Scrotal pyocele is an uncommon urological condition characterised by a purulent collection within the scrotal sac and may be associated with inflammatory conditions of the epididymis or testis. This case report describes a 69-year-old male who presented with progressive scrotal swelling, scrotal pain, and fever. The patient had a history of hypertension, coronary artery disease, hypothyroidism, and bronchial asthma. Haematological investigations showed an elevated white blood cell count of 23,200/cu. mm and platelet count of 575,000/cu. mm, while urine examination showed a turbid appearance with increased pus/WBC cells, RBCs, and epithelial cells. Scrotal ultrasonography demonstrated normal testicular size and echotexture without focal lesions, but revealed a gross left scrotal fluid collection with internal echoes. The encysted collection measured approximately 6.0 × 6.5 cm and compressed the left testis; minimal free fluid was also present in the right scrotal sac. The therapeutic approach included empirical antimicrobial therapy, analgesic and supportive treatment, while drainage and surgical procedures were discussed as management options. The case highlights the diagnostic value of ultrasonography in identifying an encysted purulent scrotal collection and assessing testicular compression. Timely recognition and appropriate multidisciplinary management are important because scrotal pyocele may be associated with severe infectious complications and possible testicular compromise.
Background: Hypokalemic periodic paralysis (HPP) is a skeletal muscle channelopathy characterised by acute episodes of muscle weakness or paralysis associated with severe hypokalaemia. Primary HPP results from inherited ion-channel mutations, whereas secondary HPP is caused by transcellular potassium shifts into cells or potassium loss, including renal and gastrointestinal losses. We describe a case of HPP associated with severe gastrointestinal fluid loss and acute quadriparesis. Case Presentation: A 44-year-old woman presented with rapidly progressive, symmetrical quadriparesis following several episodes of acute, non-projectile vomiting. Physical examination revealed marked motor weakness (power 2/5 in the upper and lower extremities; straight-leg-raising test, 0°), with preservation of cranial-nerve function, sensation, and bowel and bladder function. Investigations showed severe hypokalaemia (K, 1.66 mEq/L), with otherwise normal blood urea nitrogen, creatinine, blood glucose (106 mg/dL), and thyroid function (TSH, 0.85 µIU/mL). Electrocardiography showed a regular rate and rhythm with subtle U waves. Intravenous and oral potassium replacement increased the serum potassium level to 3.30 mEq/L by day 5. Motor strength and neurological function were fully restored to 5/5 in all four extremities. Discussion: Rapid differentiation of secondary hypokalaemic quadriparesis from acute neuromuscular emergencies, including Guillain–Barré syndrome (GBS), acute ischaemic stroke, myasthenia gravis, and acute transverse myelitis, is essential to enable early electrolyte replacement and reverse neuromuscular blockade before life-threatening respiratory or cardiovascular dysfunction develops. Conclusion: Several conditions may present with acute flaccid quadriparesis. Serum electrolytes should therefore be assessed promptly in patients with suspected hypokalemic periodic paralysis. Early testing enables rapid, readily available treatment and may avoid an unnecessary, time-consuming invasive work-up.
Diabetes-related foot ulceration remains one of the most consequential complications of diabetes mellitus, and it accounts for a disproportionate share of hospital bed occupancy, lower-limb amputation and premature death among people living with the disease. Despite four decades of mechanistic research, several international guideline cycles and a considerable volume of randomised evidence, the proportion of people who achieve durable freedom from ulceration has changed far less than the volume of published work would suggest. This review examines why. It sets out to evaluate the strength and internal consistency of the evidence underpinning current understanding of ulcer causation, classification, treatment and prevention, and to identify where confident conclusions end and extrapolation begins. Literature was identified through structured searching of biomedical bibliographic sources and citation registries, supplemented by backward and forward citation tracking and by examination of contemporary international guidance, with critical appraisal focused on design adequacy, outcome definition, risk of bias, external validity and consistency across independent replications. Five themes emerged. First, the dominant causal model of neuropathy, deformity and trauma explains ulcer onset well but predicts recurrence poorly. Second, classification systems have proliferated without a corresponding improvement in comparability, and outcome definitions remain unstandardised across trials. Third, the evidence supporting core management is uneven, with mechanical offloading resting on more robust foundations than most adjunctive technologies. Fourth, prevention research has demonstrated efficacy under monitored conditions but has repeatedly failed to demonstrate effectiveness once adherence is treated as an outcome rather than a nuisance variable. Fifth, the geographical concentration of high-quality evidence in a small number of high-income settings limits generalisability to the populations bearing the greatest burden. Additionally, this paper records a case of a 39-year-old male. Finally it was concluded that the field would benefit less from additional small trials of novel dressings than from adequately powered pragmatic studies using standardised outcomes, with ulcer-free survival rather than time to closure as the primary measure of success.
