Differential diagnosis of hepatobilliary and pancreatic diseases in children.

Emergency aid at acute liver failure.

 

                   

The liver is the largest digestive gland. It is involved in metabolic processes, the accumulation of various substances, the development of bile, promotes digestion of fats.

                This organ plays a major role in metabolism and has a number of functions

in the body, including glycogen storage, decomposition of red blood cells, plasma protein synthesis, hormone production, and detoxification. It lies below the diaphragm in the thoracic region of the abdomen. It produces bile, an alkaline compound which aids in digestion, via the emulsification of lipids. It also performs and regulates a wide variety of high-volume biochemical reactions requiring highly specialized tissues, including the synthesis and breakdown of small and complex molecules, many of which are necessary for normal vital functions.

 

                                                                                                    

 

                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                        

     

                                       Synthesis

ü Proteins are produced and secreted by the liver

                               A large part of amino acid synthesis

ü The liver performs several roles in carbohydrate metabolism:

§  Gluconeogenesis (the synthesis of glucose from certain amino acids, lactate or glycerol). Note that humans and some other mammals cannot synthesize glucose from glycerol.

§  Glycogenolysis (the breakdown of glycogen into glucose)

§  Glycogenesis (the formation of glycogen from glucose)(muscle tissues can also do this)

ü The liver is responsible for the mainstay of protein metabolism, synthesis as well as degradation.

ü The liver also performs several roles in lipid metabolism:

§  Cholesterol synthesis

§  Lipogenesis, the production of triglycerides (fats).

ü The liver produces coagulation factors I (fibrinogen), II (prothrombin), V, VII, IX, X and XI, as well as protein C, protein S and antithrombin.

ü In the first trimester fetus, the liver is the main site of red blood cell production. By the 32nd week of gestation, the bone marrow has almost completely taken over that task.

ü The liver produces and excretes bile (a yellowish liquid) required for emulsifying fats. Some of the bile drains directly into the duodenum, and some is stored in the gallbladder.

ü The liver also produces insulin-like growth factor 1 (IGF-1), a polypeptide protein hormone that plays an important role in childhood growth and continues to have anabolic effects in adults.

ü The liver is a major site of thrombopoietin production. Thrombopoietin is a glycoprotein hormone that regulates the production of platelets by the bone marrow.

 

 

              

 

                          Biliary Dyskinesia

 

               Gallbladder disease that occurs without gallstones is called biliary dyskinesia or acalculous gallbladder disease. It can be acute (arising suddenly, often as a one-time occurrence) or chronic (persistent, recurrent). Acute acalculous gallbladder disease usually occurs in patients who are very ill from other disorders. Chronic acalculous gallbladder disease may be caused by dysfunctional muscle or valve defects that impair the gallbladder’s ability to contract and release bile.

 

                        The term biliary dyskinesia refers to abnormal gallbladder function characterized by right upper quadrant abdominal pain (sometimes radiating to the upper back or shoulder blades) after eating fatty or fried foods, heavy meals with nausea/vomiting or bloating, followed by loosening of stools. The excess build up of pressure in the bile ducts is thought to be responsible for these typical gallbladder symptoms. Like gallstone disease, billiary dyskinesia is much more common in girls.

              

 

 

                                                   Etiology

                  Factors leading to biliary dyskinesia (BDK):

– Neurocirculatory dysfunction of various origins

– Deferred acute viral hepatitis

– Constitutional characteristics of the child with vegetative dystonia and

 – Neurosis

– Food allergy, atopic diathesis

– Any chronic pathology of the gastrointestinal tract (especially inflammatory)

– Parasitosis of gastrointestinal tract

– Genetic predisposition

– Chronic foci of infection in the body

– Poisoning, ecopathology, prolonged abuse of industrial food products

– Endocrine diseases (obesity, hyperthyroidism, diabetes mellitus)

                                Predisposing factors

 

                The main predisposing factors in the development of BD are: inadequate regulatory mechanisms, and innervation of the nervous system, which is characteristic of childhood, caused by hereditary high excitability and lability of the nervous system, characterized by its violation of the tone of the autonomic component and muscular weakness.

                     Leading role in the pathogenesis of BD has vegetoneurosis, leading to reductions discoordination gall bladder and sphincter apparatus. The second mechanism of BD is hormonal. In the regulation of bile intestinal hormones play an important role, among which there are both stimulating (cholecystokinin etc.) and inhibitory (glucagon, etc.), the contractile function of the gallbladder. Adverse factors affecting the autonomic nervous system and hormonal regulation, lead to impaired motor function and changes in physico-chemical and bacteriostatic properties of bile.

                   Depending on the origin of BD two types – primary and secondary are distinguished. Primary dyskinetic violation occurs due to the development of  neurohumoral regulation of the biliary system. In this regard, the primary BD often occur in children with a variety of somatoform disorders, or more familiar to our doctors, neurosis, vegetative-vascular dysfunction, diencephalic syndrome, psychosomatic syndrome in children with neuro-arthritic constitution anomaly. Important role in the development of primary BD is a violation of diet: long intervals between meals, overeating, force-feeding, abuses of oily or spicy food. Risk factors are also transferred acute infection (viral hepatitis, dysentery, salmonellosis), allergic diseases (allergic rhinitis, obstructive bronchitis, atopic dermatitis).

                      The development of secondary BD is the type of viscero-visceral reflexes in pathological states of digestive organs. As a rule, secondary dyskinetic is caused by chronic cholangitis, chronic duodenitis, chronic enterocolitis, helminthic infestation. Of particular importance is giardiasis (zhiardiaz) of the small intestine. Giardia in the mucosa of the duodenum attach to the microvilli, causing pronounced dystrophic changes in the epithelium.         

 

 

                                        Pathogenesis

 

                                 The idea that dyskinesias of the gallbladder are a purely functional disorders is currently under review. Not only hypomotoric, but even hypermotoric forms of dyskinesias occur at the level of organic changes of hepatocytes, which is a kind of primary factor contributing to the disruption of not only internal but also extrahepatic biliary tract, including the gallbladder. This pathology is a certain type of cholestasis. However, it does not exclude the role of vascular (neuro) dystonia in the development of dyskinesias of biliary system. So, two main factors lead to motility disorders:

1. Violation of the functional state of hepatocytes and disholiya (changing composition of bile)

2. Violation of neurogenic regulation of the muscular wall of GB as the central (neurocirculatory dysfunction, neurosis) and peripheral (in the pathology of the gastrointestinal tract-type viscero-visceral reflexes) genesis.

                         At the same time it is estimated that the BD may be caused by the violation of enteral secretion of hormones (cholecystokinin, motilin, and others) at chronic pathology of duodenal and small intestine. Changes of the rhythm of bile proceed in the intestine reduces the bactericidal properties of the upper gastrointestinal tract, leading to dysbiosis, intestinal dyskinesia. Long-lasting dyskinesia, causing congestion and infection of bile, throw intestinal contents in gall bladder (reflux) leads to cholecystitis. With the predominance of sympatic tone of the nervous system of patients hypotonic dyskinesia is characterized (80% of dyskinesias), with parasympatic – hypertensive.

 

                   

 

                          Different variants of sphincter of Oddi structure

 

                 

 

 

 

                                                                                                     

      

Classification

n  hypertonic-hyperkinetic dyskinesia

n  hypotonic-hypokinetic dyskinesia

 

Clinical manifestation of hypertonic-hyperkinetic dyskinesia

 

n  Duration of the disease up to 1 yr.

n  Pain syndrome

n  Dyspeptic syndrome

n  Manifestations of vegetative dysfunction, neurotic symptoms

 

Clinical manifestation of hypotonic-hypokinetic dyskinesia

 

n  Pain syndrome

n  Dyspeptic syndrome

n  Hepatomegaly

n  Gallbladder symptoms are positive

The clinic is determined by the type of dyskinesias. Most patients have symptoms of neurosis: fatigue, irritability, tearfulness, temper, headaches, palpitations, sweating. In addition, children complained of pain in the right hypochondrium, epigastrium.

                        In hypertensive form of BD children complain of paroxysmal, stabbing pain in the right hypochondrium or in the right side. Young children show umbilical area. Very rarely pain irradiates in right shoulder and shoulder blade.

The typical symptom of this state is a sharp pain in the right side during fast running or walking fast, due to additional stretching of the capsule and without an enlarged liver with increased inflow of venous blood. Particularly obvious symptom of this is manifested in physical education classes or training, while mobile games, dancing, after the errors in the diet, emotional stress.

The pain is of short duration, easily relieved by antispasmolitics. During the attack the patient may be exited, he suffers nausea, rarely vomiting, palpitations, headache, polyuria. On palpation the abdomen during the attack and after the pain is the most pronounced at the point of the projection of the gall bladder (a symptom of Kera). Outside of acute attack palpation is not painful or there is little pain sensitivity in the right hypochondrium. The liver is not enlarged. The phenomena of intoxication if they are expressed are due to major illness. In the interictal period, children feel good, but occasionally complain of pain briefly spastic character in the epigastrium, right hypochondrium and often in the umbilical region after irritating foods, carbonated drinks and cold food. The pain disappeared spontaneously or after taking antispasmolitics.

Hypotonical form of BD is characterized by almost constant, dull aching pain in his right side. Emotional stress, errors in the diet may increase the pain.

