. , . () . , . , - ( 50%), , , , - . . , , , . : , 28% ), ( 10- 11 ), . . - , , , , , , , 6- 12 . , . , , . . . , . -, , , . . , - . , , , . . , . - : ) , ) ) , ) ( ), ) , ) , ) , ) , , , ) , . ( ) ( () . , . - , : , . . , (). 94- 97% . . () () .

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Pediatric Serum Sickness

Author: Philip J Cohen, MD; Chief Editor: Harumi Jyonouchi, MD more...

Background
Serum sickness is an immune complexmediated hypersensitivity reaction characterized by fever, rash, arthritis, arthralgia, and other systemic symptoms. Von Pirquet and Schick first described and popularized the term serum sickness at the turn of the 20th century, using it to describe patients who had received injections of heterologous (nonhuman) antitoxins for the treatment of diphtheria and scarlet fever. (See Differentials, History and Physical Examination.)[1] Classic serum sickness is now rarely seen, because the use of foreign proteins is limited to antitoxins such as those used to treat botulism, gas gangrene, diphtheria, rabies, and snake and spider venom.[2] However, the use of equine and murine antisera as antilymphocyte or antithymocyte globulins and murine monoclonal antibodies for immunomodulation and cancer treatment has created a new group of medications that may cause serum sickness. (See Etiology.) Serum sicknesslike reaction (SSLR) is clinically similar to the classic or primary form described above and is attributed to many nonprotein drugs, including beta-lactam antibiotics, ciprofloxacin, sulfonamides, bupropion, streptokinase, metronidazole, allopurinol, carbamazepine, and others.[3, 4, 5, 6, 7, 8] This term has been used to describe the syndrome of a rash, arthritis, and fever within several days to weeks after drug administration. (See Etiology.) With regard to patient education, the patient and his or her family should be advised of the nature of the offending agent. Next Section: Etiology

Etiology
Serum sickness is a type III hypersensitivity reaction mediated by immune complex deposition with subsequent complement activation. The classic syndrome is caused by immunization of the host by heterologous serum proteins. Shortly after the injection of the foreign protein, the host mounts a specific antibody response to clear the foreign substance. Immunoglobulin M (IgM) antibodies usually develop 7-14 days after immunization with the antigen. When the antigen and antibody molecules are present in approximately equal molar ratios (slight antigen excess), called the zone of equivalence, cross-linking and lattice formation occur. This results in a large mass of aggregates of immune complexes deposited in various tissues, such as the internal elastic lamina of arteries and in perivascular regions. These tissue-deposited immune complexes activate complements, which lead to the clinical manifestation of the disease (eg, inflammatory changes in the renal glomeruli and in the skin).[9] Antigen cross-linking of immunoglobulin E (IgE) molecules that are bound to specific cell surface receptors and/or binding of complement split products, such as iC3b, to complement receptors (CR3/CR4) may activate mast cells and basophils, resulting in the release of the inflammatory mediators, including histamine, causing skin symptoms (urticaria). Large amounts of antigen exposure can lead to widespread deposition of complement-fixing immune complexes and the clinical presentation of serum sickness.

A patient with agammaglobulinemia lacks the ability to produce a specific antibody to antigenic challenge, including heterologous serum, and is incapable of developing serum sickness. Antithymocyte globulin (ATG) is generated by immunization of horses with human thymic tissue. The immune serum is partially purified through multiple steps, including fractionation by ionexchange chromatography.[9] However, ATG, as well as other immunosuppressive foreign proteins, such as chimeric monoclonal antibodies that consist of murine-derived antigen-binding fragment (Fab) and human-derived crystallizable fragment (Fc) portions of antibodies, have been reported to be sufficiently immunogenic to cause serum sickness. The mechanism of many of the drugs responsible for serum sicknesslike reaction is not well known. The medications may act as haptens that bind to carrier proteins (albumin or other serum proteins) that act as antigens, whereas others may create metabolites that have direct toxic effects on cells, leading to idiosyncratic delayed-type drug reactions with symptoms similar to those of serum sickness. Cefaclor has been studied for this mechanism, and its metabolites have been found to be lymphotoxic.[10, 11]

Agents that cause serum sickness

The causes of serum sickness include the following: Heterologous serum proteins - Antitoxin, antivenin, ATG, and monoclonal antibodies used in the treatment and management of various medical disorders Antibiotics - Cephalosporins, ciprofloxacin, griseofulvin, penicillins, sulfonamides, tetracyclines, metronidazole, and others Other drugs - Allopurinol, barbiturates, captopril, indomethacin, phenylbutazone, procainamide, quinidine, and thiouracil Biologic agents Streptokinase Serum sickness develops in 20-30% of patients who receive antisera for diphtheria and scarlet fever; however, most individuals develop the disease only when larger doses of the antisera are administered.[1] Similarly, higher doses of equine botulinum toxin and antisnake venom antiserum are more likely to produce serum sickness than are lower doses.[12] Serum sickness developed after antivenin for snake bites in 17% of patients,[13] 44% of patients,[14] 50% of patients,[15] and 57% of patients[16] in previously reported studies. In a subsequent review of redback spider antivenom, 3 of 32 patients who were observed for 2 weeks (10%) developed serum sickness.[17] Biologic agents such as monoclonal antibodies and ATG can also cause serum sickness. The use of ATG in bone marrow transplantation and in patients with aplastic anemia resulted in serum sickness in 86-92% of recipients.[9, 18] Infliximab, a monoclonal chimeric antibody against tumor necrosis factor (TNF), has also been shown to produce serum sickness. As reported in A Crohn's Disease Clinical Trial Evaluating Infliximab in a New Long-term Treatment Regimen I (ACCENT I), 3 of 88 patients (2%) developed serum sickness after receiving infliximab as a maintenance treatment for Crohn disease.[19] Rituximab is another chimeric monoclonal antibody on the market and is directed at CD20 expressed on the cell surface of B cells. In 2 studies that used rituximab to treat immune thrombocytopenic purpura (ITP) in children, the incidences of serum sickness were 12.5%[20] and 5.6%.[21] Other reviews have shown that serum sickness is not limited in the treatment of ITP; persons using rituximab for autoimmune diseases are also at risk.[22, 23] The humanized monoclonal antibody natalizumab (Tysabri) is a new therapeutic option for treating relapsing forms of multiple sclerosis. Humanized antibody contains murine-derived, antibody-binding

portion integrated into human antibodies by recombinant deoxyribonucleic acid (DNA) technology. Natalizumab is a monoclonal antibody directed to the 4 integrin, including 4 1 and 4 7. In one study, a delayed-infusion serum sicknesslike reaction (type III reaction) occurred in 4 of 40 patients (10%).[24] In the Natalizumab Safety and Efficacy in Relapsing-Remitting Multiple Sclerosis (AFFIRM) trial, one patient who developed a delayed serum sicknesslike reaction tested positive for antinatalizumab antibodies 5 weeks after initiation of this therapy; his symptoms persisted 12 weeks later.[25] However, the symptoms completely resolved with a short course of oral glucocorticosteroids. One case report detailed the use of omalizumab (Xolair), a humanized monoclonal antibody that blocks IgE, which caused a severe serum sicknesslike reaction in a patient using this medication to treat asthma.[26] Serum sickness caused by monoclonal antibodies will likely increase because of the dramatic rise in the use of immunomodulators of this kind. However, the use of humanized monoclonal antibodies with less murine-derived component will help reduce this risk. Many nonprotein drugs, including beta-lactam antibiotics, ciprofloxacin, sulfonamides, bupropion, streptokinase, metronidazole, allopurinol, carbamazepine, and others, have been reported to cause serum sicknesslike reactions.[3, 4, 5, 6, 7, 8] However, the incidence is much lower for antibiotics than for heterologous serum. For example, Kunnamo et al estimated that the annual incidence of druginduced serum sicknesslike reaction with acute arthritis and detectable immune complexes was 4.7 cases per 100,000 children younger than 16 years.[7] Literature surveys report a higher incidence in children treated with cefaclor compared with children treated with other antibiotics. Reviews suggest an incidence of serum sickness of 2 cases per 100,000 children for cefaclor and less than 1 case per 10 million children for cephalexin and amoxicillin.[5, 4,
8]

Previous Next Section: Etiology

Epidemiology
As previously mentioned, classic serum sickness is now rarely seen, because the use of foreign proteins is limited to antitoxins such as those used to treat botulism, gas gangrene, diphtheria, rabies, and snake and spider venom.[2] Although serum sickness may occur in individuals of any age in response to the introduction of heterologous protein, the incidence of serum sicknesslike reactions due to antibiotics, especially cefaclor, is higher in children than in adults.[8] Previous Next Section: Etiology

Prognosis
The prognosis is excellent in most cases of serum sickness, with resolution of signs and symptoms occurring in a few days. Serum sickness may recur if reexposure to the offending antigen occurs. Subsequent reactions may be more severe, with an escalating time frame compared with the original reaction. Anaphylaxis and shock from reexposure to the offending agent are possibilities. Serum sickness is usually a self-limited disorder, and symptoms resolve with time as the immune complexes are cleared from the system. The use of antihistamines, nonsteroidal anti-inflammatory drugs (NSAIDs), and corticosteroids helps to ameliorate the symptoms. Repeated and continual administration of the offending agents may lead to an immediate accelerated reaction, including cardiovascular collapse.[1]

Vasculitis, nephropathy, and respiratory complications are usually associated with the use of heterologous animal protein (antitoxin, ATG, streptokinase) and are not usually observed with drugs and other agents. Serum sicknesslike reaction is usually self-limited, with symptoms lasting only 1-2 weeks.

