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lupine-publishers-acr · 3 years

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Lupine Publishers | Epidemiological Aspects of Cardiac Decompensation Factors Renaissance Hospital N’Djamena Chad

Abstract

Introduction: Cardiac decompensation factors are numerous. Their identification allows better management of patients and limits the rate of rehospitalization. The aim of this work was to identify cardiac decompensation factors and improve their management at the renaissance hospital in N’Djamena, Chad.

Patients and Methods: This was a cross-sectional retrospective study conducted in the cardiology department at N’Djamena Renaissance Hospital, over a period of one year, from 01 January 2018 to 01 January 2019. All patients hospitalized for cardiac decompensation during this period and consented, were included.

Results: During the period of our study, 52 patients were included. The sex ratio was 1.9. The mean age was 48±9 years old. The predominant cardiovascular risk factors were arterial hypertension (37%, n = 19) and diabetes (27%, n = 14). The monthly income of our patients was in the majority of cases less than 200,000 FCFA (44%, n = 23). The main factors of cardiac decompensation were respectively, infections (18%, n = 9), supraventricular arrhythmias (16%, n = 8), changes in temperature (11%, n = 6), therapeutic nonobservance (11%, n = 6), dietary gap (10%, n = 5), and hypertensive relapses (10%, n = 5). The main etiologies of heart failure were ischemic cardiomyopathies (31%, n = 16), dilated cardiomyopathies (25%, n = 13), hypertensive cardiomyopathies (17%, n = 9), and rheumatic valvulopathies (15%). %, n = 8).

Conclusion: Rehospitalizations for cardiac decompensation are common after the first episode of hospitalization. The identification of the risk factors for this decompensation and their management make it possible to avoid these readmissions.

Keywords: Cardiac decompensation factors; Heart failure; Renaissance hospital N’Djamena characterized

Abbreviations: HF: Heart Failure; FFCA: Franc of the Financial Community in Africa; AFA: Atrial Fibrillation Arrhythmia; LV: Left Ventricle

Introduction

Heart failure (HF) is defined as a clinical syndrome characterized by chronic symptoms (dyspnea, fatigue) that may be accompanied by physical signs (crepitus, peripheral edema) caused by a structural cardiac abnormality and / or functional, resulting in decreased cardiac output [1]. It is a major public health problem because of its frequency and consequences in terms of morbidity and mortality and its economic impact on the health care system. Its prevalence is increasing because of the aging of the population but also because of the improvement of the management of many heart diseases including ischemic heart disease. It is one of the leading causes of hospitalization, morbidity and mortality, especially among the elderly [2]. Its evolution is clinically marked by periods of remission and exacerbation leading to recurrent hospitalizations. The number of readmissions for IC remains significant despite the therapeutic progress of recent years. The identification of decompensation factors and the optimization of their management could prevent these readmissions, particularly after hospitalization. The objective of this study was to identify cardiac decompensation factors and improve their management at the renal hospital in N’Djamena, Chad.

Patients and Methods

The parameters studied

This was a cross-sectional retrospective study conducted in the cardiology department at N’Djamena Renaissance Hospital, over a period of one year, from 01 January 2018 to 01 January 2019. Were included all patients readmitted for cardiac decompensation during the study period and who gave their consent.

Epidemiological characteristics: age, sex, cardiovascular risk factors (arterial hypertension, diabetes, chronic renal dysfunction with glomerular filtration rate <60ml/min / 1.73m2, obesity, dyslipidemia, alcohol, smoking), monthly cost of treatment in FFCA (1 US dollar = 593,720 FFCA). Clinical features: cardiac decompensatory factors (difference in diet, unsuitable exercise, temperature, alcohol, AFA, other rhythm disorders, hypertensive pressure, ischemic episode, anemia, bronchopulmonary infection, other infection, renal failure, poor compliance drug, hyperthyroidism, untreated sleep apnea syndrome), etiologies of HF. Electrocardiographic characteristics: arrhythmias (atrial or ventricular extrasystoles, atrial fibrillation or flutter, atrial tachycardia, ventricular tachycardia), repolarization abnormalities, sinoatrial or atrioventricular blocks. Echocardiographic features: dilated cardiac cavities, wall hypertrophy, diastolic dysfunction of the left ventricle (LV); abnormalities of left ventricular kinetics (hyperkinesia, hypokinesia, akinesia), LV systolic dysfunction (systolic ejection fraction <45%), valvular abnormality, congenital anomaly, pulmonary arterial hypertension.

Statistical Analysis

Ethics

In this study, a descriptive statistical analysis was applied using Microsoft Excel, quantitative variables were presented by their mean and standard deviation and qualitative variables were by percentages.

This work was done by obtaining the approval of the hospital management and the consent of the patients.

Results

During the period of our study, 52 patients were included. Men predominated with 65% of cases (n = 34). The sex ratio was 1.9. The average age was 48±9 years old with a minimum age of 22 years and a maximum age of 79 years. Patients were educated only in 38% of cases (n = 20). The predominant cardiovascular risk factors were hypertension (19%), diabetes (14%), dyslipidemia (11%), and 19%). The monthly income of our patients was in the majority of cases less than 200,000 FCFA. The rates were, respectively, between CFAF 100,000 and 200,000 in 44% of cases (n =23) and less than CFAF 100,000 in 33% of cases (n = 17). Only 12 patients (23%) had an income above 200,000 FCFA. The health insurance rate was observed in 13% of cases (n=7). (Table 1) shows the characteristics of the patients. The main factors of cardiac decompensation are shown in Table 2. The most frequent were respectively, infections in 18% of cases (n = 9), including 4 cases of bronchopulmonary infections (8%), supraventricular rhythm disorders in 16% of cases (n=8) including 5 cases of AFA (10%), changes in temperature especially heat with 6 cases (11%), poor therapeutic compliance 6 cases (11%), the difference diet in 10% of cases (n = 5), and hypertensive outbreaks in 10% of cases (n=5). The most common etiologies of IC (Table 3) were ischemic cardiomyopathies in 31% of cases (n=16), of which 4 patients (8%) had benefited from myocardial revascularization, dilated cardiomyopathies in 25% (n=16). = 13), hypertensive cardiomyopathies in 17% of cases (n =9) and rheumatic valvulopathies in 15% (n=8). Other etiologies were less frequent in this series such as post-embolic pulmonary heart in 6% of cases (n=3), congenital heart disease in 4% (n=2) and pericardial affections in 2% of cases (n= 1).

Table 1: Patient Characteristics.

Table 2: Cardiac Decompensation Factors.

Table 3: Etiologies of HF.