Aims: To describe the non-surgical endodontic management of a maxillary first molar with severe, symptomatic external inflammatory root resorption in an adolescent patient, and to report the 12-month outcome. Presentation of Case: A 15-year-old boy presented with spontaneous pain and marked tenderness to percussion in the maxillary right first molar (tooth 16). A periapical radiograph showed advanced external resorption, most severe in the palatal and distobuccal roots, which had become considerably shortened. Root canal treatment was started without delay. Because the resorptive tissue was richly vascularised, controlling intracanal bleeding was difficult and time-consuming despite the short canals. After haemostasis was achieved, a dense calcium hydroxide dressing was placed in all canals. Three weeks later, the patient was almost free of symptoms, and the dressing was intact with no sign of infection. As the lesion was an external inflammatory resorption, each canal was then obturated along its full length with mineral trioxide aggregate (MTA). Discussion: Early diagnosis, elimination of the microbial stimulus, and a calcium hydroxide dressing are central to arresting inflammatory resorption. Full-length MTA obturation was chosen to seal the resorptive communications and to provide a well-sealing, biocompatible barrier in the weakened roots. Conclusion: Prompt endodontic intervention with calcium hydroxide followed by MTA obturation arrested the resorption and preserved the tooth, which remained asymptomatic and functional at the 12-month review.
Situs inversus totalis (SIT) is an uncommon congenital autosomal recessive condition in which the thoracic and abdominal viscera are arranged as a mirror image of normal anatomy. Although SIT is generally an incidental and asymptomatic finding that does not affect life expectancy, it creates substantial anatomical and spatial challenges for safe surgical and anaesthetic management. We report the surgical management of a symptomatic enlarging intramural uterine fibroid with a concomitant left ovarian haemorrhagic cyst in a 36-year-old woman (gravida 3, para 3) with SIT, dextrocardia, and a right-sided aortic arch. The patient underwent total abdominal hysterectomy, bilateral salpingectomy, and left oophorectomy through a suprapubic transverse incision under combined spinal-epidural anaesthesia. The reversed pelvic anatomy required deliberate adjustment of the surgeon's right-left orientation and modification of the usual operative sequence. Intraoperatively, the surgical team carefully identified, exposed, skeletonised, divided, and ligated the pelvic vessels and uterine ligaments while preserving surrounding tissue integrity. Meticulous multidisciplinary preoperative assessment included two-dimensional echocardiography, which demonstrated concentric left ventricular hypertrophy, a left ventricular ejection fraction of 60%, and no regional wall-motion abnormality. The postoperative course was uneventful. Precise preoperative evaluation, careful documentation, multidisciplinary planning, and intraoperative spatial readjustment were central to the overall successful surgical outcome.
Background: Scleritis is a severe and potentially sight-threatening inflammatory disease of the sclera, most frequently associated with systemic autoimmune disorders. Infectious etiologies are less common but remain clinically significant, particularly those caused by herpes viruses. Early recognition is essential, as inappropriate management,especially isolated corticosteroid therapy,may worsen the disease course. Case Report: We report the case of a 15-year-old female presenting with a unilateral painful red eye associated with cutaneous herpetic lesions. Best-corrected visual acuity was 20/20 in both eyes. Ocular examination revealed localized nasal conjunctival hyperemia in the left eye without scleral nodules or necrosis. The cornea was clear with preserved corneal sensitivity, and no signs of anterior uveitis were observed. The phenylephrine test demonstrated persistence of redness with partial blanching, suggesting deep vascular involvement. Polymerase chain reaction (PCR) testing for herpes virus was positive, confirming the viral etiology. The patient was treated with systemic antiviral therapy followed by cautious introduction of corticosteroids, with a favorable clinical outcome. Conclusion: Herpetic anterior scleritis may mimic superficial inflammatory conditions such as episcleritis, particularly in early stages. PCR plays a pivotal role in confirming the diagnosis and guiding appropriate management. Prompt antiviral therapy is essential to prevent complications and ensure favorable outcomes.
