Medical Health Information

Causes of upper back pain

It is rare to hear someone complain of upper back compared to many people seeking medical help for back pain in lower back. This may be because the lower back is much more susceptible to damage and muscle fatigue place in the upper back. However, we found back pain each year to the fact that is undeniable.

It is still difficult to precise define the causes of upper back pain. Not that the medical community is divided into what should be believed, but because there are many complex reasons for common back pain. Often the physician determines that an unusual anatomy of the mental pain than eight if the diagnosis is not completely stopped: the cause or symptoms of upper back are clearly labeled.

The upper back pain

Pain is usually felt on the upper back between the shoulder blades. Although pain at this point the actual anatomic cause is likely to also be placed elsewhere. Trigger points usually closest to the muscles to bones. This is the reason why patients are often unable to pinpoint the exact location of back pain to identify.

The most common cause of upper back pain is postural problems. The upper part of the body must be properly connected to the lower body precise coordination of the components themselves and the body. The position can be achieved with the relevant parts of normal conditions. This approach is not entirely bothered, but also the status of each component, especially in parts.

With poor access often creates a problem degenerated or herniated disc. Some may also move disks. This allows pressure on the nerve roots can cause swelling. This will lead to excruciating pain and may take several months.

Most people who have pain in your upper back due to heavy displaced are women and office workers. For obvious reasons, women are more prone to this problem compared with the male population, a recent study by the statistics; the number of pins ensures that the upper back, pain is more common in women than four times higher than for men.

Causes of upper back pain vary from person to person. The basic truth remains the same cause or causes are often not correctly diagnosed the nature of the disease itself.

Hypoglycemia is the general term for any pathology involving clinical signs and laboratory signs of lack of glucose (and the transferor resurge, but that we will know after).

Circumstances occurred:

• DT1: Poor adherence, poor understanding (insulin to accommodate the pre prandial blood sugar, with meals provided, if sport after) skip a meal, insulin if taken too early basal bolus doses maladaptive if an intercurrent disease (infection, stress ...)
• DT2: sulfa, poor compliance

Acute-Alcoholization

• Pancreatic Damage: chronic pancreatitis, pancreatic cancer ...
• Another endocrine disorder: Insulinoma, adrenal insufficiency, congenital adrenal hypertrophy, Block 21 hydroxylase enzyme, Cushing disease, acromegaly
• Hepatic insufficiency
• Iatrogenic: Quinine, B, hidden Taking insulin / sulfonylurea
• Genetics: Tuner, T21
• And especially IDIOPATHIC + + + or under nutrition
• Another stuff probably

Clinical signs:
Adrenergic sweat, tachycardia, palpitation, tremor, heat. Not present if Bbloquants, Hypo repeatedly, Taking insulin for a long time, autonomic neuropathy in diabetics.

Neuro leukopenia: Hunger and painful stomach cramps, paraesthesia, cold, confusion, diplopia, epileptic fit, max coma

Hypoglycemic coma: coma without localizing sign restless, sweating + + +, pyramidal signs (bilateral Babinski, or at least I know more)

Biological signs
Glucose-venous (not capillary) <0.50 g / l (I know in mM) in the nondiabetic, <0.60 g / l in diabetic. What to do If adrenergic signs: fast + slow sugar, make the person sit + / - feet up, ECG differential diagnosis. If signs neurogly copenic: IM glucagon injection or IVD 2ampoules G30%. Emergency hospitalization. Release of the upper airway, recovery position, scope, constants, two large bore intravenous lines. Dosing insulin + C peptide (a marker of endogenous insulin synthesis, helps flush out cheaters which take insulin small hidden - psychiatrist and hospital staff whose IDE + +)
Stopping all hypoglycemic drugs, whether oral anti diabetic stop and put on insulin.
Infusion G10%
Glucose monitoring every four hours + constants

If coma, but ditto sheave emergency hospitalization + / - measures to bedridden (preventing bedsores ...)

Diagnosis after treatment:
Diabetes = plasma glucose (not hair)> 1.26 g / l fasting on two samples at two different times, practice or> 2 g / l at any time day.
HBAIC monitoring (target <7%)
OGTT for etiological confirmation: functional or organic hypoglycemia (insulinoma + +)
I pass on all supported complications of diabetes.

Prevention: If the patient is diabetic.

Reversal of diabetes education:
-Measure's lifestyle modifications + + +: Sport 3x30/sem, balanced diet 5fruits vegetables / day, 50% carbohydrate, 30% lipid (1/3saturée, 1/3polyinsaturée, 1/3monoinsaturée) 20% protein, avoid erosion, three meals / day, avoid food's high glycemic index (soda. .) taken alone, avoiding alcohol (if + + + + metformin).

CAUTION: DO NOT ALLOW FOR FOOD! Everything is permitted but in moderation.

• Observance: Do not stop treatment, do not self medicate)
• Injection techniques: deep SC, change of the site to avoid lipodystrophy ...
• Information: about emergency situations, know the risk behavior, recognize the signs, note in his notebook the dextro and injections, tell the family measures glucagon injections if needed ...

And all associated measures: Reassurance, shrink if necessary, patient associations, multidisciplinary care, care in a network of care, PEC 100% ... etc .

Situations leading to the existence of an uncontrolled SIR, MODS or MOF is many. These are situations willingly "surgical," such as trauma, burns, acute pancreatitis or situations more avidly treated in medical ICUs such as infectious pneumonia, whatever its nature, sepsis and severe infections, septicemia, pneumonia inhalations. If during the first descriptions, multiple organ failure, was readily linked to infections, it currently seems possible to describe the table above in situations where the infection does not play a fundamental role (especially in trauma cases or pancreatitis). The pathophysiology of MODS is now based on knowledge gained over the last 5 to 10 years of inflammation. Multiple organ failure is a systemic inflammatory process uncontrolled reaction to aggression whatsoever. This process involves the whole body and each organ.

The inflammatory mediators involved in this situation are very numerous, are described in more than 60 currently. In recent years, multiple studies have clearly demonstrated the role of both local and systemic mediators. Such is the case of cytokines: TNF, interleukin 1, interleukin 6, interleukin 8, PAF. These molecules can promote the inflammatory response, both at the systemic and local levels. At the local level by allowing, in the expression of adhesion molecules, the interaction between endothelial cells and circulating blood cells: platelets and coagulation activation, leukocytes and activation of chemistry granulocytic behind the production of free radicals of oxygen. At the systemic level, these molecules can activate several cellular targets locally first are the macrophage system that can auto-active "cascade."

All clinical trials, usually grouped under the term "immunotherapy of sepsis," were intended to neutralize or modulate the biological effects of these mediators, whether of anti cytokine or anti-oxidants or the last endogenous mediator: NO.

Besides the mediators, the intestine appears to play a fundamental role in the maintenance and perpetuation of inflammation at the origin of MODS and multiple organ failure. Freshly, Vallet et al have clearly shown the deleterious effect of perfusion abnormalities or ischemia-reperfusion phenomena in the mucosa and submucosa of the bowel, when situations such as shock assault septic, hypovolemic shock, trauma or burn. Under these conditions, the intestinal bacteria that colonized the intestine may pass into the lymphatic and blood circulation making the phenomenon of "bacterial translocation," now formally demonstrated in several animal models and recently even in humans. Bacteria can be found in the mesenteric lymph, liver and spleen. Under such conditions, the release of bacteria and antigens such as endotoxins or exotoxins into the bloodstream or the lymph, is likely to maintain stimulation and secretion of pro-inflammatory mediators. The liver, which represents a significant barrier to these phenomena, due to the presence of the macrophage system consists of Kupffer cells (70% of the macrophage in the body sit in the liver) has the capacity to modulate and counteract this bacterial translocation, but when liver dysfunction appears, this ability appears to decrease. The pro-inflammatory cascade, bacterial translocation, the regional anomalies and / or visceral perfusion, impaired tissue extractions of oxygen are a set pathophysiological self-activating whose resultant is a growing expectation of each org donkey defining multiple organ failure.

