Annals of Medicine and Surgery最新文献

Introduction and importance: Lithopedion (Greek for "stone baby") is an extremely rare complication of undiagnosed abdominal pregnancy where a dead fetus becomes calcified and retained for decades. This phenomenon demonstrates both a unique obstetric event and global disparities in prenatal care access.

Case presentation: A 74-year-old post-menopausal woman presented with vague abdominal discomfort. Imaging revealed a calcified mass resembling a fetal skeleton in the pelvic cavity. Her obstetric history indicated a pregnancy several decades earlier with reported intrauterine fetal death that went unmanaged due to limited medical access. Laboratory results were normal. CT imaging confirmed a densely calcified fetal structure adjacent to the uterus without surrounding inflammation. Considering her age and asymptomatic status, conservative management with regular follow-up was chosen. Six months later, she remained stable and free of symptoms. No calcified placenta or adnexal structures were identified, helping rule out alternative differential diagnoses such as calcified fibroids or teratomas.

Clinical discussion: Lithopedion forms when a dead fetus remains sterile and too large to be reabsorbed, prompting the body to encase it in calcium for protection. Most cases remain asymptomatic and are discovered incidentally in older women during imaging. Management must be individualized, balancing surgical risk and patient preference.

Conclusion: This case underlines the importance of early recognition of ectopic pregnancies, the role of imaging in diagnosis, and improved access to obstetric care. This case strongly emphasizes the role of maternal health care access, imaging availability, and timely diagnosis in preventing long-term sequelae such as lithopedion.

Traumatic brain injury (TBI) continues to be a major global cause of morbidity and mortality, with neuroinflammation recognized as a central mechanism influencing both acute and long-term outcomes. Following the initial insult, activation of glial cells, cytokine release, and blood-brain barrier disruption drive a cascade of secondary injury. While these inflammatory processes contribute to debris clearance and neurorepair, excessive or prolonged activation leads to neuronal death and chronic neurodegeneration. Recent international research has focused on modulating these pathways to enhance recovery. In the United States and Germany, trials using stem cell derived exosomes and anti-cytokine biologics have shown neuroprotective potential. In China, novel compounds such as 3-monothiopomalidomide have demonstrated efficacy in reducing microglial activation and improving behavioral outcomes in experimental TBI. Integrating these pharmacological, cellular, and imaging innovations into clinical care could transform TBI management. This letter underscores the need for global collaboration, transparent data use, and biomarker-driven neuroinflammatory modulation to optimize adult brain injury recovery.

Introduction and importance: Dextrocardia with situs solitus is an exceptionally rare congenital anomaly. Its asymptomatic nature may delay diagnosis, highlighting the need for careful prenatal and postnatal evaluation.

Case presentation: A full-term female neonate was found to have isolated dextrocardia with situs solitus following prenatal suspicion. Postnatal chest X-ray and echocardiography confirmed dextroversion with normal cardiac anatomy and function. No associated anomalies were found. The patient remained asymptomatic and was stable at 3-month follow-up.

Clinical discussion: Isolated dextrocardia with situs solitus is rare and often discovered incidentally. Our case illustrates the importance of thorough prenatal imaging and clinical follow-up to detect potential associated anomalies.

Conclusion: Even when asymptomatic, dextrocardia requires comprehensive evaluation. This case contributes to the limited literature and emphasizes the value of imaging and vigilance in similar scenarios.

Malaria remains a leading cause of illness and death in Africa, particularly affecting vulnerable populations such as children and pregnant women. Effective management of malaria relies heavily on timely access to antimalarial medications, primarily artemisinin-based combination therapies. However, drug stockouts and treatment delays are persistent challenges in many African health systems, significantly undermining malaria control efforts and contributing to increased morbidity and mortality. This review explores the multifactorial causes of drug stockouts and treatment delays, including weaknesses in procurement, supply chain management, health infrastructure, and human resources. It highlights how these systemic challenges lead to interruptions in malaria treatment, worsening disease outcomes, and facilitating the spread of drug resistance. The negative impact extends beyond clinical consequences, eroding public trust in healthcare services and pushing patients toward ineffective alternatives. To address these issues, the review underscores the need for comprehensive strategies that strengthen supply chains, improve forecasting and inventory management, and enhance healthcare delivery capacity. Integrating innovative technologies, fostering partnerships, and promoting community engagement are critical to ensuring consistent drug availability and timely treatment. Ultimately, overcoming drug stockouts and treatment delays is essential to reduce the malaria burden and advance toward elimination goals in Africa.