History and Physical Examination

History
The onset of serum sickness symptoms usually occurs 7-10 days after administration of the offending agent and correlates with the peak of circulating immune complexes. Fever, malaise, and headache are the earliest symptoms. Rash, joint pain, edema, gastrointestinal (GI) symptoms, and other symptoms follow.

Physical examination
The major physical findings include fever, rash, arthritis, arthralgia, and lymphadenopathy. The elevated temperature fluctuates between 37.5 and 40C. A rash is often the first clinical symptom and is frequently pruritic. If the causal agent was injected, the rash typically starts at the site of injection. Otherwise, the rash starts on the abdomen and spreads outward. Eruption over the rest of the body is usually symmetrical and may take any of the following forms: Urticaria (see image below) Scarlatiniform rashMorbilliform rash Polymorphous exanthema Erythema, petechiae, or purpura with a serpiginous border at the margin of palmar plantar skin

with the use of ATG[9] Urticarial rash in a child 10 days after cefaclor was administered for sore throat. Associated findings included fever, arthralgia of knees and ankles, and eosinophilia. Approximately two thirds of patients experience joint discomfort.[27] In order of decreasing frequency, the affected joints include the knees, ankles, shoulders, wrists, spine, and temporomandibular joint. Joint fluid usually yields a moderately high number of white cells. Myalgias in the arms and thighs may also occur. Lymphadenopathy coincides with the onset of other symptoms of serum sickness. The lymph nodes that receive drainage from the injection site enlarge and become tender. Other lymph nodes may also enlarge, sometimes to several centimeters in diameter. Albuminuria, microscopic hematuria, and hyaline casts are observed. Serum creatinine levels may transiently rise, and the creatinine clearance may decrease. Edema may be due to albuminuria or rash.

Nausea, vomiting, and abdominal pain are usually mild but may be confused with appendicitis and other GI disorders in children. Headache and blurred vision may develop. Other, rare symptoms include the following: Cardiovascular problems - Pericardial effusion Respiratory problems - Dyspnea, wheezing, cyanosis Proceed to Differential Diagnoses

Diagnostic Considerations
Conditions to consider in the differential diagnosis of serum sickness include the following: Systemic-onset juvenile arthritis Infectious mononucleosis Postviral synovitis Urticarial vasculitis Hypersensitivity vasculitis GI disorders Chronic idiopathic urticaria Viral exanthem Other drug reactions

Differentials
Agammaglobulinemia Appendicitis

Arthritis, Conjunctivitis, Urethritis Syndrome Kawasaki Disease Lymphoproliferative Disorders Meningococcal Infections Pediatric Henoch-Schonlein Purpura Rheumatic Heart Disease Systemic Lupus Erythematosus

Proceed to Workup

Approach Considerations
Laboratory studies
The following studies are indicated in patients with serum sickness: CBC count with differential - Leukocytosis or leukopenia, eosinophilia, or mild thrombocytopenia Erythrocyte sedimentation rate and C-reactive protein levels - Usually slightly elevated Urinalysis - Albuminuria, hematuria, active sediment Blood urea nitrogen (BUN) and creatinine levels - May be transiently elevated C3, C4, CH50 - Depressed complement levels due to complement consumption Quantitative immunoglobulins - Hypergammaglobulinemia that results from prolonged course of antithymocyte globulin (ATG) Immune complexes - C1q binding or Raji cell assays for elevated levels of immune complexes (These are possibly confirmatory but not essential for diagnosis.)

Skin biopsy
Skin biopsy is usually not indicated for serum sickness but may be considered if the etiology for vasculitis is unclear.

Histologic findings
Skin lesions reveal a perivascular lymphohistiocytic infiltrate and possible edema of perivascular stroma.[9] Immune deposits (IgM, IgE, C3, and immunoglobulin A [IgA]) seen with direct immunofluorescence (DIF) are found in superficial small blood vessels and renal glomeruli. Because of the high rate of blood flow and the filtration effect at the renal glomeruli, the immune complexes are deposited at the glomerular basement membrane. These deposits can be visualized with electron microscopy in the subendothelial and mesangial areas. These deposits lead to the activation of the complement system and the recruitment of the neutrophils. Inflammatory mediators are released, resulting in a histologic picture of glomerulonephritis.[28] Proceed to Treatment & Management

Approach Considerations
The primary therapy in patients with serum sickness is discontinuation of the offending agent. Therefore, the identification of the offending agent is of the utmost importance. Although the use of heterologous protein, such as antithymocyte globulin (ATG), is easily identified, others such as medications, may not be as obvious. Follow-up care is needed until symptoms resolve. Treatment also includes the following: Supportive care Antihistamines - For urticaria Nonsteroidal anti-inflammatory drugs (NSAIDs) - For arthritis, arthralgia, or both Steroids - When the heterologous antiserum is necessary for management of the basic disorder

Activity
No restriction of activity is necessary, although arthritis, arthralgia, or both may hamper the child's activity for several days to weeks.

Consultations
Consult an allergist/immunologist to rule out an immunoglobulin E (IgE)mediated reaction. Consult a rheumatologist to rule out other causes for arthritis or vasculitis. Consult an infectious disease specialist to choose alternative antibiotic therapy.

Inpatient care
In patients with serum sickness, if the cause of the symptoms is clear, inpatient care is unnecessary. However, in cases in which the etiology of the constitutional symptoms is uncertain, further inpatient diagnostic studies may be indicated.

Deterrence and prevention

The patient and family should be instructed to avoid using the offending agent and drugs in the same class as the offending agent. Next Section: Experimental Treatment

Experimental Treatment
All 5 patients with serum sickness experienced complete resolution of all symptoms after receiving 1 or 2 courses of therapeutic plasma exchange in a study by Tanriover et al. The authors investigated the therapeutic effects of plasma exchange as an alternative treatment for patients who underwent renal transplant and developed severe serum sickness that persisted despite systemic steroids after receiving a polyclonal antibody (ATG [Thymoglobulin] or lymphocyte immune globulin/antithymocyte globulin [Atgam]).[29] Previous Proceed to Medication

Medication Summary
The objective of medical therapy is to ameliorate the symptoms that result from deposition of the immune complexes in the various tissues. Antihistamines are useful in controlling urticarial lesions. Nonsteroidal anti-inflammatory drugs (NSAIDs) are used to treat fever and minor musculoskeletal symptoms. Corticosteroids are necessary to treat the more severe symptoms. Next Section: Antihistamines

Antihistamines
Class Summary
These agents are used to treat urticaria and pruritus. Classic H1-blocker antihistamines block the histamine-mediated increase in vascular permeability. Some second-generation antihistamines may also reduce the release of vasoactive amines. View full drug information

Diphenhydramine (Benadryl, Anti-Hist, Aler-Tab, Diphen)

Diphenhydramine is an antihistamine with anticholinergic and sedative adverse effects. It is used for treatment of allergic reactions. Previous Next Section: Antihistamines

Nonsteroidal anti-inflammatory drugs (NSAIDs)

Class Summary
This class of drugs acts by inhibiting cyclooxygenase, thereby blocking the production of prostaglandins, which are powerful mediators of inflammation. These drugs are useful in relieving fever and musculoskeletal pain. View full drug information

Ibuprofen (Motrin, Advil, Provil)

Ibuprofen is a member of the propionic acid group of NSAIDs. It has moderate efficacy and a good safety profile and is used in children for various conditions, including fever and arthritis. To avoid gastrointestinal (GI) complications, it should be taken with food. Previous

