Chronic Obstructive Pulmonary Disease

COPD is a chronic disease with periods of exacerbation and remission that evolves naturally to aggravation. Given that in COPD occurs irreversible airflow limitation and because the main cause of this disease is smoking, the treatment of COPD aims to establish prevention measures and curative measures for this disease.

Prevention of COPD benefit from these measures:

1. Fight against smoking, avoiding both active and passive smoking and conviction of the patients who smoke to quit this habit.
2. Limiting the exposure to air pollution and professional pollution by wearing masks with special filters at work.
3. Early detection and treatment of bronchitis, especially asthmatic bronchitis, occurring in childhood.
4. Prophylaxis of viral and bacterial infections in patients with obstructive pulmonary disease by using multivalent influenza vaccine in autumn, the use of antipneumococcal vaccines and antihaemophylus influenzae vaccines.
5. The research of alpha 1 antitrypsin deficiency in family members of patients suffering from emphysema, with this origin, to detect a possible partial deficit.

COPD Treatment

Curative treatment of COPD:

The immediate objectives of the treatment of COPD require healing of acute infectious exacerbations, with return to the previous stage of COPD. Installation of a exacerbation and factors that can generate the exacerbation, should be detected: respiratory infections, heart failure, pulmonary embolism, some drugs (beta blockers, tranquilizers, hypnotics, diuretics).

COPD treatment objectives are:

• Prevent disease progression;
• Relive symptoms;
• Improve health status;
• Improve exercise tolerance;
• Prevent and treat complications;
• Prevent and treat exacerbation;
• Reduce mortality;
• Prevent or minimize side effect of the therapy.

Management of COPD should be done in accordance with the standards imposed by Global Initiative for Chronic Obstructive Lung Disease (GOLD):

1. Stage I COPD (mild obstruction): reduction of risk factors by using multivalent influenza vaccine and using of short-acting bronchodilator as needed.
2. Stage II COPD (moderate obstruction): reduction of risk factors by using multivalent influenza vaccine, using short-acting bronchodilator as needed, long-acting bronchodilator and cardiopulmonary rehabilitation.
3. Stage III COPD (severe obstruction): reduction of risk factors by using multivalent influenza vaccine, short-acting bronchodilator as needed, long-acting bronchodilator,  cardiopulmonary rehabilitation and inhaled glucocorticoids if appear repeated exacerbations.
4. Stage IV COPD (very severe obstruction or moderate obstruction with evidence of chronic respiratory failure): reduction of risk factors by using multivalent influenza vaccine, short-acting bronchodilator as needed, long-acting bronchodilator,  cardiopulmonary rehabilitation,  inhaled glucocorticoids if appear repeated exacerbation, long-term oxygen therapy and surgical options such as lung transplantation should be considered.

COPD treatment scheme

Treatment of COPD is using a variety of drugs and therapeutic means, as a strategy “in steps” similar, but with some particularities, to that of the bronchial asthma. Efficiency of treatment of COPD depends on the clinical presentation and stage in which patient is diagnosed. Drugs and therapeutic resources for COPD treatment are: bronchodilators, anti-inflammatory therapy, antibiotic therapy, removal of secretions, oxygen therapy and patient rehabilitation.

Bronchodilators:

Bronchodilators are widely used in the treatment of COPD, even in cases where only bring an improvement in quality of life, not in the functional parameters. Bronchodilators are used continuously, not intermittently as in bronchial asthma.

Ways to use bronchodilators are three: inhalational (preferred), oral and injectable (subcutaneous or intravenous used in severe obstructions).

Bronchodilators

Use of bronchodilators should be preceded by assessment of bronchomotricity as follows:

• Positive bronchodilator test (increase in FEV1> 15%), which is investigated only once in the time of diagnosis, indicating a benefit of the therapy.
• If thebronchodilator test is negative or at limit, but the patient stated an subjective improvement of the symptoms, such as reduction of dyspnea, bronchodilators may be prescribed.
• When bronchodilator test is negative, these substances have no purpose.

The group of bronchodilators substances is represented by: beta 2 agonists, anticholinergics and methylxanthines.

Inhaled beta 2 agonists (with spacer) qre indicated in a proper dose, according to the severity of each case, determined by spirometry. Typically, in the case of short-acting beta 2 agonists (salbutamol, terbutaline, pirbuterol), 2 sprays used 3-4 times / day are enough. For long-acting beta 2 agonists (formoterol, salmeterol) dose is 2 sprays every 12 hours. Oral formulations of long-acting beta 2 agonists, ingested before sleep, are useful in patients with nocturnal dyspnea.

Anticholinergic medications  have a action which is installed slower than the action of beta 2 agonists, after about 15-30 minutes, but have a longer duration of action. These drugs reduce mucus secretion, which is why some authors consider this medications as a first-line drug in the treatment of COPD. The dose is 2 sprays, 3-4 times / day. May be associated with beta 2 agonists, because by combining the two classes of drugs will result a potentiating effect.

Methylxanthines or theophylline derivatives are considered to have a lower bronchodilator potential than beta 2 agonist and anticholinergics, doubled by a much greater risk of severe toxic reactions than the first two classes of bronchodilators. Therefore, methylxanthines are placed on stage three of treatment, after beta-2 agonists and anticholinergics, being given to patients with serious, sever and persistent symptoms, despite the maximal therapy with bronchodilator drugs from first two categories.

Long-acting theophylline will be taken at night before bedtime, by patients with nocturnal dyspnea, representing an alternative to long-acting beta 2 agonists. Oral dose of theophylline should be 400 – 800 mg / day with gradual increase up to 10 mg / kg / day.

For patients with severe obstructive syndromes, will be used intravenous administration of methylxanthines with serum theophylline level monitoring, which must be between 5-15 micrograms / ml.

Theophyline

Anti-inflammatory therapy:

Anti-inflammatory treatment consists of corticosteroid therapy, which has a better effect in patients with reversible obstruction and eosinophilia in sputum. Corticosteroid therapy indications are represented by patients with severe COPD and COPD exacerbations.

Cortisone preparations can be administered in three ways: intravenous, oral and inhalational.

In severe exacerbations of COPD is recommended administration of hydrocortisone hemisuccinat in total dose of 500 – 1000 mg / day for 3-4 days or methylprednisolone 1.5 mg / kg intravenously every 6 hours for 3 days (with rapid decrease in dose and interruption after another 3 or 4 days).

In COPD patients with less severe exacerbations, oral prednisone is indicated in 40 mg / day (0.5 -1 mg / kg) in a single dose for 3-4 days, with progressive decrease in dose and interruption of therapy after 7 or 10 days (total duration of treatment, about 14 days).

For the long-term oral corticosteroid therapy may benefit approximately 10% -20% of patients with severe COPD (FEV1 <1 liter). Criteria for inclusion in this alternative are:

• Unsatisfactory response to conventional therapy, correctly indicated and in maximum doses;
• FEV1 increase of more than 30%, after 2-3 weeks of administration of 40 mg of prednisone.

In long-term corticosteroid therapy, the dose should be the lowest possible (<10 mg / day), to be effective and if possible to wear the alternative management model (once every two days). Major contraindications are the appereance of complications of corticosteroid therapy, which is require the quitting of this therapy.

For inhalational corticosteroid therapy, doses are 800-1600 micrograms of beclomethasone dipropionate or equivalent doses of other preparations. In general, patients who have a bronchodilator positive test, respond to corticosteroids, but also can be made the glucocorticoid reversibility test, which attempts to identify patients with good response to long-term corticosteroid therapy.

COPD treatment

Antibiotic therapy in COPD patients:

Is use only if there is an infectious exacerbation of COPD. Antibiotic therapy is useful because it brings an immediate benefit, reducing cough and sputum and helping to lower the vital risk of severe forms of COPD.

Can be used: amoxicillin (1 g / day) or ampicillin (2-4 g / day), oxacillin (100-200 mg / day), all with a duration of 7-10 days. In high pathogenic germs infections, the indication is guided by antibiogram. In case of failure or intolerance or allergy to the antibiotics mentioned above, will be used: cephalosporins or augmentin.

