Journal scan: A review of 10 recent papers of immediate clinical significance, harvested from major international journals
From the desk of the Editor-in-Chief
Inflammatory risk and cardiovascular events in patients without obstructive coronary artery disease: the ORFAN multicentre, longitudinal cohort study
(1). Kenneth Chan et al, Published:May 29, 2024DOI:https://doi.org/10.1016/S0140-6736(24)00596-8, https://www.thelancet.com/journals/lancet/article/PIIS0140-6736(24)00596-8/fulltext
Summary
Background
Coronary computed tomography angiography (CCTA) is the first line investigation for chest pain, and it is used to guide revascularisation. However, the widespread adoption of CCTA has revealed a large group of individuals without obstructive coronary artery disease (CAD), with unclear prognosis and management. Measurement of coronary inflammation from CCTA using the perivascular fat attenuation index (FAI) Score could enable cardiovascular risk prediction and guide the management of individuals without obstructive CAD. The Oxford Risk Factors And Non-invasive imaging (ORFAN) study aimed to evaluate the risk profile and event rates among patients undergoing CCTA as part of routine clinical care in the UK National Health Service (NHS); to test the hypothesis that coronary arterial inflammation drives cardiac mortality or major adverse cardiac events (MACE) in patients with or without CAD; and to externally validate the performance of the previously trained artificial intelligence (AI)-Risk prognostic algorithm and the related AI-Risk classification system in a UK population.
Methods
This multicentre, longitudinal cohort study included 40 091 consecutive patients undergoing clinically indicated CCTA in eight UK hospitals, who were followed up for MACE (ie, myocardial infarction, new onset heart failure, or cardiac death) for a median of 2·7 years (IQR 1·4–5·3). The prognostic value of FAI Score in the presence and absence of obstructive CAD was evaluated in 3393 consecutive patients from the two hospitals with the longest follow-up (7·7 years [6·4–9·1]). An AI-enhanced cardiac risk prediction algorithm, which integrates FAI Score, coronary plaque metrics, and clinical risk factors, was then evaluated in this population.
Findings
In the 2·7 year median follow-up period, patients without obstructive CAD (32 533 [81·1%] of 40 091) accounted for 2857 (66·3%) of the 4307 total MACE and 1118 (63·7%) of the 1754 total cardiac deaths in the whole of Cohort A. Increased FAI Score in all the three coronary arteries had an additive impact on the risk for cardiac mortality (hazard ratio [HR] 29·8 [95% CI 13·9–63·9], p<0·001) or MACE (12·6 [8·5–18·6], p<0·001) comparing three vessels with an FAI Score in the top versus bottom quartile for each artery. FAI Score in any coronary artery predicted cardiac mortality and MACE independently from cardiovascular risk factors and the presence or extent of CAD. The AI-Risk classification was positively associated with cardiac mortality (6·75 [5·17–8·82], p<0·001, for very high risk vs low or medium risk) and MACE (4·68 [3·93–5·57], p<0·001 for very high risk vs low or medium risk). Finally, the AI-Risk model was well calibrated against true events.
Interpretation
The FAI Score captures inflammatory risk beyond the current clinical risk stratification and CCTA interpretation, particularly among patients without obstructive CAD. The AI-Risk integrates this information in a prognostic algorithm, which could be used as an alternative to traditional risk factor-based risk calculators.
Funding
British Heart Foundation
Nigeria rolls out novel meningitis vaccine
(2). Patrick Ashinze etal, Published:June 01, 2024DOI:https://doi.org/10.1016/S0140-6736(24)00880-8
A novel meningitis vaccine!
In March, 2024, Nigeria became the first country to introduce the Men5CV multivalent meningitis vaccine.
As one of the 26 hyperendemic countries within the African meningitis belt, Nigeria has been acutely aware of the grave threat posed by meningitis, with recent outbreaks claiming numerous lives and causing widespread suffering.
