LESSON № 3 (Practical class – 6 hours)
Topics:
1. The most common diseases of digestive systems in childhood.
2. The most common diseases of urinary systems in childhood.
3. The most common cardiovascular disease in childhood.
4. Hemorrhagic diathesis in childhood.
The most common diseases of digestive systems in childhood.
The digestive system is responsible for breaking down food, absorbing nutrients from the food, and ridding the body of waste products from the food. The digestive system consists of the:
Upper digestive tract, which includes the mouth, esophagus, and stomach.
Lower digestive tract, which includes the small and large intestines.
Liver, pancreas, and gallbladder.
DISEASES OF THE DIGESTIVE SYSTEM.
I. DISEASE OF THE MOUTH.
ACUTE STOMATITIS.
Definition.—An acute inflammation of the mucous membrane of the
mouth, occurring most frequently in children, though no age is exempt.
Etiology.—The causes that give rise to stomatitis are generally local,
though it may rise from gastric or intestinal derangements, chemical
and mechanical irritants being the most common, such as sharp edges of
broken or carious teeth; very hot drinks, such as tea and coffee; highly
spiced food; tobacco, both chewing and smoking; irritating dust inhaled
at certain work, such as lime, coal, marble, and workers in various
minerals; the corrosive acids or alkalies; and sometimes from the
decomposition of food lodged between the teeth, and fetid cavities. It
may also be caused by dentition, or follow the eruptive fevers.
Symptoms.
The inflammation is attended by the following symptoms: heat, pain, redness, and swelling. At first the mouth is dry and hot, with a burning, smarting sensation; but soon secretion is established, and mucus and saliva are found in excess. This condition is often called catarrhal stomatitis. Mastication is painful, and hot drinks, and coarse food give rise to pain. The tongue is coated, the breath is fetid, and the
child becomes peevish and cross. In a few days the disease loses its angry character, the inflammation becomes subacute, while the mouth is bathed in a ropy, offensive mucus.
Diagnosis.—The diagnosis is easily made. The red, inflamed character of the mucous membrane; the tenderness, the burning sensation, dry mouth, followed by hypersecretion of mucus, are symptoms which caot be mistaken for those of any other trouble.
Prognosis.—The prognosis is favorable, the disease usually giving way in a week or ten days.
Treatment.—This is simple and quite successful. After thoroughly cleansing the mouth with a weak solution of pyrozone, or a wash of comboracic acid, or, better still, a solution of hydrastin and chlorate of potassium, we prescribe phytolacca ten drops, and water four ounces; a teaspoonful every hour. As a mouth-wash I know of nothing to equal the phosphate of hydrastia and chlorate of potassium. If there are any gastric or intestinal complications, remedies should at once be used to correct these wrongs. If there should be fever, combine aconite with the phytolacca, and give every hour. The mouth should be kept sweet and clean. The diet should consist of liquid food; warm drinks are more agreeable than very cold or very hot fluids.
APHTHOUS STOMATITIS.
Synonyms.—Follicular Stomatitis; Disseminated Vesicular Stomatitis; Fibrinous Stomatitis.
Definition.—A variety of stomatitis, characterized by small, round, white patches upon the mucous membrane of the tongue, gums, and cheeks. Small vesicles appear upon an inflamed base, and later form small ulcers.
Etiology.—This variety usually occurs in children under three years of age, though it may occur at any period of life. It may accompany the acute infectious diseases, and occasionally occurs as an epidemic. An impoverished condition of the blood favors the disease, as well as poor hygienic surroundings; gastro-intestinal disorders also predispose to this lesion, while Strumpell believes the milk from cows suffering from the hoof and mouth disease, is an exciting cause.
The time of the year may also be considered a factor in this disease, spring and fall being the seasons when colds prevail and intestinal disturbances are common.
Symptoms.—The mouth is exquisitely tender, and, wheursing or attempting to eat, a burning sensation follows. As a result, the child is peevish and fretful. The tongue is furred, the breath is fetid, and a slight fever is occasionally noted; there may be some gastric or intestinal disturbance.
On inspecting the mouth, small vesicles are seen on the inner surface of the lips, and along the sides of the tongue, and near the frenum; they may also be found on the cheeks; these rupturing, small, white patches, surrounded by a red base are observed, which may later ulcerate. There is a free secretion of saliva and mucus, which, in the infant, dribbles from the mouth, and in older patients necessitates frequent spitting.
There may be enlargement of the submaxillary glands.
Diagnosis.—The small vesicles upon the sides of the tongue and mouth, followed by white or yellowish patches, make the diagnosis plain.
Prognosis.—The disease usually yields to treatment in a week or ten days, though some cases prove very intractable, with a tendency to recur at intervals.
Treatment.—Cleanliness is of the greatest importance, and the mouth should be rinsed with lukewarm water after each feeding. In bottle-fed babies, great care must be taken that the bottle and nipple are kept sweet and clean, the nurse being instructed to scald out the bottle after each nursing, and lay in plain cold water, or in soda or lime water.
For a mouth wash, potassium chlorate and hydrastis, or boracic acid, will prove among the best. Painting the patches with equal parts of thuja and water is also frequently beneficial. Internally, specific phytolacca is the remedy par excellence. If there is fever, add aconite to the above. Where the tissues are bluish and the breath bad, echinacea will prove more effective. Where the tongue is coated with a moist, yellow, pasty coating, potassium chlorate and hydrastis one dram, to water four ounces, a teaspoonful every hour, will give relief and the best results. Where there is hypersecretion of saliva, specific belladonna ten drops, to water four ounces, will be indicated. Dr. Webster likes the action of jaborandi for this same condition. In the adult, where the ulcers persist, apply bluestone direct to the ulcers.
THRUSH.
Synonyms.—Parasitic Stomatitis; Stomatitis Mycosa.
Definition.—A specific fungous disease of the buccal mucous surfaces, characterized by whitish or yellowish deposits, in which are found the saccharomyces albicans.
Etiology.—Predisposing causes are such as furnish a soil suitable for the propagation of the thrush fungus; such as tuberculosis, congenital syphilis, or any disease whereby the blood is impoverished. In bottle-fed children, when cleanliness is not observed, and the bottle and tube contain sour milk; in adults, typhoid fever, diabetes, and carcinoma, are fruitful causes.
The specific cause is the fungus above mentioned (saccharomyces albicans), which thrives in the changed condition of the mouth secretions, fermentation having changed the normal alkaline secretion to acid.
Symptoms.—The child is fretful and peevish, the result of the burning pain, and frequently a diarrhea, with greenish stools, occurs. On inspecting the mouth, we find the mucous membrane dry and of a dusky red color, upon which are seen the thrush spots in the form of white patches, first upon the tongue, rapidly extending to the lips,
cheeks, pharynx, and sometimes to the esophagus and stomach.
When the extension is so general, a troublesome diarrhea exists. The saliva, after a few days, becomes profuse, but is acid in character; in fact, we find an acid saliva iearly all forms. of stomatitis.
Diagnosis.—The dryness of the mouth in the early stage, the white patches, which can be readily removed without bleeding, the absence of the yellow ulcers seen in aphthous stomatitis, makes the diagnosis comparatively easy. The presence of the fungus, revealed by the microscope, makes the diagnosis positive.
Prognosis.—This is favorable unless there is marked cachexia, in which case it may be quite stubborn.
Treatment.—Remembering that the fungi thrive in an acid medium, our mouth-washes will be selected to correct this condition ; hence the alkalies are used; bicarbonate of sodium, boracic acid, potassium chlorate, etc. After each feeding, the mouth is to be carefully washed, every particle of food being removed. Sweets of all kinds are to be avoided, as they favor fermentation. The general health is to be improved by adopting more favorable hygienic conditions. Plenty of fresh air and wholesome and easily digested food will be important factors in the cure.
Phytolacca, echinacea, nux vomica, rhus tox., and others of like character, will be used. Inunction of quinine and lard will improve the condition of the skin, and act as a tonic. In all these cases we are not to overlook the great fact that the impoverished condition of the blood furnishes the soil for the development of the parasite, and remedies are to be used which will give us a better blood, and consequently a more healthy body. When we fail in this respect, the local trouble persists in spite of local treatment.
ULCERATIVE STOMATITIS.
Synonyms.—Fetid Stomatitis; Putrid Sore Mouth.
Definition.—A stomatitis characterized by the formation of ulcers on the gums and cheeks, attended by an offensive breath.
Etiology.—This is a disease of childhood, though it is sometimes met with in the adult. The predisposing causes are similar to those of aphthous stomatitis and thrush; viz., poor hygienic conditions, bad air, light, and food; poor clothing, damp and filthy quarters, and all conditions that impoverish the blood. Neglect of the mouth, and bad teeth, also favor the disease. No doubt the infectious fevers favor the generation of the virus whatever that may be. It is most likely due to a specific germ; but, as yet, the specific cause has not been discovered.
Symptoms.— “On examining the mouth, we find the gums red, swollen, and spongy, and where the ulcer is situated, a grayish, pultaceous material, on removing which, the surface is raw and bleeding. It generally commences on the front part of the gums, but gradually passes between the teeth, affects the posterior surface; continuing, it destroys the gum both before and behind, and, passing to the lips and cheeks adjacent, forms irregular ulcerations, covered by the same material. If it continues long, the tongue is swollen, and is marked by the teeth; the saliva becomes thick and very offensive, often streaked with blood, the gums bleeding at the slightest touch. The stomach is usually deranged, the bowels irregular, the tongue covered with a dirty coat, and more or less febrile action.” (Scudder.)
Diagnosis.—The soft, spongy condition of the gums, the characteristic ulceration, the foul breath, the vitiated saliva, together with the cachectic appearance of the patient, render the diagnosis easy.
Prognosis.—The disease usually yields readily to treatment, and even in those cases due to impoverished blood a cure will result in a few weeks under specific medication.
Treatment.—After thoroughly cleansing the mouth with pyrozone, boracic acid solution, or listerine, and the removal of carious teeth, we put the patient on potassium chlorate and hydrastis, both for its local and systemic use. It will fit more cases than any other remedy. For the nasty, dirty, pasty coating upon the tongue, which tells of sepsis, use sodium sulphite. If the sub-maxillary glands are involved, phytolacca will prove our best remedy. When the tissues are dusky, baptisia or echinacea will prove the better agents.
