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.
Angina pectoris is characterised by strong, oppressive pain in the chest that spreads to the neck and left arm. It is a sign of lack of oxygen in the heart. It is normally caused by a condition in the coronary arteries, which are the arteries responsible for carrying oxygen to the heart tissue.
Intense pain that appears quickly and intensifies over the course of a few minutes in the chest. It is accompanied by sweating, nausea, vomiting and can spread across the whole chest, the left arm, the neck, and the bottom part of the face.
Angina should be differentiated from the pain that can be caused by pericarditis (inflammation of the membrane surrounding the heart), from hiatal hernia (stomach hernia) and from musculoskeletal pain. It can also be confused with indigestion.
It can affect any age group in adulthood. It is very rare in children. There is a correlation with age (the risk increases as age increases), and there is a slight predominance in males.
Based on clinical observation, electrocardiogram and on determining different blood parameters that show changes in the heart muscle. Diagnosis can be made during an episode of pain, or through a stress test to highlight it, under strict medical control.
The definitive diagnostic test is cardiac catheterisation, which shows blocked areas and often allows the blockage to be cleared with the same catheter.
Electrocardiogram, echocardiogram, nuclear magnetic resonance of the heart, and also cardiac catheterisation which has a diagnostic and therapeutic aim as it can improve blockages in the coronary arteries.
Treatment is aimed at reducing the risk factors, especially tobacco, and improving blood flow in the heart, with the use of various vasodilators.
Health education is essential for those suffering from angina, in order to avoid triggers (quick and intense exercise without warming up) and risk factors (tobacco and alteration of fat content in the blood).
There are numerous coronary vasodilators and various pharmacological families. One thing they all have in common is that they improve coronary blood flow. Controlling arterial hypertension is essential to reduce cardiac effort and overloading of the surrounding vessels.
Cardiac catheterisation consists of inserting a catheter via the arm or leg that reaches the heart and uses contrast to detect coronary obstruction. It thus allows the blockage to be cleared using a dilator or by inserting a stent (an artificial object that allows the flow of blood along the coronary artery to remain open).
Cardiac surgery allows coronary reconstruction with the heart in hand, using artificial arteries or the patient's own vein, which can be taken out of other parts of the body, such as the legs. The advantage is that the reconstruction is better and the disadvantage is that it entails open surgery with the use of extracorporeal circulation.
Tobacco is a big risk factor for developing angina. It should be completed avoided. Controlling fats in the blood and moderate, constant physical exercise are very important.
It is also important to have a healthy diet and regular light or moderate exercise continued over time.
Another important aspect for those who suffer from angina is information relating to how to lead a normal life, over many years, with close monitoring of medication and the relevant tests. Many people have a long life with very few issues after having had angina, as long as the condition is closely controlled.
Cardiology, Cardiac surgery, Haemodynamics and cardiac catheterisation, Intensive care.
Delirium is an acute attention and cognitive disorder that frequently appears in elderly hospitalised patients, although it can affect anyone with a severe illness, including children.
Presentation of this mental state alteration is both acute (its onset can be quite precisely recognised) and fluctuating (there are moments in the day when the person has more manifestations). However, with appropriate interventions, it can be fully or partially reversible and even prevented.
Delirium usually involves multiple factors, but the main causes that can trigger it during hospitalisation are:
They may present with one or several of the following symptoms:
Inform the healthcare staff if you detect any of these manifestations in the person you are accompanying. In addition, bear in mind that the episode of delirium may last from hours to days in most cases, but it can also last for weeks or months.
In 40% of cases, delirium can be prevented if you follow these recommendations:
As well as implementing non-pharmaceutical measures, the medical team and nurses will analyse the possible causes of the delirium and adopt the most appropriate measures for each patient, such as diagnosing and treating infections, controlling pain, correcting dehydration, and reviewing treatment and catheter use, among other measures.
On some occasions, it will be necessary to administer medication to help control the delirium, calm the person and make them more collaborative to remove the risk of accidents and injury.
People who suffer episodes of delirium during their hospitalisation may suffer falls, bronchospasms and loss of autonomy in activities for daily living, possibly requiring more help than before hospitalisation; they may even need to stay in hospital or another centre for longer to recover their lifestyle.
In some cases, patients with delirium require subsequent follow-up due to the risk of developing cognitive impairment.
Collaboration with the family is essential, as they know the patient best and can best help to prevent some of the associated complications.
Whenever possible, it is important for the person to be accompanied by a family member or close friend, especially in their first 48 hours of admission. This will calm and reassure them.
If the companion has to go and leave the person alone, the nurses should be informed so they can supervise the necessary care.