Metastatic breast cancer represents the most advanced stage, where the accurate and rapid identification of neoplastic cells is essential for clinical management and prognostic assessment. Although immunohistochemistry is the gold standard, flow cytometry emerges as a robust and sensitive complementary diagnostic method for detecting circulating tumor cells. We report a breast cancer patient with bone marrow metastasis and demonstrate the utility of a novel flow cytometry protocol for tumor cell detection. A 39-year-old woman, with no family history of cancer, identified a right breast nodule in January 2025. Imaging studies and biopsy with immunohistochemistry confirmed invasive lobular carcinoma (ER+, PR+, HER2−). Bone scintigraphy revealed multiple metastatic lesions. Bone marrow aspiration showed infiltration by tumor cells, with flow cytometry identifying 4.0% of non-hematologic (CD45−) large cells expressing epithelial markers (Ber-EP4+, Pan-CK+++) and breast tumor markers (GCDFP-15+, CK-19+++). Peripheral blood analysis using the Bulk Lysis protocol detected 2.5% circulating tumor cells. This case highlights that standardized flow cytometry protocols provide a rapid and, reliable and non-invasive approach for detecting tumor cells in different samples. The integration of this technique into clinical practice can significantly enhance disease monitoring and early detection of metastasis in breast cancer patients.
Background: Severe depression during pregnancy with persistent suicidal ideation requires timely intervention, particularly when pharmacotherapy is ineffective. Electroconvulsive therapy (ECT) may provide rapid symptom control; however, uncertainty regarding periprocedural maternal-fetal safety and anaesthetic technique continues to influence its use. This case report describes the multidisciplinary anaesthetic management of modified ECT in a second-trimester high-risk psychiatric emergency. Case Presentation: A 26-year-old primigravida at 27 weeks and 2 days of gestation presented with recurrent major depressive disorder, nutritional decline, treatment-refractory symptoms, and persistent suicidal ideation despite sequential pharmacotherapy. Following multidisciplinary planning by anaesthesia, psychiatry, obstetrics, and neonatology teams, six sessions of modified ECT were undertaken in an operating theatre with immediate obstetric and neonatal support available. Anaesthetic Management: For each session, the patient was fasted, positioned with 15° left uterine displacement, and monitored using standard ASA monitoring. Aspiration prophylaxis was administered before treatment. After three minutes of preoxygenation, anaesthesia was induced with propofol 1 mg/kg, followed by succinylcholine 1 mg/kg. Low-pressure mask ventilation with 100% oxygen was used, and seizure adequacy was assessed clinically using the isolated arm technique. Fetal assessment comprised cardiotocography before and after the procedure, with intermittent fetal heart rate auscultation when feasible. Outcomes: Mean motor seizure duration was 32.6 ± 5.4 seconds. Maternal oxygen saturation remained at or above 96%, and transient cardiovascular responses resolved spontaneously. No aspiration, airway event, arrhythmia, hypertensive crisis, prolonged seizure, uterine contraction, or fetal heart rate abnormality occurred. Suicidal ideation resolved after treatment. At 39 weeks and 3 days, the patient delivered a healthy female infant weighing 3,120 g with Apgar scores of 9 and 9 at one and five minutes. Conclusion: Carefully planned modified ECT during pregnancy was feasible in this case when supported by multidisciplinary coordination, pregnancy-specific anaesthetic precautions, and structured obstetric surveillance.
Introduction: Drug Reaction with Eosinophilia and Systemic Symptoms (DRESS) syndrome represents an uncommon yet potentially fatal clinical condition. Drug-induced hypersensitivity reaction is characterised by fever, rash, haematological abnormalities and multi-organ involvement particularly the liver. Carbamazepine is a well-known trigger. Aim: The study presents a rare but serious adverse drug reaction, carbamazepine-induced DRESS syndrome with hepatic involvement. Case Presentation: A 29-year-old male with a seizure disorder on long term carbamazepine therapy presented with high grade fever, generalized erythematous rash, abdominal pain and jaundice. Laboratory findings showed leukocytosis, eosinophilia, elevated liver enzymes and hyperbilirubinemia. Methodology: Clinical evaluation, laboratory monitoring and causality assessment using the Naranjo scale (score 7) were performed. Carbamazepine was discontinued and replaced with levetiracetam along with supportive therapy. Discussion: Temporal association, clinical features and improvement after drug withdrawal confirmed carbamazepine induced DRESS with hepatic involvement. Conclusion: The study concludes that early recognition and discontinuation of the offending drug are crucial to prevent serious complications and ensure a favourable recovery.
