Pneumonia, Bacterial

Introduction

Background

Medical practitioners have known of pneumonia since ancient times. Hippocrates indoctrinated his students about "peripneumonia," which, for the ancient healers, had a connotation of an acute illness either with pain in the side or with severe dyspnea. The term acquired a more punctilious meaning as the study of morbid anatomy and physical diagnosis progressed over the last few centuries. Morgagni contributed the concept of solidification of the lung. Laennec, the father of pulmonary medicine, described pathological stages of the disease and showed how to diagnose them using auscultation.

Rokitansky's graphic narration helped distinguish lobar from lobular or bronchial pneumonia. Pasteur discovered Streptococcus pneumoniae in 1880, and before long, this organism was proved to be a cause of lobar pneumonia. The contemporary physicians of the 19th century were well aware of lobar pneumonia. Coope described lobar pneumonia as that "which consists of a series of changes by which the spongy pulmonary tissue is rapidly converted into a solid mass, returning afterwards, in cases that recover, to its normal condition." The modern physician, who is more adept with the x-ray viewing box than the autopsy room, has acquired sufficient familiarity with this common malady as knowledge and wisdom has been acquired over the centuries.

Pneumonia is defined as inflammation and consolidation of the lung tissue due to an infectious agent. Pneumonia that develops outside the hospital setting is considered community-acquired pneumonia. Pneumonia developing 72 hours or more after admission to the hospital is termed nosocomial or hospital-acquired pneumonia. Community-acquired pneumonia is caused most commonly by bacteria that traditionally have been divided into 2 groups, typical and atypical. Typical organisms include S pneumoniae (pneumococcus) and Haemophilus and Staphylococcus species. Atypical refers to pneumonia caused by Legionella, Mycoplasma, and Chlamydia species.

The most common atypical pneumonias are caused by 3 zoonotic pathogens, Chlamydia psittaci (psittacosis), Francisella tularensis (tularemia), and Coxiella burnetii (Q fever), and 3 nonzoonotic pathogens, Chlamydia pneumoniae, Mycoplasma pneumoniae, and Legionella pneumoniae. These atypical community-acquired pneumonias (CAPs) often cause systemic manifestations and are helpful in clinically differentiating from typical CAPs by the pattern of extrapulmonary organ involvement, which is characteristic for each atypical CAP. While zoonotic pneumonias may be eliminated from diagnostic consideration with a negative contact history, the atypical pneumonias are infrequent (approximately 15% of CAPs are atypical), difficult to diagnose, and unresponsive to beta-lactam therapy.

A definitive laboratory diagnosis of Legionella is usually based on investigations such as direct fluorescent antibody (DFA) or indirect fluorescent antibody (IFA). Antibiotics used against Legionella include macrolides, doxycycline, rifampin, quinolones, and telithromycin. Treatment is usually continued for 2 weeks although morbidity and mortality is high.

Pathophysiology

Pathogenesis of typical pneumonia

S pneumoniae generally resides in the nasopharynx and is carried asymptomatically in approximately 50% of healthy individuals. Invasive disease may occur upon acquisition of a new epithelium serotype. A strong association exists with viral illnesses, such as influenza. Viral infections increase pneumococcal attachment to the receptors on activated respiratory epithelium. Once aerosolized from the nasopharynx to the alveolus, pneumococci infect type II alveolar cells. The pneumonic lesion progresses as pneumococci multiply in the alveolus and invade alveolar epithelium. Pneumococci spread from alveolus to alveolus through the pores of Kohn, thereby producing inflammation and consolidation along lobar compartments.

A recent multivariate analysis showed an independent association between pneumococcal CAP and alcoholism. Current alcohol abuse was associated with severe CAP. No significant differences were found in mortality, antibiotic resistance of S pneumoniae, and other etiologies.

Pathogenesis of atypical infection

After aspiration or inhalation, the atypical organisms attach to the respiratory epithelial cells by a variety of mechanisms. The presence of pili on the surface of Legionella species facilitates attachment. Once adhered, the organisms cause injury to the epithelial cells and their associated cilia. Many of the pathogenetic mechanisms may be immune-mediated rather than due to direct injury by the bacteria. A host defense is mounted via cell-mediated and humoral immunity. Infection caused by atypical organisms often spreads beyond the lobar boundaries and frequently is bilateral.

Pathogenesis of nosocomial pneumonia

Aspiration plays a central role in the pathogenesis of nosocomial pneumonia. Approximately 45% of healthy subjects aspirate during sleep, and an even higher proportion of severely ill patients aspirate routinely. Depending on the number and virulence of the pathogenic organisms reaching the lower respiratory tract and on the host defense factors, pneumonia may develop. The oropharynx of hospitalized patients may become colonized with aerobic gram-negative bacteria within a few days of admission. Therefore, nosocomial pneumonia is caused predominantly by the gram-negative bacilli. However, the incidence of Staphylococcus aureus lower respiratory tract infection is increasingly common in the hospitalized and institutionalized patient and must now be considered a possible pathogen for nosocomial pneumonia.

Frequency

United States

Community-acquired pneumonia remains a common illness. Approximately 4.5 million cases of community-acquired pneumonia occur annually, and 20% result in hospitalization. Estimates of incidence of nosocomial pneumonia range from 4-7 episodes per 1000 hospitalizations. Approximately 25% of patients in intensive care units (ICUs) develop pneumonia. Overall incidence of community-acquired pneumonia is reported to be 170 cases per 100,000 persons. With advancing age, the incidence increases from 94 cases per 100,000 persons in patients aged 44 years to 280 cases per 100,000 persons in those older than 65 years. Pneumonia as a cause of hospitalization increased from 36 to 48 cases per 100,000 persons between 1984 and 1995.

Mortality/Morbidity

Pneumonia is the sixth leading cause of death in the United States and is the most common infectious cause of death. The mortality rate is reported to be 1% in the outpatient setting but may increase to up to 25% in those requiring hospital admission. In a patient with preexisting respiratory disease, onset of bacterial pneumonia may result in deterioration of respiratory status, leading to respiratory failure and death.

• Nosocomial pneumonia is the leading cause of death among hospital-acquired infections. Recent studies have shown that nosocomial pneumonia causes excessive risk of death, and the mortality rates range from 20-50%.
• Although less common in the antibiotic era, bacterial pneumonia may lead to bronchiectasis. However, lower respiratory infection with pneumococci, staphylococci, and Klebsiella species may result in bronchiectasis, especially if treatment is delayed. The damaged alveoli and small- to medium-sized airways are replaced by dilated saccules that are filled with purulent material. Ongoing chronic inflammation may gradually destroy the surrounding lung tissue.
• In patients with community-acquired pneumonia, daily activities were restricted for 24.8 days per 100 persons. Lost days of work were 8.9 days per 100 adult employees. The annual cost to treat patients with community-acquired pneumonia in the United States was 9.7 billion dollars in 1994; 92% of these costs were secondary to hospitalization. A substantial difference in cost exists between inpatient and outpatient therapy for pneumonia (US $7517 vs $264).

Sex

Incidence is greater in males than in females.

Age

Advanced age increases the incidence of pneumonia and the mortality from pneumonia.

• Elderly persons have weaker immune responses, higher risk of aspiration, and other comorbidities.
• In a 20-year US study, the mortality rate from pneumococcal pneumonia with bacteremia was 20.3%, overall. However, a higher mortality rate (37.7%) occurred in elderly patients.

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Pulmonary Eosinophilia

Introduction

Background

Pulmonary diseases associated with tissue and/or blood eosinophilia are a heterogeneous group of disorders. Various nosologies have been offered, but this article classifies these syndromes as extrinsic or intrinsic in origin. Some syndromes overlap, but this approach is convenient from the diagnostic standpoint.

Inhaled or ingested extrinsic factors, including medications and infectious agents (eg, parasites, fungi, mycobacteria), may trigger an eosinophilic immune response. This may be mild and self-limited, as in Loeffler syndrome.

Intrinsic pulmonary eosinophilic syndromes are generally idiopathic in nature. They include a diverse group of autoimmune and idiopathic syndromes ranging from blood dyscrasias to vasculitis. This group includes acute eosinophilic pneumonia (AEP), chronic eosinophilic pneumonia (CEP), idiopathic hypereosinophilic syndrome (IHES), Churg-Strauss syndrome (CSS), and eosinophilic granuloma (EG; pulmonary histiocytosis X or Langerhans cell granulomatosis).

Eosinophilia and pulmonary infiltrates have been reported in patients with AIDS, lymphoma, a variety of inflammatory lung diseases, and collagen vascular diseases (see Causes).

Asthma may manifest with marked eosinophilia, with or without infiltrates.

For additional information, see the following:

• Asthma
• Churg-Strauss Syndrome
• Pneumonia, Bacterial
• Pneumonia, Fungal
• Pneumonia, Viral
• Medscape's Pneumonia Resource Center

Pathophysiology

Tissue pathology is largely related to the release of toxic eosinophil products. These products include major basic protein, eosinophil cationic protein, and eosinophil-derived neurotoxin, which damage the respiratory epithelium, induce ciliastasis, and influence mucus production. Tissue injury may also be caused by the release of reactive oxygen species. The release of platelet-activating factor and leukotrienes contributes to bronchospasm. In some syndromes, such as tropical pulmonary eosinophilia (TPE) and CEP, interstitial fibrosis may result from chronic inflammation. Commonly, lung parenchyma is affected, but in certain extrinsic and intrinsic syndromes, other organs may be affected.

