Patent Ductus Arteriosus – Symptoms, Diagnosis And Treatment

Persistence from fetal life of the communication between the pulmonary artery and descendant  aorta is called patent ductus arteriosus. Prevalence is higher in immature newborns, about 20%, of whom 12%  are hemodynamically unstable. The incidence is 1 to 2500 -5000 of newborns to term. The ductus arteriousus is located between the left pulmonary artery and descendant aorta, distal to the origin of left subclavian artery.

Pathophysiology of patent ductus arteriosus:

At birth, the ductus arteriosus functionally closes under the action of oxygenated blood, of the decrease level of prostaglandin E2, leading to its constriction and then will appear the anatomical closure by fibrosis. Patent ductus arteriosus, depending on the size, cause a left-right shunt from the aorta to the pulmonary artery, which is leading to a volume and pressure overloading of the pulmonary circulation. Patent ductus arteriosus is a unique structure whose presence can lead to severe cardiac decompensation, but in other situations (transposition of great arteries without left-right shunt) may be saving and should be maintained until the disease is resolved by surgery.  Patent ductus arteriosus in premature infants, where development is incomplete must be destinguished from infants at term with patent ductus arteriosus, which is a congenital cardiac malformation.

Patent Ductus Arteriosus

Symptoms of patent ductus arteriosus:

Symptoms of patent dustus arteriosus are variable, from asymptomatic state to cardiovascular shock and death. The magnitude of symptoms depends on the size of  ductus arteriosus and peripheral pulmonary vascular resistances. The clinical examination may reveal a trill on auscultation, a systolic-diastolic murmur, wide apexian shock, tachycardia, hypotension. Large patent ductus arteriosus gives a murmur that sounds slowly or is absent. The left atrium and left ventricle are dilated due to increased volume of blood which is returning from the lungs. The result of this left-right shunt, is the appearance of pulmonary and systemic signs: manifestations of heart failure, tachycardia, gallop rhythm, pulmonary edema and  hepatomegaly. By decreasing of the aortic blood flow, distal from ductus arteriosus, abdominal organs perfusion will be inadequate and will appear oliguria, ileus and acidosis.

Patent Ductus Arteriosus

Diagnosis of patent ductus arteriosus:

A high degree of suspicion must exist in premature infants with cardio-circulatory imbalance immediately after birth.

1. ECG – shows signs of the left ventricle and left atrium overloading, right ventricular hypertrophy occurs later with the increasing of pulmonary vascular resistance.
2. Chest radiography – In large patent ductus arteriosus, radiography is showing signs of pulmonary overloading, signs of pulmonary edema and cardiomegaly due to left atrial and left ventricle dilatation.
3. Echocardiography – Doppler color method is showing the shunt between the large vessels and its direction. With this exploration can be examined the heart cavities left ventricle, left atrium and cardiac valvular function. Echo can exclude associated anomalies like, ventricular septal defect, interatrial septal defect, Ebstein disease.
4. Cardiac catheterization – is used more as a treatment method than as a diagnose method. Is indicated when are suspected other injuries or when pulmonary hypertension is problematic.

Natural evolution of patent ductus arteriosus:

Eisenmenger syndrome may be the final stage of a untreated patent ductus arteriosus, which evolves into irreversible pulmonary vascular disease. In this case heart-lung transplantation remains the only therapeutic solution.

Patent Ductus Arteriosus

Treatment of patent ductus arteriosus:

Once the diagnosis of patent ductus arterosus is suspected or confirmed, the treatment should be established. Thus, exist medical and surgical methods of treatment. Planning an intervention or other type of treatment is controversial, generally remaining three indicative directions: symptomatic patent ductus arteriosus must be treated, presymptomatic treatment and prophylactic treatment.

Prophylactic treatment – administration of indomethacin in premature newborns showed a success rate of closing the ductus arteriosus in 90% of cases. It is administered 10 mg/kg for 3 days. Echocardiography control can help to establish the success or the failure of the treatment.

Patent Ductus Arteriosus

Patent ductus arteriosus ligation – is indicated in all cases of symptomatic or asymptomatic patent ductus arteriosus, with left-right shunt that does not close spontaneously after drug theraphy. This treatment is done to avoid cardio-pulmonary decompensation, irreversible vascular pulmonary disease or infection. This can be done surgically or videoscopic.

Interventional treatment – consists in placing a special device at the level of patent ductus arteriosus, thus obtaining a thrombosis in most cases, local inflammatory reaction and closure of the ductus arteriosus. Although, these techniques are less invasive than surgical technique, the success rate is not 100% because there are specific complications (embolization of the device into lungs or into descending aorta).

Tetralogy Of Fallot – Symptoms, Diagnosis and Treatment

Tetralogy of Fallot is a complex congenital heart disease, classified as a cynotic heart condition, which associates four defects: ventricular septal defect, pulmonary artery stenosis  (right ventricular outflow tract obstruction), right ventricular hypertrophy and aorta dextroposition. If is present interatrial septal defect, then the disease is  called pentand of Fallot.

Tetralogy of Fallot

Morphopathology:

Tetralogy of Fallot always  associate stenosis of infundibular septum and the presence of ventricular septal defect and the aorta dextroposition. Right ventricular hypertrophy occurs as a result of ventricular overload.  Pulmonary artery stenosis is constantly present and represents the central element of tetralogy of Fallot. It may be a pulmonary valve stenosis in the right ventricular outflow tract or a hypoplasia of the pulmonary artery trunk.  Clinical picture of this defect is wide, from asymptomatic forms to extreme form in which the anatomical and functional communication between right ventricle and pulmonary artery is absent (pulmonary atresia with tetralogy of Fallot), with severe clinical expression. May be associated with tetralogy of Fallot:  right aortic arch, coronary anomalies, interatrial septal defect.

Pathophysiology of tetralogy of Fallot:

Due to increased pressure in the right ventricle, which is hindered to eject blood into pulmonary artery, will appear a right-left shunt through the ventricular septal defect that causes cyanosis and clinical hypoxic crisis. Shunt size depends on the degree of  infundibular stenosis of the pulmonary artery, ventricular septal defect size and peripheral vascular resistances. Hypoxic crises, which represents a classic complication in tetralogy of Fallot, are due to muscle spasm of the pulmonary artery which accentuates the degree of stenosis. To reduce the hypoxic crises, children are adopting a squating position, which increases peripheral vascular resistances by reducing venous return and thus, will reduce right-left shunt.

Tetralogy of Fallot

Symptoms of tetralogy of Fallot:

Symptoms are different, depending on the severity of tetralogy of Fallot complex. Some forms of tetralogy of Fallot go unnoticed at birth and first months of life. A reduced pulmonary artery obstruction and a small right-left shunt, is giving a form of disease, called “pink tetralogy of Fallot”.

