Acute mesenteric ischemia of arterial origin: importance of early revascularization

Voir aussi : F. Plumereau, S. Mucci, P. Le Naoures, J.B. Finel, A. Hamy. Ischémie mésentérique aiguë d’étiologie artérielle : intérêt d’une revascularisation précoce. Journal de Chirurgie Viscérale, Volume 152, Issue 1, February 2015, pp. 16-21. doi:10.1016/j.jchirv.2014.07.014

Early markers for myocardial ischemia and sudden cardiac death.

The post-mortem diagnosis of acute myocardial ischemia remains a challenge for both clinical and forensic pathologists. We performed an experimental study (ligation of left anterior descending coronary artery in rats) in order to identify early markers of myocardial ischemia, to further apply to forensic and clinical pathology in cases of sudden cardiac death. Using immunohistochemistry, Western blots, and gene expression analyses, we investigated a number of markers, selected among those which are currently used in emergency departments to diagnose myocardial infarction and those which are under investigation in basic research and autopsy pathology studies on cardiovascular diseases. The study was performed on 44 adult male Lewis rats, assigned to three experimental groups: control, sham-operated, and operated. The durations of ischemia ranged between 5 min and 24 h. The investigated markers were troponins I and T, myoglobin, fibronectin, C5b-9, connexin 43 (dephosphorylated), JunB, cytochrome c, and TUNEL staining. The earliest expressions (≤30 min) were observed for connexin 43, JunB, and cytochrome c, followed by fibronectin (≤1 h), myoglobin (≤1 h), troponins I and T (≤1 h), TUNEL (≤1 h), and C5b-9 (≤2 h). By this investigation, we identified a panel of true early markers of myocardial ischemia and delineated their temporal evolution in expression by employing new technologies for gene expression analysis, in addition to traditional and routine methods (such as histology and immunohistochemistry). Moreover, for the first time in the autopsy pathology field, we identified, by immunohistochemistry, two very early markers of myocardial ischemia: dephosphorylated connexin 43 and JunB.

Analysis of only 0-1 min clip or 1-4 min Clip for focal liver lesions during contrast-enhanced ultrasonography

Purpose: To evaluate the reliability of analysis of only 0-1min clips and 1-4min clips versus the entire clips in performing contrast-enhanced ultrasonography (CEUS) of focal liver lesions (FLLs). Methods: Contrast-enhanced ultrasonography (CEUS) examinations of 43 single FLLs were performed. All clips were analyzed in three ways, the entire clips, 0-1 min clips and 1-4 min clips, benign or malignant diagnosis and pathological diagnosis of each FLL were concluded by the three ways subsequently. Results: The results of correct diagnosis were assessed using Chi-square test. There was no difference with regard to benign or malignant diagnosis, between 0-1min clips and the entire clips, or between 1-4 min clips and the entire clips (p = 0.243 and p = 0.747, respectively). Moreover, no significant differences in pathological diagnosis existed between 0-1min clips and the entire clips, and 1- 4min clips versus entire clips (p=0.808 and p = 0.808, respectively). No significant differences existed among CEUS entire clip, 0-1min clip and 1-4min clip in identifying FLLs, and based on which the diagnosis of two different FLLs during CEUS with only one injection of contrast agent can be available. Conclusion: Only 0-1min clips or 1-4 min clips can be used to instead of the entre clip in performing CEUS of FLLs.

Myocardial edema after ischemia/reperfusion is not stable and follows a bimodal pattern: Imaging and histological tissue characterization

