Diagnostic et traitement des infections d'implants orthopédiques [Update on implant related infections in orthopaedic surgery. Diagnosis and treatment]

Infections associated with implants are increasingly important in modem medicine. Biofilms are the cause that these infections are more difficult to diagnose and to cure. Particularly low-grade infections are difficult to distinguish from aseptic failure, because they often present with early loosening and persisting pain. For an accurate diagnosis, clinical signs and symptoms, laboratory markers of infection, microbiology, histology and imaging examinations are needed. The treatment goal is eradication of infection and an optimal functional result. Successful treatment requires adequate surgical procedure combined with long-term antimicrobial therapy, ideally with an agent acting on biofilms.

Options chirurgicates pour l'insuffisance cardiaque terminale [Surgical options for terminal heart failure]

Terminal heart failure can be the cause or the result of major dysfunctions of the organisms. Although, the outcome of the natural history is the same in both situations, it is of prime importance to differentiate the two, as only heart failure as the primary cause allows for successful mechanical circulatory support as bridge to transplantation or towards recovery. Various objective parameters allow for the establishment of the diagnosis of terminal heart failure despite optimal medical treatment. A cardiac index <2.0 l/min, and a mixed venous oxygen saturation <60%, in combination with progressive renal failure, should trigger a diagnostic work-up in order to identify cardiac defects that can be corrected or to list the patient for transplantation with/without mechanical circulatory support.

Glomérulonéphrite rapidement progressive: une urgence diagnostique et thérapeutique [Rapidly progressive glomerulonephritis: a diagnostic and therapeutic emergency]

Rapidly progressive glomerulonephritis (RPG) is a rare clinical syndrome characterized by kidney damage that can lead to irreversible kidney failure. RPG can be caused by primary glomerular disease or can be part of a systemic autoimmune disorder. All RPG have a similar pathophysiology (proliferation of cells in Bowman's capsule and formation of crescents) and clinical evolution (rapidly progressive kidney failure with proteinuria and an active urine sediment). Immunosuppressive therapy and sometimes plasma exchanges are required. Overall- and kidney survival are closely linked to the blood creatinine level at presentation, the percentage of damaged glomeruli, and to the underlying cause. RPG is therefore a diagnostic and therapeutic emergency that needs quick referral to a nephrologist.

Reversible congestive heart failure associated with primary carnitin deficiency: report of a case and review of the literature.

A 5-year-old previously healthy boy was admitted for abdominal pain and vomiting. Physical examination showed tachypnoe (32/min), hepatomegaly and painful palpation of the upper right abdominal quadrant. Laboratory tests were normal except for elevated ammonium (202mcmol/l). Chest X-ray was performed, showing cardiomegaly and interstitial edema. Transthoracic echocardiography revealed dilated left cavities and LV hypertrophy together with a diffuse hypokinesia and LVEF of 30-40%. Diuretics and ACE-inhibitors were introduced. At that time, the differential diagnosis for the DCM included myocarditis, congenital or genetic, metabolic or autoimmune disease. The next day, the boy underwent cardiac magnetic resonance (CMR) examination, showing a severe dilatation of the LV with an end-diastolic diameter of 50mm and a volume of 150ml. LVEF was 20% with diffuse LV hypokinesia (Fig. 1). No late enhancement was present after Gadolinium injection, ruling out myocarditis. Further laboratory metabolic analysis indicated severely decreased total and free carnitin levels and low renal carnitin reabsorption, corroborating the diagnosis of primary carnitin deficiency (PCD). Carnitin substitution was initiated. The clinical condition rapidly improved. No symptoms of heart failure were present anymore. A follow-up CMR performed 9 months later confirmed the recovery. LV end-diastolic volume decreased from 150ml to 66ml, LVEF increased from 20% to 55% (Fig. 2). Late enhancement was absent after Gadolinum injection (Fig. 3).Carnitin is required for the transport of fatty acids from the cytosol into mitochondria during lipid breakdown. 75% of carnitin is obtained from food, 25% is endogenously synthesized. PCD is an autosomal recessive disorder resulting from impairment of a transporter activity, caused by mutation of the SLC22A5 gene. Incidence is about 1 in 40'000 newborns. Diagnosis is usually made at age 1 to 7. Three forms of PCD are described. In the form associated with cardiomyopathy, the disease is progressive and patient die from heart failure if not treated. Substitution of L-Carnitin leads to a dramatic improvement of disease course.This case underlines the crucial role of etiologic diagnostics in this reversible form of DCM. Early diagnostics and therapy are critical for the prognosis of the patient. This is furthermore an example of a role played by CMR in the diagnostic work-up of heart failure and its follow-up under therapy.

