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Targeted Syncope Workup in Hypercoagulable Patients
Background
Syncope presents a common diagnostic challenge due to its broad differential, ranging from benign to life-threatening conditions. Despite guidelines emphasizing a history- and physical examination- driven approach, nearly $33 billion is spent annually on syncope evaluations, often without yielding conclusive diagnoses. Here, we present a case of syncope secondary to cerebral venous sinus thrombosis, underscoring the importance of cerebrovascular imaging in select high-risk patient populations.
Case Presentation
An 80-year-old male with chronic sinusitis and history of pulmonary embolism (managed with thrombolysis and apixaban) presented due to an episode of transient loss of consciousness followed by nausea and vomiting. He denied any preceding symptoms but his wife did notice his arm move up for a few seconds. He didn’t have any headaches or post-ictal state. Physical exam showed normal orthostatic vital signs, symmetric blood pressure and radial pulses bilaterally. An extensive neurological exam was done and was unremarkable for any focal deficits including no vision changes. Initial evaluation including electrocardiogram, telemetry monitoring, transthoracic echocardiogram, and electroencephalography showed no significant abnormalities.
Chest CT angiography revealed right-sided segmental pulmonary emboli, unchanged from prior imaging. Head CT did not show any acute intracranial findings, and CT angiography demonstrated no vascular abnormality. Ultimately, an MRI brain revealed a left sigmoid sinus filling defect, suggestive of cerebral venous sinus thrombosis (CVST), in addition to chronic sinusitis. As CVST occurred while on apixaban, anticoagulation was switched to enoxaparin. He did not experience any recurrent symptoms during admission.
Conclusions
This case highlights the need for a patient- specific approach to syncope evaluation. Early neurovascular imaging may aid in prompt diagnosis and prevent unnecessary testing. CVST is a rare manifestation of venous thromboembolism and may present with symptoms mimicking vasovagal syncope, such as nausea and transient loss of consciousness. Typical symptoms of CVST include headaches, vomiting, vision changes, focal deficits, seizures, mental status changes, stupor or coma. Risk factors include prior thrombosis, hypercoagulable states like pregnancy or malignancy, obesity, OCPs, and chronic sinusitis. Noncontrast CT may miss CVST, and advanced neuroimaging is necessary for diagnosis in high-risk patients with thrombotic risk factors or symptoms suggestive of elevated intracranial pressure.
Background
Syncope presents a common diagnostic challenge due to its broad differential, ranging from benign to life-threatening conditions. Despite guidelines emphasizing a history- and physical examination- driven approach, nearly $33 billion is spent annually on syncope evaluations, often without yielding conclusive diagnoses. Here, we present a case of syncope secondary to cerebral venous sinus thrombosis, underscoring the importance of cerebrovascular imaging in select high-risk patient populations.
Case Presentation
An 80-year-old male with chronic sinusitis and history of pulmonary embolism (managed with thrombolysis and apixaban) presented due to an episode of transient loss of consciousness followed by nausea and vomiting. He denied any preceding symptoms but his wife did notice his arm move up for a few seconds. He didn’t have any headaches or post-ictal state. Physical exam showed normal orthostatic vital signs, symmetric blood pressure and radial pulses bilaterally. An extensive neurological exam was done and was unremarkable for any focal deficits including no vision changes. Initial evaluation including electrocardiogram, telemetry monitoring, transthoracic echocardiogram, and electroencephalography showed no significant abnormalities.
Chest CT angiography revealed right-sided segmental pulmonary emboli, unchanged from prior imaging. Head CT did not show any acute intracranial findings, and CT angiography demonstrated no vascular abnormality. Ultimately, an MRI brain revealed a left sigmoid sinus filling defect, suggestive of cerebral venous sinus thrombosis (CVST), in addition to chronic sinusitis. As CVST occurred while on apixaban, anticoagulation was switched to enoxaparin. He did not experience any recurrent symptoms during admission.
Conclusions
This case highlights the need for a patient- specific approach to syncope evaluation. Early neurovascular imaging may aid in prompt diagnosis and prevent unnecessary testing. CVST is a rare manifestation of venous thromboembolism and may present with symptoms mimicking vasovagal syncope, such as nausea and transient loss of consciousness. Typical symptoms of CVST include headaches, vomiting, vision changes, focal deficits, seizures, mental status changes, stupor or coma. Risk factors include prior thrombosis, hypercoagulable states like pregnancy or malignancy, obesity, OCPs, and chronic sinusitis. Noncontrast CT may miss CVST, and advanced neuroimaging is necessary for diagnosis in high-risk patients with thrombotic risk factors or symptoms suggestive of elevated intracranial pressure.
