We are the combination of four hospitals: the General Hospital, the Children’s Hospital, the Women’s Hospital and the Traumatology, Rehabilitation and Burns Hospital. We are part of the Vall d’Hebron Barcelona Hospital Campus: a world-leading health park where healthcare plays a crucial role.
Patients are the centre and the core of our system. We are professionals committed to quality care and our organizational structure breaks down the traditional boundaries between departments and professional groups, with an exclusive model of knowledge areas.
Would you like to know what your stay at Vall d'Hebron will be like? Here you will find all the information.
The commitment of Vall d'Hebron University Hospital to innovation allows us to be at the forefront of medicine, providing first class care adapted to the changing needs of each patient.
Patients with Asperger’s syndrome need a stable and predictable environment that can be easily adapted. It is key to their well-being to establish routines according to their interests, organise their time, avoid inactivity or over intense activity as well as sudden changes. Although the syndrome has no cure, appropriate treatment and involving family members can improve the quality of life of patients.
People with Asperger’s syndrome may have different requirements depending on their age, surroundings and the awareness that they have of their difficulties. For this reason, they need a tailor-made programme that responds to their specific case.
The aim of these customised programmes is to:
It is important to manage their development through different disciplines. These may include cognitive treatments, social skills programmes and occupational therapy for the patient. You also have to consider guidelines on how to resolve conflicts and how to manage pyschoeducational groups for families or caregivers.
In infants, from an emotional and attitudinal point of view, it is important to learn to identify the warning signs in their mood. In this way, we can prevent difficulties in anger management and low tolerance to frustration, since they are patients with a high degree of sensitivity to criticism. Avoid punishment as much as possible and establish more positive reinforcement strategies.
All these guidelines must be established in a space where the differences the child or adolescent presents are valued positively, including their limitations, but also their possibilities and positive aspects.
In adults, many of these characteristics continue, as Asperger’s cannot be cured. In any case, personalised treatment, involving family members and good communication with professionals can allow a better quality of life.
Dystonia is a neurological disorder characterised by involuntary muscle contractions that cause repetitive movements and tortuous and painful stances every time the patient makes a learned movement, such as walking or speaking.
Dystonia that is detected in childhood can progress rapidly and interfere in the development of the child's language and mobility, causing a physical disability that will affect them throughout life.
Dystonia is a very heterogeneous disease, which can occur for a variety of reasons:
Due to its incidence, dystonia is considered a rare disease.
Dystonia in childhood can occur in isolation or associated with other neurological and development problems. It can cause difficulty in everyday tasks such as walking, speaking, feeding oneself and taking care of personal hygiene.
When presented in isolation it is called primary dystonia and often has a genetic origin. Children who suffer from it do not usually have other health problems and their neurological development is normal. At first it manifests itself in actions such as walking, running, or writing and, later, can spread to other parts of the body and cause widespread dystonia.
Myoclonic dystonia is one of the most frequent hereditary forms of dystonia in childhood. It is characterised by the presence of sustained (dystonic) and abrupt (myoclonic) muscle contractions and psychiatric disorders such as anxiety, depression and obsessive-compulsive features. The first symptoms appear in childhood and affect the lower limbs of children, who have difficulties walking, running and with sports. This disease also affects the social relationships of these children, who have problems speaking in public or eating and drinking with friends.
Dystonia can also be associated with other neurological problems, such as spasticity, ataxia, weakness, delay in neurological development and intellectual disability. In this case we call it secondary dystonia and it is necessary to rule out neurometabolic and neurodegenerative causes.
It affects children, adolescents, and adults of all ages.
First of all, patients are subjected to a series of clinical, metabolic, neurophysiological and neuroimaging studies to classify the type of dystonia, before carrying out genetic studies. In patients with myoclonic dystonia, first of all, a Sanger sequencing study is carried out to determine the gene that causes it, and in the other patients, a complete family exome sequencing(parents and patient) is carried out or the index case (patient) based on the DNA samples available.
Being a rare and very heterogeneous disease it is difficult to reach a correct diagnosis and treatment plan. It is important to distinguish hereditary dystonia from childhood cerebral palsy, caused by brain damage at birth, since its diagnosis has very important consequences for treating the disease later.
A diagnosis in time decreases the need to carry out more diagnostic tests, making it possible to form a prognosis and to advise families on avoiding future diseases. It also has a very positive psychosocial impact on the patient and family. And most importantly, an exact diagnosis of the cause that generates the dystonia makes it possible to guide the best possible treatment for each patient, in what we call personalised medicine.
