CROUP in Children
Croup is a clinical syndrome, including a heterogeneous group diseases of larynx, infra/subglottis, trachea and bronchi, characterized by hoarseness, barking cough, stridor with or without inspiration of respiratory stress. often occurs in children.
Classification
I. Croup generally classified into two groups, namely:
A. VIRAL CROUP (laringotracheobronhotis): Characterized by prodromal symptoms respiratory infections: Respiratory tract obstruction symptoms lasted 3-5 days. Age 6-6 years. Stridor (+), Cough (all of time), Fever (+) high, duration 2-7 days, Family history (+), Predisposition by asthma (-).
B. SPASMODIC CROUP : Spasmodic cough, there is atopic factor, without prodromal symptoms, child can suddenly get respiratory tract obstruction, usually at night before take a bed, attacked for a while then return to normal.
II. Based on severity degrees, croup classified into 4 categories:
A. LIGHT: Marked by loud barking cough that sometimes arise, Stridor which can't heard when the patient take a rest or no activities and light chest retraction.
B. MODERATE: Marked by frequently barking cough, Stridor more can heard when patient less activities without respiratory distress.
C. SEVERE: Marked by frequently barking cough, Stridor inspiration more can heard when patient less activities or take a rest, and sometimes accompanied by expiratory stridor, chest wall retraction, also respiratory distress.
D. FAILED BREATH THREATENING: Cough sometimes isn't clear, stridor (+), impaired consciousness, and lethargy.
Etiology
Virus are common causes of Human Para-influenza Virus type 1 virus (HPIV-1) 60%, HPIV-2, 3 and 4, Influenza A and B viruses, Adenovirus, Respiratory Syncytial Virus (RSV) and Measles Virus.
Patophysiology
Virus transmission (mainly parainfluenza and RSV) can occur due to direct inoculation of secretion which carry the virus through the hands or by large inhalation particles entering through the eyes or nose. Virus infection in laryngotracheitis, laryngotracheobronchitis and laryngotracheobronchopneumonia usually starts from the nasopharynx or oropharynx which get down to the larynx and trachea after an incubation period of 2-8 days. Diffuse inflammation that causes erythema and edema of the mucosa wall of the respiratory tract. Larynx is the narrowest part of upper respiratory tract, which makes it very suspectible to the occurrence of obstruction. The same mucosa edema in adults and children will lead to different refinement. Mucosa edema with 1 mm thickness will cause airway narrowing by 44% in children and 75% in infants.
Mucosa edema of glottis area will cause a disruption of vocal cord mobility. edema on subglottis area can also cause symptoms of shortness of breath. Airway narrowing due to inflammation causes air turbulence that causes stridor.
In Laryngotracheitis acute edematous area, there are histologically containing cellular infiltrates in the lamina propria, submucosal and advensisia. These infiltrates contain histiocytes, lymphocytes, plasma cells, and neutrophils.
Patophysiology
Virus transmission (mainly parainfluenza and RSV) can occur due to direct inoculation of secretion which carry the virus through the hands or by large inhalation particles entering through the eyes or nose. Virus infection in laryngotracheitis, laryngotracheobronchitis and laryngotracheobronchopneumonia usually starts from the nasopharynx or oropharynx which get down to the larynx and trachea after an incubation period of 2-8 days. Diffuse inflammation that causes erythema and edema of the mucosa wall of the respiratory tract. Larynx is the narrowest part of upper respiratory tract, which makes it very suspectible to the occurrence of obstruction. The same mucosa edema in adults and children will lead to different refinement. Mucosa edema with 1 mm thickness will cause airway narrowing by 44% in children and 75% in infants.
Mucosa edema of glottis area will cause a disruption of vocal cord mobility. edema on subglottis area can also cause symptoms of shortness of breath. Airway narrowing due to inflammation causes air turbulence that causes stridor.