Next Section: Antihistamines

Corticosteroids
Class Summary
These agents elicit anti-inflammatory and immunosuppressive properties and cause profound and varied metabolic effects. They modify the body's immune response to diverse stimuli. View full drug information

Prednisone
Prednisone is a corticosteroid with salt-retention properties that is used for its potent antiinflammatory effects. Because of its well-known adverse effects, it is used only in cases in which the systemic symptoms are severe. Previous Contributor Information and Disclosures Author Philip J Cohen, MD Chief, Section of Dermatology, New Jersey Veterans Affairs Medical Center Disclosure: Nothing to disclose. Coauthor(s) Robyn Siperstein, MD Staff Physician, Department of Dermatology, University of Medicine and Dentistry of New Jersey, New Jersey Medical School Robyn Siperstein, MD is a member of the following medical societies: American Academy of Dermatology, American Medical Association, American Society for MOHS Surgery, and Sigma Xi Disclosure: Nothing to disclose. Lawrence K Jung, MD Chief, Division of Pediatric Rheumatology, Children's National Medical Center Lawrence K Jung, MD is a member of the following medical societies: American Association for the Advancement of Science, American Association of Immunologists, American College of Rheumatology, Clinical Immunology Society, and New York Academy of Sciences Disclosure: Nothing to disclose. Specialty Editor Board Mary L Windle, PharmD Adjunct Associate Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference Disclosure: Nothing to disclose. David J Valacer, MD Consulting Staff, Hoffman La Roche Pharmaceuticals

David J Valacer, MD is a member of the following medical societies: American Academy of Allergy Asthma and Immunology, American Academy of Pediatrics, American Association for the Advancement of Science, American Thoracic Society, and New York Academy of Sciences Disclosure: Nothing to disclose. Chief Editor Harumi Jyonouchi, MD Associate Professor, Division of Pulmonary, Allergy/Immunology, and Infectious Diseases, Department of Pediatrics, University of Medicine and Dentistry of New JerseyNew Jersey Medical School Harumi Jyonouchi, MD is a member of the following medical societies: American Academy of Allergy Asthma and Immunology, American Academy of Pediatrics, American Association of Immunologists, American Medical Association, Clinical Immunology Society, New York Academy of Sciences, Society for Experimental Biology and Medicine, Society for Mucosal Immunology, and Society for Pediatric Research Disclosure: Nothing to disclose. References 1. References 1. von Pirquet CF, Schick B (Translator). Serum Sickness. Baltimore: Williams & Wilkins Co; 1951. 2. Gamarra RM, McGraw SD, Drelichman VS, Maas LC. Serum sickness-like reactions in patients receiving intravenous infliximab. J Emerg Med. Jan 2006;30(1):41-4. [Medline]. 3. Ornetti P, Disson-Dautriche A, Muller G, et al. Joint symptoms in patients on bupropion therapy. Joint Bone Spine. Nov 2004;71(6):583-5. [Medline]. 4. Platt R, Dreis MW, Kennedy DL, Kuritsky JN. Serum sickness-like reactions to amoxicillin, cefaclor, cephalexin, and trimethoprim-sulfamethoxazole. J Infect Dis. Aug 1988;158(2):4747. [Medline]. 5. Heckbert SR, Stryker WS, Coltin KL, Manson JE, Platt R. Serum sickness in children after antibiotic exposure: estimates of occurrence and morbidity in a health maintenance organization population. Am J Epidemiol. Aug 1990;132(2):336-42. [Medline]. 6. Brucculeri M, Charlton M, Serur D. Serum sickness-like reaction associated with cefazolin. BMC Clin Pharmacol. Feb 23 2006;6:3. [Medline]. [Full Text]. 7. Kunnamo I, Kallio P, Pelkonen P, Viander M. Serum-sickness-like disease is a common cause of acute arthritis in children. Acta Paediatr Scand. Nov 1986;75(6):964-9. [Medline]. 8. Vial T, Pont J, Pham E, et al. Cefaclor-associated serum sickness-like disease: eight cases and review of the literature. Ann Pharmacother. Jul-Aug 1992;26(7-8):910-4. [Medline]. 9. Lawley TJ, Bielory L, Gascon P, et al. A prospective clinical and immunologic analysis of patients with serum sickness. N Engl J Med. Nov 29 1984;311(22):1407-13. [Medline]. 10.Knowles S, Shapiro L, Shear NH. Serious dermatologic reactions in children. Curr Opin Pediatr. Aug 1997;9(4):388-95. [Medline]. 11.Kearns GL, Wheeler JG, Childress SH, Letzig LG. Serum sickness-like reactions to cefaclor: role of hepatic metabolism and individual susceptibility. J Pediatr. Nov 1994;125(5 Pt 1):805-

11. [Medline]. 12.Black RE, Gunn RA. Hypersensitivity reactions associated with botulinal antitoxin. Am J Med. Oct 1980;69(4):567-70. [Medline]. 13.Offerman SR, Bush SP, Moynihan JA, Clark RF. Crotaline Fab antivenom for the treatment of children with rattlesnake envenomation. Pediatrics. Nov 2002;110(5):968-71. [Medline]. [Full Text]. 14.Shemesh IY, Kristal C, Langerman L, Bourvin A. Preliminary evaluation of Vipera palaestinae snake bite treatment in accordance to the severity of the clinical syndrome. Toxicon. Jun 1998;36(6):867-73. [Medline]. 15.Jurkovich GJ, Luterman A, McCullar K, et al. Complications of Crotalidae antivenin therapy. J Trauma. Jul 1988;28(7):1032-7. [Medline]. 16.LoVecchio F, McBride C. Scorpion envenomations in young children in central Arizona. J Toxicol Clin Toxicol. 2003;41(7):937-40. [Medline]. 17.Isbister GK. Safety of i.v. administration of redback spider antivenom. Intern Med J. Dec 2007;37(12):820-2. [Medline]. 18.Bielory L, Gascon P, Lawley TJ, et al. Human serum sickness: a prospective analysis of 35 patients treated with equine anti-thymocyte globulin for bone marrow failure. Medicine (Baltimore). Jan 1988;67(1):40-57. [Medline]. 19.Hanauer SB, Feagan BG, Lichtenstein GR, et al. Maintenance infliximab for Crohn's disease: the ACCENT I randomised trial. Lancet. May 4 2002;359(9317):1541-9. [Medline]. 20.Bennett CM, Rogers ZR, Kinnamon DD, et al. Prospective phase 1/2 study of rituximab in childhood and adolescent chronic immune thrombocytopenic purpura. Blood. Apr 1 2006;107(7):2639-42. [Medline]. 21.Wang J, Wiley JM, Luddy R, et al. Chronic immune thrombocytopenic purpura in children: assessment of rituximab treatment. J Pediatr. Feb 2005;146(2):217-21. [Medline]. 22.Sailler L. Rituximab off label use for difficult-to-treat auto-immune diseases: reappraisal of benefits and risks. Clin Rev Allergy Immunol. Feb 2008;34(1):103-10. [Medline]. 23.Medeot M, Zaja F, Vianelli N, Battista M, Baccarani M, Patriarca F, et al. Rituximab therapy in adult patients with relapsed or refractory immune thrombocytopenic purpura: long-term follow-up results. Eur J Haematol. Sep 2008;81(3):165-9. [Medline]. 24.Hellwig K, Schimrigk S, Fischer M, et al. Allergic and nonallergic delayed infusion reactions during natalizumab therapy. Arch Neurol. May 2008;65(5):656-8. [Medline]. 25.Krumbholz M, Pellkofer H, Gold R, et al. Delayed allergic reaction to natalizumab associated with early formation of neutralizing antibodies. Arch Neurol. Sep 2007;64(9):1331-3. [Medline]. 26.Pilette C, Coppens N, Houssiau FA, Rodenstein DO. Severe serum sickness-like syndrome after omalizumab therapy for asthma. J Allergy Clin Immunol. Oct 2007;120(4):972-3. [Medline]. 27.Bielory L, Yancey KB, Young NS, Frank MM, Lawley TJ. Cutaneous manifestations of serum sickness in patients receiving antithymocyte globulin. J Am Acad Dermatol. Sep 1985;13(3):411-7. [Medline]. 28.Nangaku M, Couser WG. Mechanisms of immune-deposit formation and the mediation of immune renal injury. Clin Exp Nephrol. Sep 2005;9(3):183-91. [Medline]. 29.Tanriover B, Chuang P, Fishbach B, et al. Polyclonal antibody-induced serum sickness in renal

transplant recipients: treatment with therapeutic plasma exchange. Transplantation. Jul 27 2005;80(2):279-81. [Medline].

