Journal of Medical Case Reports最新文献

Background: Compound paracetamol and amantadine hydrochloride capsules are commonly used over-the-counter medications at the primary care level. The primary component, amantadine, is excreted via the kidneys and poses a risk of accumulation in older patients, while chlorphenamine may increase the risk of delirium. This study examines the relationship between this medication and abnormal behavior by presenting case studies of two older patients and discussing clinical management strategies.

Case presentation: Case 1 involved a 78-year-old Chinese male with an estimated glomerular filtration rate (eGFR) of 87 mL/min/1.73 m², who developed visual hallucinations, delirium, and balance disturbances after five consecutive days of medication. He scored 8 on the Nursing Delirium Screening Scale. Symptoms resolved within 8 days following hydration therapy and antipsychotic treatment. Case 2 featured a 75-year-old Chinese male with an estimated glomerular filtration rate of 37 mL/min/1.73 m², who exhibited disorientation and hallucinations within 24 hours of starting the medication, scoring 10 on the Nursing Delirium Screening Scale. His symptoms completely resolved in 3 days. Both cases excluded alternative etiologies, and Naranjo Adverse Drug Reaction Probability Scale scores of 7 indicated a "probable" association between the drug and the behavioral abnormalities. Pharmacokinetic analysis revealed a strong correlation between drug accumulation, renal function status, and treatment duration.

Conclusion: The central toxicity of amantadine is significantly enhanced in older patients with renal insufficiency, and chlorphenamine may increase the risk of delirium. The risks associated with using this medication in older patients suffering from the common cold far outweigh the benefits, warranting cautious use in clinical practice; adverse reactions should be managed with prompt discontinuation of the medication and hydration to facilitate drug clearance. This study provides crucial warnings about medication safety in the older population.

Background: Therapeutic hypothermia for moderate-to-severe hypoxic-ischemic encephalopathy in neonates effectively improves neurological outcomes when initiated within 6 hours of birth. However, coagulopathy is a potential side effect of therapeutic hypothermia and requires careful monitoring for signs of hemorrhage. Uncontrolled hemorrhage is the primary exclusion criterion for therapeutic hypothermia. Herein, we report two cases of intracranial hemorrhage that, despite being massive enough to cause hypovolemic shock with anemia, could not be detected by cranial ultrasonography before the initiation of therapeutic hypothermia for hypoxic-ischemic encephalopathy.

Case presentation: One of the two Japanese newborn cases (one male and one female, 0 years old) was delivered by vacuum extraction and the other by forceps. Both infants presented with hypoxic-ischemic encephalopathy symptoms due to hypovolemic shock with anemia, without evidence of umbilical cord rupture or ultrasonographic evidence of ongoing bleeding such as intracranial or intraabdominal hemorrhage. Therapeutic hypothermia was initiated 5 hours after birth in both cases, alongside blood transfusion. One infant (male) presented with recurrent hypotension, while the other (female) developed hydrocephalus. Subsequent computed tomography or magnetic resonance imaging revealed a subdural hematoma. In one case (the male newborn), hypothermia was discontinued due to persistent bleeding, and a craniotomy was performed for hematoma evacuation.

Conclusion: These cases show that even in massive intracranial hemorrhage causing hypovolemic shock, subdural hematoma may be undetectable on bedside imaging such as cranial ultrasonography. Therefore, when therapeutic hypothermia is considered for neonates with hypoxic-ischemic encephalopathy secondary to hypovolemic shock with anemia, clinicians should be cautious and not rely solely on ultrasonography to rule out intracranial hemorrhage. Early and proactive computed tomography imaging should be performed to investigate the cause of neonatal hypoxic-ischemic encephalopathy due to hypovolemic shock with anemia.

Background: The fifth metatarsal is a major component of the lateral longitudinal arch of the foot. Damage to this area reduces foot function and impairs gait. Furthermore, immobilization used to treat fractures causes muscle weakness and contracture of the ankle joint, which impedes walking. Most studies on gait after fractures have been conducted in controlled laboratory environments, and the limitations of gait on patients' daily lives remain unclear. This case report aimed to quantitatively demonstrate the decline in gait function in daily life after a fifth metatarsal fracture and to report its duration and recovery over time.