Discussion

The limits of our work

The post-hospitalization period is conducive to rehospitalization, but long-term chronic HF patient follow-up is important because the morbidity and mortality rate remains high in this group of patients, even though many treatments have been shown to be effective. The follow-up of these patients makes it possible to optimize the therapeutics, the monitoring and to detect early the signs of decompensation. Cardiac rehabilitation plays an important role in the management of HF and should be part of the modern strategy for the management of patients with stable heart failure. This includes not only physical training, but also rehabilitation of drug treatments, control of risk factors, psychological management and finally, patient education [3]. The search for this factor that shifts a situation of balance during a decompensation is fundamental because its treatment can be very profitable. Several standards for HF support highlight the need to look for a triggering factor [4]. We studied the importance of triggers for cardiac decompensation in a population of readmitted patients who were followed for chronic HF. The main triggering factors identified were, in order of frequency, infections, atrial fibrillation, therapeutic nonobservance, temperature variations, mainly heat, uncontrolled hypertension, diet deviation, anemia, myocardial ischemia. These factors are globally found in the literature data. In this study, the first triggering factor found was the existence of an infection (18%) with bronchopulmonary infections (8%) at their head. They are promoted by decreasing the effectiveness of coughing, bronchiolar elasticity, efficiency of the mucociliary system and swallowing disorders.

The mechanisms involved in cardiac decompensation are multiple. Several studies have highlighted the important role of infections, particularly bronchopulmonary infections, in cardiac decompensation, especially in elderly patients [5-8]. The second triggering factor was a supraventricular rhythm disorder (16%), especially ACFA (10%). Suppression of atrial systole results in increased LV filling pressures and promotes the onset of HF thrust. AFA is common in HF and its prevalence increases with the severity of CI [9-13]. Cardiac decompensation was attributed to noncompliance in 8% of the cases in this study, but adherence remains difficult to assess. This non-compliance was favored by several factors in our patients; the high number of drugs with their adverse effects, given the high rate of comorbidities observed (diabetes, high blood pressure, kidney failure), the economic level which was low in almost 50% of patients and the absence of health insurance, the level of education and the influence that might have on the understanding of the disease. The therapeutic nonobservance in the HF varies in the literature from 10 to 99% according to the evaluation method used [14]. Compliance is responsible for an increase in the number of hospitalizations and a worsening of clinical signs [15]. A multidisciplinary intervention has shown its effectiveness on adherence to 30-day treatment [16] and an educational intervention has improved compliance and decreased re-hospitalization rates [17]. Anemia was found in 4 patients in our series.

This result is weak compared to data from the literature because, according to several authors, anemia is frequent during IC and is a poor prognostic factor in chronic HF [18,19], increased clinical signs, aggravation of functional status [20]. However, there is little data on the involvement of acute anemia in cardiac decompensation. In addition, the management of the etiology of HF remains essential to prevent complications and readmissions and to improve the prognosis. In our study we found that in coronary patients (31%) only 8% had benefited from myocardial revascularization, valvular patients (15%) and those with congenital heart disease (4%) had not received reparations. surgical procedures that were necessary. In our context, the identification of the decompensation factors must be of paramount importance for the clinician and should allow the improvement of the management of the pathology in particular at the preventive level. Hence the importance of educating the patient and those around him. The establishment of appropriate structures and care networks for heart failure in all regions of Chad will allow better monitoring of patients with rapid access to the specialist physician.

Our study presents several methodological limitations. First, it is a retrospective study with information gathered from the reports that sometimes did not contain all the necessary data. The size of our sample is small, we will have to lead other more representative studies in the future. And many patients have not received etiologic treatment of HF.

Conclusion

Rehospitalizations for cardiac decompensation are common after the first episode of hospitalization. The identification of the risk factors for this decompensation and their management make it possible to avoid these readmissions. Hence the importance of emphasizing access to care with appropriate therapeutic means, regular monitoring and therapeutic education

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tunisie--esthetic · 3 years

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Savoir d'avantage sur la chirurgie pour traiter les valvulopathies cardiaques en Tunisie, qui implique la réparation ou le remplacement des valvules cardiaques affectées.

#remplacement_valvulaire #réparation_valvulaire #chirurgie_cardiaque

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lerepondeurdesinsoumis · 5 years

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Après le scandale du Mediator, peut-on encore avoir confiance dans les médicaments ?

Deux mille morts, peut-être plus, deux mille victimes du Mediator, ce poison commercialisé par le laboratoire Servier... Cette molécule, de la famille des amphétamines, a provoqué chez les patients des problèmes de santé gravissimes : des valvulopathies cardiaques et de l'hypertension artérielle pulmonaire. Comment ce poison a-t-il pu être mis sur le marché ? Au début des années 1990, la toxicité d'autres médicaments du laboratoire Servier (l'Isoméride et le Pondéral) (...) - Tribune Libre from AgoraVox le média citoyen https://ift.tt/2MPmbqX via IFTTT

#actualité #éducation #société #politique #rosemar #AgoraVox le média citoyen

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magaratimes · 6 years

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#LeMonde: "Fifty years ago, in South Africa, the world's first heart transplant "

#LeMonde: “Fifty years ago, in South Africa, the world's first heart transplant “

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The Groote Shuur Hospital, which perpetuates the legacy of pioneer Christiaan Barnard, has developed a groundbreaking protocol for the operation of people with Alzheimer's disease. of valvulopathy.

At the Groote Shuur Hospital in Cape Town, South Africa , the operating theater where Christiaan Barnard performed the first heart transplant in 1967 was…

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greatestlcve · 4 years

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previscan tablets Uses, Dosage, Side Effects, Precautions

Drug Online

previscan tablets 20mg >> Generic drug of the Therapeutic class: Hemostasis and blood active ingredients: Fluindione

Important to know about Previscan?

It is prescribed in certain situations in medicine or surgery:

phlebitis (clot in a vein)

pulmonary embolism (clot in the lungs),

known heart diseases: certain disorders of the cardiac rhythm (such as atrial fibrillations), abnormalities or prosthesis of the heart valves,

some myocardial infarction.

It can be prescribed in relay of a heparin (another anticoagulant drug).

Previscan (Fluindione) Uses, Dosage, Side Effects, Precautions

Previscan indication and Uses

Emboligenic heart disease: prevention of thromboembolic complications related to certain atrial rhythm disorders (atrial fibrillation, flutter, atrial tachycardia), some mitral valvulopathies, valvular prostheses.

Prevention of thromboembolic complications of complicated myocardial infarction: mural thrombi, severe left ventricular dysfunction, emboligenic dyskinesia …, in relay of heparin.

Treatment of deep vein thromboses and pulmonary embolism as well as the prevention of their recurrence, in relay of heparin.

These indications are detailed under Dosage and Method of Administration : Biological Monitoring.

Previscan Dosage

Administration mode

ORAL WAY.

Swallow the tablets with a glass of water.

Rhythm of administration

This medicine should be administered once a day. It is best to take in the evening so that the dosage can be changed as soon as possible after the results of the INR.

Choice of the dose

Due to significant interindividual variability, the antivitamin K (AVK) dosage is strictly individual.

