A case report on sub dural hematoma in a patient on dual antiplatelet therapy

Asha Selva Malar1, Shalini H S2, Vijayakumari. D3

1Nursing Supervisor, Kauvery Hospital, Electronic City, Bangalore

2CNO, Kauvery Hospital, Electronic City, Bangalore

3Nurse Educator, Kauvery Hospital, Electronic City, Bangalore

Abstract

Subdural Hematoma (SDH) is a known complication of antiplatelet therapy, especially in elderly patients and those who are on dual antiplatelet therapy (DAPT). We report a case in an older adult on aspirin and clopidogrel after coronary stent placement who developed an acute-on-chronic SDH. This case highlights the challenges of managing intracranial bleeding in patients requiring ongoing antiplatelet therapy.

Key words: Subdural Hematoma (SDH; Dual Antiplatelet Therapy (DAPT); Percutaneous coronary intervention (PCI)

Introduction

Percutaneous coronary intervention (PCI) and dual antiplatelet therapy are common management for patients with acute coronary syndrome. Nonetheless, those treatments can provoke serious complications such as bleeding or hematomas at various anatomic sites and intracranial haemorrhage is the most feared complication of antithrombotic therapy and it can increase the risk of in-hospital death by 60%. Acute subdural hematomas are rarely reported in the literature, are generally associated with traumatic brain injury. Spontaneous acute subdural hematoma without trauma is an uncommon event, but it is a serious condition. In this article, we report a case of a spontaneous acute subdural hematoma in an elderly man receiving dual antiplatelet with clopidogrel and aspirin following percutaneous coronary intervention for acute coronary syndrome, emergency surgery was successfully performed and the patient recovered well. Early diagnosis and prompt treatment of this complication are the keys to improving the prognosis.

Case Presentation

A 74-year-old male, presented to the emergency department with the complaints of right-side weakness & numbness in UL & LL for 2 weeks. He also reported slurring of speech & imbalance while walking for the past 2–3 days. He had a history of Hypertension & was known to have coronary artery disease, post PTCA 2 years back and was on dual antiplatelet therapy (Aspirin & Clopidogrel).

Clinical Examination: On arrival

  • 74 years/Male, Average Built
  • Pulse – 128/min.
  • Blood pressure – 150/108mmHg.
  • Respiratory Rate- 20/min.
  • Temp – Afebrile.
  • Respiratory System: Bilateral air entry present
  • Cardiovascular System: S1-S2 heard, no murmur.
  • Abdomen: Soft, non-tender, bowel sounds present.
  • Neurologically Conscious, alert, oriented
  • GCS: 15/15
  • PEARL EOMs + full
  • Moving all 4 limbs
  • No cerebellar/ meningeal signs.

Diagnosis and Clinical Evaluation

CT brain showed a left front temporoparietal subacute on chronic subdural hematoma with significant mass effect on lateral ventricle and midline shift of about 9mm. His relatives were explained in detail about his clinical condition, imaging findings and plan of management with risks and complications. Cardiology reference was obtained for fitness for surgery.

He underwent Left Front Temporoparietal Craniotomy and Evacuation of Sub Dural Hematoma (Using Jayon Mini Screws and Plates). 

Post operatively he was shifted to ICU and managed with IV antibiotics, analgesics, antiemetics, PPI’s, antihypertensives, anticonvulsants and other supportive measures. His initial postoperative CT showed satisfactory evacuation with resolution of mass effect. But he developed drowsiness and worsening of right-sided weakness.

He was intubated and his repeat CT brain showed acute re-accumulation of extradural hematoma with midline shift. His relatives explained the imaging findings and the need for emergency exploration of the wound. After obtaining their consent he was shifted to OT. He underwent Wound Exploration and Evacuation of Extradural Hematoma Under General Anesthesia at midnight. Post operatively he was shifted to NSICU and managed as before. His condition improved with GCS E3V2M6, his serial CT scans showed reduction in hematoma and optimal cerebral expansion. His platelet function assay confirmed persistent activity of antiplatelet drugs (low arachidonic acid pathway).

After a short interval, the patient again developed neurological deterioration, he was noted to be drowsy, GCS E3V2M5. Repeat imaging demonstrated fresh subdural hematoma with midline shift. Relatives were re-explained about the imaging findings, and he was shifted to OT after their consent.

He underwent Wound Re- Exploration and Evacuation of Subdural Hematoma under GA. Post operatively he was shifted back to NSICU and continued to be managed as before with elective ventilation, His post op CT brain showed no fresh hemorrhage, his GCS was noted to be E4VtM6 on POD1 and he was extubated on POD1.

His follow up CT brain did not show any fresh interval changes. He gradually mobilized to chair and shifted to ward on POD3. He remained stable in the ward and is being discharged with the following advice.

