Emergencies in Pediatrics

5/27/2018 Emergencies in Pediatrics

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Emergencies in pediatrics

Department of pediatrics


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Emergencies in children

Hyperthermic syndrome

Convulsive syndrome

Neurotoxicosis

Anaphylactic shock


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Febrile syndrome\generalities

The central temperature of human

beings is, as in another animals with

warm blood, a constant, which isnaming homeothermia, in contrast

with that of animals with cold blood

(fish, reptiles, etc.) which is variable.


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Homeothermia rezults from equilibriumbetween warmth producing, orthermogenesis (alimentation, physicalexercise .), and the means to combat it,

orthermolysis (more or less abundantsweating, hydric intake - water).

There are, however, variations of central

temperature during one day by 0,6C, thelowest temperature being recorded inmorning and the highest in evening.


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It is important to know that, in

normal conditions, the children

seems to have a temperatureslightly more that the normal

temperature of adults, and can,

sometimes, to achieve38 C, and even 38,5C in evening.


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The thermic metabolism innewborn babies

Insufficient thermoproduction.

Incapacity to increase the thermic lossesin case of hyperthermia and thethermoproduction in the case ofovercooling.

Incapacity to present a febrile typicalreaction (caused by insufficientsensibility of hypothalamic neurons tothe pyrogene leucocytary substances and

big concentration of arginin-vasopressinwhich decreases the body temperature).

Only at 2-3 years in children thecircadian rhythm of corporal temperatureis establishing.


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The forms and basic mechanismsof body t0increasing

We speek about feverwhen the bodytemperature is more than 38C. A febrile

sensation can arise when the temperature

exceeds the medium normal value of 37C.

Febrile state appears when the function of

thermoregulation centers from hypothalamus is

not desturbed, but under the action of pyrogene

substances (exogenouslipopolysacharides,

or endogenousmacrophages, granulocytes,

neutrophils, eosinophils, in result ofphagocytosis the genetically determined point

of body t (set point) is changing . The febrile

states have a positive biologic character of

organism protection.


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Hyperthermic reaction(t0 higher than 38,0

38,50C), which appears on the background of

disorder and decompensation of

thermoregulation mechanisms functions(intensifying with the decompensation of

metabolism, pathologic disorders of

thermoregulation centers.

Hyperthermic reactions are often met inpediatric practice, especially in neuroinfections,

different viroses etc. and have not biologic

sense for organism. They have only pathologic

character.


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Hyperthermia corresponds to theincreasing of body central temperatureprovoked by the thermogenesis

increasing, for example, during intensivemuscular exercise and/or thediminishing of thermolysis, havingrelationship with exterior too hightemperature, diminishing of sweatingand/or insufficient hydric intake(overheating, dehydration, etc).


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Due to hyperthermia all forms of metabolismare decompensating, the endogenous

intoxication of organism increases (cascad of

intermediary metabolits), the vital centers

respiratory and cardiovascular are disturbing,the convulsions appear, the cerebral edema is

developing.

The hyperthermic reactions are not interrupted

with antipyretics, but the physical methods are

useful: the rubbings of body with humid gauze

and ensuring of local hypothermia in the region

of head and magistral vessels (towels, humid

swaddling clothes etc).


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Etiology of fever

Infectious causesViral infections

Bacterial infections

Infections with atypical germs:Mycoplasma. Chlamidia

Parasitoses

Mycoses et al.


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Etiology of fever

Noninfectious

Immunopathologic processes (collagenoses,

systemic vasculites, allergies)

Tumors (lymphogranulomatosis, lymphomas,neuroblastomas)

Intracranial traumas

Hemorrhages

Endocrine diseases Vaccination

Malignant hyperthermia etc.


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Levels of fever

Subfebrile (until 380C)

Moderated fever (38,10C39,00C)

High fever (39,00C - >)

Hyperpyrexia (more than 410C)


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urves o ever Continuous feveroscillation in 24 hrs no

more than10C (abdominal typhus)

Remittent fever - oscillation in 24 hrs more

than 10C (viral and bacterial infections) Irregularly or atypical feveroscillations are

irregularmost spread form of fever in different

pathologies

Hectic fevercorrelation between remittentand irregular fever with oscillations more than

2-3 0C

Intermittent fevershort periods of high

temperature which correlates with periods ofphysiologic temperature (tuberculosis,

purulent infections)

Recurrent feverthe alternation of febrile

crises during 2-7 days with periods of apyrexia-


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Clinical manifestations

Cardiovascular system:increase of

pulse with 8-10 beats at increasing of

fever with1 degree. In the cases of long

term febrile states manifested with highvalues the collapse, cardiac failure, DIC

syndrome are determining.