The initial dose, always probative, should be as close as possible to the equilibrium dose. It is usually 20 mg, to be adapted according to the biological results. Dosage adjustment is performed in increments of 5 mg (1/4 tablet). With Previscan (Fluindione), which has a long half-life (31 hours), a more fine dosage adjustment is made by prescription of an alternating dosage over 2 or 3 days, for example 1/2 tablet a day, 1/4 tablet the other day.

Do not use a loading dose.

In subjects at particular risk of bleeding (weight <50 kg, elderly, hepatic impairment), the initial dose is usually lower.

Biological monitoring of AVK treatment is essential and is based on INR. The equilibrium dose will be determined by adjusting the initial dose according to the INR (see below).

Dosage in elderly and elderly subjects

Treatment should be started with a lower dose. Indeed, the average equilibrium dose is lower in the elderly than in the young, usually 1/2 to 3/4 of the dose ( see section Warnings and precautions for use ).

Use in children

The experience of oral anticoagulants in children remains limited. Initiation and monitoring of treatment is a specialized service .

AVK should be avoided as much as possible in infants less than one month old.

For this oral anticoagulant, dosages in children are based only on practical experience.

The average dose to be administered per os to obtain a target INR at steady state between 2 and 3, should be calculated according to age but especially weight:

In children over 3 years , the dose per kg of body weight is similar to that of adults.

In children under 3 years , and especially before 12 months, the average doses used are higher and more variable from one child to another than in the older child.

A recommended initial dose to achieve an INR between 2 and 3 is given as an indication in the table below. It is always probative, and should be as close as possible to the expected dose at equilibrium.

In practice, for this drug, the recommended starting dose corresponds to the average doses used by specialists.

Initial recommended doses in mg / kg / day

<12 months

12 months – 3 years

> 3 years – 18 years

fluindione

1.4

0.65 – 0.70

0.37

The rate of administration (once or twice a day), the biological monitoring by the INR allowing the adaptation of the daily dose are carried out according to the same principles as in the adult. Once the target INR is reached, the interval between 2 INRs should not exceed 15 days. In children, changes in diet, drug interactions and intercurrent infections lead to significant variations in INR. In children under 3, it will be necessary to take into account a greater variability of the INR and the difficulties related to the use of this product (regurgitations, control of the catch, frequency of the blood samples …) .

Biological monitoring and dose adjustment

The adapted biological test is the measurement of the Quick time expressed in INR.

The INR or International Normalized Ratio is a mode of expression of the Quick time, which takes into account the sensitivity of the reagent (thromboplastin) used to perform the test.

This mode of expression reduces the causes of inter-laboratory variability and allows better monitoring of treatment, than the old prothrombin (PT) level.

Apart from any treatment with AVK, the INR of a normal subject is ≤ 1.2.

In the majority of situations (see table below), an INR between 2 and 3 with a target value of 2.5 is sought, which means that:

The ideal INR towards which it is necessary to tend is 2.5,

An INR less than 2 reflects insufficient anticoagulation,

An INR greater than 3 indicates an excess of anticoagulation.

In all cases, an INR greater than 5 is associated with a haemorrhagic risk (see action to be taken in case of overdose, see section Overdose ).

Rhythm of biological controls.

Before initialization of the treatment, it is recommended to check the INR in order to detect possible clotting disorders and thus be able to adapt the initial dosage as well as possible.

The first check must be made after the 3 rd taking warfarin (that is to say, the morning of the 4 th day) to track individual hypersensitivity: an INR greater than 2 ad overdose before obtaining balance and should reduce the dosage.

The second control is performed based on the results of the first INR, in order to assess the anticoagulant efficacy (as appropriate between 3 to 6 days after the 1 st control).

Subsequent controls should be performed (1-2 times per week) until the INR is stabilized, then progressively spaced up to a maximum interval of 1 month. The balance of the treatment is sometimes obtained after several weeks.

After a change of dosage, the first check should be done 3 days after a dose change, the controls should be repeated until stabilization (1-2 times per week).

Recommended INRs and treatment times

The therapeutic areas and recommended treatment times are specified in the table below, depending on the main situations. They comply with current French and international recommendations.

Relay of heparinotherapy

Due to the latency of the anticoagulant action of AVK, heparin should be maintained at the same dose for the duration of the necessary duration, at least 5 days and until the INR is in the desired therapeutic zone 2 days consecutive.

When there has been a cessation of VKA, following severe bleeding, when bleeding is controlled, and if indication for VKA is maintained, treatment with unfractionated heparin or LMWH at curative dose is recommended, concurrent with recovery AVK. It is recommended that the reintroduction of oral anticoagulation be conducted in hospital, under clinical and laboratory supervision.

In case of heparin-induced thrombocytopenia (TIH type II), it is inadvisable to introduce AVK early when heparin is stopped, because of the risk of hypercoagulability by early reduction of protein S (anticoagulant ). VKAs will be given only after initiation of a non-heparinic fast acting anticoagulant (danaparoid or hirudin) and when the platelet count is again greater than 100 Giga / L.

Missed dose

If you miss a dose, it is possible to take it within 8 hours after the usual time of administration. After this time, it is best not to take the missed dose and to resume the next dose at the usual time and the patient should not take a double dose to make up for the missed dose.

The patient will have to report an oversight during the INR check and write it down in his tracking log.

INR recommendations and duration of treatment:

Prevention of arterial and venous thromboembolic complications of emboligenic heart diseases

INDICATIONS

INR recommendations – duration of treatment

Supraventricular rhythm disorders (atrial fibrillation and atrial flutter) according to the following conditions:

target 2.5; INR 2 to 3; long-term

age

<75 years with risk factors * > 75 years **

* history of transient or established ischemic stroke, hypertension, heart failure, diabetes. In the absence of risk factor (s) before age 75, prescription of aspirin is recommended. ** after careful evaluation of the benefit / risk ratio (see section Warnings and precautions for use )

Mitral valve disease (particularly mitral stenosis ) if favoring factor (s): FA or flutter, thromboembolic history, dilation of the left atrium and / or spontaneous contrast image detected in transesophageal echography and / or intra-thrombus left atrial to the echocardiogram.

target 2.5; INR 2 to 3; long-term

Valvular prostheses

* mechanical prostheses

INR target function of prosthesis type and patient characteristics (see table below); long-term

* biological prostheses

target 2.5; INR 2 to 3; 3 months

INR recommended targets for mechanical prostheses:

Intrinsic thrombogenic risk of prostheses a

Risk factors related to the patient b

No risk factor

≥1 risk factor

Low

2.5

3.0

Way

3.0

3.5

High

3.5

4.0

has thrombogenic risk of mechanical prostheses:

Low: Prostheses that have been proven effective with moderate anticoagulation

High: old generation prostheses, especially ball

Medium: all other prostheses including recent introductions

b Risk factors related to the patient: mitral, tricuspid or pulmonary position of the prosthesis; thromboembolic antecedents; large OG> 50 mm; mitral stenosis irrespective of degree; EF <35%; some atrial rhythm disorders such as FA, flutter, atrial tachycardia.

