[Abdominal necrotizing fasciitis after caesarean delivery]. / Fasciite nécrosante de la paroi abdominale post-césarienne.

Necrotizing fasciitis (NF) is a rare infection (0,2 to 0,4/100,000 adults) of the dermis and hypodermis extending along muscular fascia1. The absence of pathognomonic symptoms makes its diagnosis difficult. Rapidly progressive, it is a life-threatening emergency whose prognosis is letal in 30 % of cases. Treatment of necrotizing fasciitis is mixed and involves aggressive surgical debridement and medical treatment with antibiotics and supportive agents. This article is presenting the case of a young woman who developed abdominal necrotizing fasciitis following a caesarean section. In forty-eight hours, the patient developed septic shock with an extensive and rapid destruction of her abdominal wall. After hysterectomy and multiple surgical debridements, evolution was favorable. After one month, a reconstruction of the abdominal wall could be performed.

La fasciite nécrosante (NF) est une infection rare (0,2 à 0,4/100.000 adultes) caractérisée par une dermo-hypodermite nécrosante s'étendant le long des fascias sous-cutanés. L'absence de symptôme pathognomonique rend son diagnostic difficile. D'évolution rapidement progressive, il s'agit d'une urgence vitale dont le pronostic est fatal dans 30 % des cas. Le traitement est mixte et associe un débridement chirurgical agressif à un traitement médical à base d'antibiotiques et d'agents supportifs. Cet article reprend le cas d'une jeune femme ayant développé une fasciite nécrosante abdominale suite à une césarienne. En quarante-huit heures, la patiente a présenté un choc septique avec une destruction extensive et rapide de sa paroi abdominale. Une hystérectomie et de multiples débridements chirurgicaux ont permis une évolution favorable. Après un mois, une reconstruction de sa paroi abdominale a pu être effectuée.

Cerebral venous thrombosis and procoagulant factors--a case study.

Cerebral venous thrombosis is a polymorphic clinical entity for which diagnosis has become more frequent with the advent of neuroradiology. The superior sagittal and transverse sinuses are frequently involved, whereas cavernous sinus thrombosis is much less frequent. Inherited resistance to the anticoagulant action of activated protein C (APC resistance), antithrombin deficiency, protein C and S deficiencies, and hyperhomocysteinemia seem to represent major causes of thrombophilia when unusual thromboembolic events (ie, before the age of 45 years) are observed. The authors present the combined occurrence of protein C and protein S deficiencies in a 32-year-old woman, manifested by extensive cerebral venous thrombosis.

Blood lactate levels are better prognostic indicators than TNF and IL-6 levels in patients with septic shock.

OBJECTIVE: Both serum levels of tumor necrosis factor-alpha (TNF alpha) and interleukin-6 (IL-6) and blood lactate levels in patients with septic shock have been shown to correlate with prognosis. The aim of the study was to define the relative predictive value of these measures. PATIENTS: 38 hospitalized patients with septic shock, including 18 survivors and 20 non-survivors. INTERVENTION: Blood TNF alpha (immunoradiometric assay), IL-6 (bioassay) and lactate (enzymatic method) levels were serially measured at the onset of septic shock and after 24 and 48 h. RESULTS: TNF alpha levels tended to be higher in the non-survivors than in the survivors at the onset of shock (204 +/- 392 vs 129 +/- 195 pg/ml, p = NS) but decreased similarly in both groups with time (p = 0.03). IL-6 levels at admission were highly variable (9656 +/- 19851 U/ml in the non-survivors and 69,222 +/- 248,804 U/ml in the survivors). Log IL-6 decreased similarly in both groups with time (p = 0.004). Admission blood lactate levels were higher in the non-survivors than in the survivors (6.11 +/- 4.78 mEq/l vs 3.49 +/- 2.00 mEq/l, p < 0.05) and decreased significantly with time in all patients (p = 0.024). However, this decrease was greater in the survivors than in the non-survivors (p = 0.003). CONCLUSION: These data indicate that the large variability in TNF alpha and IL-6 levels limit their prognostic significance in patients with septic shock. The predictive value of the trend in cytokine levels over time is not superior to that of trends in blood lactate levels.