In Laryngotracheitis acute edematous area, there are histologically containing cellular infiltrates in the lamina propria, submucosal and advensisia. These infiltrates contain histiocytes, lymphocytes, plasma cells, and neutrophils.
Clinical Manifestations
Clinical manifestations of Croup aren't preceded by such a high fever during 12-72 hours, runny nose, sore swallow, and mild cough. this condition will develop into a loud cough, the voice becomes hoarse and rough. Accompanying systemic symptoms such as fever and malaise. When severe conditions can occur shortness breath, severe stridor inspiratory, the child restless, and symptoms will worsen at night.
Treatment
1. The key management is treat of airway obstruction
2. Inhalation therapy using cold vapor to humidify respiratory tract, alleviate inflammation
3. Epinephrine Nebulation: Should be given to children with croup syndrome is accompanied by severe stridor at rest and require intubation, and children with retraction and stridor which failed by inhalation therapy
4. Corticosteroid: used to reduce edema in larynx by mucous anti inflammation mechanism. Dexamethasone given at a dose of 0,6 mg/kg/oral or IM, single dose, repeated within 6-24 hours. prednisone at a dose 1-2 mg/kg
Intubation endotracheal, conducted in patients with severe croup syndrome, which is not responsive to other therapies. The indications are hypercarbia and the threat of breath failure, there is an increasing stridor, increased frequency of breath, increased pulse rate, chest retraction, cyanosis, and impairment of consciousness.
References
1. http://www.mja.com.au/public/issues/179_07_061003/fit10207_fm.html
2. http://www.eguidelines.co.uk/user/login_newsys.php?
3. http://www.pedsradiology.com/Historyanswer.aspx?qid=303&fid=1
4. http://kidshealth.org/parent/infections/bacterial_viral/croup.html
5. http://www.nlm.nih.gov/medlineplus/ency/article/000959.htm
6. http://kamaroperasi.blogspot.com/2009/03/croup.html
7. http://pediatrics.about.com/cs/commoninfections/a/croup.htm
8. http://www.mayoclinic.com/health/croup/ds00312
9. http://www.virtualpediatrichospital.org/providers/ElectricAirway/Text/MICCroupSymptoms.shtml
Atopic Dermatitis (Eczema) in Children
Definition
Eczema can makes intolerable itching, inflammation, and sleep disorders. This disease affects about 10-20% of children. Typically the first episode befoe age 12 months and subsequent episodes will arise until a child is lost through a certain period. Most Children will recover from eczema before the of five years. A part of child will continue to have eczema until adulthood.
Etiology
There are several theories that can be associated with the etiology of AD:
1. Hereditary factors
Family history was found around 70% in all cases. In the control condition of atopic, Ig E production under the influence of a dominant gene or chromosome 11q13.
2. Imunologic
The increase of total Ig E antibodies and specific ig E in serum against antigens from food or by inhalation.
Various circumstances can exacerbate atopic dernatitis:
1. Emotional stress
2. Changes of temperature or humanity
3. Bacterila skin infection
4. Contact with substancees which are irritant clothing (especially wool)
5. Some children, food alergies can trigger atopic dermatitis.
How can food make Atopic Dermatitis?
Based on research of Double Blind Placebo Controlled Food Challenge (DBPCFC), almost 40% of infants and children with moderate and severe Atopic Dermatitis has history of food alergy. Infants an children with food allergies are generally accompanied by skin test (skin prick test) and positive specific. Ig E against various kinds of food. Despite this positive skin test to a particular food, doesn’t mean that the patient is allergic to those food, therefore, still needed a provocation test and elimination of these foods to determine for sure.
How can Inhaled Allergens make Atopic Dermatitis?
Inhaled allergens as a cause of Atopic Dermatitis (AD) can be throught contact, which can be proved by patch test, postive in 30-50% sufferer AD, or by inhalation. Postive reaction can be seen in house dust mite allergy, which one examination in vitro, 95% of AD patients contain specific Ig E postive to dust mite allergy compared to only 42% in patients with asthma ine USA. There should also be noted that AD can also be caused by other inhaled allergens such as domestic animal dander, mold or ragweed in countries with four seasons.
