Pulmonary oedema refers to extravasation of fluid from the pulmonary vasculature into
the
interstitium and alveoli of the lung.
• The
formation of pulmonary oedema may be caused by 4 major pathophysiologic
mechanisms.
Imbalance
of starling forces which are
Increased
pulmonary capillary pressure
Decreased
plasma oncotic pressure
Increased
negative interstitial pressure
Damage
to the alveolar-capillary barrier
Lymphatic
obstruction
Idiopathic
or unknown mechanism
Classification of Pulmonary Oedema
• Cardiogenic
pulmonary oedema (CPE): This is defined as pulmonary oedema due to
increased
capillary hydrostatic pressure secondary to elevated pulmonary venous
pressure.
• Non-Cardiogenic
pulmonary oedema: This includes several clinical conditions that are
associated
with pulmonary oedema based on an imbalance of starling forces other than
through
primary elevations of pulmonary capillary pressure.
Clinical Features of Pulmonary
Oedema
Symptoms
• Breathlessness
• Anxiety
• Profuse
diaphoresis
• Patients
with symptoms of gradual onset CPE (e.g. over 24 h) often report dyspnea on
exertion,
orthopnea (respiratory discomfort when supine), and paroxysmal nocturnal
dyspnea
(patient awakens gasping for air and must sit up).
• Cough
is a frequent complaint that may provide an early clue to worsening pulmonary
oedema
in patients with chronic left ventricle (LV) dysfunction.
• Pink
frothy sputum may be present in patients with severe disease.
• Chest
pain should alert the physician to the possibility of acute myocardial ischemia,
infarction,
or aortic dissection with acute aortic regurgitation as the precipitant of
pulmonary
oedema.
Physical Findings
• Tachypnea
and tachycardia
• Patients
may be sitting upright, they may demonstrate air hunger, and they may become
agitated.
• Patients
usually appear anxious and diaphoretic
• Hypertension
is often present because of the hyper adrenergic state.
• Hypotension
indicates severe LV systolic dysfunction and the possibility of cardiogenic
shock.
• Auscultation
of the lungs usually reveals fine crepitations, but rhonchi or wheezes may
also
be present.
• Rales
(crepitations) are usually heard at the bases first; as the condition worsens,
they
progress
to the apices.
• Auscultation
of murmurs can help in the diagnosis of acute valvular disorders manifesting
with
pulmonary oedema.
• Another
notable physical finding is skin pallor or mottling resulting from peripheral
vasoconstriction
and shunting of blood to the central circulation in patients with poor LV
function
and substantially increased sympathetic tone.
• Patients
with concurrent right ventricular (RV) failure may present with hepatomegaly,
positive
hepatojugular reflux (seen in the neck region) and peripheral oedema.
• Severe
cardio pulmonary oedema may be associated with a change in mental status which
may
be the result of hypoxia or hypercapnia (a condition where there is too much
carbon
dioxide
in the blood).
Differential Diagnosis,
Investigations and Treatment of Pulmonary
Oedema
Differential Diagnosis
• Pneumonia
• Pneumothorax
• Pulmonary
Embolism
• Respiratory
Failure
• Diffuse
pulmonary infections
• Aspiration
• Shock
• Acute
Respiratory Distress Syndrome (ARDS)
• Asthma
• Cardiogenic
Shock
• Chronic Obstructive Pulmonary Disease
(COPD)
• Emphysema
• Myocardial
Infarction
• Respiratory
Failure
• Diffuse
pulmonary infections
• Aspiration
• Shock
• Acute
Respiratory Distress Syndrome (ARDS)
• Asthma
• Cardiogenic
Shock
• Chronic Obstructive Pulmonary Disease
(COPD)
• Emphysema
• Myocardial
Infarction
Investigations
• Laboratory
Studies
Blood
count
Serum
electrolyte measurements
BUN
and creatinine determination
Cardiac
enzymes if available
Electrocardiogram
would be very helpful
• Imaging
Studies
Chest
radiography
Echocardiography
Note:
Most of these investigations are done at hospital levels and therefore patients
suspected
of
having pulmonary oedema must be referred for proper investigations.
Treatment of Pulmonary Oedema
• Pulmonary
oedema is life-threatening and must be considered a medical emergency
• In
the treatment of pulmonary oedema attention must be directed to identifying and
removing
any precipitating causes
• Because
of the acute nature of the problem, a number of additional nonspecific measures
are
necessary before referring the patient to the hospital, these includes
Oxygen
therapy (whenever possible)
Diuretics
e.g. furosemide (lasix)
Keep patient in semi sitting position
REFFERNCES;
• Braunwald & Fauci (2001). Harrison’s principles of
internal medicine 15th Ed. Oxford:
McGraw Hill
• Davidson, S (2006). Principles and practice of
medicine 20th Ed. Churchill:
Livingstone.
Kumar & Clark (2003) Textbook of clinical
medicine. Churchill: Livingstone.
• Douglas
Model (2006): Making sense of Clinical Examination of the Adult patient. 1st
Ed. Hodder Arnold
• Longmore,
M., Wilkinson, I., Baldwin, A., & Wallin, E. (2014). Oxford handbook of
clinical medicine. Oxford
• Macleod,
J. (2009). Macleod's clinical examination. G. Douglas, E. F. Nicol,
& C. E. Robertson (Eds.). Elsevier Health Sciences.
• Nicholson
N., (1999), Medicine of Non-communicable diseases in adults. AMREF
• Stuart
and Saunders (2004): Mental health Nursing principles and practice. 1st
Ed. Mosby
• Swash, M., & Glynn, M. (2011). Hutchison's clinical methods: An integrated approach to clinical practice.

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