[Septic iliac artery pseudo-aneurysm and spondylodiscitis L5-S1 induced by foreign body (wood shard) after intra-abdominal penetrating injury]. / Faux anévrisme iliaque et spondylodiscite L5-S1 septiques au décours d'une plaie pénétrante abdominale avec corps étranger (écharde de bois).

We report the case of a 46-year-old man, admitted in emergency department with a small penetrating abdominal wound. Haemodynamically stable, a first surgical exploration has been performed under local anaesthesia in the emergency department, showing no evidence of peritoneal penetration. Six weeks later, a foreign body adjacent to iliac artery septic pseudoaneurysm associated to a spondylodiscitis L5-S1 was showed on multislice CT and led to exploratory laparotomy which confirmed the radiologics pictures and found a jejunal perforation.

[Widerspread septic peripheral emboli from acute Enterococcus faecalis aortic valve endocarditis in a 39-year-old patient, drug addict]. / Endocardite aortique aiguë à Enterococcus faecalis avec multiples emboles septiques périphériques chez un toxicomane de 39 ans.

Enterococci have emerged in the last decades as a major cause of nosocomial or common infections and Enterococcus faecalis is responsable for 80% of all enterococcal infection. Actually, E. faecalis is the third-most-common cause of bacterial endocarditis overall and predisposing risk factors are the existence of a prosthetic valve, the age, or a previous endocarditis. Among the complications of infective endocarditis, systemic emboli are an ominous prognostic sign. Infective endocarditis still carries high morbidity and mortality rates for the patients requiring intensive care unit admission. The choice and optimal timing depend on many factors like the tolerance of the underlying cardiac disease. Indications for urgent surgical intervention are heart failure, systemic emboli, and uncontrolled sepsis despite a first adequate antibiotic therapy associating aminopenicilline and gentamicine. We report the case of a 39-year-old patient, drug-addict, admitted to the emergency department due a respiratory insuffiency, acute abdominal pain and left brachiofacial palsy and who presented a acute native aortic valve endocarditis with renal, splenic and cerebral emboli and required an urgent mechanical valvular prosthese implantation associating to a right colostomy.

Electrical parameters and ion species for active transport in human esophageal stratified squamous epithelium and Barrett's specialized columnar epithelium.

The human esophagus is lined by stratified squamous epithelium (ESSE), and in some subjects with reflux disease the distal esophagus becomes lined by Barrett's specialized columnar epithelium (BSCE). ESSE and BSCE differ both histologically and functionally, the latter evident by differences in their in vivo transmural electrical potential difference (PD), ESSE averaging -15 mV and BSCE being greater than -25 mV. In this report we examine the basis for this difference in PD. This is done by mounting endoscopic biopsies of ESSE from 25 subjects without esophageal disease and BSCE from 19 with Barrett's esophagus in mini-Ussing chambers for electrical recordings basally and after bathing solution ion replacement. The results show that the PD of human ESSE reflects a low level of active ion transport (5.1 +/- 0.8 muA/cm(2)) combined with a high level of tissue (electrical) resistance (344 +/- 34 Omega.cm(2)) and that of BSCE reflects a high level of active transport (43.6 +/- 11.6 muA/cm(2)) combined with a low level of resistance (69 +/- 8 Omega.cm(2)). Furthermore, active transport in ESSE was principally due to sodium absorption whereas in BSCE it was equally divided between sodium absorption and anion (chloride/bicarbonate) secretion, the latter through an apical membrane, 4-acetamido4'-isothiocyano-2,2'-stilbenedisulfonic acid-sensitive anion channel. As an anion-secreting tissue with bicarbonate secretory capacity more than fivefold greater than ESSE, BSCE is better suited than ESSE for defense of the esophagus against reflux disease.

[Spontaneous spinal epidural haematoma causing rapid flaccid paraplegia in a healthy 25-year-old patient]. / Hématorachis spontané avec paraplégie flasque d'installation rapide chez un patient de 25 ans sans antécédent.

