Caffeine consumption among children and adolescents has increased in recent years, largely through energy drinks. While caffeine is generally considerd as safe in low doses, current evidence suggests that high intake may provoke arrhythmias and electrocardiographic abnormalities in younger populations. This systematic review evaluates the arrhythmogenic effects of caffeine consumption in pediatric and adolescent patients. This review followed PRISMA 2020 guidelines and was registered in PROSPERO (ID 1180917). A systematic search of PubMed, EMBASE, and Cochrane CENTRAL identified studies evaluating caffeine-related arrhythmias in individuals under 19 years of age. Eligible publications included peer-reviewed studies, case reports, and case series reporting arrhythmogenic or electrocardiographic outcomes. Screening and data extraction were performed independently by two reviewers using Covidence. The search yielded 126 articles, of which 12 met the inclusion criteria. These comprised 9 case reports, 1 prospective study, 1 retrospective study, and 1 review including an unpublished case report. Across all eligible studies, a total of 39 adolescents (aged 13-18 years) were reported to have caffeine associated arrhythmias or ECG changes. Caffeine sources included energy drinks, caffeine containing tablets and powdered caffeine. Reported cardiac side effects ranged from sinus tachycardia and premature atrial or ventricular contractions to supraventricular tachycardia, ventricular tachycardia, QTc prolongation and ST-segment abnormalities. This systematic review demonstrates that high dose caffeine from sources like energy drinks, powders and tablets can induce a range of cardiac arrhythmias and electrophysiological abnormalities. Our findings underscore the need for increased awareness and improved public health education regarding the cardiovascular danger of high-dose caffeine in this population.

This is a case report of neonatal cholestasis caused by Graves' disease, accompanied by a literature review of previously published cases. Neonatal/Infantile cholestasis (NIC) is defined as an impairment in bile formation and/or flow presenting by the first year of age, typically within the first three months. Hyperthyroidism has been less frequently associated with this condition. Here, we report a case of neonatal cholestasis caused by Graves' disease and review relevant literature to summarize its clinical characteristics, and to enhance prompt and accurate recognition and diagnosis of this disease. A 28-day-old female infant was admitted to our center, presenting with jaundice, diarrhea, poor weight gain, and tachycardia. Laboratory examinations showed cholestasis, hyperthyroidism, and positive for thyrotropin receptor antibody (TRAb), confirming the diagnosis of neonatal Graves' disease. After treatment with propranolol and intravenous immunoglobulin (IVIG), the jaundice subsided, and thyroid function returned to normal. Neonatal Graves' disease must be included in the differential diagnosis of cholestasis, particularly in infants whose mothers have Graves' disease or a history of thyroid dysfunction. Early detection of hyperthyroidism in neonates with cholestasis is crucial.

Sinus tachycardia is common after heart transplantation (HTx) and may worsen graft function via increased oxygen demand and remodeling. Ivabradine, a selective If channel inhibitor, lowers heart rate independently of sympathetic activity. This meta-analysis evaluates its efficacy and safety versus standard care in HTx recipients. A comprehensive search of PubMed, Embase, WoS, Scopus, and Cochrane was conducted through September 2025. Eligible studies included randomized and non-randomized comparative trials. Data were pooled with a random-effects model to estimate mean differences (MD) for continuous outcomes and risk ratios (RR) for dichotomous outcomes. Six studies, including 852 adult HTx recipients, were included. Ivabradine consistently reduced HR across all time points. Statistical significance was reached at 24 months (MD -16.82 bpm; P=0.04) and 36 months (MD -12.94 bpm; P=0.04). A significant reduction was observed in LVMI (MD -11.10 g/m2; 95% CI -17.15 to -5.06; P<0.05; I^2=0%). While LVM and LVEF showed trends toward improvement at final follow-up (MD = -11.23 for LVM and +2.94% for LVEF), neither reached statistical significance (P = 0.06 and P = 0.48, respectively). No significant differences were found between the ivabradine and control groups regarding all-cause mortality (RR 1.16 at final follow-up; P=0.90), graft rejection (RR 1.14; P=0.87), or systolic blood pressure (MD 0.50 mmHg; P=0.83). Ivabradine lowers heart rate after heart transplantation but shows no clear benefit on mortality, rejection, or ejection fraction. It does not significantly affect blood pressure, supporting its tolerability, particularly when beta-blockers are not tolerated.