The vaccine is a result of multilaterally financed and coordinated work that took 13 years to complete; it provides protection against the five major strains of the meningococcal bacteria (A, C, W, Y, and X) following one single injection
Editorial: Alarming rise in young-onset type 2 diabetes
(3). The Lancet Diabetes & Endocrinology,: June 06, 2024DOI:https://doi.org/10.1016/S2213-8587(24)00161-X
High lights
There is a 40% increase in 5 years in the number of people diagnosed with type 2 diabetes
Type 2 diabetes, typically a condition predominantly affecting middle-aged and older adults, has become increasingly prevalent in young populations.
Young-onset type 2 diabetes is associated with greater insulin resistance, a faster decline in β cell function, and earlier and more severe complications, leading to increased morbidity and mortality, than late-onset type 2 diabetes.
At age 50 years, individuals with type 2 diabetes diagnosed at age 30 years died, on average, 14 years earlier than those without diabetes.
By contrast, less than 2 years of life are lost on average when type 2 diabetes presents after 70 years of age.
This situation is even more concerning given the rising prevalence of obesity.
Globally, obesity is now the most common cause of malnutrition.
Obesity rates in children and adults have more than doubled over the past three decades
Overweight and obesity in people younger than 40 years are the main risk factors for type 2 diabetes, and there is an inverse relationship between BMI and the age of onset.
The message is clear: there is an ongoing metabolic health crisis that poses disastrous consequences not only for the current generations and the ones to come but also for the planet.
This crisis is a setback to the advancements achieved by modern medicine
There is an urgent need to repair a broken food system which relies excessively on the consumption of highly palatable ultra-processed foods high in sugar, salt, and fats.
Reversing the growing trend in obesity is essential for preventing and reducing type 2 diabetes, especially among younger populations.
A philosophical question
Does action is a result of awareness and choice?
Do people make rational choices?
Meigs’ Syndrome
(4). Juan Jose Fernandez Diaz, etal, Published June 8, 2024, N Engl J Med 2024;390:2107, DOI: 10.1056/NEJMicm2313447,Vol. 390 No. 22
A previously healthy 51-year-old woman presented to the emergency department with a 2-month history of dyspnea. The physical examination was notable for diminished breath sounds at both lung bases and a firm, nontender pelvic mass that appeared to originate from the left ovary. A chest radiograph showed pleural effusions that were greater on the right side than on the left (Panel A). Analysis of a pleural fluid sample revealed a sterile exudate with negative cytologic findings. Computed tomography of the abdomen (Panel B, coronal view) showed a pelvic mass (asterisk) and perihepatic ascites (arrows). The CA-125 level was 1794.0 IU per milliliter (reference value, <35.0).
During a subsequent exploratory laparotomy, a left ovarian tumor was found. There were no peritoneal metastases. The solid, smooth tumor was excised (Panel C) and identified on histopathological analysis as a fibroma. Cytologic testing of the ascitic fluid was negative for a malignant condition. A diagnosis of Meigs’ syndrome — the triad of a benign ovarian tumor, ascites, and pleural effusion — was made. Meigs’ syndrome mimics ovarian cancer, but excision of the tumor results in the resolution of ascites and pleural effusion. Radiography was performed 3 weeks after surgery, at which time the patient’s symptoms, effusions, and ascites had abated.
Tuberculosis Verrucosa Cutis
(5). Juncheng Wang, et al, Published June 12, 2024,N Engl J Med 2024;390: e58,DOI: 10.1056/NEJMicm2313828,Vol. 390 No. 22
A 59-year-old veterinarian presented to the dermatology clinic with a 1-year history of a painful rash on his right hand. He had no other symptoms. On physical examination, verrucous plaques with overlying thick yellow-brown crusting were seen on the dorsum of the right hand (Panel A) and the medial aspect of the right index finger (Panel B). Biopsy of the lesion on the dorsum of the hand revealed pseudoepitheliomatous hyperplasia and tuberculoid granulomas in the dermis (Panel C, arrow; hematoxylin and eosin stain). Tissue cultures were negative, but metagenomic next-generation sequencing of the tissue identified Mycobacterium tuberculosis. An interferon-γ release assay was positive, and a computed tomographic scan of the chest was normal. A diagnosis of tuberculosis verrucosa cutis was made.