PREVENTION
As in many other situations in medicine, prevention, rather than therapeutic care, SIRS or MODS of the MOF is preferable. Some fundamentals must be observed: rapid response and appropriate shock, preoperative assessment when this is feasible risk peri-and postoperative. Intraoperative monitoring of renal hemodynamic and acid-base functions, prevention of nosocomial infections and early postoperative peri, especially in patients at risk, that is to say, diabetes, immunocompromised or receiving corticosteroids. Close monitoring of respiratory function, prevention of atelectasis, pulmonary nosocomial infection control, prevention of aspiration pneumonia, adaptation and regulation of thin and narrow terms of ventilation, to prevent barotrauma and volutrauma. Digestive decontamination seems to be part of these preventive measures. It usually involves oral administration of antibiotics: tobramycin, polymixin, antifungal and sometimes vancomycin. However, prospective evaluation of this method has not shown a major role on mortality. This statement should be qualified overall; it seems that digestive decontamination can reduce the incidence of nosocomial pneumonia, certain subgroups of multicenter studies, involving a large and heterogeneous population of patients seem to benefit from such a technique, in particularly those suffering from trauma. Even though, to date, it seems difficult to reach consensus on the real interest of digestive decontamination in mechanically ventilated patients. Gastine et al clearly demonstrate the lack of interest in terms of morbidity and mortality of this technique in patients in intensive care. More than this technique, careful monitoring perioperative and postoperative determination of risk factors, the conditioning optimal preoperative patients, reduction of immunosuppression factors seemed to be the most effective prevention.

TREATMENT
Treatment should be the correction point by point the pathophysiological mechanisms at the origin of SIRS and MODS. In this sense, several chapters deserve to be studied: hemodynamic monitoring to optimize the transport of oxygen to tissues, control of sources of infections, metabolic media are the main modes of treatment of SIRS MODS or MOF. Optimization of oxygen transport is probably desirable, but it should not be accompanied by an excess of investment dependence as therapeutic oxygen consumption-oxygen transfer does not seem to represent the fundamental regulating the therapeutic. The main purpose is to ensure the delivery of oxygen, needed by the body, by increasing cardiac output, maintaining the number of hemoglobin above 10 g · 100 mL -1, maintaining a saturation arterial oxygen> 90% to meet the metabolic demand of the different viscera.

However, there is now unrealistic about specific optimize the delivery of oxygen to each organ, being unable to control the regional variations in traffic. The best outcome of the optimization of oxygen transfer probably depends even today on the assessment and development of blood lactate due to the mathematical relationship to the relationship. Calculated, it is hardly possible the present to rely on it to optimize treatment. Under these conditions, it seems necessary to proceed step by step, by increasing cardiac output by altering preload, afterload reduction, myocardial contractility by positive inotropic drugs, for the correction of anemia and the preservation of arterial oxygen saturation. These steps follow gradually, the evolution of the hyperkinetic syndrome usually encountered in these situations and to monitor treatment effects on parameters such as PaO 2 / FIO 2, serum creatinine, blood lactate, diuresis.

When the optimization of oxygen transport is performed, metabolic support should be made. The goal is to get a balance between catabolic and nutritional intake. Excessive intake of calories appears to be relatively deleterious. Carbohydrates should probably not exceed 5 g · kg -1 per day because of the risk of hepatic lipogenesis, excess production of CO 2 when this amount is exceeded. The intake of long chain fatty acids should not exceed 1 g · kg -1 per day. The administration of protein should be between 1.5 and 2 g · kg -1 per day. The use of preparations with high concentrations of amino acids to branched-chain appears to be effective in limiting the catabolism of the body. These formulas are particularly recommended in patients that eliminate over 10 g of nitrogen per day. The use of liquid-rich oil source of "fish," containing polyunsaturated fatty acids "omega-3," appear to reduce the production of prostaglandins and leukotrienes widely produced in situations of MODS. It seems that the system is to reduce the release of interleukin 1 and TNF. Fatty acids "omega-3," arginine and certain nucleotides were introduced into special formulas for enteral nutrition to provide nutritional support for situation's qualitative hyper metabolic of MODS. Very recent work appears to have shown clinical efficacy of these regimes (reduction of nosocomial infections, shorter stay inpatient intensive care unit) Nutritional support, both qualitatively and quantitatively, seems fundamental in the therapeutic management of MODS and MOF, not least from the standpoint immunological, protein intake to prevent the relative immune suppression observed during these situations. Where possible, food should always be practiced enteral: indeed, it allows, failing to provide the caloric amount sufficient to reduce the occurrence of infectious complications of parenteral nutrition. The diet should be started as soon as possible, that is to say, one or two days after the attack in the absence of cons-indication of surgical nature.

All nutritional formulas, including elements to increase immune function will be preferred. Indeed, recent studies show that these formulas shorten the stay of patients in intensive care unit. However, no support metabolic has so far proven to improve survival of patients with SIRS, MODS or MOF. Outside of respiratory support, assistance kidneys, hemofiltration, hemodialysis, hemodynamic monitoring and supports earlier metabolic, no specific therapy currently appears to provide an improvement in survival. It should, in contrast, day after day, to check if an infectious etiology is not responsible for the perpetuation of this state (e.g. drain an abscess, excision of an infected skin wound, verify the absence of pulmonary infection site, urine or other).

In situations of trauma, stabilization of fractures performed as quickly as possible seems to improve prognosis, since it allows early mobilization. In the presence of burns, excision of burned areas, and the rapid implementation of skin grafts are all therapeutic maneuvers to minimize the effects of tissue injury. Until now, new therapies and immunotherapy, in particular, have not proven their effectiveness in these situations. The introduction of monoclonal anti-endotoxin or anti-mediators (TNF, anti-PAF anti-IL1ra) have not proven their effectiveness. Other avenues of approach are being explored, inhibition or modulation of expression of adhesion proteins, using anti-inflammatory cytokines such as IL4 and IL10. The use of antioxidants to reduce the toxicity of metabolites of oxygen (catalase, vitamin E) have been the very limited success not allowing to formal advice. However, the safety, for example, vitamin E, appears to allow its use in the initial stages of acute lung injury. Prevention of nosocomial infections in these situations, hand washing, by a duly completed antibiotic policy in the intensive care unit, through the use of disposable equipment seem to be accountable for the prevention and treatment of these situations.

EVOLUTIONARY DESCRIPTION OF THE CONSTITUTION Multiorgan failure AND hypermetabolisms.

The normal body response to injury is now well-known and has a number of cardiovascular factors, particularly tachycardia, increased contractility and cardiac output, increased oxygen consumption under the influence the secretion of catecholamines. Neuroendocrine response also includes the secretion of catecholamines natural, that of cortisol, antidiuretic hormone, the growth hormone, glucagon and insulin. Coagulation is as well activated (activation of the complement system and fibrinolytic systems). Such a response is a physiological after an assault. The maximum response is usually obtained 2-5 days after the initial insult, and then decreases bit by bit from the 7th to 10th day. Gradually reducing the total-body water takes place by a cover of diuresis with decreasing temperature and decrease of the tachycardia. In the absence of clinical signs, should be particularly vigilant because the perpetuation of this inflammatory response, may intervene.

Indeed, a number of patients maintained beyond the 10th day, whatever the organic forms of assistance offered (artificial ventilation, etc.) tachycardia, tachypnea, fever and a hyper metabolic state. This behavior is particularly common after trauma or severe infections, or following a cardiac arrest when resuscitation maneuvers were inadequate or relatively late in their occurrence. The inflammatory response is then accompanied in most cases, respiratory failure within 24 to 72 hours after the initial event. The target lung in these situations "pure" (trauma or infection) is usually the first attack. The term "ALI" in Anglo-Saxon, that is to say, Acute Lung Injury, corresponding to an acute lung includes pathophysiological conditions ranging from mild impairment in respiratory distress syndrome of the (ARDS), first described by Ashbaugh in 1967. Today, most authors agree to consider that there is a continuum between the ALI and ARDS without that one can speak of an all-or-nothing phenomenon. It seems cons rather be a phenomenon gradually evolving from a simple pathophysiologic abnormality not clinically detectable until reaching very serious life-threatening ARDS.