Extrinsic eosinophilic syndromes

• Loeffler syndrome: The pathogenesis of Loeffler syndrome is unknown but presumably reflects a hypersensitivity response to an ingested or inhaled antigen from food, medication, or an infectious agent. Many of the original cases of Loeffler syndrome were thought to be related to Ascaris infection.
• Parasitic infections: Migrating parasites traversing the lungs may cause bronchospasm, dyspnea, and pulmonary infiltrates. Embolization of microfilariae or eggs, which degenerate and expose antigens to the local immune system, leads to granuloma formation. Local elaboration of chemokines and cytokines plays a role in T-cell recruitment and granuloma formation. Persistent inflammation may lead to parenchymal necrosis and fibrosis.
• Schistosomiasis: The most common pulmonary complication is pulmonary hypertension from chronic embolization of ova.
• TPE: These patients have marked immune responses to filariae, while other individuals infected with Wuchereria bancrofti or Brugia malayi have suppressed parasite-specific immune responses. Patients with TPE rarely have signs of lymphatic filariasis. Elevated immunoglobulin E (IgE) and immunoglobulin G (IgG) levels in patients with TPE reflect polyclonal B-cell activation.
• Strongyloidiasis: Patients who are immunocompromised, including those recently prescribed systemic corticosteroids, may develop hyperinfection syndrome, in which large numbers of recently released larvae burrow through the intestine and migrate to the lungs. Sepsis and respiratory failure may result from accompanying enteric bacteremia.
• Fungal causes: Allergic bronchopulmonary aspergillosis (ABPA) is an immunologic response to Aspergillus antigens in the airways of individuals with obstructive lung disease. Both IgE-mediated and immune complex–mediated hypersensitivity responses are active. Chemokines recruit CD4+ T helper 2 antigen-specific cells to the lung. The inflammatory responses lead to airway reactivity, mucus hypersecretion, epithelial damage, bronchiectasis, eosinophilic pneumonia, and parenchymal injury and fibrosis. Aspergillus proteases likely also contribute to airway damage. Other fungi have also been found to cause a similar disorder, prompting some to suggest renaming this disorder allergic bronchopulmonary mycosis.
• Bronchocentric granulomatosis: This idiopathic condition, in which the mucosal epithelium is supplanted by epithelioid histiocytes and then by granuloma formation, is often associated with ABPA.

Intrinsic eosinophilic syndromes

• AEP: This is not associated with any history of medication usage or infection. Many patients have engaged in dusty outdoor activities, suggesting a hypersensitivity response to inhaled antigens. Eosinophilic alveolitis may be extensive, and profound hypoxemia with respiratory failure may result.
• CEP: The pathogenesis is unknown. CEP may occur in isolation and/or in association with polyarteritis nodosa, rheumatoid arthritis, scleroderma, ulcerative colitis, breast carcinoma,¹ and histiocytic lymphoma. Most patients have evidence of asthma and atopy. Although not a prominent feature, microgranulomata are occasionally seen on biopsy specimens, suggesting that an antigen-driven, T-cell–mediated process is active.
• IHES: Some patients display overproduction of chemokines,² proeosinophilic factors, including interleukin (IL)–4 and IL-5 by clonally expanded differentiation clusters 3 and 4 (CD3⁺ and CD4⁺) and Th2-like lymphocytes. These patients also have evidence of polyclonal hypergammaglobulinemia. Other patients have increased numbers of stem cells committed to the eosinophil lineage. Pulmonary involvement is manifested as wheezing, coughing, pulmonary edema, and pleural effusions. Pulmonary emboli result from a hypercoagulable state. Multiple organ systems may be affected, resulting in gastrointestinal tract dysfunction, skeletal muscle weakness (which may lead to respiratory failure), endomyocardial fibrosis, myocarditis, congestive heart failure, and/or valvular disease.
• CSS: The pathogenesis is unknown. Inhaled or ingested antigens have been proposed as causative agents in susceptible individuals. Recent reports linking the syndrome with the leukotriene inhibitors zafirlukast and montelukast in the setting of steroid withdrawal suggest these agents unmask preexisting CSS rather than suggesting that CSS is a direct causal effect of these agents. Vasculitis may affect the sinuses, central and peripheral nervous systems, gastrointestinal tract, kidneys, and heart.
• EG: The cause is unknown, but the reactive histiocytic proliferation suggests a reactive process, perhaps to an unknown antigen. Patients develop reticulonodular interstitial and cystic disease. EG is strongly associated with cigarette smoking. This may affect the lungs, bones (including the skull, resulting in diabetes insipidus), and other organs. Tissue and peripheral eosinophilia are generally not prominent features of this condition.

Frequency

United States

Intrinsic syndromes are uncommon. Regarding extrinsic syndromes, medication- or food-related syndromes are sporadic. Occasionally, outbreaks are related to contaminated food or medication, eg, L-tryptophan and toxic oil syndrome.

• Strongyloidiasis is the most common infection in the United States and is usually observed in individuals from the south, southeast, and Caribbean areas.
• Schistosoma mansoni infection is observed in the Caribbean.
• Toxocariasis (visceral larva migrans) is usually found in the southeast region of the country.
• Ascariasis, because it is prevalent worldwide, is likely to be observed in the United States.
• Among the hookworms, Necator americanus is endemic to the southeastern United States.
• Occasionally, international visitors or recent immigrants may present with other parasitic infections such as TPE and paragonimiasis.
• For fungal causes, ABPA is relatively common, with some estimates indicating that 5-10% of people who are steroid-dependent and have asthma meet the criteria. Of persons with cystic fibrosis, 10% have ABPA. Coccidioidomycosis is found predominantly in the southwestern part of the United States or among individuals with a relevant travel history.

International

Intrinsic syndromes are uncommon. Regarding extrinsic syndromes, in much of the world, parasitic infections are endemic.

• Ascaris is likely the most prevalent nematode infecting humans worldwide but tends to occur in tropical or subtropical areas.
• Ancylostoma duodenale is commonly found in the Eastern Hemisphere.
• Visceral larva migrans is found throughout the world.
• Strongyloidiasis, which usually occurs in warmer climates, has a worldwide prevalence of approximately 50-100 million individuals.
• Schistosomiasis is common in Africa, Asia, Latin America, and South America. Paragonimiasis and clonorchiasis are common in Asia.
• TPE is often observed in southern Asia, Southeast Asia, and South America. Most reported cases have occurred in ethnic Indians, while it is uncommon in Chinese persons. TPE is actually observed in a minority of patients infected with the causative filariae.

Mortality/Morbidity

• With the exception of Loeffler syndrome and drug-induced disease, these syndromes may be associated with significant morbidity. While most are responsive to corticosteroids, recognition of infection and institution of an appropriate therapy are important in preventing chronicity of symptoms and, in some cases, respiratory failure.
• Patients with IHES may develop congestive heart failure, pulmonary emboli, and multiorgan-system dysfunction. Mortality in cases of IHES has been improving with increasing therapeutic options; now, 80% of patients are surviving at 5 years and 40% are surviving at 10-15 years.
• The mortality rate in cases of CSS has been decreasing, with approximately 75% of patients surviving 5 years.

Race

• No clearly defined racial predispositions have been identified in these syndromes.
• Parasitic infections are endemic in many geographic areas, but they reflect public health conditions rather than racial predispositions.

Sex

• No sexual predilection has been noted for extrinsic eosinophilic syndromes, with the exception of TPE, which has been reported to have a male predominance at a male-to-female ratio of 4:1.
• Among the intrinsic syndromes, differences are noted. AEP is more common in men than in women, unlike CEP. CEP is twice as common in women as in men, but this sexual disparity declines with increasing age. For IHES, approximately 90% of cases are found in men and 10% are found in women. For CSS, no sexual predisposition has been reported. For EG, no sexual predominance is described. The older literature suggests a male predominance, but more recent data suggest equal distribution between sexes, possibly reflecting the changing demographics of cigarette smoking, which is thought to be etiologic.

Age

• Extrinsic syndromes tend to affect adults, but exceptions exist. Toxocariasis tends to occur in children and is often associated with geophagia. Ascariasis tends to occur in children. ABPA usually occurs in adults but may occur in children, including some patients with cystic fibrosis.
• Intrinsic syndromes generally affect adults. AEP usually occurs in persons in their third decade of life. CEP peak incidence is in the fourth decade of life. IHES usually occurs in people aged 20-50 years; however, it has also been infrequently reported in children. Most cases of CSS have been reported in adults. EG may affect individuals ranging in age from infancy to old age, but it most frequently affects patients in their second to third decade of life.

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Syringoma

Introduction

Background

Syringoma is a benign adnexal neoplasm formed by well-differentiated ductal elements. Its name is derived from the Greek word syrinx, which means pipe or tube.

Pathophysiology

Syringoma is a benign neoplasm, which is traditionally considered to differentiate along eccrine lines.

Enzyme immunohistochemical tests demonstrate the presence of eccrine enzymes such as leucine aminopeptidase, succinic dehydrogenase, and phosphorylase. The immunohistochemical pattern of cytokeratin expression indicates differentiation toward both the uppermost part of the dermal duct and the lower intraepidermal duct (ie, sweat duct ridge). However, sometimes distinguishing between eccrine and apocrine ducts is difficult and many tumors that were traditionally thought to be eccrine have recently been shown to have apocrine differentiation. Electron microscopy demonstrates ductal cells with numerous short microvilli, desmosomes, luminal tonofilaments, and lysosomes. The histogenesis of syringomas is most likely related to eccrine elements or pluripotential stem cells.

