Fatigue is an unpleasant subjective sensation, when physical activity and / or mental achieve or continue (asthenia or fatigue) requires effort. This is a subjective sensation. It is to differentiate and often confused with fatigue is a feeling of exhaustion with anticipation about the upcoming activity. Fatigue is normal and physiological.
She is often sought by athletes. It is abnormal and possibly pathological when it is extended. Usually the term “chronic fatigue” fatigue that extends beyond 6 months.
The cause of chronic fatigue is often multifactorial, rarely unique. Fatigue is a common symptom in general practice (10 to 15% of consultations) and is the sole reason for consultation in 5% of cases. The questioning is essential to identify what the patient meant by the term “fatigue”. Clinical examination should be very careful to explore the major systems of the body, and a biological minimum balance at this stage has the already be done.
Additional tests first line for an etiologic diagnosis of a state of fatigue are:
– Erythrocyte sedimentation rate, C-reactive protein;
– Complete blood count with platelet count;
– Determination of transaminases;
– Serum electrolytes, calcium, fasting glucose;
– Dipstick (search for erythrocyte, proteinuria, glycosuria);
– Possibly, chest X-ray. 2nd intention exams are:
– Serum protein electrophoresis (finding a hyper-γ-globulin polyclonal, a monoclonal component, a β-γ block, a hyper-α-2-globulin, hypoalbuminemia, etc.) ;
– Dosing of muscle enzymes, especially creatine phosphokinase (CPK);
– Assay of lactate dehydrogenase (LDH), raised in numerous diseases including blood disorders;
– Different hormone dosages: especially the TSH (thyroid stimulating hormone), but also cortisol, urinary free cortisol or pituitary hormones;
– Abdominal-pelvic ultrasound (search for tumor syndrome, hepatomegaly, splenomegaly, deep lymph nodes, etc.).
FATIGUE EXTENDED DUE TO LATE DIAGNOSIS:
Some chronic fatigue causes are easily identifiable: infectious, inflammatory, neoplastic, metabolic, hematologic or other.
Some rare diseases or diagnostic harder still can be diagnosed at this stage. The proposed list is not exhaustive.
It focuses on diseases with a specific treatment.
It is characterized by villous atrophy acquired immune-mediated, often occurring in an autoimmune context personal or family, marked by signs of malabsorption which are often very small (iron deficiency, vitamin D, folic acid, vitamin B12 or calcium), while digestive disorders are not the predominant complaint ( “patraquerie” digestive).
Diagnosis is based on the dosage of anti-transglutaminase antibodies (anti-endomysium antibodies), highly sensitive and specific. antibody assay is that the negative when there is a defi cit IgA deficiency which itself predisposes to celiac disease. If clinical conviction, must be completed by an assay of IgA (and search for IgG antibodies). Definitive diagnosis is then provided by a duodenal biopsy confirming villous atrophy.
The treatment focuses on the prescription of a gluten free diet. Wheat, barley and rye in feature and should be excluded from the diet, which requires a very specific education and possible referral to gluten-free diet products.
Sleep apnea is characterized by clinical signs of marked orientation:
– The daytime state, besides the state of fatigue, drowsiness by episodes in the day, with lower concentration of opportunities, high blood pressure, sometimes polycythemia related to nocturnal hypoxia;
– The nocturnal state, hum to look through the examination of joint about possible respiratory arrest with noisy breathing in.
Diagnosis is based on nocturnal oximetry and polysomnography (joint exploration of EEG, respiration rate and pulse oximetry).
Treatment is mainly nocturnal ventilation positive pressure. When there is excess weight, dieting is essential. Also check that there is not any obstruction or malformation of the upper airway.
Gélineau disease (narcolepsy) must also be sought by questioning: sleep with former brutal episodes of cataplexy, hypnagogic hallucinations, etc. (EEG recorded on 24 hours sleep in REM sleep).
The treatment is based primarily on modafinil (Modiodal®) which replaced tricyclic in this indication.
This is an extremely common disease, peripheral mostly by Hashimoto’s thyroiditis seen positive thyroperoxidase antibodies, which can be revealed by a state of fatigue that persists. Biological signs of thyroid insufficiency are only marked by a lack of “reserves” thyroid, with a dosage of thyroid hormone T4 remains normal, but TSH is high.
The treatment consists, after checking that there is no superimposed iatrogenic factor (especially iodine overload), to starting treatment with thyroid hormone (thyroxine) starting with a dose of 25 γ of that Lévothyrox® is gradually increased to 100 γ and often with the aim of normalizing the TSH.
Adrenal insufficiency results in a state of fatigue. The peripheral adrenal insufficiency
is usually quickly identified by skin pigmentation and hypotension. When the failure is of central origin (adrenocorticotropic deficiency in pituitary disease), the diagnosis may be more difficult:
– Especially in women when combined hormonal treatment
makes it difficult to failure diagnosis often associated gonadotropin;
– And there is no witness galactorrhea a hyperprolactinemia.
The fasting plasma cortisol assay is part of the essential balance among all tired subject.
Treatment depends on the cause (pituitary tumor, hypothalamic, hypophysitis, etc.) Or functional impairment secondary to prolonged corticosteroid therapy adrenocorticotropic. Treatment involves the prescription ofhydrocortisone, a 10 mg tablet in the morning and another at lunch, which is usually sufficient without mineralocorticoid treatment associated.