It is widely accepted that edema occurs early in the ischemic zone and persists in stable form for at least 1 week after myocardial ischemia/reperfusion. However, there are no longitudinal studies covering from very early (minutes) to late (1 week) reperfusion stages confirming this phenomenon. This study sought to perform a comprehensive longitudinal imaging and histological characterization of the edematous reaction after experimental myocardial ischemia/reperfusion. The study population consisted of 25 instrumented Large-White pigs (30 kg to 40 kg). Closed-chest 40-min ischemia/reperfusion was performed in 20 pigs, which were sacrificed at 120 min (n = 5), 24 h (n = 5), 4 days (n = 5), and 7 days (n = 5) after reperfusion and processed for histological quantification of myocardial water content. Cardiac magnetic resonance (CMR) scans with T2-weighted short-tau inversion recovery and T2-mapping sequences were performed at every follow-up stage until sacrifice. Five additional pigs sacrificed after baseline CMR served as controls. In all pigs, reperfusion was associated with a significant increase in T2 relaxation times in the ischemic region. On 24-h CMR, ischemic myocardium T2 times returned to normal values (similar to those seen pre-infarction). Thereafter, ischemic myocardium-T2 times in CMR performed on days 4 and 7 after reperfusion progressively and systematically increased. On day 7 CMR, T2 relaxation times were as high as those observed at reperfusion. Myocardial water content analysis in the ischemic region showed a parallel bimodal pattern: 2 high water content peaks at reperfusion and at day 7, and a significant decrease at 24 h. Contrary to the accepted view, myocardial edema during the first week after ischemia/reperfusion follows a bimodal pattern. The initial wave appears abruptly upon reperfusion and dissipates at 24 h. Conversely, the deferred wave of edema appears progressively days after ischemia/reperfusion and is maximal around day 7 after reperfusion.

Late onset spinal cord ischemia after thoracoabdominal aortic aneurysm open repair

The aim of this study is to evaluate if spinal cord ischemia (SCI), especially its late presentation, and can be correlated to the results of intraoperative evoked potential monitoring (IOM). Methods. This study is a physician-initiated, retrospective, single-center, non-randomized study. Data from all patients undergoing a thoracoabdominal aortic aneurysm surgical repair (TAAA SR) between January 2016 and March 2020 IOM was collected and analyzed. Results. During the study period, 261 patients underwent TAAA SR with MEP/SSEPs monitoring [190 males, 73%; median age 65 (57-71)]. Thirty-seven patients suffered from SCI, for an overall rate of 14% (permanent 9%). When stratifying patients according to the SCI onset, 18 patients presented with an early (11 permanent) and 19 with a late SCI (<24h) (11 permanent). Of 261 patients undergoing TAAA SR with IOM, 15 were excluded due to changes in the upper extremity motor evoked potentials. For the remaining 246, the association between SCI and IOM was investigated: only irreversible IOM loss without peripheral changes have been found to be a risk factor for late onset SCI (p=.006). Furthermore, given that no statistical differences were found between the two groups when no IOM changes were recorded (p=.679), this situation cannot reliably rule out any SCI in our cohort. Independent risk factors for late spinal cord ischemia onset found at multivariate analysis were smoking history (p=.008), BMI>28 (p=.048) and TAAA extent II (p=.009). The irreversible MEP change without peripheral showed a trend of significance (p=.052). Conclusions. Evoked potential intraoperative monitoring is an important adjunct during thoracoabdominal aortic open repair to predict and possibly prevent spinal cord ischemia. Irreversible IOM loss without peripheral changes was predictive of late SCI, therefore more attention should be paid to the postoperative management of this subgroup of patients.

Effetto dell' ormone tiroideo (T3) durante ex vivo lung perfusion (EVLP) sul polmone di ratto: valutazione dell'azione protettiva nel danno da ischemia riperfusione.

La perfusione polmonare extracorporea (EVLP) è una tecnica utilizzata dal 2010 per valutare e migliorare la qualità dell'organo da trapiantare e il danno da ischemia-ripefusione (IRI). Tale perfusione utilizza la soluzione di Steen, la cui composizione è solo parzialmente nota. Lo scopo è quello di identificare gli effetti di T3 su IRI polmonare ex vivo, in un modello di ratto di donatore a cuore non battente. Animali (40) randomizzati in otto gruppi e il protocollo EVLP sono stati standardizzati nel nostro centro. Sono state valutate la funzione polmonare, PEEP, la resistenza vascolare polmonare totale a 45, 60, 120 e 180 minuti di EVLP per eseguire analisi di gas, dosaggio del mediatore di infiammazione, mitocondriale libero DNA, freeT3 e freeT4. Alla fine dei campioni di tessuto polmonare sono stati congelati dal dosaggio ATP, espressione genica, DNA mitocondriale, T3. Non date le concentrazioni del produttore, abbiamo analizzato gli acidi grassi liberi, vitamine, ormoni e composizione della soluzione Steen. Risultati La soluzione di steen contiene albumina umana x2 nel siero umano (7,5-8 g/dl): le concentrazioni di ft4 e ft3 sono x2 quelle nel siero umano e vengono rilasciati dall'albumina. La concentrazione di ft4 e ft3 non è cambiata durante l'EVLP. La Steen ha alta fluorescenza per l'alta concentrazione delle molecole aromatiche (ormoni) mai descritto in precedenza. NADH e mtDNA nel perfused aumenta con danno ischemico e nel gruppo trattato con T3 Conclusione Il modello EVLP è già convalidato nella perfusione nel trapianto polmonare, ma è necessario approfondire l'effetto della Steen in termini di ormoni e analiti. L'effetto sull'IRI dell'EVLP sembra essere influenzato negativamente da un T3 troppo alto in Steen, cosa che descriviamo per la prima volta. L'ulteriore aggiunta di T3 provoca disfunzione mitocondriale e infiammazione.