Nervous system: fatigue, headache,

delirium, insomnia or somnolence.


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Respiratory systemin the first phase offever the frequency of respiration decreases,

then increases with 4 respiratory movements at

each degree of fever. In the same time, the

volume of respiration doesnt increase, buteven is decreasing being the determinant of

hypoxia appearance as a pathogenetic

mechanism of affection in fever.

Digestive systemis characterizing through the

decreasing of . motory and fermentative

activity, decreasing of gastric juice activity,

decreasing of appetite.


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Management of the child with

fever

The diagnosis is performing on the base of

thermometry, clinical manifestations of basic

disease and paraclinical routine examinations

The treatment includes following measures:

Diet

Physical methods of cooling

Using of antipyretics


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Curative management of febrile child Antipyretics:are administering at T 38 0C 1.Paracetamol: per os-dose 10-15 mg/kg each 6 no

more than 60 mg/kg/day)

per rectum: unique dose- 15-20 mg/kg

Ibuprofen- 10-15 mg/kg each 6-8 hours

If after 30-45 min. T doesnt decrease - the i/madministering of 50% sol. of analgin (metamizol)0,1 ml/year of life and 2,5% sol. of pipolfentill 1 yr- 0,01ml/kg, more than 1 yr - 0,1-0,15 ml/yr of life.Dose is repeated if over30-60 min. not effect.

In the presence of threatening signs and/or rigidity ofoccipital muscles we administer the first dose ofadequate antibacterial preparation and urgentHOSPITALIZATION .

Curative management of febrile child


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Curative management of febrile child Inwhitehyperthermia together with antipyretics the

vasodilators are administering: papaverinor no-spa1mg/kg per os or i/m. solution.

2% papaverin

- till 1 yr of life-0,1-0,2 ml, more than 1 yr -0,1-0,2 ml/yr oflife OR:

S. No-spa 0,1 ml/ yr of life OR 0,25% dibazol 0,1-0,2 ml/kg.

In hyperthermic syndr. T is measuring each 30-60 min.

After decreasing of T until 37,5 0C the hypothermic

curative measures are cancelling. Anaigin is adminstering in unique doses and no more than

3 days(.anaphylactic shock, agranulocytosis).

Acetylsalicylic acid is not administering until 15 years(Ree

syndrome).


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CONVULSIVESYNDROME


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Peculiarities of nervous systemin little age children

Immaturity of cellular elements and of nervous

fibers, which determines a diffuse affection ofthe brain.

Increased sensibility to noxious factors anddecreased threshold of excitability, which canprovoke convulsive status.

Increased hydrophilia of nervous tissue whichcontributes to rapide development of cerebraledema.

Intolerance of CNS to the immune system,which conditions the appearance of anticerebralantibodies in the case of hematoencephalicbarrier affection.

Plasticity and great compensatory possibilities

of the brain.


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Definition

Convulsions are paroxystic or rhythmicand saccadated muscular contractions,

joined in tonic, clonic or tonico-cloniccrises.

Convulsions can be by epilepticandnonepileptic(occasional) origin.

The last are released byintercurrent events (fever, metabolicdisorders, neuroinfections etc.).


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Febrile convulsions

They represent a critical disorderswhich appear in children between 6

months and 5 yrs, in associationwith fever, but without signs of .Intracranian infection and withoutafebrile crises in antecedents.

Majority of crises, until 90%,appear before 3 yrs age, with thepick of incidence at 15 months.


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Causes of febrile convulsions

Infections of nervous system.

Fever can act as the trigger factorof convulsions.

Febrile convulsions, as expressionof some genetic predispositionrelationed with age.


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Febrile convulsions

Most frequently, the crises offebrile convulsions follow thevirotic infections of respiratorytract, severe gastroenteritis caused

by Shigella or other infectionswhich provoke minimal fever by37,8038,5 0C.

Crises appear usually with the firstaccess of fever or are the firstsymptom of fever manifestation in25 42% of cases.