L'hémopéritoine spontané: diagnostic, pronostic et thérapeutiques possibles [Spontaneous hemoperitoneum: diagnosis, prognosis and possible therapeutics]

We report the case of a 58-year-old diabetic man admitted to the hospital in a comatose state due to medicamentous hypoglycemia in a context of hypovolemic acute renal failure. Hypovolemia was due to hemoperitoneum in a alcoholic patient with cirrhotic hepatic failure. CT-scan and arterial angiographies revealed a voluminous isolated hepatic mass with active bleeding suggesting the diagnosis of spontaneous bleeding from a hepatocellular carcinoma. The hemorrhage resolved after selective arterial embolization, but the patient died two weeks later from an infectious cause. The differential diagnosis of a spontaneous hemoperitoneum and possibilities of treatment in the case of ruptured hepatocellular carcinoma are discussed.

Maladie de Fabry: du diagnostic a l'enzymotherapie substitutive. [Fabry disease: diagnostic due of substitutive enzyme-therapy]

Fabry disease is a X-linked sphingolipid storage disorder resulting from the defective activity of the lysosomal enzyme, alpha-galactosidase A. Hemizygotes develop severe multisystemic disease, dominated by renal failure and progressive neurological and cardiac involvement, causing premature death. Thirty percent of heterozygotes have severe involvement of one or several organs. With developments in molecular biology, it is now possible to produce the human recombinant enzyme alpha-galactosidase A. More than 20 patients are now treated in Switzerland.

Vancomycin-intermediate Staphylococcus aureus selected during vancomycin therapy of experimental endocarditis are not detected by culture-based diagnostic procedures and persist after treatment arrest.

OBJECTIVES: Laboratory detection of vancomycin-intermediate Staphylococcus aureus (VISA) and their heterogeneous VISA (hVISA) precursors is difficult. Thus, it is possible that vancomycin failures against supposedly vancomycin-susceptible S. aureus are due to undiagnosed VISA or hVISA. We tested this hypothesis in experimental endocarditis.¦METHODS: Rats with aortic valve infection due to the vancomycin-susceptible (MIC 2 mg/L), methicillin-resistant S. aureus M1V2 were treated for 2 days with doses of vancomycin that mimicked the pharmacokinetics seen in humans following intravenous administration of 1 g of the drug every 12 h. Half of the treated animals were killed 8 h after treatment arrest and half 3 days thereafter. Population analyses were done directly on vegetation homogenates or after one subculture in drug-free medium to mimic standard diagnostic procedures.¦RESULTS: Vancomycin cured 14 of 26 animals (54%; P<0.05 versus controls) after 2 days of treatment. When vegetation homogenates were plated directly on vancomycin-containing plates, 6 of 13 rats killed 8 h after treatment arrest had positive cultures, 1 of which harboured hVISA. Likewise, 6 of 13 rats killed 3 days thereafter had positive valve cultures, 5 of which harboured hVISA. However, one subculture of vegetations in drug-free broth was enough to revert all the hVISA phenotypes to the susceptible pattern of the parent. Thus, vancomycin selected for hVISA during therapy of experimental endocarditis due to vancomycin-susceptible S. aureus. These hVISA were associated with vancomycin failure. The hVISA phenotype persisted in vivo, even after vancomycin arrest, but was missed in vitro after a single passage of the vegetation homogenate on drug-free medium.¦CONCLUSIONS: hVISA might escape detection in clinical samples if they are subcultured before susceptibility tests.

La néphropathie ischémique par athérosclérose aortorénale : diagnostic [Atherosclerotic renal artery disease diagnosis update].