Acute lung injury most often begins with an alteration of the pulmonary capillary endothelium. These cellular phenomena are due to a complex interaction involving platelets, neutrophils, endothelial cells, all mediated by numerous mediators, most prominently cytokines such as TNF, interleukin 1, interleukin 6, and interleukin-8, promoting the expression of adhesion molecules on endothelial cells. The catalytic activation of polynuclear leads to the production of proteases and oxygen-free radicals. Achieving the endothelial cell which follows, leading to an increased permeability of the alveolar-capillary membrane while allowing the passage of plasma water in the alveoli, the inflammatory cells and maintaining their own account the phenomenon interstitial and alveolar inflammation. This fluid influx and cell explain the discrepancies noted on the radiograph, and abnormal PaO 2 / FIO 2.

These pathological changes are indeed the cause of a disorder reports overall ventilation / perfusion leading to hypoxemia, decreased lung compliance. Unfortunately, these pulmonary pathophysiological changes occurring at a time when oxygen demand is increased, requiring a minute ventilation of 15 to 20 L · minimum -1, which asks the patient is unable to respond spontaneously, which led to the need use of mechanical ventilation.

If mortality from ARDS is only 50%, most often death occurs in a context not only hypoxemia, but develops gradually multiorgan dysfunction syndrome related to a secondary infection. The source of infection is most often represented by the lung, thus achieved.

After the onset of lung disease, two clinical evolutionary trends are usually recorded. The first type of evolution, which is the most common, is readily seen after trauma, burns or surgery. This evolution was described by Faist et al and Meakins as a two-stage evolution in which the first is represented by the lung and the second by the gradual development of SIRS, complicated then an encephalopathy, including hematological abnormality's leukopenia, DIC, and thrombocytopenia, gastrointestinal damage with gastrointestinal bleeding, abnormally prolonged ileus following abdominal surgery, pancreatitis or acalculous cholecystitis. There is parallel to a rapid deterioration of liver function and renal function and death usually occurs in an array of multiple organ failure between day 14 and day 21 after the assault on the body.

The second evolutionary scheme, rarely seen after trauma, but more readily stored in medical situation's assault (severe sepsis, septic shock or cardiogenic) is the development of a lung (ALI) and kidney but also almost concomitant liver, furthermore, a decrease in left ventricular contractile function, at best described by the association of hemodynamic measurements and transesophageal echocardiography. Death occurs usually a little faster around the 10th day, in an array of multiple organ failure very similar to the above-described scheme.

Along with this chronological description, and organ by organ multi-visceral disease, it is possible to record in all situations; metabolic activation is responsible for the increased demand and consumption of oxygen the body. This hypermetabolisms characteristic of all cases of SIRS, organ dysfunction or multiple organ failure is characterized, on the hemodynamic, a painting by hyperdynamic with tachycardia, increased cardiac output, fall in systemic vascular resistance and decreased arteriovenous difference.

These situations are often characterized by poor utilization of oxygen delivered to the tissue, either for reasons internal cellular mitochondrial, or for reasons of "shunt intraviscerale" performing infusion's luxury metabolically inefficient. The consequence of these phenomena is roughly appreciated by the elevation of blood lactate. Abnormalities of regional avascularization in this situation are probably largely the cause of changes in oxygen consumption calculated. However, other assumptions remain valid, such as adequacy of tissue perfusion and an inability to correct extract the tissue oxygen.

All in all, it is possible to record in this phase hyper metabolic syndrome of organ dysfunction, significant changes regarding the metabolism of carbohydrates. It seems that energy use glucose is decreased in parallel to a reduction in the activity of pyruvate dehydrogenase. Gluconeogenesis is strongly stimulated under the influence of catecholamines at the expense of amino acids, which explains the catabolism usually encountered in these patients. The final pathway of glucose metabolism is represented by hyperglycemia relatively insensitive to exogenous insulin. The elevation of serum lactate is directly related to the elevation of pyruvate, especially in all situations where there are perfusion abnormalities. Protein metabolism is also affected in all situations of SIRS and MODS. The amino acids then represent an important source of energy, they are from the catabolism of skeletal muscles and various organs. This situation hyper catabolism was thus described by the term auto-cannibalism. There is indeed, a total that increased protein catabolism, and this process is unfortunately slightly offset by the exogenous administration of amino acids.

In total, the catabolism of amino acids important carries a considerable production of urea. Parallel to the peripheral catabolism, there is an increase in hepatic protein synthesis, usually described by the term "Acute Phase Protein," however, this does not reach anabolism quantitatively the importance of catabolism, which can reach 15 to 20 g nitrogen per day. The exogenous administration of protein can promote the hepatic synthesis and provide a therapeutic target in either nutrition. Even so, when the worsening liver dysfunction, hepatic synthesis decreases significantly and most often associated with poor prognosis. Unlike situations of fasting, serum levels of ketone bodies are low in all situations of SIRS and MODS. The late stage of pre-mortem; organ dysfunction syndrome is usually accompanied by an increase in hepatic lipogenesis with a release of serum VLDL. Finally, triglyceride clearance decreases leading to an unpunctual stage of MODS, the appearance of hypertriglyceridemia. This situation of hypermetabolisms characteristic of organ dysfunction syndrome and multiple organ failure, are best described in patients subjected to therapeutic interventions and technical assistance to enable prolonged survival (mechanical ventilation, hemodialysis, hemofiltration, drug use and positive inotropic tonicardiaques). This metabolic pathway is a common often end after the assault. It differs significantly in its chronology according to two evolutionary trends that have been proposed.

Multiple organ failure

DEFINITIONS - TERMINOLOGY - CLASSIFICATION - SCORES
The multiple organ failure is a clinical, biological dating from 1970, but this concept already was raised by teams of gynecology and obstetrics in the 1940s. This "syndrome" is actually the result of the interaction of a disease or a primitive aggression of the body (trauma, infection, bruising, pancreatitis) and clinical transformation qu'imperilment evolving new therapeutic materials vital now available. A few years ago, during a state of severe shock, burns or trauma, the patient died in a very short time today the assistance ventilatory, circulatory, hemodialysis, hemodiafiltration, allowing prolonged survival in patients. It was during this period that is developing a biological and clinical entity that we are used to group together under the term multiorgan failure syndrome (MODS) (multiple organ failure syndrome in the Anglo-Saxon).

If literature was particularly abundant during the last 15 years of that entity, the definition of MODS and terminology of this syndrome are not very accurate. The term "failure" is an abnormal function of an organ, or more precisely to the abnormal expression of a clinical or biological parameter reflecting the functions of the body: ex. the serum creatinine is often referred to as "renal failure," the elevation of serum bilirubin, a "liver failure."

Recently, Marshall attempted to characterize the "dysfunction" or "failure" of a body in three ways:

1) by analyzing the degree of "abnormality" of a single functional parameter;
2) the existence of a combination of variables that "describe" a situation physiologically abnormal;
3) the need for therapeutic interventions to maintain function, e.g. dialysis.

In fact, the "ideal variable," allowing it to be the witness of organ dysfunction should be:
1) simple;
2) easily measured routinely, without error;
3) objective, independent of the clinical course;
4) a reflection of a real function of an organ;
5) little affected by transient disturbances related to resuscitation or therapeutic interventions General;
6) vary widely, even before an agonal or terminal stage;
7) a reflection of acute disturbance and not a chronic condition affecting the body;
8) be a continuous variable rather than discontinuous.

Consensus Conference conducted in the United States in 1991 attempts to distinguish the multiple organ dysfunction syndrome, sepsis, SIRS, the hypermetabolisms and introduced the term multiple organ dysfunction (MODS multiple organ dysfunction). Each term consists of fixed entities, but a clinical and biological state may evolve to produce a moving entity leading to multiple organ failure. Thus, it now seems preferable to speak of multiple organ dysfunction, a term more suited to the description of clinical and laboratory abnormalities observed after a significant stress to the body such as trauma, burns, infections, massive blood transfusions, pulmonary contusion or pancreatitis. Organ dysfunction actually covers broad physiological realities, ranging from complete failure of an organ, e.g. anuria in renal failure to a simple purely biological subclinical abnormality such as a relevant elevation of serum creatinine.

In fact, the notion of multiple organ failure has been established notably by Knauss in order to build a system aimed at better characterizing ICU patients, to assess the severity of their condition and the prognosis. Since these initial descriptions, several other definitions of organ failure have been proposed (see Table, I in Table IV ). None of the systems and none of the entities has proven to date of its superiority and its ability to describe for a specific patient's prognosis it according to the primary disease.

