Theme: «Emergency aid at infectious disease at

children»

Done By: Myrzakhanov Yerik 5 course GMF 552 group

Checked By: vice dean Musabekova Jeanne Asemkanovna

asst. of chair

Semey 2015

MINISTRY OF HEALTH OF KAZAKHSTAN SEMEY STATE MEDICAL UNIVERSITY

Chair : Pediatric and child surgeryDiscipline: Emergency medical aid Head of chair : prof. Dyussembayev

A.A

Plan Introduction Food toxic infection Infectious toxic shock Clinic and diagnostic algorithm Principles of emergency aid with position of evidence-

based medicine.

Introduction Infectious diseases of children is one of the most common reasons for seeking

emergency care. Under these conditions, in addition to aid, it is necessary to solve questions the need for hospitalization.

The absolute indications for hospitalization of children in the presence of infectious diseases:• all infectious diseases in newborns;• all infectious diseases in children of the first two years of severe intoxication;• diphtheria;• intoxication;• typhoid, paratyphoid diseases;• especially dangerous infections;• Meningococcal disease;• meningitis various etiology;• intestinal infections with intestinal toxemia and exsicosis;• viral hepatitis.

Food toxic infection Food toxic infection - a group of acute intestinal

infections resulting from consumption of foods containing opportunistic microbes and enterotoxins. Food toxic infection in children are characterized by transient phenomena of intoxication and acute gastritis or gastroenteritis.

There are two kinds of food poisoning: poisoning by toxic agent or by infectious agent.

• Food poisoning is caused by bacteria that synthesize enterotoxins. Most disease is caused by the following pathogens:

• - Klebsiella,• - Proteus,• - Tsitrobakter,• - Escherichia coli,• - Streptococcus,• - Staphylococcus aureus,• - Halophilic vibrio,• - Clostridia.

• Most of these foodborne pathogens are quite stable in the environment and is also capable multiply in foods.

The source of the pathogen in the food poisoning are often people who are engaged in cooking, sometimes animals and birds - sick or healthy bacillicarriers. They identify pathogens in the environment with the faeces. Since these bacteria are widely distributed in nature, often the source of their origin can not be established. In some cases, they may be persons with pustular skin diseases, sore throat, bacterial nasopharyngitis, pneumonia.

The mechanism of transmission of food poisoning - fecal-oral. Most often it is realized by food. Food contaminated as a result of non-compliance with sanitary conditions of their preparation and storage. Especially dangerous is the contamination of the products, not heat-treated immediately before use (jelly, salads, jelly, sour cream, etc.).

Susceptibility to foodborne diseases not high. It is believed that mostly sick people with chronic pathology of the digestive system (gastritis, gastric ulcer and duodenal ulcer, cholecystitis, colitis, etc.), As a consequence, reduced local immunity.

Pathogenesis The disease occurs by ingestion of child a substantial

amount of bacterial enterotoxins. Therefore, an important condition for the occurrence of food poisoning is an intense pre-multiplication of bacteria in the food. Having a tropism for the intestinal cells (enterocytes), toxins cause inflammation of the mucous membrane of the stomach and intestines, stimulates the synthesis of biologically active substances, the motility of the digestive tract. This gives rise to diarrhea and vomiting, loss of fluid may cause dehydration. General toxic syndrome also develop with the changes of the cardiovascular and nervous systems.

Symptoms Food poisining diseases caused by various pathogens, have similar symptoms.

The incubation period is short, usually 5-6 hours, sometimes shortened to 1 hour or extended to 12 hours. Clinic foodborne diseases cause lesions of the gastrointestinal tract as gastritis, gastroenteritis, or, occasionally, gastroenterocolitis, intoxication and dehydration. Symptoms occur suddenly and rapidly growing. There are coldness, cramping abdominal pain, often epigastric and around the navel.

Nausea and repeated vomiting that brings relief to the sick child. Later joined by diarrhea. The stools are loose or watery, fetid, up to 10 times a day or more, sometimes with mucus. Urging to stool are mostly mandatory.

The body temperature with food poisoning often low-grade or normal, rarely rises to high numbers. The skin is pale, dry and in severe cyanosis of the lips and there is toe. Tongue coated white or gray coating. Pulse frequent, blood pressure is lowered. When reusable vomiting and diarrhea symptoms of dehydration: dry and decreased skin turgor, decrease in urine output, muscle cramps limbs, tachycardia, hypotension.

First aid for food poisoning is needed immediately after the appearance of symptoms of the disease.

Emergency assistance with food poisoning include:•  Gastric lavage to remove residual food that caused the poisoning;•  Reception means that are able to adsorb toxin in the alimentary tract, and

bacteria, e.g., smectite or activated charcoal;•  Reinforced drinking mode of use of the solution rehydron;•  The use of broad-spectrum antimicrobial action (ftalazol, furazolidone);• A strict diet;•  If repeated vomiting can be taken Reglan to suppress the vomiting reflex.