Removal of secretions in COPD patients:

Removal of secretions involves several means:

1. Use of  mucolytics and expectorants drugs, like acetylcysteine (600 mg / day), ambroxol (90 mg / day), etc.
2. Orally hydration, more than 2 liters / day, associated with aerosols with distilled water or sodium chloride 9°.
3. Physical therapy includes postural drainage, by beds provided with adjustable slope (the patient’s torso is placed 15 degrees below the feet); hand chest percussion or using special devices (vibration jackets)and breathing exercises. By teaching the patient to practice diaphragmatic breathing type, will facilitate the mobilization of diaphragmatic domes.
4. Education of coughing: learning a effective coughing technique, refers both to the body positioning during coughing, and breathing control. Cough positions are: upright, with shoulders relaxed and rotate forward, head and back are slightly bent, forearms resting on thighs, bent knees and feet resting on the ground. If the patient is in bed, it will be semisitting or lying sideways, the trunk will be up and leaned in the front and knees are bent.
5. Use of of drugs that stimulate ventilation by central or peripheral mechanism (doxapram, naloxone).
6. Endoscopic aspiration  is necessary when the secretions almost completely blocks the airway and coughing is ineffective or the patient is unconscious.

Oxygen therapy in COPD patients:

There are two methods of administration of oxygen: controlled oxygen therapy and long-term oxygen therapy. Regardless of the method, the objective is to correct hypoxemia, hypercapnia and to prevent respiratory acidosis.

1. Controlled oxygen therapy, it starts concomitantly with other actions designed to combat precipitating factors of COPD. A flow of 2-4 liters / min is satisfactory, mask or nasal tube administration is intermittent (15 to 20 minutes, with intermission).
2. Long-term oxygen therapy has the benefit of the reversal of pulmonary hypertension, corrects poliglobulia, sleep and behavior disorders of patients with COPD, is reducing the prone of heart failure and prolongs the survival.

Long-term oxygen therapy

Rehabilitation of COPD patients:

Rehabilitation of patients with COPD must be planned as a individualized, long-term program which involves a multidisciplinary collaboration.

Typical components of this program are:

1. Kinesis therapy: simple or treadmill walking, ergonomic cycling, climbing stairs, etc.
2. The various techniques of physical therapy (upper extremity exercises, controlled breathing techniques), targeting the training of respiratory muscles in patients with COPD.
3. Diet high in fat and low in carbohydrate (protein content should not be changed), with positive benefits, increasing the strength of respiratory muscles, functional status and autonomy of movement. Dietary supplementation with micronutrients (phosphorus, magnesium, potassium, calcium) will strengthen the diaphragm function.
4. Intermittent mechanical ventilation in stable COPD stages, with the purpose of resting inspiratory muscles. Can be use either positive pressure ventilation (given as a regimen of 3-6 hours / day during 3 consecutive days) or with negative pressure ventilation.

Chronic Obstructive Pulmonary Disease

Chronic obstructive pulmonary disease (COPD) is a pathology characterized in terms of pathophysiology, by chronic airflow obstruction, which is caused by the association between chronic obstructive bronchitis and emphysema, with the predominance of one or another.

Airway obstruction has the following characters:

• It is chronic, meaning that the respiratory flow variations are not important during a period of several months;
• Is irreversible or partially reversible under the action of bronchodilator medication;
• It is progressive, with a slow natural evolution to aggravation.

COPD Patient

COPD is the fourth leading cause of mortality worldwide, its prevalence is in constant growth. COPD is more common in men than in women, which is explained by the greater number of men who smoke.

COPD Risk Factors And Causes

Risk factors that lead to the development of COPD are divided into certain factors and possible factors.

Certain risk factors for COPD are:

Smoking is the most important causative agent of COPD, disease six times more common in smokers than in nonsmokers. 70% – 90% of patients with COPD are smokers or have smoked. Pipe and cigar smokers have a lower risk to develop COPD than cigarette smokers, risk of developing COPD increases in relation to the number of cigarettes smoked, nicotine concentration of the cigarettes and the duration in years of this habit. The main actions of smoking on the lungs are:

• Inhibition of  macrophages and bronchial cilia motility, causing secretion stasis and increase the risk of developing pulmonary infection;
• Hyperplasia and hypertrophy of mucus-secreting glands;
• Bronchospasm by activating the vagal irritant receptors;
• Alteration of surfactant quality.

Not all smokers develop clinically significant COPD, which suggest that in the development of  COPD genetic factors are involved, which modify the susceptibility of developing the disease, depending on the individual.

Genetic susceptibility. In certain situations may be involved a deficiency of alpha 1 antitrypsin, which inhibits the protease enzyme. Proteases are secreted mainly by neutrophils, but also by macrophages and fibroblasts  and degrade proteins like  elastin and collagen. A reduce concentration of alpha 1 antitrypsin will increasing the level of proteolytic enzymes, which has as consequence the appearance of emphysema.

Premature development of emphysema and decline in pulmonary function, occur in both in smokers and nonsmokers with sever deficiency of alpha 1 antitrypsin, although smoking increasing the risk of emphysema. There are considerable variations between individuals in the severity of the emphysema.

Alpha 1 antitrypsin deficiency is relevant only in a small part of world’s population, fact that illustrates that in the development of COPD exist a interaction between genetic factors and environmental exposures.

Genetic susceptibility may be based on a bronchial hyperreactivity against various stimuli and immune deficits that increase receptivity to bacterial and fungal infections.

Air pollution. Prolonged exposure in the environment, in homes and as well in work at dust, fumes, gases and vapors is considered a causative factor for COPD. Pollutants promotes mucus hypersecretion, airway inflammation and infection and pollutants with small molecules that reach the terminal and respiratory bronchi and alveoli, triggers the goblet cell metaplasia and inflammatory processes,  mucus hypersecretion, bronchial edema and will reduce up  to obstruction the alveolar lumen. The same particles induce secretion of proteolytic enzymes, especially elastase, which can cause destruction of alveolar walls.

COPD risk factors

Possible factors for COPD are:

1. Bronchial hyperreactivity, even if not as involved as in asthma, favors the appearance of COPD.
2. Lower respiratory tract infections, especially those developed in childhood, before the age of 2 years, the majority of viral nature, especially those with respiratory syncytial virus are associated with persistent pulmonary function abnormalities.
3. Long-term passive smoking.
4. Other factors: alcohol consumption, age, male gender.

COPD Pathogenesis

COPD is characterized by chronic inflammation of the airways, lung parenchyma and pulmonary vessels, caused by exposure to cigarette smoke and other harmful particles. In this process, in different areas of the lung, number and activity of macrophages, T lymphocytes and neutrophils are increased. Activated inflammatory cells release inflammatory mediators like leukotriene B4, interleukin 8 and tumor necrosis factor alpha, able to destroy the lung structures and maintaining the inflammation.

Destruction of lung parenchyma is the major change of COPD, created by an imbalance between proteinases and anti-proteinases in the lung (imbalance between elastase hypersecretion an alpha 1 antitrypsin deficit) in favor of proteinase, and oxidative stress as a consequence of inflammation. Sources of oxidizing agents are phagocytes and the products of combustion of tobacco. Their action is complex: accentuate the enzymatic proteolysis, degrades cellular matrix components, inactivate the anti-proteases system and injures the cells that synthesize the matrix cell.

COPD Pathology

In terms of pathology, COPD is a combination of various degrees of chronic bronchitis with emphysema.

Morphological changes characteristic for COPD occur in the central airways in the peripheral airways, lung parenchyma and vessels in the lungs.

In central airways (trachea and bronchi with diameter greater than 2 mm), inflammatory cells infiltrate the covering epithelium and hypertrophy of mucus-secreting glands and increased number of goblet cells are associated with hypersecretion of mucus.

In peripheral airway (small bronchi and bronchi with diameter less than 2 mm), chronic inflammation cause repeated cycles of aggression and bronchial wall repair. Repair process result is the airway wall remodeling, with increased content of collagen and formation of ciactriceal tissue, leading to lumen narrowing and the occurrence of irreversible airway obstruction.