Dystonia in childhood is progressive and debilitating, but can be prevented with early diagnosis and the use of specific therapies depending on the identified genetic defect.
Levodopa is the treatment of choice in dopa-sensitive dystonia, caused by a defect in the synthesis of dopamine. Botulinum toxin is used to control focal dystonia. In the case of widespread dystonia, different drugs are used to decrease tremors, muscle tone, and painful spasms. And in some cases of paroxysmal dystonia, which is characterised by brief and repetitive involuntary movements during the night, antiepileptic drugs are used.
An intrathecal baclofen pump administers liquid medication through a device that is placed under the skin, and is used to treat generalised secondary forms of dystonia. It reduces pain, decreases muscle tone and spasms. It is a treatment we call symptomatic and palliative, since it does not improve the motor function of the patient.
Deep brain stimulation or globus pallidus stimulation, two electrodes are placed in the globus pallidus using a stereotaxic technique, it is the treatment of choice in primary dystonia, especially if they are widespread and do not respond to conventional medication. In these cases children can recover the function of the area affected by dystonia and improve their quality of life. It can also be useful in patients with secondary forms of dystonia, although its effectiveness is less than in primary forms of dystonia.
Performing genetic testing is the best prevention to avoid having more children affected by this disease in the same family.
Associació de Lluita contra la Distonia Mioclònica a Espanya
Associació de Malalties Neurodegeneratives amb Acumulació Cerebral de Ferro
Associació GNAO Espanya
Poliomyelitis is a highly contagious disease caused by any of the three human poliovirus serotypes, which are part of the enterovirus family. Europe was certified free of poliomyelitis in June 2002. Immunisation and vigilance of the disease continue to ensure the region is free of poliomyelitis. Post-polio syndrome has no defined causal mechanism but it affects between 20% and 80% of patients afflicted with poliomyelitis.
Initial symptoms are those of a influenza-like illness (fever, headache, joint and muscle pain, vomiting, among other things) and can last up to 10 days. Its most serious forms may cause respiratory paralysis leading to death. Post-polio syndrome presents a new neurological weakness that may be progressive or abrupt on muscles previously affected or unaffected. It may or may not be accompanied by new health problems such as excessive fatigue, muscle pain, pain in the joints, intolerance to cold, reduced physical stamina and function, and atrophy.
It mainly affects children and the mechanisms for its transmission may be through faecal-oral channels or a common vehicle (contaminated water or food).
Post-polio syndrome affects patients who have had poliomyelitis for 20 years or more.
Diagnosis is given clinically, supplemented with laboratory and electromyographic (EMG) tests.
Symptomatic treatment with analgaesics, a ventilator where necessary, gentle exercise and possibility of orthopaedic devices to prevent deformities or to enable function.
In acute diagnoses, studying secretions, stools and cerebrospinal fluid. EMG in acute and later stages for diagnosing post-polio syndrome.
Poliomyelitis has no cure but it can be prevent by vaccination.
Amyotrophic Lateral Sclerosis (ALS) is a neurodegenerative disease affecting the motor neurons in the brain and spinal cord, causing progressive paralysis of muscles, including the diaphragm. Early symptoms may include muscle weakness, difficulty speaking or swallowing, and the disease often leads to respiratory failure determining survival. Diagnosis is clinical and by exclusion, and current treatment focuses on symptom management and supportive care in multidisciplinary units.
ALS is a neurodegenerative disease caused by the death of motor neurons in the brain and the spinal cord.
There are two types of motor neuron: upper and lower. The first are found in the motor cortex and establish connections with the lower motor neurons located in the brain stem and spinal cord, which innervate muscles. When the upper motor neurons die, spasticity, weakness and hyperreflexia appear.
When the lower motor neurons die, twitching, weakness and muscle atrophy occur. Other neuron populations can also be affected, such as the temporal and frontal behavioural and executive circuits.
Epidemiologically speaking, ALS has an incidence of 1.5-2 new cases a year per 100,000 people (3 new cases are diagnosed per day in Spain). The total number of cases (prevalence) is 2-5 per 100,000. According to this data, the total number of patient with ALS in Spain is approximately 4,000 cases. This is why it is included in the rare or minority disease group.
90% of cases of ALS are sporadic (no family history). Around 10% of ALS cases are familial, usually inherited as dominant traits. The incorporation of new molecular genetics techniques in the field of research has allowed more than 25 genes involved in ALS to be identified.