Some investigators have suggested that cases of eruptive syringoma may represent a hyperplastic response of the eccrine duct to an inflammatory reaction rather than a true adnexal neoplasm. In this setting, they propose the term syringomatous dermatitis for such cases. Likewise, the scalp "syringomas" seen in scarring alopecia represent a reactive proliferation in response to the fibrosis.

Frequency

International

Syringomas are fairly common lesions.

Mortality/Morbidity

These benign tumors are largely of cosmetic significance.

Sex

Females are affected more often than males.

Age

These tumors usually first appear at puberty; additional lesions can develop later.

Clinical

History

• The lesions are asymptomatic.
• Rarely, the patient may have a family history of similar lesions. Rarely, syringomas may be associated with the Brooke-Spiegler syndrome, an autosomally dominant disease characterized by the development of multiple cylindromas, trichoepitheliomas, and occasional spiradenomas.
• Syringomas may be associated with Down syndrome.

Physical

Appearance of lesions

• Syringomas are skin-colored or yellowish, small, dermal papules (see Media File 1).
• Sometimes, the lesions may appear translucent or cystic.
• The surface can be rounded or flat-topped.
• The lesions are usually smaller than 3 mm in diameter.
• Eruptive syringomas commonly appear as hyperpigmented papules on the chest or penile shaft.

Distribution of lesions

• The lesions are usually multiple, arranged in clusters, and symmetrically distributed.
• Most commonly, lesions are limited to the upper parts of the cheeks and lower eyelids.
• Other common sites include the axilla, chest, abdomen, penis, and vulva.
• In the variant of eruptive syringoma, multiple lesions appear simultaneously, typically on the chest and lower abdomen.
• Rarely, syringomas appear as unilateral linear nevoid lesions.

Differential diagnoses and related conditions

• In rare instances, scalp syringomas can produce scarring alopecia.
• On occasion, syringomas can be associated with milia and vermiculate atrophoderma.
• Clinically, syringomas on the face are must be distinguished from trichoepitheliomas and basal cell carcinomas.
• Lesions on the eyelids may be confused with xanthelasma.
• Eruptive syringomas on the trunk can resemble disseminated granuloma annulare.

Causes

• Syringomas are frequently incidental, although some familial cases may occur.
• Eruptive syringomas (see Media File 2) are more common in African Americans and Asians than in other patients.
• Syringomas can be associated with Down syndrome.
• Clear-cell syringomas may be associated with diabetes mellitus.

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Huntington's disease

Definition

Huntington's disease is a disorder passed down through families in which nerve cells in the brain waste away, or degenerate.

Alternative Names

Huntington chorea

Causes

American doctor George Huntington first described the disorder in 1872.

Huntington's disease is caused by a genetic defect on chromosome #4. The defect causes a part of DNA, called a CAG repeat, to occur many more times than it is supposed to. Normally, this section of DNA is repeated 10 to 35 times. But in persons with Huntington's disease, it is repeated 36 to 120 times.

As the gene is passed on from one generation to the next, the number of repeats - called a CAG repeat expansion - tend to get larger. The larger the number of repeats, the greater your chance of developing symptoms at an earlier age.

There are two forms of Huntington disease. The most common is adult-onset Huntington's disease. Persons with this form usually develop symptoms in their mid 30s and 40s.

Early-onset form of Huntington disease is less common and begins in childhood or adolescence. Symptoms may resemble those of Parkinson's disease with rigidity, slow movements, and tremor.

If one of your parents has Huntington's disease, you have a 50% chance of getting the gene for the disease. If you get the gene from your parents, you will develop the disease at some point in your life, and can pass it onto your children. If you do not get the gene from your parents, you cannot pass the gene onto your children.

Symptoms

• Abnormal and unusual movements
  • Head turning to shift eye position
  • Facial movements, including grimaces
  • Slow, uncontrolled movements
  • Quick, sudden, jerking movements of arms, legs, face, and other body parts
  • Unsteady gait
• Behavior changes
  • Antisocial behaviors
  • Hallucinations
  • Irritability
  • Moodiness
  • Restlessness or fidgeting
  • Paranoia
  • Psychosis
• Dementia that slowly gets worse, including
  • Loss of memory
  • Loss of judgment
  • Speech changes
  • Personality changes
  • Disorientation or confusion

Additional symptoms that may be associated with this disease:

• Anxiety, stress, and tension
• Difficulty swallowing
• Speech impairment

In children:

• Rigidity
• Slow movements
• Tremor

Exams and Tests

The doctor will perform a physical exam. The doctor may see signs of dementia and abnormal movements. Reflexes may be abnormal. The gait is often "prancing" and wide. Speech may be hesitant or enunciation poor.

A head CT scan may show loss of brain tissue, especially deep in the brain.

Other tests that may show signs of Huntington's disease include:

• Head MRI scan
• PET (isotope) scan of the brain

DNA marker studies may be available to determine if you carry the gene for Huntington's disease.

Treatment

There is no cure for Huntington's disease, and there is no known way to stop the disease from getting worse. The goal of treatment is to slow down the course of the disease and help the person function for as long and as comfortably as possible.

Medications vary depending on the symptoms. Dopamine blockers may help reduce abnormal behaviors and movements. Drugs like tetrabenazine and amantadine are used to try to control extra movements. There has been some evidence to suggest that co-enzyme Q10 may also help slow down the course of the disease.

Depression and suicide are common among persons with Huntington's disease. It is important for all those who care for a person with Huntington's disease to monitor for symptoms and treat accordingly.

There is a progressive need for assistance and supervision, and 24-hour care may eventually be needed.

Support Groups

Huntington's Disease Society of America - www.hdsa.org

Outlook (Prognosis)

Huntington's disease causes progressive disability. Persons with this disease usually die within 15 to 20 years. The cause of death is often infection, although suicide is also common.

It is important to realize that the disease affects everyone differently. The number of CAG repeats may determine how the severity of symptoms. Persons with few repeats may have mild abnormal movements later in life and slow disease progression, while those with large repeats may be severely affected at a young age.

Possible Complications

• Loss of ability to care for self
• Loss of ability to interact
• Injury to self or others
• Increased risk of infection
• Depression
• Death

When to Contact a Medical Professional

Call your health care provider if symptoms of this disorder develop.

Prevention

Genetic counseling is advised if there is a family history of Huntington's disease. Experts also recommend genetic counseling for couples with a family history of this disease who are considering having children.

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Diseases of gums can cause barreness

The Israeli doctors have established possible communication between the bacteria causing diseases of gums, with barreness at men.

Doctor Avigdor Klinberg specializing on gingival diseases in stomatologic branch of hospital, sampled at patients of branch on treatment of barreness.

The research which is spent within three years, has shown, that at 65 % of men whose spermogram had unsatisfactory parameters, diseases of gums also have been detected, informs Rol.ru. However, at 48 % of patients with sick gums, parameters of spermogram were in the full order.

According to doctors, barreness is caused by order 500 types of the bacteria which are being a mouth, and they are capable to get into blood system and to harm to various internal bodies.

Also 50 % of men were revealed, that, in whose sperm in general are absent sperm cells, have chronic illness of gums, and bacteria causing it, also have been found in the sperm.

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Nerve Compression Syndromes

Common nerve compression syndromes include carpal tunnel syndrome, cubital tunnel syndrome, and radial tunnel syndrome. Compression of nerves often causes paresthesias; these paresthesias can often be reproduced by tapping the compressed nerve, usually with the examiner's fingertip (Tinel's sign). Suspected nerve compression can be confirmed by testing nerve conduction velocity and distal latencies, which accurately measure motor and sensory nerve conduction. Initial treatment is usually conservative, but surgical decompression may be necessary if conservative measures fail or if there are significant motor or sensory deficits.

Carpal Tunnel Syndrome

Carpal tunnel syndrome is compression of the median nerve as it passes through the carpal tunnel in the wrist. Symptoms include pain and paresthesias in the median nerve distribution. Diagnosis is suggested by symptoms and signs and is confirmed by nerve conduction velocity testing. Treatments include ergonomic improvements, analgesia, splinting, and sometimes corticosteroid injection or surgery.

Carpal tunnel syndrome is very common and most often occurs in women aged 30 to 50. Risk factors include RA or other wrist arthritis (sometimes the presenting manifestation), diabetes mellitus, hypothyroidism, acromegaly, amyloidosis, hemodialysis, and pregnancy-induced edema in the carpal tunnel. Activities or jobs that require repetitive flexion and extension of the wrist may contribute, but rarely. Most cases are idiopathic.

Symptoms and Signs

Symptoms include pain of the hand and wrist associated with tingling and numbness, classically distributed along the median nerve (the palmar side of the thumb, the index and middle fingers, and the radial half of the ring finger) but possibly involving the entire hand. Typically, the patient wakes at night with burning or aching pain and with numbness and tingling and shakes the hand to obtain relief and restore sensation. Thenar atrophy and weakness of thumb opposition and abduction may develop late.

Diagnosis

• Clinical evaluation
• Nerve conduction testing

The diagnosis is strongly suggested by Tinel's sign, in which median nerve paresthesias are reproduced by tapping at the volar surface of the wrist over the site of the median nerve in the carpal tunnel. Reproduction of tingling with wrist flexion (Phalen's sign) is also suggestive. However, clinical differentiation from other types of peripheral neuropathy may sometimes be difficult. If symptoms are severe or the diagnosis is uncertain, nerve conduction testing should be done on the affected arm for diagnosis and to exclude a more proximal neuropathy.