Atherosclerotic renal artery disease represents a cause of which little is known but not a cause to be neglected for hypertension and renal insufficiency. Even though its occurrence remains badly defined, atherosclerotic renal artery disease is constantly on the rise due to the aging population, the never prevailing hypertension and diabetes mellitus. This review aims to give a clinical profile of patients presenting with atherosclerotic renal artery disease and to discuss, in the light of study results, which diagnostic evaluation should be used considering the sequence and the benefit and risk of each in order to initiate a personalized treatment. Patients affected by atherosclerotic renal artery disease are likely to have more complications and more extensive target-organ damage than patients without renal artery stenosis. The evolution of the atherosclerotic renal artery disease is in general slow and progressive. Nevertheless, certain clinical cases manifest themselves with the onset of acute renal failure bought upon by the administration of blockers of the rennin-angiotensin-aldosterone system, or by some other causes responsible for a sudden drop in renal plasma flow (e.g., thrombosis of the renal artery). The relationship between atherosclerotic renal artery disease and atherosclerosis is complex, and mediators implicated in the pathophysiology of renovascular disease may also contribute to the progression of cardiovascular damage. An early assumption of the atherosclerotic renal artery stenosis is warranted to determine the adapted treatment (i.e., medical treatment, revascularisation...) just as the assumption and the correction of the more general cardiovascular risk factors.

Evaluation of C-reactive protein, procalcitonin, tumor necrosis factor alpha, interleukin-6, and interleukin-8 as diagnostic parameters in sepsis-related fatalities.

The aims of this study were to investigate the usefulness of serum C-reactive protein, procalcitonin, tumor necrosis factor alpha, interleukin-6, and interleukin-8 as postmortem markers of sepsis and to compare C-reactive protein and procalcitonin values in serum, vitreous humor, and cerebrospinal fluid in a series of sepsis cases and control subjects, in order to determine whether these measurements may be employed for the postmortem diagnosis of sepsis. Two study groups were formed, a sepsis group (eight subjects coming from the intensive care unit of two university hospitals, with a clinical diagnosis of sepsis in vivo) and control group (ten autopsy cases admitted to two university medicolegal centers, deceased from natural and unnatural causes, without elements to presume an underlying sepsis as the cause of death). Serum C-reactive protein and procalcitonin concentrations were significantly different between sepsis cases and control cases, whereas serum tumor necrosis factor alpha, interleukin-6, and interleukin-8 values were not significantly different between the two groups, suggesting that measurement of interleukin-6, interleukin-8, and tumor necrosis factor alpha is non-optimal for postmortem discrimination of cases with sepsis. In the sepsis group, vitreous procalcitonin was detectable in seven out of eight cases. In the control group, vitreous procalcitonin was clearly detectable only in one case, which also showed an increase of all markers in serum and for which the cause of death was myocardial infarction associated with multi-organic failure. According to the results of this study, the determination of vitreous procalcitonin may be an alternative to the serum procalcitonin for the postmortem diagnosis of sepsis.

Sensitivity and specificity of NT-proBNP to detect heart failure at post mortem examination.

NT-proBNP, a marker of cardiac failure, has been shown to be stable in post mortem samples. The aim of this study was to assess the accuracy of NT-proBNP to detect heart failure in the forensic setting. One hundred sixty-eight consecutive autopsies were included in the study. NT-proBNP blood concentrations were measured using a chemiluminescent immunoassay kit. Cardiac failure was assessed by three independent forensic experts using macro- and microscopic findings complemented by information about the circumstances of body discovery and the known medical story. Area under the receiving operator curve was of 65.4% (CI 95%, from 57.1 to 73.7). Using a standard cut-off value of >220 pg/mL for NT-proBNP blood concentration, heart failure was detected with a sensitivity of 50.7% and a specificity of 72.6%. NT-proBNP vitreous humor values were well correlated to the ones measured in blood (r (2) = 0.658). Our results showed that NT-proBNP can corroborate the pathological findings in cases of natural death related to heart failure, thus, keeping its diagnostic properties passing from the ante mortem to the post mortem setting. Therefore, biologically inactive polypeptides like NT-proBNP seem to be stable enough to be used in forensic medicine as markers of cardiac failure, taking into account the sensitivity and specificity of the test.

Migrated foreign body liver abscess: illustrative case report, systematic review, and proposed diagnostic algorithm.