Prevention of thromboembolic complications of complicated myocardial infarction: mural thrombi, severe left ventricular dysfunction, emboligenic dyskinesia …

INR- recommendations

target 2.5; INR 2 to 3;

duration of the treatment

at least 3 months (further treatment will be discussed on a case-by-case basis)

Treatment of deep vein thromboses and pulmonary embolism as well as the prevention of their recurrence, in relay of heparin

INR- recommendations

target 2.5; INR 2 to 3;

duration of the treatment

minimum duration of 3 months to be modulated according to the clinical context and the presence of modulation factors (see table below)

Clinical context of venous thromboembolism (VTE)

Duration of the treatment*

MTEV with transient major triggering factor (surgery, prolonged immobilization of 3 days or more, fracture of the lower limbs in the last 3 months)

3 months

MTEV with major persistent risk factor (cancer in treatment, antiphospholipid syndrome)

≥ 6 months, as long as the factor persists

Idiopathic MTEV

≥ 6 months

Contraindications

This medication is contraindicated in the following cases:

Known hypersensitivity to this medicine or to indanedione derivatives, or to any of the excipients,

Severe hepatic impairment

– in combination with the following drugs (see section Interactions with other drugs and other forms of interactions ):

– acetylsalicylic acid:

for anti-inflammatory doses of acetylsalicylic acid (> = 1 g per dose and / or> = 3 g per day),

for analgesic or antipyretic doses (> = 500 mg per dose and / or <3 g per day) and in the event of a history of peptic ulcer,

– miconazole used systemically or as an oral gel,

– pyrazole NSAIDs: phenylbutazone (all its forms including local),

In case of association with St. John’s Wort (plant used in herbal medicine),

In case of breastfeeding,

In patients with an allergy to wheat (other than celiac disease).

How it works Previscan

Pharmacotherapeutic group: ANTITHROMBOTICS , ATC code: B01AA .

VKA intervenes in the hepatocyte in the mechanism of vitamin K reduction. Reduced vitamin K is the co-factor of a carboxylase that converts glutamic acid to γ-carboxyglutamic acid. Four coagulation factors (factors II, VII, IX, X) and two inhibitors (C and S proteins) have γ-carboxyglutamic residues necessary for their attachment to phospholipid surfaces that catalyze their interactions. Thus, AVKs have an indirect anticoagulant effect by preventing the synthesis of active forms of several coagulation factors.

Administered orally , VKA induce hypoprothrombinemia within 36 to 72 hours.

The half-life of vitamin K-dependent coagulation factors varies from 6 h (factor VII, protein C) to 2 or 3 days (factors X, II). After administration of AVK, the first factors whose activities decrease are those whose half life is the shortest, while the last ones will be those whose half life is the longest. This is why the balance of a treatment with AVK requires several days.

The anticoagulant action can persist 3 to 4 days after stopping treatment.

The majority of clinical studies available with the AVK class have been performed with warfarin.

Previscan Side Effects

Previscan (Fluindione) Side Effects

likeall medicines, this medicine can cause side effects, although not everybody gets them.

Hemorrhagic manifestations

These are the most common unwanted and annoying effects.

In case of bleeding, even minor, an overdose should be suspected and the origin of the bleeding should be sought ( see Special Warnings ).

Tell your doctor, especially if you:

bleeding gums,

bleeding from the nose,

presence of blood in the urine,

abundant rules,

appearance of hematomas.

Tell a doctor immediately or go to an emergency medical service if you:

red or black blood in the stool,

vomiting or bloody spitting,

bleeding that does not stop.

Sometimes hemorrhage may not be externalized, only certain signs can be detected, such as:

chronic fatigue,

abnormal breathlessness,

a headache that does not yield to the usual analgesic treatment,

unexplained discomfort.

These situations should make you consult your doctor because some haemorrhages can put your life in danger.

Allergic manifestations

These manifestations are more rare than bleeding, they can be manifested by one or more of the following signs, they usually heal without sequelae after stopping treatment:

· Skin abnormalities: local edema, sudden swelling of the face and neck, itching, hives, eczema, red spots on the skin, redness spreading throughout the body with pustules, and often accompanied fever (acute generalized exanthematous pustulosis),

An abnormality of the blood count and certain biological parameters, in particular liver,

Kidney failure or worsening of pre-existing renal insufficiency,

Respiratory discomfort,

A fever

Other effects

Rare: localized skin necrosis (destruction of the skin),

Diarrhea,

Joint pain,

Alopecia (hair loss).

Cholesterol crystal embolism Some have been reported with the use of fluindione (clogging of the arteries by the migration of cholesterol crystals).

This undesirable effect is mainly manifested by a blue color of the toes, often associated with digestive disorders.

If these symptoms occur, you should consult your doctor as soon as possible to re-evaluate the fluindione treatment.

Reporting of side effects

If you get any side effects, talk to your doctor or pharmacist. This also applies to any side effects that are not mentioned in this leaflet. You can also report side effects directly via the national reporting system: National Agency for the Safety of Medicines and Health Products (ANSM) and the network of Regional Pharmacovigilance Centers – Website: https://bit.ly/2XQbWcQ

By reporting side effects, you can help provide more information on the safety of the medicine.

Previscan Interactions

There are many drugs that can interact with VKAs.

If another treatment is to be started, modified, or deleted, it is necessary to perform an INR check 3 to 4 days after each change.

Associations contraindicated

Acetylsalicylic acid (high dose aspirin)

For anti-inflammatory doses of acetylsalicylic acid (≥ 1 g per dose and / or ≥ 3 g daily)

For analgesic or antipyretic doses (≥ 500 mg per dose and / or <3 g daily) and in case of a history of peptic ulcer.

Increased risk of bleeding, especially in case of a history of peptic ulcer.

Pyrazole NSAIDs

For all forms of phenylbutazone, including local:

Increased haemorrhagic risk of oral anticoagulant (inhibition of platelet function and aggression of the gastroduodenal mucosa by nonsteroidal anti-inflammatory drugs).

Miconazole (general route and oral gel)

Unpredictable haemorrhages that can possibly be serious.

St. John’s Wort

Decreased plasma concentrations of the oral anticoagulant, due to its enzymatic inducing effect with risk of a decrease in efficacy, or even cancellation, the consequences of which may be serious (thrombotic event).

If fortuitous association, do not abruptly discontinue St. John’s wort but monitor INR before and after stopping St. John’s wort.

Associations advised against

Acetylsalicylic acid

For analgesic or antipyretic doses (≥ 500 mg per dose and / or <3 g daily) in the absence of a history of peptic ulcer disease. Increased hemorrhagic risk.

For antiplatelet doses (from 50 mg to 375 mg daily) and in case of a history of peptic ulcer. Increased hemorrhagic risk. Need for a particular control of the bleeding time.

