Meningococcal infection is an acute infectious disease that is caused by neisseria meningitidis and is characterized by the variety of clinical forms: from nasopharyngitis and healthy carrying to generalized forms (meningococcemia, meningitis, and meningoencephalitis).
Etiology: Neisseria meningitidis, Gram negative diplococci.
Epidemiology:
· Source of infection - ill person or carrier.
· Way of spreading - droplet with nasopharyngeal mucus during sneezing, coughing, speaking. –
· Susceptibility is high in children 6 mouths -5 years old. Only 15% of contact persons may be infected, 98% of them become carriers, only 2% - ill.
Classification:
Localized forms
· Meningococcal carrying,
· acute nasopharyngitis;
Generalized forms
· Meningococcemia (typical, fulminant and chronic),
· Meningitis,
· Meningoencephalitis.
Rare forms
· Meningococcal endocarditis,
· Arthritis,
· Pneumonia,
· Iridocyclitis.
More usual combined forms (meningitis + meningococcemia or meningoencephalitis + meningococcemia).
Pathogenesis
1. Inoculation and reproduction of bacteria in upper respiratory tract.
2. Development of local inflammation, lymphoid tissue hyperplasia (nasopharyngitis)
3. Bacteraemia, dissemination
4. Toxemia (meningococcemia) in fulminant form: massive bacteriemia, disintegration of microbes, endotoxemia ® infectious-toxic shock (violation of microcirculation ®DIC-syndrome ® metabolic disorders)
5. Rupture of hematoencephalic barrier meningitis, meningoencephalitis.
Diagnostic criterions
Nasopharyngitis:
· intoxication (headache, malaise, pain, fever);
· catarrhal syndrome (cough, sore throat, corryza, conjunctive hyperaemia);
· insignificant hyperemia of tonsils, soft palate, palatal arch, bright, swollen, covered by mucus back pharyngeal wall with hyper pleased follicles.
Meningococcemia is characterised by:
· acute beginning from intoxication, high temperature (39-40°C );
· prime maculopapulous rashes on the 1 day (like in measles);
· typical rashes on the 1-2nd day: purpura or petechia lesions (photo), bruises (photo). Petechia are pinpoint, may have a raised vesicular or pustular centre. Lesions are more common on the trunk and extremities but may also occurs on the palms, soles and mucosa. More fulminant meningococcal infections are often associated with extensive purpura lesions and with large, well circumscribed ecchymotic patches covering large areas of the body (photo). Necrotic bulla may develop within the ecchymotic patches with resultant sloughing. Rashes are resolved by necrosis, scarring;
· hemorrhagic syndrome (nasal bleeding, bloody vomits, hematuria).
· Other features - irritability, myalgia, arthralgia and hypotension.
Exanthema at meningococcemia
Exanthema and bruises at meningococcemia
Fulminant form:
· rapid beginning, severe toxic syndrome;
· considerable defeats from the beginning (hemorrhagic syndrome; hemorrhage in mucus membranes, skin (photo), adrenal glands, necrosis of adrenal glands known as Waterhouse-Frederixen syndrome (photo) with development of acute adrenal insufficiency, severe toxic shock syndrome);
· high lethality (at inadequate treatment).
Exanthema at fulminant meningococcemia
fulminant meningococcemia, hypostases
adrenal hemorrhage (Waterhouse-Frederikson syndrome)
Meningitis has
· sudden onset (with previous nasopharyngitis 2-3 days before in 1/3 of patients);
· toxic syndrome (hyperpyrexia);
· general cerebral syndrome:
· central repeated vomiting without nausea,
· severe diffuse headache, or in the forehead or occiput, it increases during the head movements, bright light or loud sounds;
· irritability or lethargy
· Meningeal syndrome (meningeal pose, hyperesthesia, stiff neck, positive Kerning’s and Brudzinsky’s signs, tenderness in sites of trigeminal nerve endings, suppression of skin rephlexes).
· Lethargy and obtundation usually develop and may progress to stupor or even coma.