Hypokinetic-hypotonic type of BD occurs more often in children with a predominance of sympathetic tone of the autonomic nervous system. Clinically hypomotor dyskinesia is characterized by dull, often permanent, non-intensive pain in the right hypochondrium, sometimes – the feeling of heaviness, tension in the same area. Under the influence of adverse factors the pain syndrome may be intensified, but seizures that resemble the intensity of hyperkinetic-hypertonic dyskinesia, occur rarely.   In children may be signs of dyspepsia: nausea, bitter taste in the mouth, decreased appetite. Palpation of the abdomen reveals the pain in the projection of the gallbladder. In some patients there may be positive Ortner symptom (pain in the heel of hand effleurage on the right costal arch), rarely – Musso (pain in the gallbladder that occurs after pressure on the phrenic nerve between the legs sternocleidomastoid muscle).

                               

Cholestasis is the reason of increasing of the liver, which is soft-elastic, mobile and painless. After duodenal tubing or application of holekinetics its size reduces or normalizes. It should be emphasized that in BD, except for changes in motility of biliary tract, there is a disturbance of homeostatic balance. In the body of the child may develop functional changes in the respiratory, cardiovascular, nervous and other systems. The concentration of bile lipoprotein complex reduces, which is very important in the digestion. These disorders promote dysbiosis, reducing the synthesis of vitamins.

                    An indispensable companion of the disease is dyspepsia. In children there are decreased appetite and nausea. Often, young patients caot tolerate fatty and sugary foods: after its use they have nausea and vomiting. Sometimes older children complain of a bitter taste in the mouth. Unstable stool appears.

 

 

Plan of examination

n  Fool blood count

n  Biochemical test of blood:

Ø Serum aminotransferase

Ø Serum bilirubin (predominantly the direct reacting fraction)

Ø Serum alkaline phosphatase

Ø Albumin and globulin level

n  Stool test

n  US of the abdominal cavity + cholekynetics for functional investigations

 

                             

                                                  USD of liver

 

 

 

 

                                                                        

                                                                                 S-form of gall bladder on USD

 

It is desirable to make the child fractional duodenal intubation.

Phases of bile flow may be characterized briefly as follows.

The first phase is choledochic. In response to the stimulation of duodenal wall transparent light-yellow bile appears. The time of selecting the first portion of bile, the rate of expiration portion A and the total amount of this portion are taken into account.

The second phase – a time of closed sphincter of Oddi. At this stage, the bile is not allocated. It is refractory period: if it is shortened, it means lower the tone of the sphincter of Oddi, unless extended – about hypertension sphincter.

The third phase is a time of the opening of the sphincter of Oddi (in response to the action choletcystokinetic solution) prior to the appearance of gall bile (portion B). Extension of this phase indicates obstructed bile through the cystic duct.

The fourth phase – a period of emptying of the gall bladder (it depends on the tone of his muscles and sphincter Lyutkens). Trouble (interrupted) allocation of portions after the introduction of the stimulus is a sign of stagnation of bile in the gall bladder, hypotension of its muscles and permeability of the cystic duct.

The fifth phase – the selection of hepatic bile (portion C). If, during this phase to re-enter through the probe stimulus, in some patients may be received an additional amount of gall bile (portion B), which indicates incomplete emptying of the gall bladder and hypotension of its muscles.

                          Biochemical methods are used to determine in portions B and C concentration of bile acids, cholesterol and bilirubin. In children with hyperkinetic disorders of biliary tract cholesterol and lipid complex in the portion B are lower. In hypokinesia they are increased.

                The change of parameters in the various portions of bile depends on the type of dyskinesia. In most cases, bile microscopy reveals a violation of the colloidal equilibrium of bile (an increase in the number of cholesterol crystals, calcium bilirubinate). Very often in children parasites are present in bile – vegetative forms of Giardia, opistarchos eggs, larvae Stroingyloides stercoralis and others.

                  During duodenal intubation in patients with hyperkinetic and hypertonic form of dyskinesia cystic reflex is labile and sometimes it turns out to magnesium sulphate, and sometimes – after 2-3 hours or not at all apparent. Quantity of B portion is more frequently increased, it flows slowly and is concentrated (spastic cholestasis). In patients with hypokinetic form of dyskinesia cystic reflex is variable, often weak and is observed only in the application of strong stimuli. With the weakening of the sphincter Oddi bile immediately after the introduction of the probe follows, a differentiation portions A, B, C is difficult. Portion B is taken out (more than 60 ml) and long period (time of bile in more than 25 min) due to atopic cholestasis, but the closed sphincter of Oddi is small (less than 3 minutes). The results of ultrasound and contrast cholecystography help to differentiate type of dyskinesia.

                                   Cholangiography

 

         

 

 

Cholangiography is an examination that uses X-rays and contrast medium (dye) to view your bile ducts. It is often used to see if the bile ducts are blocked, such as in obstructive jaundice, where the bile is blocked from flowing into the duodenum and spills into the blood. Obstructive jaundice can be caused by gallstones blocking the bile ducts.

 

                In the procedure, the contrast medium is injected into the body and a series of X-rays taken to reveal any gallstones, other obstructions or narrowing in the bile ducts.

              Several techniques can be used to introduce the dye into the body.

    –Percutaneous transhepatic cholangiography (PTC) .The dye is injected through the skin into the bile ducts within the liver (intrahepatic biliary ducts). This is done using ultrasound to guide where the needle goes.

    –Intraoperative cholangiography. The dye is injected directly into the bile duct during a gallbladder operation.

    –Endoscopic retrograde cholangiopancreatography (ERCP). The dye is injected into the common bile duct and the pancreatic duct through a catheter that’s passed down an endoscope. The endoscope is a thin, flexible lighted tube that is gently passed down your throat and through your stomach, until it reaches the duodenum. Irrespective of how it is introduced, once the dye is in the bile ducts, it can spread into the whole biliary drainage system. Then X-rays can be taken to show up any narrowing or blockages in the drainage system. The resulting radiographic record is called a cholangiogram.

    –Magnetic resonance cholangiopancreatography (MRCP)

 

                 Magnetic resonance cholangiopancreatography (MRCP) is a relatively new technique for viewing the bile ducts, the pancreatic duct and the gallbladder. No contrast medium has to be administered for MRCP, unlike the other techniques mentioned here. MRCP uses magnetic resonance imaging (MRI) to produce detailed pictures.      

                Magnetic resonance imaging uses radiofrequency waves directed at the body (you do not feel anything) to excite hydrogen atoms in the molecules of water in your body. This is done in a strong magnetic field, which causes the nuclei of your hydrogen atoms to align. These nuclei emit radio signals when they return to their natural alignment. The signals are used to build up a computerised image that shows differences in body tissues based on the amount of water in them. This enables extremely clear and detailed pictures to be obtained of the bile ducts and pancreatic ducts.

               

                  MRCP is an outpatient procedure that involves lying very still in an MRI scanner for several minutes at a time. The entire experience should be over in less than 20 minutes. There is no exposure to radiation, but MRCP is not suitable for people with some types of metal objects in their body — ask the centre performing the test for more details.

                 MRCP is very safe and effective, with images comparable to ERCP. However, ERCP has the added advantage that therapeutic procedures can be performed at the same time. All these things will be taken into account when deciding which test to order.

 

                The basis of treatment of sick children with BD is an integrated approach. It means that the activities must be carried out in several directions:

ü Sanitation foci of chronic infection

ü Antiparasite therapy

ü Normalization of the immune defense due to normal nutrition and regime

ü  Hypoallergization

ü Elimination of hypovitaminosis and intestinal dysbiosis.

 

                                         Nutrition

               Nutrition should be chemically, mechanically and thermally gentle (diet 5). Eating is recommended 5-6 times a day to ensure an uninterrupted separation of bile. This takes into account the morning and evening reception dairy products: yogurt, sour milk, etc. Eating should be sought on equal distribution of food during the day. Dinner should be given to children for 2-3 hours before bedtime, and without heavy meat dishes. At BD overeating is unacceptable!

 

              In acute phase extractives are excluded from the diet: pepper, mustard, horseradish, onion, garlic, sorrel, radish, smoked meat, mushrooms, pickled products, meat, fish, spicy sauce. You should not use high-melting fats: lamb, pork, beef or goose fat. Digestion of fats in BD is difficult due to the irregular income of bile in the intestine and reduce the enzyme activity of the pancreas – lipase. There is preferred vegetable oils (sunflower, olive), because their processing does not require a significant amount of bile and enzymes. There are excluded power pastry cream, paste, chocolate, cocoa, and organic coffee, chocolates, oily fish, cold meats with fat.

 

Treatment of hypertonic-hyperkinetic dyskinesia

1.     Diet N 5

2.     Spasmolitics:

platyphyllini hydrotartratis (amp. 0.2 % 1 ml)

papaverini hydrochloridum (tab. 0.01, amp. 2 % 2 ml)

no-spa (tab. 0.04 or amp. 2 % 2 ml)

3.     Choleretic:

cholagon

allocholum

cholenzynum

galstena

hepabene

Treatment of hypotonic-hypokinetic dyskinesia

1.     Diet N 5

2.     Prokinetic: motilium, domperidone (tabl. 0.01 g) 1 mg/kg/day

3.     Choleretic and cholekinetic drugs:

·        cholagon

·        allocholum

·        cholenzynum

·        galstena

·        hepabene

·        chophytol

 

 

               

                 A good therapeutic effect has physiotherapy: diadinamothermia, electrophoresis with magnesium sulfate on the liver, ozokerite applications. After the treatment the patient should be within 2-3 months to comply with a light diet. Twice a year, it is expedient to hold a course choleretic therapy, using the collection of medicinal plants, chosen in view of this type of dyskinesia.