Case presentation: This report describes a 39-year-old Japanese man who sustained a tuberosity avulsion fracture of the fifth metatarsal after slipping and falling on stairs. The fracture was immobilized with a splint, and the patient was instructed to use crutches for ambulation. The splint was removed 4 weeks post-injury, and crutches were discontinued. Daily walking was measured using inertial sensors embedded in insole devices worn on both feet. Walking speed and stride length decreased after the fracture and then gradually improved, reaching prefracture values 16 weeks postfracture. A significant decrease in the left push-off angle was observed, which decreased from approximately 77° before fracture to 54°. However, it improved weekly and reached prefracture values at 16 weeks. A decrease in the contact angle of the right foot was also observed, which took approximately 16 weeks to improve.

Conclusion: This is a case report on the temporal changes in gait pattern pre- and postfracture in a patient treated conservatively for a fifth metatarsal fracture. The fifth metatarsal fracture and subsequent immobilization strongly suggest a decrease in push-off force on the injured side during walking. This also affects the movement of the right lower limb. Decreased push-off on the fractured side reduces propulsion and limits the walking performance in daily life. Walking speed improved after 16 weeks, and this improvement was consistent with an improvement in the push-off angle. As this report measured gait in daily life, the patient's real-life mobility was affected for 15 weeks after the fracture.

Background: The management of pediatric tuberculosis involves several challenges, as illustrated in these three cases. Challenges are numerous and each case demonstrates the difficulty and delay in diagnosis, social constraints that delay the diagnosis, and drug dosing schedules that cause serious side effects in children. All three cases received the Bacillus Calmette-Guérin vaccine at birth, and each has documented confirmation of vaccination.

Case presentation: A 1-year-old Sri Lankan Muslim baby was transferred to a tertiary care center with a week-long fever of unknown origin, accompanied by recent weight faltering. Investigations revealed anemia, elevated erythrocyte sedimentation rate, and chest X-ray showing miliary changes, with a positive GeneXpert® System for tuberculosis, though gastric aspirates were negative for acid fast bacilli. GeneXpert is a molecular diagnostic system that uses real-time polymerase chain reaction technology to detect specific genetic material (DNA or RNA) from pathogens in a biological sample for the rapid and accurate diagnosis of tuberculosis. The baby was treated with antituberculosis drugs and recovered fully, and contact tracing identified the grandmother as a possible source due to a chronic cough. A 4-month-old Sri Lankan Tamil baby with fever, cough, and shortness of breath developed convulsions and was initially treated for a lower respiratory infection and possible bacterial meningitis. After transfer to a tertiary hospital and investigation, high cerebrospinal fluid protein and lymphocyte count suggested a possible tuberculosis infection and antituberculosis drugs were started. The baby developed liver dysfunction after 6 days of treatment, which resolved after discontinuing the antituberculosis drugs, and she recovered fully without sequelae after appropriate management. A 2-year-old Sri Lankan Tamil child presented with difficulty walking for 2 weeks following an accidental fall, with localized swelling and tenderness over the L4-L5 region. The child showed signs of bilateral lower limb weakness, reduced power, and exaggerated knee jerks, and had a history of contact with a father diagnosed with pulmonary tuberculosis. X-rays were performed to investigate the spinal issue, and the child had previously defaulted on tuberculosis prophylaxis after receiving isonicotinic acid hydrazide. Magnetic resonance imaging showed destruction of the L4 and L5 vertebrae with caseous material tracking and causing secondary psoas abscess.

Conclusion: Clinicians must maintain a low threshold for diagnosing tuberculosis in young children, especially those under 1 year old with malnutrition, as tuberculosis can present subtly in this age group. Performing GeneXpert® when suspected is warranted. Parental education and challenging social circumstances hinder children from getting better. The cases identify the challenges faced by clinicians.

Background: Mucormycosis is a severe opportunistic fungal infection that has become a notable complication in patients recovering from coronavirus disease 2019, particularly in individuals with preexisting diabetes mellitus or a history of corticosteroid administration. Coinfection with cytomegalovirus in immunocompromised patients with coronavirus disease 2019 is increasingly documented yet remains insufficiently acknowledged. This case is significant owing to the uncommon simultaneous occurrence of cutaneous mucormycosis and cytomegalovirus infection in a post-coronavirus disease patient, underscoring the diagnostic and therapeutic challenges associated with these dual infections.