Background
Syncope presents a common diagnostic challenge due to its broad differential, ranging from benign to life-threatening conditions. Despite guidelines emphasizing a history- and physical examination- driven approach, nearly $33 billion is spent annually on syncope evaluations, often without yielding conclusive diagnoses. Here, we present a case of syncope secondary to cerebral venous sinus thrombosis, underscoring the importance of cerebrovascular imaging in select high-risk patient populations.
Case Presentation
An 80-year-old male with chronic sinusitis and history of pulmonary embolism (managed with thrombolysis and apixaban) presented due to an episode of transient loss of consciousness followed by nausea and vomiting. He denied any preceding symptoms but his wife did notice his arm move up for a few seconds. He didn’t have any headaches or post-ictal state. Physical exam showed normal orthostatic vital signs, symmetric blood pressure and radial pulses bilaterally. An extensive neurological exam was done and was unremarkable for any focal deficits including no vision changes. Initial evaluation including electrocardiogram, telemetry monitoring, transthoracic echocardiogram, and electroencephalography showed no significant abnormalities.
Chest CT angiography revealed right-sided segmental pulmonary emboli, unchanged from prior imaging. Head CT did not show any acute intracranial findings, and CT angiography demonstrated no vascular abnormality. Ultimately, an MRI brain revealed a left sigmoid sinus filling defect, suggestive of cerebral venous sinus thrombosis (CVST), in addition to chronic sinusitis. As CVST occurred while on apixaban, anticoagulation was switched to enoxaparin. He did not experience any recurrent symptoms during admission.
Conclusions
This case highlights the need for a patient- specific approach to syncope evaluation. Early neurovascular imaging may aid in prompt diagnosis and prevent unnecessary testing. CVST is a rare manifestation of venous thromboembolism and may present with symptoms mimicking vasovagal syncope, such as nausea and transient loss of consciousness. Typical symptoms of CVST include headaches, vomiting, vision changes, focal deficits, seizures, mental status changes, stupor or coma. Risk factors include prior thrombosis, hypercoagulable states like pregnancy or malignancy, obesity, OCPs, and chronic sinusitis. Noncontrast CT may miss CVST, and advanced neuroimaging is necessary for diagnosis in high-risk patients with thrombotic risk factors or symptoms suggestive of elevated intracranial pressure.
A Rare Delayed Presentation of Immune-Related Hepatitis in a Patient Treated With Pembrolizumab
Background
Immune checkpoint inhibitors, including pembrolizumab, are associated with a spectrum of immune-related adverse events (irAEs), including immune- mediated hepatitis. Typically, this toxicity manifests within the first 14 weeks of therapy. Delayed presentations beyond one year are exceedingly rare and pose diagnostic challenges.
Case Presentation
We report an elderly patient (over 90 years old) with stage IVa squamous cell carcinoma of the lung and high microsatellite instability (MSI) who had been receiving pembrolizumab since 2023. In 2024—13 months into therapy—he presented with subjective fevers, weakness, and altered mental status. Laboratory evaluation revealed cholestatic jaundice with AST 310 U/L, ALT 291 U/L, alkaline phosphatase 860 U/L, and total bilirubin 5.7 mg/dL. Infectious workup was negative. Imaging via MRCP showed multiple scattered hepatic cysts and a small pancreatic cyst, without biliary obstruction.
Further evaluation, including serologies for hepatitis B and C, CMV, HSV, autoimmune hepatitis panel, iron studies, and ceruloplasmin, was unremarkable except for mildly elevated alpha-1 antitrypsin. Scattered liver cysts were seen on an MRI. The overall findings were most consistent with immune-related hepatitis, as pembrolizumab is known to cause both hepatocellular and cholestatic patterns of liver injury.
The patient was started on high-dose prednisone, resulting in rapid clinical and biochemical improvement. Two weeks post-discharge, liver function tests (LFTs) had markedly improved (bilirubin 1.3, AST 19, ALT 40, ALP 193). Given the severity of transaminitis and hyperbilirubinemia (AST >8x ULN, bilirubin >3x ULN), pembrolizumab was permanently discontinued. LFTs normalized after completion of the steroid taper.