In more severe forms of Fallot tetraolgie occur:

• Cyanosis;
• Hypoxic crises;
• Squating position to improve hypoxia;
• Hippocratic fingers;
• Short stature and weight deficit;
• Effort intolerance;
• Dyspnea;
• Fatigue.

Clinical examination can detect an increased apexian shock, regarding to right ventricular hypertrophy, deep systolic murmur in the area of pulmonary artery.

Diagnosis of tetralogy of Fallot:

The presence of intense cyanosis immediately after birth should lead to suspicion of a severe form of  tetralogy of Fallot. Clinical examination of an infant becoming cyanotic lately, which is not developed a properly stature and weight and in whom cardiac auscultation highlight a loud systolic murmur in the pulmonary artery, should be complemented by laboratory investigations, particularly echocardiography, which will specify the correct diagnosis.

1. Laboratory test can reveal a poliglobulia.
2. ECG – signs of right ventricular hypertrophy,  incomplete right bundle branch block and arrhythmias.
3. Chest radiography – pulmonary circulation is poor so that lung areas are hypertransparent and heart image is typical(shoe aspect), for right ventricular hypertrophy.
4. Echocardiography – identify the characteristic features of tetralogy of Fallot, the presence of ventricular septal defect, the direction of the shunt in Doppler color method, aorta dextroposition , the degree of stenosis of the pulmonary artery and right ventricular hypertrophy. Also, can be examined the valvular apparatus and integrity of the interatrial septum.  Estimation of pulmonary artery trunk size is also possible and useful.
5. Magnetic Resonance Imaging – View with accurate ventricular septal defect, right ventricular outflow tract and pulmonary artery with its distal branches.
6. Cardiac catheterization – is done only when is trying to see pulmonary artery branches and coronary artery anomalies. This exploration gives a anatomic and hemodynamic assessment of the heart and  appreciate very specific the oxygen saturation of the cardiac chambers.

Tetralogy of Fallot

Natural evolution of tetralogy of Fallot:

Without an intensive and specialized treatment newborns with severe forms of tetralogy of Fallot die. Classical form of tetralogy of Fallot become symptomatic by the age of 3-6 months, and progressively worsens. Hypoxic crises can occur but are more common in infants and characteristics by age of 2 years. The main complications are neurological injuries, pulmonary or cerebral abscess, and endocarditis in older ages.

Treatment of tetralogy of Fallot:

Medical – It is in crises of hypoxia, when the child is taking the squatting position, administration of beta blockers (propranolol) and correction of acidosis. Propranolol is useful as preventive treatment of hypoxic crisis.

Surgical – depending on the symptoms, newborn weight, the anatomically situation of the defects can be done a palliative or corrective surgery. Newborns with weight under 4 kg, hypoxic crises, symptoms, pulmonary circulation depending on patent ductus arteriosus, and underdeveloped pulmonary artery can benefit in a first stage of palliative surgery, and 6-12 months after, a total correction.

Fallot Tetralogy

Palliative surgery – Creating a systemic-pulmonary shunt, which is designed to increase pulmonary blood flow, to relief symptoms, allowing development of lung vascularization and infants development up to the final intervention.

Interventional treatment – is trying to expand right ventricular ejection way to relieve symptoms. Also peripheral pulmonart artery stenosis can be dilated.

Overall, perioperative mortality is less than 5%. Long-term survival is good, 80% of patients are asymptomatic after surgery and have 85% survival rate at 30 years after surgery.  In evolution may occur  various cardiac arrhythmias and sudden cardiac death may occur in 1% – 3% of cases.

Ventricular Septal Defect – Diagnosis And Treatment

Ventricular septal defect is a anatomically parietal defect, single or multiple, located in the interventricular septum. This defect may be isolated or associated with other cardiac malformations. It is a congenital heart malformation with left-right shunt and increased pulmonary flow.

Interventricular septum that separates the left ventricle of the right ventricle has four areas: membranous septum, inlet septum, trabecular septum and outlet septum. Lack of development of one component leads to septal ventricular defect in that area. Being classified according to their anatomical location and to their frequency, ventriculare septal defects are:

1. Perimembranos ventricular septal defect – the most common variant, is located near the tricuspid valve and is representing approximately 70-80% of all ventricular septal defects.
2. Muscular ventricular septal defect – single or multiple (“swiss cheese”), about 15% of all ventricular septal defects.
3. Infundibular ventricular septal defect – represent  5-7% of all ventricular defects and  can lead to aortic valve damage by their anatomical proximity.
4. Atrioventricular septal defect –  this type of ventricular septal defect is located in the area of atrioventricular ceiling.

Ventricular Septal Defect

Pathophysiology:

Hemodynamic changes are depending on: size of the defect, the location of the defect, lung pressure, left ventricular ejection resistance. According to these features exist:

• Small restrictive ventricular septal defect, with reduced shunt and with  pulmonary blood flow pressure / systemic blood flow pressure ratio of 1.5;
•  Moderate ventricular septal defect with moderate shunt, with pulmonary blood flow pressure / systemic blood flow pressure ratio between 1.5 and 2.5;
• Large ventricular septal defect with large shunt and pulmonary blood flow pressure / systemic blood flow pressure ratio greater than 2.5. In this case exist a significant increase pressure in the right ventricle, right atrium and will appear high blood pressure that leads to a increased resistance in  pulmonary veins and will appear vascular obstructive pulmonary disease with Eisenmenger syndrome, when the shunt reverses and becomes a right-left shunt and will appear cyanosis and congestive heart failure.

Ventricular Septal Defect

Symptoms:

It is unusual that a ventricular septal defect to give symptoms in the immediately postnatal period.

Children with small ventricular septal defect with trivial shunt are asymptomatic, discovered incidentally on clinical examination. Ventricular septal defect with moderate or large shunt, leading to installation of heart failure phenomena in the first months of life. This children presents: hepatomegaly, tachypnea, tachycardia, dyspnea, fatigue and sweating, are underweight and lung infections are common. Children with large unrestricted ventricular septal defect, will develop Eisenmenger syndrome.

Clinical examination detect on auscultation a characteristic systolic murmur and trill. In unrestricted, large ventricular septal defect, systolic murmur may be less expressive, despite the severity of the disease.

Diagnosis:

Diagnosis of ventricular septal defect is confirmed by laboratory investigations:

1. ECG. Small ventricular defects have normal ECG. Large ventricular septal defects show signs of ventricular hypertrophy and overload of the right atrium.
2. Cardiothoracic radiography. In small ventricular septal defect the radiography is normal. In large defects appear cardiomegaly and overload of pulmonary circulation.
3. Echocardiography . Bidimensional and color Doppler echocardiography reveal ventricular septal defect,  the shunt location and its direction. Interventricular septum is a complex structure with curved appearance and echo examination can miss many of ventricular defects.
4. Cardiac catheterization. Itis done only when there are discrepancies between
   echocardiographic examination and clinical manifestations. Can measure the pressures in heart cavities, and oxygen saturation in blood gases, can determine pulmonary pressure, vascular resistances. Also, can test the reversibility of pulmonary vascular disease. Can detect small muscular septal defects or other abnormalities that escaped to echo exam.