The ulcers may be touched with thuja, or with nitric acid, applied on a pine pencil. The gastric and intestinal disturbance may call for nux vomica or small doses of Podophyllin. Drop doses of Howe’s acid solution of iron is a good tonic, as well as quinia and hydrastis. To harden the spongy gums, an application of tincture of myrrh and glycerin, three times per day, is useful. The diet should be nutritious and given in fluid form.
MEMBRANOUS STOMATITIS.
Synonym.—Croupous Stomatitis.
Definition.—An inflammation of the buccal mucous membrane, characterized by the formation of a false membrane.
Etiology.—There seems to be quite a difference of opinion as to the specific cause of this form of stomatitis. Some regard the Klebs-Loeffler bacillus as responsible for it, while others contend that gonorrheal or syphilitic infection in the new-born is the primary lesion that gives rise to the disease.
Symptoms.—This form of stomatitis appears in the shape of small, irregular patches, of a grayish white color, the parts surrounding being red, painful, and hot. Of this Scudder says:
“The breath is fetid, and the submaxillary glands enlarge. As the disease proceeds, the patches of membranous exudation extend, become more or less detached, and are succeeded by others, and the intervening surfaces are red and swollen. The tongue is swollen and the mouth continually open, allowing the escape of altered saliva. The enlargement of the lymphatic glands increases, the face swells, the breath becomes more fetid, and the pulse more quick and rapid, and generally soft, open. or full and weak.” “The disease sometimes extends back to the throat, and even involves the mucous membranes further, sometimes occasioning imminent danger. It may become chronic, and continue for weeks or months.”
Diagnosis.—This is made by the membranous character of the patches.
Treatment.— “With small doses of aconite we associate phytolacca, rhus, or baptisia, as indicated. When the tissues are full, the first; if contracted and hot, with vivid redness, sometimes fissured and bloody, the rhus; and if there is dusky discoloration, the baptisia. The remedies are used in the ordinary small doses, and the phytolacca and baptisia may also be used as washes. When the tongue is broad, pallid, and dirty—a rare case—sodium sulphite is the remedy.
‘As a local application, the hydrochloric acid with honey, one part to three, four, or six, will be found as good as anything; it should be applied with a small piece of sponge attached to a stick to the membranous exudations, being careful to reach them all. At the same time a saturated solution of potassium chlorate. with a small portion of glycerin, may be frequently used. An infusion of cinchona, acidulated with hydrochloric acid, has been recommended subsequently; but I would prefer the decoction of rumex, ainus, and quercus rubra.”
GANGRENOUS STOMATITIS.
Synonyms.—Cancrum Oris; Noma; Water Cancer.
Definition.—Gangrene of the cheek and gums, affecting delicate and sickly children, rarely the adult, and characterized by a rapid destruction of tissue. The disease is generally fatal.
Etiology. — Predisposing Causes. — Age. — The disease usually occurs between the ages of two and six years, and is more frequently found in girls than in boys.
Climate.—It prevails in low moist, countries, especially in
Infections Fevers.—While the disease may be primary, it frequently follows the infectious fevers, especially measles, scarlet fever, typhoid fever, typhus fever, and pneumonia. In fact, any disease that lowers the vitality, as well as poor hygienic conditions which impoverish the blood, predispose to noma.
The Exciting Cause.—Mercurialization has been thought, by many, to be responsible for this destructive disease, and from the similarity of symptoms of this and mercurial stomatitis, there are strong grounds for the belief. The microbic theory has its adherents, but as yet no specific germ has been discovered.
Symptoms.—The disease commences with an indurated swelling, usually near the angle of the mouth. On grasping the swollen mass between the finger and thumb, we get the sensation that the induration extends through the entire cheek. Externally the affected side is swollen, and presents a blanched, glassy appearance. Internally, there is a dusky redness, in the center of which the ulcer rapidly forms; phagedenic in character, it rapidly destroys tissue, and may perforate in three or four days, though rarely before seven or eight days. The entire cheek may be involved, the tissues melting awav like a snowball in the sun. From the ulcer an ichorous fluid is discharged, and shreds of tissue slough off and are mixed with the changed and vitiated saliva. The odor is peculiarly fetid and that of gangrene. The submaxillary glands are always swollen; usually there is but little pain.
As the disease progresses, the temperature rises to 104° or 105° ; the pulse, though feeble, is rapid. In swallowing, more or less of the ichorous fluid and shreds of the gangrenous tissue enter the stomach, and a troublesome diarrhea often follows, or the patient, poisoned by the inhalations from his own necrotic cheek, finds septic lobular pneumonia complicating the already overburdened system; the prostration increases, the mind wanders, or the patient sinks into stupor, and succumbs to general sepsis. Death may occur in a few days, or be delayed three or four weeks. In exceptional cases, the patient recovers, leaving great disfigurement from cicatrization of tissue; the disease is generally confined to one side.
Diagnosis.—When fully established, the diagnosis is not difficult. The hard, indurated nodule near the angle of the mouth, the phagedenic character of the ulcer, the gangrenous tissue and foul odor, and later the perforation, can hardly be mistaken for any other variety.
Prognosis.—This is a very grave disease, and the prognosis is decidedly unfavorable, principally due to the impoverished condition of the blood, and general sepsis.
Treatment.—The local treatment will consist of first cleansing the mouth thoroughly, trimming away the gangrenous sloughs and washing the ulcer with a five per cent solution of pyrozone, or a solution of potassium permanganate. The orifice should then be packed with cotton saturated in echinacea.
Internally, give echinacea three drams, water four ounces; teaspoonful one hour, alternating with a saturated solution of hydrastin or potassium chlorate. Where the tongue is covered with a nasty, dirty, pasty coating, sodium sulphite will be used. The mineral acids will replace the above remedies if the tongue be dry and brown and sordes appear on the teeth. The treatment will be antiseptic throughout.
GLOSSITIS.
Definition.—An inflammation of the parenchyma of the tongue, usually terminating in resolution, though suppuration occasionally results.
Etiology.—This may occur as the sequel of pneumonia, or as a complication, though the exciting cause is most frequently the result of bites or stings from insects, or scalds from hot fluids, or from corrosives. Anders suggests that injuries to the tongue provide an entrance for various bacilli, which may be an exciting cause.
Symptoms.—These depend somewhat upon the form, whether a primary or a secondary lesion. In the one case, swelling of the tongue begins rapidly, soon filling the mouth, and even protruding from the lips.
The tongue may be coated, though usually it is dry, red, and glossy. There is tenderness and pain and great difficulty in swallowing. The dyspnea is distressing and sometimes endangers life. The patient is unable to talk and distress is evident in every feature. There is an increased flow of saliva, with swelling of the submaxillary glands. The pulse is rapid, and the temperature ranges from 102° to 104°. It usually runs its course in from five to seven days. Where the disease is secondary the symptoms are developed more slowly, though similar to the ones just described.
Diagnosis.—The swollen, stiff, and immobile tongue renders the diagnosis easy.
Prognosis.—It is favorable in the acute form, but must be guarded, if a complication of a grave disease.
Treatment.—Where the tongue is badly swollen and tense, I have found soft linen cloths dipped in a solution of glycerin and potassium chlorate and hydrastis, and applied to the tongue, to give the greatest relief. Alkaline washes may also be used. Internally, aconite and phytolacca are useful; bits of cracked ice may be held in the mouth, and is grateful to the patient.
I would discourage scarifying the tongue, as the relief is but momentary and the pain quite severe. Inhalations of steam from hops and tansy or eucalpytus will also give relief. If the dysphagia is great, feeding by rectum may be necessary. Where the disease is secondary, in addition to the means above mentioned, appropriate remedies should be used for the primary lesion.
. II. DISEASES OF THE SALIVARY GLANDS. HYPERSECRETION.
Synonym.—Ptyalism.
Definition.—An excessive secretion of saliva.
Etiology.—The disease may occur in a number of affections; thus it is occasionally seen iervous, emotional children, and also in hysteria, here being due to a neurosis. It is sometimes present in the acute infectious fevers, notably small-pox. It is quite common in several forms of stomatitis, as has already beeoted. Pregnancy is occasionally accompanied by an annoying flow of saliva. Certain vegetable agents cause an excessive secretion, jaborandi, muscarin, and tobacco being the most common examples, though their action is soon over.
The most frequent cause, and by far the most serious, is from the ingestion of mercury, it sometimes lasting for weeks after a patient has been thoroughly mercurialized.
Symptoms.—The mouth is constantly bathed with saliva, which necessitates frequent spitting on the part of the patient, or, in children, an almost constant dribbling. Where it is very excessive, talking is carried on with difficulty. The almost constant wetting of the lips may be attended by chapping and cracking at the angles of the mouth.
Diagnosis.—The continued dribble, or frequent emptying of the mouth of saliva, is confirmatory of the lesion.
Prognosis.—The prognosis is favorable, though in pregnancy it may continue to full term, and, in the worst cases of mercurial-ization, may persist for weeks.
Treatment.—This will depend somewhat upon the cause. In the case of stomatitis, the treatment recommended for the local disease is sufficient for a cure. If it be due to pregnancy, iris versicolor will sometimes afford relief. Where it results from mercury, potassium chlorate, both as a wash and internally, will give good results. Belladonna, especially where there is general capillary congestion, is very efficient. Atropia in 1/100 grain doses once or twice a day is useful in some very persistent cases. Small doses of jaborandi will be found beneficial.
XEROSTOMIA.
Synonym.—Dry Mouth.
Definition.—A defect or arrest of the salivary and buccal secretions.
Etiology.—In some cases it is undoubtedly a neurosis, the large majority of cases occurring in females. In many cases the cause is unknown. Diabetes is frequently attended by great thirst and dryness of the mouth, and should be considered as a causal factor.
Symptoms.—The mouth is dry, red, or parched, resulting in difficulty in mastication, deglutition, and talking. Digestion is more or less impaired, and gastric symptoms may be present.