Medial Artery Calcification (MAC) e Small Artery Disease (SAD) nei pazienti con ischemia critica degli arti inferiori: definizione dei fattori predisponenti, svilup-po di uno score prognostico, definizione istopatologica e valutazione dei risultati dell'arterializzazione delle vene dell'arto inferiore come tecnica di rivascolarizzazione

Questo studio si concentra sull'ischemia critica cronica dell'arto inferiore (CLTI), una patologia globale con gravi complicanze e impatto sociale elevato. Recentemente, la "Medial Artery Calcification" (MAC) è emersa come fattore prognostico significativo nei pazienti con CLTI e malattia grave dei vasi del piede, ma le informazioni sono principalmente retrospettive. Questa tesi esplora la relazione tra MAC e CLTI in tre sezioni. Nella sezione clinica, 248 pazienti sono stati divisi in gruppi MAC per valutare l'impatto prospettico sulla guarigione e sul salvataggio dell'arto. Nella sezione isto-patologica, campioni arteriosi di 26 pazienti sottoposti ad amputazione maggiore sono stati analizzati per comprendere la relazione tra MAC, aterosclerosi e occlusione vascolare. Nella sezione di arterializzazione, 16 pazienti sottoposti all'arterializzazione delle vene del piede (AVP) sono stati esaminati per valutare i risultati clinici prospettici. I risultati della sezione clinica indicano che la presenza di MAC severa è associata a risultati clinici peggiori nei pazienti affetti da CLTI. L'analisi isto-patologica mostra una prevalenza elevata di MAC rispetto all'aterosclerosi, con una associazione importante tra MAC e iperplasia intimale. L'AVP presenta risultati promettenti nei pazienti affetti da CLTI. In conclusione, la MAC influisce sui risultati clinici della CLTI, e l'AVP potrebbe essere una strategia efficace di trattamento.

Role Of Astrocytes In Thiamine Deficiency.

Thiamine deficiency (TD) is the underlying cause of Wernicke's encephalopathy (WE), an acute neurological disorder characterized by structural damage to key periventricular structures in the brain. Increasing evidence suggests these focal histological lesions may be representative of a gliopathy in which astrocyte-related changes are a major feature of the disorder. These changes include a loss of the glutamate transporters GLT-1 and GLAST concomitant with elevated interstitial glutamate levels, lowered brain pH associated with increased lactate production, decreased levels of GFAP, reduction in the levels of glutamine synthetase, swelling, alterations in levels of aquaporin-4, and disruption of the blood-brain barrier. This review focusses on how these manifestations contribute to the pathophysiology of TD and possibly WE.

Effectiveness Of The Endotracheal Tube Cuff On The Trachea: Physical And Mechanical Aspects.

The inflation pressure of the endotracheal tube cuff can cause ischemia of the tracheal mucosa at high pressures; thus, it can cause important tracheal morbidity and tracheal microaspiration of the oropharyngeal secretion, or it can even cause pneumonia associated with mechanical ventilation if the pressure of the cuff is insufficient. In order to investigate the effectiveness of the RUSCH® 7.5 mm endotracheal tube cuff, this study was designed to investigate the physical and mechanical aspects of the cuff in contact with the trachea. For this end, we developed an in vitro experimental model to assess the flow of dye (methylene blue) by the inflated cuff on the wall of the artificial material. We also designed an in vivo study with 12 Large White pigs under endotracheal intubation. We instilled the same dye in the oral cavity of the animals, and we analyzed the presence or not of leakage in the trachea after the region of the cuff after their deaths (animal sacrifice). All cuffs were inflated at the pressure of 30 cmH2O. We observed the passage of fluids through the cuff in all in vitro and in vivo experimental models. We conclude that, as well as several other cuff models in the literature, the RUSCH® 7.5 mm tube cuffs are also not able to completely seal the trachea and thus prevent aspiration of oropharyngeal secretions. Other prevention measures should be taken.