Tuberculosis verrucosa cutis is a type of cutaneous tuberculosis that results from direct inoculation of the organism into the skin of previously sensitized persons. Occupational exposure to mycobacteria, particularly among persons with frequent contact with livestock, is a risk factor. A 6-month course of isoniazid, rifampin, and ethambutol was initiated. At 2 months of follow-up after the start of antituberculous therapy, the rash had abated.
Multicentric Reticulohistiocytosis
(6). Fei Sun etal, N Engl J Med 2024;390:2199,DOI: 10.1056/NEJMicm2313532
A 32-year-old man presented to the rheumatology clinic with a 7-year history of skin nodules, along with swelling, pain, and morning stiffness in his fingers and knuckles. On physical examination, there were smooth nodules over the chest wall, auricles (Panel A), and dorsal surface of the distal fingertips (Panel B). There was also synovitis of the proximal and distal interphalangeal joints and metacarpophalangeal joints. Laboratory studies revealed normal inflammatory markers and negative results for rheumatoid factor and antibody against cyclic citrullinated peptide. Radiographs of the hands showed marginal erosions of multiple interphalangeal joints (Panel C, arrows).
Histopathological examination of a skin-biopsy sample obtained from a chest nodule showed histiocytes and multinucleated giant cells with abundant eosinophilic granular ground-glass–like cytoplasm in the dermis, hyperplasia of fibrous tissue, and acute and chronic inflammatory-cell infiltration. A diagnosis of multicentric reticulohistiocytosis was made. This condition is a rare systemic form of non–Langerhans-cell histiocytosis that is characterized by erosive arthritis and skin lesions. It may be misdiagnosed as rheumatoid arthritis owing to the presence of inflammatory arthritis and periarticular skin nodules. Treatment with a tapering dose of prednisone, hydroxychloroquine, and methotrexate was initiated. At the 1-year follow-up, the patient’s joint pain and skin lesions had abated.
Insulin-Induced Lipohypertrophy
(7). Nirmalya Roy etal, Published June 19, 2024,N Engl J Med 2024;390: e60
DOI: 10.1056/NEJMicm2314962,Vol. 390 No. 23
A 65-year-old man with type 2 diabetes was admitted to the hospital with hyperosmolar hyperglycemic state. Two weeks before admission, the patient’s insulin dose had been increased owing to inadequate glycemic control. The physical examination was notable for confusion and sarcopenia. There were also rubbery, subcutaneous masses on either side of the umbilicus where the patient had been repeatedly administering insulin injections — a finding known as insulin-induced lipohypertrophy.
Insulin-induced lipohypertrophy is a type of localized lipodystrophy that results from repeated subcutaneous injections at the same site. It may lead to a decreased response to insulin therapy and volatile glycemic levels. Lipohypertrophy may be difficult to detect in patients with obesity, but masses are usually palpable on abdominal examination. Patients who use subcutaneous insulin should be examined for injection-site complications at every clinic visit and should receive counseling regarding the importance of rotating injection sites to allow sites to heal. In this patient, laboratory studies were notable for a glycated hemoglobin level of 11.4% (reference range, <7). After 48 hours of treatment with insulin and intravenous fluids, the patient’s hyperosmolar hyperglycemic state resolved. He was discharged home after receiving instructions on the proper administration of subcutaneous insulin.
