Endobronchial streptokinase lysing of an obstructing endobronchial blood clot caused by massive hemoptysis has been described in the setting of sarcoidosis, cavitary histoplasmosis, and multiple myeloma. 1–3 The use of thrombolytic agents to dissolve endobronchial clots following spontaneous bleeding in patients with uremia and congestive heart failure has not been reported. We describe such a case.
A 65-year-old man was admitted to the coronary care unit for intubation and mechanical ventilation after an acute myocardial infarction complicated by pulmonary edema. The patient had chronic renal failure but did not yet need hemodialysis. He had no notable pulmonary history.
In the coronary care unit he was started on 20,000 U/day heparin for his ischemia. On the third day, while still on mechanical ventilation, he started to have a large amount of hemoptysis associated with hypotension and an acute deterioration in his blood gases. Flexible bronchoscopy revealed that bleeding was coming from the left lung, and a selective right intubation was performed. To protect the right lung, heparin was stopped. Twenty-four hours later, the endotracheal tube was repositioned in the trachea but total atelectasis of the left lung persisted. Repeat bronchoscopy showed a large blood clot occluding the left mainstem bronchus. All attempts to remove the clot, using various suctioning and biopsy techniques, were unsuccessful.
Because total lung collapse persisted for a fourth day, we decided to try local instillation of endobronchial streptokinase. A total dose of 80,000 U streptokinase was administered through the bronchoscope over 90 minutes, in aliquots of 10 mL normal saline with 10,000 U. This procedure dissolved the clot partially and the remaining fragments were suctioned easily. The left lung expanded, with improvement in patient ventilation and oxygenation. Chest radiography showed dramatic improvement. Dialysis had been initiated because of deterioration of renal function. At this point, however, all coagulation parameters and platelet counts were within normal limits: platelets, 166,000 platelets/mm3; International normalized ratio, 1.2; partial thromboplastin time, 35. The patient's workup for autoimmune disorders, including antinuclear antibody, antineutrophil cytoplasmic antibody, and anti-glomerular basement membrane, was also negative.
Four days after endobronchial lysing, endobronchial bleeding was again detected. This time, bronchoscopy localized the bleeding to both the lingual and the right middle lobe. Computed tomography of the chest revealed only bilateral alveolar opacities compatible with pulmonary hemorrhage. No other abnormalities such as bronchiectasis or lung masses were seen. A bronchial angiography was performed. No vascular abnormalities were identified; nevertheless, selective bilateral embolization was performed. The recurrent bleeding, and the social and psychologic environment of the patient, despite the small amount of bleeding, dictated this action. The bleeding subsequently stopped and the patient was extubated 4 days later and discharged from the coronary care unit.
A 3-year follow-up has not shown any remarkable events in our patient. He continues to undergo hemodialysis but otherwise is in good health without any recurrent hemoptysis.
Our case has a two interesting aspects: First, it is a case of massive, recurrent endobronchial bleeding with uremia as the only identified pathology because the patient had normal coagulation parameters and no anatomic abnormalities identified. Second, we used endobronchial streptokinase as a thrombolytic agent to dissolve a large endobronchial clot. The use of endobronchial streptokinase has not been reported in spontaneous endobronchial bleeding in a uremic patient, although it is has been reported in other situations (Table 1). 1–7 In our patient, the second bleeding episode was not related to the thrombolysis because it happened 4 days later, with normal coagulation parameters. This consisted of minor bleeding from the right middle lobe and the lingula, and was stopped successfully by bronchial embolization. Uremia can cause hemoptysis without any other identifiable etiologies. In a retrospective review of 34 uremic patients, the etiology of hemoptysis in uremic patients was undetermined in 41% of patients. 8
Bansal 7 reported a case of massive fatal hemoptysis after the instillation of 100,000 U streptokinase in one bolus. We used streptokinase in small aliquots for a total of 80,000 U, diluted in normal saline. This method appears to be safe and effective in dissolving the endobronchial clot. The reported doses of streptokinase used are 30,000 U, 50,000 U, 60,000 U, and 80,000 U (Table 1). We used 80,000 U mainly because the clot was 4 days old and we felt that a higher dose of streptokinase would be needed. Although we instilled streptokinase directly through the bronchoscope, an alternative method would be to use a plastic catheter to direct the lytic agent more easily and accurately onto the surface of the clot, as described by Thompson. 1 In hemodynamically unstable patients who cannot tolerate rigid bronchoscopy, and in whom other mechanical methods for extraction of the clot had failed, endobronchial streptokinase may be used. 3,5,6 Our case is the first in which streptokinase was used in a patient with uremia, without any other cause of bleeding. The chest radiographs were normal, even on the left side after resolution of a complete collapse of the lung that lasted for 4 days. Clinical studies describing the natural history of endobronchial clots are scarce, but it was noted previously that the longest time of bronchial obstruction followed by complete lung reexpansion was 3 days. 3
This case shows that endobronchial streptokinase can be administered safely and effectively to dissolve large, obstructing clots that cannot be removed bronchoscopically even if they persist for more than 4 days.
1. Thomson DB. Endobronchial streptokinase
to dissolve a right mainstem clot [letter]. Chest 1986; 89:904.
2. Vajo Z, Parish JM. Endobronchial thrombolysis with streptokinase
for airway obstruction due to blood clots. Mayo Clin Proc 1996; 71:595–6.
3. Arney KL, Judson MA, Sahn SA. Airway obstruction arising from blood clot. Chest 1999; 115:293–300.
4. Botnick W, Brown H. Endobronchial urokinase for dissolution of massive clot following transbronchial biopsy. Chest 1994; 105:953–4.
5. Cole RP, Groomsman GJ. Endobronchial streptokinase
for bronchial obstruction by blood clots [letter]. N Engl J Med 1983; 308:905–6.
6. Maxwell SL, Stauffer JL Endobronchial streptokinase
for relief of tracheobronchial obstruction by blood clots [letter]. Chest 1992; 101:1738–9.
7. Bansal A. Streptokinase
for endobronchial blood clots [letter]. Chest 1999; 116:587.
8. Kallay N, Dunagan D, Adair N, et al. Hemoptysis
in patients with renal insufficiency: the role of flexible bronchoscopy. Chest 2001; 119:788–94.