Case Report: An Unusual Cause for Recurrent Hemopericardium in a Patient With Dyspnea.
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SUBMITTER: Nguyen UC
PROVIDER: S-EPMC8634327 | biostudies-literature |
REPOSITORIES: biostudies-literature
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Project description:Introduction Portal hypertension is a rare complication of liver metastases. The study highlights that clinician should be aware of conditions mimicking cirrhosis with similar clinical presentation and imaging findings. Case presentation We present the case of a 29-year-old non-alcoholic lady who presented to our hospital with a history of two months of progressive, painless abdominal distension and progressively increasing yellowish discoloration of the eyes. Physical examination, laboratory investigations, and imaging tests led to a diagnosis of multiple metastases from breast carcinoma to the liver leading to portal hypertension after exclusion of other causes of portal hypertension. However, after three weeks of presentation to the hospital, the patient died before any therapeutic measures were initiated to address breast carcinoma. Clinical discussion Liver metastasis from primary breast carcinoma rarely presents with clinical symptoms of portal hypertension. Although portal hypertension secondary to pseudocirrhosis, predominantly linked to ongoing chemotherapy for known cancers, has been previously described in case studies, our case had an unusual presentation leading to diagnostic uncertainty. Conclusion Our case highlights the rare cause of liver metastasis secondary to breast carcinoma, which presented as portal hypertension. Highlights • Portal hypertension is a rare complication of liver metastases, frequently occurring in malignant diseases.• In patients with liver metastases, chemotherapy can result in areas of retracted tumor tissue and scarring, also known as pseudocirrhosis.• Although portal hypertension is secondary to pseudocirrhosis and predominantly linked to ongoing chemotherapy for known cancers, our case had an unusual presentation leading to diagnostic uncertainty.• The patient has an atypical presentation with symptoms consistent with portal hypertension and chronic liver disease without prior exposure to chemotherapy which could be due to the tumor deposits resulting in sinusoidal obstruction, subsequently leading to portal hypertension.
| S-EPMC9793164 | biostudies-literature
Project description:A 59-year-old woman with a history of a pacemaker implanted for III-degree atrioventricular block was admitted due to pocket infection. The atrial and ventricular leads were removed via the right femoral vein using a needle's eye snare. Hypoxemia was observed immediately after the removal of the lead. It was refractory to oxygen therapy. The pulse oxygen saturation (SpO2) showed 89% in the supine position and 77% in the upright position. However, the CTPA and pulmonary perfusion SPECT/CT imaging did not reveal any signs of pulmonary embolism. Pulmonary function tests and chest CT showed normal results. Transthoracic contrast echocardiography revealed a patent foramen ovale (PFO) and a right-to-left intracardiac shunt, no significant tricuspid regurgitation, without any signs of elevated right heart pressure or pulmonary hypertension. Hypoxemia was considered to be associated with the right-to-left shunt through PFO. The condition was relieved by percutaneous closure of the PFO. Refractory hypoxemia resulting from an intracardiac right-to-left shunt following pacemaker lead extraction is a rare but serious complication. Transthoracic contrast echocardiography helps in diagnosis. If the right-to-left intracardiac shunt through PFO persists irreversibly and the associated hypoxemic symptoms are significant, closure of the PFO is necessary. Transesophageal echocardiography also revealed the presence of a left-to-right shunt through PFO during cardiac systole. The closure of the PFO is also necessary to avoid long-term complications, such as chronic pulmonary hypertension and right heart failure.