· Cerebrospinal fluid (CSF) examination show: -polymorphonuclear pleocytosis, protein enlargement, high pressure of CSF, glucose and chlorides are low decreased or normal.
· local symptoms damage of 8th, 3rd, 6th, or 7th pairs of cerebral nerves, tonic-clonic seizures (brain edema), is quickly regressing;
· Infectious-toxic damage of myocardium;
· Dyspepsia: coated tongue, loss of appetite, constipation.
Features of meningitis in infants:
· intoxication, fever;
· expressed hyperesthesia (crying in case if diaper changing, taking the child);
· cerebral scream (equivalent of headache);
· Lesage’s symptom (other meningeal sins are not expressed);
· meningeal pose or head extension;
· depression of abdominal reflexes;
· expulsion and tension of large fontanel;
· diarrhea
Complications:
• infectious-toxic shock;
• acute edema-swelling of the brain;
• restriction (wedging) of oblong brain into the great cervical opening;
• convulsive syndrome;
• ependimatitis;
• DIC (disseminated intravascular coagulation) syndrome;
• pluriglandular insufficiency;
• convulsive syndrome.
Phenomena that remain:
· cerebral asthenia;
· epileptiform syndrome;
· physical and intellect retardation;
· deafness;
· blindness;
· hydrocephalus;
· Palsies, paralyses.
obstructive hydrocephalus
Laboratory tests
· Complete blood test: leucocytosis with neutrophyllosis and left shift, increased ESR
· Bacteriological investigation of nasopharyngeal mucus, blood, CSF; Bacterioscopy of blood (thick drop) and CSF;
· Clinical investigation of CSF: neutrophyl pleocytosis, protein increase, positive Pandy test, elevated pressure, slight decrease of glucose level.
· Serological IHAR, immunological methods, latex-agglutination test (presence of N.meningitidis antigens).
· Coagulogram – hyper coagulation or coagulopathy
Diagnosis example:
· Meningococcal infection, typical localized form (meningococcal carrying)
· Meningococcal infection, typical generalized combined form (meningitis + meningococcemia), complicated by toxic shock syndrome, 2nd degree
Differential diagnosis for meningococcemia should be performed with measles, scarlet fever, pseudotuberculosis; thrombocytopenia, purpura fulminance, sepsis acquired by Gram-negative strains. For meningoencephalitis differential diagnosis should be performed with meningismus in influenza; spasmophylia; viral meningitis in influenza, measles; tuberculosis meningitis.
Differential diagnosis of meningitis
Signs
|
Meningismus
|
Viral meningitis
|
Tuberculosis meningitis
|
Purulent bacterial meningitis
|
Subarachnoid hemorrhage
|
Color, transparence
|
Colorless, transparent
|
Colorless, transparent oropalescent
|
Colorless, xanthochromicor opalescent
|
White-yellow orgreen, muddy
|
bloody, after settling – xanthochromic
|
Pressure (mm.H2O),
flow out speed(drops per 1minute)
|
below 180-200
50-80
|
200-300
60-90
|
250-500
60-90
|
250-500
jet, sometimes rare drops
|
250-400
> 70 or jet
|
cytosis (in 1mkl.)
