Under-Recognized Life-Threatening Vasovagal Reflex During Chest Tube Insertion.

Chest tube insertion is a common and relatively safe procedure in an emergency setting. However, a potentially fatal complication, vasovagal reflex, may be under-recognized due to its generally mild severity. We present a case of pulseless electrical activity (PEA) requiring chest compression due to vasovagal reflex during chest tube insertion for spontaneous pneumothorax. A 23-year-old male who had a history of spontaneous pneumothorax presented with left chest pain to our emergency department. Based on point-of-care ultrasonography and chest radiography, we made a diagnosis of recurrent pneumothorax. Although he had stable vital signs and received adequate pain control, during chest tube insertion, he developed severe sinus bradycardia with a six-second pause, leading to PEA requiring chest compressions. After a few compressions, his heart rate increased and he regained consciousness. He underwent video-assisted thoracoscopic surgery for pneumothorax and was discharged without complications. Vasovagal reflex during chest tube insertion in young patients with spontaneous pneumothorax may cause severe bradycardia and cardiac arrest. Physicians should be aware of this rare but potentially fatal complication and be prepared with appropriate measures, such as pre-administration of atropine, before chest tube insertion.

Giant T waves and QT interval prolongation associated with guanfacine toxicity.

INTRODUCTION: Guanfacine is a central α2-adrenergic receptor agonist that produces drowsiness, bradycardia, hypotension, and occasionally QT interval prolongation. We discuss giant T waves associated with guanfacine toxicity. CASE SUMMARIES: Three patients presented to the hospital with histories and physical findings compatible with guanfacine toxicity. Supratherapeutic concentrations were confirmed in two of them. All three developed QT interval prolongation and giant T waves on the electrocardiogram. Giant T waves occur commonly in patients with acute myocardial infarct and hyperkalemia, as well as rarely with a number of other cardiac and non-cardiac causes. CONCLUSION: Guanfacine toxicity may cause the novel electrocardiographic finding of 'giant T wave with QT interval prolongation'. Further studies are warranted to investigate the association between the novel electrocardiographic finding and guanfacine toxicity, as well as its diagnostic utility in such cases.

Acute Abdominal Pain Without Gross Hematuria as an Atypical Initial Presentation of Renal Arteriovenous Malformation.

Congenital renal arteriovenous malformations (AVMs) occasionally manifest with recurrent gross hematuria, typically in young populations. Acute abdominal pain without previous episodes of gross hematuria in young women is frequently considered a diagnosis related to obstetric and gynecological conditions or acute appendicitis, excluding the possibility of clot retention, which is more commonly associated with the elderly. A 36-year-old woman with no history of gross hematuria presented with acute lower abdominal pain. Adnexal torsion was initially considered based on her symptoms and ultrasonography findings. However, contrast-enhanced computed tomography (CT) revealed clot retention and delayed contrast excretion in the right kidney. After bladder irrigation, she returned complaining of right flank pain. Subsequent plain CT revealed contrast pooling in the right kidney and hydronephrosis. In addition to these findings, small vessels in the right renal hilum were found to be prominent in the arterial phase on the first contrast-enhanced CT. Finally, angiography of renal arteries confirmed the diagnosis of a congenital cirsoid-type renal AVM, which was successfully treated with ethanol embolization. This case highlights the importance of understanding an atypical presentation of renal AVMs, which is acute abdominal pain, even in the absence of prior gross hematuria and the characteristic CT findings. Early diagnosis of renal AVMs is crucial for preventing potentially serious complications, including repeated clot retention and life-threatening rupture. The diverse clinical manifestations and images of renal AVMs should be recognized to facilitate prompt and accurate diagnosis.

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.

Collapse-related traumatic intracranial hemorrhage following out-of-hospital cardiac arrest: A multicenter retrospective cohort study.

