RESUMEN
BACKGROUND: Synovial sepsis of unknown origin is a rare cause of lameness in the adult horse, and a haematogenous pathogenesis has been proposed in previous cases. OBJECTIVES: To describe the features and outcome of synovial sepsis of unknown origin in adult Thoroughbred racehorses. STUDY DESIGN: Retrospective case series. METHODS: Hospital records for admissions between 2005 and 2015 were reviewed to identify adult horses diagnosed with synovial sepsis of unknown origin. Presentation, clinicopathological, microbiological and diagnostic imaging findings were recorded. Treatment methods, surgical findings, complications and long-term outcome were evaluated. RESULTS: Eleven cases were identified over the study period. Diagnosis was established from clinical examination and clinicopathologic findings, which were comparable to other aetiologies of synovial sepsis. Affected structures included synovial joints, tendon sheaths and bursae. Concurrent osteochondritis dissecans or articular cartilage lesions were evident during arthroscopic surgery in three cases. Significant intrasynovial haemorrhage was not identified. Microbial culture of synovial fluid or synovial biopsy was positive in 6/11 of cases, with all isolates being Gram-positive cocci. Of the 6 positive microbial cultures, all isolates demonstrated in vitro sensitivity to a cephalosporin antimicrobial agent. A concurrent remote wound was present in a single case. No other potential origins of bacteraemia were identified. Treatment methods included endoscopic surgery, standing multineedle lavage, intravenous regional limb perfusion, intrasynovial medication and/or systemic antimicrobial administration. All horses survived to hospital discharge. For the 6/11 cases that raced following synovial sepsis, the median period for return to racing was 221 days. MAIN LIMITATIONS: A small study population, which was retrospectively reviewed. CONCLUSIONS: Synovial sepsis of unknown origin is rare in the adult Thoroughbred racehorse and can affect a range of synovial structures. A concurrent potential source of bacteraemia is rarely identified. With appropriate management, the prognosis to return to racing is fair.
Asunto(s)
Antibacterianos/uso terapéutico , Artroscopía/veterinaria , Enfermedades de los Caballos/diagnóstico , Sinovectomía/veterinaria , Sinovitis/veterinaria , Animales , Enfermedades de los Caballos/patología , Caballos , Estudios Retrospectivos , Membrana Sinovial , Sinovitis/patología , Sinovitis/terapia , Irrigación Terapéutica/veterinaria , Resultado del TratamientoRESUMEN
Eye injuries caused by foreign bodies are a common diagnosis in many patients with an ocular emergency. A high percentage of foreign bodies are located in the cornea and are easily removed, but an intralenticular foreign body after eye injury is very rare. A 28-year-old man referred to our department with increasing loss of vision in the right eye 1 month after an accident with a hammer and chisel. At the time of admission the patient complained of a significant loss of vision and a traumatic cataract was diagnosed. The examination showed a deep stromal corneal scar and an anterior subcapsular cataract with posterior contusional rosette. Slit-lamp examination in mydriasis aroused the suspicion of an intralenticular foreign body. An X-ray examination of the right orbit was performed, but apart from a shadow, which was interpreted by the radiologists as a "pixel artefact", it revealed no presence of a foreign body. A computed tomography examination was also undertaken and confirmed the suspicion of an intralenticular foreign body, which was confirmed by an ultrasound scan. The intralenticular foreign body was removed during cataract surgery and an IOL was successfully implanted in the intact capsular bay. The day after the surgical intervention BCVA was 1.0. Every ocular trauma with a foreign body should be examined in mydriasis in order to exclude an intralenticular foreign body. Conventional X-ray images may not always be efficient enough to detect a foreign body. If an intraocular foreign body is suspected a thin-slice computed tomography examination of the orbit should be performed.
Asunto(s)
Ceguera/diagnóstico por imagen , Ceguera/etiología , Lesiones Oculares Penetrantes/diagnóstico por imagen , Lesiones Oculares Penetrantes/etiología , Implantación de Lentes Intraoculares , Adulto , Ceguera/terapia , Lesiones Oculares Penetrantes/terapia , Humanos , Masculino , Radiografía , Resultado del TratamientoRESUMEN
BACKGROUND: We report on three cases of a progressive anterior corneal degeneration with clinical characteristics of limbal insufficiency occurring in three persons in three consecutive generations of one family. The disease has not yet been described in literature. PATIENTS: A woman aged 68, her 51 years old son and his 19 years old son are affected by the disease, which suggests autosomal dominant inheritance. None of the affected family members suffers from any form of collagenosis, endocrine insufficiency, chronic dermatosis, alteration of fat metabolism or other relevant systemic diseases. There is no accompanying disease of lids and conjunctiva except of a keratoconjunctivitis sicca with alteration of the mucin phase. The youngest affected member has a binocular anterior polar cataract. In the eldest affected member we performed penetrating keratoplasty. HISTOPATHOLOGY: Revealed thinning of corneal epithelium, moderate intra- and subepithelial granulocytary infiltration, a marked hyaline thickening of Bowman's membrane. The adjacent stroma showed accumulation of granulocytes and an increased number of capillaries and fibroblasts. Posterior stroma, Descemet's membrane and endothelium were normal. There were no goblet cells in the central epithelium. CONCLUSIONS: The appearance of the disease in three consecutive generations (strongly suggesting autosomal dominant inheritance) and the progressivity are characteristics of a dystrophical process. Development of a circular pannus and infiltration of epithelium and stroma with granulocytes however classify the disease as a degeneration, clinically and pathologically similar to Salzmann's nodular degeneration and to autosomal dominantly inherited keratitis.