So, in COPD, airflow obstruction is the result of narrowing of the airways, especially those with diameter less than 2 mm. To these chronic inflammatory narrowing are added viscous mucus hypersecretion, mucosal and submucosal edema and hypertrophy and spasm of bronchial smooth muscles.

COPD

COPD Diagnosis

COPD diagnosis is palced on symptoms, clinical examination and paraclinical examination.

Symptoms

•  Chronic cough, usually the first symptom that occurs in COPD, may initially be intermittent, then become daily and often whole day and only rarely at night. In some cases, airflow limitation may occur before the cough.
• Chronic expectoration, mucous, viscous, is in small quantity.
• Dyspnea is the symptom for which patients with COPD seek medical advice. It is persistent, daily, progressive over time, exacerbated by exercise and respiratory infections.

Clinical examination:

The most important signs for diagnosis of COPD are: cyanosis, prolonged expiration (more than 5 seconds), wheezing, hypersonority at percussion, decreased vesicular murmur on auscultation and signs of chronic pulmonary cord: edema, hepatomegaly and jugular turgor.

Paraclinical examination

The following will confirm the diagnosis of COPD, estimated severity, evolution and prognosis of COPD.

• Respiratory function tests: diagnosis of COPD requires to confirm

1. Flow obstruction: showed by decreased FEV1 and FEV1/FVC report before and after administration of bronchodilator medication. Patients with COPD typically have a decrease in FEV1, and the FVC. Presence of a FEV1 <80% after administration of bronchodilator medication, associated with a report FEV1/FVC <70%, confirm the existence of the airflow limitation that is not fully reversible.
2. Changes in blood gases values: when the FEV1 is less than 40% or if are any obvious clinical signs for respiratory failure or heart failure. Reduced PaO2 (partial pressure of oxygen) with more than 8 mmHg from the normal, shows hypoxia, and increased PaCO2 (partial pressure of carbon dioxide) over 45 mmHg, shows hypercapnia.

Spirometry

• Chest X-ray: has a relatively limited role in the diagnosis of COPD. This may reveal pulmonary hyperinflation, signs of pulmonary hypertension or exclude the presence of a lung disease that produces coughing and dyspnea: lung cancer, pleurisy, pneumothorax or may reveal causes of exacerbations (pneumonia).
• CT: this is not a routine examination for COPD, its main role in highlighting the pulmonary emphysema and emphysema bubbles.
• Screening for alpha 1 antitrypsin deficiency.

Classification of COPD according to its severity:

Staging of COPD has practical importance and is an orientation for the treatment of disease.

Assessment of COPD severity is based on the intensity of symptoms, spirometry abnormalities and the presence of complications. Global Initiative for Chronic Obstructive Lung Disease (GOLD) proposes the following classification of COPD:

• Stage I: Mild COPD – characterized by mild airflow limitation ( FEV1> 80%, FEV1/FVC < 70%). Symptoms of chronic cough and sputum production may be present, but not always. At this stage, the patient is usually unaware that the lung function is abnormal.
• Stage II: Moderate COPD –  characterized by worsening air flow limitation ( 50% < FEV1 < 80%; FEV1/FVC <70%), with shortness of breath, typically developing on effort, cough and sputum production are also present. This is the stage at which patients typically seek medical  attention, because of chronic respiratory symptoms or an exacerbation of their disease.
• Stage III: Severe COPD – characterized by further worsening air flow limitation ( 30% < FEV1 < 50%; FEV1/FVC < 70% ), greater shortness of breath, reduce exercise capacity, fatigue and repeated exacerbation that almost always have an impact on patient’s quality of life.
• Stage IV: Very severe COPD – characterized by sever air flow limitation (FEV1 < 30% or FEV1 < 50% plus the presence of chronic respiratory failure; FEV1/FVC < 70%). Patient may have stage IV, very severe COPD even if the FEV1 > 30%, whenever this complications are present. At this stage, quality of life is very appreciably impaired and exacerbation may be life threatening.

COPD Clinical forms

In cases where there are sufficient elements to differentiate chronic bronchitis from emphysema, the diagnosis of COPD must specify the form of COPD:

1. COPD predominantly bronchitis (type B);
2. COPD predominantly emfizematos (type A).

In 80% of cases, COPD is mixed and in  only 20% of COPD cases are relatively pure (type A or type B), making their therapy to be similar.

COPD types

COPD Complications

1. Aggravation of chronic respiratory failure, which can be precipitated by respiratory infections, sedative medications, abdominal or chest surgery, the occurrence of pneumothorax.
2. Chronic pulmonary cord: represents hypertrophy and dilatation of the right ventricle which is caused by pulmonary hypertension. In decompensated stages is manifested by right heart failure.

COPD Evolution And Prognosis

COPD Spirometry

COPD has an evolution that is leading to deterioration in all cases, with periods of remission and exacerbations, triggered by infection.

COPD progression is translated as follows:

• Increasing the rate of decline of FEV1;
• Accentuation of the hyperinflation;
• Progressive alteration of blood gases;
• The occurrence of pulmonary hypertension in COPD patients with hypoxemia.

It is considered as an element of poor prognosis: marked tachypnea, decrease and even abolish of the vesicular murmur, tachycardia or other arrhythmias, right ventricular hypertrophy advanced changes, FEV1 <1 Liter.

Skin Wrinkles – Full Treatment Guide

Skin wrinkles are the result of the following mechanisms: skin aging, actinic lesions and oxygen free radicals from the skin.

Aging of the skin is a process of atrophy, in epiderm, the thickness of stratum corneum changes very little, but there is a epidermal papillae loss process, a reduction in the melanocytes (the cells responsible for skin pigmentation) and a decrease in Langerhans cells (cells involved in the skin immunity process).
As a result of skin skin ageing, the most important changes occur in the dermis, especially in its upper third. The total thickness of dermis decreases with age, an average of 6% per decade of life, both in women and men. Much of the dermis is lost, so that its total amount is reduced to 20% of that of a young adult. Thus there is a destruction of elastic fibers and the amount of collagen in the dermis is reduced.

Skin Wrinkles

Actinic lesions are represented mainly by the degradation and thinning of elastic fibers and decreasing in the amount of collagen.

Oxygen free radicals are the major factors involved in ultrastructural damage to skin by ultraviolet rays. Application of skin protective agencies with antioxidant effect, will reduce the skin damage induced by high doses of ultraviolet rays.

Skin Structure

The morphology of skin wrinkles:

Visible morphological changes associated with aging of the face are:

• Decrease of bone structures;
• Decrease of skin thickness and elasticity;
• Decreased adhesion of the skin on underlying layers;
• Gravitational fall of soft tissue;
• Wrinkle formation in the areas of adhesion with deep structures and areas of the muscle insertion.

Facial, around the age of 30 years appear a surplus of upper eyelid skin, fine wrinkles in the sides of the orbits and the deepening of nasal-labial grooves.

Around the age of 40 years forehead wrinkles appear and the wrinkles around the orbit and nasal-labial grooves are accentuated.

At the age of 50 years wrinkles appear on the neck and tip of the nose falls.

At the age of 60 years facial skin is much thinner and can be seen traces of decreasing in the amount of fat tissue in the temporal and buccal region. These changes continue to accumulate until death.

There are basically three types of human skin wrinkles of aging:

• Wrinkles of animation, resulting from the contraction of mimic muscles;
• Fine wrinkles caused by the breakdown of fibrin network;
• Pronounced wrinkles, deep, produced by the degradation and thinning of elastic fibers by the ultraviolet solar rays.

Therapeutic principles of correction of the wrinkles:

Basically, there are six items available in facial rejuvenation action:

1. Correction of dynamic wrinkles by controlled and temporary paralysis of the muscles by injecting botulinum toxin (Botox);
2. Improving local metabolism and revitalize the dermal structures by mesotherapy, which will reduce the wrinkles;
3. Microscopic polishing action of the skin with improving its quality and wrinkles reduction;
4. The chemical peeling and laser peeling;
5. Removing excess skin and repositioning of the deeper structures by surgical lifting, which will reduce the wrinkles;
6. Restoring volumes required in the cheeks, cheekbones or lips by fat transplantation is another therapy for correction of the wrinkels.