|
2-12
|
20-800
|
200-700
|
500-1000 andmore
|
It is hard to count in the first days,
from 5-7 day15-120
|
cytogram
lymphocytes, %
neutrophyls, %
|
80-85
15-20
|
80-100
0-20
|
40-60
20-50
|
0-30
30-100
|
from 5-7 daylymphocytes prevail
|
protein, g/l
|
0.16-0.33
|
0.33-1.0
|
1.0-3.3
|
0.66-16.0
|
0.66-16.0
|
sedimentation tests (Pandy)
|
–
|
+(++)
|
+++(++++)
|
+++(++++)
|
+++
|
Dissociations
|
Absent
|
cellular-proteinon the low level (from 8-10 day –protein-cellular)
|
protein-cellular
|
cellular-proteinon the high level
|
–
|
Fibrin pellicle
|
–
|
- in 3-5 %
|
Often rough in30-40 %
|
Often as a sediment
|
Rare
|
glucose,mmol/l
|
2.2-3.3
|
2.2-3.3
|
For 2-3 weeks1.0-2.0
|
normal
|
Differential diagnosis of meningococcemia
Signs
|
Measles
|
Rubella
|
Scarlet fever
|
Initial symptoms
|
catarrhal signs from upper airways, conjunctives during 2-4 days, intoxication
|
Increase of occipital lymph nodes, small catarrhal signs and intoxication
|
Acutely - intoxication, angina, regional lymphadenitis
|
Time of the rashes' beginning
|
on 4-5 days of the disease, with stages
|
1 day, seldom 2
|
1 day (in 20% - 2)
|
Morphology
|
maculopapulous
|
small-papulous,
|
small point-like
|
Sizes of elements
|
middle, large
|
small, middle
|
small
|
Localization
|
1 day - on the face 2 - on the face, trunk; 3 - on the face, trunk, limbs
|
on whole body, mainly on unbending surfaces of the limbs
|
mainly on bending surfaces of limbs, down the abdomen, lumbar region, face, lateral surfaces of the trunk, pale nose-labial triangle
|
Brightness and color of elements
|
bright red
|
pale-rose
|
bright
|
Further rashes' development
|
pigmentation, slight hulling
|
disappear on 3-4 days
|
gradually turn pale for 4-5 days, small, lamellar hulling
|
Catarrhal phenomena
|
expressed in first 5-6 days
|
small, short for 1-2 days
|
Not typical,
|
Oral mucous membranes
|
hyperemied, friable, enanthema, Koplick's spots
|
clear, sometimes single elements of enanthema
|
marked off, bright hyperemia, enanthema on palate, angina
|
Intoxication
|
significant, lasts 5-7 days
|
small or being absent
|
proportional to local signs, short for 1-3 days
|
Other symptoms
|
Complications (respiratory, digestive, nervous, urinary systems, eye, ears, skin)
|
increased and painful posterior neck and occipital lymph nodes
|
angina, changes on the tongue (raid, from 4-5 days "strawberry"), complications on 2-3 weeks
|
Laboratory criteria
|
leucopenia, lymphocytosis, aneosynophylia, serological reaction with measles antigen (+)
|
leucopenia, lymphocytosis, increase of the plasmatic cells' number, serological reactions with rubella antigen (+)
|
leucocytosis, shift to the left, neutrophyllosis, enlarged ESR, in pharyngeal, nasal swabs - streptococci
|
Signs
|
Pseudotubercullosis
|
Meningococcemia
|
Chickenpox
|
Initial symptoms
|
acutely with many symptoms (intoxication, intestinal changes, seldom - catarrhal signs
|
intoxication, develops very acutely, initial measles-like rash
|
Acutely, observing catarrh, intoxication, rash
|
Time of the rashes' beginning
|
on 2-8 day
|
first hours of the disease
|
On 1-2 days, appear next 3-5 days as pushes
|
Morphology
|
puncture-like, small spots, erythema
|
hemorrhagic "star-like" with necrosis in the centre
|
Polymorphic (spots, papules, vesicles, crusts)
|
Sizes of elements
|
Small, middle, large
|
from small to significant
|
middle
|
Localization
|
"hood", "mitten", "socks" signs, in skin folds, bends, around joints
|
buttocks, lower limbs, less - on trunk, hands, face
|
On whole body, on hair part of the head, seldom - on palms and soles
|
Brightness and color of elements
|
bright
|
hemorrhagic, bright, sometimes cyanotic
|
Papules are pink, vesicles - on hyperemied base
|
Further rashes' development
|
gradually disappear for 2-5 days, small, lamellar shelling
|