Ventricular Septal X-Ray

Natural evolution:

The determining factor of natural evolution is the size of ventricular septal defect. The small muscular ventricular defect may close spontaneously in the first months of life. Large ventricular septal defects, are leading to congestive heart failure and often require surgical closure during the first year of life. Children with large ventricular septal defects and increased pulmonary vascular resistance, with Eisenmenger syndrome can not be operated. Those who have moderately increased vascular resistance and with left-right shunt, may benefit from surgery.

Treatment:

Medical treatment, is prophylactic to prevent infectious endocarditis. Once installed congestive heart failure, drug therapy with cardiac tonics, diuretic and oxygen therapy, trying to improve the symptoms.

Interventional closure. The device is placed by percutaneous approach in specific sites, to close the parietal defect without affecting surrounding structures (tricuspid valve in particular). It is recommended in cases with small muscular ventricular septal defect, single or multiple, which has a higher surgical risk.

Surgery. Surgical indication is based on several factors: age, size of defect, location, direction and magnitude of the shunt and pulmonary vascular resistances. About 30% of infants with ventricular septal defect and severe symptoms are requiring closure of the defect in the first year of life. In children diagnosed with large ventricular septal defect, around the age of 4-6 weeks, 80% of these defects will reduce their size or will close spontaneously with the developing of cardiac structures. After one year of age, only a third of ventricular septal defects can close spontaneously.

Ventricular Septal Defect

Perioperative mortality is close to zero when the intervention is made early, before the onset of complications. Postoperative complications are: residual defects with significant shunt (technical defect or incomplete diagnosis), tricuspid regurgitation and atrioventricular block.

Banding of the pulmonary artery. Is generally recommended primary ventricular septal defect closure, regardless of age. Only in situations with multiple muscular septal defects, banding of the pulmonary artery is generally recommended and will be done at the age of 3-5 years.

Testicular Cancer – Symptoms, Diagnosis And Treatment

Testicular tumors are relatively rare, but serious through their rapid evolution and by the fact that usually affect young men, between 20-35 years. The etiology is unknown, but  a number of predisposing factors have been discovered:

• Genetic
• Local, in which case ectopic testicle, it was observed that testicular tumors are 40 times more common in man with ectopic testicle;
• Local injuries
• Circulatory disorders
•  Endocrine disorders
•  Viral diseases  like urlian orchitis, even if it cause testicular atrophy, can cause tumors.

Testicular Tumors Pathology

Macroscopic, the testicle with the tumor is enlarged, irregular, asymmetric, harder to touch, with hypervascularized albuginea. Testicular tumors are classified into two histological categories:

1. Germ cell tumors (90%):

• Seminoma;
• Embryonal carcinoma;
• Teratoma;
• Choriocarcinoma.

2. Gonadal stroma  and sexual cords tumors (10%):

• Leydig cell tumors;
• Sertoli cell tumors;
• Gonadoblastoma.

Seminoma is the most common tumor from the germ series testicular tumors (50%). Occurs unilaterally, has a smooth or lobulated surface, is hard, poorly demarcated, gray-white color on section. This type of testicular tumors has three forms: classic seminoma, spermatocistic seminoma and anaplastic seminoma, from which the last type is the one with the worst prognosis.

Embryonal carcinoma is the second most common type of testicular tumors (15-35%). This tumor has a gray-white color and can present areas with necrosis. It is one of the most aggressive testicular tumors, because is invading the epididymis and albugineea in 20% of cases.

Teratoma in child is invariably a benign tumor. In adult, this type of testicular tumors is considered potentially malignant, even if, morphologically,  it is well differentiated.

Choriocarcinoma is a rare form of testicular tumors, but with increased malignancy.

In approximately 50% of cases, germ cell tumors are histological mixed, many forms coexist, which is important in determining a proper therapy.

Leydig cell tumors in 90% of cases are benign. This type of tumor has a increased secretory function of androgen or estrogen or both type of hormones.

Testicular Cancer Stages

Testicular cancer extension is done quickly trough the lymphatic ways into lumbar lymph nodes. The lymphatic ways are parallel with the spermatic vein. From the lumbar lymph nodes, extension of the cancer is done trough the thoracic duct into supraclavicular lymph nodes. The lung is the firs organ, where testicular tumor metastasize.

Testicular Tumors Symptoms

Characteristic for testicular tumors is the slow and painless increase in volume of the testicle. It may take months until the patient is addressing to the doctor. Sometimes the phenomenon is associated with a minor local trauma.

In approximately 5% – 7% of cases of testicular tumors, the first symptoms of the disease are caused by metastasis:

• Back pain or lumbosacral pain by trapping nerve roots into lymph node metastases;
• Pleuropulmonary syndromes with chest pain, cough, bloody sputum (mediastinal adenopathy, pleuropulmonary metastases);
• Pathological fractures (bone metastasis);
• In some cases, gynecomastia and sexual disorders can occur (testicular tumors that secrete hormones).

Testicular Tumors Diagnosis

Clinical examination is the most important for diagnosis. Testicle is enlarged, uniform or not, smooth or lobulated and painless. Epididymis has a normal volume or can be moved by the tumor, but is always delimited by the tumor. Spermatic cord and deferens duct have a normal appearance, palpation rarely can shows their tumoral infiltration.

Testicular Tumors

• Ultrasound examination of the testis may contribute significantly to diagnosis;
• Chest radiography shows lung metastases;
• Limfography provides data on lumbar metastases.
• Cavography can show the deviation of inferior vena cava or catching of inferior vena cava in metastases.
•  Urography examination can show the deviation or catching the ureter by lumbar metastases.
• Laboratory tests may provide significant elements: human chorionic gonodotrofin (Beta HCG) and alpha fetoprotein elevated.
• Abdominal ultrasound examination and computed tomography can provide information about the presence of retroperitoneal lymph node metastasis and their size.

Percutaneous testicular puncture biopsy is strictly contraindicated because it favors the metastasis.

Evolution and prognosis of testicular tumors:

Testicular tumors generally have a rapid evolution, especially choriocarcinoma.  In case of seminoma and teratoma, the progress is slow. The prognosis of testicular tumors is severe because it affects young ages and lymphatic dissemination is rapid.

Testicular Tumor

Testicular Tumors Treatment

The treatment of testicular tumors is surgical, followed by radiotherapy or chemotherapy, depending on tumor histology. The surgery is represented by radical orchiectomy.