Background: Cerebral Venous Thrombosis (CVT) is an uncommon cerebrovascular disorder with a highly variable clinical spectrum. While headache is the most prevalent symptom, acute and severe visual impairment as the dominant presenting feature is rare and constitutes a neuro-ophthalmic emergency. Case Presentation: We report the case of a 63-year-old male with a chronic smoking history who presented with sudden-onset, progressive visual deterioration over three days, culminating in complete bilateral vision loss, accompanied by headache. An ophthalmology consultation revealed bilateral disc hyperemia. Neuroimaging, including Magnetic Resonance Imaging (MRI) and MR Venography, confirmed partial thrombosis involving the venous sinus confluence, posterior superior sagittal sinus, right transverse and sigmoid sinuses, and the right proximal internal jugular vein. The patient was managed with systemic anticoagulation and a course of high-dose corticosteroids for suspected compressive optic neuropathy. Clinical stabilization was achieved, and he was discharged on warfarin and a tapering dose of prednisolone. Discussion: This case details an atypical manifestation of CVT. The pathophysiology of acute visual failure likely involves compressive optic neuropathy, corroborated by the ophthalmoscopic finding of bilateral disc hyperemia, and possible venous congestion of the optic nerves. Management necessitates a dual strategy: immediate anticoagulation to arrest thrombus propagation and corticosteroids to mitigate secondary optic nerve insult. Conclusion: CVT should be considered in the differential diagnosis of acute, profound vision loss, particularly when accompanied by headache. Prompt diagnosis via MR Venography and expeditious, targeted intervention are critical to optimize neurological outcomes.
Posterior circulation strokes account for 20-25% of ischemic events, frequently presenting with altered sensorium, dysphagia, and limb weakness that challenge early recognition. Coexisting spinal pathology further complicates diagnosis, mandating comprehensive neuroimaging. A 68-year-old female with hypertension (amlodipine 5 mg daily) presented with a 15-day history of progressive altered sensorium, drowsiness, anorexia, dysphagia, and bilateral lower limb weakness. Initial vitals showed BP 130/80 mmHg, PR 74 bpm, SpO₂ 98% on room air. Serial assessments revealed evolving tachycardia (PR 106-116 bpm), desaturation (SpO₂ 90-98%), and hypertension (up to 160/100 mmHg). Laboratory findings included leukocytosis (WBC 17,450/mm³, neutrophils 90%), elevated CRP (13.4 mg/L), and mild hypokalemia (K⁺ 3.3 mEq/L). CSF analysis demonstrated elevated protein (157.4 mg/dL) with lymphocytic pleocytosis (40 cells/mm³). MRI brain confirmed acute posterior circulation infarction with DWI hyperintensities, while cervical spine imaging revealed a neoplastic lesion causing neural compression. Provisional diagnoses included posterior circulation stroke, neoplasia-related cervical dystonia, systemic infection, and hypertension. Management comprised intravenous antibiotics (ceftriaxone 1 g BD, piperacillin-tazobactam 4.5 g TDS, metronidazole), methylprednisolone 1 g daily, aspirin 75 mg, atorvastatin 40 mg, amlodipine 2.5 mg, and supportive therapy (pantoprazole, ondansetron, IV fluids, lactulose). Clinical improvement ensued with vital sign stabilization and resolving neurological deficits. Timely MRI-guided diagnosis and aggressive multimodal therapy yielded favorable short-term outcomes, underscoring integrated neurological care for elderly patients with multifocal crises.
Pulpal necrosis in permanent teeth with trauma-induced incomplete root development complicates treatment planning because of the presence of an open apex and thin dentinal walls. This case report aimed to evaluate the clinical and radiographic outcomes of regenerative endodontic treatment performed in a maxillary left central incisor with trauma-induced incomplete root development. In a 16-year-old female patient, an open apex, arrested root development, and periapical pathology were identified in tooth #21. Regenerative endodontic treatment, including canal disinfection, calcium hydroxide medication, induction of apical bleeding, and placement of a coronal barrier with MTA NeoPUTTY, was performed. At the 6- and 9-month follow-ups, the patient remained asymptomatic, and radiographic findings indicated continued root development. Regenerative endodontic treatment may be considered an effective approach for managing permanent teeth with trauma-induced incomplete root development.