Bilateral Peripheral Facial Palsy And Mastoid Infiltration As Symptoms Of Relapsed Acute Myeloid Leukemia.

Although Bell's palsy (BP) is the most common cause of peripheral facial palsy (PFP), other etiologies merit investigation. A 60-year-old female patient presented with recurrent bilateral PFP. Although the patient had a history of acute myeloid leukemia (AML), she had initially been diagnosed with BP-related PFP and had been treated accordingly. When the PFP recurred, additional diagnostic tests were performed. The resulting immunohistochemical profile included CD3 positivity in a few reactive T lymphocytes; positivity for myeloperoxidase in atypical cells; and focal positivity for CD34 and proto-oncogene c-kit proteins in neoplastic cells, thus confirming the suspicion of mastoid infiltration caused by relapsed AML. In patients with neoplastic disease, a finding of PFP calls for extensive investigation in order to rule out the involvement of the temporal bone.

Chasing Cardiac Physiology And Pathology Down The Camkii Cascade.

Calcium dynamics is central in cardiac physiology, as the key event leading to the excitation-contraction coupling (ECC) and relaxation processes. The primary function of Ca(2+) in the heart is the control of mechanical activity developed by the myofibril contractile apparatus. This key role of Ca(2+) signaling explains the subtle and critical control of important events of ECC and relaxation, such Ca(2+) influx and SR Ca(2+) release and uptake. The multifunctional Ca(2+)-calmodulin-dependent protein kinase II (CaMKII) is a signaling molecule that regulates a diverse array of proteins involved not only in ECC and relaxation, but also in cell death, transcriptional activation of hypertrophy, inflammation and arrhythmias. CaMKII activity is triggered by an increase in intracellular Ca(2+) levels. This activity can be sustained, creating molecular memory after the decline in Ca(2+) concentration, by autophosphorylation of the enzyme, as well as by oxidation, glycosylation and nitrosylation at different sites of the regulatory domain of the kinase. CaMKII activity is enhanced in several cardiac diseases, altering the signaling pathways by which CaMKII regulates the different fundamental proteins involved in functional and transcriptional cardiac processes. Dysregulation of these pathways constitutes a central mechanism of various cardiac disease phenomena, like apoptosis and necrosis during ischemia/reperfusion injury, digitalis exposure, post-acidosis and heart failure arrhythmias, or cardiac hypertrophy. Here we summarize significant aspects of the molecular physiology of CaMKII and provide a conceptual framework for understanding the role of the CaMKII cascade on Ca(2+) regulation and dysregulation in cardiac health and disease.

Complicações imediatas e tardias após cirurgia de reservatório ileal na polipose adenomatosa familiar

BACKGROUND: Restorative proctocolectomy is the procedure of choice to treat familial adenomatous polyposis, however it can be associated to short-term and long-term postoperative complications. AIM: To evaluate the occurrence of complications related to the surgical treatment of familial adenomatous polyposis with ileal pouch technique. METHODS: Retrospective study of 69 patients with familial adenomatous polyposis after rectocolectomy with ileal reservoir between 1984 and 2006, operated on Coloproctology Group, Medical Sciences Faculty, State University of Campinas, Campinas, SP, Brazil. The median follow-up period was 82 (2-280) months. Data obtained were surgical techniques and postoperative complications. RESULTS: The morbidity and mortality were 63.8% and 2.9%, respectively. The most frequent complications were small-bowel obstruction (17.4%), anastomotic stricture (15.9%) and pelvic sepsis (10.1%). Acute ischemia of the ileal pouch (4.3%), pouchitis (2.9%) and ileal pouch-related fistula (2.9%) had poorer frequency than others. CONCLUSIONS: The morbid-mortality was similar to the literature?s data and it is acceptable for a complex surgery in two terms like the ileal reservoir-anal anastomosis. The small-bowel obstruction was the most frequent complication. However, ischemia of the reservoir, pouchitis and pelvic sepsis were important complications and was related to the failure of the ileal reservoir.