Treatment

• Splinting
• Sometimes corticosteroid/anesthetic injection
• Sometimes surgical decompression

Changing the position of computer keyboards and making other ergonomic corrections may occasionally provide relief. Otherwise, treatment includes wearing a lightweight neutral wrist splint (see Fig. 4: Hand Disorders: Neutral wrist splint.), especially at night, and taking mild analgesics (eg, acetaminophen, NSAIDs). If these measures fail to control symptoms, a corticosteroid (eg, a mixture of 1.5 mL dexamethasone, 4 mg/mL, and 1.5 mL 1% lidocaine) should be injected into the carpal tunnel at a site just ulnar to the palmaris longus tendon and proximal to the distal crease at the wrist. If bothersome symptoms persist or recur or if hand weakness and thenar wasting develop, the carpal tunnel can be surgically decompressed by using an open or endoscopic technique.

Cubital Tunnel Syndrome

(Ulnar Neuropathy)

Cubital tunnel syndrome is compression or traction of the ulnar nerve at the elbow.

The ulnar nerve is commonly irritated at the elbow or, rarely, the wrist. Cubital tunnel syndrome is most often caused by leaning on the elbow or by prolonged and excessive elbow flexion. It is less common than carpal tunnel syndrome. Baseball pitching (particularly sliders), which can injure the medial elbow ligaments, confers risk.

Symptoms and Signs

Symptoms include numbness and paresthesia along the ulnar nerve distribution (in the ring and little fingers and the ulnar aspect of the hand) and elbow pain. In advanced stages, weakness of the intrinsic muscles of the hand and the flexors of the ring and little fingers may develop. Weakness interferes with pinch between the thumb and index finger and with hand grip.

Diagnosis

Diagnosis is often possible clinically. However, if clinical diagnosis is equivocal and when surgery is being considered, nerve conduction studies are done. Cubital tunnel syndrome is differentiated from ulnar nerve entrapment at the wrist (in Guyon's canal) by the presence of sensory deficits (on sensory testing or with Tinel's sign) over the ulnar dorsal hand and by the presence of ulnar nerve deficits proximal to the wrist on muscle testing or nerve conduction velocity testing.

Treatment

Treatment involves splinting at night, with the elbow extended at 45°, and use of an elbow pad during the day. Surgical decompression can help if conservative treatment fails.

Radial Tunnel Syndrome

(Posterior Interosseous Nerve Syndrome)

Radial tunnel syndrome is compression of the radial nerve in the proximal forearm.

Compression at the elbow can result from trauma, ganglia, lipomas, bone tumors, or radiocapitellar (“elbow”) synovitis.

Symptoms and Signs

Symptoms include lancinating pain in the dorsum of the forearm and lateral elbow. Pain is precipitated by attempted extension of the wrist and fingers and forearm supination. Sensory loss is rare because the radial nerve is principally a motor nerve at this level. This disorder is sometimes confused with backhand tennis elbow (lateral epicondylitis). When weakness of the extensor muscles is the primary finding, the condition is referred to as posterior interosseus nerve palsy.

Diagnosis

Lateral epicondylitis can cause similar tenderness around the lateral epicondyle but does not cause Tinel's sign or tenderness along the course of the radial nerve.

Treatment

Splinting allows avoidance of the forceful or repeated motion of supination or wrist dorsiflexion, reducing pressure on the nerve. If wristdrop or weakened digital extension develops, or conservative treatment fails to provide relief after 3 mo, surgical decompression may be needed.

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OHSU finds association between Epstein-Barr virus, inflammatory diseases of the mouth

2008 NOV 24 -- Researchers at Oregon Health & Science University's School of Dentistry (www.ohsu.edu/sod) have found that a significant percentage of dental patients with the inflammatory diseases irreversible pulpitis and apical periodontitis also have the Epstein-Barr virus. The Epstein-Barr virus is an important human pathogen found in more than 90 percent of the world population. It is associated with many diseases, including infectious mononucleosis, malignant lymphomas, and naspharyngeal carcinoma.

The findings are published online (www.jendodon.com/article/S0099-2399(08)00879-0/abstract) in the Journal of Endodontics, one of the leading peer-reviewed endodontology journals. The study also is expected to be published in the December 2008 (volume 34, issue 12) issue of the Journal of Endodontics.

Although the number of studies examining the role of herpesviruses in oral disease has been increasing, the majority of studies have focused on periodontitis, with no systematic attempt to examine herpesvirus in endodontic patients with varying inflammatory diseases. The OHSU study assessed the presence of human cytomegalovirus (HCMV), Epstein-Barr virus (EPV), herpes simplex virus (HSV-1), and Varicella zoster virus (VZV) in 82 endodontic patients, including patients with irreversible pulpitis and apical periodontitis, and compared them with 19 healthy patients. The goal of the study was to determine the potential association of herpesvirus with clinical symptoms, including acute pain and size of radiographic bone destruction.

Using a variety of methods, the OHSU team found the Epstein-Barr virus DNA and RNA in significantly higher percentages (43.9 percent and 25.6 percent respectively) compared with healthy patients (0 percent). Human cytomegalovirus DNA and RNA were found in measurable numbers in both endodontic patients (15.9 percent and 29.3 percent respectively) and in healthy patients (42.1 percent and 10.5 percent respectively). Herpes simplex virus DNA was found in low percentages of endodontic patients (13.4 percent) and only one patient showed the presence of Varicella zoster virus.

While a previous study examined the incidence of herpes viruses in apical periodontitis, "this is the first time irreversible pulpitis has been analyzed for the presence of herpes viruses and associated with Epstein-Barr virus," noted Curt Machida, Ph.D., OHSU professor of integrative biosciences and principal investigator, whose lab was host for the study. "The incidence of irreversible pulpitis and apical periodontitis, caused by bacteria and possibly the latent herpes virus, is painful and can greatly impair the body's natural immune system. Studies such as ours could someday lead to more effective treatments of inflammatory diseases of the mouth."

Keywords: Carcinoma, Chickenpox, Chronic Fatigue Syndrome, Cytomegalovirus, Dentistry, EBV, Endodontics, Epstein-Barr Virus, HSV-1, Hematology, Herpes Zoster Virus, Herpesvirus, Infectious Disease, Infectious Mononucleosis, Lymphoma, Oncology, Periodontitis, Pulpitis, Varicella Zoster, Varicella-Zoster Virus, Viral Research, Virology, Oregon Health & Science University.

This article was prepared by Clinical Oncology Week editors from staff and other reports. Copyright 2008, Clinical Oncology Week via NewsRx.com.

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Can Seaweed Battle Cancer?

If you read my article about the health effects of ginger, you already know that I am an avid fan of sushi. Having grown up in California where sushi is commonplace and fresh fish is caught by the hour, the delicacy consisting of raw fish, rice, spices, and seaweed, is a luxury we often take for granted. While I usually drool over the ginger, fresh fish, and soy-sauce laden rice, science might be telling me to start appreciating the thin black “skin” of seaweed wrapped around them instead.

While many beachgoers and ocean swimmers get tied up or tangled in the slimy legs of seaweed, the term “seaweed” is actually a blanket word for any variety of algae formed in the sea. Algae comes in red, green, or brown and is harvested for a number of commercial uses. Besides being an additive in some products such as toothpaste, paint, or cosmetics, seaweed is also being developed as a weight-loss tool, fertilizer, as a potential biofuel, and it could be the next “superfood” if more uses are found.

In the food spectrum, seaweed is not just used to wrap sushi or cut up into Asian-style soups. Seaweed is known around the globe as a tasty treat and can be made into pasta like spaghetti in Italy or in a type of bread in Scotland.

Seaweed has been found to be a large source of iodine, an element that is necessary for the health and maintenance of the thyroid gland and when left untreated, can lead to discomfort and possibly a goiter. The strength and elasticity found in strips of this sea-faring organism is sometimes used to dress wounds and has also been documented as used in molds for dental work. Seaweed has been used in many studies hoping to find cures or lessening agents within it against diseases like tuberculosis, annoying ailments such as arthritis or tapeworms, even the common influenza has been tested with seaweed. The results of these tests have been relatively inconclusive and no generalizations could be made.

However, most of the studies in recent years that have been done regarding the effects of seaweed, are against cancer. Hoping to find the ability to shrink tumors with algae, many researchers have devoted years to observing the patterns and data surrounding this important compound.

A 2005 study conducted at the Georgia Institute of Technology found a small strain of red algae off the coast of Fiji called Callophycus serratus, that looks promising for a new, natural cure for cancer. With ten new natural compounds from the strain to work with, researchers found that some of the compounds were born antibacterial fighters and have held up in the lab against known diseases that resist antibiotics. It was said that the natural germ-killers were made by the seaweed to ward off predators and disease. Another compound was able to kill tumor cells in the lab by being able to turn on the suicide switch in the individual cells, which scientists call a head start to a new possible line of anticancer drugs. Georgia Tech biochemists insist that they are only in the “test tube level” and many more studies will be conducted.

Four years ago the researchers speculated that if the studies continue to work, that it may take at least a decade for any of these types of drugs to become available to the public. Another downside to these findings is a common one among researchers, the dosage of the drug would have to be incredibly high in order for it to work and it may do more harm than good for the patients. Another Georgia Tech biologist Mark Hay says that curing cancer is easy, but making it easier on the patient is completely different,

“We can cure cancer with a shotgun, so curing cancer is not the problem…. Curing cancer without harming patients is a whole different thing that's very difficult to figure out. Many compounds have been found to have a negative effect on cancer cells, but almost none of them have gone to market because of adverse side effects that make them unusable.”

While it may be awhile before we are able to take seaweed capsules to ward off cancer or those extra few inches around the middle, it looks like seaweed is a great source of nutrition and shouldn’t be shooed away from the table.