Diagnosis.—The patient calls our attention to the unpleasant condition of dryness, and inspection reveals the condition.
Prognosis.—This depends upon our ability to remove the cause.
Treatment.—Jaborandi given in large doses has been found beneficial. Galvanism promises more, perhaps, than drugs. In one very persistent case, that of an old gentleman, I recommended him to chew
Chronic gastritis
The gastritis is an inflammation of a mucosa of a wall of a stomach. There are acute and chronic forms of it enough extended among children, diseases. Acute gastritis often meets among the children, especially among the children at preschool age. And chronic gastritises very often begin at younger school age. It is bound by that at entering in school the general and alimentary regimen of children sharply changes. Besides it is enlarged emotional and an exercise stress. But it often happens that the diagnosis “gastritis” is also put to one-year-old children.
Gastritis can be a brief and sudden illness (acute gastritis), a longer-lasting condition (chronic gastritis), or a special condition, perhaps as part of another medical illness.
An example of acute gastritis is stomach upset that may follow the use of alcohol or certain medications such as aspirin or nonsteroidal anti-inflammatory drugs.
Helicobacter pylori is a type of bacteria that infects the stomach. Infection with this bacteria may lead to chronic gastritis.
Gastritis is a common medical problem, with up to10% of people who come to a hospital emergency department with the complaint of abdominal pain being ultimately diagnosed with gastritis.
Gastritis can be classified on the basis of the underlying cause (eg, Helicobacter pylori, bile reflux, nonsteroidal anti-inflammatory drugs , autoimmunity, or allergic response) and the histopathologic pattern, which may suggest the cause and the likely clinical course (eg, H pylori –associated multifocal atrophic gastritis).
Other classifications are based on the endoscopic appearance of the gastric mucosa (eg, varioliform gastritis). Although some gastropathies, such as those associated with NSAID intake, exhibit minimal inflammation, these entities are discussed in this article because they are frequently included in the differential diagnosis of chronic gastritis.
Chemical or reactive gastritis is caused by injury to the gastric mucosa resulting from reflux of bile and pancreatic secretions into the stomach, but it can also be caused by exogenous substances, including NSAIDs, acetylsalicylic acid, chemotherapeutic agents, and alcohol. These chemicals cause epithelial damage, erosions, and ulcers that are followed by regenerative hyperplasia detectable as foveolar hyperplasia, and damage to capillaries, with mucosal edema, hemorrhage, and increased smooth muscle in the lamina propria.
Because inflammation is minimal or lacking in these chemical-caused lesions, gastropathy or chemical gastropathy is a more appropriate description than chemical or reactive gastritis, as proposed by the updated
No single classification provides an entirely satisfactory description of all types of gastritis. However, an etiologic classification at least provides a direct target toward which therapy can be directed, and for this reason, such a classification is used in this article. In many instances, chronic gastritis is a relatively minor manifestation of diseases that predominantly manifest in other organs or manifest systemically (eg, gastritis in individuals who are immunosuppressed).
H pylori gastritis is a primary infection of the stomach and is the most frequent cause of chronic gastritis. Cases of histologically documented chronic gastritis are diagnosed as chronic gastritis of undetermined etiology or gastritis of undetermined type wheone of the findings reflect any of the described patterns of gastritis and a specific cause cannot be identified.
Symptoms
Gastritis in children symptoms do not always mirror what is happening in the stomach. They include the following:
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· Pain described as burning, aching, and gnawing in the center just below the rib cage where the stomach is located
The pain is usually in the upper central portion of the abdomen (the “pit” of the stomach). Sometimes gastritis pain occurs in the left upper portion of the abdomen and in the back. The pain seems to “go right straight through.” People often use the terms burning, aching, gnawing, or soreness to describe the pain. Usually, a vague sense of discomfort is present, but the pain may be sharp, stabbing, or cutting.
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· A sense of discomfort |
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· Nausea and vomiting: The vomit may be clear, green or yellow, blood-streaked, or completely bloody, depending on the severity of the stomach inflammation. |
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· Feeling of fullness or burning in the upper part of the belly · In more severe gastritis, bleeding may occur inside the stomach. Any of the following symptoms can be seen as well as those already mentioned. |
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· The stomach lining when examined through a viewing instrument, the endoscope, will have minimal or no changes at all in severe cases. |
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· Belching usually either does not relieve the pain or relieves it only briefly. · Bloating · The child may appear abnormally pale · Sweating · Stool may be dark red or black in color
Symptoms of gastritis in children is more or less the same. Ø Nausea Ø Vomiting Ø Weight loss Ø Loss of appetite Ø Poor growth Ø Heartburn Children are also seen to complain of severe pain in the abdomen. The problem with these symptoms is that they are common to so many other medical conditions.
The symptoms of gastritis in children may seem to be a lot worse, as compared to adults. This could be because a child’s digestive system is immature and therefore a bit weaker. Some of the most common gastritis in children symptoms include weight loss, diarrhea, heartburn, mild nausea, tarry stools, constipation, indigestion and pain in the stomach. Hence, as soon as any of these symptoms are seen in a child, it is important to consult a doctor. Children may need to undergo a physical exam or other tests, for a proper diagnosis. Some of the tests that may be required include x rays, blood tests, stool tests and an endoscopy.
Exams and Tests · Complete blood count (CBC) showing anemia · EGD (esophagogastroduodenoscopy) and biopsy showing gastritis · Stool guaiac test to check for blood in the stools
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Gastritis Treatment
The methods used for gastritis cure may vary, based on the factors that have caused the condition. Hence, chronic gastritis treatment may vary a bit from acute gastritis treatment, since their causes are usually different. Since chronic gastritis is caused by H. Pylori infections, chronic gastritis treatment needs to focus on the eradication of the bacteria. On the other hand, acute gastritis is usually a result of alcohol abuse or excess use of NSAIDS. Therefore, acute gastritis treatment mainly includes elimination of such habits. Most health care providers advise people to take medication for treating stomach acids, so that the signs and symptoms of gastritis remain under control.
The medicines that are a part of gastritis treatment include:
Ø Antacids for neutralizing stomach acids
Ø Medication for blocking acids and promoting healing
Ø Antibiotics for destroying the H. Pylori bacteria
Ø Medication to reduce the production of acid
Unfortunately, the side effects associated with most of the medicines mentioned above can be quite strong, which is why most people prefer going in for gastritis treatment that is natural. This includes the use of simple home remedies, using natural ingredients such as fresh ginger, garlic, fennel seeds, grape leaves, licorice, carom seeds and potato juice, spinach juice and carrot juice.
Since weight plays an important part in the symptoms of this condition, it is also important for people to follow the right gastritis treatment diet plan. Foods like acidic foods, sweets, alcohol, fried food, spices, aerated drinks and fatty food should be avoided. Apart from choosing the foods that are right, it is important for people to eat small portions at frequent intervals and drink a lot of water.
Since gastritis is usually caused by poor eating habits in children, one of the main components of gastritis in children treatment includes making dietary changes. The child needs to follow a proper diet, where neither too much, nor too little food is consumed. Some of the recommendations include:
Ø Drinking coconut water often
Ø Eating a bowl of rice every day
Ø Getting a good amount of fresh fruits and vegetables
Ø Including many fiber rich foods in the diet
Ø Taking two glasses of milk
Peptic ulcer disease
A peptic ulcer is a sore on the lining of the stomach or duodenum. A common cause of peptic ulcers is infection with the H. pylori bacterium, but a class of medications called non-steroidal anti-inflammatory agents (NSAIDs), like aspirin and ibuprofen, can lead to such ulcers as well.
Contrary to popular belief, stress and spicy foods do not cause ulcers, but can exacerbate existing ones. H. pylori leads to an ulcer by attacking the mucous shield that coats the stomach and duodenum, allowing digestive acid to get through to the lining beneath. The acid and the bacteria irritate the lining and cause an ulcer. H. pylori is a well known culprit in adult peptic ulcers but may not be as common in children. Peptic ulcers are unusual in healthy children. Children who have serious medical conditions may develop peptic ulcers as a secondary condition. Also, children may be more vulnerable to the effects of NSAIDs and therefore peptic ulcers in children may be caused by such medications more often than in adults..
The pathogenesis of peptic ulcer disease is multifactorial, but the final common pathway for the development of ulcers is the action of acid and pepsin-laden contents of the stomach on the gastric and duodenal mucosa and the inability of mucosal defense mechanisms to allay those effects. Abnormalities in the gastric and duodenal mucosa can be visualized on endoscopy, with or without histologic changes. Deep mucosal lesions that disrupt the muscularis mucosa of the gastric or duodenal wall define peptic ulcers. Gastric ulcers are generally located on the lesser curvature of the stomach, and 90% of duodenal ulcers are found in the duodenal bulb.
Symptoms
· dull stomach ache or pain
· abdominal discomfort that comes and goes
· pain and discomfort that typically occur several hours after a meal or in on an empty stomach
· pain, discomfort that may be relieved by eating
· pain and discomfort that are usually relieved by antacid medications
· bloating
· gas
· nausea
· less commonly, vomiting
Diagnosis
Ø X-ray of the gastrointestinal tract
Ø Endoscopy, an exam of the stomach and duodenum with an endoscope, a thin, lighted tube with a tiny camera on the end
Ø Blood test or stool test for H. pylori
Treatment
Ø Eradication of H. pylori (when present)
Ø Acid-suppressive drugs
Ulcers caused by H. pylori are treated with a course of antibiotics to eradicate the bacterium from GI tract, as well as with drugs to reduce stomach acid, and protect the stomach lining. Ulcers caused by NSAIDs are treated by stopping the medications that caused them and by taking drugs that promote healing of the stomach lining.
Complications
Hemorrhage: Mild to severe hemorrhage is the most common complication of peptic ulcer disease. Symptoms include hematemesis (vomiting of fresh blood or “coffee ground” material); passage of bloody stools (hematochezia) or black tarry stools (melena); and weakness, orthostasis, syncope, thirst, and sweating caused by blood loss.