Acinetobacter baumannii poses a severe threat in healthcare due to its highly adaptive genome and rapid spread of multidrug and extensively drug-resistant traits. Carbapenem resistance exceeds 70% in ICUs, with cancer patients showing even higher rates, including 94.1% of isolates carrying multiple carbapenemase genes such as OXA-23-like, NDM, and KPC. These strains, largely from International Clone II, exhibit strong virulence and environmental persistence. Immunocompromised patients face poor outcomes, with septicemia mortality reaching 49.5% and risk amplified by prolonged hospitalization, mechanical ventilation, invasive procedures, and prior carbapenem exposure. Limited therapeutic options, including toxic last-line colistin, further complicate management. Emerging AI-designed nano-vaccines offer promising preventive strategies for vulnerable populations.

Introduction and importance: Transdiaphragmatic intercostal hernias (TDIHs) are rare and typically posttraumatic. The coexistence of a TDIH with congenital anomalies, such as a Morgagni hernia (MH) and chest wall defect, is exceptionally uncommon. This report details a unique case of MH associated with an ipsilateral intercostal hernia in an adult, underscoring key diagnostic and surgical challenges.

Case presentation: A 71-year-old man with multiple comorbidities presented with acute abdominal pain and a right-sided chest wall bulge. Computed tomography revealed a large right lateral diaphragmatic and intercostal hernia between the right 9th and 10th ribs, with bowel loops protruding through the intercostal defect. The symptoms spontaneously improved, and repeat imaging showed a reduction of the hernia content. Thoracotomy revealed an omental herniation through an anteromedial diaphragmatic defect (MH) and a congenital chest wall defect with stretched intercostal muscles. The MH was primarily repaired using nonabsorbable sutures, and rib approximation was performed with absorbable sutures to address the chest wall defect.

Clinical discussion: This case is remarkable for the association of two congenital defects: an MH and a TDIH. Unlike typical posttraumatic TDIHs, the intercostal defect in this case stemmed from congenital chest wall maldevelopment. Preoperative diagnosis was challenging, with the MH initially missed on imaging. This emphasizes the importance of considering congenital variants in atypical hernias.

Conclusion: To our knowledge, this is the first documented case of a TDIH occurring in conjunction with an MH, both likely congenital. Prompt recognition and tailored interventions are crucial for avoiding missed diagnoses and complications.

Introduction and clinical importance: Most malignant testicular tumors are germ cell tumors (seminomas and non-seminomatous germ cell tumors), which together account for over 90% of primary testicular cancers and predominate in men aged 15-40 years. In contrast, paratesticular sarcomas such as liposarcoma are rare and typically present in older adults. The paratesticular dedifferentiated liposarcoma (PTDDLPS) subtype is exceptionally uncommon variant, and cases showing heterologous rhabdomyosarcomatous differentiation are exceedingly rare, posing diagnostic and therapeutic challenges.

Case presentation: We report a case of 83-year-old man presented with a painless, gradually enlarging left scrotal swelling initially suspected to be a hydrocele. Ultrasonography and MRI demonstrated a heterogeneous paratesticular mass. A high inguinal orchidectomy was performed. Histopathological examination revealed dedifferentiated liposarcoma with extensive rhabdomyosarcomatous differentiation. Immunohistochemistry (IHC) showed myoglobin and MyoD1 positivity in the rhabdomyoblastic component, while MDM2 and CDK4 coexpression and molecular analysis in both lipogenic and sarcomatous areas confirmed the diagnosis. The postoperative course was uneventful and the patient was referred for multidisciplinary follow-up.

Clinical discussion: PTDDLP with rhabdomyosarcomatous differentiation in the paratesticular region is extremely rare and can mimic other sarcomas or germ-cell tumors. The correct initial surgical treatment is best performed by high inguinal (radical) orchiectomy with early spermatic cord ligation, which is crucial for minimizing scrotal contamination and local recurrence. Recognition of its biphasic morphology, IHC analysis, supported by molecular testing for MDM2 and CDK4 amplification, is essential for accurate classification and management.

