Light and Electron Microscopy
Essam Raweily, MD, MRCPath, Head Section
of Anatomical Pathology
and Hugh Anger, EM Senior Technologist
King Khalid National Guard Hospital
Jeddah, Saudi Arabia
History:
A 29-year-old male, fifteen-pack-year smoker, presented with a
one-year history of progressive shortness of breath on exertion.
His exercise tolerance was finally limited to one flight of stairs.
He denied any history of cough, chest pain, palpitations, orthopnea,
paroxysmal nocturnal dyspnea or wheezes. He denied any previous
medical illnesses and was not taking any medications. There was
no history of fever, weight-loss or night sweats. The rest of
the systemic review was unremarkable. He works as a public relations
representative. He denied any possible exposure to occupational
hazards or toxic fumes and materials. He had no risk factors for
human immuonodeficiency virus (H IV) or other infections.
Clinically his vital signs were normal. There was no cyanosis, lymphadenopathy, or clubbing. Chest examination revealed normal breath sounds and no added sounds. Cardiovascular, abdominal and CNS examinations were normal. Investigations revealed a normal complete blood count and peripheral blood morphology. Coagulation profile, urea and electrolytes were normal. Total cholesterol was 6.7 mmoill (3.55.2) and triglycerides was 2.80 mmoill (<2.3). The patient's Hepatitis B surface antigen, Hepatitis C antibody, HIV antibody, and Anti-nuclear antibodies were negative.
Pulmonary function test revealed a
restrictive pattern of moderate severity with total lung capacity
of 61%, vital capacity of 71% and transfer factor of 32% of predicted
values. Arterial blood gases revealed hypoxia of 8.9Kpa with oxygen
saturation of 94% but normal acid-base balance. His chest radiograph
showed diffuse bilateral opacities with ill-defined nodular infiltrates.
Computed tomographic (CT) scan of the chest with high-resolution
techniques revealed ground glass opacities affecting both lungs
in a 'geographic pattern'. Focal areas of lobular sparing were
present throughout the lungs. There was also a remarkable smooth
thickening of intra-lobular structures and inter-lobular septae,
with no architectural distortion, giving the appearance of a "crazy
paving" pattern. No prominent perivascular, peribronchial
disease, honeycombing changes, mediastinal or hilar lymphadenopathy
were noted.
A diagnostic bronchoscopy and transbronchial biopsy was done.
The bronchial alveolar lavage fluid was a cream-white colour.
Microscopic examination of the lavage fluid was negative for acid-fast
bacilli, fungal organisms, and gram staining organisms. Cultures
for Mycobacterium, fungal, and bacteria were all negative.
