Pneumologia
REVISTA SOCIETĂŢII ROMÂNE DE PNEUMOLOGIE
Alveolar hemorrhage syndrome –
causes and diagnostic methods
Sindromul de hemoragie alveolară – cauze și modalități de diagnostic
Abstract
The alveolar haemorrhage syndrome is an acute
condition, which requires rapid diagnosis and efficient
treatment for the multiple clinical manifestations
(dyspnoea, haemoptysis, and respiratory failure). The
conditions may occur both through endogenous and
exogenous iron loading. Multiple causes which underlie
the triggering of the alveolar haemorrhage syndrome
make the symptoms unspecific. The imaging aspect, the
bronchial endoscopy with bronchoalveolar lavage and
the histopathologic examination of the lung fragment
obtained through lung biopsy or necropsy underlie the
definitive diagnosis of this condition, at the same time
excluding the neoplastic or infectious pathology.
Keywords: alveolar haemorrhage, bronchoalveolar
lavage, hemosiderin
The alveolar haemorrhage syndrome is an acute
condition, which requires diagnosis and rapid and efficient
treatment for the multiple clinical manifestations (dysp-
noea, coughing up blood, auscultation of bilateral basal
crepitant and subcrepitant rales) and the paraclinical
changes such as anaemia, hypoxemia with suggestive nor-
mocapnia for hypoxemic respiratory failure and diffuse
lung infiltrates(1). The diagnosis is underlain by the histo-
pathologic examinations obtained through lung biopsy or
even necropsy, bronchoalveolar lavage obtained through
bronchoscopy performed with a flexible bronchoscope and
local anaesthesia, and serological tests: direct and indirect
ELISA (enzyme-linked immunosorbent assay), immuno-
fluorescence, as well as imaging examinations (thoracic and
lung X-ray and CT scan)(1,2).
The alveolar haemorrhage syndrome is not an autonomous
entity; it may have an idiopathic, autoimmune, infectious,
drug-related etiology, as well as within the context of the hema-
tologic diseases(1,2,3). It occurs not only through endogenous
loading with iron but also through exogenous loading, in work-
ers with occupational exposure to iron particles(36).
The triggering causes of the alveolar haemorrhage syn-
drome are presented in Table 1(1,2,3).
The aforementioned diseases are rare diseases, some of
them have unknown or incompletely determined etiology. In
medical practice, the most common diseases which may mani-
fest with alveolar haemorrhage are the anti-glomerular base-
ment membrane disease or the Goodpasture syndrome(2), the
Wegener granulomatosis, the systemic lupus erythematosus
and the Henoch Schonlein purpura. Among the most uncom-
mon diseases we can mention the idiopathic pulmonary hemo-
siderosis (exclusion diagnosis)(6), the diffuse alveolar
haemorrhage of infectious cause and a cause associated with
the post-administration of a medicinal product.
VOL. 66 • No. 4/2017
Rezumat Gina Ciolan,
Elena Magheran,
Sindromul de hemoragie alveolară este o suferință acută,
ce necesită diagnostic și tratament rapid și eficace din Vasile Grigorie,
cauza multiplelor manifestări clinice (dispnee, hemoptizie, Camelia Bădescu,
insuficiență respiratorie). Suferința poate să apară Cristina Teleaga
atât prin încărcare endogenă, cât și exogenă, cu fier. “Marius Nasta” Institute of
Multiplele cauze ce stau la baza declanșării sindromului Pneumophtisiology, Bucharest
de hemoragie alveolară fac ca simptomatologia să fie Corresponding author:
nespecifică. Aspectul imagistic, endoscopia bronșică cu Elena Magheran,
lavaj bronholo‑alveolar și examenul histopatologic al E-mail:elena.magheran@yahoo.com
fragmentului pulmonar obținut prin biopsie pulmonară
sau cel necropsic stau la baza diagnosticului de