Conclusion: This case emphasizes the rarity and highlights the importance of clinicopathological features, diagnostic pitfalls, and prognostic implications considering PTDDLPS with rhabdomyosarcomatous differentiation, reinforces the oncologic importance of a high inguinal approach for suspected malignant paratesticular masses in older men. IHC and molecular analyses are crucial for an accurate diagnosis, particularly in tumors with heterologous elements that may mimic other sarcomas or germ cell tumors. Early recognition and multidisciplinary management optimize local control and surveillance planning.

Introduction and importance: Idiopathic granulomatous mastitis (IGM) is a rare, benign, chronic inflammatory breast disease. It often mimics breast cancer or abscess, complicating diagnosis. Accurate identification is essential for guiding therapy, particularly in regions with high prevalence of infectious diseases such as tuberculosis.

Case presentation: A 33-year-old female presented with a 1.5-year history of bilateral painful breast masses, erythema, and sinus tract formation. Imaging demonstrated multiple hypoechoic collections and ductal alterations. Initial management targeting presumed breast abscess with antibiotics and surgical drainage provided only transient relief. Core (true-cut) biopsy revealed epithelioid granulomas with multinucleated giant cells and no neoplastic changes. Infectious causes, including tuberculosis, were excluded via negative Mantoux, sputum examination, and Ziehl-Neelsen tests. Sarcoidosis was ruled out by normal serum angiotensin-converting enzyme, absence of systemic features, and lobulocentric granulomas with mixed inflammatory cells, distinguishing IGM from the well-formed "naked" granulomas seen in sarcoidosis.

Clinical discussion: Despite negative Mantoux and Ziehl-Neelsen (ZN) staining, empirical antitubercular therapy was initiated due to the paucibacillary nature of tuberculous mastitis and the high likelihood of false-negative results in our TB-endemic region. Subsequent biopsy confirmed IGM. The patient responded excellently to tapered oral corticosteroids combined with methotrexate. This case highlights the diagnostic complexity and the importance of histopathological confirmation to distinguish IGM from infections and other granulomatous diseases.

Conclusion: Bilateral IGM is a therapeutic and diagnostic challenge due to its mimicry of malignancy and infection. Histopathology is critical for accurate diagnosis, and immunosuppressive therapy with corticosteroids and methotrexate can provide effective management, particularly in resource-limited health care settings.

Guillain-Barré syndrome (GBS) is a severe immune-driven polyneuropathy marked by the acute onset of flaccid paralysis, areflexia, and in severe cases, life-threatening autonomic or respiratory failure. Although the clinical presentation and diagnostic criteria are widely established, the precise mechanisms underlying GBS are complex and poorly understood. This review summarizes current literature on the interplay of post-infectious triggers, molecular mimicry, and host susceptibility as influenced by genetic and epigenetic variables. Infectious pathogens such as Campylobacter jejuni, cytomegalovirus, Epstein-Barr virus, and, more recently, Zika and SARS-CoV-2 operate as initiators via molecular mimicry, in which pathogen antigens imitate peripheral nerve components, triggering the formation of autoreactive antibody and T-cell responses. Acute inflammatory demyelinating polyneuropathy (AIDP) is characterized by demyelination and inflammatory cytokine responses, whereas acute motor axonal neuropathy (AMAN) is associated with ganglioside-targeting antibodies and axonal loss. Genetic polymorphisms, such as those in HLA, TLR4, MMP9, and CD1A, influence vulnerability to the disease and its progression. Given that many patients experience persistent sensory, motor, and autonomic dysfunction despite treatment, the identification of long-term complications highlights the necessity of customized rehabilitation and long-term follow-up. Traditional therapeutic techniques, such as plasma exchange and intravenous immunoglobulin, remain in use, but current trials on complement inhibitors, antibody-degrading enzymes, and mesenchymal stem cell therapies indicate a move toward mechanism-driven approaches. Despite these advances, significant knowledge gaps remain regarding predictors of poor outcomes and underlying causes of persistent disabilities and complications, highlighting the need for continued translational and clinical research.