fludrocortisone
Sources réglementaires consultées
Indications approuvées
- Substitution minéralocorticoïde dans l’insuffisance surrénalienne primaire ou secondaire, notamment la maladie d’Addison et l’hyperplasie congénitale des surrénales avec perte de sel.
Contre-indications
Absolues
- Œdème lié à une insuffisance cardiaque, une cirrhose ou une néphrose ; hypertension non contrôlée ; hypokaliémie ; choc hypovolémique.
- Hypersensibilité à la fludrocortisone ou aux excipients.
Mises en garde cliniques
- Mise en garde majeure · Surveiller la pression artérielle, le poids, les œdèmes, le sodium et le potassium ; un excès minéralocorticoïde peut provoquer hypertension, œdèmes, hypokaliémie et insuffisance cardiaque. — CIMA/AEMPS, ficha técnica 48921
- Mise en garde majeure · Utiliser la dose minimale efficace et diminuer progressivement après un traitement prolongé ; un arrêt brutal peut provoquer une insuffisance surrénalienne. — CIMA/AEMPS, ficha técnica 48921
- Mise en garde majeure · Il peut accroître la sensibilité aux infections, réactiver des infections latentes et en masquer les signes. Éviter les vaccins vivants aux doses immunosuppressives. — CIMA/AEMPS, ficha técnica 48921
Interactions médicamenteuses
- SévèreDiurétiques hypokaliémiants, laxatifs et glycosides cardiaques
Mécanisme: La perte de potassium peut être accentuée et augmenter la toxicité digitalique.
Recommandation: Surveiller le potassium et les signes de toxicité ; adapter le traitement concomitant.
CIMA/AEMPS, ficha técnica 48921
- SévèreVaccins vivants
Mécanisme: L’immunosuppression peut favoriser une infection disséminée et réduire la réponse vaccinale.
Recommandation: Éviter les vaccins vivants pendant un traitement immunosuppresseur ; planifier la vaccination avec l’équipe soignante.
CIMA/AEMPS, ficha técnica 48921
- ModéréeAntidiabétiques, diurétiques et AINS
Mécanisme: Les glucocorticoïdes peuvent compromettre le contrôle glycémique, aggraver la perte de potassium et augmenter le risque gastro-intestinal.
Recommandation: Surveiller la glycémie et les électrolytes et envisager une gastroprotection ou des alternatives selon le risque.
CIMA/AEMPS, ficha técnica 48921
Effets indésirables
Communs (≥1%)
Hypertension, œdème, hypokaliémie et céphalée
Rares mais graves
Insuffisance cardiaque et alcalose hypokaliémique
Grossesse et allaitement
Une augmentation progressive de la dose peut être nécessaire pendant la grossesse dans la maladie d’Addison ; individualiser sous surveillance étroite. La décision d’allaiter doit mettre en balance bénéfice et risque.
Bibliographie récente (PubMed)
Adrenal insufficiency is a syndrome of cortisol deficiency and is categorized as primary, secondary, or glucocorticoid induced. Although primary and secondary adrenal insufficiency are rare, affecting less than 279 per 1 million individuals, glucocorticoid-induced adrenal insufficiency is common. Primary adrenal insufficiency, which involves deficiency of all adrenocortical hormones, is caused by autoimmune destruction, congenital adrenal hyperplasia, pharmacological inhibition (eg, high doses of azole antifungal therapy), infection (eg, tuberculosis, fungal infections), or surgical removal of adrenal cortical tissue. Secondary adrenal insufficiency is caused by disorders affecting the pituitary gland, such as tumors, hemorrhage, inflammatory or infiltrative conditions (eg, hypophysitis, sarcoidosis, hemochromatosis), surgery, radiation therapy, or medications that suppress corticotropin production, such as opioids. Glucocorticoid-induced adrenal insufficiency is caused by administration of supraphysiological doses of glucocorticoids. Patients with adrenal insufficiency typically present with nonspecific symptoms, including fatigue (50%-95%), nausea and vomiting (20%-62%), and anorexia and weight loss (43%-73%). Glucocorticoid-induced adrenal insufficiency should be suspected in patients who have recently tapered or discontinued a supraphysiological dose of glucocorticoids. Early-morning (approximately 8 am) measurements of serum cortisol, corticotropin, and dehydroepiandrosterone sulfate (DHEAS) are used to diagnose adrenal insufficiency. Primary adrenal insufficiency is typically characterized by low morning cortisol levels (<5 µg/dL), high corticotropin levels, and low DHEAS levels. Patients with secondary and glucocorticoid-induced adrenal insufficiency typically have low or intermediate morning cortisol levels (5-10 µg/dL) and low or low-normal corticotropin and DHEAS levels. Patients with intermediate early-morning cortisol levels should undergo repeat early-m
Sepsis is a common condition associated with significant morbidity and mortality. Emergency physicians play a key role in the diagnosis and management of this condition. This paper evaluates key evidence-based updates concerning the management of sepsis and septic shock for the emergency clinician. Sepsis is a life-threatening syndrome, and rapid diagnosis and management are essential. Antimicrobials should be administered as soon as possible, as delays are associated with increased mortality. Resuscitation targets include mean arterial pressure ≥ 65 mmHg, mental status, capillary refill time, lactate, and urine output. Intravenous fluid resuscitation plays an integral role in those who are fluid responsive. Balanced crystalloids and normal saline are both reasonable options for resuscitation. Early vasopressors should be initiated in those who are not fluid-responsive. Norepinephrine is the recommended first-line vasopressor, and if hypotension persists, vasopressin should be considered, followed by epinephrine. Administration of vasopressors through a peripheral 20-gauge or larger intravenous line is safe and effective. Steroids such as hydrocortisone and fludrocortisone should be considered in those with refractory septic shock. An understanding of the recent updates in the literature concerning sepsis and septic shock can assist emergency clinicians and improve the care of these patients.