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Localized crises (focal, partial): I.1. Idiopathic (primary)

I.2. Symptomatic (secondary)

I.3. Cryptogenic

Generalized crises: II.1. Idiopathic

II.2. Symptomatic

II.3. Cryptogenic or symptomatic

Undetermined syndromes(with focal character

or generalized undetermined): neonatal crises,

myoclonic severe epilepsy of child, acquired

epileptic aphasia, epilepsy with peak-wave

continuous complexes during sleeping.

International classification of epilepsies,epileptic syndromes and critical disorders


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Clinical manifestations Tonic crisessudden disturbance of consciousness, axial

musculature hypertonia with members in extension, apnea,

perioronasal cyanosis, contracture of masseters, revulsionedeyes;

Tonico-clonic crisesare characterized by tonic phaseduring 10-12 seconds, followed by clonic phase with

muscular symmetric and bilateral clonuses, with shortrelaxations during until 2 minutes, the tongue wounding,sanguinolent foam, loss of urine and faeces can appear;resolutive phase is characterizing by postcritic coma with

deep, noisy respirations, bilateral midriasis; Atonic crisessudden losses of muscular tonus during

one or a few seconds, sudden falling of head on the chest.


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Loss of consciousness authenticated by

ocular revulsion.

Neuro-vegetative disorders

respiratory, irregularities of rhythm,

cyanosis; vasomotory (accesses of

pallor).


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Febrile convulsions

They appear in a child withneurologic negative anamnesis, in age

from 6 months until 5 yrs, onbackground of fever, are primarilygeneralized, duration until 15 minutes,are not repeating during the same

access of fever or in afebrility. The relatings about febrile

convulsions in heredo-collateralantecedents are possible.


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Complicated febrile

convulsions Duration more than 15 minutes, age

over 10 months, can generate the stateof convulsive status, are repeating in

series in the same day, often are focal,with lateralization, can remain motorypostcritical deficits Todd paralysis.

They will develop epilepsy in 2-3%

of cases.


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Diagnosis

It needs to exclude some infectiousdiseases with localization at CNS

level. This imposes a decision aboutthe performing of some paraclinic

investigations, lombar puncture,neuroimagistics, EEG.


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Differential diagnosis Epileptic origin of crises will be

maintained on the basis of some crises

with stereotype character recurrence,

without evidence of some trigger factors,

with typical changes on E.E.G. It is performing with the following

diseases:

primary infections of CNS;

acute encephalopathy;

syncope;

febrile delirium;


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TREATMENTof febrile convulsions in children

General principles:

Selection of optimal preparation in dependence

of convulsions type.

Selection of optimal doseusually minimal,

which allows the complete control of crises.

Respecting of anticonvulsivant monotherapy

(as exception 2-3 preparations in the treatment

resistant convulsions after exhaustion of

monotherapy), because the polytherapy canlead to chronic intoxication, undesirable

interaction of preparations with therapeutic

effect diminishing.


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Medicamentous treatment is administering dailyat the same hour for obtain a continuoustherapeutic concentration.

Optimal duration of treatment from 1 until 3

months). Interruption of treatment is performing

gradually with the clinical andelectroencephalographic monitoring.

Avoidance of factors, which releases theconvulsive crises and respecting of optimal liferegime (infections, traumas, intoxications,alcohol, caffee, concentrated tea, chocolate,

regime of sleeping - wakefulness).


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Treatment of febrile convulsions will beperforming with usual anticonvulsivantsand in specific dosage, ca celor

recomendate in tratamentul statusuluiepileptic.

The means of body temperaturedecreasing and the treatment ofinfection responsible to fever.


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Recommanded medication is the phenobarbital

or valproat, the self anticonvulsivants efficient

in febrile convulsions.

Prophylactic intermittent therapy has however a

general acception. There are a lot of

recommended protocols. But most often the

medication is performed with Diazepam per os0,3 mg/kg, Diazepam per rectum 0,5 mg/kg.


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TREATMENT OF CONVULSIVE STATUS

[after Paul Moe, Alan Seay, 1991]

Primordial measures: ABC [Aair; B -

respiration (breath); C - circulation]:

releasing of respiratiy pathways

the supply of respiration with oxygen

Maintaining of pulse, AP through optimal perfusion

of liquids 20-30 ml/kg.

Initial solution - glucose 20% i/v, 1 ml/kg.

Monitoring of sanguine gases level, ofelectrolytes, urea and of anticonvulsivants level

in the blood and of intracranial tension.