Gastric Ulcer Perforation
A peptic ulcer may penetrate the wall of the stomach. If adhesions prevent leakage into the peritoneal cavity, free penetration is avoided and confined perforation occurs. Still, the ulcer may penetrate into the duodenum and enter the adjacent confined space (lesser sac) or another organ (eg, pancreas, liver). Pain may be intense, persistent, referred to sites other than the abdomen (usually the back when caused by penetration of a posterior duodenal ulcer into the pancreas), and modified by body position. CT or MRI is usually needed to confirm the diagnosis. When therapy does not result in healing, surgery is required.
Free perforation: Ulcers that perforate into the peritoneal cavity unchecked by adhesions are usually located in the anterior wall of the duodenum or, less commonly, in the stomach. The patient presents with an acute abdomen. There is sudden, intense, continuous epigastric pain that spreads rapidly throughout the abdomen, often becoming prominent in the right lower quadrant and at times referred to one or both shoulders. The patient usually lies still because even deep breathing worsens the pain. Palpation of the abdomen is painful, rebound tenderness is prominent, abdominal muscles are rigid (boardlike), and bowel sounds are diminished or absent. Shock may ensue, heralded by increased pulse rate and decreased BP and urine output. Symptoms may be less striking in elderly or moribund patients and those receiving corticosteroids or immunosuppressants.
Diagnosis is confirmed if an x-ray or CT shows free air under the diaphragm or in the peritoneal cavity. Upright views of the chest and abdomen are preferred. The most sensitive view is the lateral x-ray of the chest. Severely ill patients may be unable to sit upright and should have a lateral decubitus x-ray of the abdomen. Failure to detect free air does not exclude the diagnosis.
Immediate surgery is required. The longer the delay, the poorer is the prognosis. When surgery is contraindicated, the alternatives are continuous nasogastric suction and broad-spectrum antibiotics.
Gastric outlet obstruction: Obstruction may be caused by scarring, spasm, or inflammation from an ulcer. Symptoms include recurrent, large-volume vomiting, occurring more frequently at the end of the day and often as late as 6 h after the last meal. Loss of appetite with persistent bloating or fullness after eating also suggests gastric outlet obstruction. Prolonged vomiting may cause weight loss, dehydration, and alkalosis.
If the patient’s history suggests obstruction, physical examination, gastric aspiration, or x-ray may provide evidence of retained gastric contents. A succussion splash heard > 6 h after a meal or aspiration of fluid or food residue > 200 mL after an overnight fast suggests gastric retention. If gastric aspiration shows marked retention, the stomach should be emptied and endoscopy done or x-rays taken to determine site, cause, and degree of obstruction.
Edema or spasm caused by an active pyloric channel ulcer is treated with gastric decompression by nasogastric suction and acid suppression (eg, IV H2 blockers). Dehydration and electrolyte imbalances resulting from protracted vomiting or continued nasogastric suctioning should be vigorously sought and corrected. Prokinetic agents are not indicated. Generally, obstruction resolves within 2 to 5 days of treatment. Prolonged obstruction may result from peptic scarring and may respond to endoscopic pyloric balloon dilation. Surgery is necessary to relieve obstruction in selected cases.
Recurrence: Factors that affect recurrence of ulcer include failure to eradicate H. pylori, continued NSAID use, and smoking. Less commonly, a gastrinoma (Zollinger-Ellison syndrome) may be the cause. The 3-yr recurrence rate for gastric and duodenal ulcers is < 10% when H. pylori is successfully eradicated but > 50% when it is not. Thus, a patient with recurrent disease should be tested for H. pylori and treated again if the tests are positive.
Although long-term treatment with H2 blockers, proton pump inhibitors, or misoprostol reduces the risk of recurrence, their routine use for this purpose is not recommended. However, patients who require NSAIDs after having had a peptic ulcer are candidates for long-term therapy, as are those with a marginal ulcer or prior perforation or bleeding.
Stomach cancer: Patients with H. pylori–associated ulcers have a 3- to 6-fold increased risk of gastric cancer later in life. There is no increased risk of cancer with ulcers of other etiology.
Chronic hepatitis in children
Hepatitis is the inflammation of the liver and can result in liver cell damage and destruction.
Hepatitis in children has many different origins or causes. A child may contract hepatitis from exposure to a viral source. The following is a list of some of the viruses associated with hepatitis:
Ø hepatitis viruses – six main types of the hepatitis virus have been identified, including hepatitis A, B, C, D, E, and G.
Ø cytomegalovirus (CMV) – a virus that is a part of the herpes virus family that can be transmitted from person to person.
Ø Epstein-Barr virus (EBV) – the virus most commonly associated with infectious mononucleosis.
Ø herpes simplex virus (HSV) – herpes can involve the face and skin above the waist, or the genitalia.
Ø varicella zoster virus (VZV) – also known as chickenpox, a complication of VZV is hepatitis.
Ø enteroviruses – a group of viruses commonly seen in children such as coxsackieviruses, hand-foot-mouth disease, and echoviruses.
Ø rubella – caused by the rubivirus, rubella is a mild disease that causes a rash.
Ø adenovirus – a group of viruses that commonly cause colds, tonsillitis, and ear infections in children. They can also cause diarrhea.
Ø parvovirus – a virus referred to as fifth disease, which is characterized by a facial rash that is described as having a “slapped-cheek” appearance.
Ø The following is a list of some of the diseases that may cause chronic hepatitis in children:
Ø autoimmune liver disease – the body’s immune system develops antibodies that attack the liver causing an inflammatory process that leads to hepatitis.
Ø chronic viral hepatitis – usually caused by hepatitis B, C, or D.
Symptoms of hepatitis
The following are the most common symptoms for hepatitis. However, each child may experience symptoms differently and some children may experience no symptoms at all.
Symptoms of acute (abrupt onset) hepatitis may include the following:
· flu-like symptoms
· fever
· nausea and/or vomiting
· decreased appetite
· not feeling well all over
· abdominal pain or discomfort
· diarrhea
· joint pain
· sore muscles
· itchy red hives on skin
Later symptoms include dark colored urine and jaundice (yellowing of the skin, and eyes).
The symptoms of hepatitis may resemble other conditions or medical problems.
Diagnosis
In addition to a complete medical history and examination by your physician, diagnostic procedures and other tests to determine the extent of the disease may include the following:
blood testing for the following:
· liver function studies
· antibody studies (to check for hepatitis)
· cellular blood counts
· bleeding times
· electrolytes
· other chemicals in the body
ultrasound – a diagnostic imaging technique which uses high-frequency sound waves and a computer to create images of blood vessels, tissues, and organs. Ultrasounds are used to view internal organs of the abdomen such as the liver, spleen, and kidneys and to assess blood flow through various vessels.
liver biopsy -a small sample of liver tissue is obtained with a special biopsy needle and examined for abnormalities.
Treatment for hepatitis:
Specific treatment for hepatitis will be determined by your child’s physician based on:
· child’s age, overall health, and medical history
· extent of the disease
· child’s tolerance for specific medications, procedures, or therapies
· expectations for the course of the disease
· opinion or preference
Treatment for hepatitis varies depending on the underlying cause of the disease. The goal of treatment is to stop damage to the liver and alleviate symptoms. Treatment may include one, or more, of the following:
Ø supportive care (healthy diet and rest)
Ø medications (to help control itching)
Ø maintaining adequate growth and development
Ø avoiding alcohol and drugs
Ø preventing the spread of the disease (if the cause is viral hepatitis)
Ø antiviral or immunomodulator medications – interferon drug therapy is an example of this drug category and is referred to as a “biologic response modifier” that can affect the immune system and has virus-fighting activities.
Ø frequent blood testing (to determine disease progression)
Ø hospitalization (may be required in more severe cases)
Ø liver transplantation (may be recommended for end-stage liver failure)
Preventing the spread of viral hepatitis:
Proper hygiene is the key to preventing the spread of many diseases, including hepatitis. Other preventative measures include:
vaccinations
Vaccinations are available for hepatitis A and B.
blood transfusion
Blood transfusions are routinely screened for hepatitis B and C to reduce the risk of infection.
antibody preparation
If a person has been exposed to hepatitis A or B, an antibody preparation (immunoglobulin) can be administered to help protect them from contracting the disease.
Dental health and overall health are closely linked. The mouth can be seen as a gateway to a large amount of micro-organisms. These can sometimes be harmful to your health, causing infections that can reach other organs of your body. They find their way either by the digestive tract or through the bloodstream.
Most dental problems are caused by bacteria or other harmful micro-organisms. These microbes are the cause of tooth decay, gum disease and abscesses of the mouth. If these dental problems are not taken care of, damaging microbes grow in the mouth and then find their way by spreading to other organs of the body. There is evidence that some systemic diseases may be caused or complicated by such oral infections.
The digestion of food begins in the mouth. Your digestive system moves foods along the digestive tract and breaks down foods so the body can absorb and use the nutrients in foods. The health of teeth, which helps break down foods, is important to how well the digestive system processes foods.
Digestive system begins in the mouth and ends at the anus. Muscles move food through the digestive tract as the digestive system breaks down the food for absorption of the nutrients the body needs for healthy growth, development and maintenance. The process of breaking down food begins with the work of the enzyme amylase in saliva, which starts breaking down some carbs in food being chewed. Saliva moistens the food and works with the muscles in the tongue and mouth to move the food into the pharynx, which is the throat passageway through which food and air travel.
Different types of teeth have different functions in eating and preparing foods for your digestive system. Incisors, which are located at the front of your mouth, are the sharpest teeth and are shaped like shovels because they cut food and push it to the back of the mouth. Canine teeth, located in the corners of the mouth, have long roots to support grasping and tearing food. Located behind the canine teeth are the premolars, which have a chewing surface that is flattened for crushing food. The molars are located in the back of the mouth, where their larger, flatter surfaces grind and chew food into smaller pieces.
Problems
Pain, misalignment, infections, gum disease, and failure to brush and floss correctly can prevent proper chewing and breakdown of foods, and slow down digestion. Missing teeth can affect alignment and the stability of remaining teeth. Partially chewed food, because of pain or missing teeth, can result in partial digestion of food and insufficient absorption of nutrients by the body. Pain caused by unhealthy teeth can lead to avoidance of some foods, such as nutritious fruits and vegetables. The loss of nutrients can include those used to build and maintain healthy teeth and gums, which can result in more oral health problems.