In the case of seminoma, radical orchiectomy is followed by radiotherapy, knowing that these tumor is one of the most radiosensitive tumor. Including metastatic forms,  survival at 5 years is possible in 90%-95% of cases.

In the case of carcinomas is performed high orchiectomy followed by chemotherapy with cisplatin, bleomycin and vinblastine.
In case of teratomas, high orchiectomy performed in most cases should be sufficient.

Rheumatoid Arthritis – Causes, Symptoms And Diagnosis

Rheumatoid arthritis is defined as a persistent inflammatory disease affecting peripheral joints symmetrically, altering the cartilage, eroding the bone and leading to ankylosis. Rheumatoid arthritis affects 1% of the general population, is more common in women than in men, the women / men ratio is 3 / 1, and most often is diagnosed between 35 and 50 years.

Rheumatoid Arthritis Causes

The exact cause of rheumatoid arthritis is unknown, but pathogenic, is accepted the existence of genetic predisposition, against which environmental antigens or endogenous antigens can cause immune mechanism which is responsible for the appearance of the inflammation in the peripheral joints.

1. Genetic predisposition. Rheumatoid arthritis is four times more common in first degree relatives of patients with seropositve rheumatoid arthritis and 10% of patients with rheumatoid arthritis have a first-degree relative with the same disease. Major genetic risk for rheumatoid arthritis is HLA DR4 in populations of northern Europe and HLA DRB 10402 in populations of southern Europe.
2. Possible antigens. There is evidence on the viral nature of antigens that can trigger a immune response in rheumatoid arthritis (Epstein Barr virus, retroviruses) or bacterial antigens (Mycoplasma arthritis, Mycobacterium tuberculosis, Proteus mirabilis).
3. Pathogenic immune process. It is supported both by the cellular argument, consisting in the presence in the synovium of a large number of lymphocytes T helper (CD4 +) and by the humoral argument: the production of local rheumatoid factor, the circulating immune complexes of IgM and IgG and the complement activation.

Rheumatoid Arthritis

Rheumatoid Arthritis Symptoms

In the onset period:

The first sign is morning joint stiffness, with a progressive duration, relevant when is exceeding 60 minutes. Joint pain occur at short intervals, especially in active movements, and swollen joints (arthritis). Joint pain and arthritis are symmetrical and most commonly interested are metacarpophalangeal joints, proximal interphalangeal (especially the finger 2 and 3) and corresponding joints from the leg. Sometimes rheumatoid arthritis, can have a onset with the inflammation of radiocarpal or of carpal joints. In 10% – 20% of cases, the onset is acute, passing sometimes in one night, from the period of apparent health, to the clinical picture of acute generalized rheumatoid arthritis.

Rheumatoid Arthritis

In the period of clinical symptoms, there are articular events and extraarticular events.

Articular manifestations. The most frequent are interested the small joints of hands, the wrists, knees and feet. In time the disease can affect the ribs, shoulders, sterno-clavicular joints, hips and ankles. In general, it might be interested any joint in the body.

• Hands. Proximal interphalangeal joint swelling, give the fingers the appearance of spindle. It is one of the early and characteristic signs. Late, will appear the deformation of the fingers;
• Fists. Radio carpal joint is constantly affected in rheumatoid arthritis. Functional is found a reduction of mobility in wrist, both in terms of flexion, and extension;
• Knees. Inflammation with edema in the knee joint, is frequently a sign of rheumatoid arthritis;
• Feet and ankles. The most common are interested metatarsophalangeal joints, with valgus deformity of the toe, causing pain in walking.

Extraarticular manifestations of rheumatoid arthritis. All extraarticular complications occur almost exclusively in patients with seropositve rheumatoid arthritis.

• Skin: subcutaneous nodule, with hard consistency and diameter about 1 cm. They occur in the joint structures, especially in areas of pressure: elbow, hand, foot, etc.;
• Muscle: swelling and eventually atrophy, especially in the interosseous muscles of hand and of foot;
• Cardiac manifestations represented by pericarditis (more frequent) and rhythm disturbances, valvular stenosis or regurgitation;
• Respiratory manifestations: pleuritis, pulmonary fibrosis;
• Ophthalmologic manifestations are rare. A particular form of rheumatoid arthritis is Sjogren’s syndrome: rheumatoid arthritis, with dry corneas, dry mouth, which may be associated with hypertrophy of the parotid glands.

Rheumatoid Arthritis

Felty syndrome is defined by the triad: rheumatoid arthritis, splenomegaly and neutropaenia.

Paraclinical examination:

1. Rheumatoid factor positive in 80% of cases,  is useful for diagnosis in a titer which is higher then 1 / 80. Rheumatoid factor is dividing rheumatoid arthritis into two classes: seropositive rheumatoid arthritis (with rheumatoid factor) and seronegative rheumatoid arthritis (without rheumatoid factor). Positivity rheumatoid factor occurs at a variable interval of time from onset of clinical disease. Usually when there are extraarticular manifestations, rheumatoid factor is present in high titers. Rheumatoid factor is present in 6% – 8% of the general population and can occur with other autoimmune diseases, which may reduce its specificity.
2. Antinuclear antibodies, occurring in 30% – 40% of cases.
3. Nonspecific inflammation tests: ESR accelerated, fibrinogen and C-reactive protein are increased.
4. Synovial fluid examination, shows the presence of leukocytes between 5.000/mm³ and 20.000/mm³, low or normal glucose, low complement and the presence of polymorphonuclear.
5. Anemia characteristic for chronic inflammation.
6. Radiological changes in rheumatoid arthritis is evolving in stages, as follows:

• Stage I (early): the presence or not of osteoporosis, but without bone erosion;
• Stage II (moderate): the presence of osteoporosis, with or without bone destruction, with or without mild cartilage damage, but without the presence of joint deformities;
• Stage III (severe): the presence of osteoporosis accompanied by bone destruction and cartilage damage, joint deformation accompanied by dislocations, but no bone ankylosis;
• Stage IV (terminal):  the presence of stage III criteria, plus fibrosis and joint stiffness .

Rheumatoid Arthritis X-Ray

     7.  Other osteoarticular imagistic examinations include bone scan and MRI, which can reveal early inflammatory changes that can not be highlighted on a standard radiography.

Rheumatoid Arthritis Diagnosis

Because the diagnosis of rheumatoid arthritis is not always easy, American College of Rheumatology proposed a series of diagnostic criteria:

1. Morning stiffness lasting at least one hour, at least 6 weeks;
2. Arthritis of three or more joints of the hand or foot, involving the simultaneous three joints, manifested by swelling, lasting at least 6 weeks;
3. Hand arthritis, at least one area of the hand joints with arthritis (metacarpophalngeal , wrist, interphalangeal joint), lasting at least 6 weeks;
4. Symmetrical arthritis, involving the same joints simultaneously;
5. Rheumatoid nodules;
6. Rheumatoid factor present;
7. Radiological changes typical for rheumatoid arthritis, which should include bone erosion or decalcification of  the bone.