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Multiple Sclerosis Relapse Rate Reduced By Nearly Half With Use of Two New Drugs

Cladribine and fingolimod, two new oral drugs, have been shown to decrease the relapse rate in people who suffer from multiple sclerosis. The drugs could become the first treatments for the disease that does not require regular injections or infusions, if they gain approval by the U.S. Food and Drug Administration (FDA).

Multiple sclerosis (MS) is a chronic and frequently disabling disease that attacks the central nervous system. According to the National Multiple Sclerosis Society, the condition affects about 400,000 Americans and is the most frequent cause of neurological disability other than trauma in people from ages 20 to 50. Symptoms vary among patients and can range from mild to severe and may cause numbness of the limbs, paralysis and even loss of vision. The progression and severity of the disease are unpredictable.

Relapsing/Remitting Multiple Sclerosis (RRMS) is one of four recognized forms of MS. However, approximately 85 percent of people presenting with Multiple Sclerosis are first diagnosed with RRMS. This form of MS is characterized by relapses that may last for days, weeks or even months, during which new symptoms can appear and old symptoms may resurface or worsen. These relapses are followed by periods of remission in which the patient fully or partially recovers from the effects that occur during relapse periods. Recovery may be gradual or practically instantaneous.

In the Phase III study of 1,200 patients with the RRMS, approximately 80 percent of MS patients who took the drug cladribine remained relapse-free for two years compared to only 61 percent of those participants given a placebo. Side effects of cladribine were mild and included headaches, colds, flu, and nausea. The patients were followed for almost two years and monitored with the use of MRI scans. The study participants all had been living with MS for an average of six to seven years, and suffered from at least one relapse in the year prior to the study.

During the study, led by Gavin Giovannoni, M.D., of the Barts and London School of Medicine and Dentistry, participants received either four courses of low-dose cladribine tablets, six courses of higher-dose cladribine tablets, or a placebo. According to Giovannoni, this means, “that individuals with MS only have to take tablets for 8 to 20 days a year. That should improve compliance.”

The study participants who received cladribine were found to be 55 to 58 percent less likely to suffer from a relapse within a year than those given a placebo. In addition, the cladribine recipients were 33 percent less likely to experience deterioration in their disabilities, such as increase in the difficulties of walking. Based on MRI scans, participants taking cladribine were also found to have considerably brain and spinal cord lesions that are typical for MS patients.

Cladribine is already licensed and marketed under the name Leustatin for the treatment of leukemia and is believed to work in the fight against MS by suppressing the autoimmune responses thought to cause the disease. Merck Serono plans to apply for FDA approval within months.

In another successful phase III study of over 1,200 patients with RRMS, 80 to 84 percent of MS patients who were given daily dosages of the drug fingolimod remained relapse-free after one year in comparison to only 67 percent of study participants who received Avonex, a typical injectable drug used to treat MS. Participants in this study had been living with MS for an average of seven years, and all had suffered from an average of two relapses within two years prior to the study. Jeffrey Cohen, M.D., of the Cleveland Clinic, led the study.

Participants taking fingolimod were found to be 38 to 52 percent less likely to suffer from a relapse within a year and also experienced fewer lesions than participants who received the Avonex injections. The length of the study was insufficient to allow conclusions to be drawn on fingolimod’s effects on disabilities. The most common side effects experienced included, headache, head colds and fatigue. However, eight cases of skin cancer as well as four cases of breast cancer did occur and it remains unclear as to whether or not fingolimod was responsible for these events.

Fingolimod also suppresses the autoimmune responses thought to cause MS. There are two other ongoing studies of fingolimod for which results are expected within a few months. The maker of the drug, Novartis, anticipates application to the FDA for approval by the end of this year.

The phase III studies for both cladribine and fingolimod were presented at the annual meeting of the American Academy of Neurology. Because both drugs suppress the autoimmune responses, concerns remain regarding the safety of long-term use, as T cells are necessary for fighting infections, and particularly viral infections. Cladribine damages the ability of the T cells to reproduce and proliferate while fingolimod locks T cells inside the lymph nodes, preventing them from traveling through the bloodstream and into the brain and spinal cord. More studies of both drugs will be required to determine safe measures for their use.

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Tincture Tonics?

When watching an older movie, particularly one that is set prior to 1950, oftentimes terms are used that are rare or extinct in modern day life. Such as when characters would faint in a scene, a smaller role would always be advised to procure the “smelling salts” because the ill person had “the vapors.” The word tincture reminds me of this old-timey speak, although I admit that I did not know exactly what one was. Apparently tinctures are still widely used today and relevant in modern alternative medicine for a variety of ailments.

Common in chemistry classes (a course I was never good in), a tincture is a solution that uses alcohol as the main ingredient acting as a solvent to dissolve the solid portion of the solution. A tincture involves the mixing of the leaves, stems, or crushed seeds of a plant/medicinal herb distilled over time in a high percentage of alcohol (usually 40 to 60, but can also be up to 90 percent ethanol alcohol).

To make a healing tincture, herb bits are placed in a small jar and ethanol is poured over them. After letting this mixture stand for several weeks, while stirring occasionally, your tincture is ready for consumption (but should only be consumed in the event of an actual ailment). This process using alcohol helps to keep the herbs lasting for many years past their normal expiration because they are living compounds. It should be noted that tinctures can also be made with vinegar, although this type doesn’t last as long as the alcohol version.

Easily stored and travel-sized, most tinctures are made in small glass or plastic vials—around one ounce in size—perfect for a first aid kit or toiletries bag. Ready to use, these tinctures are easily administered either under the tongue or a few drops mixed into water, juices, or teas.

If you do not have the resources to purchase a high-quality tincture (they can be expensive depending on the uniqueness of the herb being used, time it took the herbalist, and where you find them), it is just as easy to make one yourself. However, make sure you use a recipe so the percentages are just right and use them with caution and as recommended. Favorite alcohol-based tonics that are made as tinctures are formuated with gin, brandy, and vodka, mainly because they are the top 100-proof alcohols available for purchase. Cheap alcohol will make the tincture less effective, so buy the best you can afford (or the best-tasting in your opinion).

Tinctures are generally used for chronic pain conditions like arthritis and ongoing persistent or recurring ailments such as bronchitis, asthma, menopause, migraines, joint and muscle spasms, stomach and bowel problems such as colitis, irritable bowel syndrome, motion sickness, nausea, tremors associated with Parkinson’s disease, and many others.

These tiny potions can be taken as often as a couple of times a day or just a few times a week or monthly as necessary. Always check with your nutritionist or physician before self-medicating or using a tincture as a complement to Western medical treatments and always make sure the herbs being used or mixed are supposed to combine in order to treat your specific condition. If you happen to be on medication, also check with your healthcare provider in case you are unable to use a tincture based on alcohol content or possibly because of the drug interaction with different herbs.

Next time you watch an old movie and someone with tuberculosis needs a tincture in order to get through his or her day, maybe you (as I will) know what exactly that means, even if you don’t venture to your nearest health food store or attempt to make your own alternative tonic.

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Corneal diseases

Cornea - a front part of an external fibrous envelope of an eyeball; nonvascular, high-sensitivity, transparent, an optically homogeneous envelope with smooth, a smooth surface. Except for protective and basic function the cornea is the main refracting surface of optical system of an eye.

Diseases of a cornea makes about 25 % of the general number of diseases of eyes, and quite often are the reasons of blindness and lowering of vision.

Diseases of a cornea are rather various. Most often there are inflammatory diseases of a cornea (keratitis), differing greater variety of forms and being one of principal causes of decrease in sight and blindness, and also keratikonus. The Most frequent reasons of keratitis and keratoconjunctivitis are virus and bacterial infections.

Keratikonus - a condition of an eye at which the normal spherical form of a cornea is broken, the cornea is bent. On a surface of an eye the camber similar to a cone that leads to strong easing of sight develops.

Dystrophies and degenerations of a cornea happen primary and secondary. In a basis primary local and general infringements of a metabolism with adjournment in a cornea of products of a pathological exchange lay. Secondary dystrophies develop after transferred keratitis, traumas, burns of eyes.

For the prevention of heavy complications of diseases of a cornea are required: proper diagnostics, duly and active treatment. Various medicinal substances are applied to local treatment in the form of drops, injections. Methods of electrophoresis, phonophoresis, treatment by laser radiation are used also.

For carrying out of purposeful treatment bacterial keratitis definition of sensitivity of microflora to antibiotics by crop of defeat separated from the center is necessary.

Instruction to the patient after change of a cornea

To you the microsurgery of change of a cornea is lead. The thin seam keeping a donor fabric, can long-standing time (about one year) to remain in a cornea. It allows you to start to work with the moderate physical activity earlier. At the same time, it is necessary to remember the periodic medical control over a condition of a seam.
Durable healing of a wound after change of a cornea comes only in 6-10 months after operation. Therefore after an extract from a hospital it is necessary for you to continue the recommended treatment in house conditions. Instilling drops or loading ointments can be made the purest hands before a mirror or in a prone position, as well as by means of relatives, using those receptions with which you have got acquainted in a hospital.

During the first month to sleep it is necessary on a back or on the party opposite to the operated eye. The food can be usual, it is necessary to exclude alcoholic drinks. Surplus of sweets is not desirable. Easy gymnastic exercises without jumps, run and inclinations are useful. During rest and walks during the first year after operation it is necessary to avoid stay on the bright sun. It is impossible to sunbathe. It is possible to use the blacked out glasses. The replaced cornea during several months, and sometimes several years, has the lowered sensitivity. Therefore it is impossible to rub sharply an eye a scarf or a hand, it is necessary to be cautious at washing, to cover the operated eye during a strong wind and to avoid walks in frosty days even on the second or the next years after operation. It will help to save a cornea from damages and freezing injury.