Metronidazole-Induced Encephalopathy in a Patient Treated for Osteomyelitis
(8). David J.H. Bian et al,Publication: Annals of Internal Medicine: Clinical Cases,Volume 3, Number 6. https://doi.org/10.7326/aimcc.2023.0857
Case Report
A 73-year-old man initially presented with a 2-week history of worsening atraumatic lower back pain and leukocytosis. His medical history included type 2 diabetes mellitus, coronary artery disease, and alcohol-induced cirrhosis, coupled with typical radiological features on a magnetic resonance imaging (MRI) of the abdomen and a prior liver ultrasound. An initial lumbosacral MRI scan demonstrated a paravertebral abscess and infectious osteomyelitis at the L4-S1 vertebral levels, prompting initiation of piperacillin-tazobactam treatment (Figure 1). Initial blood cultures were negative, and urine cultures isolated pansensitive Escherichia coli, leading to a change to ceftriaxone therapy. Follow-up blood cultures isolated Bacteroides fragilis, prompting another transition to meropenem.
Figure 1. Magnetic resonance imaging findings of the lumbosacral spine. (A–C) Sagittal views of the lumbo-sacral spine in the pre-gadolinium phase (A), the post-gadolinium phase (B), and the STIR sequence (C) on initial presentation for osteomyelitis before MIE. Diffuse bone marrow edema and enhancement within the L5-S1 vertebrae were observed, highly suggestive of osteomyelitis. (D) Axial view of the lumbosacral spine in the post-gadolinium phase at the L4 vertebral level. The formation of a paravertebral fluid collection, compatible with an abscess, was observed deep to the right psoas muscle at the L4-L5 vertebral levels. MIE = metronidazole-induced encephalopathy; MRI = magnetic resonance imaging; STIR = short-tau inversion recovery.
Despite 2 weeks of antibiotic therapy, the patient developed a new onset fever, with an elevated C-reactive protein level of 61.2 mg/L. A lumbosacral MRI scan redemonstrated progressive osteomyelitis. The patient had surgical decompression and debridement of the L4-S1 vertebrae for source control. Meropenem was continued, because an abscess culture isolated B. fragilis. He recovered well postoperatively and was ambulating, with adequate oral intake and pain control. He was afebrile and cognitively intact, and the C-reactive protein level decreased to 18.5 mg/L. He was discharged with a regimen of oral moxifloxacin, 400 mg, and metronidazole, 500 mg, both twice daily, for 6 weeks.
The patient continued to recover in the month following surgery. However, around 4 weeks after discharge, he began to develop a decline in his physical and cognitive functions. He developed subacute worsening fatigue, somnolence, poor coordination and balance, and intermittent confusion. The deterioration culminated in 5 days of hallucinations, dysphagia, and dysarthria. He was readmitted to the hospital 3 weeks after the onset of these symptoms, corresponding to 3 months after he initially presented with osteomyelitis.
At the hospital, his vital signs were within normal limits (Table 1). No seizures were reported. On physical examination, he exhibited signs of delirium, such as inattention, disorganized thinking, and a fluctuating level of consciousness. His cranial nerve examination was normal, but he was unable to ambulate. Strength, reflexes, and sensations were preserved in all 4 extremities, without evidence of neuropathy. Neither pronator drift nor asterixis were observed. He had no evidence of cauda equina with no saddle anesthesia, incontinence, nor abnormal rectal tone. No tremor, rigidity, nor bradykinesia suggestive of parkinsonism were appreciated.
Table 1. Laboratory Tests Results for Patient Presenting With MIE on Admission to the Emergency Department
Laboratory Test | Value |
---|---|
Hematology | |
Hemoglobin (g/L) | 140 |
WBC (×109/L) | 5.80 |
Platelets (×109/L) | 186 |
Chemistry | |
Sodium (mmol/L) | 133 |
Chloride (mmol/L) | 100 |
Potassium (mmol/L) | 4.1 |
Creatinine (µmol/L) | 81 |
Random glucose (mmol/L) | 5.6 |
Venous blood gas | |
Bicarbonate (mmol/L ) | 21 |
Liver function tests | |
ALT (U/L) | 19 |
ALP (U/L) | 103 |
Bilirubin (µmol/L) | 23.0 |
ALP = alkaline phosphatase; ALT = alanine transaminase; MIE = metronidazole-induced encephalopathy; WBC = white blood cell count.