 

 

 

 

                   

 

                           Apparatus Refton-01-FS (DDT + HT configuration)

                        Diadynamic, electroplating, electrophoresis

 

                     

 

                                                  Ozokerite applications

 

 

 

 

                                                   Cholecystitis

 

                   Cholecystitis is inflammation of the gall bladder.

 

 

 

 

                                         Causes and pathology

 

                   Cholecystitis is often caused by cholelithiasis (the presence of choleliths, or gallstones, in the gallbladder), with choleliths most commonly blocking the cystic duct directly. This leads to inspissation (thickening) of bile, bile stasis, and secondary infection by gut organisms, predominantly E. coli and Bacteroides species.

               The gallbladder’s wall becomes inflamed. Extreme cases may result in necrosis and rupture. Inflammation often spreads to its outer covering, thus irritating surrounding structures such as the diaphragm and bowel.

             Less commonly, in debilitated and trauma patients, the gallbladder may become inflamed and infected in the absence of cholelithiasis, and is known as acute acalculous cholecystitis.

 

      

                                           Clinics

    Upper right-side abdominal pain

    Biliary colic – spasmodic upper abdominal pain

    Biliary colic after a fatty meal

    Abdominal discomfort

    Pain under right shoulder blade

 

             

 

 

                               Risk factors in Children

 

Gallstone disease is relatively rare in children. When gallstones occur in this age group they are more likely to be pigment stones. Girls do not seem to be more at risk than boys are. The following conditions may put children at higher risk:

·        Spinal injury

·        History of abdominal surgery

·        Sickle-cell anemia

·        Impaired immune system

·        Intravenous nutrition

·        Ethnicity

 

Because gallstones are related to diet, particularly fat intake, the incidence of gallstones varies widely among nations and regions. For example, Hispanics and Northern Europeans have a higher risk for gallstones than people of Asian and African descent do. People of Asian descent who develop gallstones are most likely to have the brown pigment type.

 

                                

 

                                      Genetics

 

Having a family member or close relative with gallstones may increase the risk of gallstones. Up to one-third of cases of painful gallstones may be related to genetic factors.

 

Defects in transport proteins involved in biliary lipid secretion appear to predispose certain people to gallstone disease, but this alone many not be sufficient to create gallstones. Studies indicate that the disease is complex and may result from the interaction between genetics and environment. Some studies suggest immune and inflammatory mediators may play key roles.

 

                                         Obesity

 

Obesity. Being overweight is a significant risk factor for gallstones. In such cases, the liver over-produces cholesterol, which is delivered into the bile and causes it to become supersaturated. Some evidence suggests that specific dietary factors (saturated fats and refined sugars) are the primary culprit in these cases, although studies are conflicting. Animal studies, however, suggest that obesity itself, not any particular foods, triggers the process leading to cholesterol supersaturation and the formation of stones.

 

                  Two Types of Cholecystitis:

 

1. Acute cholecystitis – this type is characterized by a sudden inflammation of the gallbladder that causes abdominal pain. Usually an attack of acute cholecystitis is hastened when a gallstone lodges in the small duct (cystic duct) leading from the gall bladder to the common bile duct.

 

 

                      Symptoms:

Ø Severe pain in the upper right part of the abdomen, just below the breastbone. Often there is also pain in the back or left shoulder blade. Pain usually starts after eating.

Ø Some patients also suffer nausea and vomiting these too are provoked by eating fried and fatty foods.

Ø Jaundice or yellowing of the eyes or skin. Sometimes when a patient has gallstones, a stone may pass out of the gall bladder and lodge in the common bile duct, obstructing the outflow of bile which causes jaundice.

Ø Fever

 

 

                                        

 

 

          2. Chronic cholecystitis – is characterized by an inflammation of the gallbladder that lasts a long time. It may be caused by repeat attacks of acute cholecystitis.

 

                                                  Symptoms:

·        Nausea

·        Abdominal pain

·        Indigestion and diarrhea, but some people don’t usually experience any symptoms. The symptoms usually come and go.     

               Cholecystitis is usually diagnosed by a history of the above symptoms, as well as examination findings. Laboratory and imaging tests (Ultrasound, Cholescintigraphy, CT Scan) are used to confirm the diagnosis and exclude other possible causes.

                   

 

 

 

Distended hydropic and hyperemic gallbladder in acute cholecystitis due to stone obstruction in the gallbladder neck or cystic duct.

 

 

              LEFT: US of a normal gallbladder after an overnight fast shows the wall as a pencil-thin echogenic line (arrow).

              RIGHT: US in the postprandial state shows pseudothickening of the gallbladder.

 

 

 

                           A                                                          B

A.The normal gallbladder wall is usually perceptible at CT as a thin rim of soft-tissue density that enhances after contrast injection.

 

 

B.   LEFT: US in patient with acute cholecystitis shows the layered appearance of a thickened gallbladder wall, with a hypoechoic region between echogenic lines

          RIGHT: At contrast-enhanced CT the thick-walled gallbladder contains a hypodense outer layer (arrow) due to subserosal oedema.  

 

            Thickening of the gallbladder wall is a relatively frequent finding at diagnostic imaging studies.

A thickened gallbladder wall measures more than 3 mm, typically has a layered appearance at sonography and at CT frequently contains a hypodense layer of subserosal oedema that mimics pericholecystic fluid.

 

                              

This is a CT scan of the upper abdomen showing cholecystitis (gall stones).

 

 

Your diet after cholecystitis treatment is as important and crucial as the surgery itself because of your body’s weakened system.

It is important to implement a cholecystitis diet to your lifestyle if you have recently had surgery or are experiencing symptoms of chelecystitis.

Acute cholecystitis symptoms can be troublesome, but do not be alarmed. Symptoms can be treated through tweaking a few things in your diet.

Below is a list of some of the best foods to add to your kitchen when implementing a cholecystitis diet.

 

 

                          

 

                               Diet

 

1. Olive Oil

 

Natural olive oil that is raw and unrefined has been proven effective in the natural remedies of acute cholecystitis. Approximately 30 ml of olive oil should be taken upon waking in the morning. You may choose to immediately follow the olive oil with about 100 ml of lemon juice or grapefruit juice. This morning cocktail should be taken every morning for weeks if necessary to eliminate waste and provide successful cholecystitis treatment. The oil can also lessen the likelihood of symptoms of cholecystitis.

 

2. Raw Beetroot Juice

 

Raw beet root juice cleanses the system and is great when a patient has experienced symptoms of cholecystitis. Drinking approximately 100 ml of beet juice twice daily will help to eliminate the possibilities of developing acute cholecystitis. Beet juice provides an effective and natural cholecystitis treatment. Beet juice can be used as a preventive measure as well.

 

3. Black Seed Oil

 

Black seed oil is a highly effective natural remedy for cholecystitis treatment. If you experience acute cholecystitis it is recommended that your cholecystitis diet include fibrous material that keeps your digestive tract moving. Black seed oil may cause highly loose stools but if taken in moderation can provide the desired effect and cleansing needed.

 

4. Hemp

 

By adding approximately two teaspoons or dessert spoonfuls to your cholecystitis diet you caaturally provide yourself with a highly effective cholecystitis treatment from the comforts of your own home. If you have been diagnosed with or experienced symptoms accompanied with cholecystitis, hemp can be beneficial to add to your diet and reduces the risk of acquiring other problems like acute cholecystitis.

 

5. Lemon Juice

 

Lemon juice is a great supplemental food to add to water or squirt on top of fish as part of your cholecystitis diet. The acid in the lemon juice breaks down fatty acids in the bile that is digesting the food.

 

6. Vinegar

 

Vinegar is an excellent supplemental food to add to dishes when cooking as a part of your cholecystitis diet. Similar to lemon juice, the acid in the vinegar breaks down fatty acids. Symptoms of cholecystitis can be greatly alleviated by incorporating vinegar and lemon juice.

 

7. Avocados

 

Avocados are a great food to add to your cholecystitis diet. They contain essential oils that are natural and are rich in vitamins your body needs.

 

8. Blackberries

 

Blackberries are rich in fiber and essential nutrients and vitamins that promote a healthy digestive system. Consuming berries every day will eliminate constipation and keep things moving at a steady rate. Your cholecystitis diet after treatment is important and at least two servings of berries each day can provide your body with important nutrients it requires to function properly.

 

9. Lecethin Granuals

 

By adding approximately two teaspoons or dessert spoonfuls of lecithin granules to your cholecystitis diet you caaturally provide yourself with a highly effective cholecystitis treatment from the comforts of your own home.

 

10. Dandelion

 

Drinking approximately 125 ml of dandelion juice daily can prevent acute cholecystitis symptoms from occurring. This is a great herb to add to your cholecystitis diet.