Referring to a broad spectrum of the autonomic symptoms, autonomic disorders, and general dysfunction of the autonomic nervous system, dysautonomia is one of the common and under-recognized comorbidities of a wide variety of systemic disease, including diabetes, autoimmune disorders, vitamin deficiencies, and hormonal dysregulation. The most common autonomic disorders encountered in clinical practice are postural orthostatic tachycardia syndrome (POTS), neurocardiogenic syncope (NCS), and orthostatic hypotension (OH), which may be undiagnosed or often mislabeled with psychiatric disorders. Typical clinical features of dysautonomia, such as orthostatic dizziness/lightheadedness, orthostatic intolerance, palpitations, exercise intolerance, cognitive dysfunction, and fatigue, should prompt a diagnostic investigation for dysautonomia, which includes an in-office 10-min stand test or a tilt table test in conjunction with other autonomic function tests if available. Treatment approach consists of non-pharmacologic and pharmacologic therapies with beta blockers, midodrine, ivabradine, pyridostigmine, fludrocortisone, stimulants, and other medications. In clinical setting, dysautonomia may present a diagnostic and therapeutic challenge in patients with various systemic disorders and may require a high index of suspicion on the part of the clinician. Importantly, diagnosing and treating dysautonomia is critical to providing comprehensive and personalized medical care to complex patients with chronic illness, who are typically highly symptomatic with multi-systemic complaints as a result of comorbid, and often undiagnosed, dysautonomia.
Orthostatic hypotension is defined as a drop in systolic blood pressure of at least 20mmHg or a drop in diastolic blood pressure of at least 10mmHg within 3minutes of standing. It is a common disorder, especially in high-risk populations such as elderly subjects and patients with neurological diseases, and is associated with markedly increased morbidity and mortality. Its management can be challenging, particularly in cases where supine hypertension is associated with severe orthostatic hypotension. Education of the patient, non-pharmacological measures, and drug adaptation are the cornerstones of treatment. Pharmacological treatment should be individualized according to the severity, underlying cause, 24-hour blood pressure profile, and associated coexisting conditions. First-line therapies are midodrine and fludrocortisone, which may need to be combined for optimal care of severe cases.
Severe pulmonary infections, including COVID-19, community-acquired pneumonia, influenza, and Pneumocystis pneumonia, are a leading cause of death among adults worldwide. Pulmonary infections in critically ill patients may cause septic shock, acute respiratory distress syndrome, or both, which are associated with mortality rates ranging between 30% and 50%. Corticosteroids mitigate the immune response to infection and improve outcomes for patients with several types of severe pulmonary infections. Low-dose corticosteroids, defined as less than or equal to 400 mg hydrocortisone equivalent daily, can reduce mortality of patients with severe COVID-19, community-acquired pneumonia, and Pneumocystis pneumonia. A randomized clinical trial of 6425 patients hospitalized with COVID-19 who required supplemental oxygen or noninvasive or invasive mechanical ventilation reported that dexamethasone 6 mg daily for 10 days decreased 28-day mortality (23% vs 26%). A meta-analysis that included 7 randomized clinical trials of 1689 patients treated in the intensive care unit for severe bacterial community-acquired pneumonia reported that hydrocortisone equivalent less than or equal to 400 mg daily for 8 days or fewer was associated with lower 30-day mortality compared with placebo (10% vs 16%). In a meta-analysis of 6 randomized clinical trials, low-dose corticosteroids were associated with lower mortality rates compared with placebo for patients with HIV and moderate to severe Pneumocystis pneumonia (13% vs 25%). In a predefined subgroup analysis of a trial of low-dose steroid treatment for septic shock, patients with community-acquired pneumonia randomized to 7 days of intravenous hydrocortisone 50 mg every 6 hours and fludrocortisone 50 μg daily had decreased mortality compared with the placebo group (39% vs 51%). For patients with acute respiratory distress syndrome caused by various conditions, low-dose corticosteroids were associated with decreased in-hospital mortality (34% vs