How relation between Allergic dermatitis and bacteria infection?
AD patients had a tendency to be accompanied by bacterial skin infection, usually Staphylococcus aureus, viruses and fungi. Staphylococcus can be found in 90% lesions of patients with AD and the number could reach 107 colony per cm square on the part of the lesions. Infections caused by staphylococcus bacteria will be released a toxin that works as a superantigen, activating macrophages and T lymphocytes, which then release histamine. Therefore, patients with AD with complicated infected by bacteria should be given a combination antibiotics against Staphylococcus and topical steroid drugs.
Histopathology
The appearance may look dependent on the course of the disease from a sufferer. In patients without skin lesions, the histopathological will have a mild hyperkeratosis, hyperplasia epiderm and mild inflammatory cell (lymphocytes) in the derm. In patients wich acute lesions, histopathological will have an intracellular edema (spongiosa) in the epiderm and intracellular edema.
If Chronic, the lesions will be lycenification, hystopatological will appear hyperplasia epiderm accompanied by the extension of the rete ridges, striking hyperkeratosis, and mild spongiosis. The number of Langerhans cells in the epidermis increases and mononuclear inflammatory cells in the derm is dominated by macrophages. Histopathological appearance of non-specific atopic dermatitis and in accordance with various other phases so the histopathological dermatitis is not used as parameter for diagnosis.
Clinical manifestations
Clinical Manifestations of atopic Dermatitis is itching, the presence of macular erythematous, chapel, or papulovesikel, which crusted eczematous area, lychenification and excoriations. Dryness of the skin and secondary infections. Based on the clinical appearance and age, Atopic dermatitis is divided into three types, namely:
A. Infant
Usually arisses at the age two months-two years. Generally begin as an itchy enough eritematous plaque on the check accompanied by development of intraepidermal vesicle which ruptured, then ruptured vesicle produces skin lesions with local damp crust. Predilection for the flexures, front and sides of the neck, eyelids, forehead, face, wrists, and dorsa of the feet and hands
B. Children
Usually arises at the age 4-10 years. The rash often appears and come back only on one several regions, especially the upper arm, elbow, or behind the front of the knee. Lesions are usually less eksudatif or not wet begin with a fairly itchy erythematous, scaly little chapel of infiltrates.
C. Adult
TYPE Acute
Poorly defined erythematous plaques, with or without scale Excoriations occur as a consequence of scratching and rubbing. Secondarily infected sites: pustules (usually follicular), crusts.
Chronic Lichenification a thickening of the skin with accentuation of skin markings, which results from repeated rubbing or scratching: diffusely lichenified areas; nodular lichenification (may be confused with prurigo nodularis)
Chronic Recurrent Papular and lichenified plaques, excoriations, pustules, erosions, dry and wet crusts, and cracks (fissures)
DISTRIBUTION Often generalized, with predilection for the flexures, front and sides of the neck, eyelids, forehead, face, wrists, and dorsa of feet and hands
Poorly defined erythematous plaques, with or without scale Excoriations occur as a consequence of scratching and rubbing. Secondarily infected sites: pustules (usually follicular), crusts.
Chronic Lichenification a thickening of the skin with accentuation of skin markings, which results from repeated rubbing or scratching: diffusely lichenified areas; nodular lichenification (may be confused with prurigo nodularis)
Chronic Recurrent Papular and lichenified plaques, excoriations, pustules, erosions, dry and wet crusts, and cracks (fissures)
DISTRIBUTION Often generalized, with predilection for the flexures, front and sides of the neck, eyelids, forehead, face, wrists, and dorsa of feet and hands
1. Stigmata of atopic dermatitis: there are several clinical features and stigmata that occur in AD, namely: “WHITE DERMATOGRAPHISM” Scratches on the skin will cause redness AD patients within 10-15 second, followed by vasoconstrition that causes white line within the next 10-15 minutes. It is paradoxal vascular reactions of adaptation to changes in temperature in patients with AD. If AD had sufferer limb cold exposure, will be an accelerated cooling and heating deceleration compared with normal people.