The most common diseases of urinary systems in childhood.
The urinary tract is the network of organs and tubes that process and carry urine out of the body. The kidneys, ureters, bladder, and urethra are part of the urinary tract.
Urine is made in the kidneys. It flows through tubes (ureters) to the bladder. The bladder stores urine. And another tube, the urethra, carries urine to the outside of the body.
Urinary system parts and their functions:
two kidneys – a pair of purplish-brown organs located below the ribs toward the middle of the back. Their function is to:
· remove liquid waste from the blood in the form of urine.
· keep a stable balance of salts and other substances in the blood.
· produce erythropoietin, a hormone that aids the formation of red blood cells.
The kidneys remove urea from the blood through tiny filtering units called nephrons. Each nephron consists of a ball formed of small blood capillaries, called a glomerulus, and a small tube called a renal tubule. Urea, together with water and other waste substances, forms the urine as it passes through the nephrons and down the renal tubules of the kidney.
two ureters – narrow tubes that carry urine from the kidneys to the bladder. Muscles in the ureter walls continually tighten and relax forcing urine downward, away from the kidneys. If urine backs up, or is allowed to stand still, a kidney infection can develop. About every 10 to 15 seconds, small amounts of urine are emptied into the bladder from the ureters.
bladder – a triangle-shaped, hollow organ located in the lower abdomen. It is held in place by ligaments that are attached to other organs and the pelvic bones.The bladder’s walls relax and expand to store urine, and contract and flatten to empty urine through the urethra.
two sphincter muscles – circular muscles that help keep urine from leaking by closing tightly like a rubber band around the opening of the bladder.
nerves in the bladder – alert a person when it is time to urinate, or empty the bladder.
urethra – the tube that allows urine to pass outside the body. The brain signals the bladder muscles to tighten, which squeezes urine out of the bladder. At the same time, the brain signals the sphincter muscles to relax to let urine exit the bladder through the urethra. When all the signals occur in the correct order, normal urination occurs.
Urinary tract infections (UTIs) are common in kids. By the time they’re 5 years old, about 8% of girls and about 1-2% of boys have had at least one.
In older kids, UTIs may cause obvious symptoms such as burning or pain with urination (peeing). In infants and young children, UTIs may be harder to detect because symptoms are less specific. In fact, fever is sometimes the only sign.
Most UTIs are caused when bacteria infect the urinary tract, which is made up of the kidneys, ureters, bladder, and urethra. Each plays a role in removing liquid waste from the body. The kidneys filter the blood and produce urine; the ureters carry the urine from the kidneys to the bladder; and the bladder stores the urine until it is eliminated from the body through the urethra.
An infection can occur anywhere along this tract, but the lower part — the urethra and bladder — is most commonly involved. This is called cystitis. If the infection travels up the ureters to the kidneys, it’s called pyelonephritis and is usually more serious.
Although bacteria aren’t normally found in the urine, they can easily enter the urinary tract from the skin around the anus (the intestinal bacteria E. coli is the most frequent cause of UTIs). Many other bacteria, and some viruses, can also cause infection. Rarely, bacteria can reach the bladder or kidneys through the blood. Bacterial UTIs are not contagious.
UTIs occur much more frequently in girls, particularly those around the age of toilet teaching, because a girl’s urethra is shorter and closer to the anus. Uncircumcised boys younger than 1 year also have a slightly higher risk of developing a UTI.
Other risk factors for developing a UTI include:
· an abnormality in the structure or function of the urinary tract (for example, a malformed kidney or a blockage somewhere along the tract of normal urine flow)
· an abnormal backward flow (reflux) of urine from the bladder up the ureters and toward the kidneys. This condition, known as vesicoureteral reflux (VUR), is present at birth, and about 30% to 50% of children with a UTI are found to have it.
· poor toilet and hygiene habits
· the use of bubble baths or soaps that irritate the urethra
· family history of UTIs
UTIs are highly treatable, but it’s important to catch them early. Undiagnosed or untreated UTIs can lead to kidney damage, especially in kids younger than 6.
Signs and symptoms of UTIs vary depending on the child’s age and on which part of the urinary tract is infected. In younger kids and infants, the symptoms may be very general. The child may seem irritable, begin to feed poorly, or vomit. Sometimes the only symptom is a fever that seems to appear for no reason and doesn’t go away.
Neonates with urinary tract infection (UTI):
Ø Jaundice
Ø Fever
Ø Failure to thrive
Ø Poor feeding
Ø Vomiting
Ø Irritability
Infants:
Ø Poor feeding
Ø Fever
Ø Vomiting
Ø Strong-smelling urine
Ø Abdominal pain
Ø Irritability
Preschoolers:
Ø Vomiting
Ø Abdominal pain
Ø Fever
Ø Strong-smelling urine
Ø Enuresis
Ø Urinary symptoms: Dysuria, urgency, frequency
School-aged children:
Ø Fever
Ø Vomiting
Ø Abdominal pain
Ø Flank/back pain
Ø Strong-smelling urine
Ø Urinary symptoms: Dysuria, urgency, frequency
Ø Enuresis
Ø Incontinence
Adolescents are more likely to present with typical urinary symptoms; adolescent girls are more likely to have vaginitis (35%) than UTI (17%).
Ø ain, burning, or a stinging sensation when peeing
Ø an increased urge to urinate or frequent urination (though only a very small amount of urine may be produced)
Ø fever (though this is not always present)
Ø frequent night waking to go to the bathroom
Ø wetting problems, even though the child is toilet taught
Ø low back pain or abdominal pain in the area of the bladder (generally below the navel)
Ø foul-smelling urine that may look cloudy or contain blood
Diagnosis
Physical examination findings in UTI can be summarized as follows:
· Costovertebral angle tenderness
· Abdominal tenderness to palpation
· Suprapubic tenderness to palpation
· Palpable bladder
· Dribbling, poor stream, or straining to void
Urine collection methods for diagnosis include the following:
· Suprapubic aspiration
· Catheterization: The most commonly used collection technique in infants and younger children
· Midstream clean catch: Adequate for older children
· Urinalysis
The gold standard for diagnosing urinary tract infections (UTIs) is the isolation of a pathogen from a urine culture obtained via suprapubic aspiration.
However, because it may take as long as 48 hours for a urine culture to be positive, urinalysis is ofteeeded to help make the initial diagnosis of UTI.
Urinalysis for presumptive diagnosis of UTI includes the following:
· Bright-field or phase-contrast microscopy of centrifuged urinary sediment
· Gram stain of uncentrifuged or centrifuged urinary sediment
· Nitrite and leukocyte esterase test: Positive test means UTI likely
· Nitrite test: Positive test means UTI probable
· Leukocyte esterase test: Positive test is nonspecific
· Voiding cystourethrography
The following types of pediatric patients should undergo voiding cystourethrography after a first febrile UTI:
· Patients in whom treatment fails after 48-72 hours
· Patients with an abnormal voiding pattern (dribbling of urine)
· Infants and children in whom good follow-up is not assured
· Patients with an abdominal mass
· Infants and children with recurrence of a febrile UTI
Management
Antibiotic agents for parenteral treatment of UTIs include the following:
· Ceftriaxone
· Cefotaxime
· Ampicillin
· Gentamicin
Antibiotic agents for the oral treatment of UTIs include the following:
· Sulfisoxazole
· Trimethoprim/sulfamethoxazole
· Amoxicillin/clavulanic acid
· Cephalexin
· Cefixime
· Cefpodoxime
· Nitrofurantoin
Glomerulonephritis
Glomerulonephritis is a type of kidney disease that involves the glomeruli — very small structures in the kidneys that supply blood to units in the kidneys that filter urine — called the nephrons. During glomerulonephritis, the glomeruli become inflamed and impair the kidney’s ability to filter urine.
Glomerulonephritis can be acute (a sudden attack of inflammation) or chronic (coming on gradually).
Glomerulonephritis may develop after a bacterial infection, like strep throat, or it may be caused by a chronic condition.
Etiology:
a) bacterial (Group A streptococci, staphylococcal) infection;
b) Viral ( hepatitis B, mononucleosis);
c) Fungal ( histoplasmosis );
d) Parasitic (toxoplasmosis)
Classification:
Acute glomerulonephritis.
I a) with nephritic syndrome – renal edema, arterial hypertension, hematuria, proteinuria;
b) with nephrotic syndrome – marked edema, high proteinuria ( 3 gr per day and more ), hypoproteinemia, blood cholesterol is increased;
c) with nephrotic syndrome, adding arterial hypertension, hematuria;
d) with urinary syndrome
II Renal function : normal, damaged, acute renal insufficiency.
Chronic glomerulonephritis.
a) nephrotic form – marked edema, high proteinuria ( 3 gr per day and more ), hypoproteinemia, blood cholesterol is increased;
b) hematuric form – hematuria with proteinuria;
c) mixed form – edema, hypertension, and urinary syndroms.
Nephrotic syndrome
II Renal function :
normal
Damaged (Chronic renal insufficiency)
III Activity of renal process
Period of exacerbation
Period of partial remission
Period of full clinical and laboratory remission
Subacute (malignant) glomerulonephritis
-Without disorders of renal function
-With disorders of renal function
-Chronic renal insurfficiency
Symptoms of glomerulonephritis in children
In mild cases, there may be no symptoms; the disease is only discovered by a routine urine test or when chronic kidney failure develops.
For some it may present with fluid retention, and nephrotic syndrome is diagnosed after testing shows heavy proteinuria and hypoalbuminaemia.
When present, symptoms may include:
· Blood-stained, brown, smoky or foamy urine
· Reduced amounts of urine (although sometimes it is increased)
· Tiredness
· Lethargy
· Nausea
· Vomiting
· Hiccups
· Itching
· Sore throat
· Headaches
· Problems with breathing
· Rash
· Weight loss
· Joint pains
· Pale skin
· Fluid accumulation in the tissues
· High blood pressure
· Seizures
Diagnosis and treatment of glomerulonephritis
Glomerulonephritis must be diagnosed by a doctor, following
Urine tests
· urinanalysis
· Nechyporenko’s test
· Kakovsky-Addis test
· Ambyrze’s test
· urine culture
· Zimnitskiy’s test
Blood tests
· Fool blood count
· Biochemical test of blood
o Serum level of electrolytes
o total protein, albumin and globulin level
o cholesterole
o residual nitrogen, blood urea, creatinine
Throat swabs (to look for a bacterial infection),
Ultrasound scan of the kidneys or eventually a biopsy (where a small sample of tissue is taken from the kidney through a needle).