NSAIDs (except pyrazole NSAIDs see contraindicated combinations)

Increased bleeding risk of oral anticoagulant (aggression of the gastroduodenal mucosa by nonsteroidal anti-inflammatory drugs).

If the association can not be avoided, close clinical and biological monitoring.

Fluorouracil (and, by extrapolation, tegafur and capecitabine)

Significant increase in the effect of oral anticoagulant and hemorrhagic risk.

If it can not be avoided, more frequent control of the INR. Adjustment of oral anticoagulant dosage during cytotoxic therapy and 8 days after discontinuation.

Associations subject to precautions for use

Allopurinol

Increased effect of anticoagulant and hemorrhagic risk (decreased hepatic metabolism).

More frequent control of the INR.

Possible adaptation of oral anticoagulant dosage during treatment with allopurinol and 8 days after discontinuation.

Aminogluthetimide (described for warfarin and acenocoumarol)

Decreased effect of oral anticoagulant (increase in hepatic metabolism).

More frequent control of the INR.

Possible adaptation of oral anticoagulant dosage during treatment with aminogluthetimide and 2 weeks after discontinuation.

Amiodarone

Increased effect of oral anticoagulant and hemorrhagic risk.

More frequent control of the INR.

Possible adaptation of oral anticoagulant dosage during amiodarone treatment and 8 days after discontinuation.

Androgens

Variation of the anticoagulant effect (modification of hepatic synthesis of coagulation factors with tendency to increase the effect of oral anticoagulant).

More frequent control of the INR.

Possible adaptation of oral anticoagulant dosage during androgen therapy and 8 days after discontinuation.

Enzymatic inducing anticonvulsants (carbamazepine, fosphenytoin, phenobarbital, phenytoin, primidone)

Decrease (or, rarely, increase with phenytoin) of the effect of oral anticoagulant by increasing its hepatic metabolism by the inducing anticonvulsant.

More frequent control of the INR.

Possible adaptation of oral anticoagulant dosage during treatment with the inducing anticonvulsant and 8 days after discontinuation.

Antidepressants selective serotonin reuptake inhibitors (citalopram, escitalopram, fluoxetine, fluvoxamine, paroxetine, sertraline)

Increased effect of oral anticoagulant and hemorrhagic risk.

More frequent control of the INR.

Possible adaptation of oral anticoagulant dosage during the association period and after discontinuation.

Aprepitant

Risk of reduction of the effect of the oral anticoagulant by increasing its hepatic metabolism by aprepitant.

More frequent control of the INR.

Adaptation of the dosage of the oral anticoagulant during and after the combination.

Azathioprine

Decreased effect of oral anticoagulant by increasing its hepatic metabolism.

More frequent control of the INR.

Possible adaptation of oral anticoagulant dosage to initiation of immunosuppressive (or cytotoxic) therapy and after discontinuation.

Benzbromarone

Increased effect of oral anticoagulant and hemorrhagic risk.

More frequent control of the INR.

Possible adaptation of oral anticoagulant dosage during benzbromarone treatment and after discontinuation.

Bosentan

Decreased effect of oral anticoagulant by increasing its hepatic metabolism.

More frequent control of INR and possible adjustment of oral anticoagulant dosage.

Cephalosporins (cefamandole, cefoperazone, cefotetan, ceftriaxone)

Increased effect of oral anticoagulant and hemorrhagic risk.

More frequent control of the INR.

Possible adaptation of oral anticoagulant dosage during cephalosporin treatment and after discontinuation.

Cimetidine (at doses ≥ 800 mg / day)

Increased effect of oral anticoagulant and hemorrhagic risk (decrease in hepatic metabolism).

More frequent control of the INR.

Possible adaptation of oral anticoagulant dosage during cimetidine treatment and 8 days after discontinuation.+ Cisapride

Increased anticoagulant effect and haemorrhagic risk.

More frequent control of the INR.

Possible adaptation of oral anticoagulant dosage during treatment with cisapride and 8 days after discontinuation.

Colchicine

Increased effect of oral anticoagulant and hemorrhagic risk.

More frequent control of the INR.

Possible adaptation of oral anticoagulant dosage during colchicine treatment and 8 days after discontinuation.+ Colestyramine

Decreased effect of oral anticoagulant (decreased intestinal absorption).

Take colestyramine away from oral anticoagulant (more than 2 hours, if possible)

+ Cyclines

Increased anticoagulant effect and haemorrhagic risk.

More frequent control of the INR.

Possible adaptation of oral anticoagulant dosage during cyclin treatment and after discontinuation.

Danazol

Increased haemorrhagic risk by direct effect on coagulation and / or fibrinolytic systems.

More frequent control of the INR.

Adaptation of the dosage of vitamin K antagonist during treatment with danazol and after discontinuation.

Econazole

Regardless of the route of administration of econazole:

Increased effect of oral anticoagulant and hemorrhagic risk.

More frequent control of the INR.

Possible adaptation of oral anticoagulant dosage during and after discontinuation of econazole.

Fibrates

Increased effect of oral anticoagulant and hemorrhagic risk.

More frequent control of the INR.

Possible adaptation of oral anticoagulant dosage during treatment with the combination and 8 days after discontinuation.+ Fluconazole, itraconazole, voriconazole

Increased effect of oral anticoagulant and hemorrhagic risk.

More frequent control of the INR.

Possible adaptation of oral anticoagulant dosage during azole treatment and 8 days after discontinuation.+ Fluoroquinolones (ofloxacin, pefloxacin, enoxacin, lomefloxacin, moxifloxacin, ciprofloxacin, levofloxacin, norfloxacin)

Increased effect of oral anticoagulant and hemorrhagic risk.

More frequent control of the INR.

Possible adaptation of oral anticoagulant dosage during fluoroquinolone treatment and after discontinuation.

Glucocorticoids (except hydrocortisone as replacement therapy) (general and rectal)

Possible impact of corticosteroid therapy on the metabolism of the oral anticoagulant and that of the coagulation factors.

Haemorrhagic risk specific to corticosteroids (digestive mucosa, vascular fragility) at high doses or prolonged treatment for more than 10 days.

When the association is justified, reinforce the surveillance: biological control at the 8th day, then every 15 days during the corticotherapy and after its stop.

For methylprednisolone (0.5 to 1 g bolus): increased effect of oral anticoagulant and hemorrhagic risk.

INR control 2 to 4 days after the bolus of methylprednisolone or in the presence of any haemorrhagic signs.

Griseofulvin

Decreased effect of oral anticoagulant by increasing its hepatic metabolism with griseofulvin.

More frequent control of the INR.

Possible adaptation of oral anticoagulant dosage during treatment with griseofulvin and 8 days after discontinuation.

Low molecular weight and related heparins and unfractionated heparins (at curative doses and / or in the elderly)

Increased haemorrhagic risk

When relaying heparin with oral anticoagulant, strengthen clinical monitoring.