You can follow the prevention recommendations and also bear in mind the following:
Chronic fatigue syndrome, also known as myalgic encephalomyelitis, is a condition characterised by chronic and incapacitating fatigue when exerting little effort, which does not improve with rest. Over time this causes dysfunction of the neurological, immune, endocrine and metabolic systems. Its severity is very variable. In some cases physical and cognitive capacity may be significantly affected, disabling patients and limiting their quality of life. In other cases, people with the condition may lead a relatively active 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:
Kidney disease encompasses a wide range of conditions that compromise the normal functioning of the kidneys. Their main purpose is to purify the blood of different composites, regulate their composition of mineral salts and acidity and contribute to the normal formation and maintenance of bones. They also support the creation of red blood cells and regulate arterial pressure.
Kidney disease is measured by the stage of renal insufficiency, which increases from 1 to 5; the most advanced stage at which the kidneys have ceased to function. During stages 1 to 4 there are different medical treatments that can slow or compensate for renal insufficiency. At stage 5, patients have to undertake extrarenal purification techniques such as haemodialysis or peritoneal dialysis. In this case, the possibility of a kidney transplant will always be considered, which would allow a normal life free from dialysis but would require taking immunosuppressant medication to prevent rejection of the transplanted organ.
The treatment of kidney failure has four fundamental pillars: controlling high blood pressure when present, managing elevated urea levels, addressing mineral salt imbalances (sodium, potassium, calcium, phosphorus, magnesium), and controlling acidosis and anemia.
Renal insufficiency is usually detected with a simple blood test. Symptoms tend to be tiredness and generally feeling unwell caused by a build-up of urea, anaemia or both factors together. The patient may also have a headache if their arterial pressure is high.
All age groups. In childhood, there is often a genetic cause. In adults, it may be due to other illness such as diabetes, immune diseases or infectious diseases. It may also manifest due to the late appearance of genetic diseases in adults.
Renal insufficiency is diagnosed with a simple blood test. Establishing the cause of the renal insufficiency is more complicated. Often, a kidney biopsy and genetic testing will be needed.
Typical tests include blood tests, ultrasound, nuclear magnetic resonance imaging, kidney biopsy and genetic testing.
Initial treatment consists of substituting or compensating for the aforementioned alterations. During later stages, haemodialysis or peritoneal dialysis may be used, and in the case of terminal renal insufficiency, a kidney transplant may be carried out; from a deceased or a living donor.
Drinking a reasonable amount of water a day contributes to good kidney function.
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
Hereditary metabolic diseases (HMDs) are a group of rare genetic disorders. The genetic defect causes a structural alteration in a protein that is involved in one of the metabolic pathways, causing it to block the affected pathway. As a consequence, this causes a build up of substances that may be toxic for the body and a deficiency of others that it needs.
Hereditary metabolic diseases (HMD) are chronic progressive multi-system illnesses that may appear at any age and that in most cases pose diagnostic and therapeutic challenges. Our Unit has been recognised as a leader within Spain (CSUR) and Europe (ERN) for this pathology and takes part in the neonatal screening programme in Catalonia. We are the only centre in Catalonia to offer complete care from paediatrics to adults with particular expertise in lysosomal storage disorders.
HMDs are divided into:
- Intermediary metabolism HMD: usually with acute symptoms.
- HMD related to the organelles (lysosomal storage disorders, peroxisomal diseases, mitochondrial disorders and endoplasmic reticulum storage diseases): chronic presentation with no decompensations (with the exception of some mitochondrial disorders)
Multiple systems in the body are affected and different organs and systems are involved with varying symptoms depending on the disorder and the patient’s age. These disorders require a coordinated approach to care and programmes to manage the transition to adulthood.
Many symptoms become evident during childhood in the form of delayed physical growth and delayed psychomotor development. There may be associated heart problems, kidney conditions, and at times decompensations leading to liver or kidney failure and neurological impairment. In the case of organelle disorders, symptoms are chronic and affect the bones and organs of the senses in greater measure. They are more common in adults than intermediary metabolism disorders.
Diagnosis is carried out by:
They are chronic disorders that need to be treated in specialised centres with multidisciplinary teams to provide support for all related health problems.
The following may be necessary, depending on the type of disorder:
Prevention consists of thorough genetic and reproductive counselling if there is a family history of the disease. Early diagnosis of some diseases through the neonatal screening programme enables effective treatment and improved prognosis.
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.
Psoriasis is a non-infectious inflammatory skin condition. It is chronic and shows up as pinky-red skin lesions covered with scaly silvery-white dead skin cells. It normally appears between 15-35 years old but can do so at any age.