Treatment depends on various factors including the cause, the histological picture (the microscopic appearance of cells and tissues), the severity of kidney failure, the child’s age and general health. If an infective cause is found it may be treated with antibiotics but in most cases, the cause is unclear and there’s no cure; treatment aims to slow the disease, prevent complications and help the kidneys to do their job.
Possible treatments include fluid restriction, a diet low in protein, salt and potassium, diuretics (tablets that increase urine production), blood pressure medicines, antibiotics, steroids and drugs that suppress the immune system. In severe cases, kidney dialysis may be needed.
Further help for children with glomerulonephritis
It’s vital that children with glomerulonephritis get specialist care. In some cases the condition improves fairly quickly, but in others chronic renal failure develops. Under such circumstances, long-term therapy may be needed, including kidney dialysis and possibly a kidney transplant, with many implications for the wellbeing of the child.
The most common cardiovascular disease in childhood.
CARDITIS
Carditis, or inflammation of the heart, is most conveniently broken down into three categories:
Pericarditis – Inflammation of the pericardium
Myocarditis – Inflammation of the heart muscle
Endocarditis – Inflammation of the endocardium
MYOCARDITIS (nonrheumatic)
ETIOLOGICAL AGENTS:
Many species of viruses, bacteria, chlamydia, rickettsia, fungi and protozoans can cause myocarditis. However, viruses are the most important infectious agents. Of these, the enteroviruses are the single most important group.
OVERVIEW OF DISEASE:
The disease is an infection of the myocardium or muscle of the heart. The virus is ingested in fecally-contaminated water and/or food and eventually, either directly or indirectly, reaches the heart. There may be a prior skin infection before heart effects are seen. The virus invades the heart muscle cells and causes necrosis of the cells and clinical effects.
PATHOLOGY:
Necrosis of myofibers is seen initially and this may be either patchy or diffuse. An acute inflammatory reaction with polymorphonuclear leukocytes may be seen during the first few days of infection, and this is promptly followed by a mononuclear leukocyte cellular infiltrate by the end of the first week. Late changes include fibrosis and loss of myofibers.
Myocardial cell damage appears to occur in several ways:
a. Direct viral damage (e.g., with the Coxsackie B virus).
b. Inhibition of humoral and macrophage-mediated immunity early in the infection.
c. T-cell mediated cell lysis late in the disease.
DIAGNOSIS:
In infants and young children the disease progresses rapidly, beginning with fever, tachycardia and listlessness and progressing with signs and symptoms of CNS, gastrointestinal, liver and myocardial involvement. Cardiac failure may be evident within a few days of onset of the illness.
In older children and adults the illness usually progresses more slowly with generalized manifestations of viral infections localized to:
a. Respiratory tract
(1) Moderate fever
(2) Cough
(3) Coryza
b. Abdomen
(1) Pain
(2) Nausea
(3) Vomiting
Myocardial involvement becomes manifest one or two weeks after the initial illness with:
a. Fever
b. Malaise
c. Fatigue
d. Dyspnea (labored or difficult breathing)
e. Palpitations (tachycardia)
f. Altered heart sounds (muffled, transient pericardial rubs)
g. Chest pain
h. Electrocardiographic changes
i. Cardiomegaly
j. Pulmonary congestion
k. Abnormal laboratory findings:
(1) Increased sedimentation rate
(2) Increased leukocyte count
(3) Increased myocardial isoenzymes
(a) Serum Glutamic Oxaloacetic Transaminase (SGOT)
(b) Creatinine Phosphokinase (CPK)
(c) Lactic Dehydrogenase (LDH)
TREATMENT:
Viral myocarditis is typically a mild disease and responds well to bed rest. Bacterial, fungal and protozoan myocarditis can be treated with the appropriate antibiotics. Glucosteroids and other immunosuppressive drugs are CONTRAINDICATED.
ENDOCARDITIS
Endocarditis, inflammation of the membrane lining the chambers of the heart and covering the cusps of the various valves, is caused directly by microbial colonization of the endocardium or indirectly by induction of autoimmunity, as in acute rheumatic fever. Direct colonization is termed infective endocarditis and is caused by microorganisms physically present in endocardial lesions know as vegetations. The disease may be either acute or chronic.
ETIOLOGY:
Almost all bacteria and many fungi, when they get into the blood stream, can cause infective endocarditis. However, 80% of the cases are caused by streptococci or staphylococci.
OVERVIEW:
Relatively avirulent microorganisms derived from the normal flora of the body cause most cases of infective carditis. They gain access to the blood intermittently, as a result of minor trauma to the mucosa of the oropharynx, gastrointestinal tract or genitourinary tract. Such transient bacteremias usually occur without ill effects but they will lead to endocarditis in patients with an underlying cardiovascular lesion or with a suppressed immune system. Intravenous drug abusers commonly have infective endocarditis due to Staphylococcus aureus from contaminated needles. Blood-borne organisms are deposited on the downstream side of the valves where they colonize and cause disease.
PATHOLOGY:
As bacteria colonize the endocardium, they form vegetations which vary in size from tiny bodies to masses large enough to occlude valve orifices. Often, they are soft and friable and only loosely attached to the endocardium. Thus, they break off easily to form arterial emboli. Fungal vegetations tend to be bulky, giving rise to large emboli. Apart from the propensity to generate emboli, there is no correlation between size of vegetation and severity of endocarditis.
The bulk of the vegetation is an amorphous mass of fibrin and platelets containing colonies of microorganisms. There may be inflammatory cells attached to the vegetation. There are four consequences to the formation of this vegetation:
a. Organisms within the vegetation are protected from antibodies, complement, and leukocytes
b. Organisms within the vegetation are metabolically inactive, replicating at an unusually slow
rate, rendering them relatively resistant to the action of many antimicrobics
c. Healing is slow because macrophages and fibroblasts must spread through the vegetation
and endothelial cells must grow over the surface.
d. Emboli are generated when vegetations break off; these cause infarcts.
Abscesses may develop by direct invasion of the valve rings of the heart near the vegetations. These are common with pyogenic cocci but rare with other organisms.
CLINICAL SYMPTOMS:
The interval between the colonization of the endocardium and the onset of symptoms is two weeks. Death can occur about 6 weeks after colonization if the disease goes untreated. The initial symptoms are those of any infection:
a. Low grade fever
b. Anorexia
c. Fatigue
d. Weight loss
e. Anemia
f. Splenomegaly
Serologic findings include:
a. Hypergammaglobulinemia
b. High levels of rheumatoid factor
c. High levels of antinuclear antibody
d. High levels of circulating immune complexes
The circulating immune complexes give rise to skin manifestations which include:
a. Splinter hemorrhages
b. Petechia
c. Osler’s nodes
d. Janeway’s lesions
Common Peripheral Manifestations of Infective Endocarditis.
Roth spots
Urinary findings may include:
a. Proteinuria
b. Microscopic hematuria
c. Red blood cell casts
Heart murmur is present at some times during the disease but is generally not constant. If the tricuspid valve is damaged to the extent that there is tricuspid regurgitation, Carvallo’s sign will be present; this is augmentation of the pan-cystolic murmur by inspiration.
DIAGNOSIS:
Because the clinical features of the disease can be quite variable and ofteonspecific, diagnosis is mainly based on laboratory tests. Blood culture and serologic testing are the most important. Always use venous blood to isolate the organism. A positive blood culture with some or all of the symptoms listed is needed to obtain the diagnosis.
TREATMENT:
Antibiotic therapy must persist for at least 14 days, even if symptoms disappear prior to that time. A combination of antibiotics, rather than a single antibiotic, is always used. If no organism has been isolated after repeated attempts the recommended therapy is:
Ampicillin, given IV every 4 hours + Gentamycin, given every 8 hours.
If an organism has been isolated, then the antibiotic regimen is based on the species of the etiologic agent, the age of the patient and the extent of the disease. The regimens are complex and are listed in various reference books.
If antibiotic therapy is not successful surgical removal of infected endocardium may be necessary. This is especially true with fungal infections and when the patient has an intracardiovascular prosthesis.
Nonspecific therapy includes:
· Bed rest
· Low salt diet
· Alleviation of congestive heart failure
· Control of fever
· Transfusion to maintain a hematocrit close to 30%
Acute rheumatic fever
Rheumatic fever (acute rheumatic fever or ARF) is an autoimmune disease that may occur after a group A streptococcal throat infection that causes inflammatory lesions in connective tissue, especially that of the heart, joints, blood vessels, and subcutaneous tissue.
The disease has been described since the 1500s, but the association between a throat infection and rheumatic fever symptom development was not described until the 1880s. It was associated with scarlet fever (rash caused by streptococcal exotoxins) in the 1900s. Prior to the broad availability of penicillin, rheumatic fever was a leading cause of death in children and one of the leading causes of acquired heart disease in adults. The disease has many symptoms and can affect different parts of the body, including the heart, joints, skin, and brain. There is no simple diagnostic test for rheumatic fever, so the American Heart Association’s modified Jones criteria (first published in 1944 and listed below) are used to assist the physician in making the proper diagnosis.
Jones criteria are guidelines decided on by the American Heart Association to help doctors clinically diagnose rheumatic fever.
Two major criteria or one major and two minor plus a history of a streptococcal throat infection are required to make the diagnosis of rheumatic fever.