You can watch TV, go to museums, cinema and theatre if it is not connected with difficult and close moving to transport. It is possible to start the usual or limited work in 2-4 months depending on a condition of the operated eye and working conditions. Expansion of the general mode should be carried out one step at a time, however during the first year work with a slope of a head downwards, outdoor games, run, heavy physical work is absolutely counter-indicative. After an output for work do not forget to show to the oculist each 2-3 months within the first year after operation, especially if it is not removed an encircling stitch.

In case of occurrence of reddening and an ache in an eye, and blear-eyedness to you it is necessary for photophobia to see a doctor promptly. Only early the begun treatment can prevent deterioration of vision.

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Dystonia and Botox Injections

The first thing you notice about "Joey" is that his head is turned and tipped to one side; his left ear rests on his hunched-up left shoulder. He has to turn his whole upper body to look at you. Joey has torticollis, also known as cervical dystonia, meaning that his neck muscles are in an involuntary spasm that forces his head into its painful, abnormal position.

Can affect any part of the body
Dystonia--those painful muscle spasms--can affect any part of the body including:

• eyelids (blepharospasm)
• face (oromandibular)
• vocal cords (dysphonia)
• arms, legs, or trunk

"Writer's cramp" is dystonia in the hand or arm muscles.

Causes
Dystonia affects people of all ages and ethnic backgrounds. Some forms of it can be inherited; researchers have identified more than 10 genes or chromosome locations associated with the disorder. Dystonia may also occur due to birth injury, traumatic injury, toxins (such as manganese), certain medications (such as haloperidol), stroke, or be part of another disorder such as Parkinson's disease. It generally develops gradually, and symptoms can appear at any age.

Diagnosis
There is no specific test for dystonia, so it is usually diagnosed based on the symptoms. Dystonia can come and go, so some people who experience it may have a hard time convincing health care providers that it exists. The spasms may change significantly with different actions. For example, hand dystonia may occur when trying to write but not during other activities.

Treatment
For most people with dystonia, the disorder does not shorten life, but it does cause pain and discomfort, and may interfere with basic activities such as walking, dressing, or eating.

There are a number of medications that can treat dystonia, either alone or in combination. One of the most common treatments is Botox (botulinum toxin) injections (marketed as Vistabel in Europe). Dysport is another brand available in Europe. Another formulation of botulinum toxin used is called Myobloc (U.S.) or Neurobloc (Europe).

Botox injections
Although most people in the U.S. know Botox as a vanity treatment for facial lines, it was originally developed in 1989 as an orphan drug to treat dystonia and muscle spasms. Injection of the drug causes weakness in the targeted muscle, thus relaxing the spasm and relieving dystonia.

Information for this article was taken from:
- Molloy, F. M. (2002). Botulinum toxin (Botox): Dystonia treatment. eMedicine, accessed at http://www.emedicine.com/neuro/topic585.htm
- Dystonia Medical Research Foundation

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Shigellosis

What Is It?

Shigellosis is an infection of the colon (large intestine) caused by Shigella bacteria. Shigellosis is also called bacillary dysentery because it can cause severe diarrhea. However, the infection often causes only mild symptoms.

Shigella can be found in water polluted with infected sewage. Bacteria commonly enter the body through a contaminated drinking supply. Shigella bacteria also can be found on food that has been rinsed with unclean water, grown in fields contaminated with sewage, or touched by flies that have touched feces. Shigella bacteria can reach the mouth on dirty fingers that have touched items soiled with feces, including dirty diapers, toilets and bathroom fixtures. Outbreaks of shigellosis are most common in areas where sanitation is poor, and in places where people live under confined or crowded conditions. Shigella also can be passed from person to person during anal-oral sex.

Worldwide, an estimated 140 million people develop shigellosis each year, and about 600,000 die. Most of these deaths occur in developing countries among children under age 5. In the United States, only 20,000 cases are reported each year, but the actual number of infections is probably more than 200,000 per year. Shigellosis is more common among children ages 1 to 4. Children of this age are especially at risk because they are starting to use the toilet and often forget to wash their hands. Infants are at the highest risk of becoming seriously ill from a Shigella infection.

Symptoms

Although health experts don't know why, some people take in Shigella bacteria without becoming ill. Others develop only a brief fever, or a brief fever with mild diarrhea that goes away on its own. About 25% of patients, however, develop high fever, abdominal cramping and severe diarrhea that can contain blood, mucus and pus. These people can have 10 to 30 bowel movements each day, along with a persistent urge to have a bowel movement that can lead to rectal prolapse (an abnormal protrusion of the rectum). Rarely, Shigella bacteria can affect other parts of the body far from the digestive tract. When this happens, there can be seizures, confusion or coma, kidney failure, arthritis, rashes or other symptoms.

Diagnosis

Your doctor will ask about your symptoms and about the appearance of your bowel movements. He or she will ask if you have recently traveled to developing countries, been in contact with people who have severe diarrhea, or might have been exposed to contaminated pools, lakes or food.

Your doctor will diagnose shigellosis based on a physical examination and the results of laboratory tests. These tests include taking a swab of your rectum or a sample of your stool (feces). If you have signs of dehydration (excessive loss of body water) or significant blood loss, additional blood tests may be necessary.

Expected Duration

In most otherwise healthy people with mild shigellosis, diarrhea goes away on its own within five to seven days. However, in very young children, the elderly or people with chronic illnesses, shigellosis can be severe and can lead to life-threatening dehydration and other complications within a few days.

Prevention

There is no vaccine to protect against shigellosis. To prevent the spread of Shigella bacteria, you should:

• Practice good hygiene, especially frequent handwashing.
• Wash your hands immediately after changing a child's diaper, especially if the child has diarrhea.
• Dispose of soiled diapers in closed-lid garbage cans.
• Swim only in lakes and pools whose water quality is monitored by local health officials.
• When traveling to developing countries, drink only water that has beeb treated or boiled eat only foods that have been cooked thoroughly. Never eat unpeeled fruits, and always peel fruits yourself immediately before eating them.

Treatment

If you have a mild case of shigellosis, you probably won't need treatment because your symptoms will probably go away on their own. Sometimes, doctors may prescribe antibiotics if there are very young or very old members in a household who could get the infection.

If you have a severe case of shigellosis, your doctor will prescribe fluids to treat dehydration and an antibiotic based on how you became infected. For example, if you became infected with shigellosis in the United States, your infection probably will respond to common antibiotics such as ampicillin (Polycillin, Totacillin, Omnipen), trimethoprim-sulfamethoxazole (Bactrim, Septra and other brand names), tetracycline (sold under many brand names), or ciprofloxacin (Cipro). However, if you became infected during travel to a developing country, the infecting strain of Shigella is more likely to be resistant to these common antibiotics, and you may need a newer or less common antibiotic.

The use of antidiarrheal medicines to slow bowel movements is controversial. It can take longer to clear the bacteria from the lower intestine and the illness caused byt he infection could become more severe.

When To Call A Professional

Call your doctor if you develop severe diarrhea, especially if the bowel movements contain blood or mucus. Call your doctor whenever you have a fever and severe diarrhea. Seek immediate attention if you have signs of dehydration, such as very dry mouth and lips, and lightheadedness when you stand, whether or not you are thirsty.

Prognosis

In developed countries, most people with shigellosis recover completely. In underdeveloped countries, the risk of complications, including death, is signifcantly higher.

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Factors and the conditions causing irritation of a dental pulp

The irritation of a pulp of a tooth can arise owing to caries of a teeth, as a result of preparation of a tooth and carious cavities, under influence a filler material, owing to penetration of microorganisms at not tight seal, at an exposure dentin.

Caries of a tooth serves as a principal cause of changes in a pulp and its inflammations. Already at initial damage dentin fibrilloblasts react adjournment secondary and formation of a layer scleroid dentin (adjournment of salts of calcium on walls of dentinal canaliculus) down to full occlusion of dentinal canaliculus. These processes should be considered as display of protective mechanisms of a pulp on action of a cue.

At processing of a caries and destruction of enamel of a bacterium get in dentin, however the inflammation of a dental pulp does not arise. It is established, that first signs of an inflammation come, when carious the cavity is separated from a pulp by a layer of 1,1 mm [Reeves R., Stanley H. R., 1996], i.e. the pulp practically is not infected up to an instant of penetration of microorganisms in secondary dentin [Massler, Pawlak J., 1977].

Preparation of a cavity without use of a water spray leads to its damage. Thus probability of damage of the in direct proportion area of preparation and depth of damage. Thus, preparation of a tooth under vinirs or artificial crownwork without due cooling serves a serious risk factor for a pulp.

Filler materials. There are the numerous data specifying irritating influence various of filler materials. From cements the most expressed adverse action renders silicate though specify, that it is shown at formation of a clearance between edge of enamel and dentin as microorganisms nestle close in dentin [Brannstrom, 1979].

Composites also are considered as irritating materials. First of all, toxicity of composites of the first generation was marked. Materials let out now as specify numerous supervision, render insignificant influence on a pulp.

During many years use of bondings was studied at sealing. It is proved, that improvement of a compounding bondings has allowed to achieve favorable reaction of a pulp to used composites.

Regional permeability as considers a number of researchers, is a principal cause of irritation of a pulp after sealing. The leading part thus belongs to microorganisms. With the purpose of the prevention of the specified changes in a pulp it is recommended to spend padding fabrics of a tooth and use bonding systems.