The complete blood count, liver profile, and chemistry panels were unremarkable (Table 1). A brain MRI scan demonstrated no acute infarction or hemorrhages. However, hypersignaling on the bilateral dentate nuclei was observed, consistent with MIE (Figure 2A–C). Following this finding, metronidazole was discontinued. A lumbosacral MRI scan demonstrated persistent osteomyelitis at the L4-S1 vertebral levels and piperacillin-tazobactam was restarted. The symptoms of delirium improved rapidly, and the patient remained consistently alert and oriented with normal recall and improving mobility. He was discharged with a regimen of piperacillin-tazobactam for 8 weeks.
Figure 2. Magnetic resonance imaging findings in MIE. (A–C) Axial views of the dentate nuclei in the FLAIR (A), the DWI (B), and the ADC (C) map imaging sequences 3 months after initial manifestation of osteomyelitis. No acute infarction, intracranial hemorrhages, midline shift, hydrocephalus, mass lesions, or brain herniations were visualized. However, these imaging sequences demonstrated symmetrical hypersignaling in the DWI and FLAIR sequences without restriction of both dentate nuclei. These findings were highly suggestive of MIE. (D and E) Axial views of the dentate nuclei in the FLAIR (D) and the DWI (E) sequence imaging done 3 months after the diagnosis of MIE and 6 months after the patient’s initial presentation for osteomyelitis. Axial views demonstrated complete resolution of the DWI and FLAIR sequence abnormalities in the bilateral dentate nuclei, suggestive of complete resolution of MIE.
- Sagittal view of the corpus callosum in the FLAIR sequence 3 months after diagnosis of MIE. Of note, the corpus callosum does not demonstrate any signaling abnormalities on the FLAIR imaging, follow-up imaging, and on initial presentation. ADC = apparent diffusion coefficient; DWI = diffusion-weighted imaging; FLAIR = fluid-attenuated inversion recovery; MIE = metronidazole-induced encephalopathy; MRI = magnetic resonance imaging.
A repeat brain MRI performed 11 weeks after MIE presentation showed complete resolution of the abnormalities in the dentate nuclei (Figure 2D–E). Of note, the corpus callosum was unaffected on his initial and follow-up MRI scans (Figure 2F). On his follow-up examination 5 months post-MIE presentation and 8 months after initial presentation of osteomyelitis, his osteomyelitis had resolved, and he was no longer taking any antibiotics. Additionally, there were no sequelae of MIE or recurrence of neurologic abnormalities.
Discussion
Metronidazole is known to penetrate through the blood-brain barrier, with extensive distribution in the brain (2). It is metabolized in the liver and excreted in the kidneys. Renal or hepatic dysfunction may result in build-up of metronidazole, leading to central nervous system toxicity (3). However, the exact mechanism is unknown. Because MIE shows similar clinical and imaging findings to Wernicke encephalopathy, it has been hypothesized that thiamine deficiency may be a contributor to MIE (3, 4). Alston and colleagues demonstrated that metronidazole can react with thiamine in the gastrointestinal tract through bacterial thiaminase in vitro (4). This reaction produces a thiamine analogue that can competitively inhibit the downstream action of thiamine and can lead to thiamine deficiency–like findings (5). A recent systematic review by Sørenson and colleagues of 136 MIE patients from case series and case reports identified various risk factors for MIE (3). In their study, the average duration of treatment with metronidazole before symptom onset was 47.2 days. Higher cumulative doses of metronidazole and longer treatment durations were associated with an increased risk for MIE. Patients with difficult-to-treat infections, such as osteomyelitis, complications of inflammatory bowel disease, and large abscesses necessitating extended antibiotic therapy, were at higher risk for MIE (3). Chronic hepatic and renal impairments were also more prevalent (3). Our patient’s risk factors were cirrhosis and having received a prolonged metronidazole regimen for osteomyelitis.