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Intravenous anticonvulsivant treatment:

diazepam 0,1-0,3-0,5 mg/kg (20mg) can be

repeated after 5-20 min, its maximal action is

after 20 min: can provoke respiratorydepression;

lorazepam 0,05-0,2 mg/kg (has more

prolonged that diazepam action);

phenitoin (diphenin) 10-20 mg/kg;

phenobarbital 10-20 mg/kg.

Correction of metabolic disorders (acidosis,

etc.).


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If the convulsions are repeated again, it isintroducing:

phenitoin 5 mg/kg and phenobarbital 5 mg/kg;their concentration in blood is monitoring, the

respiration and blood pressure are maintainingin the normal limits;

i/v paraldehid 4% or per rectrum 0,1-0,3 ml/kg(1:1 with the olives oil)

valproic acid in suspension 30-60 mg/kg per osor per rectum.

After convulsive status resolving the phenitoinand phenobarbital (5-10 mg/kg) and calcium

preparations will be administered.


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Prognosis

In febrile convulsions it is favorable.

In 70% of cases only oneself convulsivant

epizod will be exist and in 9 % of cases over 3

episods will be exist.

Higher risk of recurrence of FC is more in

children before 1 year. After 4 yrs the risk of

recurrence constitutes10 %.

The risk of epilepsy development is by 4times more in children with febrile convulsions.


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Hypocalciemic convulsions

Hypocalciemic convulsions (tetanic convulsions,spasmophilia)provoked by low concentration of Ca.

More frequent - in the age of 6 months-1,5 yrs.

Clinical picture: 1. Local convulsions:

Convulsions of mimic musculature Hand of obstetrician

Plant and fingers in position of flexion

Laryngospasm (noisy inspiration, screaming of

cock) 2. Generalized convulsions with loss of

consciousness until a few minutes. Convulsions canbe repeated in the type of epileptic status and are

finishing at the normalizing of ions level.


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Emergency treatment

In soft convulsionsis administering Sol. 10% ofcalcium chloride or calcium gluconate 0,1-0,15g/kg/day

In severe accesses- Sol.10% of calcium gluconate0,2 ml/kg i/v slow after dissolving in Sol. 5% ofglucose 2 times.

If the convulsions are continuing- Sol. 25% ofmagnesium sulphate o,2 ml/kg/ i/m and Sol. 0,5%seduxen 0,05-0,1 ml/kg i/m/

HOSPITALIZATION after the treatment ofconvulsions in the somatic department, the childcontinues to receive the Ca preparations 1 monthand vitamin D3.


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Respiratory-affective convulsions They present accesses of convulsive apnoe which appear in the

crying of children. Trigger factors: frightening, pain, joy, abusive alimentation

In the time of crying the child retains respiration, the cyanosisof teguments and buccal cavity mucosae is developing.

Due to hypoxia the child can loose the consciousness at shorttime period, tonic or clonico-tonic convulsions can appear.

EMERGENCY CARE:

To create an average of calming.

To apply the measures for reflectory restoring of respiration. Consultation of neurologist and sedative treatment.

Neurotoxicosis Etiology


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Neurotoxicosis - Etiology Infectious factors(viral, bacterial, mixt), intestinal

infections

Premorbid pathologic factors:

- perinatal pathology of central nervous system

- age peculiarities of CNS

- craniocerebral intranatal trauma - intrauterine asphyxia

- prematurity

- retardation in the intrauterine development

- anemia, rickets - congenital malformations

- states of immunodeficiency or immunocompression


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Clinical syndromes in neurotoxicosis cerebral syndromes:

- hyperthermia

- convulsions

- hypertensive-hydrocephalic

- meningeal

- by neuro-hormonal insufficiency somatic syndromes

- respiratoriy insufficiency

- cardiovascular insufficiency

- hepatic insufficiency

- renal insufficiency

- suprarenal insufficiency

- hematopoetic insufficiency


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Clinical manifestations I degree

State of consciousness psychomotory excitation

Sleeping superficial with interruption

Convulsions preconvulsive/clonic state

Pupils of the eye moderated narrowing

Cranial nerves without pathology Hyperkinesis tremor of extremities

Bulbar disorders absent

Muscular tonus increased

Big fontanelle soft tensioned

Meningeal signs occipital stiffness

Vegetative disorders hyperemia, after that pallor

C f


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Clinical manifestations II degree