It is relatively easy to diagnose when there is an obvious attempt fatigue, but the diagnosis may be delayed in myasthenias skeletal. We must identify the signs of bulbar intermittent diplopia, swallowing disorders and respiratory disorders.
Diagnosis is provided by:
– Electromyography with repetitive stimulation test;
– Sometimes supplemented by a study in single fiber, if the clinic conviction is sufficient;
– And by a dosage of antirécepteurs antibodies to acetylcholine (positive in 85% of cases).
Treatment is symptomatic: cholinesterase inhibitors, or Mestinon® Mytélase®, spread throughout the day and usually very effective.
It is also etiologic “; in the young, can be directed towards:
– Thymectomy, especially if there is a thymic enlargement or thymic tumor;
– And / or to an immunological referred to treatment (corticosteroids, immunosuppressants and in acute cases: plasmapheresis and / or intravenous immunoglobulin).
Myopathy and myositis:
The diagnosis of myopathy associated with hypokalemia, hypocalcaemia or congenital enzyme disease (McArdle disease, for example) may be disregarded if it is not thought to check the serum electrolytes, serum calcium and CK levels . A painful lameness of non-vascular and non-neurological stress imposes an electromyogram and stress tests with determination of lactic acid (in search of muscle glycogen storage disease or mitochondrial cytopathic), preceding a muscle biopsy study histochemical.
Polymyositis usually associate with fatigue muscle pain, joint pain and often Raynaud’s syndrome, sometimes pulmonary involvement.
The diagnosis is provided by the existence of an inflammatory syndrome with elevated ESR, elevated CPK and immunological markers (antinuclear antibodies with vis-à-vis specific soluble nuclear antigens essentially anti-JO1 type).
The treatment of metabolic or enzymatic myopathy requires specialist advice, and for the treatment of inflammatory myopathies (corticosteroids, immunosuppressants, possibly supplemented by immunoglobulin infusions).
It is characterized by a genetic iron overload (85% of the HFE gene mutation, the most common being H282Y and H63D). This recessive genetic disease is often characterized by:
– First, abnormal fatigue;
– Followed by the appearance of the signs of liver damage, endocrine, metabolic or joint.
Diagnosis is provided by measuring the coefficient of saturation of transferrin (> 45%) and by a ferritin is elevated without other inflammatory or cytolytic cause.
The treatment is particularly effective on fatigue and consists of “bloodletting” first repeated every week, and with longer intervals that allow desaturation. The objective is to achieve a ferritin levels less than 50 ng / mL.
They are characterized by a state of cytolysis may be intermittent, hence the importance of renewing the determination of transaminases. When there is a history that finds predisposing circumstances, think to look for infection with hepatitis C.
The treatment of hepatitis C is based on peginterferon plus ribavirin, and treatment of chronic active hepatitis immune-mediated (dosage smooth antimuscles antinuclear antibodies with liver biopsy) requires specialized care usually with a corticosteroid and immunosuppressive therapy.
Parkinson’s disease can be taken early to a state of fatigue due to the difficulty of getting started and stiffness.
The treatment must take into account the long evolution of the disease and must use a comprehensive strategy (expert opinion).
STATEMENTS OF FATIGUE IDIOPATHIC:
They cover topics tired from “always” (often psychasthenic). This is usually of subjects with a personality disorder or a pathological neurotic.
Psychotherapy support may be helpful.
CHRONIC FATIGUE SYNDROME:
Chronic fatigue syndrome is defi ned by slightly different criteria in different countries (USA, UK, Australia), which are broadly the following:
– Beginning which can be spotted in time fatigue “acquired”;
– No relief by rest;
– Reduction in activity of at least 50% (disability);
– And often associated with other subjective complaints: headache, musculoskeletal pains, sleep disturbances, impaired concentration.
No objective criteria could be highlighted, and post-viral etiology can not be formally documented. It is therefore a heterogeneous framework whose prevalence is probably very low (less than 0.1% in general practice and around 0.1 to 0.5% in specialized areas).
The treatment is not specific for the syndrome.
The key is to insist, for those patients whose suffering is real, on the recognition of triggering factors and the management, with particular emphasis on maintenance factors and aggravation.
It is thus possible to have a certain effectiveness.
We must believe the patient without necessarily believing illness … keep the hope of an improvement, not to multiply the additional tests when there is no clinical orientation. We must give ourselves the means to resolve socio-economic problems and professionals who do not fail to appear.
The therapies are ineffective or dangerous:
– Immunotherapy (and especially
– Prolonged rest which causes muscle deconditioning and conversely a too rapid recovery without “bearing” essential activity, source of intolerance and deepening unrest by an effect of “feed-back” negative.
The treatments are usually helpful:
– Recovery ‘progressive’ physical activity;
– The cognitive behavioral-inspired therapies that are the only ones proven their effectiveness.
The treatments discussed in terms of cases are:
– Antidepressant treatment, avoiding sedative antidepressants and focusing on serotonergic antidepressants;
– The lifestyle advice (removal of alcohol, terms of quality sleep, etc.);
– Dietary treatments and multivitamins;
– And, in exceptional cases, treatment with the Hydrocortisone which in some cases has been in small doses (5 to 10 mg) be useful (to be reserved for specialists). Treatment with DHEA has not proved its effectiveness.