Thyroid hormones: levothyroxine, liothyronine sodium, thyroxines, tiratricol

Increased oral anticoagulant effect and haemorrhagic risk (increased metabolism of prothrombin complex factors).

More frequent control of the INR.

Possible adaptation of oral anticoagulant dosage when initiating treatment for hypothyroidism or overdose of thyroid hormones. Such control is not necessary in patients undergoing stable thyroid replacement therapy.

HMG CoA-reductase inhibitors (atorvastatin, fluvastatin, rosuvastatin, simvastatin)

Increased effect of oral anticoagulant and hemorrhagic risk.

More frequent control of the INR.

Possible adaptation of the dosage of the oral anticoagulant.

+ Macrolides (azithromycin, clarithromycin, dirithromycin, erythromycin, josamycin, midecamycin, roxithromycin, telithromycin, troleandomycin)

Increased oral anticoagulant effect and haemorrhagic risk.

More frequent control of the INR.

Possible adaptation of oral anticoagulant dosage during macrolide treatment and after discontinuation.

Mercaptopurine

Decreased effect of oral anticoagulant by increasing its hepatic metabolism.

More frequent control of the INR.

Possible adaptation of oral anticoagulant dosage to initiation of immunosuppressive (or cytotoxic) therapy and after discontinuation.

Nevirapine, Efavirenz

Decreased effect of oral anticoagulant by increasing its hepatic metabolism.

More frequent control of INR and possible adjustment of oral anticoagulant dosage.

Nitro-5-imidazoles (metronidazole, ornidazole, secnidazole, tinidazole)

Increased effect of oral anticoagulant and hemorrhagic risk by decreasing hepatic metabolism.

More frequent control of the INR.

Possible adaptation of oral anticoagulant dosage during treatment with these imidazoles and 8 days after discontinuation.

Orlistat

Increased effect of oral anticoagulant and hemorrhagic risk.

More frequent control of the INR.

Possible adaptation of oral anticoagulant dosage during orlistat treatment and after discontinuation.

Paracetamol

If paracetamol is taken at maximum doses (4 g / d) for at least 4 days, there is a risk of an increase in the effect of the oral anticoagulant and the risk of haemorrhage.

More frequent control of the INR.

Possible adaptation of oral anticoagulant dosage during paracetamol treatment and after discontinuation.

Pentoxifylline

Increased haemorrhagic risk

More frequent control of the INR.

Possible adaptation of oral anticoagulant dosage during treatment with pentoxifylline and 8 days after discontinuation.

Proguanil

Risk of increased oral anticoagulant effect and risk of bleeding.

More frequent control of the INR.

Possible adaptation of oral anticoagulant dosage during treatment with proguanil and after discontinuation.

Propafenone

Increased anticoagulant effect and haemorrhagic risk. Invoked mechanism: inhibition of oxidative metabolism of oral anticoagulant.

More frequent control of the INR.

Possible adaptation of oral anticoagulant dosage during and after discontinuation of propafenone.

Rifampicin

Decreased effect of oral anticoagulant (increase in hepatic metabolism).

More frequent control of the INR.

Possible adaptation of oral anticoagulant dosage during rifampicin treatment and 8 days after discontinuation.

Ritonavir

Variation of the effect of the oral anticoagulant, most often in the direction of a decrease.

More frequent control of the INR.

Possible adaptation of oral anticoagulant dosage during ritonavir therapy.

Sucralfate

Decreased digestive absorption of oral anticoagulant.

Take sucralfate away from oral anticoagulant (more than two hours if possible).

Sulfamethoxazole, sulfafurazole, sulfamethizol

Increased effect of oral anticoagulant and hemorrhagic risk.

More frequent control of the INR.

Possible adaptation of oral anticoagulant dosage during anti-infective treatment and 8 days after discontinuation.

Tamoxifen

Risk of increased anticoagulant effect and haemorrhagic risk.

More frequent control of the INR.

Possible adaptation of the dosage of the oral anticoagulant.

Tibolone

Increased oral anticoagulant effect and haemorrhagic risk.

More frequent control of the INR. Possible adaptation of oral anticoagulant dosage during tibolone treatment and after discontinuation.

Tramadol

Risk of increased effect of oral anticoagulant and risk of bleeding.

More frequent control of the INR.

Possible adaptation of oral anticoagulant dosage during tramadol treatment and after discontinuation.

Viloxazine

Increased anticoagulant effect and haemorrhagic risk.

More frequent control of the INR.

Possible adaptation of oral anticoagulant dosage during viloxazine treatment and after discontinuation.

Vitamin E ≥ 500 mg / day (alpha-tocopherol)

Increased effect of oral anticoagulant and hemorrhagic risk.

More frequent control of the INR.

Possible adaptation of oral anticoagulant dosage during vitamin E treatment and after discontinuation.

Associations to consider

+ Alcohol

Possible variations of the anticoagulant effect: increase in case of acute intoxication, decrease in case of chronic alcoholism (increased metabolism).

+ Platelet antiaggregants

Increased haemorrhagic risk

+ Acetylsalicylic acid at antiaggregant doses (50 mg to 375 mg daily) in the absence of a history of peptic ulcer.

Increased hemorrhagic risk.

+ Thrombolytics

Increased haemorrhagic risk

Special problem of antibiotics

Many cases of increased activity of oral anticoagulants have been reported in patients receiving antibiotics. The marked infectious or inflammatory context, the age and the general state of the patient appear as risk factors. In these circumstances, it appears difficult to distinguish between the infectious pathology and its treatment in the occurrence of the imbalance of the INR. However, some classes of antibiotics are more involved: these include fluoroquinolones, macrolides, cyclins, cotrimoxazole and certain cephalosporins, which in these conditions make it necessary to strengthen INR surveillance.

Special problem of anticancer

Due to the increased thrombotic risk of tumor diseases, the use of anticoagulant therapy is common. The large intra-individual variability of coagulability during these conditions, coupled with the possibility of an interaction between oral anticoagulants and anticancer chemotherapy, imposes, if it is decided to treat the patient with oral anticoagulants. , increase the frequency of INR checks.

PreviscanWarnings and Precautions

Previscan (Fluindione) Warnings and Precautions

Special warnings

Before deciding on the initiation of AVK treatment, particular attention will be paid to the cognitive functions of the patient as well as to the psychological and social context, due to the constraints of the treatment.

This medicine is generally not recommended:

· In case of haemorrhagic risk.

The decision to start or continue treatment with AVK should be based on the benefit / risk ratio specific to each patient and situation. Risky situations include the following:

organic lesion likely to bleed,

recent neuro-surgical or ophthalmological intervention or possibility of surgical revision,

recent or evolving gastro-duodenal ulcer

esophageal varices,

uncontrolled hypertension,

history of haemorrhagic stroke (except in cases of systemic embolism),

· In case of severe renal impairment (creatinine clearance <20 ml / min),

· In combination with (see section 4.5):

o acetylsalicylic acid:

§ for analgesic or antipyretic doses (> 500 mg per dose and / or <3 g per day) in the absence of a history of peptic ulcer

§ for anti-aggregating doses (from 50 mg to 375 mg daily) and in case of a history of peptic ulcer.

o NSAIDs (except pyrazole NSAIDs: phenylbutazone, see section 4.3),

o 5-fluorouracil and, by extrapolation, tegafur and capecitabine.

