Ministry of Health of the Republic of Moldova, State Medical and Pharmaceutical University Nicolae Testemitanu, Medical Students and Residents Association
Abstract
State Medical and Pharmaceutical University “Nicolae Testemitanu”, Chisinau,
Republic of MoldovaIntroduction: Massive hemoptysis is an uncommon but life-threatening emergency. The loss
of at least 600 ml of blood within a 48-hour period has been associated with a high mortality rate.
Although most commonly hemoptysis caused by valvulopathies is not massive enough to be life
threatening, have been reported cases of asphyxia after pulmonary hemorrhage in patients with
mitral stenosis. Hemoptysis and occurrence of pulmonary edema associated with end stage and
severe mitral stenosis would be an indication for early surgery.
Aim of the study: To assess the clinical, laboratory aspects and the presentation of a clinical
case with massive hemoptysis and mitral stenosis occurred at mature age.
Material and methods: The patient was hospitalized, examined, evaluated in Hospital "Saint
Trinity", Chisinau.
Results: Patient aged 45 years was hospitalized in Emergency Department due to pulmonary
hemorrhage (>21/24 hours) and hemorrhagic shock. From anamnesis, the patient is known with
rheumatic heart defect - mitral stenosis at the age of 25 years. It is of interest that massive
hemoptysis in this patient occurred as a first manifestation of mitral stenosis. He administered
anticoagulation therapy - Warfarin. Physical examination on admission revealed a normal weight
patient in critical condition. Relative limits were deflected: left heart border - by 4 cm and right -
by 2 cm, arrhythmic heart sounds, atrial fibrillation, diastolic murmur, distended jugular, peripheral
edema at the calves, lower liver edge - 4 cm below the right costal border.
Echocardiographic examination revealed the patient's hardened, calcified aorta walls, indurated
annulus and aortic valves, calcified, with formation of the moderate regurgitation (II degree), mitral
annulus calcification, mitral valves endured pronounced calcified stenosis formation, transmitral
pressure gradient - 36 mmHg., mitral orifice area - 1,5 cm2, considerable dilatation of the left atrium,
right atrium, moderate dilatation of the right ventricle, asymmetrical hypertrophy of the left ventricular
myocardium, ejection fraction - 60%. Tricuspid valve insufficiency - IIIrd gr. Pulmonary artery valve
insufficiency - IInd gr. Severe pulmonary hypertension, pulmonary artery pressure - 68 mmHg. Initial
treatment consisted from antishock therapy (ice bag. airway maintenance, oxygen 2-4 1/min, permanent
venous access, fluid resuscitation, hemostasis and hemodynamic correction), (3-blockers and digitalis
administration. Patient's general condition improved by stopping hemoptysis and reducing dyspnea, but
pulmonary bleeding complications required a special intervention-the reference to cardiac surgeon.
Conclusion: Our patient's history and clinical course illustrate that severe hemoptysis may
complicate moderate degrees of mitral stenosis. The patient had the high thromboembolic risk
necessitated anticoagulation therapy. Mitral valve operation would appear to be beneficial in
cessation of hemoptysis