Raised pulmonary arterial pressure

  • High altitude pulmonary oedema
  • Massive PE
  • Pulmonary veno-occlusive disease
  • Post pneumonectomy
  • Air embolism

Negative pressure pulmonary oedema

  • Airway obstruction
  • Re-expansion pulmonary oedema, eg. following the drainage of a particularly large pleural effusion
 

Radiological features of acute pulmonary oedema

 There are two distinct radiological phases. The interstitial phase is the fluid filling up spaces between acini; the alveolar phase is where that fluid floods the air spaces. Both phases tend to appear at the same time in ICU patients, at least in the context of fluid overload and heart failure.

  • Interstitial pulmonary oedema may develop first.
  • Small pulmonary vessels lose their definition on the radiograph; blurring occurs. This can be mistaken for something
  • Peribronchial cuffing occurs: the blood vessels which follow the bronchi become engorged, and thus causes a "cuffed" appearance. These cuffs are usually the most prominent around the hila.
  • Kerley B lines may appear - these are linear shadows created by collections of septal fluid; they tend to be most prominent near the peripheries of the lungs, because the fissures are seen side-on.
  • Thickening of fissures also occurs for the same reason; think of them as really big Kerley lines.
  •  Pleural effusions may form
  • "Bat Wing" oedema is  alveolar oedema in a non-gravity-dependent distribution, and is usually seen in hyper-acute heart failure, eg. if there is acute mitral incompetence due to papillary muscle rupture.

Discriminating between cardiac and non-cardiac causes of acute pulmonary oedema

Question 29.1 from the second paper of 2008 asked how you would go about telling them apart, besides taking a careful history and performing a thorough exmaination. Realistically, history and examination will give you most of the answers. For instance, the first sentences of a telephone handover will reveal that the patient has recently had a pneumonectomy while holidaying in the Himalayas. Therefore, the real question is how to distinguish capillary leakage syndromes from cardiac causes of pulmonary oedema.

The college answer suggested TTE, BNP, PICCO and PAWP measurement.

Investigations to Help Discriminate Between Cardiac and Non-Cardiac Causes of Acute Pulmonary Oedema
Investigation Cardiogenic pulmonary oedema Non-cardiogenic pulmonary oedema
History
  • Chest pain
  • Paroxysmal nocturnal dyspnea or orthopnea
  • Worsening exercise tolerance
  • Pneumonia, sepsis, aspiration, high altitude, drug overdose, recent lung transplant, recent pleural effusion drainage, all the obvious stuff.
Examination
  • S3 gallop: suggests an elevated end-diastolic LV pressure; a highly specific finding with low sensitivity.
  • Mitral stenosis or regurgitation murmur
  • Raised JVP
  • Cool extremities
  • Low JVP
  • Warm vasodilated extremities
  • Vigorous strong pulses
ECG findings
  • Ischaemia
  • Heart block
  • Arrhythmia
  • Right ventricular strain, eg. as in PE
Troponin
  • Can confirm cardiac ischaemia
  • May be elevated in renal failure, sepsis, SAH, etc...
Brain natriuretic peptide (BNP)
  • More than 100pg/ml suggests that CCF is contributing to the APO
  • Less than 100pg/ml in ED or 200pg/ml in ICU suggests that the oedema is non-cardiogenic (eg. it may be ARDS)
Chest Xray
  • Cardiac causes of APO usually have more perihilar infltrates. Classical "bat wing" appearance is rare in non-cardic pulmonary oedema
  • Cardiomegaly is a clue
  • One may be able to see engorged pulmonary veins.
  • Non-cardiac APO tends to feature peripheral lung infiltrates. However, all sorts of ARDS look the same on Xray.
  • In massive PE the oedema will be irregular (i.e. limited to areas which are still perfused) whereas the rest of the lung will be oligaemic.
Echocardiography
  • Gold standard for diagnosis of cardiac structural and functional disease, but does not rule out non-cardiac causes. It is possible to have both poor baseline LV function and acute pulmonary oedema of a totally non-cardiogenic cause. 
  • Massive PE and similar things can be found on TTE.
  • A normal TTE all ut excludes cardiac causes of APO.
Swan-Ganz catheter
  • PAWP is valuely related to LA filling pressure, and a PAWP over 18mmHg suggests either cardiogenic APO or volume overload.
  • A normal or increased cardiac output, combined with a normal PAWP, all but excludes cardiogenic causes of APO 

Weirdly, the use of BNP to discriminate between different causes of pulmonary oedema has attracted some strongly pejorative comments from the LITFL audience. Its use in the context of emergency medicine was somehow viewed as wasteful and lazy, a crutch of the amateur. The real man examines the patient and takes a full history, they might say. However, BNP has been well validated in that setting (Maisel et al, 2002) and appears to be more accurate than any historical information, physical examination findings or other laboratory investigations.   Karmapaliotis et al (2007) also investigated this issue in the ICU setting, where one may not have the luxury of good history or examination.  At a cut-off twice as high as in the ED (≤ 200 pg/ml), BNP had a specificity of 91% for ARDS. However, it must be pointed out that these studies excluded patients with known severe systolic dysfunction. BNP is also raised in renal failure and sepsis (like troponin), and has the additional limitation of rarity and expense. The downtown hospitals of rural Nebrahoma may not have BNP kits available to every breathless patient.

References

Karmpaliotis, Dimitri, et al. "Diagnostic and prognostic utility of brain natriuretic Peptide in subjects admitted to the ICU with hypoxic respiratory failure due to noncardiogenic and cardiogenic pulmonary edema." CHEST Journal 131.4 (2007): 964-971.

Monnet, Xavier, et al. "Assessing pulmonary permeability by transpulmonary thermodilution allows differentiation of hydrostatic pulmonary edema from ALI/ARDS." Intensive care medicine 33.3 (2007): 448-453.

Ware, Lorraine B., and Michael A. Matthay. "Acute pulmonary edema." New England Journal of Medicine 353.26 (2005): 2788-2796.

 

Gluecker, Thomas, et al. "Clinical and radiologic features of pulmonary edema." Radiographics 19.6 (1999): 1507-1531.

 

Karmpaliotis, Dimitri, et al. "Diagnostic and prognostic utility of brain natriuretic Peptide in subjects admitted to the ICU with hypoxic respiratory failure due to noncardiogenic and cardiogenic pulmonary edema." CHEST Journal 131.4 (2007): 964-971.

 

Maisel, Alan S., et al. "Rapid measurement of B-type natriuretic peptide in the emergency diagnosis of heart failure." New England Journal of Medicine 347.3 (2002): 161-167.