Conclusions
This case highlights a rare instance of delayed immune-related hepatitis occurring over a year after initiation of pembrolizumab, far beyond the typical window of onset. Clinicians should maintain a high index of suspicion for irAEs even in late stages of immunotherapy, particularly when common etiologies are excluded. Prompt recognition and corticosteroid treatment can lead to favorable outcomes, even in older patients.
Background
Immune checkpoint inhibitors, including pembrolizumab, are associated with a spectrum of immune-related adverse events (irAEs), including immune- mediated hepatitis. Typically, this toxicity manifests within the first 14 weeks of therapy. Delayed presentations beyond one year are exceedingly rare and pose diagnostic challenges.
Case Presentation
We report an elderly patient (over 90 years old) with stage IVa squamous cell carcinoma of the lung and high microsatellite instability (MSI) who had been receiving pembrolizumab since 2023. In 2024—13 months into therapy—he presented with subjective fevers, weakness, and altered mental status. Laboratory evaluation revealed cholestatic jaundice with AST 310 U/L, ALT 291 U/L, alkaline phosphatase 860 U/L, and total bilirubin 5.7 mg/dL. Infectious workup was negative. Imaging via MRCP showed multiple scattered hepatic cysts and a small pancreatic cyst, without biliary obstruction.
Further evaluation, including serologies for hepatitis B and C, CMV, HSV, autoimmune hepatitis panel, iron studies, and ceruloplasmin, was unremarkable except for mildly elevated alpha-1 antitrypsin. Scattered liver cysts were seen on an MRI. The overall findings were most consistent with immune-related hepatitis, as pembrolizumab is known to cause both hepatocellular and cholestatic patterns of liver injury.
The patient was started on high-dose prednisone, resulting in rapid clinical and biochemical improvement. Two weeks post-discharge, liver function tests (LFTs) had markedly improved (bilirubin 1.3, AST 19, ALT 40, ALP 193). Given the severity of transaminitis and hyperbilirubinemia (AST >8x ULN, bilirubin >3x ULN), pembrolizumab was permanently discontinued. LFTs normalized after completion of the steroid taper.
Conclusions
This case highlights a rare instance of delayed immune-related hepatitis occurring over a year after initiation of pembrolizumab, far beyond the typical window of onset. Clinicians should maintain a high index of suspicion for irAEs even in late stages of immunotherapy, particularly when common etiologies are excluded. Prompt recognition and corticosteroid treatment can lead to favorable outcomes, even in older patients.
Background
Immune checkpoint inhibitors, including pembrolizumab, are associated with a spectrum of immune-related adverse events (irAEs), including immune- mediated hepatitis. Typically, this toxicity manifests within the first 14 weeks of therapy. Delayed presentations beyond one year are exceedingly rare and pose diagnostic challenges.
Case Presentation
We report an elderly patient (over 90 years old) with stage IVa squamous cell carcinoma of the lung and high microsatellite instability (MSI) who had been receiving pembrolizumab since 2023. In 2024—13 months into therapy—he presented with subjective fevers, weakness, and altered mental status. Laboratory evaluation revealed cholestatic jaundice with AST 310 U/L, ALT 291 U/L, alkaline phosphatase 860 U/L, and total bilirubin 5.7 mg/dL. Infectious workup was negative. Imaging via MRCP showed multiple scattered hepatic cysts and a small pancreatic cyst, without biliary obstruction.
Further evaluation, including serologies for hepatitis B and C, CMV, HSV, autoimmune hepatitis panel, iron studies, and ceruloplasmin, was unremarkable except for mildly elevated alpha-1 antitrypsin. Scattered liver cysts were seen on an MRI. The overall findings were most consistent with immune-related hepatitis, as pembrolizumab is known to cause both hepatocellular and cholestatic patterns of liver injury.
The patient was started on high-dose prednisone, resulting in rapid clinical and biochemical improvement. Two weeks post-discharge, liver function tests (LFTs) had markedly improved (bilirubin 1.3, AST 19, ALT 40, ALP 193). Given the severity of transaminitis and hyperbilirubinemia (AST >8x ULN, bilirubin >3x ULN), pembrolizumab was permanently discontinued. LFTs normalized after completion of the steroid taper.
Conclusions
This case highlights a rare instance of delayed immune-related hepatitis occurring over a year after initiation of pembrolizumab, far beyond the typical window of onset. Clinicians should maintain a high index of suspicion for irAEs even in late stages of immunotherapy, particularly when common etiologies are excluded. Prompt recognition and corticosteroid treatment can lead to favorable outcomes, even in older patients.