Increasing breathlessness, hyperkalaemia and thrombocytosis in a patient with chronic obstructive pulmonary disease

Citation
Isa. Hassan et al., Increasing breathlessness, hyperkalaemia and thrombocytosis in a patient with chronic obstructive pulmonary disease, HOSP MED, 62(9), 2001, pp. 572-573
Citations number
4
Language
INGLESE
art.tipo
Article
Categorie Soggetti
General & Internal Medicine
Journal title
HOSPITAL MEDICINE
ISSN journal
1462-3935 → ACNP
Volume
62
Issue
9
Year of publication
2001
Pages
572 - 573
Database
ISI
SICI code
1462-3935(200109)62:9<572:IBHATI>2.0.ZU;2-Y
Abstract
A 72-year-old gentleman with no past history of chronic obstructive pulmona ry disease (COPD) was admitted with a history of progressive shortness of b reath, increasing over the preceding 2-3 months, His exercise tolerance was decreasing and he was unable to climb stairs without becoming breathless. He described a cough on most days productive of creamy white sputum but he hod never coughed up any blood, He denied wheeze, ankle oadema, orthopnoea or paroxysmal nocturnal dyspnoea. There was no history of chest pain. He wa s not on any medication and had no allergies. He was an ex-smoker. He smoke d an average of 20 cigarettes a day (one packs for almost 30 years) giving him a total of 30 pack years of smoking. He denied drinking alcohol. There were no symptoms referable to any other system, On examination, he was breathless, cyanosed and tachycardic with a pulse of 120 regular, blood pressure of 160/70 mmHg, and temperature of 37.7 degree sC. His oxygen saturation on air was 77%. Heart sounds were normal. Jugular venous pressure was not visible and there was a slight pitting oedema of h is right foot. He hod widespread reduced breath sounds on respiratory exami nation with widespread inspiratory crackles. Abdominal and neurological exa minations were unremarkable. Initial investigations showed haemoglobin 11.9 g/dl (normal range (NR) 13-1 8 g/dl) with normal red cell indices. His white cell count was 16.9x10(9)/l itre (NR 4-11x10(9)/litre), platelets 1339x10(9)/litre (NR 140-440x10(9)/li tre), sodium138 mmol/litre (NR 133-148 mmol/litre), potassium 6.9 mmol/litr e (NR 3.5-5.5 mmol/litre). Urea, creatinine, bicarbonate, glucose calcium, creatine kinase and liver function were all normal. Blood gases on air show ed marked hypoxic with a pH of 7.38, PaCO2 6.1 kPa and PaCO2 7.6 kPa. Oxyge n saturation was 81.3% and his bicarbonate level was 32.6 mmol/litre. Chest X-ray showed normal heart size with prominent peri-hilar vasculature and t here were some interstitial change in the right lower zone with a small rig ht basal effusion. Subsequent repeat chest X-ray showed the lungs to be hyp erinflated but clear, with the effusion having resolved Electrocardiography showed a sinus tachycardia, On spirometry his forced expiratory volume in 1 second was 1.12 litres (40% of predicted), forced vital capacity was 2.1 litres (59% of predicted) giving a ratio of 53%. Gas transfer corrected to his haemoglobin (DLCO CORR) was 14.17 (59% of predicted) and the ratio of h is gas transfer to alveolar volume (DL/VA ) was 3.89 (101% of predicted). He was initially thought to be having an infective exacerbation of COPD and was treated as such with steroids, nebulisers, antibiotics and prophylacti c subcutaneous heparin, He had a good clinical response to these. However, on noting his raised platelet count, aspirin 150 mg was started and a perfu sion lung scan arranged, The latter showed segmental defects, particularly in the left lung field, with the appearances suggesting pulmonary emboli (F igure 1), In view of his asymmetric ankle oedema a venogram of his right le g was arranged. This proved negative. His relatively raised potassium level was thought to be spurious and a repeat check on a lithium heparin blood s ample gave a reading of 4.3 mmol/litre (NR 3.5-5.5 mmol/litre). A bone morr ow trephine was reported as markedly hypercellular. There was hyperplasia o f white cell series with numerous mature forms and reduced erythropoiesis w hich was normoblastic, Megakaryocytes were markedly increased in numbers, m any occurring in small clusters with dysmorphic hyperlobated nuclei and abu ndant cytoplasm, There was no increase in the blastic component, lymphocyte or plasma cell population or of reticulin fibrosis within the marrow. The appearances were consistent with a myeloproliferative disorder and were in keeping with on essential thrombocythaemia, Ultrasound scan showed normal l iver, kidneys and spleen, With the results of the perfusion scan the patien t was anticoagulated with warfarin and started on allopurinol and hydroxyru rea. He was mobilized and made an uncomplicated recovery.