The exposure of dentin can occur after loss of a seal, as a result of deleting fabrics, at erosion, etc., that is accompanied by sensitivity action of irritating factors. Sensitivity can arise also at an exposure cervical dentin because canaliculus of dentin become opened.

The sheeting (direct) provides:

1) clarification of a surface of a pulp;

2) drying of a cavity;

3) imposing on the naked pulp of medical paste;

4) a seal from zinc oxide eugenic acid cement;

5) imposing of a constant seal.

Most widely used materials for protection of a pulp contain all calcium hydroxide. As a result of it above a site of an exposure it is postponed secondary dentin, forming the dentin bridge. Consider, that formation of a barrier occurs not due to the calcium containing in a material, closing a pulp.

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Colitis - a problem of intestines

Very often at people the wrong opinion concerning such disease as colitis is created. They assume, that colitis is a gripe. However, this incorrect assumption. The word colitis has occurred from the Greek word "kolon" which is translated as a large gut. Actually colitis is an inflammatory disease of a mucous membrane of thick intestines.

Colitis in sharp forms pass very violently, but during too time it is very fast. Chronic colitis in turn proceed very long and languidly. Sharp colitis are very often accompanied by an inflammation of thin guts and a stomach. The medicine knows some types of colitis. Among them: ulcer, infectious, ischemic, medicinal, radiating and some other types of colitis. Ulcer colitis it is accompanied by occurrence of chancres in paries of intestines. At ischemic prick blood badly reaches intestines.

There is a big number of the reasons of occurrence colitis. It can be intestinal infections, an infection in a bilious bubble or a pancreas, long application of antibiotics, infringement of blood supply of a gut. If to speak about a wrong feed it also influences formation of colitis. More often this abusing flour and animal food, also a spicy food and alcohol. If at you a dysbacteriosis of intestines, worms, a bad heredity or a food allergy, quite probably, that you become "hostage" of colitis. One more very frequent factor of occurrence of colitis is the wrong mode of day, a frequent mental or physical overstrain.

The basis of any colitis includes damage of a mucous membrane of a gut. If colitis is caused by an intestinal infection then disease passes with rough influence on an organism. During the moment of disease various bacteria and parasites get on a mucous membrane of a gut and start it to damage. During this moment in a gut of the patient there is an inflammatory process. Because of it the wall of a gut swells. The gut cannot normally function any more. The wrong operating mode causes desires on defecation, a diarrhea and painful sensations in a stomach. At the patient at prick constantly the temperature raises.

First attributes of colitis are a pain in the field of a stomach and a unstable chair. Rumbling and a swelling of a stomach can disturb the patient. In a dung there can be a slime or blood. The person with colitis feels slackness, weakness. The given disease proceeds more often, approximately, some weeks.

If happens you got a colitis, it is necessary for you to address necessarily to the gastroenterologist. Only him can put you the correct diagnosis. Also you should hand over the analysis кала and to pass some researches on various devices.

Treatment of any kind of colitis requires a special diet. All other treatment is appointed depending on the reasons of disease. If at you has appeared colitis because of an intestinal infection then to you will necessarily appoint antibiotics. In case of if you became the owner of this disease because of application of a plenty of medicines then all medical products are canceled.

Medicinal therapy, physiotherapy, psychotherapy – all this methods of treatment colitis. Sanatorium treatment of this disease very well helps.

Colitis, as well as all other diseases, requires duly treatment. For this reason leave all businesses on then and engage for the beginning in the health. Visiting of the gastroenterologist will help you to get rid from colitis and to feel far more confidently and better.

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How is Down Syndrome Diagnosed?

How is Down's Syndrome Diagnosed?

Down syndrome is diagnosed one of two ways, either during pregnancy or shortly after birth. The diagnosis is always based on the presence of an extra number 21 chromosome on a karyotype (a picture of an individual's chromosomes).

At Birth

The diagnosis of Down's syndrome is usually made soon after birth because of some subtle differences in the baby's appearance. Children with Down syndrome have some distinctive facial features and physical characteristics that may lead your doctor to suspect that your baby has Down syndrome.

Some of the features include:

• A flat facial profile, flat nasal bridge and somewhat small nose
• Almond shaped eyes with epicanthal folds
• A small mouth with a slightly enlarged tongue
• A big space between the first and second toe
• Small broad hands with short fingers and a little finger that curves inwards.
• A single palmar crease on their hand
• Reduced muscle tone (hypotonia) which results in floppiness

If the doctor suspects that the baby has Down syndrome, a chromosome test called a karyotype, will be ordered. It usually takes a few days to get the results of this blood test. It is almost always a shock when a baby is diagnosed with Down syndrome but there are some things that you can do to get through the first few months.

During pregnancy

Screening versus Diagnostic Testing

There are two kinds of testing that can be done during a pregnancy - diagnostic testing such as amniocentesis and chorionic villi sampling (CVS), and screening testing such as ultrasound (sonogram) and maternal serum screening tests. A screening test can never give you a firm diagnosis - a screening tests simply tells you if you have a slightly higher risk to have a baby with Down syndrome. A diagnostic test on other hand, gives you a firm diagnosis.

Down syndrome can be diagnosed in pregnancy by diagnostic tests such as amniocentesis or chorionic villi sampling (CVS). These are considered optional tests during pregnancy which means that it is your choice whether or not to have this testing. It is recommended that women considering testing speak with a genetic counselor to review their risks and to discuss risks and benefits of these procedures before making their decision about testing

The results of amniocentesis and CVS will give you a picture of the fetus’s chromosomes and the diagnosis of Down syndrome is very straightforward. Infants with Down syndrome have an extra number 21 chromosome for a total of 47 chromosomes rather than 46.

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Dermatitis

Dermatitis is an inflammatory process arising in integuments. Its reason can become various physical or chemical factors of an environment. The degree of influence of the harmful agent sometimes depends on individual sensitivity of an organism, in this case it is a question of the allergic nature of disease. It takes place both at external contact with cue, and after its hit inside of an organism. Depending on it, distinguish contact forms of illness and toxicoderma.

Ordinary contact reactions result from hit on a leather of caustic chemical substances, for example, acids or alkalis. Depth and the area of defeat thus neatly depends on concentration, area and time of influence of the negative factor. At long-standing contact to small dozes of toxin pathological process gets chronic character, and at lots — immediately there is a sharp reaction. It is accompanied by reddening of a leather, formation of bubbles, a suppuration, occurrence of hypostases, pains, burnings and an itch.

As a rule, its reason are solar burns, significant differences of temperatures, toxic substances of a vegetative or animal origin, cosmetic and perfumery means, medicinal creams and ointments. As most often meeting form sharp dermatits the attrition and the water callouses formed on a leather owing to mechanical friction serves. Usually on palms of hands it is observed after heavy physical work, and on stops — as a result of long carrying close footwear. At people with excess weight quite often attritions arise on a body between folds of a leather.

For chronic process bluish painting of integuments, occurrence of cracks, a thickening of a horn layer and a peeling is characteristic. The reason of similar reactions can become various fungoid, bacterial or virus infections, strong diaphoresis, especially in a combination to synthetic clothes. To cause the allergic form of disease some foodstuff are capable. At children such condition has received the name of a diathesis. More often it is connected with the use in food of dairy products, citron, nuts, eggs.

Constant stay in a condition of stress provokes occurrence or strengthening of negative symptoms of dermatitis. It is necessary to comply with caution to people with a dry leather, especially in cold and windy weather. During this period for protection of the open sites of an integument it is necessary to use special creams. For preventive maintenance of disease it is necessary to adhere strictly to the safety precautions at the reference with dangerous substances on work and houses, in time to eliminate activators of infections, with caution to approach to use of medical products.

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Lyme disease and related tick-borne infections

Highlights

Lyme Disease Rates Double in Past 15 Years

The annual number of people newly infected with Lyme disease has doubled from around 10,000 cases per year in the early 1990s to about 20,000 cases per year now. Improved diagnosis and reporting probably contribute to this increase. In the United States, Massachusetts, New Jersey, and Pennsylvania have reported the highest number of Lyme disease cases in recent years. People ages of 5 - 14 years and 45- 54 years are at highest risk for contracting Lyme disease.

New Guidelines for Treatment of Neurological Lyme Disease

Most cases of Lyme disease can be prevented or cured with prompt antibiotic treatment following a deer tick bite. However, neurological complications can later develop in some patients. In 2007, the American Academy of Neurology released new guidelines for the treatment of nervous system Lyme disease. The guidelines recommend that patients with severe disease receive a 2 - 4 week course of intravenous antibiotics (penicillin, ceftriaxone, or cefotaxime). Patients with milder neurological cases may do well with a 2 - 4 week course of oral doxycycline. No guidelines currently recommend long-term antibiotic treatment for any stage or complication of Lyme disease.

Introduction

Lyme disease is the most commonly reported tick-borne disease in the United States. Vector-borne infections are transmitted by insects.

Borrelia Burgdorferi

The Lyme disease infection in the U.S. is caused by a spirochete called Borrelia (B.) burgdorferi. A spirochete is a bacteria-like organism with a cylinder-like shape surrounded by an outer membrane.

Lyme researchers have the completion of DNA encoding of B. burgdorferi. Researchers learned that certain proteins coat its outer surface. These proteins, collectively called Osp, are responsible for attaching the spirochete to cells in humans and other mammals.