Wrinkles Types

Non-surgical procedures in the treatment of wrinkles :

Chemical peeling and laser peeling:

Fine wrinkles will be removed through a chemical peeling technique, which involves the application of acid on the skin surface, singly or in combination (glycolic acid, mandelic acid, trichloroacetic acid or phenolic acid), producing a well-controlled deep burn, whose healing result will be a skin rejuvenation, through action at microscopic level. For similar effects can be appealed at the thermal effect of the CO2 laser (laser peeling).

Immediately after a medium peeling will appear brown scabs, which are starting to fall spontaneously after 2-3 days. After the fall of scabs, often there is a slight pink discoloration that can persist up to 2 or 3 weeks. Although, it is not a pure surgical intervention, it can be accompanied by some discomfort for several days, especially when the entire face is treated. Reintegration in social life is usually done after 3 to 4 weeks after treatment when the swelling is decreased and the red spots of the face will disappear.

Is not recommended sun exposure earlier than 8 weeks after surgery, because hyperpigmentation may occur in treated areas, which may become permanent.

Chemical Peeling

Botulinum toxin:

Botulinum toxin is used as a cosmetic treatment of facial wrinkles under the name of Botox in the U.S.A  and in Europe under the name of Dysport.

The principle of action of botulinum toxin is directed to the terminal neuromuscular junction, blocking chemical synaptic mediators and causing temporary paralysis of involved muscle groups.

Therefore, the target muscle groups lose the ability to shrink and the muscle relaxation will produce the stretching of the skin, which will be without wrinkles. Both relaxed muscles and relaxed skin will benefit from a local vasodilation with a rich oxygenation of the skin, which will have a brighter color and will be without wrinkles.

This changes are installed differently from case to case, being modified by age and sex. Although, usually within 24 hours appear the first effects of injected botulinum toxin, correct evaluation is done after 7-14 days.

All these changes are temporary and therefore, it is always necessary the reinjection or returning to treatment in 4-6 months.

Contraindications of treatment with botulinum toxin are:

• In people allergic to one or more components of the botulinum toxin, such as albumin;
• In people with diseases that cause the overall decrease of muscle strength, such as myasthenia gravis;
• In people under treatment with antibiotics;
• In people under treatment with non-steroidal anti-inflammatory drugs;
• The presence of infections in the face region;
• Pregnancy and lactation;
• Minor patients who have not obtained parental consent.

Botulinum Toxin

Surgical procedures in the treatment of wrinkles:

Subperiosteal facial lifting:

This technique was applied initially to lift the the cheek and forehead fine tissue, the technique being later extended to the periorbital dissection and around the zygomatic body, to correct the cheek position.

Subperiosteal facial lifting can be done on the entire length of the upper jaw and on the nasal bones, to get a good effect of reducing wrinkles in the cheek and to get a good effect in reduction of  nasal-labial groove.

Subperiosteal facial lifting complications are:

• Injury to the branches of facial nerve (buccal, mandibular or temporal branch);
• Skin flap necrosis, especially common in smokers;
• Alopecia (hair loss) that may occur due to errors in temporal incision placement.

Nasal-labial contour:

Nasal-labial contour is harder to correct than the wrinkles in the chin or the wrinkles in the mandibular region. To solve the nasal-labial grooves have been proposed the following solutions:

• Subcutaneous procedures that are stretching the cheek skin;
• Direct excision of skin;
• Exogenous collagen injection;
• Autologous fat injections or dermo-adipose grafts.

Nasal-Labial Fold Correction

Zygomatic region:

In the ideal face, from the aesthetic point of view, zygomatic region is more prominent. The increasing of the region can be made by:

• Use of silicone implants, bioceramic implants or restyline implants;
• Autologous fat transplant.

Cervico facial liposuction:

When is combined with face lifting, liposuction can be applied percutaneously, before the lifting of the skin or under direct viewing through an open approach. Facial liposuction technique manage to remove the fat excess without detaching the skin and presents little risk of damage the facial nerve. Complications have been reported as the appearance of skin depressions and the appearance of fibrous streaks in the subcutaneous tissue.

Currently, liposuction is indicated for the removal of fat excess from the neck and removal the wrinkles from the neck.

Correction of lip aging:

As for lips, changes due to aging occurs as follows:

• A greater distance between the basis of nasal septum and upper lip vermilon (the red of the upper lip);
• Less exposed vermilion (thin lips);
• Relative loss of the  amount of vermilion.

These can be corrected by:

• Removing the excess skin from the basis of nose or from the vermilion;
• Correction of vermilion by injection with collagen, autologous fat or restyline.

Lip Correction

Frontal lifting:

Frontal muscles are extensions of the frontal cranial aponeurosis and are inserted into the supraorbital dermis.

Innervated by the frontal branches of the facial nerve, vertically fibers of the frontal muscle contract to raise eyebrows, producing transverse wrinkles along the forehead. Tonus and frontal muscle contraction help to maintain the eyebrow position.  Frontal muscle must resist to the gravitational forces and to the periorbital muscle action that pushes the eyebrow down.

Lower movement of the eyebrows is the combined result of the action of the procerus muscle, corrugator supercilli muscle and orbicularis oculi muscle.

Prolonged hyperreactivity of the upper facial muscles produces three types of wrinkles:

• The transverse raising of the forehead with the appearance of  transverse wrinkles of the forehead (frontal muscle);
• Eyebrows ptosis, with the appearance of wrinkles around the orbits (corrugator and orbicularis muscles);
• Vertical wrinkles at the root of the nose (procerus muscle).

Forehead Wrinkles

If the main objective is raising eyebrows, then in this case, the most effective technique involves the complete release of soft tissue adhesions from the orbital groove, in this way is kept intact the frontal muscle.

On the other hand, if the primary purpose is to reduce the transverse wrinkles of the forehead, the recommended procedure is the incision and excision of the frontal muscle, in this way,the release of soft tissue along the orbit groove no longer needed.

To achieve simultaneous eyebrows lifting and forehead wrinkle reduction, is required the release of soft tissue along the orbit groove and the incision and excision of the frontal muscle.

To reduce the transverse wrinkles of the forehead is also recommended the using of botulinum toxin injections.

Patau Syndrome Or Trisomy 13 – Causes, Symptoms And Caryotype

Trisomy 13 or Patau syndrome is the least common and most severe of autosomal trisomy, showing multiple abnormalities, most of which are incompatible with life. The clinical presentation of Patau syndrome was made in 1957 by Bartholini, but his authorship belongs to Patau, because he specifies the chromosomal etiology of the syndrome.

The incidence of Patau syndrome is 1 / 4000 – 1 / 10000 newborns. It is more common in girls, because boys have a reduced rate of survival. Mortality is high, 80% of patients with Patau syndrome die within the first month of life, 10% survive until age of one year.

Patau Syndrome

Causes:

There is a significant association between advanced maternal age and Patau syndrome. Aneuploidy arise mainly due to non-disjunction in primary maternal meiosis.

The clinical presentation of Patau syndrome:

Patau syndrome is characterized phenotypically by:

1. Head: microcephaly, scalp defects, malformed and lowset ears.
2. Facial: sloping forehead, nose broad and flat, hypertelorism, hypotelorism, ocular anomalies such as microophthalmia or anophthalmia, absence of iris, cataract, iris coloboma, cleft lip and cleft palate.
3. Neurologic: Holoprosencephaly, in which the brain is not divided completely into halves, is often present and is generally signaled by the presence of midline facial defects.
4. Limbs: polydactyly or sindactyly.
5. Cardiac malformations: represents 80% of all malformations: patent ductus arteriosus, ventricular septal defect, interatrial septal defect, dextrocardia.
6. Genitourinary malformations: polycystic kidney, renal duplicaton, double ureter, testicular agenesis and cryptorchidism in boys, clitoral hypertrophy and two-horned uterus in girls.
7. Capillary hemangiomas on the face, forehead and neck.

Baby with Patau syndrome

Karyotype:

• Patau syndrome homogeneous or uniform trisomy, karyotype is 47, XX+13 or 47, XY+13;
• Patau syndrome in mosaic or mosaic trisomy, karyotype is 47,XX+13 / 46,XX or 47,XY+13 / 46,XY.

