A 38-year-old HIV-positive female, recently started on antiretroviral therapy, presented in extremis. She had features suggestive of an HIV-associated cardiomyopathy complicated by the following problems: a four-day-old stroke, extensive deep venous thrombosis, and massive pulmonary embolism. She received intravenous streptokinase with rapid improvement, both haemodynamically and, unexpectedly, neurologically. Our case illustrates that a positive outcome is potentially possible where the two conditions coincide.
A 38-year-old female presented with a 2-day history of dyspnoea and pleuritic chest pain. She had developed a right sided hemiplegia 4 days before the current presentation. She was HIV positive with a CD4 count of 180, and she was receiving highly active antiretroviral therapy.
On examination she was distressed, with a respiratory rate of 30 breaths per minute, a low-volume pulse of 130 beats per minute, and a blood pressure of 70/30 mm Hg. The jugular venous pressure was markedly elevated. On palpation, the apex beat was myopathic and displaced, there was a left parasternal heave and palpable pulmonary component of the second heart sound. Auscultation revealed a loud pulmonary component of the second heart sound (P2) and a third heart sound at the left sternal edge. Her right leg was markedly swollen. She had a dense right hemiplegia with absent power on the right.
Chest X-ray showed an increased cardiothoracic ratio. ECG showed a sinus tachycardia and left bundle branch block without features of acute right ventricular strain. Doppler ultrasound confirmed an extensive right-sided deep vein thrombosis.
A helical CT pulmonary angiogram demonstrated multiple defects in major branches of both pulmonary arteries and multiple areas of pulmonary infarction (Figure
(a) Axial computerised tomography pulmonary angiogram showing filling defect in pulmonary artery. Similar filling defects were found at multiple levels of the pulmonary artery vasculature. (b) Coronal computerised tomography pulmonary angiogram showing multiple filling defects in the pulmonary artery and a triangular hypodensity in the right lower lung, which is most likely a pulmonary infarct.
(a) Axial computerised tomography (unenhanced) brain showing a wedge-shaped hypodensity in the left frontopareital area with extension across both gray and white matter, which is in keeping with a cerebral infarct. (b) Axial computerised tomography (enhanced) brain showing hyperdensity in the left-hand side in the area of previous ischaemia. (c) Coronal computerised tomography (enhanced) brain showing hyperdensity in the left-hand side in the area of previous ischaemia.
Full blood count and routine chemistry were unremarkable. A D-dimer test was positive and troponin T concentration was normal. Our final diagnosis was that of HIV infection, probable HIV-associated cardiomyopathy, deep venous thrombosis, and acute massive pulmonary thromboembolism.
The patient was unstable, tachycardic, and severely hypotensive. Though mindful of her stroke, we administered streptokinase according to the standard protocol. Her haemodynamic status improved markedly, and blood pressure normalised. Signs of pulmonary hypertension improved. A repeat CT pulmonary angiogram showed partial resolution of the pulmonary emboli. To our surprise, her neurological signs improved remarkably as well, with an improvement in muscle power over several hours to near normal. A repeat CT brain scan now demonstrated a rim of enhancement around the infarction, reported as a haemorrhage, though subsequently suggested to represent an area of luxury perfusion.
She maintained her initial clinical improvement and improved further over subsequent days on standard therapy for heart failure. Intercostal drainage was required for a large right haemorrhagic pleural effusion secondary to pulmonary infarction. She was discharged after 18 days on warfarin.
Risk factors for thrombosis in our patient included immobility, dilated cardiomyopathy, and her HIV status. HIV is an independent risk factor for thrombosis. Antiretroviral therapy does not appear to significantly increase risk of venous thromboembolism in HIV-positive patients [
Our patient demonstrated global myocardial impairment, probably on the basis of an HIV-associated cardiomyopathy. Her sudden deterioration and acute onset of pulmonary hypertension suggested the onset of “clinically massive” or high-risk pulmonary embolism [
An ischaemic stroke within the past 6 months is accepted as an absolute contraindication to thrombolysis [
We believed our patient to be unsuitable for embolectomy. With her informed consent, we proceeded to thrombolysis despite the stroke. In response to thrombolysis, the patient improved dramatically and repeat CT angiography revealed partial resolution of the thrombi. To our surprise, there was a prompt, marked improvement in the patient’s neurological status.
Thrombolysis is now recommended as initial treatment for ischaemic stroke presenting within 3 hours [
There are three case reports of patients with coexistent pulmonary embolism and stroke given thrombolysis. Pelletier et al. [
During the evolution of an ischaemic stroke, there is a gradient of hypoperfusion [
European Cooperative Acute Stroke Study (ECASS) III, a randomized, placebo-controlled, phase-three trial, tested the efficacy and safety of rt-PA administered 3 to 4.5 hours after symptom onset [
In summary, thrombolysis proved safe and effective, and it was accompanied by unexpected neurological improvement.