Urticarial rash in a child 10 days after cefaclor was administered for sore throat. Associated findings included fever, arthralgia of knees and ankles, and eosinophilia.

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Definition
An allergy is an exaggerated immune response or reaction to substances that are generally not harmful. See also: Allergic conjunctivitis Allergic reactions Allergy testing Allergy to mold, dander, dust Atopic dermatitis (eczema) Contact dermatitis Drug allergies Food allergies Hay fever (allergic rhinitis)

Causes, incidence, and risk factors

Allergies are relatively common. Both genetics and environmental factors play a role. The immune system normally protects the body against harmful substances, such as bacteria and viruses. It also reacts to foreign substances called allergens, which are generally harmless and in most people do not cause a problem. But in a person with allergies, the immune response is oversensitive. When it recognizes an allergen, it releases chemicals such as histamines. which fight off the allergen. This causes itching, swelling, mucus production, muscle spasms, hives, rashes, and other symptoms, which vary from person to person. Common allergens include pollen, mold, pet dander, and dust. Food and drug allergies are common. Allergic reactions can also be caused by insect bites, jewelry, cosmetics, spices, and other substances. Some people have allergy-like reactions to hot or cold temperatures, sunlight, or other environmental triggers. Sometimes, friction (rubbing or roughly stroking the skin) will cause symptoms. A specific allergy is not usually passed down through families (inherited). However, if both your parents have allergies, you are likely to have allergies. The chance is greater if your mother has allergies. Allergies may make certain medical conditions such as sinus problems, eczema, and asthma worse.

Symptoms
Allergy symptoms vary, but may include: Breathing problems Burning, tearing, or itchy eyes Conjunctivitis (red, swollen eyes) Coughing Diarrhea Headache Hives Itching of the nose, mouth, throat, skin, or any other area Runny nose Skin rashes

 Stomach cramps Vomiting Wheezing What part of the body is contacted by the allergen plays a role in the symptoms you develop. For example: Allergens that are breathed in often cause a stuffy nose, itchy nose and throat, mucus production, cough, or wheezing Allergens that touch the eyes may cause itchy, watery, red, swollen eyes. Eating something you are allergic to can cause nausea, vomiting, abdominal pain, cramping, diarrhea, or a severe, life-threatening reaction Allergens that touch the skin can cause a skin rash, hives, itching, blisters, or even skin peeling Drug allergies usually involve the whole body and can lead to a variety of symptoms

Signs and tests

The health care provider will perform a physical exam and ask questions such as when the allergy occurs. Allergy testing may be needed to determine if the symptoms are an actual allergy or caused by other problems. For example, eating contaminated food (food poisoning) may cause symptoms similar to food allergies. Some medications (such as aspirin and ampicillin) can produce non-allergic reactions, including rashes. A runny nose or cough may actually be due to an infection. Skin testing is the most common method of allergy testing. One type of skin testing is the prick test. It involves placing a small amount of the suspected allergy-causing substances on the skin, and then slightly pricking the area so the substance moves under the skin. The skin is closely watched for signs of a reaction, which include swelling and redness. Skin testing may be an option for some young children and infants. Other types of skin tests include patch testing and intradermal testing. For detailed information, see:Allergy testing Blood tests can measure the levels of specific allergy-related substances, especially one called immunoglobulin E (IgE). A complete blood count (CBC), specifically the eosinophil white blood cell count, may also help reveal allergies. In some cases, the doctor may tell you to avoid certain items to see if you get better, or to use suspected items to see if you feel worse. This is called "use or elimination testing." This is often used to check for food or medication allergies. The doctor may also check your reaction to physical triggers by apply heat, cold, or other stimulation to your body and watching for an allergic response. Sometimes, a suspected allergen is dissolved and dropped into the lower eyelid to check for an allergic reaction. This should only be done by a health care provider.

Treatment
Severe allergic reactions (anaphylaxis) require treatment with a medicine called epinephrine, which can be life saving when immediately given. The best way to reduce symptoms is to try and avoid what causes your allergies in the first place. This is especially important for food and drug allergies.

There are several types of medications available to prevent and treat allergies. Which medicine your doctor recommends depends on the type and severity of your symptoms, your age, and overall health. Specific illnesses that are caused by allergies (such as asthma, hay fever, and eczema) may require other treatments. Medications that can be used to treat allergies include: ANTIHISTAMINES Antihistamines are available over-the-counter and by prescription. They are available in many forms, including: Capsules and pills Eye drops Injection Liquid Nasal spray

CORTICOSTEROIDS Anti-inflammatory medications (corticosteroids) are available in many forms, including: Creams and ointment for the skin Eye drops Nasal spray Lung inhaler

Patients with severe allergic symptoms may be prescribed corticosteroid pills or injections for short periods of time. DECONGESTANTS Decongestants can help relieve a stuffy nose. Decongestant nasal spray should not be used for more than several days, because they can cause a "rebound" effect and make the congestion worse. Decongestants in pill form do not cause this problem. OTHER MEDICINES Leukotriene inhibitors are medicines that specifically block the substances that trigger allergies. Zafirlukast (Accolate) and montelukast (Singulair) are approved for those with asthma and indoor and outdoor allergies. ALLERGY SHOTS Allergy shots (immunotherapy) are occasionally recommended if the allergen cannot be avoided and symptoms are hard to control. Allergy shots keep your body from over-reacting to the allergen. Regular injections of the allergen are given, with each dose slightly larger than the previous dose until a maximum dose is reached. They do not work for everybody and require frequent doctor's visits.

Support Groups
See: Asthma and allergy support group

Expectations (prognosis)
Most allergies can be easily treated with medication. Some children may outgrow an allergy. This is particularly true of food allergies. However, as a general rule, once a substance has triggered an allergic reaction, it continues to affect the person.

Allergy shots are most effective when used to treat those with hay fever symptoms and severe insect sting allergies. They are not used to treat food allergies because of the danger of a severe reaction. Allergy shots may require years of treatment, but they work in most cases. However, they may cause uncomfortable side effects (such as hives and rash) and dangerous outcomes (such as anaphylaxis).

Complications
Anaphylaxis (life-threatening allergic reaction) Breathing problems and discomfort during the allergic reaction Drowsiness and other side effects of medicines

Calling your health care provider

Call for an appointment with your health care provider if: Severe symptoms of allergy occur Treatment for allergies no longer works

Prevention
Breast-feeding children for at least 4 months or more may help prevent atopic dermatitis cow milk allergy, and wheezing in early childhood. However, changing a mother's diet during pregnancy or while breast-feeding does not seem to help prevent allergy-related conditions. For most children, changing diet or special formulas does not seem to prevent these problems. If there is a family history of eczema and allergies in a parent, brother, or sister, discuss the infant feeding with your child's doctor. The timing of introduction of solid foods in general, as well as use of several specific foods, can help prevent some allergies. There is also evidence that infants exposed to certain airborne allergens (such as dust mites and cat dander) may be less likely to develop related allergies. This is called the "hygiene hypothesis" and sprang from observations that infants on farms tend to have fewer allergies than those who grow up in environments that are more sterile. Once allergies have developed, treating the allergies and carefully avoiding those things that cause reactions can prevent allergies in the future.

References
Wallace DV, Dykewicz MS, Bernstein DI, Blessing-Moore J, Cox L, Khan DA, et al. The diagnosis and management of rhinitis: an updated practice parameter. J Allergy Clin Immunol. 2008 Aug:122(2). Kurowski K, Boxer RW. Food allergies: detection and management. American Family Physician. 2008 June:77(12). Bielory L, Friedlaender MH. Allergic conjunctivitis. Immunol Allergy Clin North Am. 2008 Feb;28(1):43-58, vi.
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Definition
An allergy is an exaggerated immune response or reaction to substances that are generally not harmful. See also: Allergic conjunctivitis Allergic reactions Allergy testing Allergy to mold, dander, dust Atopic dermatitis (eczema) Contact dermatitis Drug allergies Food allergies Hay fever (allergic rhinitis)

Causes, incidence, and risk factors

Allergies are relatively common. Both genetics and environmental factors play a role. The immune system normally protects the body against harmful substances, such as bacteria and viruses. It also reacts to foreign substances called allergens, which are generally harmless and in most people do not cause a problem. But in a person with allergies, the immune response is oversensitive. When it recognizes an allergen, it releases chemicals such as histamines. which fight off the allergen. This causes itching, swelling, mucus production, muscle spasms, hives, rashes, and other symptoms, which vary from person to

person. Common allergens include pollen, mold, pet dander, and dust. Food and drug allergies are common. Allergic reactions can also be caused by insect bites, jewelry, cosmetics, spices, and other substances. Some people have allergy-like reactions to hot or cold temperatures, sunlight, or other environmental triggers. Sometimes, friction (rubbing or roughly stroking the skin) will cause symptoms. A specific allergy is not usually passed down through families (inherited). However, if both your parents have allergies, you are likely to have allergies. The chance is greater if your mother has allergies. Allergies may make certain medical conditions such as sinus problems, eczema, and asthma worse.