The clinical manifestations of MIE are diverse. Sørensen and colleagues observed that the most prevalent symptoms were dysarthria (63%), gait instability (55%), limb discoordination (53%), delirium (41%), and polyneuropathy (30%) (3). Seizures, dysphagia, and myoclonus could also be present (3). In our patient, presenting symptoms included dysarthria, dysphagia, gait ataxia, and delirium.
Metronidazole-induced encephalopathy should be suspected when a patient presents with cerebellar dysfunction and symptoms of encephalopathy in the context of recent metronidazole use. The differential diagnosis for encephalopathy with delirium, gait ataxia, and dysarthria is broad and includes Wernicke encephalopathy, Marchiafava-Bignami disease, and hepatic encephalopathy. The diagnosis of MIE relies heavily on brain MRI findings of hyperintense lesions of the dentate nuclei and the splenium of the corpus callosum, distinguishing MIE from other encephalopathies (Table 2).
Table 2. Differential Diagnosis of MIE and Detailed Table Listing Medical Conditions Resembling MIE With Common Clinical and Imaging Findings.
Differential Diagnosis | Typical Clinical Manifestations | Typical CNS MRI Findings |
---|---|---|
Wernicke encephalopathy | Ataxia, gait instability, altered mental status, oculomotor disturbances, polyneuropathy | Bilateral symmetrical T2 hyperintense lesions in the periventricular regions of the mammillary body, medial thalamus, floors of the 3rd and 4th ventricles, periaqueductal gray matter, and midbrain tectum |
Marchiafava-Bignami disease | Altered mental status, seizures, gait instability | Cystic degeneration of the corpus callosum |
Hepatic encephalopathy | Altered mental status, rigidity, dysarthria, resting or kinetic tremor, dysdiadochokinesia | Hyperintense lesions of the globus pallidum on T1 imaging. Increased glutamine/glutamate peak and decreased myoinositol and choline signals on PMRS |
Chronic methyl bromide intoxication | Neurobehavioral changes (e.g., apathy, aphasia, decreased libido, etc.), dysarthria, ataxia, chorea, extrapyramidal deficits, visual disturbances | T2/FLAIR-hyperintense lesions in the dentate nuclei, splenium of corpus callosum and the brainstem |
Antibiotic-associated encephalopathy type 1 (penicillin, cephalosporins) | Seizures, myoclonus (symptom onset occurs within days on treatment initiation) | Normal MRI |
Antibiotic-associated encephalopathy type 2 (procaine, penicillin, sulfonamides, fluoroquinolones, macrolides) | Psychosis (symptom onset within days of treatment initiation) | Normal MRI |
Antibiotic-associated encephalopathy type 3 (metronidazole) | Dysarthria, ataxia, dysmetria, altered mental status | Bilateral and symmetrical hyperintense lesions of cerebellar dentate nuclei, dorsal medulla, dorsal pons, midbrain, and splenium of the corpus callosum on T2 and FLAIR |
CNS = central nervous system; FLAIR = fluid-attenuated inversion recovery; MIE = metronidazole-induced encephalopathy; MRI = magnetic resonance imaging; PMRS = proton magnetic resonance spectroscopy.
Management of MIE is cessation of metronidazole and supportive care. Patients usually recover rapidly after discontinuation of metronidazole. Our patient’s case followed a similar course, rapidly improving after metronidazole discontinuation. No medications are currently approved to treat MIE. Certain medications have been used anecdotally. In a case report by Li and colleagues, methylprednisolone therapy successfully treated the neurologic symptoms of MIE. The authors hypothesized that corticosteroids could reduce the inflammatory effects of MIE, leading to quicker recovery (6). In a case report, Matta and colleagues successfully used high-dose thiamine to treat a patient with MIE with known malnutrition whose condition did not improve after metronidazole cessation. It was hypothesized that malnutrition and metronidazole had additive effects, causing severe thiamine deficiency (7).