Table I. Definitions of organ failure (OSF)
1. Cardiovascular failure (presence of at least one of the following)
- Heart 54 b · min -1
- Mean Arterial Pressure 49 mmHg
- Ventricular tachycardia and / or ventricular fibrillation
- PH 7.24 with PaCO2 mmHg
2. Respiratory failure (presence of at least one of the following)
- Respiratory rate 5 or 49 c · min -1
- PaCO 2 50 mmHg
- 2 AaDO 350 mmHg (713 AaDO 2 = FIO 2 - PaCO 2 - PaCO 2)
- Ventilation at day 4 of organ failure
3. Renal failure (presence of at least one of the following criteria in patients without chronic renal failure)
- Diuresis 479 ml/24 h or 159 mL / 8 h
- Creatinine 3.5 mg/100 ml
4. Hematologic failure (presence of at least one of the following)
- Leukocytosis 1000 / m 3
- Plaquetttes 20 000 mm 3
- Hematocrit 20%
5. Neurological failure
- Score of Glasgow 6, in the absence of sedation

Table II. Definitions of organ failure
1. Cardiovascular failure
- Heart 54 b · min -1
- Mean Arterial Pressure 49 mmHg
- Ventricular tachycardia and / or ventricular fibrillation
- PH 7.24 with PaCO2 49 mmHg
2. Respiratory failure
- Respiratory rate 5 or 49 c · min -1
- PaCO 2 50 mmHg
- 2 AaDO 350 mmHg
- Ventilation at day 4 of organ failure
3. Renal failure (in patients without chronic renal failure)
- Diuresis 479 ml/24 h or 159 mL / 8 h
- Urea and 214 mg/100 mL
- Creatinine 3.5 mg/100 ml
4. Hematologic failure
- Leukocytosis 1000 / m 3
- Chips 20 000 mm 3
- Hematocrit 20% (in the absence of chronic renal failure)
5. Neurological failure
- Score of Glasgow 6 (in the absence of sedation)
6. Liver failure
- Acute clinical failure associated with P 0.66 100 mmHg
- Heart 50 b · min -1
- Ventricular tachycardia or ventricular fibrillation or cardiac arrest or myocardial infarction
2. Respiratory failure
- Respiratory rate 5 or 49 c · min -1
- Mechanical ventilation for at least 3 days or with FIO 2> 0.4 and PEEP> 5 cmH 2 O
3. Renal failure (in patients without chronic renal failure)
- Creatinine 280 m mol · L -1 (3.5 mg · dL)
- Purification extrarenal
4. Neurological failure
- GCS 6 (in the absence of sedation)
5. Hematologic failure
- Hematocrit 20%
- Leukocytosis 300/mm 3
- Chips 50 000/mm 3
- DIC
6. Liver failure
- Clinical jaundice or total bilirubin 51 m mol · L -1 (3 mg · dL -1)
- ALT> 2 ×
- Hepatic encephalopathy
7. Gastrointestinal failure
- Acute ulcer bleeding (requiring more than 2 units sanguines/24 pm)
- Acute pancreatitis haemorrhagic, acute acalculous cholecystitis, necrotizing enterocolitis,
gastrointestinal perforation

Table IV. Definitions of organ failure
1. Respiratory failure (at least one of the following)
- PaCO 2 <60 mmHg with FIO 2 = 0.21 - Artificial ventilation 2. Cardiovascular failure (at least one of the following criteria in the absence of hypovolemia) - Systolic blood pressure <90 mmHg with signs of peripheral hypoperfusion - Use of inotropic or vasopressor drugs to maintain systolic blood pressure> 90 mmHg
3. Renal failure (at least one of the following criteria in the absence of chronic renal failure)
- Serum creatinine> 300 m mol / L
- Urine output <500 ml/24 h or <180 mL / 8 h - Need for renal replacement therapy 4. Neurological failure (at least one of the following) - Score of Glasgow 6 (in the absence of sedation) - Acute onset of a delirium 5. Liver failure (at least one of the following) - Bilirubin> 100 m mol / L
- Alkaline phosphate> 3 ×
6. Hematologic failure (at least one of the following)
- Hematocrit 20%
- Leukocytosis <000/mm 3 2
- Platelets <40 000/mm 3

As shown in Tables I to IV, the definitions vary greatly from one author to another. And Knauss (Table I) does not include liver failure; Chang (Table II) uses the OSF Knauss taking into account liver failure. Tran (Table III) a special place in heart rhythm disturbances and gastrointestinal failure, whereas Fagon (Table IV) defines a different way from other authors, liver failure in a system failure; score body (ODIN). These four systems based on the presence of clinical and laboratory abnormalities affecting various vital systems (cardiovascular, respiratory, renal, hepatological hematological, neurological) through their differences, reveal much uncertainty that currently exists on the actual definition of 'organ failure and its prognostic significance. This results from the concept "syndromic" to this question: dysfunction syndrome or multiple organ failure or uni is a combination of parameters "deviant" clinical and laboratory findings occurring after very different pathophysiological processes. Therefore, the consequences of organ dysfunction on the prognosis of a patient are variable and are more useful in the analysis of targeted populations. Thus, the use of the concept of multiple organ failure or organ failure classification is put forward in a more "humanitarian and economic" as pathophysiologic: avoid excessive prolongation of the agony of patients accompanied with loss of dignity for them, suffering for the entourage and by dehumanization of "medicine" can be a purpose served by the established prognosis by the extent of organ failure.

In addition, an unnecessary prolongation of life, represents a considerable cost to zero profits, "expense" that could be used in a better way for other patients. To this end economic and humanitarian, some computer algorithms were developed to assess the "predictions" from the extent of organ failure coupled with severity ratings.

To refine this methodology, some recent publications have attempted to describe the syndrome of organ failure in targeted populations, e.g. in elderly trauma victims. In this population, validation of organ failure scores is significantly different and allows better management of these patients by defining multiple stages of organ failure: a pre-failure stage, a stage of failure compensated by assistance and a stage of decompensation beyond any therapeutic resource. In the same vein, recent studies have attempted to validate systems failure including "six bodies" in children.

In general, after all validations, seven organ failures are the organ dysfunction syndrome (respiratory failure, renal, hepatic, cardiovascular, hematologic, gastrointestinal, neurological). Each of these organ dysfunctions found in more than half of the published descriptions constitute the organ dysfunction syndrome.
The description of each of this organ failure is at best described by the variations attributed to a single variable reflecting a physiological abnormality, such as the PaO 2 / FIO 2 to the lung. This way of describing organ dysfunction seems better to variables using the nature of the therapeutic interventions necessary to maintain the function: e.g the use of mechanical ventilation or the use of a certain level of PEEP. The description by a single variable, also appears preferable to the combination of composite variables: e.g for ARDS, the association of hypoxemia with bilateral infiltrates on the chest radiographs in the absence of a rise in pulmonary capillary wedge pressure. Satisfactory and physiological markers corresponding to the criteria identified as necessary and sufficient for the description of organ dysfunction, are five in number, PaO 2 / FIO 2 to the respiratory system, elevation of serum creatinine for renal dysfunction, elevated serum bilirubin for hepatic dysfunction, platelet counts for hematologic dysfunction Glasgow Coma Score and for central nervous system dysfunction.
Markers to describe dysfunction of the cardiovascular system or the gastrointestinal system are not optimal. The five markers described above are validated and correlated with mortality in intensive care independently. Hypotension is relatively validated in terms of predicting mortality. Assessment of gastrointestinal dysfunction using a continuous marker has not been achieved to date. The combination of each of these variables increases the predictive power of mortality in a population of resuscitation. These descriptions, statistically validated, allow the use of organ dysfunction scores, based on these physiological parameters to assess for phases II and phase III, the efficacy of new treatments.

What is bowel infarction?
All tissues in the body depend on the continuous and stable supply of oxygen, and the oxygen is transported in the blood. If it gets too little blood, and thus as well brief oxygen to an area of ​​the body, developed signs of oxygen deficiency. This can result in loss of function or pain. If it becomes a full stop of the blood supply, it will cause the area received its supply of oxygen through the blood vessel dies. At the heart is called angina when blood supply is so small that it causes pain, and heart attack when blood flow stops completely a stop in a blood vessel to the brain leading to stroke, also known as stroke. If one of the major arteries to the intestine becomes clogged, a section of the intestine developed signs of oxygen deficiency, and eventually dies if you do not have time to deal with this quickly enough. This is known as intestinal infarction.

