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PubMed · 14206711

[DOUGLAS' ABSCESS].

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D DORDEVIC CAMBA. 1964. [DOUGLAS' ABSCESS].. https://pubmed.ncbi.nlm.nih.gov/14206711/

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[Perforation of the esophagus with a mediastinal abscess].

INTRODUCTION: Surgical voice rehabilitation after total laryngectomy is still only a partially solved problem. Because of easy handling and rare complications, the Provox voice prosthesis has become common in voice rehabilitation. CASE REPORT: The 69 year old patient underwent laryngectomy, selective bilateral neck dissection and the implantation of a Provox voice prosthesis because of a glottic squamous cell carcinoma (pT(4), pN(0), M(0)). Postoperative healing ensued without any complications. During adjuvant radiochemotherapy, the patient developed distinctive cervical edema which led to a tilting of the Provox prosthesis. Due to a perforation of the posterior esophageal wall, the patient developed a pronounced mediastinal abscess which was relieved through a transcervical mediastinotomy. Antibiotic therapy led to a partial remission of the symptoms. CONCLUSION: Severe complications may not only occur during the early phase of surgical voice rehabilitation, but also at a much later stage, after completion of the healing process. A voice prosthesis which is too long or generates pressure from a radiogenic edema, cannula and finger pressure used to close the tracheostoma is transmitted through the prosthesis and may lead to a perforation of the posterior esophageal wall. In particular, when the tissue is injured during the course of radiotherapy, this type of complication should be taken into consideration.

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Cases from the Osler Medical Service at Johns Hopkins University.

PRESENTING FEATURES: A 70-year-old African American man was admitted with a history of fever, chills, and malaise of several days' duration. His past medical history was notable for end-stage renal disease requiring hemodialysis, coronary artery disease, and aortic stenosis requiring a bioprosthetic aortic valve replacement. On the day of admission, the patient was noted to have a shaking chill while undergoing dialysis through his catheter and was admitted to the hospital. He complained of pain at the catheter insertion site, shortness of breath, and dyspnea on exertion, but denied chest pain. On physical examination, the patient had a temperature of 100.4 degrees F, with a heart rate of 64 beats per minute, blood pressure of 127/72 mm Hg, and an oxygen saturation of 97% on room air. He was a mildly obese man in no apparent distress. He had shotty cervical lymphadenopathy and a right subclavian dialysis catheter in place, with erythema and pus at the entry site. His jugular venous pressure was 10 cm H(2)O. Lung examination showed bibasilar rales. Heart sounds were normal, with no rub or gallop. He had a 2/6 systolic ejection murmur best heart at the left sternal border as well as a 3/6 holosystolic murmur at the apex that radiated to his left axilla. Examination of the abdomen and extremities was unremarkable. The patient's neurological examination was unremarkable, and he was alert and oriented to person, place, and time. Laboratory studies showed an elevated white blood cell count of 16,700 cells/microL. His blood urea nitrogen level was 43 mg/dL and his serum creatinine level was 4.9 mg/dL. Multiple blood cultures grew methicillin-resistant Staphylococcus aureus. An admission, chest radiograph showed no infiltrate. An admission electrocardiogram showed normal sinus rhythm with first degree atrioventricular block, left anterior fascicular block, and left ventricular hypertrophy. shows rhythm strips from lead II electrocardiograms 5 months before admission (top), on admission (middle) and 5 days after admission (bottom). What is the diagnosis?

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Class II MHC: sweetening the peptide only diet?

MHC molecules typically bind peptides to create ligands for the T cell antigen receptor. In this issue of Cell, report an unexpected association of class II MHC molecules with processed zwitterionic polysaccharides from pathogenic bacteria. The complexes appear to modulate the T cell dependent pathology of abscess formation.

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