Small, disappear gradually, significant, leave "dry" necrosis
|
After desquamation of the crusts - a slight pigmentation
|
Catarrhal phenomena
|
Not typical
|
are absent, in 30-40% on previous 2-3 days - nasopharyngitis
|
Moderate,
|
Oral mucous membranes
|
Possible hyperemia of the pharynx, tonsils,
|
hyperemia and groiness of back pharyngeal wall, hypertrophy of follicles
|
On pink background - polymorphic elements
|
Intoxication
|
expressed, long-lasting (2-3 weeks)
|
sharply expressed
|
Small or moderate
|
Other symptoms
|
arthritis, myocarditis, diarrhea, hepatitis, abdominal syndrome, lymphoproliferative symptom, kidneys, nervous system damage, pneumonia
|
meningitis, encephalitis, arthritis, iridocyclitis, endocarditis, aortitis, pneumonia, pleurisy
|
Seldom: generalized visceral forms, meningoencephalitis
|
Laboratory criteria
|
leucocytosis, shift to the left, high ESR, Indirect hemagglutination reaction with special diagnosticum (+), separation of Y. pseudotuberculosis from excrements
|
leucocytosis, shift to the left, neutrophyllosis, high ESR, in nasopharyngeal swab, thick drop of blood - meningococci
|
Leucopenia, lymphocytosis, serological: binding complement reaction with Chickenpox antigen (+)
|
Treatment of nasopharyngitis includes:
1. Antibacterial therapy with rifampicin 10 mg/kg/daily for 3-5 days or macrolides (erythromycin 30-50 mg/kg/daily, spiramycin, azythromycin 10 mg/kg/daily) or chloramphenicol 30-50 mg/kg/daily;
2. Bed rest up to the normalization of body temperature,
3. Adequate rehydration with oral fluids (lemon tea, raspberry tea, warm alkalic drinks
4. Vitaminized milk-vegetable food;
5. Control of fever (when the temperature is more than 38.5-39˚C); in children before 2 mo and in case of perinatal CNS damage, seizures in the history, severe heart diseases – when the temperature is up to 38˚C with acetaminophen (paracetamol 10-15 mg/kg not often than every 4 hours (not more than 5 times per day) or ibuprophen 10 mg/kg per dose, not often than every 6 hours.;
6. Antiseptic fluids locally (gurgling), ultraviolet insolation of the pharynx.
Generalized forms before transporting (prehospital treatment):
1. Oxygen therapy by water-wet oxygen;
2. To perform the peripheral venous puncture;
3. Infusion therapy by isotonic salt solutions (0.9 % sodium chloride solution or sodium chloride solution + potassium chloride + calcium chloride dihydrate + sodium lactate) in a volume 20 ml/kg body weight for 20 minutes;
4. Antibacterial therapy – cefotaxim for one occasion dose 75 mg/kg (when on the hospital stage application of solutions which contain in the composition a calcium (Ringer’s solution and others like that) or ceftriaxon for one occasion dose 50 mg/kg (when infusion of preparations of calcium at subsequent therapy is not needed) intravenously droplet. Possibly application of chloramphenicol for one occasion dose 25 mg/kg intravenously stream;
5. Glucocorticoids only intravenously (prednisolon, hydrocortisone) in a dose 10 mg/kg (by prednisolon);
6. Antipyretic therapy (in the case of necessity) – (paracethamol 10-15 mg/kg, Ibuprofen 5-10 mg/kg through a mouth, methamisol sodium 50 % IV 0,1 ml/yrs of life;
7. Anticonvulsant therapy (in the case of necessity) – diazepam in a single dose 0.3-0.5 mg/kg (not more than 10 mg on one injection);
8. Transporting of patients with the severe forms of meningococcemia is carried out by the reanimation brigades of first-aid.
An algorithm of meningococcemia intensive care in the specialized hospital:
1. Providing of communicating of respiratory tracts and adequate breathing
2. Providing of venous access. At fulminant forms MI must be provided 2 venous accesses simultaneously.
3. At presence of refractive shock, progressive increase of intracranial pressure, cramps – intubation of trachea and acquired pulmonary ventilation.