The diagnosis of rheumatoid arthritis requires the presence of at least four of the seven criteria listed.

To give a full diagnosis of rheumatoid arthritis should be taken into account the functional classification of the disease:

• Class I: Any activity is possible;
• Class II: normal activities are possible, despite the pain and discomfort represented by limiting the mobility of one or more joints;
• Class III: low functional capacity, are possible only a few of the normal activities (is possible Self-care);
• Class IV: immobilization in bed or wheelchair, usually self-care measures are impossible.

Bladder Cancer – Causes, Symptoms, Diagnosis And Treatment

Bladder cancer is the most common malignancy of the urinary tract. The age group most affected is between 50-70 years. Is four times more common in men than in women.

Causes of bladder cancer:

The main factors that predispose to bladder cancer are:

1. Occupational factors. Has been shown that workers in chemical industry, who are working with aniline dyes, which are composed of aromatic amines, will develop bladder cancer after a while. Latency period is about 6 to 20 years. These substances produce bladder cancer only if are excreted in urine.
2. Food factors. Nitrites and nitrates in preserved foods would be considered having a carcinogenic role. Artificial sweeteners like saccharin by it’s content oh cyclohexylamine, can also cause bladder cancer.
3. Chronic irritation of the bladder by lithiasis, chronic cystitis, schistosomiasis is a potential cause of bladder. In countries where infection with Schistosoma haematobium, a parasite, is endemic, bladder cancer is more common and occurs in young age. Bladder mucosal inflammatory changes associated with removing of the parasites eggs, lead to transformation of epithelial metaplasia.
4. Has been shown that smoking in particular, but also drinking tea and coffee and analgesic abuse (phenacetin) can lead to the development of bladder cancer.

Morphopathology:

Bladder tumors are almost entirely (98%) malignant. They can be primitive or secondary.   Primitives bladder tumors are mostly epithelial (carcinomas) rarely mesenchymal (sarcomas). Secondary bladder tumors, are propagated from the neighboring organs (cervix, uterine body, prostate, rectum, sigmoid colon, appendix) to the wall of the bladder or are represented by metastasis  (gastric cancers, lung cancer).

Epithelial tumors include transitional cell carcinomas, the most common histological form (90%), epidermoid carcinomas (3-7%), adenocarcinomas (1%) or other rare forms.

Macroscopic, can be found two types of lesions:

• Papillary lesion, with the growth into bladder cavity with narrow base of implantation, single or multi-center, variable size, sometimes presenting secondary changes like necrosis, haemorrhage and ulceration;
• Infiltrative lesion with granular surface, which consists of a thickening of the lining, without producing an obvious intraluminal mass and includes areas of variable extention.

Both types of injury can take two forms:

• Non invasive, superficial, without exceeding the basal membrane;
• Invasive, exceeding the basal membrane with progressive infiltration of all layers of the bladder wall.

Bladder Cancer

Extension of bladder cancer occurs both locally, exceeding the bladder wall and invade nearby organs (into invasive forms) and distance by invading other organs like brain, lung, bone and liver.
Staging of bladder cancer:

To assess tumor invasion and the level of differentiation has been proposed the classification of bladder cancers after TNM (tumor, lymph nodes, metastasis) system:

Tumor:

• Tis: in situ carcinoma;
• T1: tumor limited to mucosa;
• T2: tumor infiltrating bladder muscle;
• T3: tumor infiltrating entire thickness of bladder;
• T4: tumor infiltrating neighboring organs and fixes the bladder to the pelvic wall;

Lymph nodes:

• No: without involving the regional lymph nodes;
• N1:  involvement of a single lymph node with a diameter under 2 cm;
• N2: involvement of a single lymph node , with a diameter between 2-5 cm or multiple lymph nodules less than 5 cm diametre;
• N3 involving  lymph nodes with a diameter greater than 5 cm;
• Nx: the invasion of lymph nodes can not be determined.

Metastasis:

• Mo: without metastases;
• M1: metastasis are present;
• Mx: can not establish the existence of metastasis.

Symptoms of bladder cancer:

Hematuria is the most important clinical sign. It can be painless and capricious. Can appear events that occur frequently in cystitis: pyuria or hypogastric pain. Ureteral obstruction in cases of tumor invasion is present with low back pain, fever sometimes as a sign of infection. Rarely, patients can present symptoms of metastasis: abdominal pain, bone pain or weight loss.

Bladder Cancer Staging

 Diagnosis of bladder cancer:

Diagnosis of bladder cancer is put after symptoms and paraclinical examinations, which are represanted by:

• Cystoscopy shows the tumor, her appearance (papilomatos or plan), location, size and  number;
• Ultrasound examination, transabdominal, may reveal the tumor, but does not provide significant data about the local extension;
• CT is useful in assessing the local extension of primary tumor and to establishing the presence of metasasis;
• Urinary cytology, can show the existence of malignant cells. It is useful both for primary diagnosis and for monitoring the treated patients.

Evolution of bladder cancer:

All bladder cancers have a high potential for relapse.

Superficial bladder cancer have a long term evolution because the recurrences can be controlled and treated.

Invasive tumors that infiltrate the bladder wall have a severe evolution, characterized by relapses, lymph node invasion and early metastases, especially in the liver, lungs and bones.

Bladder Cancer

Treatment of bladder cancer:

Bladder cancer is treated in a complex and difficult way. The treatment  must be based on proper and early diagnostic of the bladder cancer.

Superficial tumors ( stages Tis, T1, T2) benefit of transurethral resection (TUR). Survival beyond five years is about 70%. Adjuvant therapy after surgery is applied to prevent the relapse and the progression of the tumor. It consists of local or systemic chemotherapy or endovesical immunotherapy.

In the case of local chemotherapy are used endovesical instillation with various agents like : Epodyl, Mitomycin C and Doxorubicin. Systemic chemotherapy is using methotrexate-cyclophosphamide-cisplastin association.

Endovesical immunotherapy  is made with BCG vaccine instillation because it has a immunostimulant effect, or with interferon, which has antiproliferative and immunostimulant action.

Tracking of these patients is made by cystoscopy, urography and urine cytology every 3 months during the first year, every 6 months for the next two years, and then annually.

Invasive tumors (stages T2, T3) have radical surgery.

Surgery is major and is indicated in patients with bladder cancer and a good general condition. The best results are obtained in conditions of preoperative and postoperative radiotherapy. In these situations, the rate of survival beyond five years can reach 35-40%.

Transurethral resection may be a surgical alternative for bladder cancer. It is applicable to patients with small tumors, well differentiated, with superficial muscle invasion  and to those patients who have contraindications for radical intervention.