 

                                Treatment:

 

        Patient will need to stay in the hospital, and are given antibiotics (intravenously) to treat infections and other medications are also given to control abdominal pain and vomiting.

       CC is most often treated by the surgical removal of the gall bladder to prevent symptoms from coming back. In some chronic cases if the risk of surgery is high or if the symptoms are not severe the doctor may simply recommend a diet that is low in fat.

 

 

 

                                        Giardia lamblia or Giardiasis

 

                   Giardia lamblia contaminates surface water all over the world and can cause an unpleasant prolonged intestinal illness known as giardiasis, or beaver fever.

Giardia lamblia is a protozoan, a single-celled parasite that lives in the intestines of people and animals. For the lucky, its presence causes no symptoms. For the less fortunate, G. lamblia causes an intestinal parasitic disease—giardiasis—that is always unpleasant, and may be prolonged.

                              Giardia cell

  

              Giardia lamblia is found in feces and in contaminated water supplies. People ingest the infective cysts of the parasite when they drink contaminated water or accidentally ingest fecal material on contaminated food items, hands, or other objects.

 

                Giardia lamblia is resistant to chlorination and can survive water treatment. Unfiltered water supplies, particularly those drawn from surface supplies, have often been the source of outbreaks of giardiasis. Many animals can carry the parasite, including cats, dogs, sheep, cattle, muskrats and beavers (the source of the commoame “beaver fever”). Infected people can cause an outbreak as well: contaminated hands can spread the parasite to food or objects.

 

 

               Giardia lamblia is much larger than bacteria, but still too small to be seen without a microscope. There are two stages, called cysts and trophozoites. Cysts are oval—watermelon shaped—and contain two pairs of nuclei that look like spherical eyes, along with a collection of other thread-like structures. Trophozoites are shaped like teardrops, with a broad rounded end and a pointy end that tapers off. The parasite alternates between the two stages.

                              

                The cyst stage is very resilient; it survives well in cool damp conditions and even in very cold water in winter. This is the stage that people swallow. In the small intestine, the cyst breaks down, releasing two trophozoites, which attach to the intestinal lining and divide to produce more trophozoites.

 

                        Intracellular Metabolism and biochemistry

 

              Giardia relies on glucose as its major energy source and breaks glucose down into ethanol, acetate and carbon dioxide. However, it can also use arginine as an energy source. The mitochondria of Giardia possess unique biochemical pathways that suggest that it diverged from other eukaryotes at an early stage in evolution.

 

B vitamins and bile salts are necessary for Giardia to survive, and a low-carbohydrate diet was shown in mice to reduce the number of Giardia organisms present.

 

   Primary endosymbiosis is believed to have given rise to heterotrophs, and secondary endosymbiosis is believed to have given rise to the photoautotrophic eukaryotes. 

                 Some trophozoites are carried away in the intestinal flow, especially when the host has diarrhea. As they move through the intestine, some secrete a resistant wall and become cysts.

Trophozoites and cysts of Giardia lamblia are passed in the stool. The trophozoites die quickly, but the cysts survive a long time in the right conditions.

Cysts are swallowed by another unsuspecting host and the process begins all over again.

                              Clinics

Ø Abdominal pain

Ø Watery diarrhea

Ø Foul smelling gas and burping

Ø Mild fever, sometimes with chills

Ø Malabsorption

 

                    In chronic infection, intermittent diarrhea alternating with normal stools and sometimes even constipation.

 

                               Treatment             

 

It’s probably impossible to completely avoid coming in contact with Giardia lamblia, but you can lessen your chances of catching it:

Never drink untreated water from surface sources—rivers, streams, lakes. Treat water with filtration or a chemical treatment that kills protozoa.

              When traveling in countries where sanitation is poor, drink bottled water and avoid uncooked vegetables that you do not peel yourself (with clean hands).

Practice good hygiene at all times: wash hands thoroughly after using the toilet and before handling food.

 

If you do catch giardiasis, take heart: you are not the first—Giardia lamblia cysts have been recovered from preserved human stools that are over two thousand years old. Two thousand years ago, this parasitic disease would have run its course, but today there are drugs that are usually very effective at killing the parasite.

 

 

Drug	Treatment duration	Possible Side Effects
Metronidazole	5–7 days	Metallic taste; nausea; vomiting; dizziness; headache; disulfiram-like effect; neutropenia
Tinidazole	Single dose	Metallic taste; nausea; vomiting; belching; dizziness; headache; disulfiram-like effect
Nitazoxanide	3 days	Abdominal pain; diarrhea; vomiting; headache; yellow-green discolouration of urine
Albendazole	5 days	Dizziness; headache; fever; nausea; vomiting; temporary hair loss

 

 

                       Acute and chronic pancreatitis

 

 

                          

 

                      Acute pancreatitis is a rare finding in childhood but probably more common than is generally realized. This condition should be considered in the evaluation of children with vomiting and abdominal pain, because it can cause significant morbidity and mortality. Clinical suspicion is required to make the diagnosis, especially when the serum amylase concentration is normal. Recurrent pancreatitis may be familial as a result of inherited biochemical or anatomic abnormalities. Patients with hereditary pancreatitis are at high risk for pancreatic cancer.      

                       Pancreatitis is a disease process with multiple triggers that may cause activation of proteases within the pancreas. It is rare in children, and the causes are more varied in children than in adults (70 to 80 percent of adult cases are related to either alcohol intake or gallstones). In about 25 percent of childhood cases, the etiology is unknown, but trauma, multisystem disease and drugs account for most identified causes.

 

 

                               

 

 

                Acute pancreatitis is inflammation of the pancreas that occurs suddenly and usually resolves in a few days with treatment. Acute pancreatitis can be a life-threatening illness with severe complications. Each year, about 210,000 people in the United States are admitted to the hospital with acute pancreatitis.1 The most common cause of acute pancreatitis is the presence of gallstones—small, pebble-like substances made of hardened bile—that cause inflammation in the pancreas as they pass through the common bile duct. Chronic, heavy alcohol use is also a common cause. Acute pancreatitis can occur within hours or as long as 2 days after consuming alcohol. Other causes of acute pancreatitis include abdominal trauma, medications, infections, tumors, and genetic abnormalities of the pancreas.

                                                       

                                                 Symptoms

 

                Acute pancreatitis usually begins with gradual or sudden pain in the upper abdomen that sometimes extends through the back. The pain may be mild at first and feel worse after eating. But the pain is often severe and may become constant and last for several days. A person with acute pancreatitis usually looks and feels very ill and needs immediate medical attention. Other symptoms may include:

·        a swollen and tender abdomen

·        nausea and vomiting

·        fever

·        a rapid pulse

 

                Severe acute pancreatitis may cause dehydration and low blood pressure. The heart, lungs, or kidneys can fail. If bleeding occurs in the pancreas, shock and even death may follow.

                                       Diagnosis

 

                While asking about a person’s medical history and conducting a thorough physical examination, the doctor will order a blood test to assist in the diagnosis. During acute pancreatitis, the blood contains at least three times the normal amount of amylase and lipase, digestive enzymes formed in the pancreas. Changes may also occur in other body chemicals such as glucose, calcium, magnesium, sodium, potassium, and bicarbonate. After the person’s condition improves, the levels usually return to normal.

 

                     Diagnosing acute pancreatitis is often difficult because of the deep location of the pancreas. The doctor will likely order one or more of the following tests:

Serum Markers for Determining Diagnosis and Prognosis in Acute Pancreatitis           

Laboratory test	Time of onset (hours)	Purpose	Clinical observation/limitations
Alanine transaminase	12 to 24	Diagnosis and etiology	Associated with gallstone pancreatitis; threefold elevation or greater in the presence of acute pancreatitis has a positive predictive value of 95 percent in diagnosing acute gallstone pancreatitis
Amylase	2 to 12	Diagnosis	Most accurate when at least twice the upper limit of normal; amylase levels and sensitivity decrease with time from onset of symptoms
C-reactive protein	24 to 48	Predictive of severity	Late marker; high levels associated with pancreatic necrosis
Interleukin-6	18 to 48	Predictive of severity	Early indication of severity
Interleukin-8	12 to 24	Predictive of severity	Early indication of severity
Lipase	4 to 8	Diagnosis	Increased sensitivity in alcohol-induced pancreatitis; more specific and sensitive than amylase for detecting acute pancreatitis
Phospholipase A2	24	Predictive of severity	Associated with development of pancreatic necrosis and pulmonary failure
Procalcitonin	24 to 36	Predictive of severity	Early detection of severity; high concentrations in infected necrosis
Trypsinogen activation peptide	Within a few hours	Diagnosis and predictive of severity	Early marker for acute pancreatitis and close correlation to severity

 

-Abdominal ultrasound

            Sound waves are sent toward the pancreas through a handheld device that a technician glides over the abdomen. The sound waves bounce off the pancreas, gallbladder, liver, and other organs, and their echoes make electrical impulses that create a picture—called a sonogram—on a video monitor. If gallstones are causing inflammation, the sound waves will also bounce off them, showing their location.