Elevated lactate levels and high anion gap metabolic acidosis are hallmarks of Metformin-associated lactic acidosis, a rare but potentially fatal complication of Metformin therapy. Although the incidence of MALA is low, it carries a significantly high mortality rate, particularly in cases where diagnosis and treatment are delayed. Early recognition is therefore essential to improve clinical outcomes and reduce the risk of fatality. MALA is most commonly associated with underlying conditions such as sepsis, hypoxia, or renal impairment, all of which can impair lactate clearance and exacerbate metabolic disturbances. However, it is important to note that MALA can also occur in the absence of these traditional risk factors, making diagnosis more challenging. This highlights the need for clinicians to maintain a high index of suspicion even in atypical presentations. In this case, a patient with type 2 diabetes mellitus who had been receiving long-term metformin therapy presented with symptoms including nausea, vomiting, and altered mental status following a short episode of fever. Despite having normal renal function, laboratory investigations revealed severe metabolic acidosis, with a blood pH of less than 7.2 and markedly elevated lactate levels. These findings are consistent with a diagnosis of MALA, suggesting that metformin accumulation or altered metabolism may have contributed to the condition. The probable cause of the patient’s metabolic disturbance was attributed to metformin, despite the absence of common predisposing factors such as renal dysfunction. This case underscores the importance of recognising that MALA can develop even in patients who appear clinically stable and do not exhibit typical risk factors. Timely identification and intervention are therefore critical in preventing severe complications and improving patient outcome.
Cerebral venous sinus thrombosis (CVST) is an uncommon form of intracranial thrombosis characterised by the formation of a blood clot within the cerebral venous drainage system, including the dural venous sinuses, cortical veins, and the deep venous structures such as the vein of Galen system. Which is considered a subtype of venous thromboembolism. Common presenting features of CVST are symptoms of raised intracranial pressure, headaches, seizures, focal neurological deficits and altered sensorium. Seventy percent of CVST cases result from a hypercoagulable state.It also refers to acute Thrombosis or blood clots that can lead to strokes. Oral contraceptive pills (OCPs) are extensively utilised both for contraception and for the treatment of various gynaecological disorders, providing substantial benefits to women’s health. Nevertheless, their administration is also linked to a spectrum of potential adverse health effects. We report a case of female patient presented with intermittent fever, headache, dizziness, generalized weakness, and gastrointestinal symptoms. She had a history of hypothyroidism and was recently diagnosed with PCOS, for which she was on combined oral contraceptives. Initial evaluation indicated anemia and minor metabolic abnormalities. Persistent neurological symptoms followed by seizures prompted further evaluation with contrast-enhanced CT (Computed Tomography) of the brain, which showed haemorrhagic venous infarcts in the left temporo-occipital region with surrounding edema, leading to the diagnosis of Cerebral Venous Sinus Thrombosis likely associated with oral contraceptive use. The suspected drug was discontinued, and treatment with low-molecular-weight heparin was initiated. The patient improved clinically and was discharged in stable condition. This case highlights the risk of oral contraceptive-associated CVST and the importance of early diagnosis and prompt anticoagulation.
Post-dural puncture headache is an important complication of neuraxial anaesthesia and may be particularly disabling in obstetric patients during the early postpartum period. Although many cases respond to conservative measures, persistent symptoms may interfere with ambulation, breastfeeding, and maternal recovery and may require an epidural blood patch. This retrospective case series describes the clinical response to intravenous neostigmine–atropine in six obstetric patients with post-dural puncture headache that persisted despite 48–72 hours of conservative management. Post-dural puncture headache was diagnosed clinically on the basis of orthostatic headache occurring within five days of neuraxial anaesthesia, after exclusion of alternative causes where clinically indicated. All patients received intravenous neostigmine 20 μg/kg with atropine 10 μg/kg, diluted in 20 mL of normal saline and administered over five minutes under haemodynamic monitoring. Pain severity was assessed using a 10-point visual analogue scale. Outcomes included change in headache severity, need for repeat dosing, requirement for epidural blood patch, recurrence before discharge, and adverse effects. The six patients were aged 26–31 years. Four developed headache after spinal anaesthesia with a 25G Quincke needle, and two after accidental dural puncture during labour epidural placement with an 18G Tuohy needle. Baseline visual analogue scale scores were 7–8 after conservative therapy. Following treatment, final scores decreased to 1–2 within 10–16 hours. Five patients required a second dose at 8 hours. No patient required epidural blood patch during the hospital stay, and no clinically significant adverse effects were observed. Intravenous neostigmine–atropine was associated with improvement in headache severity in this small series of obstetric patients with persistent post-dural puncture headache. Larger controlled studies are required to confirm efficacy, safety, optimal dosing, and durability of response.