As a consequence of the continuous decrease in motor neurons, symptoms of the disease appear. These usually depend on the location of the motor neurons undergoing the most advanced processes of degeneration. In most patients (70%) the first symptom is loss of strength with muscular atrophy in the hands or clumsiness when walking, with frequent falls. In approximately 25% of patients, the first symptom is difficulty talking or swallowing, which indicates that degeneration of the bulbar motor neuron population is the most intense. There are also other possibilities for clinical presentation of this disease, although much less frequent: respiratory failure, weight loss or unexplained lack of energy (asthenia), cramps and twitches in the absence of muscle weakness, spasticity in legs, rapid mood changes or cognitive impairment.
In advanced phases, the disease can also paralyse the eye muscles. In the final stages of the disease, paralysis of the respiratory muscles leads to respiratory failure, which is often the cause of death.
The condition particularly affects people aged between 40 and 70. The incidence is greater in men (3:2.2 per 100,000) in sporadic forms. The age of first onset of symptoms reaches its peak between 58 and 63 years old in sporadic cases and between 47 and 52 years in familial forms. Incidence decreases markedly after the age of 80. The risk of suffering ALS is 1:400 for women and 1:350 for men.
The differing ways in which ALS manifests is one of the two reasons for a delay in suspected diagnosis of the disease, which can be up to 15 months. The other is that there is no test or biomarker to objectively confirm the diagnosis in the initial stages of the condition. A diagnosis of ALS is a diagnosis of exclusion, based on clinical criteria and conducting tests (MRI, clinical analysis, genetic tests, electromyography, EMTC, neuropsychological exam, nuclear medicine techniques and others) to rule out other illnesses with similar clinical findings. In most specialised ALS units, the disease diagnostic criteria used are the revised El Escorial criteria and the Awaji-shima criteria.
There is currently no medication that can cure or stop the disease. Riluzole and Edaravone are the only medications approved for ALS treatment, although their effect on survival is moderate (months).
The European (EFNS) and American (ANA) associations of neurology recommend that patients with ALS be treated in specialised centres, where possible in multidisciplinary units, so that they might be prepared for any complications. These units should offer solutions to control the symptoms, including the use of a feeding tube, control of saliva secretions, cough assist devices, respirators for mechanical ventilation, technology to improve the patient’s ability to move around and facilitate communication in patients who have lost the ability to speak.
These multidisciplinary units are the centres preferred by those running new drug trials.
The reality is that there is currently no effective treatment, although patients and their relatives often desperately search online for miracle drugs that might cure the condition. ALSuntangled, a group made up of 80 international experts in ALS, was born with the aim of protecting these patients from the numerous products advertised. It mission is to review the veracity and safety of the alternative treatments offered online that have not gone through the proper regulatory channels. It publishes its results in the official magazine for the disease and on its website.
Diagnostic imaging techniques (MRI, CAT, PET), electrophysiology (electromyography, EMTC, PESs), laboratory analysis (haematology, biochemistry, antibodies, hormones, enzymes, serology, genetics), respiratory functional tests, gasometry, pulse oximetry, overnight pulse oximetry, capnography, BMI, calorimetry, lumbar puncture, functional scale for the disease (ALS-FRS-R). A muscular biopsy may be required in exceptional cases. It is advisable to admit the patient in order to arrange for testing and offer them a report on discharge detailing the ALS diagnostic category and degree of functional repercussion (ALS-FRS-R).
Although various environmental risk factors have been suggested (geographic, occupational, dietary habits, proximity to electrical channels, contact with pesticides or other neurotoxins), there is no agreement on preventative measures to take.
In family forms, it is possible to offer genetic counselling to people with a desire for offspring.
During the natural course of the disease, complications often appear that may be prevented and treated. Among the most significant are malnutrition, respiratory failure, hypersalivation, spasticity, pain, loss of independent movement and communication, depression, anxiety, sleep disorders, bed sores, cognitive deficits and burden on carers.
Chronic fatigue syndrome, also known as myalgic encephalomyelitis, is a condition characterized by severe and persistent fatigue that does not improve with rest. It can affect neurological, immune, and metabolic systems and significantly impact daily life. Common symptoms include extreme tiredness, muscle pain, cognitive difficulties, and sleep disturbances. Treatment focuses on symptom management and improving quality of life.
Even through the cause of chronic fatigue syndrome is not yet known, it is being actively researched. It is thought the condition may be brought on by a combination of physical and psychological factors. These include viral or bacterial infections, recent negative or traumatic experiences, mental stress, depression and nutritional deficiencies. It is important to study the accompanying symptomatology: pain, sleep disorders, headaches; and cognitive, neurological, neurovegetative and immunological symptomatology in order to reach a proper diagnosis.