Spinal cord stimulation (SCS) is an effective therapeutic option for refractory neuropathic pain, but infectious complications, particularly epidural abscess, are rare and carry high morbidity. Evidence describing the inpatient rehabilitation course following urgent surgical decompression in patients with radiographic cord compression but largely preserved neurologic function remains limited, and standardized functional outcomes are seldom reported. We present the case of an 84-year-old woman with severe dextroscoliosis, kyphosis, and chronic axial back pain who underwent an outpatient SCS trial. Five days later, on the day of lead removal, she presented with fever (maximum temperature 38.5 °C), tachycardia, leukocytosis (white blood cell count 11.58 K/μL), markedly elevated inflammatory markers (C-reactive protein 312 mg/L on repeat testing after an initial erroneously high reading, procalcitonin 10.11 ng/mL, and erythrocyte sedimentation rate 63 mm/hr), and urinary retention. Thoracic MRI demonstrated a dorsal-predominant epidural collection from T8-T12 with cord compression and adjacent paraspinal cellulitis. She underwent urgent T8-T12 decompressive laminectomies and was treated for methicillin-resistant Staphylococcus aureus bacteremia with daptomycin. Following acute care, she completed a 23-day inpatient rehabilitation admission. Functional progress was tracked with the seven-point functional independence measure (FIM). The FIM motor sub-score improved from 47 on admission to 68 on discharge (a 21-point gain). Pain, monitored with the Numeric Rating Scale (NRS), decreased from 6/10 on admission to 2/10 on discharge with a multimodal analgesic regimen. By discharge, she ambulated 300 feet independently without an assistive device and was modified independent on 12 steps. This case suggests that inpatient rehabilitation may be safely delivered to selected older adults with radiographically severe but clinically preserved post-SCS epidural abscess. It also supports the routine reporting of FIM-based outcomes in this rare scenario.

Uterine carcinosarcoma (UCS), also known as malignant mixed Müllerian tumor (MMMT), is a biphasic neoplasm characterized by the presence of carcinomatous (epithelial) and sarcomatous (stromal tissue) elements. It frequently presents at an advanced stage and can mimic primary ovarian carcinoma on clinical and radiological evaluation, particularly when diagnosed after hysterectomy for presumed benign disease. To our knowledge, this represents one of the few reported cases of metastatic UCS from Sub-Saharan Africa. We report a case of advanced UCS in a 59-year-old postmenopausal woman who presented to a tertiary referral center in Northern Tanzania with a 6-month history of gradual-onset, progressive abdominal pain and distension. Physical examination revealed pallor, tachycardia, bilateral lower limb edema, and a large, irregular abdominopelvic mass. Contrast-enhanced CT scan demonstrated a massive heterogeneously enhancing abdominopelvic mass (24 × 22 × 12 cm) with central necrosis, diffuse peritoneal carcinomatosis, omental caking, and diaphragmatic deposits. Findings were also notable for hepatic surface scalloping, multiple liver lesions, bulky necrotic retroperitoneal lymphadenopathy, moderate ascites, and innumerable bilateral pulmonary nodules, suggestive of advanced ovarian malignancy with widespread metastases. Histopathological review of the archived hysterectomy specimen and an umbilical wedge biopsy revealed a biphasic tumor with atypical glandular (carcinomatous) and spindle cell (sarcomatous) components, including frequent mitoses and necrosis. Immunohistochemistry (IHC) showed cytokeratin positivity in tumor cells within the carcinomatous component and desmin positivity in the sarcomatous component. Based on clinicopathological correlation, the diagnosis was confirmed as UCS, FIGO stage IVB. A multidisciplinary tumor board recommended neoadjuvant carboplatin and paclitaxel chemotherapy followed by interval cytoreductive surgery. Before treatment initiation, she developed progressive bilateral lower limb swelling suggestive of deep vein thrombosis. Empirical anticoagulation with unfractionated heparin was started. However, she suddenly deteriorated after an assisted fall, with loss of consciousness and respiratory distress. The presumed cause of death was highly suggestive of massive pulmonary embolism, although confirmatory imaging or postmortem examination was not available secondary to cancer-associated venous thromboembolism (VTE), occurring in the setting of advanced stage IV uterine carcinosarcoma with extensive peritoneal, hepatic, and pulmonary metastases.

Although Brugada syndrome has traditionally been considered a primary electrical disease, accumulating evidence supports the presence of subtle structural abnormalities, particularly involving the right ventricular outflow tract. Nevertheless, the identification of overt myocardial scar and biventricular arrhythmogenic substrate should prompt consideration of an alternative diagnosis. We report the case of a 51-year-old man presenting with syncope during a febrile illness and a transient spontaneous type-1 Brugada ECG pattern. Initial evaluation was unremarkable. However, Holter monitoring revealed multifocal ventricular ectopy, including non-sustained ventricular tachycardia (NSVT) with both left and right bundle branch block morphologies, suggesting biventricular origin. Cardiac magnetic resonance showed a non-ischemic subepicardial scar, and electroanatomical mapping identified additional right ventricular abnormalities. Programmed stimulation induced sustained ventricular arrhythmias. These findings supported the presence of an underlying biventricular structural scar cardiomyopathy presenting with a fever-induced type-1 Brugada ECG pattern. The patient underwent transvenous ICD implantation. This case highlights the importance of a comprehensive multimodal diagnostic approach.