Symptoms
Allergy symptoms vary, but may include: Breathing problems Burning, tearing, or itchy eyes Conjunctivitis (red, swollen eyes) Coughing Diarrhea Headache Hives Itching of the nose, mouth, throat, skin, or any other area Runny nose Skin rashes Stomach cramps Vomiting Wheezing

What part of the body is contacted by the allergen plays a role in the symptoms you develop. For example: Allergens that are breathed in often cause a stuffy nose, itchy nose and throat, mucus production, cough, or wheezing Allergens that touch the eyes may cause itchy, watery, red, swollen eyes. Eating something you are allergic to can cause nausea, vomiting, abdominal pain, cramping, diarrhea, or a severe, life-threatening reaction Allergens that touch the skin can cause a skin rash, hives, itching, blisters, or even skin peeling Drug allergies usually involve the whole body and can lead to a variety of symptoms

Signs and tests

The health care provider will perform a physical exam and ask questions such as when the allergy occurs. Allergy testing may be needed to determine if the symptoms are an actual allergy or caused by other problems. For example, eating contaminated food (food poisoning) may cause symptoms similar to food allergies. Some medications (such as aspirin and ampicillin) can produce non-allergic reactions, including rashes. A runny nose or cough may actually be due to an infection. Skin testing is the most common method of allergy testing. One type of skin testing is the prick test. It involves placing a small amount of the suspected allergy-causing substances on the skin, and then

slightly pricking the area so the substance moves under the skin. The skin is closely watched for signs of a reaction, which include swelling and redness. Skin testing may be an option for some young children and infants. Other types of skin tests include patch testing and intradermal testing. For detailed information, see:Allergy testing Blood tests can measure the levels of specific allergy-related substances, especially one called immunoglobulin E (IgE). A complete blood count (CBC), specifically the eosinophil white blood cell count, may also help reveal allergies. In some cases, the doctor may tell you to avoid certain items to see if you get better, or to use suspected items to see if you feel worse. This is called "use or elimination testing." This is often used to check for food or medication allergies. The doctor may also check your reaction to physical triggers by apply heat, cold, or other stimulation to your body and watching for an allergic response. Sometimes, a suspected allergen is dissolved and dropped into the lower eyelid to check for an allergic reaction. This should only be done by a health care provider.

Treatment
Severe allergic reactions (anaphylaxis) require treatment with a medicine called epinephrine, which can be life saving when immediately given. The best way to reduce symptoms is to try and avoid what causes your allergies in the first place. This is especially important for food and drug allergies. There are several types of medications available to prevent and treat allergies. Which medicine your doctor recommends depends on the type and severity of your symptoms, your age, and overall health. Specific illnesses that are caused by allergies (such as asthma, hay fever, and eczema) may require other treatments. Medications that can be used to treat allergies include: ANTIHISTAMINES Antihistamines are available over-the-counter and by prescription. They are available in many forms, including: Capsules and pills Eye drops Injection Liquid Nasal spray

CORTICOSTEROIDS Anti-inflammatory medications (corticosteroids) are available in many forms, including: Creams and ointment for the skin Eye drops Nasal spray Lung inhaler

Patients with severe allergic symptoms may be prescribed corticosteroid pills or injections for short periods of time.

DECONGESTANTS Decongestants can help relieve a stuffy nose. Decongestant nasal spray should not be used for more than several days, because they can cause a "rebound" effect and make the congestion worse. Decongestants in pill form do not cause this problem. OTHER MEDICINES Leukotriene inhibitors are medicines that specifically block the substances that trigger allergies. Zafirlukast (Accolate) and montelukast (Singulair) are approved for those with asthma and indoor and outdoor allergies. ALLERGY SHOTS Allergy shots (immunotherapy) are occasionally recommended if the allergen cannot be avoided and symptoms are hard to control. Allergy shots keep your body from over-reacting to the allergen. Regular injections of the allergen are given, with each dose slightly larger than the previous dose until a maximum dose is reached. They do not work for everybody and require frequent doctor's visits.

Support Groups
See: Asthma and allergy support group

Expectations (prognosis)
Most allergies can be easily treated with medication. Some children may outgrow an allergy. This is particularly true of food allergies. However, as a general rule, once a substance has triggered an allergic reaction, it continues to affect the person. Allergy shots are most effective when used to treat those with hay fever symptoms and severe insect sting allergies. They are not used to treat food allergies because of the danger of a severe reaction. Allergy shots may require years of treatment, but they work in most cases. However, they may cause uncomfortable side effects (such as hives and rash) and dangerous outcomes (such as anaphylaxis).

Complications
Anaphylaxis (life-threatening allergic reaction) Breathing problems and discomfort during the allergic reaction Drowsiness and other side effects of medicines

Calling your health care provider

Call for an appointment with your health care provider if: Severe symptoms of allergy occur Treatment for allergies no longer works

Prevention
Breast-feeding children for at least 4 months or more may help prevent atopic dermatitis cow milk allergy, and wheezing in early childhood. However, changing a mother's diet during pregnancy or while breast-feeding does not seem to help prevent allergy-related conditions. For most children, changing diet or special formulas does not seem to prevent these problems. If there is a family history of eczema and allergies in a parent, brother, or sister, discuss the infant feeding

with your child's doctor. The timing of introduction of solid foods in general, as well as use of several specific foods, can help prevent some allergies. There is also evidence that infants exposed to certain airborne allergens (such as dust mites and cat dander) may be less likely to develop related allergies. This is called the "hygiene hypothesis" and sprang from observations that infants on farms tend to have fewer allergies than those who grow up in environments that are more sterile. Once allergies have developed, treating the allergies and carefully avoiding those things that cause reactions can prevent allergies in the future.

References
Wallace DV, Dykewicz MS, Bernstein DI, Blessing-Moore J, Cox L, Khan DA, et al. The diagnosis and management of rhinitis: an updated practice parameter. J Allergy Clin Immunol. 2008 Aug:122(2). Kurowski K, Boxer RW. Food allergies: detection and management. American Family Physician. 2008 June:77(12). Bielory L, Friedlaender MH. Allergic conjunctivitis. Immunol Allergy Clin North Am. 2008 Feb;28(1):43-58, vi.

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 1. .. . 2005; 4: 97110. 2. Morice A.H. Chronic cough. Breathe 2006; 3 (2): 164. 3. Bolser D.C. Cough suppressants and pharmacologic protussive therapy (ACCP evidencebased clinical practice guidelines). Chest 2006; 129: 238S249S. 4. Guo R., Pittler M.H., Ernst E. Herbal medicine for the treatment of COPD: a systematic review. Eur. Respir. J. 2006; 28: 330338. 5. Irwin R.S. et al. Diagnosis and management of cough. ACCP evidencebased clinical practice guidelines. Executive summary. Chest 2006; 129: 1S23S. 6. Belvisi M.G., Geppetti P. Cough: current and future drugs for the treatment of chronic cough. Thorax 2004; 59: 438440. 7. Morice A.H. et al. Opiate therapy in chronic cough. Am. J. Crit. Care Med. 2007; 175: 312315. 8. Rimsza M.E., Newberry S. Unexpected infant deaths associated with use of cough and cold medications. Pediatrics 2008; 122: e318e322.