The major criteria for diagnosis include
· arthritis in several joints (polyarthritis), or migratory polyarthritis (joint inflammation), which usually presents first and occurs in 45% of patients and most commonly affects the large joints such as the knees
· heart inflammation (carditis), (inflammation of the heart), which occurs in 60% of patients is the most severe symptom of ARF and can result in permanent damage to the heart valves, and can be life threatening;
· nodules under the skin (subcutaneous nodules or Aschoff bodies), which are firm, painless lumps most frequently found around the wrists, elbows and knees. These are present in only 2% of patients
· rapid, jerky movements (Sydenham’s chorea), occurs in 30% of patients and is a movement disorder comprising of purposeless volatile movements of the face and arms. This was also called St. Vitus’ dance, which was named after the patron saint of the “mania dancers” of the middle ages
· skin rash (erythema marginatum), which occurs in 5% of patients and often described as a “serpiginous” with a wavy and snakelike appearance which has distinct erythematous (red) borders or “margins”
The minor criteria include
· fever, is often present during the acute infection with group A strep and is present during the initial phase of rheumatic fever.
· high ESR (erythrocyte sedimentation rate, an laboratory sign of inflammation),
· joint pain (arthralgia),
· EKG changes (electrocardiogram), and
other laboratory findings (elevated C-reactive protein, elevated or rising streptococcal antigen test).
Treatment :
Aims of treatment-
Ø Eradication of initiating streptococcal infection by a therapeutic course of penicillin.
Ø Treatment of acute carditis
Ø Treatment of extracardiac manifestations
Ø Specific treatment of congestive cardiac failure
Eradication of initiating streptococcal infection by a therapeutic course of penicillin-
The patient with acute rheumatic fever with whatever manifestations should be given a therapeutic course of antibiotic to eradicate residual streptococci which may be difficult to isolate.
A ten day course of oral penicillin or Inj Benzathine penicillin in single IM inj 1,20,000 IU in children above 60kg and 600,000 IU in children below 60kg. If patient is sensitive to penicillin – oral erythromycin 20mg/kg/day in three divided dose can be given for 10 days. Tetracyclines and sulphonamides are not used.
Bed rest –
Recommended duration and strictness of bed rest is variable. Reason for bed rest is to reduce cardiac work and to avoid use of involved joints.
In those patients with only arthritis 3 weeks, bed rest is advised. Generally patients with polyarthritis or arthralgia become asymptomatic by 2nd or 3rd week and also if at all carditis is going to develop it develops within 3 weeks. After three weeks, ambulatory bed rest is given.
In those patients with murmur of mitral &/or aortic regurgitant murmur but without cardiomegaly or CHF- two weeks complete bed rest and next two weeks gradual ambulatory bed rest is given.
In those patients with murmur and cardiomegaly without CHF, 4 weeks strict bed rest followed by 2 weeks ambulatory bed rest is given.
In those patients with murmur, cardiomegaly and CHF, strict bed rest is given until CHF is completely controlled and ambulatory bed rest is given for 4 weeks after anti-inflammatory therapy has been stopped.
Anti-inflammatory drugs –
Aspirin and steroids are the two anti-inflammatory agents of choice for treatment of acute rheumatic fever. Both drugs suppress inflammation, joint manifestations as well as acute phase reactions. There is a little or doubtful effect on erythema marginatum, subcutaneous nodules, chorea as well as on long term complication of arthritis. Aspirin is effective for arthritis but steroids are far superior to aspirin in case of severe carditis.
Why aspirin is not given in severe carditis?
· High dosage aspirin increases O2 consumption of myocardium and increases workload on heart and so precipitates CHF.
· It has been shown that if only aspirin is used in carditis, during the course of aspirin the patient can develop pericardial rub which never happens during steroid course.
· Aspirin exerts no specific effect on lesion of acute rheumatic process at any site but produces excellent symptomatic relief of arthritis and fever.
· There is not yet proven evidence that steroids reduce incidence and severity of residual rheumatic heart disease but there is definite impression that death during acute attack of carditis is prevented.
Duration of treatment:
With either drug, duration is 6 weeks or until patient’s clinical condition improves and ESR has returned to normal. Both drugs should be given for 4 weeks and then tapered off slowly iext 2 weeks. To avoid or minimize rebounds addition of aspirin towards the end of steroid treatment is quite useful.
Occasionally, it is necessary to continue the steroid treatment for longer periods of time especially in patients who remain in heart failure with other decongestive measures. If the patient remain in CHF beyond 3 – 4 months of steroid and other decongestive measurers one should seriously think of surgery.
In very severe CHF, methyl prednisolone parenterally should be used followed by oral prednisolone.
Aspirin : 100 – 120 mg/kg/day.
Prednisolone: 2 – 3 mg/kg/day
( maximum 60mg/day. )
Congestive heart failure In patients who present with heart failure, digitalis and diuretics are considered. Digitalis i.e. digoxin was previously contraindicated since some patients are extremely sensitive to the glycoside. It can be used if one remains on low dosage schedule.
Chorea – Isolated chorea is treated symptomatically since neither aspirior steroids have any effect on the course. The combination of phenobarbitone and chlorpromazine works well, if not haloperidol can be used.
Prophylaxis :
The story of rheumatic fever does not end with the completion of anti-inflammatory treatment and normalization of acute phase reactants. Every patient of acute rheumatic fever is a candidate for continuous prophylaxis as risk of recurrent attack of acute rheumatic fever continue.
The method of choice is monthly intramuscular injection of 1.2 mega units of benzathine penicillin and at times every three weeks. In case of genuine penicillin allergy, sulfonamides (0.5gm/daily <
The point of confusion is when to stop prophylaxis. If a patient presents with severe carditis or with recurrent episodes of Acute Rheumatic Fever, prophylaxis is considered for life. For moderate carditis, prophylaxis till 16 years and for mild or no carditis for 3 years from last episode should be given.
Hemorrhagic diathesis in childhood.
Hemorrhagic syndrome (Latin hemorrhagia – bleeding) is a clinical manifestation of the tendency of an organism to repeated bleedings and hemorrhages under the influence of insignificant trauma and so spontaneously.
The group of diseases, the clinical symptom of which is hemorrhagic syndrome are united under the name of hemorrhagic diathesis.
Hemorrhagic diathesis cases are divided into 3 basic groups.
The classification is based on the prevalence of the damage of one of three factors participating during hemostasis in the pathogenesis of the diseases:
1. Blood coagulation system.
2. The quantity and quality of thrombocytes.
3. Vascular wall (normally, the blood cells do not pass through it).
Classification of hemorrhagic diathesis
1. Coagulopathy – the basis of pathogenesis is a disordered blood coagulation system (hemophilia, etc.).
2. Thrombocytopathy – diseases are caused by the disorder in the formation and components of thrombocytes (Werlhof’s disease, etc.).
3. Angiopathy – the basis of the pathology is the disorder of the vascular wall (Henoch-Schonlein purpura, etc.).
HEMOPHILIA
Hemophilia – one of the kinds of coagulopathy – is an inherent disease, with prolonged (from several hours to several days) bleeding, caused by the disorder of blood clotting system.
Etiopathogenesis – the disease is genetically transmissed to the grandson from the grandfather through the healthy mother of the child who is the carrier of hemophilia. Only male gender suffers from it. However, some exceptions are possible: if the mother is a carrier of hemophilia, and the father has this disease then their daughter may suffer from hemophilia. It is necessary to note that the heredity of the disease (Fig. 178) is established only in 1/2-3/4 parts of its cases.
Pathogenesis of diseases is the disorder of the first phase of blood clotting: the presence of antihemophilic factors in the patient in less quantity than normal breaks the formation of plasmic thromboplastin, which results in the prolongation of blood-clotting time; leading to prolonged bleeding.
3 basic forms of hemophilia are differentiated depending on the prevailing lack of one of the antihemophilic factors:
1. Hemophilia A (=classical) – the deficiency of factor VIII (= antihemophilic globulin A). This is the most often form – 80% from the total quantity of patients.
2. Hemophilia B – the deficiency of factor IX (=plasma thromboplastin component). Its frequency is about 10-15%.
3. Hemophilia C – the decrease in the activity of factor XI (=plasma thromboplastin antecedent). The frequency of it is about 3-5%. Thus, in the basis of hemophilia lavs the disorder of the mechanism of the secondary internal hemostasis.
The clinical signs appear in the majority of patients at early childhood age, very rare in adult.
Complaints, external symptoms and the data of the objective examination, in all kinds of hemophilia are identical:
(a) Bleedings from the remains of the umbilical cord in a newborn.
(b) Bleedings in children of the breast-feeding age at teething, in grownups – while tooth extraction.
(c) Bleedings at insignificant trauma of skin (shaving, cut, bruise, scratches).
(d)Bleedinqs from the mucous membranes of nose, mouth, gastrointestinal path, in the urinary passage which can lead to posthemorrhagic anemia.
(e) Hemarthrosis. for which the increase in volume and tenderness of joints is characterized, can be accompanied by hyperthermia. Numerous hemarthrosis, when blood does not absorbed completely, can result in the deformation of joints, development of the contracture (restriction of the movements in a joint), ankylosis (full immobility in a joint) and physical inabilities of the children.
(f) Bruises and hematoma are the result of hemorrhages in the skin, subcutaneous, muscular tissue and in retroperitoneal space. The proceeding of hemophilia is characterized by periodicity – i.e. the periods of an aggravation (they happen quite unexpectedly, can be present even on the background of therapeutic prophylaxis of the disease) are replaced by the periods of remission of different duration (from several weeks to several years).
In childhood the disease frequently gets the severe form with high death rate (up to 75%). After 20 years the relief of clinical symptoms and rarer occurrence of aggravations are marked.
Diagnostic parameters of the laboratory investigation:
• The prolongation of blood clotting time (by Lee-White – from tens minutes to several hours).
• The prolongation of plasma recalcification time.
•Reduction of antihemophilic factors in plasma.
Attention! Analyses of the primary hemostasis (the quantity of thrombocytes. the parameter of clot retraction, etc.) and thrombin time in patients with hemophilia are within the limits of norm.
Treatment:
1. General measures:
Avoid severe injury, encourage non-violent exercises e.g. swimming.
Careful dental hygiene and regular dental examination.
Avoid intramuscular injections.
Avoid aspirin.
Vaccinate against hepatitis B.
Surgery is avoided, whenever possible, but wheecessary it should be carried out under cover of replacement therapy arid in a hospital which has the laboratory facilities for monitoring the response to this therapy.