4. Infusion therapy by salt solutions, by colloid solutions for blood circulation stabilizing.
5. Correction of hypo- and hyperglycemias
6. Antibacterial therapy
7. support of hemodynamics in case of refractive shock (dopamine, Dobutaminum, epinephrinum, norepinephrinum).
8. Purposeful correction of acid-basic balance and water-electrolyte disorders.
9. At presence of signs of adrenal insufficiency and/or refractive to adequate doses of sympathomimetics – Glucocorticoids intravenously. Preparation of choice is hydrocortisone as daily infusion or every 6 hours.
10. Treatment of hyperthermia (paracethamol, Ibuprofen, methamisol sodium, physical methods of cooling).
11. Anticonvulsant therapy (diazepam, sodium oxybutiratis, barbiturates, phenitoin).
12. Treatment of DIC-syndrome.
13. At growth of intracranial hypertension, head cerebral edema:
• location of bed with elevated head end on 30 °;
• acquired pulmonary ventilation;
• control of plasma osmolarity (within the limits of 300-310 mosmol/l);
• glycemia control;
• control of hyperthermia and cramps;
• effective cardiac output or insignificant increase of arterial pressure;
• at the terms of stable hemodynamics manitol and furosemid injection.
Indexes
|
Points
|
Systolic pressure (<
Systolic pressure (<
Dermal-rectal temperature gradient > 3°С
Estimation of comma by
Worsening of the state during last hour
Absence of meningism
Widespread purpura, large ecchymoses
A deficit of bases is in arterial or capillary blood > 8,0
|
3
3
3
2
2
1
1
|
Maximal estimation
|
15 points
|
At estimation by the Glasgow Glasgow
An algorithm of meningococcemia intensive care in the specialized hospital:
1. Providing of communicating of respiratory tracts and adequate breathing
2. Providing of venous access. At fulminant forms MI must be provided 2 venous accesses simultaneously.
3. At presence of refractive shock, progressive increase of intracranial pressure, cramps – intubation of trachea and acquired pulmonary ventilation.
4. Infusion therapy by salt solutions, by colloid solutions for blood circulation stabilizing.
5. Correction of hypo- and hyperglycemias
6. Antibacterial therapy
7. support of hemodynamics in case of refractive shock (dopamine, dobutaminum, epinephrinum, norepinephrinum).
8. Purposeful correction of acid-basic balance and water-electrolyte disorders.
9. At presence of signs of adrenal insufficiency and/or refractive to adequate doses of sympathomimetics – Glucocorticoids intravenously. Preparation of choice is hydrocortisone as daily infusion or every 6 hours.
10. Treatment of hyperthermia (paracethamol, Ibuprofen, methamisol sodium, physical methods of cooling).
11. Anticonvulsant therapy (diazepam, sodium oxybutiratis, barbiturates, phenitoin).
12. Treatment of DIC-syndrome.
13. At growth of intracranial hypertension, head cerebral edema:
• location of bed with elevated head end on 30 °;
• acquired pulmonary ventilation;
• control of plasma osmolarity (within the limits of 300-310 mosmol/l);
• glycemia control;
• control of hyperthermia and cramps;
• effective cardiac output or insignificant increase of arterial pressure;
• at the terms of stable hemodynamics manitol and furosemid injection.
Antibacterial therapy
Intravenous infusion of cefotaxim or ceftriaxon. At mild and moderate forms of meningococcemia benzylpenicillin is possible (reserve antibiotics are ampicillin, ceftriaxon, cefotaxim or chloramphenicol), in case oh hypersensitivity to beta-lactams chloramphenicol is used. For protecting from a nosocomeal infection (if necessary) the second antibiotic should be given (amikacin 15 mg/kg/day, nethylmicin – to the children before 1 year 7.5-9 mg/kg, to the elder children – 6-7.5 mg/kg).