The patient must be informed and educated to follow his treatment. In particular, we must insist on the need:

take treatment without forgetting, every day at the same time;

perform regular biological control (INR), in the same laboratory;

be very vigilant about the associated drugs, which can disrupt the balance of treatment ( see section 4.5 ).

Delivery to the patient and use of the information and monitoring booklet provided for AVK treatment are recommended.

The vitamin K intake of the diet should be regular so as not to disturb the balance of the INR. The foods richest in vitamin K are: cabbages (curly, Brussels sprouts, white cabbage, broccoli, …), spinach, asparagus.

Due to the latency of several days, VKAs are not an emergency treatment.

The risk of a haemorrhagic accident is greatest during the first months of treatment. Surveillance must therefore be particularly rigorous during this period, especially when returning home to a hospitalized patient.

In case of bleeding during anticoagulant therapy, overdose should be sought by the practice of an INR see section 4.9. In the absence of overdose, the origin of the bleeding will be sought and if possible treated. In addition, a transient therapeutic adaptation will be discussed according to the indication and the situation.

Lumbar puncture should be discussed taking into account the risk of intra-spinal bleeding. It should be deferred whenever possible. It is an invasive procedure that justifies the stopping of AVK treatment with a relay if necessary by heparin, or even the neutralization of AVK treatment in case of emergency (see paragraph Surgery or invasive medical dices under AVK below).

During anticoagulant therapy, avoid intra-muscular injections that may cause hematomas.

Immune-allergic manifestations may occur, requiring cessation of treatment (see section 4.8).

Impairment of renal function occurring at the start of treatment necessitates the consideration of the role of fluindione and the diagnosis of renal immunoallergic disease. If this is confirmed, the treatment should be interrupted and corticosteroid therapy may be proposed, and started at the earliest after diagnosis.

This pathology is mainly observed in patients with end-stage renal failure treated by dialysis or in patients with known risk factors such as protein C or S deficiency, hyperphosphatemia, hypercalcemia or hypoalbuminemia. Rare cases of calciphylaxis have been reported in patients taking anti-vitamin K, also in the absence of kidney disease. When calciphylaxis is diagnosed, appropriate therapy should be initiated and discontinuation of Previscan (Fluindione) should be considered.

Low dose AVK-aspirin combination:

In patients with an indication of AVK and requiring low doses of aspirin (75-100 mg) because of a confirmed arterial pathology, low-dose AVK-aspirin combination should be based on an individual thrombotic risk assessment. embolic and hemorrhagic.

Contraception is desirable in women of childbearing ageb.

Recommendation when traveling abroad:

Préviscan (fluindione) is marketed only in France. If the patient travels abroad, he / she must carry with him the quantity sufficient to follow his treatment during his stay and know the name in the INN that must appear on the order.

This medicine contains lactose. Its use is not recommended in patients with galactose intolerance, Lapp lactase deficiency or glucose or galactose malabsorption syndrome (rare hereditary diseases).

This medicine can be given in case of celiac disease. Wheat starch may contain gluten, but only in trace form, and is therefore considered safe for patients with celiac disease.

Embolisms of cholesterol crystals can occur during treatment with anticoagulant, including fluindione. This effect is rare but potentially severe, with a high mortality rate.

It is manifested by a skin syndrome (blue toe syndrome) that may be accompanied by renal failure and / or visceral syndrome. Neurological signs can appear in severe forms.

Embolisms of cholesterol crystals may occur weeks to months after the start of treatment, mainly in the presence of cardiovascular co-morbidities, including atherosclerosis and / or in case of vascular surgery.

If the diagnosis of cholesterol crystal embolism is confirmed, treatment with fluindione should be discontinued. If anticoagulant therapy is considered necessary, consider switching to another non-vitamin K anticoagulant.

Precautions for use

In the elderly and elderly, the risk of haemorrhage is high. Therefore, the initiation of antivitamin K treatment, as well as the continuation of this treatment, should be done only after careful evaluation of the benefit / risk ratio.

The decision of treatment and its follow-up must take particular account of the specific risks related to the field:

frequency of associated pathologies and therapeutic associations,

frequency and severity of haemorrhagic accidents, particularly related to the risk of falling,

risk of impairment of cognitive functions leading to a risk of mistaking.

The risk of overdose, particularly at the start of treatment, should be carefully monitored.

In case of severe renal insufficiency, this drug is generally not recommended. However, in cases where it is used, initial doses should be lower and INR monitoring closer.

The dosage will be adapted and the surveillance increased in case:

moderate hepatic impairment,

hypoprotidemia,

during any intercurrent pathological event, in particular an acute infectious episode.

In case of known congenital deficiency of protein S or C, the administration of AVK should always be done under the guise of heparinotherapy and, in the case of severe deficiency of protein C (<20%), the infusion of concentrate of Protein C during the introduction of AVK can be discussed to prevent the occurrence of cutaneous necrosis observed at the introduction of VKA.

Surgery or invasive medical procedures under AVK

In case of surgery or invasive medical procedures, several attitudes are possible and should be discussed according to the thrombotic risk specific to the patient and bleeding risk, particularly related to the type of surgery.

Procedures that can be performed without interrupting VKA

Treatment with AVK with INR maintenance in the usual therapeutic zone (2 to 3) may be continued in certain surgeries or invasive procedures, which cause infrequent, low intensity or easily controlled bleeding. Local haemostasis may be necessary. However, taking other drugs that interfere with haemostasis, or the existence of co-morbidity, increases the risk of bleeding and may lead to the choice of interruption of VKAs. These situations include: skin surgery, cataract surgery, rheumatology of low risk haemorrhagic, some oral surgery, some acts of digestive endoscopy.

Situations that require relaying by heparin, if the interruption of AVK is necessary for a programmed act

If the interruption of AVK is necessary for a programmed act, when the risk of thromboembolism according to the indication of treatment with AVK is high , a pre and post-operative relay by a heparin with curative doses (unfractionated heparin or LMWH) if they are not contraindicated) is recommended.

The interruption will be done 4 to 5 days before the intervention under the supervision of the INR, intervention when the INR is lower than 1.5 then resumption of the AVK treatment in post-operative under cover, possibly, of a heparinothérapie both that the INR is less than 2.

In patients with mechanical heart valves, the pre- and post-operative relay is recommended regardless of the type of mechanical valve prosthesis.

In ACFA patients, the high thromboembolic risk is defined by a history of transient or permanent ischemic stroke, or systemic embolism.