Routine measures to prevent MIE are generally not required for most patients, because metronidazole is usually well tolerated. For at-risk groups, including those with hepatic and renal disease who require extended metronidazole regimens, close follow-up should be arranged (3). Recently, the landmark trial Oral versus Intravenous Antibiotics for Bone and Joint Infection (OVIVA) demonstrated that oral antibiotics are an excellent option for treating osteomyelitis in comparison with intravenous antibiotics, which may lead to increased use of oral metronidazole (8). With a movement toward use of oral antibiotics for infections requiring prolonged treatment courses, clinicians should be aware of MIE as a possible complication of extended metronidazole therapy (8).
Oral antibiotics are increasingly used to treat osteomyelitis. Metronidazole is a well-tolerated antibiotic with excellent oral absorption. Clinicians should be aware of MIE, a rare complication in at-risk patients who present with typical neurologic symptoms. The disease is confirmed on MRI, and metronidazole should be discontinued when MIE is suspected. The prognosis after metronidazole cessation is excellent.
Postherpetic Abdominal Pseudohernia
(9). Enrique de-Madaria, et al ,Published June 26, 2024, N Engl J Med 2024;390:2308,DOI: 10.1056/NEJMicm2400595,VOL. 390 NO. 24
A 78-year-old man presented to primary care clinic with a 5-day history of constipation and flank bulge. Eight days before presentation, he had received a diagnosis of herpes zoster of the left flank and had begun to take valacyclovir. On physical examination, scabbed herpes zoster lesions were seen along the T12 dermatome (Panel A). There was also an outpouching of the left lower abdominal wall without any underlying masses or fascial defects (Panels A and B). Computed tomography of the abdomen was notable only for a protrusion of the left lower abdominal wall (Panel C, axial view, arrow). Electromyography of the left rectus abdominis muscle showed a focal axonal neuropathy. A diagnosis of postherpetic abdominal pseudohernia was made. In patients with herpes zoster, motor complications may occur if the virus spreads from its typical location in the sensory dorsal root ganglia to the motor axons of the ventral roots. Abdominal pseudohernia is one such motor complication that results from paralysis of the abdominal wall muscles in the affected dermatome. Postherpetic visceral neuropathy has also been described and was thought to be the cause of this patient’s constipation. Reassurance about the favorable prognosis of this condition was given. After 5 months, the patient’s skin changes, constipation, and pseudohernia had abated.
Ocular Bee Sting
Talia N. Shoshany etal, Published June 22, 2024,N Engl J Med 2024;390: e64,DOI: 10.1056/NEJMicm2400652,VOL. 390 NO. 24
A 55-year-old man presented to the ophthalmology clinic with worsening vision and pain in his right eye after having been stung by a bee in that eye 2 days earlier. On the day of the bee sting, the stinger had been removed at a local emergency department. On physical examination at the current presentation, vision in the right eye was limited to counting fingers. The intraocular pressure in the right eye was 16 mm Hg (reference range, 12 to 21). A slit-lamp examination with fluorescein dye —, which stains epithelial defects yellow-green — was performed. It showed conjunctival injection, inferior corneal edema, and an infiltrate at the nasal limbus with a piece of retained stinger (Panel A, arrow). A hyphema, which was attributed to iris trauma from the buried stinger and bleeding iris vessels, was also observed (Panel A, asterisk). Jeweler’s forceps were used to remove the stinger remnant (Panel B; Panel C shows the stinger remnant at 100× magnification). Ocular bee stings warrant referral to an ophthalmologist owing to the severe inflammation that may result from the injury, as well as the possibility of a retained stinger in the eye. Topical antibacterial and prednisolone eye drops were prescribed. At 5 months of follow-up, the visual acuity in the right eye had improved to 20/25.