A 59-year-old man presented with a 2 week history of sudden onset dyspnea and a week history of cough. Dyspnea was initially noticed during daily routine activities but progressively to dyspnea at rest. Cough was productive of about 2.5 ml of yellowish sputum per bout. There was no associated chest pain, fever, orthopnea, or paroxysmal nocturnal dyspnea. There was no history of lower limb swelling or calf pain, no significant weight loss, or drenching night sweats. He had had 3 doses of moderna (mRNA 1273) COVID 19 vaccine, with the booster dose taken about a month before the onset of symptoms. There were associated anorexia, generalized body pain, joint pain, and weakness, and was bed bound for weeks. There was no significant past medical history. He does not smoke a cigarette or drink alcohol. No family history of any significant medical conditions.
At presentation, he was conscious and alert, no pale, afebrile, anicteric, and well hydrated with no pitting pedal edema. Oxygen saturation was 87% in room air and 95% with supplemental oxygen via nonrebreathe mask at 5 liter/min. Respiratory rate was 30 cpm, no trachea deviation, and bronchial breath sounds with coarse crepitation were heard in the right middle lung zone. Pulse rate was 123 bpm, regular and full volume, blood pressure was 100/85 mmHg and apex beat was not displaced.
Complete blood count, serum electrolytes, urea and creatinine, lipid profile were essentially normal. ESR (Erythrocyte Sedimentation Rate) was 10 mm/hour and CRP (C - reactive protein) was 78.1 mg/L. Sputum gene expert test was negative for Mycobacterium Tuberculosis and sputum culture yielded no growth.
An initial assessment of atypical community acquired pneumonia was made. He was admitted and commenced on intravenous antibiotics, intravenous fluids, and continued on supplemental oxygen. He was subsequently reviewed by the respiratory and cardiology teams due to lack of significant improvement and worsening dyspnea. He gave a history of a similar event about a year prior.
Electrocardiography (ECG) showed sinus tachycardia. Compressive ultrasonography (CUS) of lower limb vessels was essentially normal. Computed tomography pulmonary angiography (ctpa) revealed nearly occlusive pulmonary embolism of the right and left pulmonary arteries with features of possible early pulmonary hypertension. There were also fibrotic streaks on the anterior aspect of the right middle lung lobe and evidence of thoracic spondylosis. (Figure 1) The echocardiogram revealed a dilated right atrium, dilated right ventricle, grade 1 diastolic dysfunction, moderate pulmonary hypertension, and poor right ventricular systolic function with an ejection fraction of 75.18% and minimal pericardial effusion.
An assessment of bilateral pulmonary embolism was made and the patient was moved to the Intensive Care Unit (ICU). He was commenced on Subcutaneous Enoxaparin 80 mg 12 hourly immediately. IV streptokinase 250,000 units was given over 30 minutes and then followed up by 100,000 units after 1 hour. On subsequent reviews, he continued to make sustained clinical improvement. He was moved from the ICU to the medical ward on the 19th day of admission with oxygen saturation of 95-99% on an oxygen concentrator and was commenced on Tab Warfarin 7.5 mg nocte and Tab Sildenafil Citrate 20 mg twice daily. During his admission, he had serial complete blood count, electrolyte, urea and creatinine, and clotting profile tests done. (Table 1) The possibility of a hypercoagulable state was considered, however, protein C and S assays were within normal limits. He was weaned off oxygen on the 28th day of admission.
On the 33rd day of admission, he was discharged home on 7.5 mg of warfarin with oxygen saturation of 96% in room air. He came for follow-up in the chest clinic 2 weeks after discharge. Breathlessness and cough have completely subsided and the patient is alive and well. A repeat thrombophilia workup was not done as the patient could not afford it. Follow-up echocardiography was done with showed a mildly dilated right atrium and ventricle, grade 1 diastolic dysfunction, mild to moderate pulmonary hypertension, and ejection fraction of 81.6%. No evidence of pericardial effusion was seen.