Prenatal diagnosis:

Patau syndrome is suspected because of prenatal ultrasound detected changes: nuchal translucency, heart defects, neural tube defect  and the certainty diagnosis can be made by cytogenetic analysis of amniotic fluid or of fetal blood and chorionic villi biopsy.

Genetic consultation:

Genetic counseling and genetic testing is aimed especially for the parents carriers of 13 chromosome translocation and have a child with Patau syndrome, to prevent the recurrency of this chromosomal anomalies, the risk is 1%.

Edwards Syndrome Or Trisomy 18

Trisomy 18 was described separately, both by Edwards and by Smith in 1960. Edwards syndrome is the second autosomal trisomy after Down syndrome.

The incidence of Edwards syndrome at birth is 1 / 6000-8000 of live births. Approximately 95% of the products of conception with Edwards syndrome are removed during intrauterine life, and about 80% of newborns who have Edwards syndrome are girls. One year survival rate is 5% – 10%.

Edwards Syndrome

Causes:

In 95% of cases, Edwards syndrome is a homogeneous trisomy, mosaicism and translocations are present in small percentage. Extra chromosome 18 is responsible for the phenotypic manifestations, namely the region 18q11 – q12.

The incidence of Edwards syndrome increases with maternal age, so in about 90% of cases, the excess chromosome is of maternal origin.

The clinical presentation of Edwards Syndrome:

Edwards syndrome phenotype is characterized by:

1. Head: microcephaly, narrow bifrontal diameter and prominent occiput, which gives the skull characteristic appearance of “bird head”.
2. Facial presents: microphthalmia, short and horizontal palpebral fissure, hypertelorism, micrognathia, small mouth, cleft lip, cleft palate, malformed and lowset ears.
3. Upper limbs: is characteristic contracture of the  hand, clenched hands with the index finger overriding the middle finger and the fifth finger overriding the fourth finger.
4. Foot: it has a characteristic form of  rocker-bottom feet with prominent calcanei.
5. Neurological manifestations: psychomotor retardation, hypertonia, myelination defects, agenesis of corpus callosum.
6. Malformations of organs and systems:

• Cardiac malformations: in 90% of the cases, appear ventricular septal defect, interatrial septal defect, persistent ductus arteriosus, coarctation of the aorta;
• Pulmonary malformations: pulmonary hypoplasia with abnormal lobulation;
• Gastrointestinal malformations: omphalocele,  intestinal malrotation, atresia of the esophagus, ileum atresia, anal imperforation;
• Genitourinary malformations: polycystic kidney, double ureter, unilateral renal agenesis, cryptorchidism and hypospadias in boys, labial and ovarian hypoplasia in girls.

Edwards Syndrome

Karyotype:

• Edwards syndrome homogeneous or uniform trisomy in 95% of cases, the karyotype is:  47,XX+18 or 47,XY+18;
• Edwards syndrome in mosaicism or mosaic trisomy in about 5% of cases, the karyotype is: 47,XX+18 / 46,XX or 47, XY+18 / 46 XY;
• Edwards syndrome with translocation, very rare.

Edwards Syndrome

Prenatal diagnosis:

Prenatal diagnosis in Edwards syndrome can be established by ultrasound, which will highlight maternal polyhydroamnios, due to defective sucking and swallowing reflexes of the fetus in utero and then olighydroamnios due to renal malformations, unique umbilical artery and fetal hypotonia. To confirm the diagnosis of Edwards syndrome, karyotype is done by sampling the amniotic fluid, chorionic villi or fetal blood.

Genetic consultation:

Edwards syndrome recurrence risk is 1%, but this risk increases substantially if parents are carriers of a balanced translocations. The risk of recurrence should be established for each case in accordance with structural rearrangements, and segregation mode.

Mitral Regurgitation – Symptoms, Diagnosis And Treatment

Return of a volume of blood from the left ventricle into the left atrium during ventricular systole as a result of incompetence of closing of mitral valvular apparatus characterize mitral regurgitation.

Causes:

Various pathological processes can affect one or more constituents of the mitral valvular apparatus, resulting a lack of closure of the two mitral cuspe. Rheumatic disease still represents a etiology in some underdeveloped countries while degenerative and ischemic diseases passed on first place as the etiology of mitral regurgitation. Mitral valve prolapse is a disease with a not enough clarified etiology, which may progress to severe mitral regurgitation that requires surgery. Endocarditis, by the destruction process of the endocard can lead to mitral regurgitation. In terms of installation of mitral regurgitation phenomena, exist an acute form with sudden onset, either by rupture of the cusps, cordage in cardiac ischemic disease or endocarditis and chronic mitral regurgitation that progresses slowly.

Mitral Regurgitation

Pathophysiology:

It is different in acute form of mitral regurgitation from the chronic form of mitral regurgitation, because  the regurgitant volume, overload suddenly the left atrium and pulmonary circulation and lead to pulmonary edema and cardiogenic shock. In this situation is needed emergency surgery to save patient’s life. In the chronic form of mitral regurgitation, adaptive mechanisems  represented by left ventricle and left atrium hypertrophy, keep for a long period of time the patients asymptomatic. With the overcoming of this phase and installation of cardiac decompensation phenomena, left and right ventricular pressure will be increased, pulmonary pressure will be increased and patients become severely symptomatic.

Symptoms and diagnosis of mitral regurgitation:

Chronic mitral regurgitation can be tolerated for years without symptoms. In time, will appear asthenia, dyspnea, orthopnoea, nocturnal attacks of dyspnea, palpitations and peripheral edema. In the acute form of mitral regurgitation which is more common in coronary artery disease, myocardial infarction with rupture of cordage, sudden and severe symptoms are installed which are evolving to acute pulmonary edema and cardiogenic shock. The clinical examination show a hyperdinamic apexian shock, move left by left ventricle hypertrophy. On auscultation, it is heard a characteristic holosistolic murmur, with irradiation in the left axilla.

Mitral Regurgitation

Once the suspicion of the existence of mitral regurgitation by physical examination the patient is fully investigated for objective assessment of lesion severity.

Cardiothoracic radiography. Initial, cardiac silhouette is normal, then increases by the increasing of the left atrium and left ventricle, in advanced forms, reaching impressive size.

Electrocardiogram. Reflected the left atrium and left ventricle hypertophy , by changing the P wave, which becomes “mitral” and changing QRS axis deviation to the left. Atrial fibrillation once installed, can remain even after surgery. The presence of  acute or chronic coronary artery disease, sequelae of myocardial infarction with Q wave, may explain some forms of mitral regurgitation which are unknown by the patient until then.

Echocardiography. Is an indispensable investigation by the information brought about the etiology of mitral regurgitation disease and its consequences. More, intraoperative echocardiography is indispensable when is tempted the mitral valve reconstruction. The value of echocardiography in the diagnosis of mitral regurgitation is important, because:

• Confirm and quantify the mitral regurgitation and the repercussions on the left ventricular function;
• Identify the mechanism of regurgitation, ring expansion, retraction or rupture of cordage;
• Investigate the other valves: aortic, tricuspid and pulmonary valve;
• Rate functional or structural tricuspid regurgitation and pulmonary hypertension;
• Orientate the surgical option, for replacement of the mitral valve or mitral valve plasty;
• Tracing the consequences of a myocardial infarction;
• Periodic monitoring of asymptomatic forms of mitral regurgitation, to choose the optimal time for surgical intervention.

Mitral Regurgitation Diagnosis

Cardiac catheterization. It is required to confirm or rule out coronary artery disease as a etiologic mechanism. In patients with known angina pectoris, sequelae of a myocardial infarction and those with cardiovascular risk factors irrespective of age and accuracy of echocardiography, cardiac catheterization is indicated. Rate and quantify with high sensitivity regurgitant blood volume, left ventricular function, pulmonary hypertension and tricuspid regurgitation.

