A Case Report of Under-Recognized Conditions in Pulmonary Embolism: Patent Foramen Ovale and Right Ventricular Thrombus.

Pulmonary embolism (PE) is a potentially life-threatening condition that presents with a spectrum of clinical symptoms ranging from asymptomatic to hemodynamic instability. The early diagnosis in the emergency department is often challenging. Although the association between patent foramen ovale (PFO) and thromboembolic events in patients with PE is well-documented, the significance of the presence of PFO in patients with PE may be underrecognized. In addition, the occurrence of right ventricular thrombus (RVT) in PE is a rare but significant complication with implications for disease management. We report a case of acute-on-chronic PE with concurrent bilateral renal infarction due to a paradoxical embolus, alongside RVT. A 35-year-old male presented at our emergency department with complaints of sudden onset abdominal pain. Bilateral renal infarction was identified on a contrast-enhanced computed tomography (CT). Point-of-care ultrasound showed suggestive findings of PE and RVT. Subsequently, a pulmonary CT angiography confirmed bilateral PE, a PFO, and RVT. The patient was effectively managed with thrombolytic therapy, with extracorporeal membrane oxygenation on standby. This case highlights the need to recognize the diverse clinical manifestations of PE and the importance of considering coexisting PFO and RVT in affected patients. The diagnosis of PE can be complex when symptoms overlap with arterial thrombosis, such as renal infarction secondary to a PFO. In addition, RVT, although uncommon, is a serious complication in patients with PE that may require careful evaluation for thrombolytic or anticoagulant therapy. It is critical to consider the possibility of a PFO in all cases of PE, even in the absence of arterial embolism, and to promptly evaluate for RVT prior to initiating treatment.

QT-Interval Prolongation Associated with Supratherapeutic Guanfacine Concentration: A Case Report.

INTRODUCTION: Guanfacine, an alpha-2 adrenergic agonist, is used to treat attention deficit hyperactivity disorder (ADHD). Although cardiovascular effects including hypotension and bradycardia are common adverse effects of guanfacine, the effect of guanfacine on QT intervals remains unclear. The association between the serum concentration of guanfacine and its toxicity has also not been fully investigated. CASE REPORT: This is a case of a 21-year-old woman with ADHD who developed repeated presyncope 1 day before admission. She was taking 3 mg of extended-release guanfacine and 50 mg of sertraline. On admission, she had bradycardia and hypotension. An electrocardiogram (ECG) showed a QT interval of 0.68 s and a QTcF interval of 0.648 s. The QT intervals were manually measured and corrected by the Fridericia formula (QTcF = QT/RR1/3). Although she denied taking an overdose of guanfacine and other drugs, we suspected guanfacine toxicity. The serum guanfacine concentration was 13.0 ng/mL on admission and decreased to 3.2 ng/mL on day 1 and 0.4 ng/mL on day 2. Changes in QTcF intervals and her vital signs correlated with serum guanfacine concentrations. CONCLUSION: Supratherapeutic serum guanfacine concentrations may induce QT prolongation.

Severe Recurrence of Neuroleptic Malignant Syndrome: Usefulness of Dexmedetomidine for Antipsychotic Withdrawal.

Neuroleptic malignant syndrome (NMS) is a potentially fatal side effect that occurs in patients taking antipsychotics. Patients with NMS are often forced to rechallenge antipsychotic medications to control the underlying psychiatric symptoms. We present a case of severe recurrence of NMS in a patient in whom the administration of antipsychotics was restarted two days after NMS resolution. A 19-year-old man with somatic symptom disorder had been transported for fever, tachycardia, rigidity, and disturbance of consciousness. He was taking atypical antipsychotics with poor medication compliance. A diagnosis of NMS was made, and he was treated with administration of dantrolene sodium and benzodiazepines under tracheal intubation. On day 2, he was extubated. On day 4, his symptoms of NMS improved, but psychiatric symptoms rapidly exacerbated. He and his family strongly insisted on discharge, and we therefore unavoidably restarted the administration of antipsychotics. On day 37, he was retransported, and a diagnosis of recurrence of NMS was made. Blood examination showed marked deterioration of acute kidney injury and disseminated intravascular coagulation compared to those at the first admission. Without the administration of antipsychotics, his psychiatric symptoms were poorly controlled. Administration of dexmedetomidine helped his agitation to be well controlled without antipsychotics for two weeks. Short-term restart of antipsychotic drugs in patients with NMS may result in more severe NMS relapse. Dexmedetomidine may be useful for NMS patients when the administration of antipsychotics cannot be restarted. When antipsychotics are unavoidably rechallenged in patients with NMS, the risk of severe relapse should be taken into consideration, and dexmedetomidine may be used for prolongation of the withdrawal period.

D-dimer measurement is useful irrespective of time from the onset of acute aortic syndrome symptoms.