Local measures may be used to arrest the bleeding from small wounds by pressure, immobilization and cold compresses.
2. Replacement therapy : The blood products used for replacement therapy include :
A. Fresh frozeti plasma : used in emergency since it can be readily available. Every 1 ml contains 1 unit of factor VIII.
B. Cryoprecipitate : each bag contains 125 units of factor VIII.
C. Factor =V111 concentrates : available in vials containing 250 and 500 units to be reconstituted in 25 ml. Doses: For usual hemarthrosis : 25 units/kg/12 h. For hematuria & GIT bleeding 50 units/kg/12 h. For CNS bleeding 50-75 units/kg/8 h.
D. Desmopressin: a vasopressin analog stimulates a transient increase in factor VIII levels. It is useful in mild cases.
E. Antifibrinolytic therapy as Epsilon aminocaproic acid : Used for the prevention or treatment of oral hemorrhage because salivkis rich in fibrinolytic enzymes.
Complications of hemophilia :
1. Joint deformities secondary to hemarthrosis.
2. Spontaneous or post-traumatic intracranial hemorrhage.
3. Hepatitis and AIDS.
4. Inhibitors to factor VIII develop in about 10% of all hemophiliacs leading to a poor clinical response to therapy.
Hemophilia B : (Factor IX Deficiency): X-linked recessive trait.
Clinical Picute : similar to hemophilia A.
Treatment: Fresh frozen plasma or factor IX concentrate.
Hemophilia C : (Factor XI Deficiency): Autosomal recessive trait affecting males and females equally
Clinical Picute; similar to hemophilia A.
Treatment: Fresh frozen plasma.
WERLHOF’ S DISEASE (=IDIOPATHIC THROMBOCYTOPENIC PURPURA)
In different sources of the medical literature till now Werlhof’s disease (German doctor of the 18 th century) – one among the different kinds of Thrombocytopathy – has many names. From the second specified name attentive students understood the following details of the pathological process of disease: in pathogenesis the primary factor is the thrombocytopenia, and the basic clinical symptom – purpura. In this case, in the basis of Werlhof’s disease lays the disorder of one of the links of primary hemostasis, particularly – of thrombocytes.
Etiopathogenesis – at present the cause of Werlhof’s disease is still not known.
According to etiology, there are two forms of the disease (in our native practice: idiopathic thrombocytopenic purpura is a general name of a group of diseases):
1. Hereditary (very rare).
2. Acquired which under different modern theories is divided into two forms:
(a) Primary (but still there are several theories of its etiology):
• The disorder of the bone marrow by slowing down the process of maturition megakaryocytes and separation of thrombocytes.
• The delay in the release of thrombocytes and their increased hemolysis in spleen.
• The immune theory according to which antithrombocytal autoantibodies destroy the thrombocytes in blood, and so influence pathologically the process of their separation in the bone marrow.
(b) Secondary – the occurrence of thrombocytopenia is promoted by viral infections, intoxication of miscellaneous genesis, endocrine and psychological disorders, medicines (especially vaccination), food and other factors.
However, irrespective of etiology, the main change in structure of blood at Werlhof’s disease is the reduction in the quantity of thrombocytes -thrombocytopenia. As it is mentioned above, simultaneously there is a decrease in the function of thrombocytes concerning the epithelia of blood vessels.
The following clinical signs of pathological process are observed :
(a) Arising of hemorrhages at any surface of skin and of naked mucous membranes, with the following characteristic symptoms:
• Asymmetric.
• Polymorphic – of different sizes (from petechia to ecchymosis).
• Polychrome (different colors) – as hemorrhages arise one by one at different times, simultaneously their color depends on the duration of the occurrence from red – claret (fresh) to blue-green and yellow color (in some days); the skin gets a characteristic look – ‘the leopard skin’ (our term).
(b) Bleedings :
• From mucous membranes of the nose, oral cavity, urinary bladder, gastro-intestinal tract, lungs, kidneys, etc.
• In the elder girls abundant menstrual bleedings.
(c) There can be hemorrhages into brain, pleura, retina of eyes.
Diagnostic parameters of the laboratory investigation (Fig. 172 B):
• Thrombocytopenia (can be up to several units).
• Prolongation of the duration of capillary bleeding according to Duke (10-20 minutes and more).
• Prolongation or absence of the clot retraction.
• Violation of the parameters of the analyses of adhesive-aggregative functions of thrombocytes.
• Positive tests for capillary wall resistance.
• During significant bleeding develops- posthemorrhagic anemia – the reduction of the indexes of erythrocytes and hemoglobin.
Treatment:
1. Bed regime
2. Good feeding
3. Prednisone (1-2 mg/kg/day for 2-4 weeks) are given to shorten the period of severe thrombocytopenia.
6. Chronic ITP not responding to medical treatment.
7. Symptomatological treatment: hemostatic hubka, epsilon aminocaproic acid, dicinon, adroxon, vitamines, treatment anemy/
HENOCH-SCHONLEIN PURPURA
Henoch-Schonlein purpura (=anaphylactoid purpura; our terminology – Schonlein– Henoch disease=hemorrhagic vasculitis) (German doctors of the 19 th century) – is one of kinds of angiopathy.
The basic mechanism of the disease is an inflammation and lesion of the walls of capillaries and fine vessels in the form of increased permeability.
According to the modern data, in the basis of hemorrhagic vasculitis the disorders of thrombocytal and coagulation system of blood clotting are of great importance. But the disease is occurred as a result of the violation of the link of primary hemostasis. mainly – the walls of arteriole-precapillaries, capillaries and venules (panvasculitis).
Etiopathogenesis – is not established completely to the present. It is supposed, that the damage of the vascular wall occurs under the influence of infections as Henoch– Schonlein purpura mostly develops in 2-4 weeks after tonsillitis, influenza, otitis or other infectious diseases. Sometimes the disease is shown on the background of the food and medicinal allergy. Thus, the pathogenesis of hemorrhagic vasculitis has the infectious or toxic-allergic character, when on the walls of the vessels immune complexes settle and damage them. Due to the increased permeability which has arisen, plasma and erythrocytes pass into the surrounding tissue through the vessels.
Clinical signs – in children the hemorrhagic vasculitis can be observed more often than in adult persons.
Depending on the place of lesion, 4 basic syndromes of the disease were described.
1. Dermal syndrome – the important and constant clinical sign of it are hemorrhages on the skin with following characteristics:
(a) Rashes – more often petechia (the rash can be spotty – papule).
(b) Symmetry of the occurrence.
(c) The place of the occurrence – is mostly around joints, especially talocrural, on extensor surfaces of extremities and buttocks.
(d) Simultaneous occurrence of all rashes and consequently all hemorrhages are of the same color (at first red, in some days the colour becomes yellow in color).
(e) For rashes the periodic appearance of it is often typical – in some days, and sometimes in 2 weeks after the first rash, the new elements of fresh hemorrhage appear.
2. Articular syndrome quite often arises simultaneously with the dermal syndrome, therefore it is also called dermo-articular – usually talocrural, knee and radiometacarpeal joints in which there is pain, edema and hyperemia of skin. The process is short – 2-3 days.
3. Abdominal syndrome, in the pathology of which there are hemorrhages into the wall of the intestines and mesentery, reminds the clinical features of ‘acute abdomen’:
(a) Periodic pain in the abdominal cavity – the child is restless wandering; a particular localization is not characteristic for the pain, on the contrary – migration takes place (i.e. the place of its location varies during anamnesis and at palpitation).
(b) The patient takes the compelled position – presses the legs to the stomach or takes knee-elbow position.
(c) Vomiting, it can also be with blood.
(d) Diarrhea, it can be with blood as well.
(e) Paleness, suffering expression in the face.
(f) Dry tongue covered with white coating-fa) Tachycardia. 4. Renal syndrome arising usually on the 2nd – 4 th week of the pathological process.
In the analysis of urine renal syndrome will be shown by:
(a) Hematuria (erythrocytes are present in urine).
(b) Proteinuria (protein in urine).
Sometimes hemorrhages in brain result in:
1) Spasms.
2) The general meningeal syndrome. The process on the whole has a favorable prognosis.
Pathognomonic laboratory data are not present during Henoch-Schonlein purpura. All parameters specifying the quantitative and qualitative value of thrombocytes, and also the analysis of the secondary hemostasis at Henoch-Schonlein purpura are always within the limits of the norm. It is the indispensible differential-diagnostic symptom as a professional help to the doctor in such a form of hemorrhagic diathesis. And the only tests that can be positive are the tests for capillary wall resistance. The moderate leukocytosis with a small shift to the left and increase in ESR may be seen in the general blood test.
Treatment
1. Bed regime
2. Hypoalergic diet
3. Antibacteriac medcine at acute infectiones diseases
4. Heparin is base method of treatment (250-300 U/kg/day) 1-2 weeks
5. Anteagreganti (curantil or trental)
6. Prednisoloni at abdominal and jonit syndrome (1,5mg/kg/day) till 2 weeks
7. At nefrotic syndrome we dive prednisolone+curantili+heparine+leikeran
8. Ascorutine, halascorbin
9. Plasmapheres
Bibliography
а) Basic
1. Ra-Id Abdulla Heart Diseases In Children: A Pediatrician’s Guide / Ra-Id Abdulla. – Springer, 2011 – 486 p.
2. Maureen R. Nelson. Pediatrics / Maureen R. Nelson. – NY: Demos Medical Publishing, 2010. – 259 p.
3. Vicky R. Bowden. Pediatric Nursing Procedures / Vicky R. Bowden, Cindy Smith Greenberg. –
4. Ronald M. Perkin. Pediatric Hospital Medicine: Textbook of Inpatient Management / Ronald M. Perkin, Dale A. Newton, James D. Swift. – Lippincott Williams & Wilkins, 2008 – 924 p.
b) Additional
http://www.hopkinschildrens.org/pediatricgi/
http://www.seattlechildrens.org/clinics-programs/nephrology/
http://www.medicinenet.com/congenital_heart_disease/article.htm
Prepared by ass.prof. Luchyshyn N.Yu., MD, PhD
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