Ixodes Ticks

The vector that carries B. burgdorferi in the U.S. Northeast and North Central states is the Ixodes scapularis tick. The Ixodes scapularis tick goes through three stages over the course of about two years:

• It is born from eggs as a larva.
• It develops into the nymph stage.
• It develops into the adult stage.

The Cycle of Infection

Cycle of Infection in the Northeast and North Central U.S. For Lyme disease to exist in these regions, three factors must come into close contact:

• The Borrelia (B.) burgdorferi spirochete
• The spirochete's host, the Ixodes scapularis tick
• The mammal for the tick to bite

The following describes the most common cycle in the Northeast and North Central U.S. by which the Lyme disease infection eventually reaches a person:

• The cycle of infection is related to the tick's life cycle, which requires 2 years to complete. The tick typically first picks up the spirochete during its larva stage, when it needs a blood meal to mature further.
• The tick's initial meal is typically blood from the white-footed mouse, which is commonly infected with Borrelia burgdorferi. After it dines on the infected blood, the tick then becomes a carrier of this spirochete.
• Borrelia burgdorferi lodges in the tick throughout one of both of its following life stages, nymph and adult. It is during these stages that the infection is passed on to other animals, including humans. Nymph ticks emerge around mid-June and can be about the size of poppy seeds. They are very difficult to spot and are estimated to be responsible for 90% of all Lyme disease cases. Adult ticks can be as large as a raisin after feeding, and easy to spot, but they usually prefer their dinner on the white-tailed deer.
• The infected nymph or adult tick crawls (it does not fly or jump) onto another animal, which can be mice or larger animals, such as deer, birds, or humans. If the tick bites these animals, it may then infect them with the B. Burgdorferi spirochete. (It should be noted that infected humans cannot pass the spirochete on to other humans by any means, including infected blood or urine or sexual contact.)
• A tick can feed for several days while being imbedded in the skin, after which it falls off. The tick's bite is painless, however, so only about half of people with Lyme disease recall being bitten.

Cycle of Infection in the Northwest. In the Northwest, the infecting insect is the Western blacklegged tick, Ixodes Pacificus. Here, the frequency of Lyme disease is much lower than in the other two regions because the animal carrier of the infection is the dusky-footed wood rat. This animal is bitten and infected by the Ixodes neotomae tick, which does not bite humans. The actual tick that spreads B. burgdorferi to people is Ixodes pacificus, which must feed first on an already infected wood rat.

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Diagnostics and treatment of tinea

A tinea represents a fungoid infection which can amaze set of parts of a body of the person. Below we shall designate sites of a body on which can appear dermatosis.
The-part of a head covered by hair.
- A smooth leather of a trunk.
- Nails.
- Stops of legs.
- Inguinal area.
- A skin of the face on which the vegetation settles down.

The given infection is widely widespread. If in time to undertake elimination of illness and to observe all doctor's instructions such effective treatment will give the favorable forecast. But can be and so, that at the started illness the chronic form tinea develops.
Infection tinea occurs at direct contact to the sick person, or through the polluted subjects. Among these subjects there can be a footwear, towels or mats in bathroom. The activator of disease tinea is the fungus.

Treatment of illness individually, depends on the form of its display. At disease of tinea it is necessary to address to the doctor. In fact depending on the form of disease of defeat of a leather differ on appearance and duration of existence of illness.

From a tinea of a hair parts of a head basically suffer children, and is characterized by occurrence small, one step at a time extending papules on a head, as well as a peeling, loss of hair on the amazed sites. Also on seat of papule can be formed inflamed, furuncular-like units.
At disease of a tinea of a smooth skin, papules extend on any sites of a skin, there are flat formations, dry, covered by scaly crust or damp, covered by crusts. Depending on a degree of their increase, the centers of spots are cleared, giving a classical picture of a leather in the form of circles.

A tinea nails begins with tips of one or more nails on legs or hands. In the second case disease is shown far less often, than in the first. Illness leads to a gradual thickening of nails, variation of their color, a curvature. Under them the substance formed from of died cells accumulates. As a result, the nail can be completely destroyed.
A tinea stop causes finely lamellar peeling of a skin, occurrence of bubbles between fingers. In heavy cases the infection can lead to inflammatory process of all the stops, described a strong itch and a pain at walking.

A tinea of an inguinal areas it is characterized by occurrence red, with precise borders, spots in an inguinal areas. The designated spots can extend on buttocks, internal surfaces of a hips and external genitals.
At diagnostics of a tinea, it is carried out scrape from the amazed sites of a leather. The received material investigate by means of a microscope.
A tinea, as a rule, it is treated by preparations for external application. Local treatment proceeds within two weeks after disappearance of symptoms. Also, at treatment of a tinea use the open damp bandages.

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Hernias at children: inguinal, umbilical, a hernia of a white line of a stomach. Symptoms. Methods of treatment.

Hernia is an outwandering bodies from a cavity in norm them borrowed through properly existing or pathologically generated aperture with conservation of an integrity of envelopes, their covering, or availability of conditions for this purpose.
Let's consider a hernia of a forward belly wall of a stomach. It is the most widespread surgical pathologies at children. An original cause of progress of hernias - defect of progress of a belly wall. However there are some features which we shall consider separately.

Umbilical hernia. For 4-5 day after a birth of the child the umbilical cord disappears. The umbilical ring consists of two parts. The bottom part where pass umbilical arteries and a uric channel, are well reduced and form a dense cicatricial fabric. In the top part there passes a umbilical vein. Its walls thin, have no muscular environment, are badly reduced in the further. Quite often at weak peritoneal band and patent to a umbilical vein the umbilical hernia is formed. Except for it the major factor promoting occurrence of this pathology, frequent increase of intrabelly pressure is. It can be caused, for example, frequent we cry the child.
The aperture in the top part of a umbilical ring can be wide, and not trouble the child. But in case of small defect with firm edges concern of the child probably. As a rule, a umbilical hernia always can be reduced. The restrained umbilical hernia to meet in an adult practice more often. However we quite often should operate children with unreducible hernias (when hernial contents are attached to an internal wall of a leather of a forward belly wall by solderings).

Experience of out-patient supervision of children with the umbilical hernias diagnosed at early age, allows to tell with confidence, that to 5-7 years age often there comes self-healing. Liquidation of a hernia is assisted with strengthening a belly wall. It certainly massage, laying of children on a tummy, gymnastics. Surgical treatment it is begun not earlier than 5 years age. Properly and accurately lead operation, allows to eliminate a hernia with good cosmetic effect. As a rule, relapses does not happen.

Hernia of "a white line" stomach (anteperitoneal adipoma). If to lead a line between omphalus and ensiform shoot of a brest is and there is "a white line" stomach. At a direct muscle of the stomach, shaping given area, is from 3-6 tendinous crosspieces. In seat of intersection of these crosspieces and "a white line" stomach sometimes there are small defects. In them it is often stuck out anteperitoneal fat. If they settle down in immediate proximity from a umbilical ring, them name paraumbilical (periomphalic) hernias. Unfortunately, these hernias are not inclined to spontaneous closing. Treatment only operative, similar to operation at a umbilical hernia.

An inguinal hernia. Very frequent surgical disease at children. As a rule, all hernias at children of early age congenital. What reasons of occurrence of this pathology? It is a lot of opinions in this occasion at children's surgeons. It and weakness of a forward belly wall and feature of a structure inguinal areas and nonclosure vaginal a shoot abdominal membrane and a heredity. We shall try under the order, on an example of an congenital inguinal at the boy.
About from 6-th month of intra-uterine progress of the boy orchis fall from a belly cavity in marsupium on inguinal to the channel. Therefore these hernias name slanting. For presentation present itself, that on a tube (vaginal to a shoot abdominal membrane) as on the lift, orchis, conducted by the lowering mechanism from a belly cavity goes down in marsupium. Then under the plan there is a closing a pipe (vaginal shoot abdominal membrane) and by that the termination of the message between belly completely and marsupium. If it does not occur, at increase of intrabelly pressure in the nonclosure vaginal shoot of abdominal hernia membrane leaves contents of a belly cavity. It is an inguinal hernia.
What for to an organism to strain and stretch a stomach when there is an opportunity to dump a superfluous pressure in "hernial contents". And frequently the child grows and … increases hernial bulge. Treatment of the given pathology only operative. Technically to carry out it at the child easier is more senior 1 year. However quite often operation is shown to the child at once at statement of the diagnosis. To wait dangerously. Occurrence of terrible complication - infringement inguinal hernias is possible. Hernial bulge in inguinal areas earlier that arising disappearing suddenly became firm, the child has begun to worry and has begun to cry, there was a vomiting, refusal of meal. At touch up to firm "bulla" in a groin to the child it is very painfull!!!
Most likely, there was an infringement inguinal hernias. To not give food, not give water and it is urgent to bring the child to the hospital. Muscles of a stomach have restrained contents of a hernial bag. It can be a site of a gut, a bladder or ootheca at girls. If urgently to not help the child after a while the site, deprived blood supplies, can be sphacelous, i.e. become lifeless. In that case treatment very heavy and long. In my practice there were 2 cases, hernial contents at the restrained hernia were a site of a blind gut with again changed an appendicular shoot. It was necessary to lead simultaneously with celotomy.

Believe, it is better to not lead up to infringement. To operate the child with a hernia it is necessary healthy, with good analyses and in the daytime. And it is possible only at scheduled operation. Every year in our branch, about to 500 children with the given pathology, scheduled operative interventions are spent. Operations last about 15-20 minutes, pass under a mask narcosis and the control of skilled anaesthesiologists. And here, after the small period of rehabilitation - your child is completely healthy. We have made all in time and properly.

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