We describe a patient with an alveolar haemorrhage that probably arose due to malignant hypertension. A 26-year-old man noticed a cough with clear sputum 10 days before admission to the hospital. Six days before admission, he flew from Miyazaki to Osaka, and returned 4 days before admission. Two days before admission, he developed exertional dyspnoea and haemoptysis. He had at least a 3 year history of hypertension, but treatment was not administered.
Upon admission, his vital signs were as follows: blood pressure, 210/150 mmHg; pulse rate, 128 beats/min and respiratory rate, 32/min. A fundus revealed severe hypertensive changes consisting of retinal haemorrhage, soft exudates and papilloedema. Laboratory data revealed 3.1 mg/dl creatinine, 2.2 g/dl albumin, haemoglobin 13.0 g/dl, platelets 6.0 x 104/µl, C-reactive protein 20.0 mg/dl, haptoglobin <8 mg/dl, and the absence of antinuclear antibody, MPO-antinuclear cytoplasmic antibody (ANCA), PR3-ANCA and anti-glomerular basement membrane antibody. Plasma renin activity was 31.2 ng/ml/h and plasma aldosterone concentration was 492 pg/ml. Ultrasonic cardiograph revealed a conspicuous thickening of the left ventricular wall (LVPWTd 22 mm).
Bronchial intubation and mechanical ventilation was applied, since the patient had become drowsy during admission. Chest computed tomography examination showed a prominent bilateral dense pulmonary infiltration indicating alveolar haemorrhage. Bronchoalveolar lavage (BAL) fluid contained increased numbers of red blood cells. Hypertension was controlled at 150/90 mmHg with a calcium antagonist, ß-blocker and angiotensin II blockade. We performed a kidney biopsy and obtained 30 glomeruli. The capillary walls of almost all of them were thickened and wrinkled. Crescent formation was absent. A small artery showed onion peel thickening with a narrowed lumen. An immunofluorescent study did not detect immunoglobulin or complement deposition.
The mechanism of how malignant hypertension can cause alveolar haemorrhage remains unclear, but humoral factors might be involved in the alveolar capillaries [1]. A careful review of the patient's medical history showed that the symptoms worsened after flying to Osaka. Since planes on this route travel at 8000 m, the patient would have been subjected to the equivalent of 20002500 m of altitude and 0.70.8 atm of air pressure [2]. We supposed that this patient had mild congestive heart failure and/or airway inflammation, that could cause more hypoxia than in normal subjects. High-altitude pulmonary oedema is a life-threatening condition caused by rapid ascent to altitudes >2500 m [3]. Grissom et al. described a patient who developed high-altitude pulmonary oedema after rapidly ascending a mountain [4] and in whom BAL findings confirmed alveolar haemorrhage. We speculated from these reports and the present findings that flying at high altitude could trigger alveolar haemorrhage in the presence of underlying conditions such as malignant hypertension, mild congestive heart failure and airway inflammation.
Conflict of interest statement. None declared.
First Department of Internal Medicine Miyazaki Medical College University of Miyazaki Japan Email: ysato{at}med.miyazaki-u.ac.jp
References
|