Natural evolution:

The prognosis of these patients depends on the etiology,  the severity of mitral regurgitation and left ventricular function. Evolution even in patients with significant mitral rehurgitation may be spread over decades until decompensation. But once decompensation installed, the operator risk increases and postoperative results are weaker, facts that should be taken into account, when choosing the best time for surgical intervention. Dilatation of left atrium with atrial fibrillation installation, will increase up to  10% – 20%, the  incidence of cerebral embolic complications and peripherals embolic complications. The study revealed that 80% of patients with mitral regurgitation remain alive at 5 years and 60% at 10 years . Natural evolution is much worse in mitral regurgitation due to coronary disease.

Treatment:

Medical treatment. Prophylaxis of infectious endocarditis in patients with known mitral regurgitation is very important. Vasodilators, antiarrhythmics for atrial fibrillation, diuretics and anticoagulant treatment improves much the clinical status, but should not delay the surgical intervention, until will appear severe left ventricular decompensation.

Surgical treatment. It is only rational treatment to a point in the evolution of mitral regurgitation. Surgical decision and the best time is harder to assess. The current trend is that the surgical intervention should be done sooner, before left ventricular decompensation and the recommendation is to be used reconstructive techniques rather than mitral valve replacement.

Mitral Valve Replacement

Surgical indication is made depending on the severity of mitral regurgitation, clinical status of patients, symptomatic or asymptomatic and the effects on left ventricular function:

• Symptomatic patients with severe mitral regurgitation and ventricular dysfunction, left ventricular ejection fraction < 60% and end-systolic diameter of left ventricle > 45 mm;
• Asymptomatic patients with mitral regurgitation,  when the echocardiographic data and angio show left ventricular dysfunction;
• Mitral regurgitation with atrial fibrillation, because after surgery is likely to return to sinus rhythm.

Aortic Regurgitation – Symptoms, Diagnosis And Treatment

The inability of aortic valve, due to pathological processes, to close during the ventricular diastole, with the return of a quantity of blood from aorta to the left ventricle, define the aortic regurgitation.

Aortic valve regurgitation occurs when the aortic valve does not work properly. To understand this, you must know the normal mechanism of action of the aortic valve. Aortic valve works like an open gate in a unique way so that blood from the left ventricle (the heart’s main pump) can pass into the aorta (main artery that leaves the heart). From the aorta, oxygenated blood passes into the smaller arteries and then throughout the entire body to nourish tissues. When the heart rests between beats, the aortic valve closes to prevent blood flowing back into his heart.

Causes:

Various pathological processes may affect the elements of the aortic root, resulting acut or chronic aortic regurgitation.

Acute aortic regurgitation:

• Acute aortic dissection;
• Endocarditis;
• Trauma;
• Postinterventional (balloon dilation of aortic stenosis);

Chronic aortic regurgitation:

• Rheumatic;
• Congenital;
• Aneurysms of ascending aorta;
• Marfan Syndrome;
• Severe high blood pressure with long evolution;
• Ankylosing spondylitis, rheumatoid arthritis, giant cell aortitis;
• Ehler-Danlos syndrome;
• Reiter’s syndrome.

Aortic Regurgitation

Pathophysiology:

Return of blood from the aorta into the left ventricle during diastole, due to aortic valve incompetence, is the essential haemodynamic change, that condition the appearance of heart modifications. If is a acute aortic regurgitation, then a massive and sudden volume of regurgitant blood surprises the left ventricle, of normal size, not adapted. The result is a fast and brutal increase of pressure in the left atrium and left ventricle with acute ventricular failure, acute pulmonary edema and cardiogenic shock. In these situation is needed emergency surgery to save the patient’s life. If the installation of aortic regurgitation is progressive, then the left ventricle adapts for a long time by its dilation and will increase its compliance, to maintain a normal end-diastolic pressure. Patients are asymptomatic during this period. Heart grows to a certain point, the compliance will decrease, end-diastolic pressure in left ventricle will increase, systolic function is depressed and will appear left ventricular failure and patients will be symptomatic with signs of heart failure, effort and sleep dyspnoea, fatigue and pulmonary edema.

Aortic Regurgitation

Symptoms and diagnosis of aortic regurgitation:

A long period of time patients are asymptomatic. Then, will appear symptoms like dyspnoea, palpitations, fatigue, sweating and angina pectoris. Clinical examination will revel  a large pulse, “celer et altus” (Corrigan pulse), the Musset sign (rhythmic tilt of the head), Hill sign (femoral blood pressure is 60 mmHg higher than brachial) blood pressure have divergent values, strong apexian shock and musical aortic systolic murmur.

After examining the patient, paraclinical investigations will specify the exact severity of aortic regurgitation, the effects on the heart, on other valves and on coronary system.

Radiological examination. Highlight the size of the left ventricle, left atrium and of the aorta. In early forms, the radiography is normal, then will appear a dilated left ventricle, a dilated ascending aorta  and signs of pulmonary stasis.

Electrocardiogram. Normal at first, then will appear signs of  left ventricular hypertrophy, arrhythmias, atrial fibrillation and sometimes can appear ischemic changes.

Echocardiography. Transthoracic and transoesophageal performed in two-dimensional mode and Doppler mode will bring crucial elements in deciding the treatment of atrial regurgitation. Ecocardiography is useful in the diagnosis of the aortic regurgitation because:

• Confirm an asses the acute aortic regurgitation;
• Confirm the diagnosis of chronic aortic regurgitation;
• May specify the etiology of aortic regurgitation, aortic dissection, endocarditis with vegetation;
• Rate the effects on left ventricle;
• Evaluates the condition of the mitral, tricuspid and pulmonary valve and the pulmonary hypertension;

Aortic Regurgitation

Cardiac catheterization. Is routinely performed in all patients over 40 years to investigate the coronary system, dilation of aortic root or if are other vascular associated disease, carotid system and peripheral arteries. This exploartion rate the severity of aortic regurgitation, size and function of the left ventricle, valvular lesions associated, pressure in the heart chambers, pulmonary vascular resistance and will perform the calculation of the pulmonary hypertension.

Treatment:

Medical treatment. In asymptomatic patients is not required any treatment in the absence of hypertension. It is recommended only general measures, hygienic-dietary, elimination of cardiovascular risk factors (smoking, obesity), infectious endocarditis prophylaxis and regular monitoring of the disease. If the symptoms will appear, then is recommended vasodilatators to reduce regurgitant volume, converting enzyme inhibitors, reevaluate the patient for surgical indication before will appear severe decompensation of the heart.

Aortic Regurgitation

Surgical treatment. Optimal timing for surgery in aortic regurgitation is more difficult to be choose than for aortic stenosis due to the long asymptomatic evolution of the disease. Surgical indication in asymptomatic patients with severe aortic regurgitation is controversial, due to good natural evolution of the disease. On the other hand,ventricular decompensation once occurred, can reduce the chances of recovery of the cardiac function and the survival rate after surgery. Surgical indications accepted by most authors are:

• Asymptomatic patients with progressive heart enlargement, progressive left ventricular hypertrophy, reduction of left ventricular ejection fraction <45% or end-diastolic diameter of the left ventricle > 70 mm;
• Symptomatic patients with angina pectoris or heart failure;
• Acute aortic regurgitation;
• Acute bacterial endocarditis with severe aortic regurgitation and risk of septic embolism.

Aortic Stenosis – Symptoms, Diagnosis And Treatment

stenosis represents a reduction of the aortic valve opening due to pathological processes that lead to thickening, fibrosis, calcification and its merger with the formation of a barrier to the left ventricular outflow tract.

Causes:

Congenital lesions predominate in younger patients (bicuspid valve, unicommissural valve), in which the process of fibrosis and calcification will amplify  over time. Degenerative etiology is prevalent in old age, in which the cusps are restrained by calcium deposits.

Aortic Stenosis

Pathophysiology:

Valvular aortic stenosis, by the obstacle that is representing in the way of left ventricular ejection, cause an increase in the cardiac  afterload (cardiac labor) and in the gradient between left ventricle and aorta. The heart is reacting by concentric left ventricular hypertrophy, in the first phase of compensation, until the adaptive reserves are depleted when the left ventricle begins to dilate and will appear heart failure phenomena.