Aplicação do escore MELD em pacientes submetidos a transplante de fígado: análise retrospectiva da sobrevida e dos fatores preditivos a curto e longo prazo

BACKGROUND: The model for end-stage liver disease (MELD) was developed to predict short-term mortality in patients with cirrhosis. There are few reports studying the correlation between MELD and long-term posttransplantation survival. AIM: To assess the value of pretransplant MELD in the prediction of posttransplant survival. METHODS: The adult patients (age >18 years) who underwent liver transplantation were examined in a retrospective longitudinal cohort of patients, through the prospective data base. We excluded acute liver failure, retransplantation and reduced or split-livers. The liver donors were evaluated according to: age, sex, weight, creatinine, bilirubin, sodium, aspartate aminotransferase, personal antecedents, brain death cause, steatosis, expanded criteria donor number and index donor risk. The recipients' data were: sex, age, weight, chronic hepatic disease, Child-Turcotte-Pugh points, pretransplant and initial MELD score, pretransplant creatinine clearance, sodium, cold and warm ischemia times, hospital length of stay, blood requirements, and alanine aminotransferase (ALT >1,000 UI/L = liver dysfunction). The Kaplan-Meier method with the log-rank test was used for the univariable analyses of posttransplant patient survival. For the multivariable analyses the Cox proportional hazard regression method with the stepwise procedure was used with stratifying sodium and MELD as variables. ROC curve was used to define area under the curve for MELD and Child-Turcotte-Pugh. RESULTS: A total of 232 patients with 10 years follow up were available. The MELD cutoff was 20 and Child-Turcotte-Pugh cutoff was 11.5. For MELD score > 20, the risk factors for death were: red cell requirements, liver dysfunction and donor's sodium. For the patients with hyponatremia the risk factors were: negative delta-MELD score, red cell requirements, liver dysfunction and donor's sodium. The regression univariated analyses came up with the following risk factors for death: score MELD > 25, blood requirements, recipient creatinine clearance pretransplant and age donor >50. After stepwise analyses, only red cell requirement was predictive. Patients with MELD score < 25 had a 68.86%, 50,44% and 41,50% chance for 1, 5 and 10-year survival and > 25 were 39.13%, 29.81% and 22.36% respectively. Patients without hyponatremia were 65.16%, 50.28% and 41,98% and with hyponatremia 44.44%, 34.28% and 28.57% respectively. Patients with IDR > 1.7 showed 53.7%, 27.71% and 13.85% and index donor risk <1.7 was 63.62%, 51.4% and 44.08%, respectively. Age donor > 50 years showed 38.4%, 26.21% and 13.1% and age donor <50 years showed 65.58%, 26.21% and 13.1%. Association with delta-MELD score did not show any significant difference. Expanded criteria donors were associated with primary non-function and severe liver dysfunction. Predictive factors for death were blood requirements, hyponatremia, liver dysfunction and donor's sodium. CONCLUSION: In conclusion MELD over 25, recipient's hyponatremia, blood requirements, donor's sodium were associated with poor survival.

Dyskinesia induced by phenytoin

Phenytoin is an effective antiepileptic drug, although, it can be associated with many side effects, including dyskinesia. OBJECTIVE: To describe the clinical characteristics of phenytoin induced dyskinesia. METHODS: We investigated the occurrence of involuntary movements in patients followed at our adult and pediatric epilepsy clinics during the period of one year. RESULTS: Three patients presented with phenytoin-induced dyskinesia: one adult with axial and orofacial dyskinesia, and two children with choreoathetosis. They did not have other signs of phenytoin intoxication and had complete recovery after phenytoin withdrawal. CONCLUSION: Phenytoin induced dyskinesia may occur during either chronic or initial treatment and with normal serum phenytoin levels. However, it occurs most often in patients on polytherapy, usually after increasing dosage and with toxic serum levels. Other signs of phenytoin intoxication may be present in these patients, but often the dyskinesia is the only side effect, which may delay the diagnosis and treatment. The clinical characteristics of the involuntary movements vary and may be focal or generalized, most often characterized by choreoathetosis and dyskinesias. These may last for hours, days or even years, but frequently disappear completely after phenytoin withdrawal.