 

A wavy, ‘spastic’ appearance                             Enlarged, irregular,

of the duodenum,                                          hypoechoic pancreatic body with

thought to be secondary                                surrounding hyperechoic mesentery

to pancreatitis.                                               imaged in a sagittal plane, caudal to the

                                                                      gall bladder and cranial and dorsal to

                                                                      the    duodenum..                                                                                                                

                                                                  

              

 

-Computerized tomography (CT) scan. The CT scan is a noninvasive x ray that produces three-dimensional pictures of parts of the body. The person lies on a table that slides into a donut-shaped machine. The test may show gallstones and the extent of damage to the pancreas.

Pancreas edema in pancreatitis

 

                           

-Endoscopic ultrasound (EUS). After spraying a solution to numb the patient’s throat, the doctor inserts an endoscope—a thin, flexible, lighted tube—down the throat, through the stomach, and into the small intestine. The doctor turns on an ultrasound attachment to the scope that produces sound waves to create visual images of the pancreas and bile ducts.

                                      

-Magnetic resonance cholangiopancreatography (MRCP). MRCP uses magnetic resonance imaging, a noninvasive test that produces cross-section images of parts of the body. After being lightly sedated, the patient lies in a cylinder-like tube for the test. The technician injects dye into the patient’s veins that helps show the pancreas, gallbladder, and pancreatic and bile ducts.

    

                     Magnetic resonance cholangiopancreatography                                          

                                             Treatment

 

                Treatment for acute pancreatitis requires a few days’ stay in the hospital for intravenous (IV) fluids, antibiotics, and medication to relieve pain. The person cannot eat or drink so the pancreas can rest. If vomiting occurs, a tube may be placed through the nose and into the stomach to remove fluid and air.

              Unless complications arise, acute pancreatitis usually resolves in a few days. In severe cases, the person may require nasogastric feeding—a special liquid given in a long, thin tube inserted through the nose and throat and into the stomach—for several weeks while the pancreas heals.

 

                 Before leaving the hospital, the person will be advised not to eat fatty meals. In some cases, the cause of the pancreatitis is clear, but in others, more tests are needed after the person is discharged and the pancreas is healed.

                                        Complications

 

            Gallstones that cause acute pancreatitis require surgical removal of the stones and the gallbladder. If the pancreatitis is mild, gallbladder removal—called cholecystectomy—may proceed while the person is in the hospital. If the pancreatitis is severe, gallstones may be removed using therapeutic endoscopic retrograde cholangiopancreatography (ERCP)—a specialized technique used to view the pancreas, gallbladder, and bile ducts and treat complications of acute and chronic pancreatitis. Cholecystectomy is delayed for a month or more to allow for full recovery. 

                 If gallstones are present in the common bile duct, the surgeon may perform a sphincterotomy. A small incision is made through the endoscope, which enlarges the opening of the common bile duct into the duodenum. The stones can then pass through.

                 If an infection develops, ERCP or surgery may be needed to drain the infected area, also called an abscess. Exploratory surgery may also be necessary to find the source of any bleeding, to rule out conditions that resemble pancreatitis, or to remove severely damaged pancreatic tissue.

 

                     Pseudocysts—accumulations of fluid and tissue debris—that may develop in the pancreas can be drained using ERCP or EUS. If pseudocysts are left untreated, enzymes and toxins can enter the bloodstream and affect the heart, lungs, kidneys, or other organs.

 

 

 

                In rare cases, acute pancreatitis can cause breathing problems. Hypoxia, a condition that occurs when body cells and tissues do not get enough oxygen, can develop. Doctors treat hypoxia by giving oxygen to the patient. Some people still experience lung failure—even with oxygen—and require a respirator for a while to help them breathe.

 

 

 

 

                          Chronic pancreatitis

 

                   Chronic pancreatitis is inflammation of the pancreas that does not heal or improve—it gets worse over time and leads to permanent damage. Chronic pancreatitis, like acute pancreatitis, occurs when digestive enzymes attack the pancreas and nearby tissues, causing episodes of pain. 

               The chronic form of pancreatitis can be triggered by one acute attack that damages the pancreatic duct. The damaged duct causes the pancreas to become inflamed. Scar tissue develops and the pancreas is slowly destroyed.

 

Other causes of chronic pancreatitis are

·        hereditary disorders of the pancreas

·        cystic fibrosis—the most common inherited disorder leading to chronic pancreatitis

·        hypercalcemia—high levels of calcium in the blood

·        hyperlipidemia or hypertriglyceridemia—high levels of blood fats

·        some medicines

·        certain autoimmune conditions

·        unknown causes

 

             Episodes of abdominal pain and diarrhea lasting several days come and go over time and can progress to chronic pancreatitis. A diagnosis of hereditary pancreatitis is likely if the person has two or more family members with pancreatitis in more than one generation.

                                              Clinics

 

Most patients with chronic pancreatitis experience upper abdominal pain, although some  have no pain at all. The pain may spread to the back, feel worse when eating or drinking, and become constant and disabling. In some cases, abdominal pain goes away as the condition worsens, most likely because the pancreas is no longer making digestive enzymes.

                        Other symptoms include

§  nausea

§  vomiting

§  weight loss

§  diarrhea

§  oily stools

 

         Patients with chronic pancreatitis often lose weight, even when their appetite and eating habits are normal. The weight loss occurs because the body does not secrete enough pancreatic enzymes to digest food, so nutrients are not absorbed normally. Poor digestion leads to malnutrition due to excretion of fat in the stool.

                                             Diagnosis

 

             Chronic pancreatitis is often confused with acute pancreatitis because the symptoms are similar. As with acute pancreatitis, the doctor will conduct a thorough medical history and physical examination. Blood tests may help the doctor know if the pancreas is still making enough digestive enzymes, but sometimes these enzymes appear normal even though the person has chronic pancreatitis.

 

In more advanced stages of pancreatitis, when malabsorption and diabetes can occur, the doctor may order blood, urine, and stool tests to help diagnose chronic pancreatitis and monitor its progression.

 

After ordering x rays of the abdomen, the doctor will conduct one or more of the tests used to diagnose acute pancreatitis—abdominal ultrasound, CT scan, EUS, and MRCP.

                                                      Treatment

 

                 Treatment for chronic pancreatitis may require hospitalization for pain management, IV hydration, and nutritional support. Nasogastric feedings may be necessary for several weeks if the person continues to lose weight.

                   When a normal diet is resumed, the doctor may prescribe synthetic pancreatic enzymes if the pancreas does not secrete enough of its own. The enzymes should be taken with every meal to help the person digest food and regain some weight. The next step is to plan a nutritious diet that is low in fat and includes small, frequent meals. A dietitian can assist in developing a meal plan. Drinking plenty of fluids and limiting caffeinated beverages is also important.

 

                                                     Complications

 

 

 

                       As with acute pancreatitis, ERCP is used to identify and treat complications associated with chronic pancreatitis such as gallstones, pseudocysts, and narrowing or obstruction of the ducts. Chronic pancreatitis also can lead to calcification of the pancreas, which means the pancreatic tissue hardens from deposits of insoluble calcium salts. Surgery may be necessary to remove part of the pancreas.

                     In cases involving persistent pain, surgery or other procedures are sometimes recommended to block the nerves in the abdominal area that cause pain.

 

When pancreatic tissue is destroyed in chronic pancreatitis and the insulin-producing cells of the pancreas, called beta cells, have been damaged, diabetes may develop. Patients with a family history of diabetes are more likely to develop the disease. If diabetes occurs, insulin or other medicines are needed to keep blood glucose at normal levels. A health care provider works with the patient to develop a regimen of medication, diet, and frequent blood glucose monitoring.

 

 

 

 

                               Chronic hepatitis

              Chronic hepatitis is inflammation of the liver that lasts at least 6 months.

                Common causes are hepatitis B and C viruses and drugs.

Many patients have no symptoms until the liver has become severely scarred.

              Chronic hepatitis can result in cirrhosis, with an enlarged spleen, fluid accumulation in the abdominal cavity, and deterioration of brain function. A biopsy is done to confirm the diagnosis.

Drugs, such as antiviral drugs or corticosteroids, may be used, and for advanced disease, liver transplantation may be needed.

 

           

                  Chronic hepatitis, although much less common than acute hepatitis, can persist for years, even decades. In most people, it is quite mild and does not cause significant liver damage. However, in some people, continued inflammation slowly damages the liver, eventually resulting in cirrhosis (severe scarring of the liver), liver failure, and sometimes liver cancer.

          Cirrhosis

  

              CLASSIFICATION

·             Viral

Ø Hepatitis B

Ø Hepatitis C

Ø Hepatitis D

•     Autoimmune

•     Drug induced

•     Metabolic

                 

 

                                            Causes

             Chronic hepatitis is usually caused by one of the hepatitis viruses. Hepatitis C virus causes about 60 to 70% of cases, and at least 75% of acute hepatitis C cases become chronic. About 5 to 7% of hepatitis B cases, sometimes with hepatitis D co-infection, become chronic. Hepatitis A and E viruses do not cause chronic hepatitis.

             Certain drugs can cause chronic hepatitis, particularly when they are taken for a long time. They include isoniazid, methyldopa, nitrofurantoin and, rarely, acetaminophen. 