Symptoms:

Three symptoms are suggestive for aortic stenosis:

• Angina pectoris;
• Syncope:
• Sudden death.

In advanced stages of cardiac decompensation occurs: effort and rest dyspnea, palpitations by installation of atrial fibrillation, cerebral embolism(stroke) or systemic embolism, fatigue and risk of infective endocarditis. Some patients remain asymptomatic for a long period of time. Even in these cases there is risk of sudden death, which is why tracking and treatment of these patients is important.

Aortic stenosis degrees:

Normally the aortic orifice area in adults is 3-4 cm².

Depending on the degree of narrowing, aortic stenosis is classified in:

• Large aortic stenosis (between 2.5 cm² and 1.5 cm²);
• Moderate aortic stenosis (between 1.5 cm² and 1cm²);
• Severe aortic stenosis (less than 1 cm²).

Aortic Stenosis

Natural evolution:

Patients with aortic stenosis remain asymptomatic for years despite the severe obstruction. A moderate aortic stenosis (aortic orifice area between 1 to 1.5 cm²), remains without complications, but 40% of patients with hemodynamically significant stenosis develop symptoms over the next 1 or 2 years. The onset of the symptoms like angina pectoris, syncope, shortness of breath after a long period of evolution of aortic stenosis, marks the beginning of cardiac decompensation and the aortic stenosis should be treated to avoid sudden death. Most studies have shown that the sudden death have a incidence of 1% in asymptomatic patients, but in those symptomatic, the incidence of sudden death is 20% – 30%.

Life expectancy is 1 or 2 years for patients with heart failure phenomena, 2 or 3 years in those with syncope and 4 or 5 years, in patients with angina pectoris. Among patients with severe aortic stenosis, medically treated, 50% die in 2 years, half of them by sudden death.

Knowing the natural evolution of aortic stenosis,  helps the physician to take the most appropriate measures in some point in the evolution of the disease.

Clinical and paraclinical diagnosis of aortic stenosis:

Diagnosis by physical examination of  the patient is easily made by characteristic elements like loud and rough systolic murmur  in aortic focal, with irradiation to the neck vessels, large apexian shock, pectoral thrill and pulse “parvus et tardus” (late and slow).

Clinically diagnosed patients are subjected to laboratory tests that cuts and nuanced the diagnosis of aortic stenosis:  ECG, cardiothoracic radiography and cardiac echocardiography. Of these, echocardiographic study in M-mode, two-dimensional mode and Doppler mode, confirm the diagnosis, staging the aortic stenosis and asses the aortic valve lesions.

Echocardiography is useful in aortic stenosis because:

• Specifies the diagnosis of aortic stenosis and severity of injury;
• Assessing the heart size and function, left ventricular dimension in systole and diastole andventricular hypertrophy;
• Assessment of the mitral valve, tricuspid valve and pulmonary hypertension;
• Regular reassessment of asymptomatic patients with aortic stenosis;
• Tracking the hemodynamic changes in pregnant women with aortic stenosis.

Aortic Stenosis Diagnosis

Ultrasound tracking of patients with asymptomatic severe aortic stenosis shall be done at 6-12 months and in those with moderate aortic stenosis at 2 years.

Exercise testing is not indicated in patients with severe aortic stenosis, being even dangerous, and the information are insignificant.

Cardiac catheterization. Is performed in all patients proposed for surgery, which risk factors for coronary heart disease, to assess the coronary system. Also when there is a discrepancy between clinical features and echocardiographic data, cardiac catheterization, accurately measure the transvalvular flow, the gradient between the aorta and left ventricle, the aortic effective orifice area and left ventricular function.

Treatment:

Medical treatment. In patients known with aortic stenosis, is done the prophylaxis of  infectious endocarditis in the case of dental maneuvers or gynecological surgery, by administering antibiotics during this period. Associated hypertension is also accordingly treated. Evolution in patients with severe aortic stenosis which is treated with drugs is unfavorable, with 50% mortality at two years, half of them by sudden death.

Surgical treatment. Surgery represents the treatment of sever aortic stenosis, especially if is symptomatic. The goal of surgery is to eliminate symptoms, prevent sudden death, improved ventricular function, increased life expectancy and active reintegration of patients into family and society.

Aortic Stenosis Valve Replacement

Indications for surgery in aortic stenosis:

• Severe aortic stenosis in newborns;
• Severe aortic stenosis, symptomatic at any age;
• Moderate aortic stenosis associated with coronary lesions;
• Moderate aortic stenosis associated with other valve lesions that have surgical indication;
• Aortic stenosis in asymptomatic patients who have ventricular dysfunction, ventricular hypertrophy, severe hypotension or ventricular tachycardia during exercise.

Postoperative evolution. Complications:

Operative mortality in elective interventions is less than 3%, increasing in extreme ages, newborns, elderly, emergency operations, the presence of endocarditis and associated pathology.

Immediate postoperative complications are dominated by bleeding, disturbances in heart conduction, embolic stroke, low cardiac output syndrome, kidney failure and respiratory failure. In the long run the survival is 75% at 5 years and 60% at 10 years, with risk of endocarditis, complications of anticoagulant treatment, bleeding or valve clogging, cerebral or peripheral embolism.  All these complications depend on the parameters of the patient before surgery (cardiac function, age), surgical technique and postoperative care.

Atrioventricular Septal Defect – Diagnosis And Treatment

Atrioventricular septal defect is a complex, congenital cardiac defect affecting  interatrial septum, interventricular septum, mitral and tricuspid valvular apparatus. Spectrum of injuries is high, from simple forms of atrioventricular defects to sever forms of atrioventricular septal defcts with changes of valvular apparatus (cuspe and cordage of the mitral valve and tricuspid valve). The incidence of this malformation is 4% – 6% of all congenital cardiac malformations.  Often id associated with other anomalies such as Down syndrome or Ellis van Credeld syndrome (ectodermal dysplasia, polydactyly).

Partial form of atrioventricular septal defect:

Associate large interatrial septal defect, situated immediately above the atrioventriculare valve, and mitral valve modifications because it is presenting three clefts (normally, mitral valve has two clefts). Tricuspid valve is rarely affected.

An important element to be known is that the subvalvular apparatus, in the case of partial form of atrioventricular septal defect presents anomalies  in 20% of the cases,  compared to full form of atrioventricular septal defect, where the subvalvular apparatus presents anomalies in only 3% of  the cases. This element gives otherwise, the difficulty of mitral valve repair, a big number of reinterventions and the need to change the valve after a few years after the first surgery.

Atrioventricular Septal Defect

Pathophysiology:

In pathophysiological terms, atrioventricular septal defect acts as a ostium secundum interatrial septal defect, which is associated with a mitral valve defect that is accentuating pulmonary stasis, increases the risk of pulmonary vascular disease and will lead to installation of Eisenmenger syndrome.

Symptoms and diagnosis of partial form of atrioventricular septal defect:

On clinical examination are seen  precordial shock due to a hyperdynamic right ventricle,  systolic murmur on the right ventricular outflow tract (due to increased blood flow), halved second cardiac sound  and systolic murmur of mitral regurgitation which is significant.

1. ECG – left axial deviation of the heart, right ventricular conduction disturbances and left anterior hemiblock;
2. Chest radiography – X-ray shows cardiomegaly due to enlargement of the right atrium and right ventricle. Pulmonary hypervascularization with stasis.
3. Echocardiography – that specifies the diagnosis in 2 D or in three-dimensional reconstruction of the heart, which will give anatomical and functional information about the heart and about the mechanism of mitral and tricuspid valve regurgitation.
4. Cardiac catheterization – passage of the probe from the aorta, trough interatrial septal defect, into the right atrium, will certify the diagnosis. This exploration is bringing anatomical and functional  information about the heart and valves, hemodynamic pressure, gas saturation of blood in the heart cavities and particularly can appreciate pulmonary hypertension and pulmonary vascular resistances.

Natural evolution of partial form of atrioventricular septal defect:

If atrioventricular septal defect is not diagnosed at birth, becomes symptomatic in the first years of life. Children have a short stature and weight deficit, signs of congestive heart failure, dyspnea, fatigue, recurrent lung infections. Once diagnosed, to avoid complications, is indicated that the surgery to be done around the age of 4 years. Diagnosis of atrioventricular septal defect in adulthood should be seen as an exception rather than a rule.