Procedure-1

Left Fronto temporoparietal craniotomy and evacuation of sub dural hematoma (using Jayon mini screws and plates) under GA

Operation notes:

  • Patient positioned supine on head ring with shoulder support, painted and draped
  • Scalp incised, musculocutaneous flap raised.
  • Craniotomy done,
  • Dura opened as a flap based on middle meningeal artery.
  • Dark altered blood with thick subdural membranes noted.
  • SDH evacuated and membranes excised.
  • Subdural space washed thoroughly with warm saline till returning fluid was clear from all corners.
  • Hemostasis achieved, subdural drain placed.
  • Dura closed with prolene.
  • Bone flap repositioned and fixed with Mini screws and plates.
  • Wound closed in layers, scalp stapled

Procedure-2

Wound exploration under general anesthesia

Operation notes:

  • Patient positioned supine on head ring with shoulder support, painted and draped
  • Surgical explored, musculocutaneous flap elevated
  • Bone flap removed, extra dural collection of blood noted
  • Diffuse ooze noted from dural surface, no arterial spurters were noted
  • Hemostasis achieved, with surgical, gel foam and thorough saline wash
  • Hitch sutures applied to dura anchoring to peri cranial under surface
  • Hemostasis achieved, drain placed subgaleally
    • Wound closed in layers, Scalp stapled.

Procedure-3

Wound re- exploration and evaluation of subdural hematoma under general anesthesia. Operation notes:

  • Patient positioned supine on head ring with shoulder support, painted and draped
  • Wound re- explored, musculocutaneous flap raised.
  • Dura re-open by releasing prolene sutures
  • Sub dural hematoma noted, evacuated thoroughly
  • Subdural space washed thoroughly with warm saline till returning fluid was clear from all corners.
  • Hemostasis achieved, subdural drain placed.
  • Dura closed with prolene.
  • Subgaleal drain placed, wound closed in layers
  • Scalp stapled.

Discussion

Acute subdural hematoma is generally associated with traumatic brain injury, acute spontaneous subdural hematoma (ASSDH) without trauma is rare, serious entity. Dual antiplatelet therapy with clopidogrel and aspirin is routinely prescribed after coronary artery stenting, plays a critical role in secondary prevention among patients with acute coronary syndrome and has decreased the rates of re-infarction and stent thrombosis after percutaneous coronary intervention.

Our patient had an acute subdural hematoma after PCI under dual antiplatelet therapy; however, he did not show any signs of coagulopathy, thrombocytopenia or head trauma. Antiplatelet agents are frequently used, and their haemorrhagic complications occur usually at skin or gastrointestinal sites. Serious bleeding event can occur with antiplatelet therapy and intracranial haemorrhage is the most feared complication of antithrombotic therapy and may lead to severe morbidity and mortality unless diagnosed and treated early.

Therefore, early diagnosis and treatment of subdural hematoma is very important because the mortality rate is estimated at 60–76.5% of cases. Here, we describe a case of spontaneous acute subdural hematoma in a patient with ischemic heart disease receiving dual antiplatelet therapy (with Aspirin and clopidogrel) following percutaneous coronary intervention.

He recuperated with no residual neurological deficits. Rapid discontinuation of all the antiplatelet drugs and hematoma evacuation was performed with a favourable evolution. Early diagnosis and prompt treatment of this complication resulted in a good result in this patient. Surgical evaluation should be urgent, and a brain CT scan be performed as quickly as possible.

Management of haemorrhagic patients under antithrombotic therapy is very difficult. Resuming the treatment could lead to recurrence bleeding, on the other hand, suspension or stopping of treatment could expand the thrombotic risk. Early diagnosis and surgical intervention are often essential for hematomas with significant mass effects. Treatment may be managed by nonoperative conservative approach in selected cases.

In our case, rapid discontinuation of all the antiplatelet drugs and surgical hematoma evacuation were performed with a favourable evolution. The patient’s neurological status improved steadily. A repeat CT 48 hours later showed any interval changes. During follow up CT he remained asymptomatic with no recurrence of SDH.

Our patient was satisfied with the quality of our management.

Conclusion

This case highlights the increased vulnerability of patients on dual antiplatelet therapy to sub dural haematoma. Prompt recognition, imaging and coordinated management can lead to excellent outcomes while balancing the competing risks of bleeding and thrombosis.

Acute subdural hematomas in acute coronary syndromes are scarce but critical conditions after percutaneous coronary intervention (PCI). The use of this antiplatelet therapy requires the cardiologist be vigilant of this possible side effect. Opportune management and a correct strategy in secondary prevention of bleeding events are crucial factors to decrease morbidity and mortality in these patients and to improve the prognosis.

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