Bladder Cancer Treatment

Neoadjuvant chemotherapy is especially useful for patients with bladder cancer and lymph node metastases. Good results are obtained with the combination of Methotrexate, Vinblastine, Adriamycin and Cisplatin.

In the case of bladder cancer with visceral metastases, palliative methods, chemotherapy and radiotherapy remain the only alternative.

Lung Cancer – Risk Factors, Symptoms And Diagnosis

Lung cancer consists in developing of malignant tumors in the lungs, with a  starting point in bronchial and lung structures. Worldwide, lung cancer is the first cause of  mortality, ranking first place among cancers which can occur in men and third among cancers in women. Lung cancer incidence is increasing in proportion to the frequency of smoking and air pollution, age of maximum incidence is between 45 and 60.

Lungs X-rays

Lung Cancer Risk Factors

The most important risk factors for lung cancer development are carcinogenic factors, genetic factors and dietary factors.

1. Chemical carcinogens are smoking, air pollution and occupational pollution.

• Smoking is the most important factor, is responsible for 85% of lung cancers. In pulmonary cancer counts the number of cigarettes smoked per day, length in years of this habit, the onset of smoking at young ages, the presence of cigarette filter. A less important role it has smoke.
• Air pollution occurs with certain substances detected in the air, especially in urban areas, which are identical to those found in cigarette smoke (benzopiren). In industrialized regions, the rate of death by lung cancer is 2-5 times higher than in rural areas.
• Professional pollution it increases the frequency of lung cancer, especially if is associated with smoking. Occupational hazards are responsible for developing pulmonary cancer, like asbestos, iron oxides, arsenic (from pesticides, glass industry), tar, chromium and nickel.As these factors are very diverse you should check out the specific chemical hazard that relates to you; for example, if you work in the insulation industry you might be interested mesothelioma related articles.
• Radioactive carcinogens are represented uranium and polonium.

2.  Genetic factor lies in genetic susceptibility to the environmental factors involved in the development of lung cancer based on aggregation of cases in some families.

3.  Food factor. Recent studies confirm an inverse relationship between cancer and consumption of fruits and vegetables, and the existence of protective substances, like antioxidants (vitamins A, C, E and selenium).

Lung-Cancer

Pathology

Lung cancer is polymorphic and heterogeneous, and in terms of pathology can be:

1. Epidermoid carcinoma (squamous cell) has a frequency of approximately 29% and often is located in the large bronchi. Metastasize late and therefor is operable and with the best prognosis. Is less sensitive to chemotherapy and radiotherapy.
2. Small cell carcinoma has a frequency about 18%, is usually located in the large bronchi. Metastasize early, diffuse and varied, being considered the most aggressive form of cancer. Usually, it is considered that at the time of diagnosis, cancer reached the systemic dissemination stage and, therefore, is inoperable.
3. Adenocarcinoma has a frequency of about 32%, more frequently located peripherally. Has a severe evolution, because of early metastasis and is less sensitive to chemotherapy and radiotherapy.
4. Large cell carcinoma has a frequency of about 9%, is located peripherally. Usually, is  presented like a large mass, over 10 cm.

From the clinical, prognostic and therapeutically point of view is useful the classification of pulmonary cancer in:

• Small cell carcinoma, aggressive, with poor prognosis receiving chemotherapy;
• Non small cell carcinoma, including the rest of  types which were described, with something better prognosis and which are treated with surgery, chemotherapy and radiotherapy according to the stage in which the cancer is discovered.

Lung Cancer Symptoms And Clinical Diagnosis

Currently lung cancer diagnosis is established late, which contributes decisively to the bad results of therapy. Early diagnosis of pulmonary cancer is currently the only way to improve the prognosis of this disease.

Signs of the respiratory function:

• Cough is the symptom most consistently and most important for diagnosis, if the patient is paying attention since the first weeks after appearance and after changing its character. Coughing can occur in a smoker patient but also in nonsmokers and has the following characters: persistent, dry, irritating nature, rebellious to treatment with antitussives. If the patient is chronically coughing, lung cancer diagnosis may be suggested by: changing of tonality, the increase in intensity, in duration, declined  answer to antitussives drugs. Any old cough that gets worse  should be suspected as caused by lung cancer;
• Hemoptysis (coughing blood) can be of variable intensity;
• Dyspnea is caused by compression or obstruction of the trachea and of the large bronchi;
• Chest pain occurs in late stages of pulmonary cancer;
• Infectious episodes  (pneumonia, lung abscess).

Signs of locally extension:

• Dysphonia;
• Superior Vena Cava compression syndrome, characterized by dizziness, headache, swelling in pelerine;
• Claude Bernard Horner syndrome, characterized by enoftalmie, miosis, reduction of palpebral fissure;
• Pleurisy by invasion of the pleura;
• Heart rhythm disturbances that reflect the  extension of tumor in pericardium and heart.

Signs given by metastases:

Metastatic potential of lung cancer is increased, about 60% – 70% of patients having metastases at presentation to the doctor. The most common organs in which metastasize lung cancer are: bone, brain, adrenal glands, bone marrow, lymph nodes.

Paraneoplastic syndromes, induced by the secretion of hormones and peptides by the tumor, are manifested through signs which appear at distance from neoplasia, they may precede by months to years the tumor manifestations, disappear after treatment and occur in case of relapse. These are:

• Bone: digital clubbing, painful and swollen joints;
• Nervous system: sensory-motor neuropathy, cerebellar syndrome;
• In muscle: polymyositis and dermatomyositis;
• Endocrine: gynecomastia, hyperthyroidism, Cushing’s syndrome;
• Vascular and hematologic: migratory thrombophlebitis, anemia, thrombocythemia, thrombocytopenia;
• Skin: acanthosis nigricans;
• Renal: Nephrotic syndrome;
• Metabolic: lactic acidosis, hyperuricemia.

Lung-Cancer

General symptoms, include fever, weight loss, fatigue, anorexia, aversion to tobacco in smokers.

Lung Cancer Diagnosis

Lung Cancer Diagnosis

1. Chest radiography is fundamental, but unfortunately, many times, when lung cancer is evident radiographically, the diagnosis is delayed.
2. CT scan is useful for determining the nature of a chest mass, based on tomographic density, highlighting the mediastinal lymph damage, emphasizing the extension of lung cancer in the mediastinum, pleura and ribs. Abdominal sections will be done for the examination of  the liver and adrenal glands.
3. Bronchoscopy is a important paramount because it allows the biopsy of the tumors and assessment of tumor extension.
4. Cytological examination of sputum may show the existence of tumor cells.
5. Laboratory tests, provide little information such as acceleration of ESR, serum calcium, serum sodium levels, potassium levels can be changed. Tumor markers are of a limited importance, because they are not specific.
6. Functional respiratory exploration (spirometry) indicates whether surgery is possible or not.
7. Other paraclinical: brain CT, scintigraphy, bone MRI, marrow biopsy, abdominal ultrasound to detect metastases.