Case presentation: The purpose of this report is to discuss a 56-year-old man of South Asian/Pakistani descent with a history of diabetes mellitus and hypertension. He was diagnosed with post-coronavirus disease pneumonia with an anterior abdominal wall lesion that did not resolve after treatment for cutaneous mucormycosis, which was diagnosed on histopathology. Liposomal amphotericin B was administered intravenously, and the patient underwent surgical wound debridement. However, the patient was readmitted owing to sepsis and had a cytomegalovirus reactivation confirmed by polymerase chain reaction testing. Ganciclovir was given intravenously. The patient's health continued to deteriorate until he died from complications of his disease in spite of receiving aggressive medical and surgical treatment.

Conclusion: This case illustrates the need for prompt recognition and treatment of concurrent opportunistic infections in patients who are immunocompromised owing to coronavirus disease 2019. A multidisciplinary proactive approach will be necessary to improve survival and patient outcomes in similarly complex patient cases.

Background: This report details a case of AGXT gene mutation in a male patient, 9 years 6 months old, Portuguese ethnicity, with history of nephrocalcinosis and recurrent nephrolithiasis in childhood, which progressed to chronic kidney disease. It illustrates the diagnostic and therapeutic implications of identifying an AGXT c.33dup (p.Lys12Glnfs156) variant in a patient with primary hyperoxaluria type 1. Recognizing nonresponsive genotypes prevents unnecessary prolonged treatment and allows earlier evaluation for advanced therapies such as liver transplantation or RNA interference therapy.

Case presentation: A nine-year-old boy, white, with consanguineous parents and family history of early-onset end-stage renal disease, presented with recurrent nephrolithiasis and bilateral nephrocalcinosis since age 6 year. Initial evaluation revealed hyperoxaluria and elevated serum oxalate, confirming clinical suspicion of primary hyperoxaluria type 1 without pyridoxine response. At age 14 years, he developed acute renal failure due to obstructive urolithiasis and Acinetobacter baumannii infection, requiring ureteroscopic lithotripsy and intravenous antibiotics. Partial renal recovery followed, with stable function (estimated glomerular filtration rate ≈ 40 mL/min/1.73 m²) and no recurrence during longitudinal follow-up. At age 16 years, homozygosity for the primary hyperoxaluria type 1 gene, variant c.33dup (p.Lys12Glnfs*156), was identified, confirming primary hyperoxaluria type 1. Family screening revealed two asymptomatic siblings (ages 7 and 9 years) who were heterozygous carriers of the same variant. Lumasiran therapy was initiated for this patient as a disease-modifying treatment to reduce oxalate production and stabilize renal function.

Conclusion: Primary hyperoxaluria type 1 remains a diagnostic and therapeutic challenge, particularly in resource-limited settings. Identification of specific AGXT variants offers key prognostic and therapeutic insights. Early genetic testing in children with unexplained nephrocalcinosis or recurrent nephrolithiasis may be cost-effective, enabling timely diagnosis, targeted treatment, and family screening while reducing the long-term burden and healthcare costs associated with end-stage renal disease.

Background: Blastocystis hominis infection in patients with Parkinson's disease may exacerbate gut microbiota dysbiosis, potentially worsening neurological symptoms; however, such associations remain speculative without microbiome data. Targeted interventions to restore gut microbial balance could mitigate disease progression and improve patient outcomes.

Case presentation: An 86-year-old Caucasian male presented to the emergency department with severe watery diarrhea, up to six episodes per day, of 1 month duration. The patient's diarrhea was nonbloody and nonmucoid. He denied fever, nausea, vomiting, abdominal pain, bloating, loss of appetite, or anal itching. There was no history of weight loss, fatigue, or systemic symptoms. A stool sample was examined microscopically using normal saline, revealing Blastocystis hominis cysts (the burden was not quantified) and a rare white blood cell count. The sample was concentrated using acetylacetate and ether. Additional tests, including Clostridioides difficile and other common infectious pathogens, were ruled out in our patient to address alternative infectious etiologies.The patient was started on intravenous ciprofloxacin and metronidazole, resulting in an improvement in diarrhea consistency and frequency until the resolution of symptoms within 4 days of initiating intravenous therapy. The patient also reported mild improvement in his Parkinson's disease symptoms by the end of hospitalization, though objective neurologic post-treatment scoring (eg. Unified Parkinson's Disease Rating Scale) was not performed.

