Intrapleural instillation of thrombolytic agents has been useful in the treatment of hemothorax when thoracostomy tube drainage is ill-starred We present a patient who perform the operations indicated ined acute hypoxemic respiratory failure following the intrapleural instillation of the pair streptokinase and urokinase 24 h apart.

Intrapleural instillation of thrombolytic agents has been useful in the treatment of hemothorax when thoracostomy tube drainage is ill-starred We present a patient who perform the operations indicated ined acute hypoxemic respiratory failure following the intrapleural instillation of the pair streptokinase and urokinase 24 h apart. Hypoxemia greatest in number likely resulted from a direct efficiency of the products of fibrinolysis in succession the pulmonary circulation.

Complications of the therapeutic use of intrapleural thrombolytic agents are infrequent. Although intravascular administration has been associated with adult respiratory distress syndrome (ARDS) in brace patients,1,2] intrapleural instillation has not been previously reported to lead to pulmonary complications. We not long ago observed a patient who perform the operations indicated ined two episodes of severe hypoxemia related to the instillation of pair different thrombolytic agents.

CASE REPORT

A 58-year-old man with sick sinus syndrome exhibited an iatrogenic right hemothorax following placement of a permanent transvenous cardiac pacemaker. Clos thoracostomy tube drainage to suction was not sufficient in completely evacuating the hemothorax.

in succession the fourth day after tube placement, 250000 U of streptokinase was instilled intrapleurally. Eight hours following instillation, the patient evolveed severe hypoxemia and basilar crackles. Physical examination did not indicate a cardiac cause. He remained afebrile and had no hemoptysis or arrhythmias. He had none previously received a thrombolytic agent. Baseline cardiac ejection fraction was 65 percent The arterial vital fluid gas (ABG) values on 100 percent oxygen were pH of 744 [PCOsub2] of 31 mm Hg and [POsub2] of 73 mm Hg Prior to the instillation of streptokinase, the ABG values in succession 2 L/min nasal cannula [Osub2] were pH of 737 [PCOsub2] of 35 mm Hg and [POsub2] of 81 mm Hg The chest radiograph showed bilateral interstitial and alveolar infiltrates, diffuse mass loss, and the previously observ blunting of the right costophrenic angle. Pulmonary artery catheterization revealed a pulmonary artery constraining force (PAP) of 24/6 mm Hg pulmonary capillary wedge press (PCWP) of 5 mm Hg and cardiac output (CO) 64 L/min. Fibrinogen plain was 489 mg/dl (control, 175 to 400) prothrombin time was 133 s (control, 11.4 s), partial thromboplastin time of 226 s (control 25.7 s), and platelet reckon of 310,000/[mu]l.

Four hours after administration of aerosolized [beta]-agonists, intravenous corticosteriods, and diphenhydramine, the patient's condition was improved and ABG values had turn backed to baseline. The chest tube drained 500 ml of hemorrhagic fluid, moreover drainage then decreased. Urokinase, 450000 U was instilled intrapleurally forward the following day. Seven hours after instillation, the patient make knowned the same adverse reaction and answer to treatment as with streptokinase. The chest tube drained 300 ml throughout the next 2 days and then was remov united month later, he was asymptomatic, and his chest radiograph had reverted to baseline.

DISCUSSION

The therapeutic uses of intrapleural thrombolytic agents have been reported for throughout 40 years.[3] The newer purified agents used to treat empyema and hemothorax have been reported to be safe and effective.[4,5] Adverse events have been limited to excitement erythema, and edema of the chest wall adjacent to the chest tube, and a certain number of decrease in hemoglobin which may be proper to the primary process. couple cases of ARDS associated with the use of intravenous and intra-arterial streptokinase have been reported.[1,2] We are unaware of previous reports of methodical hypoxemia or pulmonary edema associated with the use of intrapleural thrombolytic agents.

A cardiogenic cause of this patient's acute hypoxemic respiratory failure was exclud by the agency of the normal PCWP. An immunologic cause may have been suspected if the hypoxemia had followed the use of streptokinase no other than but urokinase lacks antigenicity. It is doubtful that the two preparations contained impurities that would cause hypoxemia. The no other than compound common to both preparations is albumin which is not reported to lead to hypoxemia in humans or when infused into animals.[6]

It is unlikely that the patient's hypoxemia was owed to alveolar hemorrhage, since he had a mildly elevated fibrinogen flat This is in concordance with earlier observations that there are no important measurable consequences on systemic fibrinolysis caused by means of intrapleural instillation of streptokinase.[7] Plasma plasminogen, [[alpha].sub.2]-antiplasmin, fibrinolytic activity, and thrombin time do not change after intrapleural instillation of thrombolytics. In fact, the systemic fibrinogen plain is commonly elevated since it is an acute phase reactant, despite an increase in fibrin degradation effects (FDP).[7] These FDP are likely generated during fibrinolysis in the pleural space and are then rapidly transferred into the systemic circulation. Rapid systemic uptake has been documented when other agents are instilled intrapleurally.[8]

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