Lung cancer prognosis is restricted because of late diagnosis, but also because of the early metastasis of this type of cancer. With complete treatment, life expectancy at 5 years, in patient with lung cancer is 10%.

New Drug Shows Promise In Reversing Leukemia

A particularly difficult to treat form of leukemia is based on changes in the DNA to cause massive destruction in white blood cells, according to a study at Children’s Hospital Boston and Dana-Farber Cancer Institute. The research team in partnership with a biotechnology company showed that a new drug has the ability to stop these changes, even to stop cancer growth. The drug is one of the first that targets a vulnerability caused by a genetic rearrangement in leukemia gene (MLL).

New Drug

Researchers knew for some time the cause of MLL leukemia (alterations in DNA structure and proteins associated with it, and not in the genetic code itself). These epigenetic changes start promoting cancer genes that ultimately leads to leukemia. The most important thing is that researchers have shown that they can reverse the process.

Although childhood leukemia is a cancer with very good therapeutic results, those cancers caused by mutations in the MLL gene have devastating consequences. It was found that a portion o on chromosome 11, where the gene MLL can be normally found, breaks and sticks with parts of other chromosomes to form new proteins. These new proteins alter the normal function of MLL protein that leads to cancer. These arrangements in the MLL gene can be observed in about 10% of all children and adults diagnosed with myeloid leukemia or acute lymphoblastic leukemia and who, in many cases do not have a good response to conventional cancer treatment. Normally the rate of successful treatment of childhood leukemia is about 75-90%. Leukemia caused by rearrangement of the MLL gene has a therapy success rate of 50%. Scientists must now find new methods for treating these patients.

The culprit behind the changes in the MLL gene is an enzyme called Dot1l. The researchers injected the mice with leukemia cells that lacked Dot1l, and the mice remained healthy, unlike the mice that were injected with cells with active Dot1l enzyme. Further studies revealed a small molecule called EPZ004777, which has the power to inhibit the Dot1l enzyme. Mice with leukemia  treated with EPZ004777 survived longer.
This discovery could revolutionize the oncology field, as researchers announced that enzymes like Dot1l are very active in many types of cancers.

Gastric And Duodenal Ulcer

Gastric and duodenal ulcer (peptic ulcer) represent a circumscribed disruption of gastric or duodenal wall continuity, single or multiple,which is accompanied by a fibrous reaction. These interruptions can penetrate gastric or duodenal mucosa and can reach up to the serous.

Peptic ulcer until recently represented a disease with chronic, cyclical evolution, in which the peptic factor was incriminated. The concepts of  this pathology, in recent years, have changed a lot, making peptic ulcer from a disease in which acid secretion was required (“No acid, No ulcer”), a disease caused by an infectious agent (Helicobater pylori).

Peptic Ulcer

Besides involvement in the development of peptic ulcers, Helicobacter pylori is involved in the development of chronic gastritis, gastric lymphoma and gastric cancer.

The prevalence of peptic ulcer is 5% – 10% in the general population, but prevalence based on pathological studies is 20% -30% in men and 10% – 20% in women. The current trend is a marked decrease in the prevalence of peptic ulcer due to eradication of Helicobacter pylori infection.

Causes:

1. Infection with Helicobacter pylori, once acquired, remains in the body for life, if is not treated.Helicobacter pylori infection is manifested as a acute gastroduodenitis, which becomes chronic and will be responsible for peptic ulcer development. Helicobacter pylori acts on gastric mucosa, both directly and indirectly by increasing acid secretion. Direct mechanism is determined by the inflammatory process made by toxins secreted by Helicobacter pylori, which generates an acute gastritis, which becomes chronic. Indirect mechanism is represented by the fact that bacteria secrete urease, leading in this way to a alkaline gastric juice, which stimulates secretion of gastrin and acid hypersecretion. Due to, acid hypersecretion that reaches the duodenum, here are some changes which consist in transforming the duodenal epithelium in gastric epithelium (gastric metaplasia). In duodenum, Helicobacter pylori can not develop on the duodenal lining, it can only develop in areas with gastric metaplasia.
2. Hypersecretion of acid gastric juice.
3. Bile acids, are another aggressive factor with ulcerogenic effect through the mechanism of emulsification of lipids from the lining cells of the stomach.
4. Smoking: certainly a factor that is decreasing alkaline pancreatic secretion and stimulate the acid secretion.
5. Potentially ulcerogenic drugs: aspirin and NSAIDs and the administration of corticosteroids in large doses and for a long period of time.
6. Individual, genetic factors, there are studies showing familial aggregation of peptic ulcer (peptic ulcer prevalence increased in first degree relatives of the patients), and the existence of genetic markers (blood group O).
7. Other factors often incriminated, are represented by stress, chronic alcohol consumption and various diets.

Diagnosis of peptic ulcer:

Clinical diagnosis of peptic ulcer is based on the classic symptomatology with rhythmicity and regularity. The character of pain is related to eating (hunger pain), the appearance of pain in spring and autumn is a typical signs that may suggest a peptic ulcer. Lately, more ulcer are frequent discovered by endoscopy in the a

Peptic Ulcer

bsence of typical symptoms. Thus, any epigastric dyspepsia should be suspected as an peptic ulcer. Sometimes, the onset may be dramatic with upper gastrointestinal bleeding or perforation.

Other symptoms that may occur in peptic ulcer are vomiting, changes in appetite and dyspeptic symptoms (belching, bloating, early satiety).

Paraclinical diagnosis is made by demonstrating the presence of peptic ulcer  and by demonstrating the existence of Helicobacter pylori infection.

1. Digestive endoscopy, is a highly sensitive diagnostic method because it allows accurate assessment of the ulcer, by recognizing the lesion, by demonstrating it’s activity and by demonstrating the presence of a hemorrhage. Moreover, endoscopy allows biopsies in peptic ulcers which can highlight the benign or malignant character of the lesion. Evaluation of a healed peptic ulcer is also done by endoscopy which can demonstrate the existence of the scar.
2. Radiography of peptic ulcer, may be a complementary method of diagnostic, especially when is suspected a gastric emptying disorder (pyloric stenosis).
3. Determination Helicobacter pylori, the causative agent of most peptic ulcers, is a compulsory element in the diagnosis of peptic ulcer. Determination of Helicobacter pylori is made by direct methods and indirect methods.

• Direct methods require endoscopy with biopsy. The presence oh Helicobacter pylori is determined by histological examination.
• Indirect methods dose not require endoscopy and are represented by the determination of  Helicobacter pylori antibodies from the plasma and respiratory tests. Helicobacter pylori antibodies, also can be detereminated in saliva and eradication of Helicobacter pylori infection can be demonstrated by determination of bacteria in the stool (fecal test antigen against Helicobacter pylori). The most sensitive indirect methods of diagnosis of infection with Helicobacter pylori are respiratory tests and fecal antigen anti Helicobater pylori.