Surgical treatment of partial form of atrioventricular septal defect:

Surgical treatment aims to solve the two defects: closing interatrial septal defect and mitral valve plasty. Mitral valve repair is the key to long-term success. If repair is not possible, then mitral valve should be replaced by a mechanical or biological valve. Approximately 10% of the mitral plasty reach the second valve replacement surgery. The pericardial patch used for closing interatrial septal defect, can damage the atrioventricular node with the apparition of temporary or permanent heart block, which is requiring pacemaker implantation.

Atrioventricular Septal Defect

Complete form of atrioventricular septal defect:

This type of disease associates interatrial septal defect, ventricular septal defect and  atrioventricular valvular defects (mitral and tricuspid). This type of atrioventricular septal defect can be associated with other anomalies such as tetralogy of Fallot, transposition of the great arteries and Down syndrome.

Symptoms and diagnosis of complete form of atrioventricular septal defect:

Infants with complete form of atrioventricular septal defect, presented  frequent respiratory infections and a lack of appropriate physical development,  signs of congestive heart failure, dyspnea, tachycardia, pulmonary stasis and hepatomegaly. Clinical examination can detect a sistolic murmur of  the right ventricular outflow, sistolic murmur on the bottom left of the sternum, which is proving the presence of a ventricular septal defect and a mitral regurgitation murmur.

Diagnosis is indicated by paraclinical investigations and in particular by echocardiography.

Atrioventricular Septal Defect

1. ECG – are described in the partial form of atrioventricular septal defect.
2. Chest radiography – marked cardiomegaly and pulmonary stasis.
3. Echocardiography – is the examination which is expected to confirm the diagnosis of atrioventricular septal defect. Study 2 D and 3 D reconstruction gives precise anatomical data on interatrial septal defect, ventricular septal defect, valvular apparatus, cardiac cavity size and functional data about the shunt direction, magnitude of the shunt and ventricular function.
4. Cardiac catheterization – Is giving characteristic image of swan neck by higher and anterior position of  the aortic valve in relation with mitral valve. This investigation is useful to assess the degree of pulmonary hypertension, because many children have severe obstructive vascular disease by the age of 2 years.

Complete form of atrioventricular septal defect can progress to congestive heart failure in the first months of life and require surgery. The major risk is the development of obstructive pulmonary vascular disease, severe pulmonary hypertension that would make surgery risky or contraindicated.

Treatment of complete form of atrioventricular septal defect:

Surgical treatment – It is indicated at any age. Total correction of atrioventricular septal defect can be done in the first months of life depending on the severity of symptoms and pulmonary hypertension. Creating a competent atrioventricular apparatus is the key of success for short and long term, of  this intervention. Residual mitral valve regurgitation is usually the one that indicate the need for reinterventions.

Postoperative mortality of atrioventricular septal defect rate is below 5%. Survival at 20 years is 70%. Reinterventions for residual mitral regurgitation rate is around 10%.  At reintervention it is tried a new valve repair or the replacement with mechanical valvular prosthesis.

Coarctation Of The Aorta – Diagnosis And Treatment

Coarctation of the aorta is defined as a stenosis on aortic track present at birth, which can be anatomically located in the aortic arch, descending aorta or abdominal aorta. The most common form of coarctation of the aorta is the one in which the narrowing  is found distal from the origin of  left subclavian artery. The incidence of coarctation of the aorta is 5% – 10% of all congenital cardiac malformations. Can appear as isolated injury or associated with: bicuspid aortic valve, patent ductus arteriosus, ventricular septal defect, Turner syndrome, aneurysms of Willis polygon and hemangiomas.

Pathophysiology of coarctation of the aorta:

Hemodynamic manifestations depend on the degree of stenosis, presence of other associated defects and the presence of ductus arteriosus. The presence of  an narrow area at the level of aorta, will create a anatomically barrier and a functional gradient between the above are and the distal area . So the above area will be permanently hypertensive and the distal area hypoperfused. To maintain an adequate circulation, distal to the abdominal organs, the body will develop a collateral circulation through intercostal arteries and mammary arteries.

Coarctation of Aorta

Diagnosis of coarctation of the aorta:

Coarctation of the aorta can be suspected by clinical examination, due to stenosis severity and the association with other defects and is confirmed by paraclinical investigations. Presence of hypertension in young people, can attract attention. Pulse can be well beaten in radial arteries and decreased and late in the femoral arteries. On auscultation in the interscapular space is charged a intense systolic murmur. The presence of collateral circulation give a crescendo-descrescendo murmur. If coarctation of the aorta is associated with bicuspid aortic valve (40% of cases), then will appear a  aortic regurgitation murmur.

1. ECG -signs of left ventricular hypertrophy.
2. Chest radiography – In children, X-ray shows cardiomegaly and signs of pulmonary stasis. In adolescents and adults may be present the classical, pathognomonic sign of coarctation of the aorta – coastal erosion (coastal rosary) and signs of left ventricular hypertrophy with increased cardiac shadow.
3. Echocardiography – performed 2D, color Doppler, is helpful in diagnosis of coarctation of the aorta by identifying the area of stenosis and will calculate the presional gradient.This investigation is helpful for the exploration of aortic valve, mitral valve, interatrial and interventricular septum integrity, the reaction of the left ventricle and is an indispensable examination. Prenatal detection by fetal Echo is quite difficult, although exist  indirect signs that are suggesting the possibility of coarctation of the aorta.
4. MRI – Provides images with high accuracy, identify  the anatomical form and the location of the coarctation of the aorta and the presence of collateral circulation. It is mainly used  for the postoperative tracking of restenosis or the development of  a local aneurysm.
5. Cardiac catheterization – is rarely necessary in children. It is used to exclude other associated defects when echocardiography and clinical status are inconsistent. In adults over 45 years is indicated to assess the coronary arteries. Cardiac catheterization is use to measure the pressional gradient from the narrowing. Gradient below 20 mmHg, shows a medium coarctation of the aorta and more than 20 mmHg indicate surgical solution.

Coarctation Of Aorta

Natural evolution of coarctation of the aorta:

In severe forms of coarctation of the aorta associated with other defects, the child may present at birth congestive heart failure, severe acidosis, distal hypoperfusion. In these cases, is needed immediate and complex treatment both medical and surgical. Asymptomatic forms can reach adulthood in the third or fourth decade of life when they are detected because of elevated blood pressure, intense headache, epistaxis,  cramps or bleeding strokes. Causes of death include: coronary heart disease, rupture / dissection of aorta, endocarditis, aortic valve lesions, intracerebral hemorrhage.

coarctation of aorta X-Ray

Treatment of coarctation of the aorta:

Medical – in infants with severe stenosis, congestive heart failure, renal failure, metabolic acidosis, medical urgent measures are needed: resuscitation, intubation, infusion of prostaglandin to keep the ductus arteriosus permeable and interventional or surgical procedures (balloon dilatation).

Surgical – It is necessary at any age, urgent to save newborn lives or elective to prevent complications of coarctation of the aorta. There are several surgical techniques that attempt to resolve the area of stenosis.

Interventional method – can be made of emergency in infants with critical situation, when is trying the dilation of the area with stenosis, with a balloon.  Shall be made in adults with dilation and stent placemen, in case of  postsurgical restenosis. In case of an aneurysmal dilatations may be inserted a stent-graft.

Coarctation Of Aorta

Postoperative complications  can be: damage of the recurrent or phrenic nerve, chilotorax, hypertensive crisis, paralysis by medullary ischemia. In the long run, especially when the surgical intervention is done after age of 15,  hypertension may persist after surgery.

Prognosis:

Untreated coarctation of the aorta may reach the age of 35, and 20% even up to 50 years. If  surgery is done before 14 years, then the survival rate to 20 years is 90% and the survival after this 20 years is 80%. Women operated by coarctation of the aorta can have children, but the pregnancy  is considered with high-risk. Native or residual stenosis of the aorta is a contraindication for pregnancy.