Evans syndrome is an uncommon autoimmune hematological disorder characterized by the coexistence or sequential development of autoimmune hemolytic anemia and immune thrombocytopenia. Its occurrence with antiphospholipid antibody syndrome, cystic fibrosis, chronic pancreatitis, insulin-dependent diabetes mellitus, pulmonary tuberculosis, and nocardiosis creates a highly complex diagnostic and therapeutic situation. We report the case of a 33-year-old male with multiple established autoimmune, genetic, metabolic, and infectious comorbidities who presented with acute left lower limb pain and swelling for three days. Clinical examination showed erythema, tenderness, and swelling of the affected limb. Doppler ultrasonography confirmed deep vein thrombosis. Laboratory evaluation showed anemia, thrombocytopenia, and markedly raised D-dimer. The patient had a background of Evans syndrome, double-positive antiphospholipid antibody syndrome, next-generation sequencing-confirmed cystic fibrosis, chronic pancreatitis, insulin-dependent diabetes mellitus, pulmonary tuberculosis on anti-tubercular therapy, and nocardiosis. He had recently received eltrombopag for severe thrombocytopenia following a hemolytic episode. The thrombotic event was considered to be temporally associated with eltrombopag use in the presence of an underlying prothrombotic antiphospholipid antibody profile. Management included anticoagulation with enoxaparin, discontinuation of eltrombopag, continuation of anti-tubercular therapy, immunosuppressive therapy, insulin treatment, analgesia, and supportive care. During hospitalization, limb pain and swelling improved, and the platelet count increased to 0.60 lac/cu.mm by Day 10. This case highlights the importance of individualized risk assessment when using thrombopoietin receptor agonists in patients with prothrombotic autoimmune disease and emphasizes the need for coordinated multidisciplinary management in complex multisystem overlap presentations.
Background: The long-term ingestion of external corticosteroids can lead to iatrogenic Cushing’s syndrome and are known to be adverse drug reactions that are prevented. There are many nonspecific symptoms associated with iatrogenic Cushing’s syndrome that often mimic other dermatologic or systemic conditions and may therefore go undetected. If there has been long-term use of an external corticosteroid, there are also considerations if the external corticosteroid is withdrawn suddenly. It can lead to a delayed crisis. Case Report: 53-year-old hypertensive female patient presented with skin thickening and hyperpigmentation over the abdomen and the lower extremities; generalized pruritus; exertional dyspnea; weakness; recent history of a chest pain; and fall. The patient reported medical history of taking chronic non-steroidal anti-inflammatory medication and external corticosteroids for joint pain. Clinical examination showed pallor, mild pedal edema, hypertension, skin atrophy, and scaliness. When laboratory tests were performed, low serum cortisol levels, concentric left ventricular hypertrophy with diastolic dysfunction Grade I, mild anemia, thrombocytopenia, hyperbilirubinemia, and mild renal impairment were obtained. Treatment/ Results: The patient was treated with antihypertensives, supportive care, gradual tapering of steroids and dermatology consult. Conclusion: This case demonstrates that there is chronic adrenal suppression from due to long-term exposure of corticosteroids. Low cortisol level confirms the diagnosis of Cushing’s syndrome due to exogenous steroid use as compared to endogenous causes. In the evaluation of abnormal skin or systemic changes, always ask the patient about use of corticosteroids; it is important to taper corticosteroids appropriately so sudden withdrawal does not result in a crisis
Background: Acute suppurative parotitis is uncommon in infants and is rarely observed beyond the neonatal period. When bilateral, its clinical presentation may resemble viral parotitis, cervical lymphadenitis, or deep-neck-space infection. Early high-resolution ultrasonography may help identify a potentially drainable collection or abscess. Case Description: A 9-month-old, fully immunised girl presented with upper respiratory catarrh of 10 days' duration, low-grade fever for 2 days, and a painful, rapidly enlarging right parotid swelling for 1 day. Marked systemic inflammation was evident (CRP, 356.59 mg/L), and microcytic hypochromic anaemia was noted. High-resolution ultrasonography of the right parotid region showed a large, heterogeneous parotid gland with increased Doppler vascularity and reactive cervical lymphadenitis, without a drainable fluid collection. Intravenous cefotaxime and amikacin, together with empirical oral cloxacillin, were initiated. After 48 hours, the swelling had progressed to involve both parotid glands. Following paediatric surgical review, antimicrobial therapy was escalated to intravenous meropenem, vancomycin, and metronidazole to cover possible multidrug-resistant pathogens, including MRSA and anaerobes. Because of the parents' concerns regarding the child's condition, they declined planned surgical exploration and further invasive investigation; this refusal was formally documented in the medical record. The patient improved promptly with the intensified conservative regimen, became afebrile within 48 hours, and showed a marked reduction in CRP. She was discharged on oral linezolid and levofloxacin, recovered uneventfully, and had no recurrence at follow-up. Conclusion: Early sonographic assessment and escalation of antimicrobial therapy to cover suspected MRSA and anaerobes may support conservative management when serial imaging shows no organised, drainable abscess.