The cause of this disease is an alteration of the immune system that causes an inflammatory chain reaction in the body’s defence mechanisms that results in excessive production of skin cells.
It appears as pinky-red patches covered with silvery-white scaly skin. It mostly appears on elbows, knees, the lower back and the scalp, but can also occur on other parts of the body.
Up to a third of people with psoriasis may go on to develop joint problems, or psoriatic arthritis, characterized by inflammation of the joints. This is generally intermittent and asymmetric and mainly occurs in the fingers, toes and lower spine.
It most commonly appears as skin lesions, which can sometimes itch or become sore, especially if the skin cracks or is broken. There are different types of psoriasis:
Aside from skin lesions, people with psoriasis may develop psoriatic arthritis, which occurs as pain, heat and reddening around the joint and being unable to move the joint. In its advanced stages, there may be deformities, pain in the heels and back pain.
It affects 2-3% of the world population. 10-30% of sufferers develop arthritis, which can occur at any time, although it is more likely between 30-50 years old.
Diagnosis is by observation of the lesions and the areas around them. Specialists may sometimes perform a skin biopsy to confirm diagnosis and to rule out other conditions that may appear similar or have the same symptoms.
There are currently different treatments to alleviate symptoms and signs, and which also cure the skin lesions in most cases. The dermatology specialist will decide the most suitable treatment for each patient, depending on the type of psoriasis, where it is on the body, the severity, and type of patient.
There are three types of treatment:
Oral herpes is an infection in the lips, mouth and gums caused by the herpes simplex virus (HSV-1) and which shows up as small painful blisters called herpes labialis, commonly known as cold sores.The herpes simplex infection is very contagious, common and endemic throughout the world. It is normally acquired in childhood and lasts a lifetime.
Herpes caused by the HVS-1 virus is spread by mouth-to-mouth or skin contact with ulcers or saliva and the area around the mouth and lips. It can also be spread to the genitals, resulting in genital herpes.
Although uncommon, it can be transmitted from an infected mother to her baby during birth.
Usually, herpes labialis (or the cold sore virus) is asymptomatic and most people infected do not realise. When it appears, it does so as painful blisters or ulcers on or around the mouth. People with this condition notice a feeling of stinging, tingling or burning in the affected area.
After the first infection, the blisters may periodically reappear, varying from person to person.
According to the WHO, 67 % of the population is infected with HSV-1.
Diagnosis is done in a medical centre, in other words, through examination of the patient. If there is any doubt, the specialist may request virological culture tests on the blisters during the initial stages of the disease to confirm it.
Antiviral medications such as aciclovir, famciclovir and valaciclovir are the most effective to treat those infected with HSV-1. However, despite reducing the intensity and frequency of symptoms, they do not cure the infection.
Eczema is a skin condition characterised by the appearance of small vesicles and which exudes fluid. Flaking skin produced by the disease can cause itching, inflammation and pain. It is the skin’s inflammatory response to external or internal stimuli and there are two types: endogenous (or atopic), and exogenous (or contact). Often called dermatitis, eczema has different clinical presentations and may have several different causes.
The existence of other diseases, allergies, contact with irritants and genetic inheritance are some of the causes of eczema.
Endogenous or atopic eczema is an atopic disease typically found in patients with rhinitis, conjunctivitis, asthma and dermatitis, and usually presenting as hypersensitive dry skin. It is often related to allergic reactions or external stimuli such as exposure to pollen, dust, fur, and urticaria, viral infections and bacterial skin infections.
Exogenous or contact eczema is the allergic or irritative reaction to chemical substances that have come into contact with the skin and that the body interprets as toxic.
Eczema shows up as skin lesions made up of itchy scaly red patches on different parts of the body. Sometimes there may be an inflammatory reaction in the area of the outbreak that may give rise to serum-filled blisters.
Figures show that around 30% of patients with eczema have a family history of atopic disease in the family. Atopic eczema can appear when a child is just a few months old and in these cases it does so on the scalp, face and nappy area. It usually disappears during puberty, leaving the skin dry, and in some cases, signs of atopy such as urticaria or asthma.
Contact eczema appears in patients sensitive to a particular substance, called an allergen. The affected person will have a skin reaction each time they are exposed to this substance.
Suspected diagnosis of each type of eczema must be carried out through studying the patient's medical history. In most cases, diagnosis is clinical, in other words, the dermatologist will diagnose the condition after examining the patches on the skin. If there is any doubt, a skin biopsy can confirm diagnosis.
For contact eczema, a patch test will be needed to determine the allergen responsible for the patient’s patches of eczema.
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