State of consciousness inhibition until sopor Sleeping pronounced somnolence

Convulsions repeated tonicoclonic

Pupils of the eyes miosis, < fotoreaction

Cranial nerves rarely - III and VII pair

Hyperkinesis disorders of coordination

Bulbar disorders seldom after convulsions

Muscular tonus diminished Big fontanelle diminished

Meningeal signs moderately pronounced

Vegetative disorders hyperhydrosis,

acrocyanosis or cyanosis

Cli i l if i


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Clinical manifestations III degree

State of consciousness sopor-coma Sleeping sopor-coma

Convulsions tonico-clonic/status

Pupils of the eyes miosis or midriasis

Cranial nerves III,IV,VI,VII,IX

Hyperkinesis not characteristic

Bulbar disorders characteristic

Muscular tonus pronounced diminishing Big fontanelle hypotone, no pulsation

Meningeal signs pronounced or disappear

Vegetative disorders hyperthermia/hypothermia

sallowgrey cyanosis


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Pathogenetic treatment

ALL children with neurotoxicosis are

hospitalized

Prehospital treatment:

antipyretic therapy

anticonvulsivant therapy

antibioticotherapy corticotherapy

in II-III degree - diuretics


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Anaphylactic shock Pathogenetic mechanismis represented by

marked vasodilatation, decreased venous return anddepletion of intravascular volume through the loss atcapillary level, at which a moderate depression ofmyocardial function can be associated.

More frequent causes: - antibiotics, especially from betalactamides group

(penicilline on first place)

- insect bites, serum, vaccines, gammaglobulins i/v,

blood transfusion, excess of antigen during specifichyposensibilization for asthma and pollinosis

Allergic food, excess of pneumoallergens


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Anaphylactic shock/clinical picture

-onset is often very rapid, with respiratory signs:sneezing, cough, running nose, dyspnea, wheezing,cyanosis, sometimes signs of severe obstruction ofsuperior respiratory pathways(inspiratory stridor,laringean edema). Even pulmonary edema can

appear.

- cardiovascular signs: pericordial pains,palpitations, feeling of weakness, cardiacarrhythmias, marked hypotension, syncope

- digestive signs: nausea, vomiting, abdominalpains, diarrhea

- cutaneous signs: pallor,urticarian erruptions,angioneurotic edema.

A h l ti h k/t t t


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Anaphylactic shock/treatment Primary measures

Medicament of choice-Sol. 0,1% adrenalin

(vasoconstrictor effects,beta 1 inotrop positive andbronchodilator effects) i/m or i/v o,1 ml/yr (no morethan 1,0 ml) of life dissolved in 5 ml isotonic sol.

Block of further allergen absorption: proximal

cuff(on 30min.) and local infiltration with adrenalin Prednisolon 5 mg/kg

Antihistaminics: Sol. 1% dimedrol 0,05ml/kg(no morethan 0,5 ml in a child until 1 yr of life and1,0 ml in

older 1 yr). Pipolphen is not administering (markedhypotensive effect)

Obligatory contriol of Ps and AP

Anaphylactic shock/treatment


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Anaphylactic shock/treatment After primary measures:

- i/v S. 0,1% adrenalin o,1 ml/yr of life in10 ml of

isotonic sol. - prednisolon 2-4 mg/kg, or hydrocortison 4-8 mg/kg,

or 0,4% dexamethason 0,3-0,6 mg/kg

- volemic loading 20-30 ml/kg isotonic or Ringer sol.

During 20-30 min. Then, if the hemodynamics is notrestored - Reopolygliucin or polyglucin 10 ml/kg.

- If BP remains low- each 10-15 min. the Sol. 0,1%adrenalin 0,05-o,1 ml/yr of life (no more than 5 mg)

or Sol. 1% mesaton o,1 ml/yr of life (no more than1,0 ml)

- In the absence of effect - Dopamin 8-10mkg/kg/min under control of Ps and AP


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Anaphylactic shock/treatment In bronchospasm:

oxygenotherapy

Ensuring of respiratory pathways permeability (atnecessity even tracheostomy or tracheal intubation),ventilation

Sol. 2,4% euphyllini 0,5-1,0 ml/yr of life (no morethan 10 ml) i/v in get with 20 ml of isotonic sol.

At necessity - cardio-pulmonary reanimation

After according of emergency care -HOSPITALIZATION in emergency department.


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ATTENTION!

Emergencies in Pediatrics

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