Use of intravenous (IV) tissue plasminogen (tPA) as a fibrinolytic therapy for acute ischemic stroke is a standard acute phase treatment. The common complication of tPA is hemorrhage, especially intracranial. But, there are other rare sites of bleeding. We present one such rare case of a patient developing spontaneous hemopericardium after IV tPA for acute ischemic stroke.

All eligible acute ischemic stroke patients should be thrombolysed within 3 hours of last known normal and to a more selective group of eligible acute stroke patients, (based on ECASS III exclusion criteria) within 4.5 hours of last known normal [1-4] tPA is the most commonly used agent for thrombolysis, given its neurological benefits at 3 months and long term [2]. But, complications are also associated with the use of tPA. Hemorrhage is one such serious complication of tPA. However, the coagulation factors that may potentially increase the risk of bleeding, after tPA, are not well understood. But, an early transient coagulopathy associated with elevated International normalized ratio (INR) in stroke patients treated with tPA has been reported [5,6]. The term post- tPA coagulopathy is used for an early transient coagulopathy associated with documented elevated INR> 1.5 within 24 hours of tPA infusion without a known cause [6].

A 61-year-old gentleman, known case of hypertension, presented to Emergency department with sudden onset of left sided weakness since 1.5 hours with progressive weakness leading to inability to walk or hold objects by left hand. No history of slurred speech, chest pain, loss of consciousness or dyspnea. Patient was hemodynamically stable, with a GCS-15/15. Pupils were bilaterally equal and reactive to light. Power on left upper limb was 0/5 and left lower limb was 2/5. An MRI brain (stroke protocol) was done (Figure 1), which suggested an acute right frontal and parieto-occipital- right Middle cerebral artery (MCA) territory patchy infarcts. Neck Doppler done suggested bilateral multiple plaques in carotid bulbs and proximal Internal Carotid Artery without significant stenosis.

Figure 1: DWI MRI Images showing acute right MCA territory infarcts.

The right vertebral artery was hypoplastic with non- visualization of distal vertebral artery Va segment. Electrocardiogram showed ST depression in leads 1, aVL and tall T waves in chest leads, Troponin I-0.02ng/ml, INR -1.2. As the patient presented within the window period for thrombolysis, he was administered IV tPA after obtaining consent. Gradually, left lower limb power improved to 3/5 over 3 hours and patient remained hemodynamically stable.

At the end of 3 hours, patient developed hypotension (Blood Pressure-74/40mm Hg). Hypotension was managed with fluid resuscitation. Pupils were bilaterally equal (2mm) and reactive to light and there was no further worsening of neurological deficit. A bedside 2D Echocardiography (Figure 2) was suggestive of concentric Left Ventricular (LV) hypertrophy, grade 1 LV Diastolic dysfunction, mild pericardial effusion around Right Ventricle, Right Atrium, Apex (0.9cm) and anterolateral wall (0.6cm) with Ejection Fraction 0.55, non- collapsing Inferior venacava and no regional wall motion abnormality. After around half an hour, patient developed a second episode of hypotension (70/30 mm Hg) requiring vasopressor support, and drop in GCS (E2V3M3) with reactive and normal pupils. 

Figure 2: 2D Echo showing a pericardial effusion.