Background: Sudden loss of consciousness as a result of cardiac arrest can cause severe traumatic head injury. Collapse-related traumatic intracranial hemorrhage (CRTIH) following out-of-hospital cardiac arrest (OHCA) may be linked to poor neurological outcomes; however, there is a paucity of data on this entity. This study aimed to investigate the frequency, characteristics, and outcomes of CRTIH following OHCA. Methods: Adult patients treated post-OHCA at 5 intensive care units who had head computed tomography (CT) scans were included in the study. CRTIH following OHCA was defined as a traumatic intracranial injury from collapse due to sudden loss of consciousness associated with OHCA. Patients with and without CRTIH were compared. The primary outcome assessed was the frequency of CRTIH following OHCA. Additionally, the clinical features, management, and consequences of CRTIH were analyzed descriptively. Results: CRTIH following OHCA was observed in 8 of 345 enrolled patients (2.3%). CRTIH was more frequent after collapse outside the home, from a standing position, or due to cardiac arrest with a cardiac etiology. Intracranial hematoma expansion on follow up CT was seen in 2 patients; both received anticoagulant therapy, and one required surgical evacuation. Three patients (37.5%) with CRTIH had favorable neurological outcomes 28 days after collapse. Conclusions: Despite its rare occurrence, physicians should pay special attention to CRTIH following OHCA during the post-resuscitation care period. Larger prospective studies are warranted to provide a more explicit picture of this clinical condition.

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.

CT chest-cerebral angiography for basilar artery occlusion caused by pulmonary arteriovenous malformation.

Early diagnosis of basilar artery occlusion (BAO) based only on clinical findings is challenging. We present a fully recovered case of BAO caused by pulmonary arteriovenous malformation (PAVM) that was diagnosed early using a protocol for CT angiography (CTA) and promptly treated with endovascular therapy (EVT). A woman in her 50s complained of vertigo with normal level of consciousness (LOC). On arrival, her LOC decreased to a Grass Coma Scale score of 12, and we performed a CT chest-cerebral angiography protocol. Head CTA showed BAO, and an intravenous tissue plasminogen activator was administered, followed by EVT. Chest contrast-enhanced CT showed PAVM in segment 10 of the left lung, which was treated with coil embolisation. For patients with a complaint of vertigo, BAO should be suspected, even if they have an initially normal LOC. A CT chest-cerebral angiography protocol is useful for prompt diagnosis and treatment of BAO and can reveal undetermined causes.

Unusual cause of retroperitoneal hemorrhage: Acute deep vein thrombosis.

Retroperitoneal hemorrhage is rarely associated with acute deep vein thrombosis (DVT). We present a case of retroperitoneal hemorrhage due to disruption of the external iliac vein associated with acute DVT, which was carefully treated with an anticoagulant. A 78-year-old woman complained of acute abdominal pain. Contrast-enhanced computed tomography (CT) showed left retroperitoneal hematoma and venous thrombosis from just above the bifurcation of the inferior vena cava to the left femoral vein. She was admitted for conservative treatment without an anticoagulant. The next day, she developed pulmonary embolism (PE), but administration of an anticoagulant was not started because of the possibility of rebleeding. Forty-four hours after the onset of PE, unfractionated heparin was administrated intravenously. After initiation of anticoagulation, retroperitoneal hemorrhage did not expand and PE did not get worse. Follow-up contrast-enhanced CT suggested May-Thurner syndrome (MTS). She was uneventfully discharged home on the 35th day with oral warfarin. Retroperitoneal hemorrhage is rarely caused by acute DVT in the case of potential causes such as MTS. In such cases, the timing of initiation of anticoagulation is difficult considering the possibility of rebleeding from retroperitoneal hemorrhage. We should start anticoagulation based on both the state of hemostatic and preventive procedures for PE. Learning objective: Retroperitoneal hemorrhage is rarely caused by acute deep vein thrombosis because of the iliac vein rupture. The subsequent occurrence of pulmonary embolism (PE) makes it more complicated and critical because treatment strategies for these two conditions are the opposite: hemostasis versus anticoagulation. The initiation of administration of an anticoagulant should be determined based on status of patients, the procedures of hemostasis, and prevention of PE.

Understanding the Trajectory to a Diagnosis of Tetanus: A Descriptive Study.