How frequently is this?
In contrast to myocardial infarction and ischemic stroke is the intestine a rare condition. The gut has a very good and diverse blood supply. If a vein is damaged, it is adjacent veins that can take over the job. Moreover, it appears that the artery of the intestine is more robust and resistant to atherosclerosis is the cause of diseases of the heart and brain. It might be because the gut trimmer many times a day?

Bowel Infarction occurs primarily in elderly people who are weakened by another disease, and who also have atherosclerosis disease in other parts of the body.

What are the symptoms?
The disease usually occurs with intense acute pain in the stomach. Nausea and vomiting accompany the pain, and after a relatively short time, there is bowel movement that is often bloody. In a few hours, this develops into a critical state with declining circulation and blood poisoning when bacteria spread from the intestines into the body.

Some may experience a less dramatic course of events, i.e. the blood vessels more gradually become clogged. In such cases, the pain in my stomach could come and go, and the cause can be difficult to prove. However, when one or more blood vessels eventually become completely closed, the disease gets the dramatic sequence as described above.

How is the disease?
This is a disease that requires urgent surgical treatment. At a surgery attempts to restore blood flow to the area that is damaged. If the condition persisted for more than a few hours, there is usually nothing to do but to remove the section of an intestine that has lost blood supply. This is fairly major surgery, and the danger of blood poisoning and congestion of the heart is large. In general, the faster the diagnosis is made and treatment can start, the better the prognosis. However, even with the greatest expertise available, this is an acute disease condition associated with high risk of death, perhaps as much as 50%.

The goal of treatment is the reconstruction of the aorta if there is a danger that it may burst, that is, if an aneurysm of the aorta is further than 5.5 cm. If the aneurysm has ruptured, emergency surgery will be needed to save the life of the patient.

The treatment is surgery that can be done either by unclosed surgery or by internal reinforcement of the hearth. At open surgery removed the damaged section of aorta and replace it with an artificial vein, called Vascular. Some aneurysms can be treated with an internal reinforcement (stent) is inserted from one or both groins. Any such treatment is dependent on aneurysm appearance, and the hospital's experience with the method.

Surgery is necessary in case of leakage or cracking of the aneurysm. Other reasons for surgery can be a pain, blockage in the ureters because of aneurysm, blood clot, resigned from the aneurysm. If the checks show that the aneurysm is growing (more than 1 cm per annum) or size of 5.5 cm, it is also the basis for operation. These are large and comprehensive interventions with high risk of complications. The following factors argue against surgical treatment due to complication risk: Heart attack last six months, heart failure, lung failure with breathlessness at rest, cancer with reduced life expectancy and renal failure.

Aneurysm of the aorta is at most a sign that blood vessels elsewhere in the body can be damaged by atherosclerosis. It is therefore, very important to slow the atherosclerosis process by whatever means available. This means that you have to stop smoking - this is crucial for the further development of the disease and to withstand an operation. Moreover, it is appropriate to cholesterol-lowering treatment, and careful blood pressure treatment to anyone with elevated blood pressure.

Is a limited expansion of the vessel partition of the aorta? The expansion is at least twice as wide as the nearest normal part of the vein. In practice, this means an extension of the main artery of more than three cm. Aneurysms can be shaped or coil-shaped bag.

The figures for incidence are uncertain. The incidence seems to increase, and it is probably hidden because of sudden death as a result of non-diagnosed aneurysms that burst in autopsy material available in bukdelen aneurysm of the aorta at 2-4% by the age of 50-60 years. The condition is four times as common in men than women.

What causes aortic aneurysms?
Atherosclerosis, which weakens the vessel wall, is the main cause. Risk factors for aneurysm is another blood disease, high blood pressure and smoking, family history of aneurysms of the aorta bukdelen; injury, inflammation, syphilis and connective tissue diseases are rare predisposing factors.

How aortic aneurysm diagnosed?
All aneurysms are typically symptom-free - unless they expand rapidly, or if they burst. Symptoms can sometimes arise from pressure on the surrounding structures: the abdominal aorta can cause spinal and intestinal pain, usually persistent. Chest section of the aorta can cause chest pain or symptoms caused by pressure on the esophagus, voiced cord nerve or the body's major samleare. There may be coughing blood as a result of compression of the trachea or bronchi (small airways) or hoarseness due to pressure on the left part of the vocal cord nerve.

Aneurysms in the groin and hamstrings can sometimes be known by the doctor. Aneurysm of the aorta can be detected as a random pulsating tumor in the abdomen. Fast-growing aneurysms can cause soreness in the stomach. Aneurysm of the thoracic portion of the aorta is most often incidental to findings on a radiograph of the chest.

Examination by ultrasound can show the size and extent of the aneurysm. In particular, aneurysms of the aorta appear well on ultrasound. The survey is used to control for monitoring any growth. CT (X-Drum) provides accurate measurements and shows the anatomy well, and is a significant alternative to ultrasound. It may also be relevant to X-ray examination with contrast of the aorta before any operation.

How are long-term prospects of aortic aneurysm?
An aortic aneurysm may be asymptomatic for life. Large aneurysms that expand, will eventually cause symptoms such as pain in the back / upper abdomen or symptoms caused by compression of the body hovedsamleare, esophagus or trachea. If the expansion continues, this will cause the aneurysm burst and sudden death.

Long-term outlook will depend on the aneurysm size and localization. Aneurysms of the aorta that is less than 5 cm, have little chance of rupture. Aneurysms are more than 7 cm, 3 of four cases of rupture within five years if one is not operated. An aneurysm operated gives life expectancy as the general population, provided that you do not have a concurrent cardiac disease.

A complication of an aneurysm is life-threatening bleeding, failure of blood supply to heart muscle, stroke, kidney failure and lack of blood supply to the bowel. Other complications include blood clots, infection of Vascular arrbrokk and Vascular leakage.

The aorta is the main artery extending from the heart. In the chest, cavity departs from arteries (arteries) to the head and arms; the abdominal cavity departs from arteries to the organs in the stomach. The aorta ends in the pelvis where it splits into two and goes down in each of the legs and changes its name to the iliac artery.

It's called aortal dissection when there is a tear in the aorta so that blood entering the wall of the blood vessel, and means that the inner layers of the vessel wall separate from the outer layer. The symptoms of aortic dissection are sudden, severe chest pain or abdominal pain. These come in seconds, and can radiate between the shoulder blades and back of the back.

It is 60-80 new cases of this complication every year.

What causes aortic dissection?
Aortic dissection caused by a weakness in hovedpulsarens wall. This can be inherited, be a result of atherosclerosis or damage caused by surgery or accidents. Blood flows into the blood vessel wall, and pushes its way along the vessel wall. This can cause the aorta burst, giving rise to a very serious and life-threatening bleeding. In the elderly it is most often atherosclerosis and high blood pressure that cause, among younger are inborn connective tissue diseases or congenital valvular error's more frequent causes.

Aortic dissection is a hyper-acute condition in which it is required with immediate admission to the hospital for treatment.

How is the diagnosis?
The diagnosis is suspected assuming the typical symptoms, and patients will be immediately admitted to a hospital. The condition can be confused with acute myocardial infarction, or not as much frequently with blood clots in the lungs in hospitals, the diagnosis by CT examinations, or so-called echocardiography or less by MRI.

How is the condition?
Treatment depends on where in the main artery dissection is done. Dissection of the first and the ascending portion of the aorta is most severe (so-called type A dissection) and is often sought surgery as quickly as possible. If there exists only dissection of the descending portion of the aorta, the results are best with conservative treatment, i.e., strict blood pressure treatment and monitoring and operation.

What is the prognosis?
Untreated the prognosis poor mortality is about 20% before the patient reaches the hospital, and approx. 30% during the hospital stay. If treatment is successful, it is found 10-year survival after discharge up to 60%.