The most typical symptom is intense tiredness and fatigue that is not cured by rest and that limits daily life. Fatigue should last more than six months for diagnosis to be confirmed.
Other common symptoms are:
It affects young people, mainly women, between twenty and forty years old. Although there are no studies of its prevalence in the Spanish population, in other countries it affects 0.07% to 0.3% of people.
A general blood test is used along with imaging tests to carry out a differential diagnosis with other causes of persistent fatigue. The basic imaging tests are a chest x-ray and an abdominal ultrasound. A psychopathological assessment is required prior to definitive diagnosis to:
In the case of CFS, as with many immunoinflammatory diseases, there is no specific diagnostic test available; a diagnosis is therefore reached by fulfilling the Fukuda criteria.
Primary criteria (both must be present):
Unexplained and persistent or recurring chronic fatigue (minimum 6 months), which appears again or comes on suddenly and which is not as a result of recent exertion. Does not significantly improve with rest. Produces a considerable decrease in levels of occupational, educational, social or personal activity. Exclusion of other illnesses that may cause prolonged fatigue.
Additional symptoms (occurring concurrently, 4 or more of the related signs and symptoms must be present and be persistent or recurring over 6 months following the onset of fatigue):
There is no treatment to cure chronic fatigue syndrome, but the symptoms can be improved:
There is currently no treatment to cure chronic fatigue syndrome, but symptoms can be improved:
Diagnosis of chronic fatigue syndrome (CFS) is purely clinical, but a general blood test and imaging tests are useful to carry out a differential diagnosis with other causes of persistent fatigue.
The general blood test should include:
Minority diseases, also called rare diseases, are those that affect between 5% and 7% of the population. They are very varied, affecting different parts of the body with a wide range of symptoms that change both between diseases and within the same disease.
It is estimated that some 30 million people in the EU, 3 million in Spain, and around 350,000 in Catalonia suffer from one.
The complexity of most rare diseases requires multidisciplinary care involving expert professionals from different medical specialties, personalized nursing management, psychological support, and social work, among other services.
At Vall d’Hebron, more than 200 specialist professionals care for over 40,000 patients with rare diseases. We are one of the hospitals in Spain that treats the highest number of rare conditions and one of the leading centers in Europe in this field. As of 2025, we are part of 20 European Reference Networks for rare diseases (ERN), 43 Spanish reference centers (CSUR), and the 12 expertise networks of the Department of Health (XUEC). This makes the hospital a highly specialized center for caring for these diseases throughout the entire life journey—from birth to adulthood—through a networked system that allows sharing resources and expertise with other hospitals and centers in the region.
The professionals across the various units and centers aim to improve patient access to diagnosis, information, and personalized care, as well as support research through:
The Rare Diseases Committee aims to establish a common framework for rare disease care at the hospital, identify and align the different initiatives (clinical, training, and research), deploy prioritized action lines, and monitor and evaluate outcomes in order to propose and implement improvements.
The concentration of patients with rare diseases increases knowledge and promotes research. Our Research Institute (VHIR) is a leader in both basic and clinical research. More than 14 basic research groups focus on studying rare diseases to improve diagnosis and develop new therapeutic approaches. We are the center in Spain with the highest number of clinical trials involving orphan drugs, including gene therapies, and we have a leading unit dedicated to the development of advanced therapies.
For more information, you can contact the rare disease team at: minoritaries@vallhebron.cat
Alzheimer’s disease (AD) is the most common neurodegenerative disease worldwide. First described in 1906, it was known for years as senile dementia, but today we know that most cases of senile dementia are AD. WHO data states that it affects over 50 million people worldwide and this is set to triple by 2050. It is the main cause of disability in the elderly and the second specific cause of death in Spain.
In certain areas of the brain of someone with Alzheimer’s, two proteins (amyloid-beta and tau) are progressively produced over several years, forming deposits that eventually damage and destroy the neurons, leading to the progressive loss of higher-level cognitive brain functions such as: memory, language (aphasia), the ability to perform learned motor functions (apraxia), and to recognise different sensory stimuli (agnosia), reasoning and judgement, and changes in mood, behaviour and personality. Although the etiology of the disease is unknown, we do know of many factors that contribute to its appearance.
AD manifests in various ways. The signs and symptoms are specific to each individual and the characteristics of how the dementia develops will be different for each person.