Evolution of peptic ulcer:

Over the past 20-30 years, the evolution of peptic ulcer was improved and is mostly favorable, complications were reduced significantly, and cases that are requiring surgery are relatively rare. The introduction of anti Helicobacter pylori therapy led to a decrease of ulcer recurrences.

Complications:

The possible complications of peptic ulcer are:

• Upper gastrointestinal bleeding, is the most common complication, approximately 15%;
• Perforation;
• Pyloric stenosis;
• Malignancy of the ulcer, the risk of developing this complication is low.

Peptic Ulcer

Peptic ulcer treatment:

In peptic ulcer is generally recommended to be avoided  acidic foods and spicy foods. Smoking is banned because it turned out that is delaying ulcer healing, in contrast diet and the abolition of caffeine have not been shown to hasten the healing process of ulcerous lesion.  Excluding coffee in full pain relapse may be recommended. In patients with active peptic ulcer is prohibited consumption of NSAIDs, aspirin and corticosteroids.

Drug therapy consists in administration of:

Antisecretory drugs, like histamine H2 receptor blockers (ranitidine, famotidine) or proton pump inhibitors (omeprazole, lansoprazole), for a period of 6-8 weeks.

Treatment schemes for eradication of Helicobacter pylori infection:

Indications for treatment for eradication of Helicobacter pylori infection is contained in the Maastricht European consensus, they are:

• Active peptic ulcer or peptic ulcer in the past and complicated peptic ulcer;
• Gastric lymphoma;
• Atrophic chronic gastritis;
• After gastric resection for gastric cancer;
• First-degree relatives of patients with gastric cancer.

Schemes to eradicate the Helicobacter pylori infection are containing proton pump inhibitors (omeprazole, lansoprazole) combined with two antibiotics. The schemes use triple or quadruple therapy.

Triple therapy is used in practice for a period of 7 to 10 days and in case of failure is passes to quadruple therapy for a period of 10 days.

Checking Helicobacter pylori eradication is done by endoscopy with biopsy.

Endoscopic treatment is aimed especially in peptic ulcer complications.

Surgical treatment of peptic ulcer has decreased greatly, with the appearance of current drug treatment. Absolute indications for surgery are perforation and penetration of the peptic ulcer.

Cholelithiasis

Cholelithiasis, is a relatively common disease, over 10% of the adult population of European countries have this disease. In most cases, cholelithiasis is discovered during a routine abdominal ultrasound, but also can give symptoms.

Cholelithiasis

Causes:

The main causes incriminated in the development of cholelithiasis are:

• Genetic predisposition;
• Female gender: the ratio women / men being 2-3/1;
• Obesity;
• Age;
• Dyslipidaemia;
• Diabetes;
• Hypertriglyceridaemia.

Pathogenesis of cholelithiasis:

Cholelithiasis, occurs as a consequence of breaking the existing balance in the bile, where cholesterol, bile acids and lecithin are in a balance that ensures cholesterol solubilisation. An increase in the elimination of cholesterol (in dyslipidemia, the sudden loss weight, diabetes, obesity) or on the contrary, a decrease in bile acid secretion will lead to breaking the balance that ensures cholesterol solubilisation at its precipitation in the gallbladder, with cholesterol crystals development. Biliary stasis is another factor that favors the appearance of gallstones.

Diagnosis of cholelithiasis:

Clinical diagnosis of cholelithiasis can be put when appear a biliary colic or a dyspepsia that may suggest a biliary pain. It should be noted that  cholelithiasis is often asymptomatic or partially symptomatic and its diagnosis is made incidentally.

Paraclincal diagnosis of cholelithiasis is by abdominal ultrasound, which may reveal the presence of gallstones, as well as their number. Echo-endoscopy can be used as a diagnostic method in cases of cholelithiasis with uncertain ultrasound diagnosis.

Computer tomography (CT) can determine the calcium content of gallstones.

Classification of cholelithiasis:

A modern concept of cholelithiasis is the classification in:

1. Symptomatic cholelithiasis, it is the one that generates biliary colic.  Biliary colic represents a intense or violent pain in the epigastrium or right hypochondrium , lasting about 30 minutes. Nausea, vomiting and headache, occurring in outside of biliary colic, dose not represent symptomatic cholelithiasis.
2. Asymptomatic cholelithiasis is the form of the disease that does not cause biliary colic.

Cholelithiasis

Evolution:

Evolution of cholelithiasis is often unpredictable. In general, symptomatic cholelithiasis generates biliary colic, relatively frequent, which can be complicated by acute cholecystitis. Often asymptomatic cholelithiasis remain asymptomatic throughout life, but some clinical studies have shown that about 20% of asymptomatic cholelithiasis became symptomatic after 10 years of evolution.

Complications of cholelithiasis include:

• Biliary colic;
• Acute cholecystitis;
• Migration of gallbladder stones in coledoc;
• Vesicular hydrops;
• Acute pancreatitis;
• Gallbladder cancer.

The prognosis of cholelithiasis:

Cholelithiasis has often a good prognosis because symptomatic cases are most often solved by surgery and the asymptomatic forms are kept under surveillance.

Treatment of cholelithiasis:

Currently there is almost a consensus that asymptomatic cholelithiasis should be observed and not solved by surgery. Since only 1% -2% of the cases become symptomatic every year, observation of  asymptomatic cholelithiasis seems the most logical solution, remaining as if symptoms appear, to decide the therapy.

Symptomatic cholelithiasis  will be treated. Most often, the treatment will be surgical and rarely will be  performed by non-surgical techniques. With the introduction of laparoscopic cholecystectomy, was ensured a short period of hospitalization and minimal postoperative complications. This technique treats mostly uncomplicated cholelithiasis and acute cholecystitis or  vesicular hydrops.

Cholelithiasis

Non-surgical treatment techniques of cholelithiasis are drug litholysis and shock wave lithopripsy, less used lately due to the high degree of occurrence of the relapse.

Drug litholysis is addressed to cholesterol gallstones, preferably small. Treatment consists of administration of ursodeoxycholic acid or combined with chenodeoxycholic acid, for a period of 3 to 12 months, until the complete dissolution of gallstones apper. Chance of success is about 50% and the risk of relapse within 5 years is 10%. Supervision is done by abdominal ultrasound.

Shock Wave Lithotripsy, consists in bombing of cholesterol stones with shock waves. It is addressed to unique gallstones or less numerous stones, preferably less than 15 mm. Fragments will be dissolved by the administration of bile acids (ursodeoxycholic acid), up to complete disappearance of all fragments of stones from the gallbladder.