Pyogenic liver abscess is a severe condition and a therapeutic challenge. Treatment failure may be due to an unrecognized ingested foreign body that migrated from the gastrointestinal tract. There has recently been a marked increase in the number of reported cases of this condition, but initial misdiagnosis as cryptogenic liver abscess still occurs in the majority of cases. We conducted the current study to characterize this entity and provide a diagnostic strategy applicable worldwide. To this end, data were collected from our case and from a systematic review that identified 59 well-described cases. Another systematic review identified series of cryptogenic-and Asian Klebsiella-liver abscess; these data were pooled and compared with the data from the cases of migrated foreign body liver abscess. The review points out the low diagnostic accuracy of history taking, modern imaging, and even surgical exploration. A fistula found through imaging procedures or endoscopy warrants surgical exploration. Findings suggestive of foreign body migration are symptoms of gastrointestinal perforation, computed tomography demonstration of a thickened gastrointestinal wall in continuity with the abscess, and adhesions seen during surgery. Treatment failure, left lobe location, unique location (that is, only 1 abscess location within the liver), and absence of underlying conditions also point to the diagnosis, as shown by comparison with the cryptogenic liver abscess series. This study demonstrates that migrated foreign body liver abscess is a specific entity, increasingly reported. It usually is not cured when unrecognized, and diagnosis is mainly delayed. This study provides what we consider the best available evidence for timely diagnosis with worldwide applicability. Increased awareness is required to treat this underestimated condition effectively, and further studies are needed.

Fibrose rétropéritonéale: cause rare d'insuffisance rénale postrénale, a ne pas méconnaître [Retroperitoneal fibrosis: a rare cause of postrenal kidney failure, no to be missed].

We report the observation of a fifty years old man, admitted in the emergency room for bilateral lumbar pain and hyperkaliemic metabolic acidosis, and postrenal kidney failure induced by bilateral hydronephrosis. Radiographic exploration and histologic studies of biopsy confirmed an idiopathic retroperitoneal fibrosis that clinically and biologicaly responded to three seances of hemodialysis, and insertion in each uretere of one double J stent, and long term corticotherapy. The retroperitoneal fibrosis is a little common inflammatory disease, characterized by the development of a fibrous mass around the retroperitoneal structures. His diagnostic means evolved. On the other hand, his treatment was the object of no checked controlled and randomized trial. This article proposes an updating of the knowledge on this subject.

Early prediction of response to sunitinib after imatinib failure by 18F-fluorodeoxyglucose positron emission tomography in patients with gastrointestinal stromal tumor.

PURPOSE: Positron emission tomography with (18)F-fluorodeoxyglucose (FDG-PET) was used to evaluate treatment response in patients with gastrointestinal stromal tumors (GIST) after administration of sunitinib, a multitargeted tyrosine kinase inhibitor, after imatinib failure. PATIENTS AND METHODS: Tumor metabolism was assessed with FDG-PET before and after the first 4 weeks of sunitinib therapy in 23 patients who received one to 12 cycles of sunitinib therapy (4 weeks of 50 mg/d, 2 weeks off). Treatment response was expressed as the percent change in maximal standardized uptake values (SUV). The primary end point of time to tumor progression was compared with early PET results on the basis of traditional Response Evaluation Criteria in Solid Tumors (RECIST) criteria. RESULTS: Progression-free survival (PFS) was correlated with early FDG-PET metabolic response (P < .0001). Using -25% and +25% thresholds for SUV variations from baseline, early FDG-PET response was stratified in metabolic partial response, metabolically stable disease, or metabolically progressive disease; median PFS rates were 29, 16, and 4 weeks, respectively. Similarly, when a single FDG-PET positive/negative was considered after 4 weeks of sunitinib, the median PFS was 29 weeks for SUVs less than 8 g/mL versus 4 weeks for SUVs of 8 g/mL or greater (P < .0001). None of the patients with metabolically progressive disease subsequently responded according to RECIST criteria. Multivariate analysis showed shorter PFS in patients who had higher residual SUVs (P < .0001), primary resistance to imatinib (P = .024), or nongastric GIST (P = .002), regardless of the mutational status of the KIT and PDGFRA genes. CONCLUSION: Week 4 FDG-PET is useful for early assessment of treatment response and for the prediction of clinical outcome. Thus, it offers opportunities to individualize and optimize patient therapy.

Tuberculose miliaire chez une personne âgée: diagnostic inattendu à l'autopsie [Miliary tuberculosis: unexpected autopsy finding in an elderly person].

Miliary tuberculosis is a rare disease that is difficult to diagnose because of its non-specific presentation. It should be suspected in elderly patients who complaint of failure to thrive, unexplained fatigue and weight loss. Using a clinical situation where the diagnosis was made only at autopsy, we briefly review the epidemiology of miliary tuberculosis and propose recommendations for the diagnosis and the prophylaxis of latent tuberculosis. Finally, we discuss criteria to perform epidemiological investigations among close contacts in this situation.