Background and objective Tetanus is a rare but potentially fatal disease in developed countries, including Japan. It is very difficult to diagnose this condition early because of its broad symptomatology and the lack of familiarity with tetanus among both physicians and patients. In this study, we aimed to describe the clinical manifestations of tetanus and to examine as to which departments/branches of medicine patients consult in order to provide helpful information for diagnosing this challenging condition. Materials and methods This was a descriptive, retrospective study conducted at a single tertiary hospital from January 2011 to December 2021. Patients with generalized tetanus, cephalic tetanus, and local tetanus presenting to our emergency department were included in the study. We examined the clinical manifestations and departments that patients with tetanus visited first. Additionally, the initial diagnosis and diagnostic evaluation before the diagnosis were examined. Results Of the total 10 patients included in the study, nine had generalized tetanus and one had cephalic tetanus; the common initial manifestations were neck stiffness (30%), dysarthria (20%), and trismus (20%). Of note, 80% of patients also complained of dysphagia before the diagnosis. Patients first visited various departments, including a dental clinic (30%) and the department of otorhinolaryngology (20%). Only two patients were accurately diagnosed with tetanus at the first department they visited. Physicians performed head imaging for all the patients. Conclusions Based on our findings, in Japan, patients with tetanus present with symptoms that physicians interpret or suspect to be associated with disorders of the central nervous system. Meanwhile, patients themselves tend to consider the symptoms as indicative of oral or dental issues. Further prospective studies involving a larger number of participants are needed to investigate the clinical course of tetanus until the establishment of a diagnosis.

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.

Blood cultures should be collected for acute cholangitis regardless of severity.

BACKGROUND: Despite the high frequency of bacteremia in acute cholangitis, the indications for blood cultures and the relationship between the incidence of bacteremia and severity of acute cholangitis have not been well established. This study examined the association between the 2018 Tokyo Guidelines (TG18) severity grading for acute cholangitis and incidence of bacteremia to identify the need for blood cultures among patients with acute cholangitis in each severity grade. METHODS: Patients with acute cholangitis who visited our emergency department between 2019 and 2020 were retrospectively investigated. Patients administered antibiotics within 48 h of hospital arrival, whose prothrombin time-international normalized ratios were not measured, or who were suspected of false bacteremia were excluded. RESULTS: Out of the included 358 patients with acute cholangitis, blood cultures were collected from 310 (87%) patients, of which 148 (48%) were complicated with bacteremia. As the TG18 severity grading increased, the frequency of bacteremia increased (Grade I, 35% [59/171]; Grade II, 59% [48/82]; Grade III, 74% [42/57]; P <0.001). Agreement with the TG18 diagnostic criteria (unfulfilled, suspected, or definite) was not different between patients with and without bacteremia; however, 36% (14/39) of the patients with "unfulfilled" criteria were complicated with bacteremia. CONCLUSIONS: As the severity of acute cholangitis increased, the frequency of bacteremia increased; however, the incidence of bacteremia was high even in mild cases and cases that did not meet the TG18 diagnostic criteria. Blood cultures should be collected regardless of the severity of acute cholangitis for patients who visit the emergency department.

Potential Fatal Complication of Neurofibromatosis Type 1: Acute Upper Airway Obstruction Due to Ruptured Transverse Cervical Artery Aneurysm.

Neurofibromatosis type 1 (NF1) can cause vascular complications even in undiagnosed NF1 patients. A ruptured aneurysm of the branches of the subclavian artery is a rare but life-threatening event, and the hemorrhage can cause upper airway obstruction. We present a case of NF1 patient with a ruptured transverse cervical artery aneurysm, which led to a nearly obstructed airway. A 52-year-old man who was not previously diagnosed with NF1 presented with sudden pain from the left shoulder to the neck. Since childhood, he has had multiple cutaneous neurofibromas and café-au-lait macules, and freckling in the bilateral axillae. His swollen left side of the neck and left shoulder suggested a hematoma, which compressed the upper airway. Contrast-enhanced computed tomography revealed a cervical hematoma caused by a ruptured aneurysm of the transverse cervical artery. We performed awake fiberoptic intubation because a difficult airway was predicted and surgical airway management may have been impossible due to the anterior cervical hematoma. His airway was secured, and his aneurysm was successfully treated by coil embolization. Based on his cutaneous findings, he was finally diagnosed with NF1. Those who have café-au-lait macules and cutaneous neurofibromas may present with acute cervical hematoma, and it is important to consider the possibility of ruptured aneurysms in the neck region. When patients develop an acute cervical hematoma that causes an acute upper airway obstruction, emergency physicians should consider awake fiberoptic intubation to secure the airway.