: www.rmj.ru, rss-farm.ru

Otita medie acut tratat inadecvat evolueaz n alte forme de otit medie (otita medie

Otita medie constituie o boal cu cea mai mare rspndire n copilria mic. Majoritatea copiilor (pn la 90%) sufer cel puin o dat n via de otit medie acut (OMA), 74 % copii - au 3 i mai multe episoade. Analiza datelor statistice n anii 19922007 arat c 30 % de prescripii ale antibioticelor pentru copii n lume sunt pentru tratamentul OMA. Nectnd c OMA se ntlnete la orice vrst, boal este cea mai prevalent n copilria mic. Pn la 60-80 % din copii au ca minimum un episod de otit medie n primul an de via, 8090 % - la 23 ani. Cea mai mare incidena de OMA se ntlnete ntre 6 i 24 luni de viaa. [2, 3, 6, 7, 18, 20 ] Diagnosticul otitelor medii acute la copii de vrst mic este dificil. Otita medie decurge relativ asimptomatic n 40 60 % de cazuri, anume la copii n primii ani de via. Semnele locale specifice la debutul afeciunii au un caracter nepronunat i instabil, se manifest prin nelinitea copilului nespecific, reacia neadecvat la adresarea prinilor, ce se agraveaz treptat cu meninerea procesului patologic n urechea medie. Toate acestea sunt cauzele adresrii cu ntrziere la medic. Lipsa diagnosticului oportun i a tratamentului adecvat a OMA duce la dezvoltarea complicaiilor grave vitale mastoidita, sepsis, meningita, etc. [2, 5, 7, 9, 18,20 ] exudativ, otita medie recidivant, otita medie adeziv) n 60 % de cazuri. Aceste forme se caracterizeaz prin hipoacuzie - la nceput uoar, dar progresiv, care ntre timp devine stabil i ireversibil. Aprecierea strii auzului de ctre copil i prini este insuficient. Pn n prezent n Republica Moldova nu este implementat sistemul de screening al auzului la copii, astfel nct la mai mult de 80 % din pacieni se diagnostic ntmpltor n timpul examenului profilactic. Influena hipoacuziei asupra vieii sociale a copilului (dezvoltarea psiho-emoional, formarea vorbirii i a intelectului) este semnificativ. [1, 5, 10, 17, 19]-0Datorit particularitilor anatomo-fiziologice ale urechii medii i a ntregului organism al copilului (fon alergic, dezvoltare incomplet a imunitii .a., ca rezultat al OMA se poate dezvolta otita medie cronic supurat cu riscul dezvoltrii complicaiilor intracraniene. [5, 17 ] CLINICE: - anamnestice o evaluarea factorilor de risc OMA o acuze caracteristice ale copilului sau schimbri n comportamentul copilului o durata bolii - fizice o semne otoscopice o semne generale de infecie acut o semne de proces inflamator n cile de respiraiePARACLINICE: (dup necesitate i posibilitate)

- Obligatoriu o hemoleucograma o sumarul urinei - Recomandate o Examenul audiologic n cazurile ndoielnice (impedansmetria, audiometria)EVALUAREA SEVERITII: - manifestri de impregnare infecioas (febr, greuri, vom, anorexie, astenie - manifestri de insuficien respiratorie (dispnee, etc.) - manifestri neurologice dereglri ale tractului gastro-intestinal Pacientul nu necesit spitalizare (lipsesc criteriile de spitalizare) Se va administra tratament conser vator complex la domiciliu A doua vizit activ - peste 48 de ore de tratament Se va aprecia eficacitatea tratamen tului Se va reevalua necesitatea spitali Contactul telefonic a 2-a zi (dup 24 de ore de la iniierea tratamentului) Pacientul prezint criterii de spitalizare: - vrsta pn la 1 an - comorbiditi importante - ineficiena tratamentului complex iniiat la domiciliu - imposibilitatea ngrijirii adecvate la domiciliu sau dorina prinilor copilului de a se trata n condiii de staionar Cel puin un criteriu de internare: - manifestri neurologice - afectarea cilor respiratorii inferioare - dereglri gastro-intestinale - hiperleucocitoza (>25 x 109 /l) i sau mrirea VSH (>35 mm/or)Caseta 1. Clasificarea OMA la copii conform formelor [2, 10] Otita medie acut Otita medie acut, evoluia prelungit (subacut) Otita medie acut recidivant Otita medie acut, forma latent Otita medie acut cataral Otita medie acut supurat Caseta 2. Clasificarea OMA la copii conform fazelor [5, 19 ] Faza preperforativa Faza perforativa Faza de recuperare Caseta 3. Agenii etiologici n dezvoltarea OMA [ 3, 6, 12, 13,16] Ageni microbieni: Streptococcus pneumoniae Haemophilus influenzae

 Branhamella catarralis Stafilococii Pneumococii Anaerobi Virui Ciuperci Hlamidii. Not: Primii trei ageni microbieni cauzeaz aproximativ 90 % din OMA 11 Caseta 4. Factorii de risc n dezvoltarea OMA [ 4, 5, 7, 8, 11, 12, 13, 14, 15] Devieri n perioada de dezvoltare antenatal i intranatal; Procese inflamatorii n perioada postnatal; Alimentaia iraional i artificial, avitaminoza, bolile infecioase; Infecia de vecintate - rinitele, faringitele, sinuzitele, vegetaiile adenoide; Infeciile acute frecvente ale cilor respiratorii; Imaturitatea imunitii copilului; Vrst fraged (factori locali anatomo-topografici ale tubei auditive i factori generali ai or ganismului); Malnutriia; Procese alergice; Predispoziia ereditar; Bolile infectocontagioase, etc. Not: Screening-ul factorilor de risc se va face obligatoriu la toi copii pn la vrst de 3 ani i la necesitate copiilor pn la vrst de 7 ani (vezi Anexa 1) La copiii cu cel puin 3 factori de risc n prezena semnelor clinice generale i/ori dere glrilor n comportament (caseta 7) se va efectua obligatoriu otoscopia. Caseta 6. Acuzele copilului de vrst 3 ani i mai mare cu OMA, faza preperforativ[3, 19] Otalgie (dureri n ureche) Scdere de auz Zgomote auriculare Cefalea (dureri de cap) Caseta 7. Acuzele prinilor a copilului de vrst pn la 3 ani cu OMA, faza preperforativ [2, 5, 7, 20] Nelinitea copilului, agitaie Dereglri n atenie i reacia neadecvat la adresare Dereglri de somn Dereglri de alimentaie (inapeten) La copiii primului an de via dereglri gastrointestinale (vom, diaree) Caseta 8. Examenul obiectiv general Semne generale de infecie acut (febr, cefalee, slbiciune, inapeten, etc.) Semne de infecie a cilor de respiraie (rinorea, congestie nazal, tuse, etc.) Manifestri neurologice (nelinite, agitaie, dereglri ale somnului, vom, greuri, convulsii) Dereglri gastro-intestinale (inapeten, vom, diaree) Caseta 10. Indicaii pentru consultul medicului ORL Vrsta de pn la 1 an a copiilor cu suspecie la OMA; Dificulti n stabilirea diagnosticului de OMA; n lipsa efectului tratamentului conservator a OMA pe parcursul primelor 3 zile dup iniiere; Otita medie acut evoluia prelungit (subacut) Otita medie acut recidivant

 Otita medie acut forma latent OMA, forma de gravitate medie Riscul dezvoltrii complicaiilor (febr, vom, grea, convulsii, agitaii, somnolen, semne meningiene) la copii cu OMA Asimetria feei la copilul cu OMA Caseta 11. Criteriile de spitalizare a copiilor cu OMA OMA la copiii primului an de via OMA la copiii cu suspiciu la dezvoltarea complicaiilor (febr nalt, vom, grea, convulsii agitaii, somnolen, semne meningiene) OMA evoluia prelungit (subacut) OMA recidivant OMA forma latent OMA la copiii cu patologia asociat (dereglri gastro-intestinale, pneumonia, pielonefrita) OMA la copiii cu lipsa dinamicii pozitive dup tratament conservator ambulator OMA la copiii din familia vulnerabil Caseta 13. Tratamentul conservator complex Fr antibioticoterapie Indicaii: Perioada iniial (primele 2 3 zile de la nceputul semnelor infecioase faza preperforativ starea general a copilului este relativ satisfctoare, suportabil din anamnez: copilul cu dezvoltare fizic normal prima otit n via, sau rar (una n civa ani) infecii respiratorii - rar semnele locale nu sunt pronunateDurata tratamentului fr antibioticoterapie 3-4 zile Coninutul tratamentului fr antibioticoterapie: Preparate antipiretice: Paracetamol (Efferalgan), doza max. 25 mg/kg, apoi 12,5 mg/kg fiecare 6 - 8 ore sau 60 mg/kg/24 ore, sau Ibuprofen (Nurofen) 5-10 mg/kg la fiecare 4-6 ore. Preparate antihistaminice: Difenhidramin (Dimedrol) sau Clemastin sau Cloropiramin (Suprastin) 5- 10 mg/kg/zi, per os Tratamentul nazofaringelui: lavaj nazal, preparate vazoconstrictoare Oxymetazolin (Nazol), Xilometazolin (Galazolin), Nafazolin (Naftizin) Tratament local: picturi otice antiinflamatoare i analgezice Otinum, Otipax Nota: Reevaluarea strii generale i locale a copilului - peste 34 zileCaseta 14. Tratamentul complex inclusiv antibioticoterapie Indicaii: lipsa efectului de la tratament ant iviral, antiinflamator n timp de 3 zile otita medie acut pe parcursul ultimei luniantibioticoterapie pe parcursul ultimei luni vrst copilului pn la 1 an nceputul recidivelor de otit medie pn la 6 luni otita medie acut recidivant otita medie acut, evoluia prelungit otita medie acut supurat, faza perforativ otita medie acut, evoluie clinic grav Indicaii pentru tratament cu antibioticoterapie 10 zile: otita medie acut supurat, faza perforativ otita medie acut, evoluie clinic grav Durata tratamentului cu antibioticoterapie 710 zile (sub control otoscopi ndicaii pentru tratament cu antibioticoterapie 10 zile otita medie acut pe parcursul ultimei luni antibioticoterapie pe parcursul ultimei luni vrst copilului pn la 7 ani nceputul recidivelor de otit medie pn la 6 luni otita medie acut recidivant