In patients with a history of MTEV, the high thromboembolic risk is defined by an accident (DVT and / or PE) less than 3 months old, or idiopathic recurrent thromboembolic disease (number of episodes> 2, at least one accident without triggering factor).

In other cases , the post-operative relay by a heparin with curative doses is recommended when the recovery of AVK within 24 to 48 hours postoperatively is not possible due to the unavailability of the enteral route.

Case of non-valvular atrial fibrillation (FANV) stable in ambulatory:

In patients treated for ambulatory stable non-valvular atrial fibrillation (FANV), when initiating therapy, the use of a heparin-AVK relay should be avoided since, in this context, this relay is not indicated and increases. the hemorrhagic risk without reducing the arterial thromboembolic risk.

Preoperative management of the patient for surgery or urgent invasive procedure at risk of bleeding

In the event of surgery or invasive procedure URGENT (an urgent act is defined by a time of intervention not allowing to reach a goal of an INR <1,5, or 1,2 in neurosurgery) at risk haemorrhagic ( abdominal surgery, orthopedic surgery, neurosurgery, lumbar puncture), the measurement of the INR must be performed at the patient’s admission.

The action to take is as follows:

Administration of prothrombin complex concentrates (CCP also known as Kaskadil and Octaplex PPSBs) is recommended.

Combination of 5 mg vitamin K with the administration of prothrombin complex concentrates, unless correction of haemostasis is required for less than 4 hours. Enteral administration should be preferred where possible.

Completion of an INR within 30 minutes after the administration of the CCP and before performing the recommended surgery or invasive procedure. In case of insufficiently corrected INR, it is recommended to administer a supplement of CCP dose, adapted to the value of the INR according to the recommendations of the SPC of the drug.

Performing an INR 6 to 8 hours after the antagonization is recommended.

Drive and use machines

Not applicable.

Previscan and PREGNANCY / BREAST FEEDING / FERTILITY

Pregnancy

With all the vitamin K antagonists, a malformation syndrome has been described in the human species in about 4 to 7% of pregnancies between 6 and 9 weeks of amenorrhea (malformations of the bones of the nose, epiphyseal punctures); a cerebral fœtopathy occurs in 1 to 2% of cases beyond this period.

A possibility of embryonal or fetal loss is reported throughout the duration of the pregnancy.

Therefore, in women of childbearing age, contraception is desirable when using vitamin V antagonists.

In pregnant women, the prescription of antivitamin K must be exclusively reserved in cases where heparin can not be used.

If vitamin K antagonists are used during pregnancy, heparin should be switched from 36

th week of gestation. The prenatal diagnosis will be adapted to the period of intrauterine exposure to vitamin K antagonists. Breastfeeding:

Breastfeeding is contraindicated during treatment.

What should I do if I miss a dose?

If you forget to take Previscan (Fluindione) 20 mg, quadresectable tablet, never take the same dose twice in the same day.

Missed medication may be “caught up” within 8 hours after the usual time of administration. After this time, it is best not to take the missed dose and to resume the next dose at the usual time.

Remember to report an oversight during an INR check and note it in your log book.

What happens if I overdose from Previscan?

An overdose can be manifested by:

the appearance of bleeding,

an INR greater than 5, with or without associated bleeding.

If you take more Previscan (Fluindione) 20 mg, quadresectable tablet than you should: consult your doctor immediately, if possible the one following you.

In some cases, it will simply be necessary to modify the dose; in other cases, treatment will have to be done urgently.

What is Forms and Composition?

FORMS and PRESENTATIONS

Quadresectable 20 mg tablet (slightly convex, cruciform fracture on both sides, pink): Box of 30, blister packs of 15.

COMPOSITION

p cpFluindione (DCI)20 mg

Excipients: dried wheat starch, lactose, talc, alginic acid, dried potato starch, stearic acid, red iron oxide (E172).

Excipients with known effect: lactose, wheat starch.

NOT’s

Edrug-online contains comprehensive and detailed information about drugs available in the medical field, and is divided into four sections:

general information:

Includes a general description of the drug, its use, brand names, FAQs, and relevant news and articles

Additional information:

General explanation about dealing with the medicine: how to take the medicine, the doses and times of it, the start and duration of its effectiveness, the recommended diet during the period of taking the medicine, the method of storage and storage, recommendations in cases for forgetting the dose and instructions to stop taking the drug and take additional doses.

Special warnings:

For pregnant and breastfeeding women, the elderly, boys and drivers, and use before surgery.

Side effects:

It treats possible side effects and drug interactions that require attention and its effect on continuous use.

The information contained in this medicine is based on medical literature, but it is not a substitute for consulting a doctor.

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previscan tablets Uses, Dosage, Side Effects, Precautions

Drug Online

previscan tablets 20mg >> Generic drug of the Therapeutic class: Hemostasis and blood active ingredients: Fluindione

Important to know about Previscan?

It is prescribed in certain situations in medicine or surgery:

phlebitis (clot in a vein)

pulmonary embolism (clot in the lungs),

known heart diseases: certain disorders of the cardiac rhythm (such as atrial fibrillations), abnormalities or prosthesis of the heart valves,

some myocardial infarction.

It can be prescribed in relay of a heparin (another anticoagulant drug).

Previscan (Fluindione) Uses, Dosage, Side Effects, Precautions

Previscan indication and Uses

Prevention of thromboembolic complications of complicated myocardial infarction: mural thrombi, severe left ventricular dysfunction, emboligenic dyskinesia …, in relay of heparin.

Treatment of deep vein thromboses and pulmonary embolism as well as the prevention of their recurrence, in relay of heparin.

These indications are detailed under Dosage and Method of Administration : Biological Monitoring.

Previscan Dosage

Administration mode

ORAL WAY.

Swallow the tablets with a glass of water.

Rhythm of administration

This medicine should be administered once a day. It is best to take in the evening so that the dosage can be changed as soon as possible after the results of the INR.

Choice of the dose

Due to significant interindividual variability, the antivitamin K (AVK) dosage is strictly individual.

The initial dose, always probative, should be as close as possible to the equilibrium dose. It is usually 20 mg, to be adapted according to the biological results. Dosage adjustment is performed in increments of 5 mg (¼ tablet). With Previscan (Fluindione), which has a long half-life (31 hours), a more fine dosage adjustment is made by prescription of an alternating dosage over 2 or 3 days, for example ½ tablet a day, ¼ tablet the other day.

Do not use a loading dose.

In subjects at particular risk of bleeding (weight <50 kg, elderly, hepatic impairment), the initial dose is usually lower.

Biological monitoring of AVK treatment is essential and is based on INR. The equilibrium dose will be determined by adjusting the initial dose according to the INR (see below).

Dosage in elderly and elderly subjects

Treatment should be started with a lower dose. Indeed, the average equilibrium dose is lower in the elderly than in the young, usually ½ to ¾ of the dose ( see section Warnings and precautions for use ).