Conclusion: This case highlights the need to consider parasitic infections in patients with Parkinson's disease presenting with chronic diarrhea. While we hypothesize that B. hominis infection may transiently worsen Parkinson's disease symptoms through inflammatory or microbiota-mediated pathways, this remains speculative in the absence of microbiome sequencing or objective neurologic evaluation. Further studies integrating clinical, microbiological, and microbiome analyses are warranted.

Background: Bee stings account for approximately 14% of anaphylactic reactions and are the second most common trigger after food allergies. The body's response to bee venom can range from allergic reactions to systemic toxicity, with a mortality rate of 15-25%. Survivors might develop complications such as acute kidney injury, hypertension, anemia, rhabdomyolysis, liver damage, heart attack, and breathing difficulties, depending on the number of stings. In this case series, we discuss two pediatric patients who experienced acute kidney injury following a bee sting, emphasizing the risk of severe systemic complications in children.

Case presentation: We report two Black African boys with bee sting-induced acute kidney injury: an 11-year-old and a 7-year-old, both with swelling and reduced urine output. Both underwent three hemodialysis sessions and recovered renal function. A year later, the 11-year-old's kidneys were normal, but the 7-year-old was lost to follow-up.

Conclusion: Bee stings, the second leading cause of fatal anaphylaxis after food allergies, can cause serious complications. This case series emphasizes the importance of early detection and swift treatment to improve outcomes.

Background: Viral acute retinal necrosis is a rare acute uveitis characterized by peripheral necrotizing retinitis with severe functional damages. We reported an unusual case of varicella zoster virus acute retinal necrosis starting with optic nerve involvement.

Case presentation: A 55-year-old immunocompetent Caucasian woman presented with pain in the left eye and signs of papillitis with enlargement of the blind spot. Visual function rapidly decreased because of ocular inflammation within a few days. After ophthalmological and systemic tests, a diagnosis of varicella zoster virus acute retinal necrosis was made. A prompt treatment with intravenous acyclovir and early vitrectomy was performed.

Conclusion: Optic disc involvement preceding retinal necrosis in varicella zoster virus acute retinal necrosis is a diagnostic challenge. A prompt diagnosis and treatment are pivotal to manage these patients, avoiding severe visual damage.

Introduction: Gestational trophoblastic disease is the term used to describe the heterogeneous group of interrelated lesions that arise from abnormal proliferation of placental trophoblasts. The clinical presentations of gestational trophoblastic tumor are vaginal bleeding, uterine enlargement greater than expected for gestational dates, hyperemesis, secondary clinical hyperthyroidism, and less common presentations such as pregnancy-induced hypertension in the first or second trimester and theca lutea cyst torsion. It is a rare incident to find uterine rupture due to a molar pregnancy. Most uterine ruptures reported so far were all malignant histologic types of the spectrum.

Case presentation: We present a case of ruptured uterus as a complication of complete molar pregnancy presenting with shock and severe anemia. A 37-year-old Ethiopian gravida 6 para 5 with 5-month amenorrhea came with vaginal bleeding, abdominal pain, and symptoms of anemia. Her hemoglobin was 2.8 g/dl, and there was a honeycomb-appearing endometrial mass and free fluid in the general peritoneum. She underwent emergency laparotomy, where a hysterectomy was done for cornual uterine rupture. She was followed with serial serum human chorionic gonadotropin and declared cured after 6 months of surveillance.

Conclusion: Even though it is rare, a ruptured uterus in a molar pregnancy can be a catastrophic complication, presenting with massive hemoperitoneum and hemorrhagic shock. Hysterectomy, along with vascular filling with crystalloid and transfusion of blood products, can save a patient's life. Patients can be followed with serial serum human chorionic gonadotropin for any transformation to gestational trophoblastic neoplasia.