Drug Related

•     Dose related: 6 MP, methotrexate and acetaminophen

•     Idiosyncratic: phenytoin, phenobarbital and carbamezipine

 

Ø Acetaminophen	Ø Erythromicin
Ø Halothane	Ø Estrogen
Ø Valporic Acid	Ø Anabolic steroids
Ø Isoniazide	Ø Ceftriaxone
Ø Sulfonamides	Ø Cyclophosphamide
Ø Phenytoin	Ø OCP
Ø Methotrexate	Ø Chlorpromazine
Metabolic Ø Wilson Disease
Ø Alpha 1 anti-trypsin deficiency
Ø Tyrosiniemia
Ø Niemann-Pick disease type 2
Ø Glycogen storage Disease IV
Ø Cystic Fibrosis
Ø Galactosemia
Ø Bile Acid Synthetic Abnormalities

 

           

             Wilson’s disease, a rare hereditary disorder involving abnormal retention of copper in the liver, may cause chronic hepatitis in children. Other causes include alcoholic hepatitis, fatty liver not due to alcohol use (nonalcoholic steatohepatitis), and alpha1-antitrypsin deficiency (a hereditary disorder).

             No one knows exactly why a particular virus or drug causes chronic hepatitis in some people but not in others or why the degree of severity varies. In many people with chronic hepatitis, no obvious cause can be found. In some of these people, the chronic inflammation resembles inflammation caused by the body attacking its own tissues (an autoimmune reaction, but this connection has not been proven. This type of inflammation called autoimmune hepatitis, is more common among women than men.

 

                                         Clinics            

 

           In about two thirds of people, chronic hepatitis develops gradually without causing any obvious symptoms until cirrhosis occurs. In the remaining one third, it develops after a bout of acute viral hepatitis that persists or returns (often several weeks later).

           Symptoms often include a vague feeling of illness (malaise), poor appetite, and fatigue. Sometimes affected patients also have a low-grade fever and some upper abdominal discomfort. Jaundice is rare.

                        

 

                Complications of chronic liver disease and cirrhosis may eventually develop. They can include an enlarged spleen, spiderlike blood vessels in the skin, redness of the palms, and accumulation of fluid in the abdominal cavity. Liver malfunction may lead to deterioration of brain function (hepatic encephalopathy), particularly in people with cirrhosis due to hepatitis C.

            

                                       Spiderlike blood vessels in the skin

 

                         Redness of the palms

   

  Skin hemorrhagies                                   Pigmentation of skin

                      Nose hemorrhagies

         Autoimmune hepatitis may cause other symptoms that can involve virtually any body system, especially in girls. Such symptoms include acne, cessation of menstrual periods, joint pain, lung scarring, inflammation of the thyroid gland and kidneys, and anemia. Often there are scratches of the skin.

                    

               Scratches and formed as a result of these cracks on the skin are a gateway for infection.

               In many people, chronic hepatitis does not progress for years. In others, it gradually worsens. The outlook depends partly on which virus is the cause:

          Chronic hepatitis C leads to cirrhosis, which develops over a period of years, in about 15 to 25% of people. The risk of liver cancer is increased but only if cirrhosis is present.

                                       

                 There are many signs of cirrhosis that provider may find. It may have red palms or small spider-like veins on the face or body.         

             Cirrhosis: Another problem caused by high pressure in the veins of the liver is ascites. Fluid leaks out into the belly and it begins to fill it up. This can make the abdomen enlarge like a balloon filled with water. The legs can get swollen too.

                  Chronic hepatitis B tends to worsen, sometimes rapidly, and increases the risk of liver cancer.

           Chronic co-infection with hepatitis B and D causes cirrhosis in up to 70%.

           Autoimmune hepatitis can be effectively treated in most people, but some develop cirrhosis, with or without liver failure.

                Chronic hepatitis caused by a drug may completely resolve once the drug is stopped.

 

                                               Diagnosis

                   Discrimination between hepatitis A and B is becoming easier as the serologic and clinical characteristics of each type become better known. Hepatitis A is generally a benign pediatric illness with few sequelae. In contrast, hepatitis B is more often associated with complications and may progress to chronic liver disease in as many as 10% of cases. Chronic persistent hepatitis appears to be a benign disorder not requiring therapy. Occasionally related etiologically to virus B, chronic active hepatitis is often associated with severe clinical illness. However, it generally responds to steroid therapy, at least initially, and may be arrested or cured.

                    

                        Diagnostic criteria related to CH include the following                        

                Chronic hepatitis B: HBsAg positive for more than six months, serum HBV DNA greater than 20,000 IU per mL (lower values of 2,000 to 20,000 IU per mL often occur with HBeAg-negative chronic hepatitis B), persistent or intermittent elevation in alanine transaminase (ALT) or aspartate transaminase (AST) levels, and liver biopsy showing chronic hepatitis with moderate or severe necroinflammation.

 

                  Inactive HBsAg carrier state: HBsAg positive for more than six months, HBeAg negative and anti-HBeAg positive, serum HBV DNA less than 2,000 IU per mL, persistently normal ALT and AST levels, liver biopsy confirming absence of significant hepatitis.

 

                Resolved hepatitis B: known history of acute or chronic hepatitis B or the presence of anti-hepatitis B core antigen (anti-HBcAg) with or without anti-HBsAg, HBsAg negative, undetectable serum HBV DNA (very low levels may be detectable with sensitive prostate-specific antigen assays), and normal ALT levels. Hepatitis B S Ag > 6 months

•     Variable biochemical tests

•     Congenital ( 85% rate) or acquired

•     Other Markers: DNA PCR, HBe Ag, Anti-HB c , Anti- HB e

•     1-5% of acute attacks become chronic

•     70 % cirrhosis

•     HCC carcinoma ( monitor alpha fetoprotein)

 

                 Doctors may suspect hepatitis C when patients have typical symptoms, when blood tests to evaluate liver function are abnormal, or when they have had hepatitis C before. Blood tests are done and may help establish the diagnosis, identify the cause, and determine the severity of liver damage. However, a liver biopsy is essential for a definite diagnosis. The liver biopsy also enables a doctor to determine how severe the inflammation is and whether any scarring or cirrhosis has developed. The biopsy may help identify the cause of hepatitis. Occasionally, a biopsy needs to be done more than once.

                      

                                   Liver biopsy

 

                If people have chronic hepatitis B, ultrasonography and blood tests to measure alpha–fetoprotein levels are done annually to screen for liver cancer. Levels of alpha–fetoprotein (a proteiormally produced by immature liver cells in fetuses) usually increase when liver cancer is present. People with chronic hepatitis C are screened similarly, but only if they have cirrhosis.

 

 

                                        Elastography 

 

           Elastography is based on liver ultrasound, but has a huge difference to the normal imaging technique of ultrasound of the liver. It uses mechanical waves that are sent through the liver. The speed of these waves through tissue provides data about the condition and stiffness of the liver and thus can indicate a liver fibrosis. Elastography might become a completely non-invasive substitute for Biopsy.

                   

                       Important techniques in this field include:

                                 Transient Elastography

 

Transient elastography makes it possible to measure the elasticity (stiffness) of tissue painlessly using ultrasound. This new method provides a particular benefit for populations at risk (haemophiliacs, transplant patients, etc.) and patients who refuse a biopsy.

                                 

                       Transient elastography

 

                                                             Contrast Harmonic Imaging

Contrast harmonic imaging (CHI) is a new Doppler technology using the non-linear properties of ultrasound contrast agents. CHI is promising to further improve the differential diagnosis of liver lesions and the detection of metastases.

                               Magnetic Resonance Imaging (MRI)                                                          

  A new technique uses a modified form of Magnetic Resonance Imaging (MRI) to accurately measure the elasticity of the liver. By applying vibrations to the liver, MRE obtains pictures of the mechanical waves passing through the organ. The wave pictures are then processed to generate a quantitative image of tissue stiffness.

Noninvasive Approaches Offer Substantial Market Potential in Liver Disease                                                                                                                 

                                      Diagnostics

Novel noninvasive liver diagnostics tests have a good potential to revolutionize the diagnosis in hepatology. Up to now liver biopsy is widely considered the diagnostic gold standard for the diagnosis of liver fibrosis and liver cirrhosis. However, biopsy as an invasive procedure is not appropriate for all patients with liver disease. There fore noninvasive liver diagnostics tests might play a significant role in the management of patients with liver disease.

 

  Abdominal ultrasound shows hyperechoic fibrotic tissue around the portal vein (p) and the hepatic hilus. (a: aorta, v: vena cava; p: portal vein; gb: gallbladder).

    

                                           Encephalopathy

                   A liver that is working poorly may not be able to get rid of toxic substances like ammonia (which comes from the intestines), and it may allow these substances to go into the brain and cause confusion.

                Besides confusion, toxins in the brain cause changes in sleep, mood, concentration, and memory. If it gets really bad, it can even cause a coma.

These are all symptoms of hepatic encephalopathy. If there is encephalopathy, may be problems driving, writing, calculating, and performing other activities of daily living. Signs of encephalopathy are trembling and hand “flapping.”

                                

 

                Encephalopathy may occur when there is an infection or internal bleeding, and it may also occur if patients are constipated or take too many water pills or take tranquilizers or sleeping pills. 

                                                                  

                

                 Algorithm for the management of chronic HBV infection. (ALT = alanine transaminase; HBeAg = hepatitis B e antigen; HBsAg = hepatitis B surface antigen; HBV = hepatitis B virus.)                                    