 otita medie acut, evoluia prelungit

Coninutul tratamentului cu antibioticoterapie: Antibioticoterapie (caseta 15) Preparate antipiretice: Paracetamol (Efferalgan), doza max. 25 mg/kg, apoi 12,5 mg/kg fiecare 6 - 8 ore sau 60 mg/kg/24 ore, sau Ibuprofen (Nurofen) 5-10 mg/kg la fiecare 4-6 ore. Preparate antihistaminice: Difenhidramin (Dimedrol) sau Clemastin sau Cloropiramin (Suprastin) 5- 10 mg/kg/zi, per os Mucolitice (Acetilcisteina, Carbocisteina) Tratamentul nazofaringelui: lavaj nazal, preparate vazoconstrictoare Oxymetazolin (Nazol), Xilometazolin (Galazolin), Nafazolin (Naftizin) Tratament local: picturi otice antiinflamatoare i analgezice Otinum, Otipax - n faza preperforativ, picturi antibacteriale neototoxice, care conin Ciprofloxacin sau Ofloxacin -n faza perforativ)
Caseta 15. Alegerea antibioticoterapiei pentru OMA la copii Tratamentul antibacterial este indicat de la a 3 - 4 zi dup instalarea OMA i include antibioticoterapie Peniciline semisintetice (Amoxicilin 80100 mg/kg n 34 prize sau Ampicilin 80100 mg/kg n 4 prize i/m) Asocieri b-lactamine cu inhibitori de b-lactamaz:Amoxicilin + acid clavulonic (Augmentin, Klamoks, Amoxiclav 50100 mg/kg n 23 prize) Cefalosporine (Cefalexin 2550 mg/kg n 3 4 prize per os, Cefotaxim 70100 mg/kg n 2 prize i/m Dup indicaii (tratament antibacterian cu peniciline semisintetice i/sau cefalosporine n ultima lun sau alergia la aceste preparate) macrolide sau combinaii de sulfamide cu trimetoprim.Caseta 16. Indicaii pentru tratamentul chirurgical Lipsa efectului dup tratament conservator Indicaiile locale - bombaj MT, la copiii mari bombaj MT pe parcursul 3 zile de tratament intensiv, persistena i intensificarea durerii n ureche i n procesul mastoidian, intensificarea hipoacuziei, apariia ameelii, sau reaciei labirintului) Indicaiile generale - persistena i intensificarea semnellor de intoxicaie pe parcursul 3 zile de tratament intensiv, febra permanent, cefalea pronunat la copiii mari, semnele de meningism)Caseta 21. Supravegherea pacienilor cu OMA Control medicului de familie peste o lun Control medicului ORL (otoscopic optic, pneumatic peste o lun dup OMA Control audiologic (audiometria, impedansmetria) peste o lun dup OMA Consultul specialitilor dup indicaii peste o lun dup OMA. Caseta 22. Complicaiile OMA Mastoidita Sepsisul Paralizia nervului facial Meningita Abcese intracranieneMedicamente:

 Peniciline semisintet ice, asocieri b-lactamine cu inhibitori de blactamaz, cefalosporine, macrolide, combinaii de sulfamide cutrimetoprim. Preparate antipiretice Preparate antihistaminice Preparate vazoconstrictoare Picturi otice antiinflamatoare i analgezice Picturi antibacteriene neototoxice A.8. Definiiile folosite n document Amigdalita cronic este inflamaia cronic a tonsilelor palat ine ce se manifest prin angini repetate. Anginele sunt cauzate de ageni microbieni (bacterii, virusuri, fungi). Copii: Persoane cu vrsta egal sau mai mic ca 18 ani. A.9. Informaia epidemiologic Inflamaia cronic a tonsilelor palat ine constituie una din cele mai frecvente patologii ORL. Circa 10 50% din populaie sufer de Amigdalit cronic [5]. Problematica tonsilitelor cronice a depit limitele tiinei otorinolaringologice. Aceast patologie fiind tot mai des studiat dectre reprezentanii medicinii teoretice i clinice de diferite specialiti (imunologia, alergologia, pediatria, reumatologia, nefrologia). Anual sunt elaborate preparate medicale noi, metode contemporane de tratament i investigaii a amigdalitei cronice. Cu toate acestea, afectarea tonsilelor palat ine este n continuare o maladie de mare inciden att la copii ct i la maturi. Procesele autoimune prezente n esutul limfatic amigdalian favorizeaz dezvoltarea complicaiilor sistemice n organism i nrutesc patogenia lor [8]. Organizaia Mondial a Sntii apreciaz c amigdalita este cauza a mai mult de 120 de afeciuni ale organismului uman. Deci, amigdalita prin consecinele sale asupra sntii populaiei nu prezint numai o problem medico-biologic ci i una social.C. 1. ALGORITMI DE CONDUIT C. 1.1 Algoritmul general de conduit al pacientului cu Amigdalit cron c Prima vizit CLINICE: - anamnestice o acuzele pacientului o durata bolii o angini suportate n trecut o boli asociate - fizice o semne locale de Amigdalit cronic o schimbri n articulaii, schimbri la sistemul cardiovascular, renal ExaminriPARACLINICE: - Obligatoriu o hemoleucograma o sumarul urinei o ECG - Recomandare o examenul bacteriologic la flor de pe tonsilele palatine o examenul biochimic al sngelui o proteina C reactiv, antistreptolizinaO, factorul reumatoidEVALUAREA SEVERITII: - manifestri de subfebrilitate - abcese peritonsilare n anamnez - manifestri cardiovasculare - manifestri renale manifestri gastroduodenalePacientul se ia la eviden Pacientul se ea la eviden de medicul

de familie cu consultul ORL Consultaia medicilor specialiti de alt profil dup necesitate Tratament conservator 2 ori pe an de medicul ORL Se va aprecia eficacitatea tratamentului i necesitatea spitalizrii Se evalueaz criteriile de spitalizarePacientul prezint criterii de spitalizare: - Angini frecvente dup tratamentul conservator - Abcese paratonsilare n anamnez - Patologii asociate cardiovasculare n remisie - Patologii asociate renale n remisie - Patologii asociate gastroduodenale n remisie Pacientul trebuie spitalizat!Caseta 1. Clasificarea amigdalitei cronice Amigdalit cronic compensat. Amigdalit cronic decompensat. Recidive de angini. Patologii asociate.Caseta 2. Agenii etiologici n dezvoltarea amigdalitei cronice Ageni microbieni streptococii, stafilococii, pneumococii, anaerobi; Virusuri adenovirui, Ciuperci Hlamidii. Caseta 3. Factorii de risc n dezvoltarea amigdalitei cronice Devieri n perioada de dezvoltare antenatal, intranatal i postnatal; Alimentaia iraional i artificial, avitaminoza, bolile infecioase; Infecia de vecintate - rinitele, faringitele, sinuzitele, vegetaiile adenoide; Infeciile acute frecvente ale cilor respiratorii; Anginele i peritonsilitele repetate; Influena nefavorabil a diferitor factori ai mediului extern - ageni chimici i iradierea mrit; Alergia; Factori anatomotopografici (aezarea amigdalelor palatine la intersecia a dou tracte: respirator i digestiv, ce duce la traumatizarea esutului amigdalian, aciunea permanent i mrit a antigenilor mediului nconjurtor); Imaturitatea imunitii copilului; Predispoziia ereditar; Bolile infectocontagioase i hematologice etc.C.2.4. Conduita pacientului cu Amigdalit cronic Caseta 4. Paii obligatorii n conduita pacientului cu Amigdalit cronic 1. Controlul profilactic a populaiei cu scop de depistare activ a amigdalitei cronice 2. Culegerea anamnezei 3. Examinarea clinic5. Evaluarea riscului de complicaie tonsilar (consultaia specialitilor) 6. Deciderea asupra tacticii de tratament (conservator versus chirurgical) 7. Efectuarea tratamentului