Although clinical presentation of a spinal epidural compressive haematoma is well recognized, causing acute radicular pain shortly followed by cord compression syndrome, its aetiology may pose a quandary. Rare and most commonly seen after trauma, spinal surgery, epidural anaesthesia, anticoagulation therapy, vascular malformation or coagulopathy (haemophilia), spinal epidural haematoma (SHE) can be spontaneous. Surgical decompression remains the mainstay treatment especially when the prognosis depends on the interval to surgery and the severity of preoperative neurological deficit. We report the case of a healthy 25-year-old man who presented, three days after an acute back pain, a flaccid paraplegia with urinary retention. Magnetic resonance imaging of the spinal column identified a compressive SHE extending from T3 to T6, requiring an early laminectomy. After decompression, clinical outcome revealed a complete recovery excepted some mild sensibility trouble remains.

Effect of luminal acidity on the apical cation channel in rabbit esophageal epithelium.

Esophageal epithelial cells contain an apical cation channel that actively absorbs sodium ions (Na(+)). Since these channels are exposed in vivo to acid reflux, we sought the impact of high acidity on Na(+) channel function in Ussing-chambered rabbit epithelium. Serosal nystatin abolished short-circuit current (I(sc)) and luminal pH titrated from pH 7.0 to pH > or = 2.0 had no effect on I(sc). Circuit analysis at pH 2.0 showed small, but significant, increases in apical and shunt resistances. At pH < 2.0, I(sc) increased whereas resistance (R(T)) decreased along with an increase in fluorescein flux. The change in I(sc), but not R(T), was reversible at pH 7.4. Reducing pH from 7.0 to 1.1 with H(2)SO(4) gave a similar pattern but higher I(sc) values, suggesting shunt permselectivity. A 10:1 Na(+) gradient after nystatin increased I(sc) by approximately 4 muAmps/cm(2) and this declined at pH < or = 3.5 until it reached approximately 0.0 at pH 2.0. Impedance analysis on acid-exposed (non-nystatin treated) tissues showed compensatory changes in apical (increase) and basolateral (decrease) resistance at modest luminal acidity that were poorly reversible at pH 2.0 and associated with declines in capacitance, a reflection of lower apical membrane area. In esophageal epithelium apical cation channels transport Na(+) at gradients as low as 10:1 but do not transport H(+) at gradients of 100,000:1 (luminal pH 2.0). Luminal acid also inhibits Na(+) transport via the channels and abolishes it at pH 2.0. These effects on the channel may serve as a protective function for esophageal epithelium exposed to acid reflux.

[Delayed discovery of congenital diaphragmatic hernia: diagnostic difficulties. A report of two cases]. / Les hernies diaphragmatiques congénitales de révélation tardive: difficultés diagnostiques. A propos de deux cas.

Delayed revelation of congenital diaphragmatic hernias (CDH) is not uncommon and can represent 5-30% of total CDHs. Time before diagnosis may be prolonged, sometimes to the adult period. Respiratory and gastrointestinal symptoms are frequent but not specific. The clinical presentation of delayed CDH may thus mislead the practitioner. Diagnosis can be approached and/or confirmed by plain radiography. Outcome is usually favorable after surgery. We report two cases of delayed CDH and we discuss the difficulty of diagnosis.

Calcium-switch technique and junctional permeability in native rabbit esophageal epithelium.

The Ca(2+)-switch technique was used to investigate the nature of the barrier governing (paracellular) permeability across the junctions of "native" rabbit esophageal epithelium. This was done by mounting esophageal epithelium in Ussing chambers to monitor transepithelial electrical resistance (R(T)), a marker of junctional permeability. When exposed to Ca(2+)-free Ringer solutions containing EDTA, R(T) declined approximately 35% below baseline over 2 h, and this decline reversed within 2 h by restoration of (1.2 mM) Ca(2+)-containing, normal Ringer solution ("Ca(2+)-switch technique"). Junctional resealing, i.e., increased R(T) on Ca(2+) replacement, was assessed by the Ca(2+)-switch technique and shown to be 1) specific for Ca(2+), with only Mn(2+) among substituted divalent cations yielding partial resealing; 2) a function of extracellular Ca(2+) levels because maneuvers (BAPTA/AM or A23187 exposure) to alter intracellular Ca(2+) had no effect; 3) dose dependent, requiring as a minimum > or =0.5 mM Ca(2+) and 1.2 mM Ca(2+) for optimization; and 4) independent of protein synthesis because it was not inhibited by cycloheximide. Resealing was also inhibited by luminal antibodies or synthetic peptides to the extracellular domain of E-cadherin. Immunohistochemistry revealed E-cadherin within all layers of stratum corneum in Ca(2+)-free but not Ca(2+)-containing solution. The present investigation documents, using the Ca(2+)-switch technique, that esophageal epithelial junctions contain a major Ca(2+)-dependent component and that this component reflects adhesion between the extracellular domains of E-cadherin containing a histidine-alanine-valine recognition sequence.