 

                                                            Treatment

 

If a drug is the cause, the drug is stopped. If another disorder is the cause, it is treated.

 

           Hepatitis B and C: People with progressive chronic hepatitis B or C are usually given antiviral drugs. For hepatitis B, entecavir, adefovir  or lamivudine is usually used. These drugs are taken by mouth, as is telbivudine , a new drug for which little information is available. Interferon-alpha or pegylated interferon-alpha, given by injection under the skin, may be used instead of an oral drug. Hepatitis B tends to recur once drug treatment is stopped and may be even more severe. Thus, an antiviral drug may need to be taken indefinitely.

                  For hepatitis C, pegylated interferon-alpha plus ribavirin is most effective. This combination may stop the inflammation. After taking these drugs for 6 months to 1 year, 45 to 75% of patients improve and have no further problems.

                       Antiviral drugs used to treat chronic hepatitis commonly cause side effects. Lamivudine may have fewer side effects than the others. These drugs should not be taken by patients who have certain conditions:

·        Advanced cirrhosis due to hepatitis B

·        A transplanted organ

·        A reduced number of blood cells (cytopenia), such as red blood cells (anemia)

·        Substance abuse.

 

If family members and close contacts of people with chronic hepatitis B have not been vaccinated, they should be. They are also given hepatitis B immune globulin. Such measures are not necessary for chronic hepatitis C.

                Autoimmune Hepatitis: Usually, corticosteroids (such as prednisone) are used, sometimes with azathioprine , a drug used to suppress the immune system. These drugs suppress the inflammation, relieve symptoms, and improve long-term survival. Nevertheless, scarring in the liver may gradually worsen. Stopping these drugs usually leads to recurrence of the inflammation, so most people have to take the drugs indefinitely.

 

                                         Complications:

                    Regardless of the cause or type of chronic hepatitis, complications require treatment. For example, treating ascites involves restriction of salt consumption, bed rest, and sometimes drugs. If brain function deteriorates, eliminating protein from the diet can help.

                                    Liver Transplantation

                    Transplantation may be considered for patients with severe liver failure. However, in patients who have hepatitis B or hepatitis C, the virus tends to infect the transplanted liver. In patients with hepatitis B, the virus tends to severely damage the transplanted liver over months or a few years, but taking lamivudine may improve the outcome. In patients with hepatitis C, the virus virtually always recurs in the transplanted liver, but the infection is usually so mild that people are likely to survive for many years.

  

             This gift of new life brings its own set of potential complications and requires lifelong medications to prevent rejection. Liver transplantation is considered for people in situations such as these:

§  When other medical or surgical treatments have failed to correct the life-threatening problems caused by cirrhosis

§  To treat some cancerous tumors of the liver or bile ducts such as hepatocellular carcinoma

§  To correct abnormalities in metabolism or anatomical function that may limit long-term health and are cured by liver transplant

§  Children who are born with congenital disorders

 

In the pediatric experience, survival of both the recipient and the transplanted liver (graft) at 1 year is about 90%. Donor complications have been very few. 

 

 

                            Prevention                                    

              There have been safe and effective, active and passive immunisation preparations for hepatitis B for more than 30 years. Worldwide, the primary mode of transmission of the virus is from mother to newborn baby. The earlier this infection is acquired the more likely chronic hepatitis will evolve.

 Perinatal transmission can be effectively interrupted by passive immunisation of the newborn baby with hepatitis B immune globin, together with a series of three active vaccinations starting at birth and given over the subsequent 6 months of life.

             Universal vaccination throughout the world has been underway to varying degrees for many years and ultimately should sharply reduce the prevalence of hepatitis B disease, in particular the risk of HCC. An estimated 400 million people now have active hepatitis B.

                         Unfortunately, there are neither passive nor active vaccines for hepatitis C virus. Most hepatitis C in the world is a result of parenteral transmission either by transfusion of blood products or, more commonly, re-use of syringes, needles, or both. The introduction of blood-donor screening for hepatitis C virus some 16 years ago, as well as hepatitis B virus 35 years ago in developed countries, has virtually eliminated post-transfusion hepatitis. Unfortunately, in underdeveloped countries, particularly in rural areas, blood products remain infected. Concerted efforts toward implementing sterile technique and the use of disposable needles and syringes, mainly in health-care settings, are much needed. A more difficult challenge is the worldwide prevention of illicit drug use, as well as treating infected drug users.

 

                       For those already infected with hepatitis C, most will develop chronic hepatitis. 30% will develop cirrhosis over a 30-year period and will subsequently develop associated complications, in particular HCC. Pegylated interferon with ribavirin can successfully eradicate this viral infection in around 50% of patients.  However, this therapy is expensive and the treatment is fraught with side-effects. There are phase II clinical trials underway assessing the safety and efficacy of orally administered antivirals (eg, protease and polymerase inhibitors) that hopefully will eventually lead to even more effective therapy with fewer side-effects. The incidence of HCC secondary to chronic hepatitis C is rising. Some of these patients can be treated with liver transplantation and tumour ablative techniques but, unlike hepatitis B, recurrent infection with hepatitis C virus is almost 100% in recipients of liver transplantation.

 

 

                     Acute liver failure

Acute liver failure (ALF) is a broad term and encompasses both fulminant hepatic failure (FHF) and subfulminant hepatic failure. It is a rare but potentially fatal disease, especially if complicated by hepatic encephalopathy and impaired protein synthesis. Incidence of acute liver failure is low only about 2000 cases annually occurring in the US.

 More than 350 million people worldwide are inflicted by Hepatitis B Virus and about 170 million by Hepatitis C. 20% of those patients with chronic viral hepatitis might develop liver cirrhosis which might end in the need of a liver transplantation (LTx).

Today many patients in hepatology who develop acute liver failure recover with supportive treatment but with continued deterioration or having adverse prognostic factors, orthotopic liver transplantation (OLT) is often required. Approximately 6% of OLTs performed in the United States are for fulminant hepatic failure (FHF). Prior to orthotopic liver transplantation (OLT) for FHF, the mortality rate was generally greater than 80%. However, with improved intensive care, the prognosis is much better now than in the past, with some series reporting approximately a survival rate of 60%.

                                  Infectious Acute Liver Failure

 

In many countries viral hepatitis is a common cause for FHF, especially hepatitis A and hepatitis B, it is extremely uncommon in hepatitis C. Survival rates in HAV patients with FHF are about 50-60%, much more favourable than the outcome for patients with other hepatitis. These patients account for a substantial proportion (10-20%) of the pediatric liver transplants in some countries despite the relatively mild infection that is observed in many children infected with HAV. In the developing world, acute HBV infection dominates as a cause of FHF.

 

Another cause for an infectious acute liver failure may be a sepsis.

A hepatic coma is observed relatively rarely and is connected with the severe diseases which will destroy liver parenchima(infectious viral hepatitis, cirrhosis of liver, poisoning by mushrooms). It is conditioned by insufficiency of detoxin function of liver which promote to penetration of toxins in CNS. At a hepatic coma in most cases the comatose state develops gradually, thus deep disorders of consciousness are rarely.

                                             

 

                       Other causes for acute liver failure include:

o   Acute Fatty Liver (as a result of pregnancy, tetracyclines, alcohol or Reye syndrome)

o   Multi Organ/Liver Failure after heart surgery

o   The HELLP (hemolysis, elevated liver enzymes and low platelets) syndrome occurs in 0.1-0.6% of pregnancies and usually is associated with preeclampsia.

o   Wilson’s Disease (hereditary copper accumulation) may infrequently present with acute liver failure. Without OLT, this is almost uniformly fatal.

o   Ischemic Liver Failure after surgical procedures and occlusion of hepatic artery.

o   Cryptogenic Acute Liver Failure (for nearly 15% of patients in the US, the cause of the acute liver failure remains indeterminate)

 

                              Clinical Criteria

Ø Prolonged jaundice (ie. beyond 14 days age)

 Plus:

Ø Pale stools

Ø Dark urine

Ø Failure to thrive

Ø Hepatomegaly

 

Other presentations:

Ø Coagulopathy

Ø Abnormal antenatal scan ~5%

Ø Splenomegaly / portal hypertension (late signs)

 

 

                                     Investigations

·        Liver function tests

·        Conjugated Bilirubin raised >100 umol/L (normal <20 umol/L)

·        Raised Alkaline Phosphatase, ALP >600 iu/L (normal <500 iu/L)

·        Gamma GT >100 IU/L (normal 20-40).

·        Albumin + Coagulation: usually normal at presentation

·        Abdominal Ultrasound

·        Hepatomegaly

·        Absent / contracted gallbladder after 4 hour fast

·        HIDA or TEBIDA (N-tert–butyliminodiacetic acid + phenobarbitone pre-treatment 3-5 days) hepatobiliary scanning

·        Good hepatic uptake, reduced / absent excretion to intestine.

