Management of Co-occurring Intracranial Hemorrhage and Fatal Pulmonary Embolism: A Case Report

Introduction

Intracranial hemorrhage (ICH) can be a life-threatening condition, and when it occurs in combination with fatal pulmonary embolism (PE), it presents a complex and challenging clinical scenario. This case report details the management of a patient who experienced both ICH and high-risk PE, highlighting the difficulties and considerations in such a situation.

Case Presentation

In August 2018, a 67-year-old woman with a history of hypertension and poorly controlled blood pressure was admitted to the emergency department after being unconscious for 1 hour. Brain computed tomography (CT) revealed hemorrhage in the left basal ganglia, cerebellum, and brain stem, with a hematoma that had 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 (ICU), where 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 was 100+/min, and blood pressure was 120–140/80–90 mmHg without vasoactive drugs. The hematoma was partly absorbed, and the lateral ventricle drainage tube was still in situ.

Thirteen days later, her condition suddenly worsened, and she presented with tachypnea, hypoxia, and human-machine confrontation. Bedside sedation was administered to relieve the confrontation, but her blood pressure decreased to 88/64 mmHg, and norepinephrine was intravenously injected at a dose of 10.7 mg/min. Despite initial considerations that the hypotension was caused by the sedative, 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. Deep venous thrombosis in the lower extremities was not found. 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.

Diagnosis and Initial Management

Based on these findings, the patient was diagnosed with acute high-risk PE with contraindications to thrombolysis due to her recent history of massive ICH. Systemic thrombolysis was avoided. Cardiothoracic surgeons and interventional physicians were consulted, but the hospital was not equipped for pulmonary embolectomy, catheter-directed treatment, and extracorporeal membrane oxygenation (ECMO). Additionally, 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.

Further Worsening and Treatment

However, her blood pressure continued to decline, and her 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. To save the patient, an intravenous administration of 10-mg alteplase bolus was immediately started, with the intention of giving another 40 mg within 2 hours at 20 mg/h. The UFH infusion was stopped during alteplase infusion.

Response to Treatment

After 23 minutes, her blood pressure increased to 159/74 mmHg under intravenous norepinephrine administration at 200 mg/min. Her PaO₂ in arterial blood gas increased to 93.3 mmHg on a FiO₂ of 1.00 after 90 minutes. 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 hours. The norepinephrine administration was completely stopped within 20 hours.

Follow-up and Outcome

Brain CT scans were performed 3, 48, and 72 hours after thrombolysis. The repeated brain CT scans revealed that the hematoma caused by the original hemorrhage was similar to that before thrombolysis, but new mild hemorrhage occurred in the cerebral falx. CTPA was not repeated due to renal dysfunction caused by tissue hypoperfusion. Two weeks later, the patient was transferred to the ward for further rehabilitation.

Discussion

Intracranial hemorrhagic patients with certain risk factors, such as higher age, greater weight, a bedridden status, infection, and delay in timely initiation of venous thromboembolism (VTE) chemoprophylaxis, are prone to VTE. Co-occurring ICH and high-risk PE are critical conditions for both patients and physicians. While medical technologies have advanced, systemic thrombolysis can still be an effective measure in emergency situations such as shock and cardiac arrest. In this case, a lower dose of alteplase (25 mg) was effective and safe.

Conclusion

This case report demonstrates the complexity of managing co-occurring ICH and fatal PE. It highlights the importance of careful consideration of treatment options, balancing the risks and benefits, and the need for close monitoring of the patient’s condition. Further research is needed to optimize the management of such patients and improve outcomes.

doi.org/10.1097/CM9.0000000000001291

Was this helpful?

YesNo

0 / 0