Most patients (85% of cases) present the typical form (amnestic or hippocampus), which starts with the symptom of episodic progressive memory loss in relation to recent events and difficult taking in new information, and thereby losing the ability to adapt to new situations. Discrete constructional apraxia. Loss of fluidity of speech with normal comprehension. Early and persistent depression, anxiety or apathy (most common), with a substantial decline in initiative, motivation and interest, and with indifference and passivity.
In the mid stages, the disease presents loss of remote memory. Temporal and spatial disorientation. Ideomotor and ideational apraxia occur as well as constructional apraxia. Speech continues to worsen and comprehension issues are added to the loss of fluidity and anomia. Visual and body image agnosia (somatagnosia) develops. The mid stages are when sleep and psychiatric disorders are most evident, including becoming agitated at night, being restless, delirium (being unable to distinguish what is reality: delusional jealousy, confusing TV programmes with real life) and hallucinations (false sensory perceptions: hearing voices, seeing insects).
In the late stages, patients present severe agnosia, a loss of bladder and bowel control, become mute or almost mute, and present motor function alternations such as overall stiffness and a stooped posture. Approximately 10% present epileptic seizures. All patients show obvious weight loss during this final stage.
In around 15% of patients with AD, memory may be relatively preserved until the late stages. These are atypical forms or variants (without memory loss in the early stages) which may present in three forms: with behavioural or personality changes, with visuospatial alterations, or with changes to language as the earliest and predominant symptom of the disease. As it progresses, the other symptoms described as the typical form of the disease also appears. These atypical forms of AD are more common in cases where the onset occurs at a younger age.
Daily activities (DA) are progressively affected: first there is a reduction in work and social activities (advanced daily activities); followed by changes to everyday activities (handling domestic objects, money, cooking, housework), and in the late stages, basic daily activities are affected (washing, dressing, eating, bladder and bowel control). In the final stage, patients enter a vegetative state and die as the result of an intercurrent illness: the time from diagnosis to death is usually around » 5-10 years.
The prevalence and incidence of the disease increases after 65 years of age. It therefore affects 5% of the population over 60, 20% of those over 80 and 30% of those over 90. In Spain there are 800,000 people with the condition. The real figure is undoubtedly much higher, however, as the first symptoms are sometimes difficult to distinguish from those that naturally appear with age. For this reason it is an underdiagnosed disease, with around 1 in 3 people with AD believed to be undiagnosed.
Fewer than 5% of cases of AD are hereditary. This is known as familial or inherited AD and occurs through autosomal dominant inheritance. The clinical picture includes an earlier onset of the condition (before 65 years old) and a faster evolution.
The remaining 95% (sporadic AD) present the combination of risk factors for the development of the disease together with genetic alterations, together making the patient susceptible to the disease.
Apart from genetic factors, other risk factors for developing the disease are: ageing; gender (from 65 it is more common in women); vascular risk factors such as high blood pressure, diabetes or obesity; lifestyle (smoking, alcohol, lack of physical activity, lack of intellectual activity, little social interaction); previous head injuries, and chronic sleep disorders. People with Down syndrome (trisomy 21) have an extra copy of the gene that encodes the amyloid precursor protein (APP) making them more susceptible to AD at a younger age. Chronic sleep problems increase the risk of AD. Interrupted sleep increases levels of the amyloid-beta and tau protein.
Due to the fact that pathological alterations (amyloid deposit following tau) begin in the brain 15-20 years before symptoms appear, there are currently considered to be 3 stages of the disease:
Although there is currently no cure for the disease, there are treatments that can delay or slow the progression of the disease for a time, improving quality of life for these people. Drug treatments are: cholinesterase inhibitors (rivastigmine donepezil, galantamine) that act to facilitate cholinergic neurotransmission and are licensed for the symptomatic treatment of light or moderate AD, and memantine, a non-competitive glutamatergic NMDA receptor antagonist, which decreases levels of glutamate (an excitotoxin that destroys neurons when released chronically and in excess) and is licensed for the mid and late stages of the disease.
In addition to these treatments, proper management of lifestyle factors is very important, such as: correcting any hearing loss, reducing smoking and drinking, proper management of blood pressure and diabetes, a balanced diet, avoiding obesity, doing regular physical activity, preserving and encouraging social contact. Together with the above, cognitive stimulation is useful during a large part of the progression of the disease.
There are currently 400 studies assessing the efficacy and safety of different treatments in patients with AD.