Do not use the medication immediately after the procedure, gastric lavage.

Pediatric Toxic Shock Toxic shock syndrome (TSS) is a multisystem disease manifested

by sudden onset of fever, chills, hypotension, and rash. Multisystem involvement may cause vomiting, diarrhea, myalgia, mucous membrane hyperemia, mental confusion, renal dysfunction, hepatic abnormalities, and thrombocytopenia.

TSS is caused by toxin-producing strains of staphylococci (staphylococcal TSS) and streptococci (streptococcal TSS). Both causes are discussed in this article. Todd et al first described staphylococcal toxic shock syndrome in 1978. The association of TSS with menstruation and tampon use was established in 1980. Cases of TSS caused by streptococci were first reported in the mid-1980s.

FindingsStaphylococcal Toxic Shock Syndrome

Streptococcal Toxic Shock Syndrome

Age 15-35 y 20-50 ySex More common in

females Males and femalesLocal invasive disease Absent PresentGeneralized erythroderma Present Absent

Nausea, vomiting, or diarrhea >90% of patients Uncommon

Bacteremia Uncommon 60% of patients

Toxins implicated TSST-1; enterotoxins B and C

Streptococcal pyrogenic exotoxins A and B

Mortality rate 3.3% 30%

The following table summarizes key distinctions between staphylococcal and streptococcal TSS.

Toxic shock syndrome starts suddenly, often with high fever (temperature at least 102°F [38.8°C]), a rapid drop in blood pressure (with lightheadedness or fainting), confusion, vomiting, diarrhea, headache, or muscle aches.

A sunburn-like rash may appear anywhere on the body, including the palms of the hands and the soles of the feet. A person also might have bloodshot eyes and an unusual redness under the eyelids or inside the mouth (and in the vagina in females). The area around an infected wound can become swollen, red, and tender, but might not even appear infected.

Other symptoms can include confusion or other mental changes, decreased urination, fatigue and weakness, and thirst.

If TSS is untreated, organs such as the liver and kidneys may begin to fail, and problems such as seizures, bleeding, and heart failure can develop.

DiagnosisUsing the criteria for case definition of Staphylococcal Toxic Shock Syndrome4 in paediatric practice is complicated by communication difficulties, diminished prodromal period in children and the requirement to include desquamation in the diagnosis (this occurs up to two weeks later and only if the illness is allowed to progress).

Pragmatic criteria for diagnosis of Staphylococcal TSS in children1 include:-1. Pyrexia . 39oC2. Irritability3. Diarrhoea +/- vomiting4. Lymphopaenia with a commonly normal total white cell count5. Rash (commonly non-specific diffuse maculopapular)

Not all of these features need to be present to make the diagnosis.Hyponatraemia is commonly seen. Other haematological changes such as thrombocytopaenia and coagulopathy may be late developments in children.

Staphylococcal Toxic Shock Syndrome

DiagnosisStreptococcal TSS commonly arises from invasive soft tissue infections viz. necrotising fasciitis,cellulitis and myositis. Diagnosis is confirmed by the isolation of Group A Streptococcus from anormally sterile site (blood, CSF, peritoneal fluid, tissue biopsy) together with clinical signs ofseverity :-• Hypotension / shock• Two or more of the following:-

Renal impairment Coagulopathy (thrombocytopaenia or disseminated intravascular coagulation) Hepatic involvement (elevated transaminases and bilirubin) Respiratory Distress Syndrome Generalised erythematous, macular rash (may desquamate) Soft tissue necrosis (gangrene, necrotising fasciitis, myositis)

In children, coagulopathy and rash may be late signs and should not be relied upon.

Streptococcal Toxic Shock Syndrome

Management TSS is rapidly progressive with high mortality. Suspected

cases should be managed on the Paediatric Intensive Care Unit. Consultant advice and support should be sought from the PICU, Burns and Paediatric Renal teams.

Management as per standard septic shock guidelines6 should be commenced including active fluid resuscitation, early use of vasopressors and inotropes, establishment of central access and intubation mechanical ventilation if required. Note that unlike “warm shock” TSS usually displays high systemic vascular resistance and may be refractory to inotropes.

ManagementIn general, after the history and physical, if the patient has low blood pressure and multiorgan involvement characterized by two of the above listed symptoms of organ dysfunction (renal, lung, liver, skin, or blood), the clinical diagnosis of TSS is made, according to CDC criteria. A confirmation of the diagnosis is done by isolation of bacteria from a normally sterile site; the bacteria should be identified as capable of producing exotoxin that either is, or functions like, TSST-1.