certitudine al acestei afecțiuni, excluzând în același
timp patologia neoplazică sau infecțioasă.
Cuvinte‑cheie: hemoragie alveolară, lavaj bronholo-
alveolar, hemosiderină
The Goodpasture syndrome is a rare condition, with a
prevalence of 1 to one million(2). The pathogenic mechanism
is not fully known, being considered an autoimmune disease.
Recent studies show the role of the environmental factors
(aromatic hydrocarbons, iron ores, silicon oxide) and behav-
ioural factors (smoking) in determining the evolution of the
disease(2,3,4). The microscopic examination describes diffuse
alveolar haemorrhage, macrophages loaded with hemosiderin,
without vasculitis or septum necrosis(1). The definitive nature
of the diagnosis is given by the presence of the anti-glomerular
basement membrane antibodies in the plasma. The anti-glo-
merular basement membrane antibodies may be identified
using ELISA method and immunofluorescence(1,3,4).
The Henock-Schonlein purpura is clinically charac-
terised by palpable purpura, arthritis with arthralgias, gas-
trointestinal bleeding and renal and pulmonary
diseases(1,13,16). Although the number of reported cases is very
small, being more frequently encountered in children than
in adults, we recall the occurrence of the siderophages within
the first 24-48 hours from the onset of the lung alveolar
haemorrhage(1).
The diffuse alveolar haemorrhage in systemic lupus
erythematosus represents a severe complication of this
disease, being associated with increased morbidity and mor-
tality(9-12). Diffuse alveolar haemorrhage occurs more com-
monly in women, the ratio women/men being 6:1, compared
to the lupus disease – 9:1(10). The mechanism for the occur-
rence of the alveolar haemorrhage seems to be the immune-
mediated destruction of small blood vessels and of the
alveolar septums(10,11). From a histopathological point of
view, the lung capillarity is described with the impairment
of the alveolar microcirculation. Macrophages appear being
loaded with hemosiderin in the alveoli and the occlusion of
the septal alveolar capillaries(12).
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Table 1 Causes of the alveolar haemorrhage syndrome(1,2,3)
Idiopathic pulmonary hemosiderosis
Idiopathic pulmonary hemosiderosis and glomerulonephritis
Vasculitis and collagenosis:
Systemic lupus erythematosus
Wegener granulomatosis
Idiopathic thrombocytopenic purpura
Goodpasture’s syndrome
Necrotizing cryoglobulinemic vasculitis
Henoch-Schonlein purpura
Granulomatosis with polyangiitis, formerly
Wegener granulomatosis, is characterised by necrotizing
granulomatous inflammation of the upper and lower airways
and vasculitis of small vessels(1,13-15). At microscopic examina-
tion, the presence of necrotizing granulomatous inflamma-
tion and of necrotizing vasculitis at the level of the lung
parenchyma is an important argument for the diagnosis of
granulomatosis with polyangiitis(1,13). The presence of the
erythrocytes in the alveolar interstitial, of hemosiderin and
fibrinoid necrosis is owed to the extravasation of blood in
the alveoli(13). The bronchoalveolar lavage liquid includes
macrophages loaded with hemosiderin(15).
Idiopathic pulmonary hemosiderosis is a rare cause
of pulmonary alveolar haemorrhage, occurring in over 80%
of cases in children(6). The diagnosis of idiopathic pulmo-
nary hemosiderosis can be established when the other eti-
ologies have been excluded(6). It is characterised biologically
by iron-deficiency anaemia; radiologically by diffuse pul-
monary infiltrates, and clinically by cough, moderate degree
dyspnoea and haemoptysis(5-8). Allergies, autoimmunity,
genetic factors and environmental factors underlie the