 

                                             Percutaneous liver biopsy

ü Portal fibrosis

ü Cholestasis

ü Biliary duct proliferation

                                                 Differential Diagnoses

ü Alpha-1-antitrypsin deficiency

ü All causes of Neonatal Jaundice

 

A clinic is characterized by psychical excitation with the signs of hallucinations, dellirium, conditioned reflexes are low-spirited with saving of unconditioned reflexes. Muscular tone and tendon reflexes are promoted, quite often there are the meningeal signs. An icterus is a permanent sign. As a result of change of formation of prothrombini and oppression of thromocytopoesis there are bleeding from a skin and mucus membranes. Breathing is deep, toxic, from a mouth sweetish smell of fresh liver is hearihg. Tachycardia, increased tones of heart, arterial blood pressure is low. A liver at first is enlarged. In the period of development of coma quickly becomes soft and decrteased (yellow dystrophy of liver). In a blood: hyperbilirubinemia due to direct faction, hypernitrogenemia, hyperproteinemia. In urine: aminiaciduria, proteinuria, cylinduria, billiar pigments.

 

Signs	Hypochloremic		Hepatic	Acetonemic (nondiabetic)
Previous or basic disease		Diseases which are accompanied by vomit	Disease of liver: infectious hepatitis, hepatocholengitis, innate and acquired cirrhosis of liver	Having a fever diseases, cyclic acetonemic vomit
Beginning		Slow	Gradual	Gradual
Consciousness		Gradual loss of consciousness	Gradual development of the comatose state, which passes through all stages, but rarely reaches to the deep coma, hallucinations and delirium	Oblivion, somnolence, passes through all stages, sopor, coma
Motive activity		Adynamia, tetania, hyperreflection, catalepsy, fibric convultions	Spastics, that reaches to contructure, increased reflexes, meningeal symptims	Blood pressure is low, and reflexes are reduced
Convultions		–	–	Rarely
Breathing		Encreased, superficial, unpleasant smell from a mouth	Deep, toxic (Kussmaul), smell of raw liver (meat)	Deep, toxic, strong smell of acetone from a mouth
Cardio-vascular changes		Deaf tones, low АP speed-up soft pulse, arrhythmia	Tachycardia, palpitation, blood pressure  is low, soft incomplete filling pulse	Deaf cardiac tones, soft pulse low АP
Changes of digestion		Absence of appetite, diarrhea and vomit	Vomit, pneumatic stomach, increase of spleen	Absolute absence of appetite, massive vomit
Liver		Depending on the basic disease	Decreased	Increased, sickly
Eyes		Pupils wide	Pupils are extended	Without the changes
Skin		Turgor is diminished and elasticity	Dry icteric or subicteric, slightly swollen, point hemorrhage	Dry, pale, cheeks are red
Edemata		Absent	Small	Absent

 

 

 

 

 

 

 

Blood	Leucocytosis hypochloremia, alcalosis	Direct billirubin (+++), increase of products of disintegration	Hypochloremia, acidoketonemia absence of hyperglucemia
Urine	Oliguria, anuria, albumen (+), a little amount of form elements	Billirubin (++), at acute yellow atrophy decreases, aminoacidiria (leycini, tirosini), insignificant albuminuria	Acetone, acetovinegar acid, glucosuria (-)

 

Help on a prehospital stage at a hepatic coma

1.     Oxygentherapy by an oxygen pillow.

2.     At convultions – 20 % solution of Oxybutiratis sodium  50-100 mg/kg of  mass  intravenously streamly slowly on 10-15 ml 10 % Glucose or 0,5 % solution of Seduxeni 0,1 ml/kg of of mass intravenously streamly or intramuscular.

3.     After help and at diminishment of clinical sings hospitalization. During transporting  intravenous in drops introduction of isotonici solution of sodium  chloride.

Help on a hospital stage

1.     Infusion therapy. Common amount of liquid for introduction – 60-70 % age-old necessity: 2/3 day’s volume the liquid – Glucose 5-10 % solution, other (1/3 liquids) are expanders, salt solutions (Reopoliglucini, isotonic solution of sodium  chloride, the Ringer solution).

2.     Cocarboxylazae   5 mg/kg  of mass, 5 % solution of ascorbinati sodium 150-500 mg intravenously streamly.

3.     Glucocorticoids ( Prednisoloni  a 5-10 mg/kg  of mass on day) by even doses in 3-4 hours without the nightly interruption  intravenously streamly.

4.     Intravenously in drops ingibitors of proteolysis: Trasiloli, Gordox to 100 000-250000 U  daily, Contricali to 50000 U  daily (in 3-4 introductions).

5.     At hypokaliemia intravenously in drops 4 % or 7,5 % solution of potassium  chloride in a dose 2 mmol/kg  daily (1 ml 7,5 % to solution contains   1 mmol/l of potassium).

6.     Syngrom therapy:

–         at convultions: 20 % solution of Oxybutiratis sodium  50-100 mg/kg of  mass or 0,5 % solution of Seduxeni 0,1 ml/kg of of mass intravenously streamly slowly on 10 ml 5-10 % Glucose;

–         at  edema syndrome: 1 %  of Lasix solution  1-3 mg/kg of  mass daily intramuscular or intravenously streamly; Mannitoli 1-3 g/kg of  the mass on one introduction (as 30 % solution)  intravenously in drops;

–         at cardiac insufficiency:  0,06 % Corgliconi  solution or Strophantini 0,05%  0,01-0,015 ml/kg intravenously streamly on  10 ml isotonici solution of sodium  chloride;

–         at a hemorrhagic syndrome: 5 % solution e–aminocaproni acids 0,1 ml/kg of  the mass for one occasion dose intravenously in drops; 1 % solution of Vicasoli 0,5-1,0 ml intramuscular 1-2 times per day ; 10 % solution of  calcium gluconati a 1 ml/yr of  life  intravenously streamly; Fibrinogeni intravenously in drops 1,5-2 mg/kg of  the mass daily.

7.     Antibiotics (Pennicillini, Cephalosporins).

8.     In absence of effect from base treatment — replaceable blood transfusion, hemosorbtion, amino acid dialysis with next Plasmophoresis, transplantation of liver.

 

Reye Syndrome  (acute hepatic encephalopathy) is a malignant syndrome at the infectious diseases. Conditioned superfluously by acute hepatic insufficiency with the metabolic disturbance, that arises up at the acute viral diseases treated by the high doses of salicylics. Inherent to the children, thus than junior child, the more frequent it meets.

                                               Definition

 

Reye syndrome is sudden (acute) brain damage (encephalopathy) and liver function problems of unknown cause.

 

The syndrome has occurred with the use of aspirin to treat chickenpox or the flu in children. However, it has become very uncommon since aspirin is no longer recommended for routine use in children.

                                      

 

 Causes

 

Reye syndrome is most often seen in children ages 4 – 12. Most cases that occur with chickenpox are in children ages 5 – 9.In pathogenesis the main role has a toxicoinfective influence on a liver. In a few days unrestrained vomit, severe motive and psychical excitability which in a few hours passes to delirium and deep coma without tonico-clonic convultions, appears from the beginning of illness. In most cases a coma is accompanied by severe disorders of breathing, hemorrhages. The increase of liver and icterus are not present. A diagnosis is confirmed by the considerable increase of transaminases, lactatdehydrogenasis, by the decline of blood coagulation factors (П, V, VI, ІХ, Х), hypoglicemia, by hypernitrogenemia.

  

 

 

Reye’s syndrome is a very rare disorder that damages many parts of the body, especially the brain and the liver. For unknown reasons, some of the cells that make energy (mitochondria) stop working correctly, causing severe illness. The most serious problems are swelling of the brain and problems with the breakdown of fat, which causes it to build up in the liver and other organs. The illness can be fatal, especially if not detected early and treated appropriately.

                               Reye’s syndrome Treatment

 

          Treatment depends on the symptoms, but all patients with Reye’s syndrome need to be treated in a hospital and monitored closely. Treatment focuses on protecting the brain against irreversible damage by preventing or reducing brain swelling.

 

                         Specific treatments may include:

 

·        Giving fluids containing sugar and salts intravenously (into a vein)

·        Medications (for example, to decrease brain swelling or treat problems caused by liver failure)

·        Intubation (inserting a tube that helps with breathing) to protect the lungs and also reduce brain swelling

·        Patients with more serious disease typically are treated in an intensive care unit.

 

 

                                     Reye’s syndrome Prevention

 

              Although a clear link between aspirin and Reye’s syndrome has not yet been proven, experts agree that to prevent Reye’s syndrome, the safest approach is never to give aspirin or aspirin-containing medicines to children. Read labels carefully. Look for the word aspirin and other words that also mean aspirin: acetylsalicylate, acetylsalicylic acid, salicylic acid and salicylate. Wheecessary, non-aspirin medicines, such as acetaminophen (Tylenol), should be used instead.

 

Referens:

A – Basic:

1.     Pediatrics. Textbook. / O. V. Tiazhka, T. V. Pochinok, A. N. Antoshkina et al. / edited by O. Tiazhka – Vinnytsia : Nova Knyha Publishers, 2011 – 584 pp. : il.ISBN 978-966-382-355-3

2.     Nelson Textbook of Pediatrics, 19th Edition Kliegman, Behrman. Published by Jenson & Stanton, 2011, 2608.  ISBN: 978-080-892-420-3.

3.     Illustrated Textbook of Paediatrics, 4th Edition.  Published by  Lissauer & Clayden, 2012, 552 p. ISBN: 978-072-343-566-2.

4.     Denial Bernstein. Pediatrics for medical Students. – Second edition, 2012. – 650 p.