Antibiotic
|
Optimum way ofinjection
|
Day's dose
|
Amount of injection
|
Ceftriaxon
|
Bolus, slow IVinfusion
|
100 mg/kg
|
2
|
Benzylpenicillin
|
Bolus IV
|
300-500 thousands of IU/kg
|
6-8
|
Сhloramphenicol
|
Bolus IV
|
100 mg/kg
|
2-4
|
Cefotaxim
|
Bolus, slow IVinfusion
|
150 mg/kg
|
2-4
|
Ampicillin
|
Bolus IV injection
|
injection
|
300 mg/kg
|
Duration of antibacterial therapy at MI is 7-10 days.
Infusion therapy is performed in the hyperhydratation regime
• Solutions are entered intravenously, stream.
• Isotonic crystalloid solutions (sodium chloride, Ringer’s solution, sodium chloride + potassium chloride + calcium chloride dehydrate + sodium lactate) are entered in a dose 20-30 ml/kg during the first 20 minutes.
• Colloid solutions (derivates of hydroxethylen starch of ІІІ generation) are entered with the speed of 20-40 ml/kg/hour.
• In case of ITSH immediate infusion of crystalloid solutions 20 ml/kg during the first 20 minutes with subsequent infusion of colloid solution in a dose 10-20 ml/kg in next 20 minutes.
• In case of fulminant forms of MI it is expedient to connect crystalloid and colloid solutions in correlation 2:1.
• If infusion 60-90 ml/kg of salt solution or 20-40 ml/kg of colloids during the first hour of treatment appeared uneffective, then in such cases there is a necessity for application of sympathomimetics and respirator support.
• Stimulation of urination by saluretics in case of oliguria, anuria – (furosemide 1-2 mg/kg) expedient only in case of hemodynamics stabilizing (satisfactory perfusion, arterial pressure, central venous pressure).
• Application of glucose solutions, especially water is impermissible in case of ITSH, metabolic acidosis and cerebral edema. They do not stay too long in the vessels, strengthen the edema of cells, brain edema. Water solutions of glucose can be appointed only after stabilizing of hemodynamics, normalization of perfusion and liquidation of acidosis. By the unique testimony for infusion of glucose for patients with shock and head cerebral edema there can be hypoglycemia. The level of glucose must be supported within the limits of 3.5-8.3 mmol/l. At the level of glucose less than 3.5 mmol/l the correction by 20-40 % glucose solution is used, at the level over 10-11 mmol/l – insulin.
• Metabolic acidosis is corrected by intravenous infusion of sodium bicarbonate at blood pH below 7.1-7.2.
• Infusion therapy must remove electrolyte disorders also (hypocalcaemia, hyperkalimia, hypokalimia).
• Meningitis is not an in indication for IV therapy limitation in case of effective hemodynamics maintenance.
• After shock liquidation protracted infusion therapy is need.
• The calculation of volumes for infusion therapy is done on the basis of physiologic necessity, correction of deficits of water and electrolytes, taking into account pathological losses, level of glucose, general albumen, state of alimentary canal, and degree of cerebral edema.
• One of aspects of infusion therapy there is a necessity of partial parenterally feed in after shock period. Its basis is infusion of 10-20 % glucose solutions with insulin and amino acids solutions.
Sympathomimetic and inothrope support of hemodynamics.
• Application of inothrope preparations for children with refractive to infusion therapy shock – dopamine as permanent intravenous infusion 10 мcg/kg/min, if ineffective – increase the dose to 20-30 мcg/kg/min. At decreased cardiac output Dobutaminum is appointed in the same doses, as dopamine.
• If, without regard of dopamine administration in the dose of 20-30 мcg/kg/min, hypotension is saved, expedient is application of norepinephrinum or epinephrinum from 0.05 to 3мcg/kg/min. If dopamine is ineffective quite often it is succeeded to obtain the substantial improvement of hemodynamics by the combined application of Dobutaminum and norepinephrinum.
Glucocorticoids
• Glucocorticoids are appointed at presence or suspicion on acute adrenal insufficiency and/or refractivity to the sympathomimetics.
• Hydrocortisone is a medicine of choice. Possible is prednisolone application.
• Preparations are entered every 6 hours.