Corticosteroids increase blood interleukin-10 levels during cardiopulmonary bypass in men.

BACKGROUND: Interleukin (IL)-10 is a potent antiinflammatory cytokine inhibiting the release of tumor necrosis factor--alpha (TNF-alpha) and IL-8 by activated macrophages and polymorphonuclear leukocytes. Cardiopulmonary bypass (CPB) represents a unique situation where an inflammatory reaction is predictably induced. The present study examined the influence of CPB on the release of TNF-alpha, IL-1 beta, IL-8, and IL-10 and also defined the effects of pretreatment with corticosteroids on the release of these cytokines. METHODS: The study included 22 patients undergoing coronary artery bypass graft operations, including eight control patients and seven patients who received dexamethasone, and seven patients who received methylprednisolone 4 hours before the operation. Cytokines were measured with the enzyme-linked immunosorbent assay technique before treatment, before anesthesia induction, immediately before heparin administration, before aorta declamping, 10 minutes and 90 minutes after aorta declamping, and 4 hours after the end of CPB. RESULTS: In the control patients the TNF-alpha levels and especially the IL-8 levels increased during CPB and reached their maximal levels 4 hours after CPB. IL-10 levels rose moderately and transiently, reaching peak values 90 minutes after aorta declamping. Notably, administration of corticosteroids prevented IL-8 release but increased IL-10 levels, which were tenfold higher than in the control group 90 minutes after aorta declamping (dexamethasone, 271 +/- 128 pg/ml; methylprednisolone, 312 +/- 213 pg/ml; control, 17 +/- 12 pg/ml, p < 0.05). IL-1 beta was not detected in any group of patients. CONCLUSIONS: The present data indicate that IL-10 is released together with proinflammatory cytokines during and after CPB and that pretreatment with corticosteroids markedly enhances this release. The release of IL-10 may play an important role in the antiinflammatory effects of corticosteroids.

Clinical and biological significance of interleukin-10 plasma levels in patients with septic shock.

Interleukin-10 is a potent macrophage-deactivating cytokine that inhibits lipopolysaccharide-induced tumor necrosis factor production. We determined the plasma levels of immunoreactive interleukin-10 in 16 patients with septic shock and in 11 patients with circulatory shock of nonseptic origin. In septic shock, interleukin-10 levels peaked during the first 24 h (median: 48 pg/ml) and decreased progressively till Day 5. In nonseptic shock, interleukin-10 plasma levels also increased during the first 24 h but to a lesser extent (median: 17 pg/ml). In septic shock patients, interleukin-10 plasma levels were positively correlated with tumor necrosis factor (r = 0.8, p = 0.01) and with parameters of shock severity including lactate levels (r = 0.56, p < 0.05) and correlated negatively with blood platelet counts (r = -0.65, p < 0.05). The decreased production of tumor necrosis factor-alpha and interleukin-6 after in vitro incubation of whole blood from septic shock patients with lipopolysaccharide was not influenced by in vitro neutralization of interleukin-10. We conclude that interleukin-10 is produced in patients with circulatory shock of septic and nonseptic origin and that the production of this anti-inflammatory cytokine during septic shock correlates positively with the intensity of the inflammatory response.

Administration of anti-TNF antibody improves left ventricular function in septic shock patients. Results of a pilot study.

In this pilot study, murine monoclonal anti-TNF antibody (2 mg/kg) was administered to ten patients within 24 h of septic shock which persisted after initial resuscitation with intravenous fluids and adrenergic agents. This treatment resulted in a reduction in heart rate (from 122 +/- 10 to 113 +/- 10 beats per minute at 4 h, p less than 0.01) associated with an increase in LVSWI (from 26.5 +/- 5.6 to 31.5 +/- 10.5 g.m2 at 2 h, p less than 0.05), indicating in the absence of change in cardiac filling pressures, an improvement in ventricular function. Arterial oxygenation improved concurrently in six patients. These changes, however, appeared transient. The improvement in cardiac function following anti-TNF antibody administration in patients is in keeping with recent experimental studies indicating the role of TNF in the myocardial depression characterizing septic shock.