Inside the hollow portion of bone is a spongy core called bone marrow. This is wherever stem cells are formed. Stem cells are undeveloped cells can build up hooked on components of blood: red blood cells bring oxygen approximately the body, white blood cells which exchange blow's infectivity, and platelets that facilitate blood to clog and discontinue minor bleeding.

Acute lymphoblastic leukemia is stem cell's cancer in the marrow bone that produces lymphocytes. The word "severe" means that cancer cells reproduce quickly and transfer the standard cells in the blood and marrow bone. In addition, as the number of diseased lymphocytes in the blood and bone marrow increases, it will be produced fewer red blood cells and platelets. If a marrow bone is incapable of generate sufficient healthy lymphocytes, the patient will not be proficient at fight infections.

Leukemia cells preserve to go with the spread metastasize or blood to further organs in the body where they can begin to create new tumors. Common symptoms of Acute lymphoblastic leukemia are persistent fever, fatigue, bleeding, bruising occurs easily, and enlarged lymph nodes.

Chemotherapy is the main treatment and aims to destroy the leukemia cells to normal cells can grow. Radiation therapy, biological therapy and bone marrow transplant may also be used if the chemotherapy does not produce the desired result. Acute lymphoblastic leukemia is the most common cancer among younger children. Luckily, ca. 80% of all children with Acute lymphoblastic leukemia healed.

Doctors and nurses will be your best informants if you or your child has acute lymphoblastic leukemia. It is important to discuss with your doctor who treatment is most suitable for you or your child.

The skeleton is the body's framework and also protects the internal organs. The hip joint carries most of the body weight. As a person's age, the bones become thinner and more fragile, increasing the risk of injury.

The hip joint is located in the pelvis. It connects the body (torso) with the legs and supports the weight of the body. The bones of the pelvis - the pubis, ischium and ileum - form a ball joint to the thigh bone, the femur, the body's longest legs. Injuries and age wear can damage the joint, which increases the risk of hip fractures and hip fractures. A hip fracture in most cases repaired with the insertion of an artificial hip joint.

During the operation, with the insertion of a new hip, hip socket cleaned of all cartilage and degenerative changes. A plastic cup sited in the inflated hip socket. The apex of the thigh bone is impassive, and a metal ball attached to the top of the leg. Metal ball attached to a short metal stem which is inserted into the marrow of the femur to make certain immovability to the prosthesis.

The patients and elderly patients with osteoporosis are at increased risk for hip fracture and may need hip replacement surgery. There are several potential complications associated with this procedure that should be discussed with your doctor before surgery.

What can I do?
The purpose of treating carotid stenosis is usually to prevent strokes and drips. Such preventive treatment should ideally begin in childhood, with a healthy diet, physical activity and no smoking.

However, it is never too late with these lifestyle changes. Even if you already have atherosclerosis, the risk to die or have serious heart disease can be greatly reduced if you make any changes.

Most important of all is to stop smoking. Stopping smoking will almost immediately reduce your risk, while having a number of other positive health consequences.

Diet is important and you should eat lots of fruits, vegetables and fish, while the fat content should be reduced. In particular, animal fats should be avoided. Animal fats found in meat, meat products and dairy products like cheese and whole milk.

You should also make sure to be physically active. Light and moderate intensity is sufficient, such as walking.

Good treatment of diabetes, high cholesterol and high blood pressure reduces the risk, and overweight can benefit from weight loss.

Eczema is a skin disease that affects more and more children in families predisposed to allergy. Several studies show that eczema is due in part to advances in medicine, with advances in vaccines and vaccines, antibiotics, and then simply hygiene, have protected the child against many infectious diseases. However, at the same time, these improvements have altered the immune system. The emergence of new allergens and pollution are also implicated in increasing eczema.

The first outbreak of eczema usually occurs within three months. In infants, lesions are mainly at the scalp, face, neck, arms and legs. A topic dermatitis or eczema, is particularly rife in the first year of life. It often improves around the age of two to three years, with lesions localized mainly in the folds of the elbows and knees, then usually disappears during childhood. However, some children were still minute dry patches that can also persist until puberty. In general, the eczema flare evolves in stages: at first, appear to itch subsequently the skin becomes red and dotted with small vesicles barely visible, while giving a grainy appearance. Then the vesicles swell, causing a scratching which causes the rupture of these short blisters with oozing more or less important. The last phase of the thrust is that scabs who fall within a few days and leave the skin red before healing of the eczema flare. In all cases, the child's skin is always dry even outside attacks.

Currently, there is no way to effective prevent eczema. In families at risk, we advise mothers to breastfeed their babies, or if they cannot or do not wish, to feed him with a hypoallergenic milk and does not start food diversification before the fifth month. Eczema is a chronic disease, and no physician can make it disappear. However, we can reduce the number and intensity of relapses and the child to relieve suffering minimized.

In case of eczema flare, treatment relies on creams or ointments containing cortisone. Topical corticosteroids are necessary to treat eczema: they reduce inflammation and allow the skin to recover. Feel free to apply sufficient cream from the start, then you can space out the application as an improvement alternating with cream sanitizer based on copper or zinc. If super infection occurs frequently due to scratching, antibiotics may be prescribed. In addition to standard therapy against eczema, do not forget the emollient creams. They apply alternating with topical corticosteroids (morning or evening) on ​​areas less red. If contemporary corticosteroids were used correctly, three-quarters of a topic dermatitis resistant no longer exist. In rare cases, eczema is very severe.

Definition
Eczema is a noncontiguous skin disease-forming or red placards to an ill-defined edge.

Clinical signs

• Inflammation
• Desquamation of the skin
• Redness
• Blisters

Contact eczema

The contact dermatitis follows the skin contact with a product.

It occurs in two steps:

• Awareness
• The skin reaction

• Adrenocorticoid
• Eviction of the contact

Atopic eczema
Atopic eczema or atopic dermatitis, eczema is hereditary and is linked to colds or asthma.

Treatment

• Drought prevention: no bath, cotton clothes, moisturizer
• Eviction allergens: dust mite, ventilated room at room temperature
• Adrenocorticoid
• Antihistamine for itching

Should the condition be treated?
Many have no symptoms or symptoms of carotid stenosis Although these patients with asymptomatic carotid stenosis have an increased risk of strokes and drips, so the research does not show any convincing benefit from surgical intervention in these.

Blood-thinning medications, known as acetylsalicylic acid (e.g. Albyl-E ®) reduces the risk of such as stroke and TIA. Most people with carotid stenosis should use these drugs for life.

People with high cholesterol may benefit from cholesterol-lowering drugs, particularly so-called statins (e.g. simvastatin).

In sum, mainly those with significant tightening and clear symptoms and signs of narrow veins, it may be appropriate surgical treatment. Such operations usually occur when the surgeon removes plaques inside the artery (endarterectomy), or by a short tube inserted and prevents the area quickly becomes clogged again (stenting).

In patients who have had a drip (TIA) as a result of narrow Halske, it seems that early intervention - within two weeks - gives better results than later intervention. Several experts have called for prompt surgical treatment even at a stroke, provided that the patient is stable and have limited neurological outcome. Rapid and effective diagnosis and treatment of these patients are important. There are some significant discrepancies in treatment practices, which highlight the need for clearer guidelines for the surgical treatment of carotid stenosis.

The most important preventative treatment, however, you do yourself.

Vitiligo Treatment can be aimed at restoring the normal pigment or destroying the pigments. To restore function of the skin and improve appearance of the person, Vitiligo is manageable though; today, many ways to change the appearance of vitiligo without addressing its underlying causes. Treatment options may include the following:

• Exposure to intense ultraviolet light UVB therapy, for example
• Drugs administered orally, for example, trimethylpsoralen
• Medicines applied to the skin as creams, corticosteroids, immunosuppressants or repigmenting.

The skin may be inserted or removed from normal areas and placed in the areas of vitiligo. In the future, the pigment cells of the skin can be cultured in the laboratory and used for the treatment of stakeholders. Mild cases, vitiligo pale marks that obscure products or other cosmetic camouflage solutions to be hidden. Affected person is pale - skin, if necessary, avoid the sun, the patches can be made less visible. However, sun exposure can also play the pigmented melanocytes.