BACKGROUND: In acute aortic syndrome (AAS) screening, D-dimer is a well-established biomarker whose usefulness has been scarcely studied with respect to its measurement timing. We aimed to evaluate the effectiveness of D-dimer-based AAS screening focused on the time interval between AAS onset and D-dimer measurement. METHODS: We retrospectively analyzed consecutive patients diagnosed with AAS who visited our hospital between 2011 and 2021. For the primary analysis, we divided patients according to the quartiles of the time interval between AAS symptom onset and D-dimer measurement. D-dimer level ≥ 0.5 µg/mL and age-adjusted D-dimer ≥ [age (years) × 0.01] µg/mL (minimum of 0.5 µg/mL) were defined as positive. The primary endpoint was the comparative ability of D-dimer to detect AAS within and between each time quartile. In an exploratory secondary analysis, we reported patient and AAS characteristics in the subgroup of patients who underwent repeat D-dimer measurement within 48 h of the first D-dimer measure. RESULTS: The 273 AAS patients were divided into four groups based on quartiles of the time interval (Group 1, ≤1 h; Group 2, 1-2 h; Group 3, 2-5 h; and Group 4, >5 h). There were no significant differences in D-dimer levels or in the proportions with positive D-dimer (Group 1: 97%, Group 2: 96%, Group 3: 99%, Group 4: 99%; P = 0.76) or positive age-adjusted D-dimer (Group 1: 96%, Group 2: 90%, Group 3: 96%, Group 4: 97%; P = 0.32) between the groups. Of the 147 patients who had D-dimer re-measured, nine had negative D-dimer levels on either the primary or secondary measurement. Of these nine patients, eight had AAS with a thrombosed false lumen and one with a patent false lumen had a short length of dissection. In all nine patients, D-dimer levels remained low (maximum of 1.4 µg/mL). CONCLUSION: D-dimer levels were elevated from the early stages of AAS. The clinical utility of D-dimer is not affected by the time interval from AAS onset to D-dimer measurement, but rather is influenced by AAS characteristics.

Unexpectedly Prolonged Serotonin Syndrome and Fatal Complications Following a Massive Overdose of Paroxetine Controlled-Release.

Symptoms caused by a selective serotonin reuptake inhibitor (SSRI) overdose are often mild and can be managed with supportive care and close monitoring, even when complicated by serotonin syndrome. There are limited pharmacokinetic data regarding massive overdoses of paroxetine, and the severity of an SSRI overdose is likely to be underestimated. We describe a fatal case of severe serotonin syndrome and acute respiratory distress syndrome (ARDS) following an overdose of controlled-release paroxetine. A 53-year-old male with depression presented with altered consciousness. He had ingested controlled-release paroxetine along with other medications. On arrival, he had ocular flutter and myoclonus, and blood examinations revealed acute kidney injury and rhabdomyolysis, which suggested serotonin syndrome. Computed tomography (CT) showed pharmacobezoars in the esophagus and stomach. Symptoms of serotonin syndrome and hypotension persisted despite administration of high doses of vasopressors with endotracheal intubation. We performed endoscopic decontamination to remove pharmacobezoars from the stomach. Finally, he developed severe ARDS and died due to respiratory failure on day 23. Sequential serum concentrations of paroxetine were 5.38 µg/mL at admission and 3.21 µg/mL on day 7, both above lethal levels. This case highlights the potential for fatal complications and prolonged toxicity in the case of a massive overdose of controlled-release paroxetine. We should recognize that such an overdose may be life-threatening and should consider aggressive interventions including endoscopic decontamination. A better understanding of the pharmacokinetics of a massive SSRI overdose would be helpful for optimal management.

Potential of unenhanced computed tomography as a screening tool for acute aortic syndromes.

AIMS: Contrast-enhanced computed tomography (CE-CT) is the gold standard for diagnosing acute aortic syndromes (AAS). Unenhanced computed tomography (unenhanced-CT) also provides specific findings for AAS; however, its diagnostic ability is not well discussed. This study aims to evaluate the potential of unenhanced-CT as an AAS screening tool. METHODS AND RESULTS: We retrospectively examined AAS patients who visited our hospital between 2011 and 2021 to validate the diagnostic value of unenhanced-CT alone and along with the aortic dissection detection risk score (ADD-RS) plus D-dimer. Acute aortic syndrome was assessed as detectable using unenhanced-CT with any of the following findings: pericardial haemorrhage, high-attenuation haematoma, and displacement of intimal calcification or a flap. Of the 316 AAS cases, 292 (92%) were detectable with unenhanced-CT. Twenty-four (8%) cases undetectable with unenhanced-CT involved younger patients [median (interquartile range), 45 (42-51) years vs. 72 (63-80) years, P < 0.001] and patients more frequently complicated with a patent false lumen (79% vs. 42%, P < 0.001). Acute aortic syndrome-detection rate with unenhanced-CT increased with age, reaching 98% (276/282) in those ≥50 years of age and 100% (121/121) in those ≥75 years of age. With the ADD-RS plus D-dimer, there was only one AAS case undetectable with unenhanced-CT among patients ≥50 years of age, except for cases with the ADD-RS ≥1 plus D-dimer levels of ≥0.5 µg/mL. CONCLUSION: Acute aortic syndromes in younger patients and patients with a patent false lumen could be misdiagnosed with unenhanced-CT alone. The combination of the ADD-RS plus D-dimer and unenhanced-CT could minimize AAS misdiagnosis while avoiding over-testing with CE-CT.