Dilated intercellular spaces and shunt permeability in nonerosive acid-damaged esophageal epithelium.

OBJECTIVES: It has recently been established that patients with nonerosive reflux disease have on biopsy within esophageal epithelium a lesion known as dilated intercellular spaces (DIS). METHODS: To further explore the nature and implications of this lesion, in vitro models of nonerosive acid and acid-pepsin damage were created in Ussing chamber-mounted rabbit esophageal epithelium. Using these models circuit analysis and permeability studies were carried out, the latter using dextran of varying size and human epidermal growth factor (EGF). RESULTS: Luminal HCl, pH 1.1, or HCl, pH 2.0 + pepsin, 1 mg/ml, for 30 min significantly reduced transepithelial electrical resistance (RT) but produced no gross erosions or histologic evidence of cell necrosis. Transmission electron microscopy, however, documented the presence of DIS. Circuit analysis on healthy esophageal epithelium showed that shunt resistance (RS) was much lower than apical membrane, basolateral membrane and transcellular resistances (Ra, Rb, and Rcell, respectively) and approached that of RT. Further, circuit analysis on acid and acid-pepsin damaged tissues showed that the declines in RT resulted from declines in RS. Moreover, the declines in RT (and so RS) were associated with a linear increase in permeability to 4 kD dextrans as well as an increase in permeability to 6 kD EGF and dextrans as large as 20 kD. CONCLUSIONS: In nonerosive acid-damaged esophageal epithelium DIS develop in association with and as a marker of reduced transepithelial resistance and increased shunt permeability. This change in shunt permeability upon acid or acid-pepsin exposure is substantial, permitting dextran molecules as large as 20 kD (33 A) to diffuse across the epithelium. Also, this shunt leak enables luminal EGF at 6 kD to diffuse across the acid-damaged epithelium and by so doing enables it to access its receptors on epithelial basal cells. We hypothesize that the shunt leak of EGF may in part account for the development of a reparative phenomenon on esophageal biopsy in patients with nonerosive reflux disease known as basal cell hyperplasia.

Physiological and morphological effects of alendronate on rabbit esophageal epithelium.

Alendronate, an aminobisphosphonate, produces as a side effect a topical (pill induced) esophagitis. To gain insight into this phenomenon, we assessed the effects of luminal alendronate on both esophageal epithelial structure and function. Sections of rabbit esophageal epithelium were exposed to luminal alendronate at neutral or acidic pH while mounted in Ussing chambers to monitor transmural electrical potential difference (PD), short-circuit current (I(sc)), and resistance (R). Morphological changes were sought by light microscopy in hematoxylin and eosin-stained sections. Impedance analysis was used for localization of alendronate-induced effects on ion transport. Luminal, but not serosal, alendronate (pH 6.9-7.2), increased PD and I(sc) in a dose- and time-dependent manner, with little change in R and mild edema of surface cell layers. The changes in I(sc) (and PD) were reversible with drug washout and could be prevented either by inhibition of Na,K-ATPase activity with serosal ouabain or by inhibition of apical Na channels with luminal acidification to pH 2.0 with HCl. An effect on apical Na channel activity was also supported by impedance analysis. Luminal alendronate at acidic pH was more damaging than either alendronate at neutral pH or acidic pH alone. These data suggest that alendronate stimulates net ion (Na) transport in esophageal epithelium by increasing apical membrane sodium channel activity and that this occurs with limited morphological change and no alteration in barrier function. Also alendronate is far more damaging at acidic than at neutral pH, suggesting its association with esophagitis requires gastric acid for expression. This expression may occur either by potentiation between the damaging effects of (refluxed) gastric acid and drug or by acid-induced conversion of the drug to a more toxic form.