Background: Simple bone cyst (SBC) is a rare intraosseous pseudocyst of the jaws that lacks an epithelial lining. It is most commonly seen in children and adolescents and is usually detected incidentally because patients are often asymptomatic. Aims: This study aims to present an incidental case of a simple bone cyst in a paediatric patient detected during radiographic evaluation of a retained primary maxillary incisor and to emphasise the importance of a multidisciplinary diagnostic approach for accurate diagnosis and management. Case Report: A 12-year-old female patient presented with a retained primary maxillary left central incisor and delayed eruption of the permanent successor. Panoramic radiography revealed two mesiodens associated with the unerupted permanent maxillary left central incisor. An incidental radiolucent lesion was also observed in the mandibular left premolar region between teeth 34 and 35. Further evaluation using cone-beam computed tomography showed a well-defined radiolucent cavity with mild buccolingual expansion and intact cortical plates. Surgical exploration revealed an empty bone cavity and histopathological examination showed fibrovascular connective tissue with focal haemorrhage and haemosiderin deposition, supporting the diagnosis of SBC. One-year follow-up demonstrated satisfactory bone healing without recurrence. Conclusion: This case highlights the importance of careful radiographic assessment in paediatric patients, as clinically silent lesions may be discovered during investigation of unrelated dental concerns. A combination of clinical, radiographic, and histopathological findings is essential for establishing an accurate diagnosis and appropriate management.
Background: Tubercular meningitis (TBM) is the most severe form of central nervous system tuberculosis, and its course is frequently complicated by vasculitis, tuberculomas, and ischaemic infarcts. When acute vasculitic cortical-subcortical infarcts occur alongside active cavitary pulmonary tuberculosis and chronic alcohol dependence, both diagnostic reasoning and day-to-day management become considerably more difficult. Case Description: A 49-year-old man receiving anti-tubercular therapy (ATT) for pulmonary tuberculosis, with a 20-year history of heavy alcohol use, presented with sudden involuntary movements of all four limbs, generalised weakness, and slurred speech. He was drowsy but rousable, with severe dysarthria, left-sided hypertonia, and an extensor left plantar response. Contrast-enhanced brain MRI showed features of TBM, a well-defined ring-enhancing caseating tuberculoma with central liquefaction (~2.0 × 1.0 × 2.0 cm) in the left parietal lobe, and acute multifocal cortical-subcortical vasculitic infarcts in the left insular cortex and left temporo-parietal lobes. CSF analysis showed early neutrophil-predominant pleocytosis (52 cells/cumm; 85% neutrophils and 11% lymphocytes), raised protein (48.5 mg/dL), borderline glucose (45.0 mg/dL), and elevated adenosine deaminase (ADA) of 12.0 U/L. Chest imaging revealed cavitary consolidation with air-fluid levels in the right lung and bilateral consolidation. He was admitted to the ICU for airway protection and subsequently developed alcohol withdrawal delirium, which was controlled with haloperidol and quetiapine. Pulsed corticosteroids, a modified ATT regimen, mannitol, antiplatelet therapy, and thiamine repletion resulted in marked clinical improvement. Conclusion: This case highlights how early neuroimaging and CSF biomarkers can identify uncommon vascular complications of neurotuberculosis when microbiological confirmation is elusive. Managing severe TBM alongside cavitary pulmonary disease and alcohol withdrawal delirium requires close multidisciplinary coordination and an adaptive management plan as complications arise.