| S-EPMC10461397 | biostudies-literature
Project description: Not available
| S-EPMC10689292 | biostudies-literature
Project description:BackgroundHaemothoraces are a reported but extremely rare complication of pacemaker implantation. Haemothoraces can be a consequence of lead perforation through the right ventricle (RV) and pericardium into the pleural space, direct lung or vascular injury during access.Case summaryA 72-year-old woman presented 24 h after a pacemaker implantation with chest pain and shortness of breath. Computed tomography of the chest confirmed perforation of the RV lead into the left pleural cavity with a large left sided haemothorax. Following percutaneous drainage of the left sided haemothorax, the patient became haemodynamically unstable necessitating emergent sternotomy. During surgery, the extra-cardiac portion of the pacing lead was cut, the RV repaired and a large haematoma evacuated from the left pleural space. Despite this, the patient remained hypotensive, and further exploration showed a bleeding intercostal artery that had been lacerated by the pacing lead. This was treated by electrocautery, and the patient's haemodynamic status improved. The RV lead remnant was removed transvenously via the subclavian vein, and the patient was left with a single chamber atrial pacemaker.DiscussionPrompt recognition of RV lead perforation and its associated sequalae, often utilising multi-modality imaging, is vital to enable transfer to a centre with cardiac surgical expertise. In this case, the perforating RV lead lacerated an intercostal artery, and this was only identified at the time of surgery. In order to minimize the risk of perforation, multiple fluoroscopic views should be used, and care should be taken during helix deployment.
| S-EPMC9113347 | biostudies-literature
Project description:A 55-year-old former professional athlete reported out of proportion dyspnea on exertion. After a detailed cardiac investigation, a cardiopulmonary exercise test on an ergocycle demonstrated an abnormal and non-physiological ventilatory response characterized by a sharp rise in ventilation followed by a decrease while exercise workload was progressively increasing. This was accompanied by noisy breathing. A laryngoscopy with direct visualisation of larynx and vocal cord during voluntary eucapnic hyperventilation confirmed the diagnosis of exercise-induced laryngeal obstruction. The patient was treated with speech therapy and all the symptoms resolved. A second cardiopulmonary exercise test showed a normalisation of the ventilatory pattern during exercise. This case demonstrates the importance of recognizing the symptoms of an exercise-induced laryngeal obstruction regardless of age, and the effectiveness of the speech therapy on symptoms and on exercise testing.
| S-EPMC6997562 | biostudies-literature
Project description:BackgroundThe use and utility of novel oral anticoagulants has been increasing in clinical practice due to their relatively lower incidence of side effects such as intracranial haemorrhage, particularly in the elderly, when compared with vitamin K antagonists. Rivaroxaban is a factor Xa and prothrombinase inhibitor indicated for stroke and venous thromboembolism prophylaxis in non-valvular atrial fibrillation as well as treatment of venous thromboembolism.Case summaryA patient with history of paroxysmal atrial fibrillation on Rivaroxaban presented with generalized malaise, lightheadedness, and dizziness. The patient was found to be in profound cardiogenic shock despite unremarkable cardiac enzymes. Electrocardiogram revealed rate controlled atrial fibrillation and T-wave inversions in the inferolateral leads without associated electrical alternans. Bedside echocardiogram revealed a large pericardial effusion consistent with cardiac tamponade physiology. Following anticoagulation reversal, the patient underwent urgent pericardiocentesis yielding haemorrhagic fluid, with subsequent improvement in haemodynamic status. Despite the presence of retroperitoneal lymphadenopathy on previous computed tomography of the abdomen and concern for underlying malignant effusion secondary to lymphoma, cytology of the fluid revealed no evidence of malignant cells and follow-up flow cytometry and bone marrow biopsy were unremarkable.DiscussionWhile hemopericardium is not listed as a known side effect of Rivaroxaban, previous cases of hemopericardium secondary to Rivaroxaban have been described in the literature secondary to pre-disposing risk factors including CYP450 drug interactions or cardiac device implantations. In this case, the patient experienced a spontaneous hemopericardium on Rivaroxaban without any previously elucidated risk factors or evidence of malignancy.
| S-EPMC7898561 | biostudies-literature
Project description:Abstract Background Remote monitoring has emerged as a complement to in-person care for patient with cardiac implantable electronic devices (CIEDs). It provides the care team with information about device integrity, programming issues, or other medical data (i.e. arrhythmias) and since 2015 has been recognized as a part of standard management by the Heart and Rhythm Society for all patients with CIEDs. However, while it can provide invaluable information to providers, the volume of generated data can increase the risk of oversight. We present a novel case of apparent device malfunction that on closer scrutiny was obvious, but provides a lesson in the mechanisms by which data can be artifactual. Case summary A 62-year-old male presented after his cardiac resynchronization therapy-defibrillator (CRT-D) alerted him that his device was at an elective replacement interval (ERI). He underwent an uncomplicated generator exchange; however, 2 weeks later, a remote alert showed that his device was at ERI and all impedances were above the upper limit. Device interrogation the following day demonstrated that the new device was functioning appropriately and his home monitor had in fact paired with his old generator. He obtained a new home monitor, and subsequent remote transmissions have demonstrated that his device is functioning appropriately. Discussion This case demonstrates the importance of careful review of details from home-monitoring data. While concerning for device malfunction, there could be alternative causes when alerts are generated by remote monitoring. To our knowledge, this is the first report of this mechanism of alert via a home-monitoring device and should be considered when reviewing unusual remote download data.