Known preventions strategies work on the risk factors for the disease: healthy habits, controlling vascular risks (high blood pressure, diabetes, etc.), a higher level of education, changes to lifestyle (essentially increasing physical activity) giving up toxic habits (smoking and drinking). All of the above can reduce cases of AD by 35-40%, or at least delay its onset.
Education and mental activity stimulate the connections in the brain and increase the cerebral reserve capacity, so it is very important to remain mentally active.
The Dementia Unit in the Neurology department is in charge of diagnosing and looking after patients with Alzheimer’s. The unit includes neurologists with expertise in diagnosing and managing the different pathologies that can occur with dementia (changes to cognitive and behavioural functions that result in changes to daily life) as the main manifestation. Neuropsychologists, nurses and social services and healthcare staff also play a very important role in the Unit.
Other units and departments involved in the diagnosis and monitoring of these patients are: Primary Care, Nuclear Medicine, Neuroradiology, Psychiatry, Pathological Anatomy, Genetics.
Parkinson's disease is a dysfunction of the basal ganglia caused by degeneration of the cells that produce dopamine in the substantia nigra.
It is a progressive neurodegenerative disease of the central nervous system that affects the parts of the brain involved in controlling and coordinating movement, muscle tone and posture.
The prevalence of Parkinson’s in Catalonia is 229 in every 100,000 people.
This is focused on empowering patients and their carers to achieve behavioural changes within their own control and to motivate them to continue treatment long term. It centres on reducing medication and gaining quality of movement. The main goal is functional independence for the individual and general physical condition from the onset of the disease. It is all geared towards minimising secondary complications and the risk of falls.
There are a growing number of studies emphasising that aerobic activity may have a neuro-protective effect. Likewise, during treatment, preventing inactivity, falling and fear of getting around or falling is stressed.
Neuromuscular disease is a chronic illness that results in serious disability, loss of independence, and with significant psychosocial consequences. Respiratory alterations are the main cause of morbidity and mortality in patients with neuromuscular diseases. They are significantly affected by the evolution of the disease and are the reason for multiple hospital admissions where the patient’s life is seriously endangered.
The main causes of respiratory impairment are hypoventilation due to weak inspiratory muscles and a lack of ability to cough due to weak expiratory muscles. Ventilatory support via non-invasive mechanical ventilation or tracheotomy can prevent or reverse ventilatory failure in these patients.
The loss of expiratory strength means that patients are unable to expel bronchial secretions. If the bulbar muscles are also affected and patients run the risk of inhaling saliva, the contents of the mouth or food, this can induce multiple respiratory infections, pneumonia and atelectasis which results in obstruction of the airway and seriously endangers the patient's life.
The combination of non-invasive mechanical ventilation to assist coughing decreases morbidity and hospital admissions for these patients.
There are currently around 60,000 people with the condition in Spain.
In the Cardiorespiratory Rehabilitation Unit, we monitor maximal inspiratory and expiratory pressure (MIP and MEP) and peak expiratory flow (PEF), also known as peak cough flow (PCF) and carry out spirometry.
Treatment goals are focused on controlling the evolution of the ventilatory failure and avoiding or improving episodes of respiratory failure. To achieve these objectives, manual techniques or equipment have to be used. These are techniques to encourage pulmonary expansion, manually assist coughing, and others.
One very important objective is to train the main carer in physiotherapy techniques in order to avoid possible complications in the respiratory system.
Anticoagulant therapy involves the use of medications that reduce the blood’s ability to clot in order to prevent the formation of thrombi. It is used in thromboembolic diseases and in patients at risk of embolism to protect circulation.
There are different types of anticoagulants: injectable or oral.
Low molecular weight or unfractionated heparin. Should be started at therapeutic doses as soon as thrombosis is suspected, even before the diagnosis is confirmed, or as prophylaxis (prevention), at prophylactic doses, when the person has one or more risk factors that could trigger a venous thromboembolism (such as hip or knee replacement surgery). They are administered at fixed doses according to the patient’s weight, the type of thrombosis being treated or risk factor being controlled.
They are used as maintenance therapy when oral anticoagulants are contraindicated (e.g. pregnancy) or have been ineffective.
They are used as maintenance treatment (longer use) and are given on confirmation of the diagnosis of deep vein thrombosis or pulmonary embolism. There are two types of oral anticoagulants: vitamin K antagonists and direct-acting.
The anticoagulant treatment is controlled with blood tests or capillary blood tests (by pricking the patient's finger). Monitoring of patients on anticoagulant treatment is done by haematology and haemotherapy specialists.
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