Vitiligo is a disease with complex causes. People with vitiligo seem to inherit a genetic predisposition toward the disease. The disease can be caused by a variety of precipitating causes. Many people report that their vitiligo first appeared to follow a traumatic event or stressor. The main symptom is the loss of skin color. The hair that grows in the affected areas also lacks color. In addition, individuals may have alterations of the pigment of the retina or the iris of the eye. Once diagnosed, the treatment of vitiligo is necessary. It's important to fight other diseases causing the Vitiligo.

The extreme cases of vitiligo can be unattractive and may affect the prognosis of an individual and social interaction. Sometimes the best treatment for this disease is available to all special treatments. Skinned people should avoid tanning of normal skin as white skin without pigment vitiligo has no natural protection against the sun. Therefore, these areas are easily sunburn, and patients have an increased risk of skin cancer. Avoid the sun as much as possible, especially when it is most intense to avoid burns.

Makeup, skin self-compounds or dyes is a simple way of disguising vitiligo is less significant. It can be used to reveal areas of white beauty elegance. The use of sunscreen is not the burning of the affected areas. Multangulum skin and oral medications are available for more severe cases. These pieces may have unwanted side effects when selected to ensure that multangulum. The sunscreens and cover - ups are not satisfactory, consult your doctor can recommend treatment to others.

Autologous transplantation, depigmentation of the skin and repigmentació therapies were other options are severely affected. However, the treatment of choice for white light / depends on the number of sites and their dispersion. It is recommended to treat this patient preference. Everyone responds differently to treatment of vitiligo, and a particular treatment does not work for everyone. These treatments can be used in conjunction with medical or operative treatment current treatment options for Vitiligo medicinal, surgical, and there are other therapies.

For some patients with severe cases, treatment for vitiligo is more practical to remove the residual pigmentation of normal skin. This makes the body color of a white solid. On the other hand, some people with this disorder to opt for depigmentation of chemistry. It's made by a chemical called hydroquinone monobenzylether and lasts over a year to complete. This process is irreversible and generally ends with concluded or nearly complete depigmentation. In children, treatment of vitiligo is usually done through the proposed protection measures and solar cover.

Repigmentació therapy is done through topical corticosteroids. Creams containing corticosteroid compounds can be effective in returning pigment to small areas of affected skin. These agents can weaken the skin and therefore, should be used for the supervision of a dermatologist. Treatment of Vitiligo also should pay attention to psychological well-being of the person.

People with vitiligo are in no doubt to stumble on the best treatment of vitiligo in our world herbal cure vitiligo oil useful for fighting disease and Vitiligo. Cure Vitiligo Oil guaranteed 100% clinically confirmed enduring treatment for both brands Leukoderma and vitiligo. This is a special herbal formula designed to contain the Coconut Oil, Root Berbers, psoralea corylifolia, and black cumin these herbs collectively in a fixed quantity of that defeat and cure vitiligo. Of Cure Vitiligo, Oil comprises solely of herbs, so you have less or no side effects.

Question and Answer Vitiligo

A: The choice of treatment depends on the type of vitiligo patients who would have preferred. In our time, when awareness is widespread, it is assumed that patients know that not all treatments work for them, and some of them may or may not work for a particular patient. Any choice of treatment should be done in consultation with the doctor. Regarding the cost of treatment is concerned, can vary from $ 100s of dollars for a few dollars. Furthermore, in this case is absolutely necessary to make a careful selection. Below are resources available for Vitiligo / Leukoderma, topical steroid therapy, homeopathic therapy, ayurvedic, herbal therapy, surgical therapy.

Q: What is the best treatment for vitiligo?
A: The best remedy for the vitiligo patients is a better choice for him. The vitiligo cannot be left or roots, but the white spots of vitiligo can be delivered according to a series of treatments available. Below is a list of attainable treatments, therapy with topical steroids, homeopathic therapy, ayurvedic, herbal therapy, surgical therapy.

Q: How does vitiligo herbal treatment?
A: herbal treatments always instinctively by the human body as it is made from natural ingredients. Nature has a hidden treasure of herbs; the value has been identified. The ancient Egyptians and Chinese have used herbs to treat many diseases. Herbal treatment of diseases has contributed to medical science in many ways. When science cannot provide a cure for a disease herb are solving our problems. Cure Vitiligo Oil is a pure herbal product that is a blend of natural ingredients, false buckthorn root, coconut oil, black cumin and Psoralea coryfolia. Root false buckthorn and cumin stimulate the immune system as it is considered an autoimmune disease vitiligo. Coryliforlia Psoralea is a photosensitized agent increases the effect of tanning. Coconut oil acts as an agent for softening and smoothing. The combination of these four ingredients in a way that a product is herbal Cure Vitiligo Oil does wonders for the skin. The product eliminates the white spots of vitiligo. It is a clinically proven and guaranteed success.

Q: What is the appearance of vitiligo? Who is more likely to suffer, men or women or children?
R: Vitiligo is characterized by the appearance of white patches of the skin. These spots appear when the melanocytes that produce melanin (the cells of these cells are present naturally in the skin produce melanin which is brown-black pigment that normally determines skin color) are destroyed. How exactly these melanocytes are destroyed; Noy's science has been able to give a direct answer, because this disease is very little known. Many causal factors have been proposed from which the disorder Autoimmue seems more plausible. About this theory, an autoimmune reaction against melanocytes is encouraged both his body and destroyed or made dysfunctional. As an outcome the melanocytes discontinue sustained melanin and an attribute white patch of vitiligo appears this exacting area on the body. Vitiligo is a rare disease on the skin. It affects only 1 to 2% of the world today. It affects both sexes and all races. It can happen to anyone, whether men or women or children. People with vitiligo are prone to give birth to children with vitiligo, vitiligo, but by itself is not genetic. For most patients, patches occur in approximately 40 year of their lives, and the patches can spread slowly.

Carotid stenosis is common incidental findings when the doctor listens to the neck vessels with a stethoscope. The doctor can then listen to "trick" of blood that passes the narrow site. Listening to the neck vessels, however, says little about the extent of the lost no mention, and it may be desirable to do an ultrasound (color Doppler ultrasound) to get a better picture of it.

Other times you get suspected condition only when there is a stroke or repeated drip (TIA) ultrasound of neck vessels as part of the report. Patients with carotid stenosis are at increased risk of stroke shortly after TIA, and should therefore be investigated within a short time (less than two weeks).

Sometimes, usually in advance of the operation, is made ​​known as angiography. This is a survey, taking X-ray film of the neck, while the injected contrast fluid in blood vessels.

Contrast fluid will not pass through X-rays, so that the outline of the neck vessels produced by X-ray film. This makes it easier to judge. How much is narrowing?

Most people have no symptoms of carotid stenosis (it is asymptomatic). Many do not they have the condition, or it can be found randomly by medical examination. These individuals tend elevated risk of drips and stroke later.

People who have already had the drip or stroke once, have a higher risk of recurrence.

Stroke and the drip can take in many ways. So-called TIA-attack is brief (lasting less than 24 hours), and the symptoms go to way back. At the stroke can result in permanent damage. Common symptoms include weakness strength, temporary blindness, loss of sensing ability, difficulty speaking, sudden dizziness, fainting or balance.

Often, only one of these symptoms are present.

Calcification of Halske (carotid stenosis)

What causes carotid stenosis?
Calcification ( hardening of the arteries ) in Halske due to fatty deposits on the inside of the vessels that carry oxygen-rich blood to the brain. Such fatty deposits called an aterom. A plaque is a major aterom mass. The development of a plaque starts with cholesterol "dig" into the wall of the vein. The body tries to repair this damage, the formation of scar tissue that makes the vessel wall thicker and stiffer and the blood vessels narrower. As more cholesterol is deposited, the vessel walls thicken and blood flow inside the vessel is reduced further. This is known in medical terminology for atherosclerosis.

What causes atherosclerosis?
A certain degree of atherosclerosis is very common among people in nearly everyone Western countries, although the incidence varies. In most development begins as early as the age of 20, and increases with age. Atherosclerosis is the main cause of many cardiovascular diseases, including heart attacks, angina and stroke.

Although atherosclerosis, to a degree, is a natural part of aging process, there are several factors that may have calcification to go significantly faster. Many of these things can greatly affect themselves.

Smoking is one of the main causes of atherosclerosis. In smoking starts earlier calcification, occurs much faster and have more serious consequences than in non-smokers.