| S-EPMC10127937 | biostudies-literature
Project description:BackgroundAtrial dissociation (AD) is described as the existence of two simultaneous electrically isolated atrial rhythms. Theoretically, detection of dual atrial rhythms with a sufficiently high rate by pacemaker can lead to automatic mode switching and associated pacemaker syndrome. Such a clinical observation has not been reported before in the literature.Case summaryAn 87-year-old female with Ebstein's anomaly status post-tricuspid valve annuloplasty and tricuspid valve replacement and a dual-chamber pacemaker presented with congestive heart failure 1 week after undergoing atrial lead revision. Interrogation of her dual-chamber pacemaker revealed two atrial rhythms: sinus or atrial-paced rhythm and electrically isolated atrial tachycardia (AT). Sensing of both atrial rhythms by the pacemaker led to automatic mode switching, which manifested as ventricular paced rhythm with retrograde P waves on electrocardiogram. Adjusting the atrial lead sensitivity to a level higher than the sensing amplitude of AT restored atrial paced and ventricular sensed rhythm, which resulted in resolution of heart failure symptoms.DiscussionRegardless of the cause of AD, there must be electrical insulation between the two rhythms for their independent coexistence in the atria. Atrial dissociation can lead to pacemaker syndrome from automatic mode switching. If the sensing amplitude during sinus rhythm is significantly larger than that of AT, adjusting the atrial lead sensitivity would solve the issue, as in the present case. Otherwise, atrial lead revision, pharmacotherapy, or AT ablation should be considered.
| S-EPMC8765788 | biostudies-literature
Project description:We describe a case of an 88-year-old woman with a severe bluntly ematic pericardial effusion. Radiological and laboratory examinations excluded all the most common causes of hemopericardium, and the diagnosis of spontaneous hemopericardium associated with the treatment with rivaroxaban was made. This is the first case report describing a hemopericardium in a patient treated with rivaroxaban who did not take other herbal products or drugs that may significantly increase rivaroxaban blood levels. This report emphasizes the need for the careful use of new oral anticoagulants, and the importance of taking in mind uncommon side effects. Spontaneous hemopericardium should be considered in these patients.
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Project description:Aminoacyl-tRNA synthetases (ARSs) are enzymes responsible for attaching amino acids to tRNA, which enables protein synthesis. Mutations in isoleucyl-tRNA synthetase (IARS1) have recently been reported to be a genetic cause for growth retardation, intellectual disability, muscular hypotonia, and infantile hepatopathy (GRIDHH). In this study, we reported an additional case of compound heterozygous missense variations c.701 T > C (p.L234P) and c.1555C > T (p.R519C) in IARS1, which were identified using medical exome sequencing; c.701 T > C (p.L234P) was a novel variant, and c.1555C > T (p.R519C) was found in GnomAD. Unlike other reported patients, this individual presented prominently with recurrent liver failure, which led to her death at an early age of 19 months. She also had significant growth retardation, muscular hypotonia, chubby and flabby face, recurrent loose stools, and abnormal brain computed tomography (CT), while zinc deficiency and hearing loss were not present. Studies in zebrafish embryo modeling recapitulated some of the key phenotypic traits in embryo development, neurodevelopment, liver development, and myogenesis, demonstrating that these variations caused a loss of gene function in IARS1. We have found a novel mutation point c.701 T > C (p.L234P) in IARS1. Compound heterozygous mutations of c.701 T > C (p.L234P) and c.1555C > T (p.R519C) in IARS1 are pathogenic, which can cause GRIDHH in child.
| S-EPMC9172121 | biostudies-literature