• The calculation of dose is done by prednisolone 10 mg/kg. Glucocorticoids are appointed as adjuvant therapy of purulent meningitis. Dexamethazonum is a medicine of choice 0.15 mg/kg х 4-6 times per day during 2-4 days.
Treatment of DIC-syndrome
• Therapy of DIC-syndrome assumes administration of heparin in a dose 50-200 EU/kg per day, under control of coagulogram indexes.
• At presence of hypercoagulability a dosage is applied to 150-200 EU/kg, that in combination with infusion, antibacterial and antiagregant therapy lead to the rapid normalization of coagulogram indexes.
• The criterion of efficiency of heparin therapy is lengthening of coagulation time in 2-3 times from an initial index.
• In transitional and hypocoagulation phases of DIC-syndrome fresh-frozen plasma in a dose 10-20 ml/kg as a fast, stream infusion in combination with heparin in a dose 25-50 EU/kg is applied. If necessary plasma is entered again.
• The criterion of such therapy efficiency is an increase of fibrinogen level to 1.5-2 gs/l, prothrombine index increase over 60 %, stopping of mucosal bleeding, and bleeding from the places of injections.
• In phase of incoagulability and fibrinolysis the inhibitors of proteases are given: contrical in a dose of 1000 EU/kg, and other in equivalent doses.
A diet in case of intensive therapy
• For warning of translocation of intestinal microflora at the severe forms of meningococcemia early tube enteroalimentation have to begin at once after stabilizing of hemodynamics, in absence of enteroplegia displays.
• In the beginning of infants feeding optimal is application of lactose-free formulas which also contain prebiotics.
• Formulas can be entered through a nasogastric tube.
• Infants who have breastfeeding will achieve pasteurized breast milk.
Care of skin, prophylaxis and treatment of skin necroses
• At meningococcemia is needed a careful care of skin, prophylaxis of bedsores, treatment of skin by antiseptic fluids.
• At presence of deep skin and soft tissues defects there can be necessary a necrectomy and plastic closing of a skin defect or amputation of distal segments of extremities.
• Expedient treatment of necrotizing surfaces by antiseptic aerosols, creams which contain silver sulphodiasinum.
• Carotinoids applications speed up cicatrisation of necroses.
• Not deep necroses heal over independently and do not need treatment.
• At arthritis – NSAIDs, warm on joints, massage, gymnastics.
• At iridocyclitis – nicotine acid, nitrate of sodium in a temporal area.
• At pneumonia – combination of antibiotics, oxygenation, physiotherapy.
• At carditis – bed rest, cardiac glycosides, cardiothrope medicine.
• At hypertensive syndrome – diacarb (acethasolamid) + asparkam according the
syndrome severity.
Discharge the patient:
• clinically healthy, with normal CSF analyses;
• with one documented negative nasopharyngeal culture which is performed in 3 days after antibiotic therapy.
Dispensarization for 2 years by paediatrician, in case of meningitis, meningoencephalitis – also neurologist.
Prophylaxis:
1. Sanation of carriers by erythromycin, chloramphenicol, ciprofloxacin or rifampin for 3-5 days;
2. Quarantine for 10 days, contacts inspection with one bacteriological test of nasopharyngeal culture;
3. Disinfection.
References:
1. Current therapy in pediatric infectious diseases – 2 edited by John D. Nelson, M. D. – B.C. Decker inc. Toronto, Philadelphia, 1988, - P. 134-138, 285.
2. Ambulatory pediatric care (edited by Robert A. Derchewitz; - 2 nd ed. – Lippincot – Raven, 1992. – P. 570-574; 255.
3. Principles and Practice of Pediatric Infectious Diseases. / Edited by Saran S. Long, Larry K. Pickering, Charles G. Prober, Philadelphia , Pa
Additional:
1. Textbook of Pediatric Nursing. Dorothy R. Marlow; R. N., Ed. D. –London
2. Pediatrics ( 2nd edition, editor – Paul H.Dworkin, M.D.) – 1992. – 550 pp.
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