pathophysiology of idiopathic pulmonary hemosiderosis
without being able to provide data in this regard(1,8). Under
microscopic examination, intraalveolar haemorrhage, mac-
rophages loaded with hemosiderin and different degrees of
interstitial fibrosis are described(1).
The association between the pulmonary infections
and the diffuse alveolar haemorrhage is rarely reported.
Pathogenic germs act both upon immunocompromised
patients and upon immunocompetent patients(17). In the
immunocompetent patients, the most common agents incrim-
inated for the production of diffuse alveolar haemorrhage are
the flu virus (H1N1), the Malaria and Leptospirosis parasites,
as well as Staphylococcus aureus, and in the immunocompro-
mised hosts, the diffuse alveolar haemorrhages are caused by
bacteria of types Mycoplasma and Legionella, and viruses such
as the adenovirus and Cytomegalovirus(18,19). The microscopic
examination shows the congestion of the alveolar capillaries,
210
Medicines:
Cytostatics
Amphotericin B
D penicillin
Heart and vascular diseases:
Congestive heart failure
Mitral stenosis
Pulmonary hypertension
Pulmonary veno-occlusive disease
Pulmonary embolism with infarction
Arteriovenous aneurysms
Various:
Lymphangioleiomyomatosis
Severe haemorrhagic pneumonia
Tuberous sclerosis
Bone marrow transplant
Hematologic diseases
Severe coagulopathy
the focal alveolar destruction with formation of hyaline mem-
branes and macrophages ­loaded with hemosiderin(17-19).
During recent years, diffuse alveolar haemorrhage has
been reported following the administration of medicinal prod-
ucts such as vincristine(20), rituximab(21), itraconazole(21) and
heparin with small molecular mass(22). The difficult diagnosis
of the alveolar haemorrhage syndrome, the late identification
of the cause and the lack of therapy lead to increased risk of
evolution towards exitus of these patients.
From a clinical perspective, the alveolar haemorrhage
syndrome does not have specific symptoms, and may mani-
fest through cough, small and repeated haemoptysis, which
can be associated or not with respiratory failure(23).
Haemoptysis is absent in 30% of the patients, blood cannot
reach the upper airways in order to be exteriorised as haem-
optysis, due to the high alveolar volume which absorbs
important blood quantities(33).
The alveolar haemorrhage syndrome is biologically
characterised through variable anaemia with a much decreased
value of serum iron. The sudden decrease in haemoglobin
within 24-48 hours and the X-ray of the interstitial and alveo-
lar infiltrates increase the probability of diffuse alveolar haem-
orrhage(9). The unspecific inflammatory syndrome (much
increased ESR) is present, and the serologic tests specific to
each disease may be useful for supporting the diagnosis. Thus,
in Goodpasture syndrome can be used the plasma identifica-
tion of the anti-glomerular basement membrane antibod-
ies(1,3,4) and of the linear deposits of IgG and the C3 fraction of
the complement(1-4), in systemic lupus erythematosus the pres-
ence of increased titres of autoantibodies of the double-strand-
ed DNA type, lupus anticoagulant, anti beta2-GP1, anti SM,
anti Ro, anti RNP, hypocomplementemia are useful (11), and in
the Henock Schonlein purpura granular deposits of IgA and
the C3 fraction of the complement(14,18).
From a functionally respiratory point of view, the
restrictive syndrome with the reduction in the vital capac-
ity, the total lung capacity and the residual volume, and the
lack of bronchial obstruction prevails. The gaseous transfer
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 Pneumologia
REVISTA SOCIETĂŢII ROMÂNE DE PNEUMOLOGIE