8. Profilaxia acutizrilor (n caz de tratament conservator) 9. Supravegherea 4. Examinarea paraclinicCaseta 5. Acuzele bolnavului cu Amigdalit cronic Angine n anamnez; Durere i nepturi n gt preponderent la rece; Senzaii de corp strin, arsur i uscciune n gt; Accese de tuse uscat; Miros neplcut din gur; Sforit prin somn; Dureri n regiunea cordului i articulaiilor; Oboseal fizic i intelectual.Caseta 6. Examenul obiectiv Prezena de coninut patologic n cripte (puroi, cazeum); Roeaa stlpului palat in anterior (simptomul Gize); Edemaierea stlpilor palatini anteriori, mai ales n partea polului superior (simptomul Zac); Hiperemia, infiltraia i edemaia stlpilor palatini anteriori (simptomul Preobrajenschi); Microabcese i microchisturi n esutul tonsilelor palat ine; Gena ganglionar (ganglionii subangulomandibulari mrii, puin dureroi la palpare). Investigaiile paraclinice Analiza general de snge Sumarul urinei ECG Biochimia sngelui: bilirubina fraciile ei, ALT, AST, testul cu timolTestele reumatice (ant istreprolizina-O, proteina C reactiv) Antibioticograma Consultul medicului ORL Consultul medicului pediatru Consultul reumatologului Consultul nefrologului i/sau urologului Tabelul 2. Diagnosticul diferenial al amigdalitei cronice [4] Criterii Amigdalita cronic Faringita cronic Anamneza Angini repetate Acutizri de faringite acute Status localis Coninut patologic n cripte Prezent Absent Gena ganglionar Prezent Ca regul absent Roeaa i edemaierea stlpilor palatini anteriori Prezent Ca regul absent Tuse uscat Ca regul prezent Ca regul prezent Peretele posterior faringian schimbat: atrofie; hiperemie; hiperplazie Nemodificat Modificat Patologia gastroduodenal Ca regul absent Ca regul prezent

 Influena factorilor nocivi Ca regul absent Ca regul prezent Caseta 7. Criteriile de spitalizare a pacienilor cu Amigdalit cronic Amigdalita cronic decompensat (tratament chirurgical)Caseta 8. Indicaii pentru tratamentul conservator Pacieni cu Amigdalit cronic compensat Pacieni cu Amigdalit cronic decompensat care au contraindicaii pentru intervenie chi rurgical Pacieni cu Amigdalit cronic decompensat care refuz operaia.Caseta 9. Tratamentul conservator Local: nlturarea focarului de infecie din tonsilele palatine prin splarea criptelor cu sol. antisep ce (sol. Nitrofura 1:5000; sol. Dioxidin 1%; sol. Miramistin 0,01%; sol.Nucin 0,2%) Badijonarea mucoasei tonsilelor palatine cu soluii (Lugol; Iodinol; Clorofillipt) Aplicarea aerosolilor Inhalipt; Benzidamin (Tantum-Verde) Ultrasunet pe proiecia tonsilelor palatine (7-10 edine) General: Preparate antihistaminice (2 ori pe zi): (Difenhidramin,Prometazin, Clemastin,cloropinamin, Mebnidrolin) Preparate imunostimulatoare (Timolin, Timogen, Tactivin, Ribomunil, Bronho-munal, Prodigiozan, IRS-19, Levamizol, Imudon) Vitaminoterapie Retinoli acetas (Revit), Retinoli palmitas (Aevit) Clirea organismului Caseta 10. Indicaii pentru tratamentul chirurgical Amigdalit cronic, forma decompensat. Amigdalit cronic, forma decompensat. a. infecia amigdalian recurent cu 3 acutizri infecioase pe an n ultimii 3 ani sau 5 episoade infecioase fiecare din ultimii 2 ani sau 7 acutizri n ultimul an, fr efect al tratamentului conservator. b. abces periamigdalian acut sau recurent. c. complicaii la distan : reumatism, glomerulonefrit, septicemie.Caseta 15. Supravegherea pacienilor cu Amigdalit cronic compensat Medicul de familie Indic consultul medicului ORL de 2 ori pe an pentru efectuarea tratamentului conservator Indic analiza general a sngelui, urina sumar, ECG o dat pe an. Indic consultul altor specialiti dup indicaii pentru excluderea altor patologii pentru sanarea altor focare de infecii Medicul ORL Petrece tratament conservator local i general de 2 ori pe an n condiii de ambulatoriu; Scoate de la eviden pacientul tratat de amigdalit cronic compensat dup 3 ani de trata-ment efectiv; Stabilete diagnoza de Amigdalit decompensat i indic tratament chirurgical.Caseta 16. Complicaiile amigdalitei cronice Abcese peritonsilare Artrite Reumatism Miocardite Nefrite

Alergia alimentara la copii

Oualele, laptele, soia, graul, alunele sau rosiile reprezinta 90 la suta din produsele alergice doua alimente alergice pentru micuti. Datele cercetarii arata ca cel putin 5-8% dintre copii mici sunt alergici la aces mici, unii pot depasi varsta de cinci ani.

Alergia alimentara, simptome Copii predispusi la alergia alimentara au o respiratie suieratoare si dificultati de inspiratie si expiratie. In acelasi tim urtricanie, varsaturi, diaree, greata, umflaturi in jurul gatului si durere abdominale. Aceste semnale sunt redate ime acestea pot fi severe. O reactie severa este anafilaxia. Alergia alimentara la copil (una dintre cele mai grave) poate umflarea mucoasei bucale si a gatului, scaderea tensiunii, soc si in cele din urma moartea. In general, alergiile alimentare reprezinta intoleranta organismului la anumite alimente, de aceea pot provoca vars exemplu, una dintre aceste reactii pot sa apara la copii cu intoleranta la lactoza. Acest lucru apare atunci cand organ de multa lactaza, o eczima necesara pentru a digera lactoza, zaharul din laptele de vaca si alte produse lactate.

Alimentele si alergia a) . Laptele Alergia la laptele de vaca este foarte frecventa la copii; studiile arata ca un procent de 2, 5% din sugari. Numerosi c de lapte, precum laptele de capra sau de oaie. De obicei, alergia este indrepatata impotriva uneia sau a ambelor pro din lapte si lactoza nu pot provoca alergia, insa pot cauza intoleranta alimentara. Un procent de peste 85 la suta din mentionat si faptul ca 10% dintre acesti copii sunt alergici si la carnea de vita. Alergia la lapte reprezinta riscul dez

b) . Ouale Aceasta alergie prezinta aceleasi procentaj (2, 5%) ca si alergia copiilor la lapte. Copii pot fi alergici la albus sau ga depaseste varsta de 5 ani, dezvoltand in acelasi timp alergiile nazale si astmul. Intr-un timp se folosea vaccinul MMR, in cazul copiilor cu algerici la ou.

c) . Soia Fiind o leguminoasa prezenta in diverse alimente, soia afecteaza doar 0, 3% dintre copii, in special pe cei mici. Rar micutilor.

d) . Graul Proteinele prezente in boabele de grau provoaca alergia, dar in cazuri minime. Cei mai expusi acestui risc sunt cop cereale: ovaz si orz.

e) Arahidele Un procent de 0, 6 din totalul populatiei este predispusa acesteia. Alergia la alune poate fi asociata cu o reactie pute bronsic. Doar 20% dintre copii sunt alergici la varsta maturitate, de aceea alergia la arahide este specifica mai mult

O alta categorie de copii este alergica la nuci (cam 0, 5%) . La inceput alergia la nuci este severa, dar poate fi inlatu

f) . Fructele de mare Pestii, crustaceele si molustele sunt alte alimente care pot provoca aparitia reactiilor alergice. S-au semnalat cazuri Este recomandat evitarea consumulului acestora.