Management of Co-occurring Intracranial Hemorrhage and Fatal Pulmonary Embolism: A Case Report
Introduction
Patients with intracranial hemorrhage caused by hemorrhagic stroke, brain trauma, or brain tumor resection are prone to venous thromboembolism (VTE). VTE includes pulmonary thromboembolism (PTE) and deep venous thromboembolism. PTE, especially high-risk PTE, has a high mortality rate. Coexisting intracranial hemorrhage and high-risk PTE present a clinical dilemma. Patients with high-risk PTE require fibrinolysis; however, recent intracranial hemorrhage is an absolute contraindication to fibrinolysis due to the potential for fatal recurrent intracranial hemorrhage. This case report presents the clinical details of a patient who was successfully resuscitated despite these challenges.
Case Presentation
In August 2018, a 67-year-old woman was admitted to the emergency department after being unconscious for 1 hour. She had a several-year history of hypertension as well as poorly controlled blood pressure. Brain computed tomography (CT) revealed hemorrhage in the left basal ganglia, cerebellum, and brain stem, and a hematoma that ruptured into the ventricle. She underwent craniotomy and hematoma evacuation in the cerebellum and brain stem, followed by decompressive craniectomy and lateral cerebral drainage. After the operation, she was admitted to the intensive care unit. She was bedridden and relied on tracheal intubation for mechanical ventilation. Her oxygen saturation (SaO2) level was 100% on a fraction of inspiration oxygen (FiO2) of 0.3; heart rate, 100+/min; and blood pressure, 120–140/80–90 mmHg without vasoactive drugs. The hematoma was partly absorbed, and the lateral ventricle drainage tube was still in situ.
Clinical Deterioration and Diagnosis
After 13 days, her condition suddenly worsened, and she presented with tachypnea, hypoxia, and human-machine confrontation. To relieve the human-machine confrontation, she received bedside sedation. Her blood pressure decreased to 88/64 mmHg, and norepinephrine was intravenously injected at a dose of 10.7 mg/min. We initially considered that the hypotension was caused by the sedative; however, her blood pressure gradually decreased, and the norepinephrine dose used to maintain the blood pressure was increased gradually. Her arterial blood gas results were as follows: pH, 7.28; partial pressure of carbon dioxide, 39.3 mmHg; and arterial oxygen pressure (PaO2), 64.9 mmHg on a FiO2 of 1.00. Electrocardiography revealed sinus tachycardia. Bedside echocardiography did not show any obvious abnormalities. We found no deep venous thrombosis in the lower extremities. CT pulmonary angiography (CTPA) revealed multiple filling defects in the bilateral main pulmonary arteries and their branches. The hypersensitive troponin T value was 0.177 ng/mL, while that of N-terminal pro-brain natriuretic peptide was 482.8 ng/L. On the basis of these findings, we considered the patient as having acute high-risk PTE with contraindications to thrombolysis.
Treatment Strategy
Given her recent history of massive intracranial hemorrhage, systemic thrombolysis was avoided. We consulted cardiothoracic surgeons and interventional physicians; however, our hospital was unfortunately not equipped for pulmonary embolectomy, catheter-directed treatment, and extracorporeal membrane oxygenation (ECMO). Furthermore, her condition did not allow long-distance transfer. Therefore, unfractionated heparin (UFH) infusion was started as an initial intravenous bolus of 80 units/kg followed by 18 units·kg⁻¹·h⁻¹ to maintain the activated partial thrombin time (APTT) between 50 and 70 s. However, her blood pressure declined and SaO2 level persisted. Her blood pressure still decreased to 78/63 mmHg under intravenous norepinephrine at 400 mg/min. The PaO2 in arterial blood gas decreased to 31.1 mmHg on a FiO2 of 1.00.
Emergency Thrombolysis
To save the patient, we immediately started an intravenous administration of 10-mg alteplase bolus and intended to give another 40 mg within 2 h at 20 mg/h. The UFH infusion was stopped during alteplase infusion. Her blood pressure increased to 159/74 mmHg under intravenous norepinephrine administration at 200 mg/min after 23 min. Her PaO2 in arterial blood gas increased to 93.3 mmHg on a FiO2 of 1.00 after 90 min. However, mild bleeding occurred at multiple sites, including the airway, ear, nose, mouth, vagina, and artery puncture point. To balance the treatment effectiveness and bleeding risk, the alteplase infusion was stopped at a total dose of 25 mg, and UFH infusion was restarted once the APTT decreased to <70 s. Her ventilator parameters recovered within 10 h. The norepinephrine administration was completely stopped within 20 h.
Post-Thrombolysis Monitoring
Brain CT scans were performed 3, 48, and 72 h after thrombolysis. The repeated brain CT scans revealed that the hematoma caused by the original hemorrhage was similar to that before thrombolysis; however, new mild hemorrhage occurred in the cerebral falx. We did not repeat CTPA because of renal dysfunction caused by tissue hypoperfusion. Two weeks later, the patient was transferred to the ward for further rehabilitation.
Discussion
Intracranial hemorrhagic patients with higher age, greater weight, a bedridden status, infection, and delay in timely initiation of VTE chemoprophylaxis are prone to VTE. Co-occurring intracranial hemorrhage and high-risk PTE are critical conditions for both patients and physicians. Fortunately, medical technologies have progressed rapidly, and more options such as catheter-directed thrombolysis, pulmonary embolectomy, and ECMO are now available. However, systemic thrombolysis is still an effective measure for patients with co-occurring intracranial hemorrhage and high-risk PTE in emergency situations such as shock and cardiac arrest. A lower dose of alteplase (25 mg) was effective and safe for our patient.
Conclusion
This case highlights the complexities and challenges in managing patients with co-occurring intracranial hemorrhage and high-risk pulmonary embolism. The successful use of a lower dose of alteplase in this patient underscores the importance of individualized treatment strategies in critical care settings. Further research and clinical guidelines are needed to optimize the management of such complex cases.
doi.org/10.1097/CM9.0000000000001291
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