The treatment for TSS varies from patient to patient; however, the following treatments are fairly common. Patients with TSS usually will be treated with two or more of the following treatments:

Intravenous fluids to treat shock IV antibiotics Deep surgical cleaning of any infected wounds Cardiac medications to help treat low blood pressure Oxygen and/or mechanical ventilation as needed Blood products if needed Dialysis for patients with kidney failure Hospitalization in an intensive-care unit

It is possible to reduce the chances of developing TSS. Menstruating females should minimize use of items like tampons, diaphragms, and sponges. Tampons should be changed frequently, and superabsorbent tampons should be avoided. Anyone diagnosed with TTS has a higher risk of reinfection; women diagnosed with TSS should avoid tampon use in the future. Early treatment of wounds, especially deep wounds, can help prevent 

Principles of emergency aid with position of evidence-based medicine.

Causes and Source Control Ensure a careful survey for infectious focus. Any

surgical wounds should be considered potential sources of infection. If evidence of wound infection, wide debridement is suggested. Do not delay surgical intervention for medical imaging. Necrotising fasciitis or necrotising myositis is a surgical emergency requiring aggressive debridement. In females, vaginal examination for foreign bodies such as tampons should be considered.

Antimicrobial Therapy Inadequate initial antimicrobial therapy markedly increases mortality

and discussion with microbiology at the earliest availability is important. Empirical therapy to cover both Staphylococcal TSS and Group A Streptococcal disease is advised, for example high-dose flucloxacillin. Clindamycin should also be included in all initial antimicrobial regimes due to demonstrated reduction in toxin production.

Vancomycin is not advised as a first-line antibiotic due to the low prevalence of MRSA in the paediatric population while flucloxacillin has better bactericidal efficacy. For patients with history of non-severe penicillin allergy, cefuroxime and clindamycin are recommended. For patients with history of severe penicillin allergy, clindamycin with vancomycin or linezolid is advised.

Intravenous Immunoglobulin (IVIG) IVIG is recommended as an adjunctive therapy in children with severe

toxin-related infection showing failure to improve despite best standard care7. Intravenous immunoglobulin should be considered in patients in whom there has been no clinical response within the first six hours of aggressive therapy8. IVIG for this indication should be at the request of a PICU Consultant only. An IVIG request form must be submitted to the immunoglobulin panel. There is no conclusive evidence or guideline for IVIG dosage for this indication. Therefore adoption of the recommended dose for PVL-SA / adult TSS is recommended. Total dose of 2g/kg is suggested (rounded down to the nearest whole vial). It is reasonable to consider repeat administration after 48 hours if there remains a poor response to treatment. Human Intravenous Immunoglobulin (IVIG) may rarely induce thromboembolic events including myocardial infarction, cerebrovascular accident, pulmonary embolism and deep vein thrombosis. Caution is therefore advised in the prescription and administration of high dose immunoglobulin in patients with pre-existing risk factors for arterial or venous thrombotic events.

Evidence for the use of IVIG in paediatrics and neonates

Results of trials on intravenous immunoglobulin (IVIG) as adjunctive therapy for sepsis have been conflicting. A prospective single-centre case-control study suggested IVIG conferred a significant reduction in mortality in PICU sepsis patients9; adjunctive use of IVIG in sepsis and septic shock is advocated in the 2008 Surviving Sepsis guidelines6. However, meta-analysis in adults and children has failed to conclusively support the use of IVIG in sepsis and septic shock10,11. There is growing evidence that IVIG therapy has no effect upon the outcome of suspected or proven neonatal sepsis11,12. Evidence for the use of IVIG in Staphylococcal Toxic Shock Syndrome in children is graded as III on the basis of case reports, in vitro studies and extrapolation from adult studies7 and is recommended for use as a short-term therapy of medium (blue) priority in the event of clinical rationing.

References Young A and Thornton K. Toxic Shock Syndrome in Burns: Diagnosis and Management.

Arch Dis Child Educ Pract Ed 2007; 92: 97-100 2. Descloux E et al. One in Five Mortality in Non-Menstrual Toxic Shock Syndrome Versus

No Mortality in Menstrual Cases in a Balanced French Series of 55 Cases. Eur J Clin Microbiol Infect Dis 2008; 27: 37-43

3. Lamagni T et al. Epidemiology of Severe Streptococcus pyogenes disease in Europe. J Clin Microbiol 2008; 46: 2359-2367

4. Wharton M et al. Case Definitions for Public Health Surveillance. MMWR Recomm Rep 1990; 39: 1-43

5. Working Group on Severe Streptococcal Infections. Defining the Group A Streptococcal Toxic Shock Syndrome: Rationale and Consensus Definition. JAMA 1993; 269: 390-391

6. Dellinger R et al. Surviving Sepsis Campaign: International Guidelines for the Management of Severe Sepsis and Septic Shock: 2008. Crit Care Med 2008; 36: 296-327

7. Department of Health Clinical Guidelines for Intravenous Immunoglobulin Use. 2011 www.ivig.nhs.uk

Medically Reviewed by a Doctor on 12/9/2014 Joseph S Bushra, MD, FAAEM Charles Patrick Davis, MD, PhD

Paediatr Drugs. 2005;7(1):11-25. Toxic shock syndrome in children: epidemiology, pathogenesis, and management. Chuang YY1, Huang YC, Lin TY.

Thanks for attention!