A 69-year-old woman with a history of hypertension presented with a generalized petechial rash and shortness of breath of 3 days duration.
The rash was nonpruritic, painless, and started at the thighs, but rapidly disseminated to the rest of the body.
She had progressive dyspnea on exertion, with a significant decrease in exercise tolerance.
She denied fever, headache, dizziness, hemoptysis, or bleeding from anywhere.
There was no history of new drug use, unusual food intake, contact with any sick persons, or recent travel.
Her only medication was enalapril, which she had been taking for several years.
The patient denied any use of recreational drugs, tobacco, or alcohol.
On admission, she was afebrile, normotensive with mild tachypnea (respiratory rate of 22 breaths per minute).
Physical examination revealed scattered petechial rash, more prominent in lower extremities, nonpalpable and nonblanching.
Chest auscultation revealed coarse crackles bilaterally.
Cardiovascular, abdominal, and neurological examinations were normal.
There was no palpable lymphadenopathy or visceromegaly.
Laboratory examination revealed thrombocytopenia (platelets 7000/μL), anemia (hemoglobin 10.8 mg/dL and hematocrit 34%), and leukocytosis (white blood cells [WBCs] 11,600/μL).
The coagulation profile was normal, which excluded disseminated intravascular coagulation.
Arterial blood gas on ambient air revealed a partial pressure of oxygen (PaO2) of 64 Torr, a partial pressure of carbon dioxide (PaCO2) of 37 Torr (pH 7.45), and an increased alveolar-arterial gradient (44 Torr).
Diffuse airspace consolidation was found on chest roentgenogram (Fig.1A).
Computed tomography (CT) of the chest showed diffuse ground glass alveolar opacities and patchy infiltrates (Fig.1B, C).
She was started on broad-spectrum antibiotics and received intravenous steroids.
Peripheral smear showed giant platelets and occasional small platelet clumps, with no schistocytes.
A flexible fiber-optic bronchoscopy (FFB) showed normal mucosa with no endobronchial lesions (Fig.2A).
Serial aliquots of BAL fluid (BALF) turned more hemorrhagic, confirming the bronchoscopic diagnosis of DAH (Fig.2B).
Cytology of BALF showed a substantial amount of hemosiderin-laden macrophages, further supporting the diagnosis.
All BALF cultures and gram stains were negative.
The patient remained with severe thrombocytopenia and hypoxia despite steroids and platelets transfusion.
High doses of pulse steroids and intravenous immunoglobulins (IVIGs) were added with clinico-radiological improvement.
A bone marrow aspirate was morphologically normal.
Additional laboratory studies failed to reveal an etiology for secondary thrombocytopenia (Table ​1), supporting the diagnosis of ITP.
Steroids were gradually tapered.
Repeat chest radiograph showed almost complete resolution of bilateral infiltrates (Fig.3).
Platelet count returned to normal by week 10 after admission without any additional therapies (Fig.4).