factor through the alveolar capillar membrane (TLCO) is

also decreased. In the blood gases analysis, the decrease of
PaO2 and PaoCO2 is initially noticed during exercise and
subsequently at rest, the alveolo-capillar gradient increas-
ing during exercise.
The imaging aspects, both the simple lung X-ray (Figure
1) and the high resolution computed tomography (Figure 2)
are not specific to this condition. The high resolution com-
puted tomography (HRCT) with a thickness of the tomo-
graphic cups of under 1 mm is highly superior to the standard
chest X-ray and the standard chest computed tomography
with 3-5 mm sections(25,28). On the standard chest X-ray,
interstitial syndromes (fine reticular, reticulonodular and
infiltrative “wooly” opacifications), condensation processes
and micronodules can be noticed. In the computed tomogra-
phy with a thickness of the tomographic cups of under 1 mm, Figure 1. Front lung X-ray in a patient with pulmonary
lesions of “mat glass”, reticular opacifications, nodules and alveolar haemorrhage – reticulonodular opacifications in the
micronodules are present. The X-ray differential diagnosis right lower part of the thorax

Figure 2. CT scan of the thorax – bilateral diffuse pulmonary infiltrates, aspect of “ground-glass”

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is performed first of all with carcinomatous lymphangitis,

Figure 3. Macroscopic aspect of the bronchoalveolar lavage
liquid within an alveolar haemorrhage syndrome
secondary lung tuberculosis, Pneumocystis pneumonia, viral
pneumonias, brochopneumonia and the respiratory distress
syndrome of the adult.
Bronchoscopy with bronchoalveolar lavage under-
lies the diagnosis of the alveolar haemorrhage syndrome,
not by showing remarkable and characteristic endobron-
chial changes, but rather through the possibility of per-
forming the bronchoalveolar lavage, with a flexible
bronchoscope and local anaesthesia(30).
Bronchoalveolar lavage is performed through instil-
lation in the bronchial tree, in any territory or preferably at
the level of the lingula or the middle lobe, due to a good
recovery, of a quantity of saline solution between 100 and
300 ml. The sterile saline solution is used at a temperature
of 37°C or at an environmental temperature in order to avoid
the occurrence of bronchospasm. The proper cooperation of
the patient and the gentleness of the examining physician
lead to a satisfactory recovery of the instilled liquid, approxi-
mately 70% of the total liquid used in lavage. The recovery
of the instilled liquid also depends on the sealing and stabil-
ity of the fibrobronchoscope at the level of the bronchia
where lavage is performed. The liquid used in the lavage
changes its aspect gradually, during the aspiration, depend-
ing on the moment of the bleeding(34,35). It may be transpar-
ent, rose-coloured, dark red, orange red or brown(24) (Figure
3). As bleeding is older, the aspect of the aspirated liquid is
darker. The colour is given by the erythrocytes mixed with
macrophages which contain hemosiderin(34). If bleeding is
recent, the only indicator is represented by the erythrocytes

a b

c d

Figure 4. Cytological aspect in the alveolar haemorrhage syndrome – macrophages loaded with hemosiderin and erythrophages
a, b, c) the May-Gruenwald-Giemsa staining – macrophages loaded with hemosiderin
d) iron colour – hemosiderin in the macrophages is coloured in blue with the help of this colour (Prussian blue)

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REVISTA SOCIETĂŢII ROMÂNE DE PNEUMOLOGIE

Table 2 The GOLDE score

GOLDE score
Normal values 4-25
Mild 25-100
Moderate 100-300
Severe 300-400

Table 3
Normal cells of the bronchoalveolar
lavage (BAL) liquid
Cytology Figure 5. Intraoperative aspect in a patient with a
Total cell count <13x106 pulmonary alveolar haemorrhage syndrome. Atypical
Macrophages > 84% resection at the level of the left lower lobe.
Lymphocytes < 15%
Neutrophils < 3% The largest values of the GOLDE score have been identi-
Eosinophils < 0.5% fied in the idiopathic pulmonary hemosiderosis, due to the
disease becoming chronic. In the alveolar haemorrhage syn-
Mast cells < 0.5%
drome, in addition to the macrophages loaded with hemosi-
Plasmocytes 0% derin, the total cell count is increased even in patients who
have leukopenia in the peripheral blood. After the occupa-
in a high number in the liquid used for lavage. If at least 72 tional exposure to iron, the erythrocyte fragments are miss-
hours have passed from the alveolar bleeding, macrophages ing and the phagocytes are coloured anthracotically. Normal
with hemosiderin are identified in the liquid(32) (Figure 4). cells in the BAL liquid are shown in Table 3.
In optic microscopy the Prussian blue colour is used for The surgical lung biopsy remains the gold standard in
identifying the hemosiderin (Figure 4). the diffuse alveolar haemorrhage syndromes, whose cause
Based on the number of positive macrophages and the could not be established through less invasive diagnosis meth-
colour intensity, the GOLDE score is determined, indicating ods. The transbronchial biopsy does not provide sufficient
the severity of the syndrome (Table 2). data for supporting the diagnosis(9). The surgical intervention

a b

c d

Figure 6. Histopathological aspect of the lung alveolar haemorrhage – stains ensured with haematoxylin - eosin
a and b) images taken with the 10x lens – the alveolar spaces include red blood cells and siderophages with endoluminal obstructive
character; c) image taken with the 40x lens (see the green arrow) – interalveolar septums thickened in certain areas through fibrosis
and through the presence of a reduced interstitial inflammatory infiltrate; d) image taken with the 40x lens (see the green arrow) –
hyperplasia of pneumocyte 2

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is performed after the preanesthetic and presurgical examina-
tion in all the patients who have an indication of pulmonary
biopsy, but who have a contraindication regarding the perfor-
mance of this intervention. Through minimum thoracotomy
under general anaesthesia, several lung fragments are col-
lected from the most relevant areas in the HRCT examination,
even though from the point of view of the approach, the mid-
dle and lingula lobes are the most accessible ones to the sur-
geon(26) (Figure 5). The need for pulmonary biopsy also results
from the fact that the medicinal treatment is changed in
50-60% of the cases after obtaining the histopathologic
examination(27).
In the microscopic examination of the biopsy or necropsy
fragments of lung parenchyma, numerous red blood cells and
siderophages with obstructive character are noticed. The
alveolar septums are thickened, in certain parts, through
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