Person with high-fat content in the blood is more prone to atherosclerosis. This is especially stout in the form of cholesterol. Blood fat content is influenced, to some extent, by the food we eat, but also genetic factors are important.

Other risk factors include being male, female after menopause, have diabetes or high blood pressure.

How is the diagnosis?
It can be very difficult to distinguish this disease from atherosclerosis disease. Atherosclerosis, however, most often affects people over 40 years. Complaint at Burgers disease is also clearly more prominent in the feet and hands than the usual atherosclerosis. Moreover, we can get help from the relatively typical medical history, with inflammation in superficial veins in the early stages. If you are referred to a specialist in vein disease, it will be necessary to do ultrasound and possibly X-ray of your arteries to identify the disease as feasible.

What is the treatment?

Self-Treatment
The only really effective measure for this disease is smoking cessation. If you do not stop smoking, the disease always gets worse even if you get different treatment. Furthermore, avoid tight footwear can prevent circulation. It pays to keep your feet warm for the cold pulls the blood vessels together. You should avoid medications that can cause the blood vessels to constrict, such as migraine medications and beta blockers in hypertension. Check with your doctor if you have questions. A good advice is also to go for a walk of 15-30 minutes each day, because exercise improves circulation in the legs (forming more blood vessels). If you have problems with your feet, making it difficult for you to go, it can be customized insoles and footwear to ease symptoms. To help the blood circulation in the legs at night it is wise to raise the head end to the bed by 20-30 centimeters. The bed rest should especially heel protected from pressure damage by bandages or padding foam.

Another treatment
There are medications that can expand the blood vessels thereby improving blood circulation unfortunately, the effects from these medications uncertain and variable. Some patients will still be able to have some benefit from such drugs.

The surgical options are relatively limited, because this is a disease that primarily affects small blood vessels.

The conclusion is that the best treatment. We have is smoking cessation.

What is the treatment?
The main goal of treatment is to get the patient out of the destructive phase of illness and into a good phase (remission) and to prevent organ damage.

The treatment can be roughly divided into three phases:

• Induction of remission
• Maintenance Treatment
• Relapse Treatment

Severity and extent share the patients into three groups:

• It localized or early disease.
• Generalized disease with threatening organ damage
• Severe and life-threatening illness

The drug treatment usually consists of a combination of corticosteroids and chemotherapy (e.g., methotrexate and cyclophosphamide). After an intensive treatment period of 3-6 months (induction of remission) escalating doses down and continue with maintenance therapy. It often lasts for up to 24 months, but in some cases, it lasts longer and rarely is life-long treatment is required. New, so-called biological therapies, have been shown to give good results in cases where the ordinary treatment fails.

What is calcification of Halske?

Calcification of Halske (carotid stenosis) is a relatively common condition in older people. The disease occurs when calcium deposits from sticking through the wall of the neck vessels and makes them narrower.

Carotid stenosis occurs primarily in older people. About 10% of 80-year-olds have the condition. Most people have no symptoms or symptoms, and we call this asymptomatic carotid stenosis occasionally minute piece of plaque loose and follow the flow of blood to the brain. This could cause a small drip or stroke.

This is called asymptomatic carotid stenosis. The condition occurs most commonly in people who also have calcification in blood vessels elsewhere in the body.

It is estimated that around. 20% of all cerebral infarcts - the most common type of stroke - caused by blood clots from the carotid arteries.

What are the symptoms?
In its early stages, it is common inflammation of the superficial veins from the arms or legs. The signs of these are redness and soreness of the skin over the inflamed vein. These changes usually return within 2-3 weeks, but the skin afterwards we can see increased pigmentation; that is, the darker spots. Because of the mild symptoms are often overlooked condition of both patient and physician.

Later in the course you get symptoms of poor blood circulation, usually in the legs' periodic pain in feet and possible attach the walk is typical. The pain continues when a halt. Other symptoms of poor blood circulation are coldness, pallor, numbness, tingling or burning sensation.

As the disease worsens pain will become more frequent and more prolonged, and eventually you will have pain in the legs even at rest. In severe cases, one can see the wound (which is difficult to grow), and gangrene as a result of poor circulation.

Burgers disease is also called thromboangiitis obliterans, which means inflammation that clogs the arteries. This disease is characterized by persistent or recurrent inflammation of the small and medium-sized blood vessels. This leads to contractions and blood clots and prevents blood supply, especially to the legs. It is not the same as atherosclerosis, although symptoms can be similar.

What is the reason?
We do not know the exact cause of the disease, but there is a clear correlation with smoking.

Who is affected?
It affects only people who smoke. In northern Europe, the disease is rare in southern Europe it is more frequent. Burgers disease less than 1% of those referred to a specialist because of poor blood circulation. 95% of patients are men, and the disease onset usually before 40 years of age.

How are long-term prospects?
If you stop smoking right away, the prospects are good! If you continue to smoke, there is the great risk that you will end up having to amputate parts of the arms or legs due to gangrene.

Laboratory tests are important to determine which organs are involved, to rule out other diseases and to monitor disease and treatment over time.

Often is an increased number of white blood cells (leukocytosis), low blood count (anemia) and low platelet count (thrombocytopenia). Since the medications used to treat the condition, can inhibit the production of blood cells, it is important to check these blood values ​​during treatment or soon to be able to reveal that there is no bone marrow suppression.

Furthermore, blood erythrocyte sedimentation rate (ESR) and CRP are usually elevated, but non-specific samples and elevations may occur with many other diseases.

Disease must be followed with measurements of blood tests that show kidney function and liver function, since these are the organs that can be affected by the disease.

Antibody samples are important to clarify the vascular disease / vasculitis exists. It's about so-called ANCA tests (ANCA = cytoplasmics antibodies antineutrophil).

Scientists know little about the disease, but the various blood vessel inflammation caused the formation of antibodies that attack the body's own tissues, so-called autoimmune diseases. The result is blocked blood vessels and circulatory failure to the tissues that receive blood supply from their waited years. This can lead to bleed in the surrounding tissues and in some cases, impaired vascular development of ballooning of the blood vessels, aneurysms.

What is the prognosis?
Patients with widespread vascular inflammation (systemic vasculitis) are at increased risk for other diseases as a result of injuries from the underlying disease and the aggressive treatment. Serious side effects may occur especially in the first year of treatment.

Many patients with vasculitis will have a relatively benign, self-limiting illness - especially if the disease is confined to the skin. Patients with aggressive disease, ANCA-associated vasculitis smakar must start treatment as soon as possible to ensure a better prognosis. New treatments have improved the prognosis of vasculitis.

A distinction is made between 10 different types of vasculitis. Most occur in small blood vessels, fewer found in the larger blood vessels.

Small vessels


Churg-Strauss syndrome
An infection that primarily occurs in the airways and is associated with asthma. The inflammation is found in small to medium-sized vessels.

Cutaneous leukocytoclastic angiitt
A condition found only in the skin, and that is not spread around the body or in the kidneys.

Essential cryoglobulin misk vasculitis
An inflammation that affects the smallest blood vessels: capillaries, venules or arterioles. It attacks the very skin and kidneys.

Henoch-Schonlein purpura
The immune substances affecting capillaries, venules or arterioles. The disease typically attacks the skin, intestines and kidneys, but it also has joint pain or arthritis. The condition occurs in children.

Microscopic polyangiitis
Inflammation and destruction of capillaries, venules, or arterioles, but also small and medium-sized arteries may be approached. Severe kidney inflammation (necrotizing glomerulonephritis) is very common.

Wegener's granulomatosis
Inflammation of the airways and damage to capillaries, venules, arterioles and arteries. Severe kidney infection is common.

Medium-sized vessels

Kawasaki disease
Inflammation of the arterial wall, especially in the cardiac coronary arteries, but also the main artery (aorta) and veins may be involved. It occurs in young children.

Polyarteritis nodosa
A severe inflammation of the wall to the medium to small arteries without kidney damage or vasculitis in arterioles, capillaries and venules.

Large vessels


Giant cell arteritis
Inflammation of the aorta and its major branches. Especially frequent is the temporal artery the attack (temporalisarteritt), a condition associated with polymyalgia rheumatic.

Takayasu arteritis
Inflammation of the aorta and its major branches.