NAWFEL BEN-HAMOUDA

Dr. NAWFEL BEN-HAMOUDA

Lausanne University Hospital (CHUV), Lausanne, Vaud, Switzerland
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Research Focus & Metrics

Academic Career Length

19Years (2008-Present)

(Calculated once Scilit publication data is synced: current year − year of first publication + 1)

Representative Publications

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17 June 2019 in Nutrition in Clinical Practice
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Journal Article
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MAMarco Altarelli
Marco Altarelli
NBNAWFEL BEN-HAMOUDA
NAWFEL BEN-HAMOUDA
ASAntoine Schneider
Antoine Schneider
MBMette M. Berger
Mette M. Berger

1 July 2017 in Critical Care Medicine
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Journal Article
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ARAndrea O. Rossetti
Andrea O. Rossetti
DQDiego F. Tovar Quiroga
Diego F. Tovar Quiroga
EJElsa Juan
Elsa Juan
JNJan Novy
Jan Novy
RWRoger D. White
Roger D. White
ARAlejandro A. Rabinstein
Alejandro A. Rabinstein
Objective: The prognostic role of electroencephalography during and after targeted temperature management in postcardiac arrest patients, relatively to other predictors, is incompletely known. We assessed performances of electroencephalography during and after targeted temperature management toward good and poor outcomes, along with other recognized predictors.Design: Cohort study (April 2009 to March 2016).Setting: Two academic hospitals (Centre Hospitalier Universitaire Vaudois, Lausanne, Switzerland; Mayo Clinic, Rochester, MN).Patients: Consecutive comatose adults admitted after cardiac arrest, identified through prospective registries.Interventions: All patients were managed with targeted temperature management, receiving prespecified standardized clinical, neurophysiologic (particularly, electroencephalography during and after targeted temperature management), and biochemical evaluations.Measurements and Main Results: We assessed electroencephalography variables (reactivity, continuity, epileptiform features, and prespecified “benign” or “highly malignant” patterns based on the American Clinical Neurophysiology Society nomenclature) and other clinical, neurophysiologic (somatosensory-evoked potential), and biochemical prognosticators. Good outcome (Cerebral Performance Categories 1 and 2) and mortality predictions at 3 months were calculated. Among 357 patients, early electroencephalography reactivity and continuity and flexor or better motor reaction had greater than 70% positive predictive value for good outcome; reactivity (80.4%; 95% CI, 75.9–84.4%) and motor response (80.1%; 95% CI, 75.6–84.1%) had highest accuracy. Early benign electroencephalography heralded good outcome in 86.2% (95% CI, 79.8–91.1%). False positive rates for mortality were less than 5% for epileptiform or nonreactive early electroencephalography, nonreactive late electroencephalography, absent somatosensory-evoked potential, absent pupillary or corneal reflexes, presence of myoclonus, and neuron-specific enolase greater than 75 µg/L; accuracy was highest for early electroencephalography reactivity (86.6%; 95% CI, 82.6–90.0). Early highly malignant electroencephalography had an false positive rate of 1.5% with accuracy of 85.7% (95% CI, 81.7–89.2%).Conclusions: This study provides class III evidence that electroencephalography reactivity predicts both poor and good outcomes, and motor reaction good outcome after cardiac arrest. Electroencephalography reactivity seems to be the best discriminator between good and poor outcomes. Standardized electroencephalography interpretation seems to predict both conditions during and after targeted temperature management.

1 June 2013 in Resuscitation
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HEHarald Engel
Harald Engel
NBNAWFEL BEN-HAMOUDA
NAWFEL BEN-HAMOUDA
KPKatharina Portmann
Katharina Portmann
FDFrederik Delodder
Frederik Delodder
TSTamarah Suys
Tamarah Suys
MOMauro Oddo
Mauro Oddo

29 October 2022 in Journal of Clinical Medicine
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ZLZied Ltaief
Zied Ltaief
NBNAWFEL BEN-HAMOUDA
NAWFEL BEN-HAMOUDA
VRValentina Rancati
Valentina Rancati
ZGZiyad GUNGA
Ziyad GUNGA
CMCarlo Marcucci
Carlo Marcucci
LLLucas Liaudet
Lucas Liaudet
Vasoplegic syndrome (VS) is a common complication following cardiovascular surgery with cardiopulmonary bypass (CPB), and its incidence varies from 5 to 44%. It is defined as a distributive form of shock due to a significant drop in vascular resistance after CPB. Risk factors of VS include heart failure with low ejection fraction, renal failure, pre-operative use of angiotensin-converting enzyme inhibitors, prolonged aortic cross-clamp and left ventricular assist device surgery. The pathophysiology of VS after CPB is multi-factorial. Surgical trauma, exposure to the elements of the CPB circuit and ischemia-reperfusion promote a systemic inflammatory response with the release of cytokines (IL-1β, IL-6, IL-8, and TNF-α) with vasodilating properties, both direct and indirect through the expression of inducible nitric oxide (NO) synthase. The resulting increase in NO production fosters a decrease in vascular resistance and a reduced responsiveness to vasopressor agents. Further mechanisms of vasodilation include the lowering of plasma vasopressin, the desensitization of adrenergic receptors, and the activation of ATP-dependent potassium (KATP) channels. Patients developing VS experience more complications and have increased mortality. Management includes primarily fluid resuscitation and conventional vasopressors (catecholamines and vasopressin), while alternative vasopressors (angiotensin 2, methylene blue, hydroxocobalamin) and anti-inflammatory strategies (corticosteroids) may be used as a rescue therapy in deteriorating patients, albeit with insufficient evidence to provide any strong recommendation. In this review, we present an update of the pathophysiological mechanisms of vasoplegic syndrome complicating CPB and discuss available therapeutic options.

1 February 2017 in Nutrition
Verified
Journal Article
Closed access
NBNAWFEL BEN-HAMOUDA
NAWFEL BEN-HAMOUDA
MCMélanie Charrière
Mélanie Charrière
PVPierre Voirol
Pierre Voirol
MBMette M. Berger
Mette M. Berger

Verified
Journal Article
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MBMette M. Berger
Mette M. Berger
OPOlivier Pantet
Olivier Pantet
ASAntoine Schneider
Antoine Schneider
NBNAWFEL BEN-HAMOUDA
NAWFEL BEN-HAMOUDA
Inpatients are threatened by global malnutrition, but also by specific micronutrient (i.e., trace element and vitamins) deficiencies that frequently are overseen in the differential diagnosis of major organ dysfunctions. Some of them are related to specific geographic risks (iodine, iron, selenium, zinc, vitamin A), while others are pathology related, and finally many are associated with specific feeding patterns, including low dose enteral feeding. Among the pathologies in which laboratory blood investigations should include a micronutrient outwork, anemia is in the front line, followed by obesity with bariatric surgery, chronic liver disease, kidney disease, inflammatory bowel disease, cardiomyopathies and heart failure. The micronutrients at the highest risk are iron, zinc, thiamine, vitamin B12 and vitamin C. Admission to hospital has been linked with an additional risk of malnutrition—feeding below 1500 kcal/day was frequent and has been associated with a structural additional risk of insufficient micronutrient intake to cover basal needs. Although not evidence based, systematic administration of liberal thiamine doses upon admission, and daily complementation of inpatients’ food and enteral feeding solutions with multi-micronutrient tablets might be considered.