Alveolar hemorrhage (AH) is a clinical syndrome with diverse etiologie
s both immune and nonimmune. The defining pathological feature of AH i
s the presence or absence of pulmonary capillaritis. The antineutrophi
l cytoplasmic antibody (ANCA) related vasculitis and systemic lupus er
ythematosus are the commonest causes of immune AH with pulmonary capil
laritis, whereas Goodpasture's syndrome and idiopathic pulmonary hemos
iderosis are common causes of immune AH without pulmonary capillaritis
. The major nonimmune causes of AH are primarily drug induced, or due
to hematological malignancy and disorders of coagulation. Clinical fea
tures of AH include: dyspnea, fever, hemotypsis, bilateral crackles an
d pallor. Hypoxemia and bilateral diffuse airspace disease on the ches
t radiograph with relative sparing of the bases and apices which most
often clears within 48 hours after its onset further characterize this
syndrome. The major clinical implications of this syndrome are its po
tential to cause respiratory failure in severe cases and its sequelae
of pulmonary fibrosis with associated morbidity and disability. In add
ition, AH may be the initial manifestation of a systemic immune disord
er which can be managed optimally if recognized early. The diagnosis o
f AH is confirmed by bronchoalveolar lavage by demonstrating a progres
sively bloody return on successive aliquots of instilled saline or hem
osiderin laden macrophages in the bronchoalveolar lavage fluid. The op
en lung biopsy remains the gold standard for the diagnosis of AH but i
s reserved for inapparent cases in whom corticosteroids and immunosupp
ressive therapy may be life saving. Serologic testing and examination
of the urine sediment are useful adjuncts to the diagnosis. The treatm
ent of AH is primarily supportive while an attempt is made to determin
e its etiology and initiate specific therapy. Glucocorticoids and cycl
ophosphamide are the cornerstones of therapy in immune AH with adjunct
ive plasmapheresis in life-threatening cases.