2. Palm crease fold increment in the palm of the hand striking thought it is not typical sign for the AD.
3. Dennie Morgan lines or extra folds of skin under the eyes.
4. Buffed Nails Syndrome: nails look shiny because it’s always due to a sense of sangal itch scratched.
5. Allergic Shiner: is often found in patients with allergic disease due to repeated rubbing and scratching under the eye tissue with the consequents stimulation of melanocytes and increased melanin accumulation.
6. Hyperpigmentation: caused by continous scratching
7. Pilaris Keratotic: Dry skin, scaly, cracked and follicular hyperkeratotic
8. Delayed Blanch: injection of acetylcholine to patitient atopic mild erythema will delayed. This is caused by vasocontriction or increased capilarry permeability.
9. People with excessive sweating tend to sweat a lot so that AD increased pruritus
Diagnosis
A. Major Criterias (>3)
1. Pruritus
2. Typhical morphology and distribution:
- Infants and Children: the location most in face and extensor
3. Dernatitis are chronic recurrent
4. History of atopic patients or their families
B. Minor Criterias (>3)
1. Xerosis
2. Reactivation of the fast type skin test
3. Elevated levels of Ig E
4. Dermatitis on the mammary areola
5. Keilitis
6. Recurrent conjunctivitis
7. White dermographism/blanch delayed
Management
Epiglottitis in Children
a. Definition
Epiglottitis is an infection which attacks epiglotits and supraglotis structure, makes acute airway obstruction and cause death if not treated. Acute epiglottis an emergency so that the diagnosis should be established as quickly as possible, but must be done quickly and precisely in order to reduce mortality. The situation that is potentially deadly and dramatic this usually occurs in
children aged 2-7 years, peak incidence occurs at age 3.5 years.
b. Etiology
Epiglotitis almost always caused by Hemophilus influenza type B. Other causes are S. aureus, S. pneumonia, C.albicans, viruses and trauma.
c. Clinical manifestations
Epiglotitis marked by a sudden high fever and severe sore throat, shortness of breath, followed by symptoms of progressive airway obstruction quickly, can deteriorate into total obstruction of breathing and death.In younger children initially good general condition, often appear either before sleep but then wake up at night with high fever, afoni, protruding tongue, accompanied by severe breathing (respiratory disstres) moderate or severe stridor with inspiration.
Older children, initially complained of sore throat and dysphagia, the patient prefers a sitting position, body bent forward with his mouth open and neck extension. Respiratory crisis can occur within minutes or start 3-4 days after the occurrence of rhinitis. Inconvenience or substernal chest pain under the front there and could often compounded by coughing. When the condition getting worse, patients may be disturbed by the sound of whistling during respiration (may ronkhi), chest pain, and sometimes by shortness of breath.
d. Diagnosis
The diagnosis is based on the discovery of a large epiglottis, swollen and red cherries, with checks or direct laryngoscopy. On radiological examination showed picture thumb sign.
Thumb Sign
e. Treatment
Provision of oxygen
Provision of weight adjusted intravenous fluids and hydration status
Provision of Salin Sulfate inhalation
Intubation or tracheostomy
Antibiotics
Antibiotics given intravenously in the form of third-generation cephalosporins (cefotaxim or ceftriaxone), sefotaxim (50-100 mg / kg / day in three divided doses) for 7-10 days and free child fever two days, while ceftriaxone (50-100 mg / kg / day) can be given a single dose for 5 days.
References
1. http://www.waent.org
2. http://www.virtualpediatrichospital.org
3. http://emedicine.medscape.com
4. http://www.drugs.com/cg/acute-epiglottitis-in-children.html
5. http://www.privatehealthcare.co.uk/diseases/ear-nose-throat/epiglottitis-children
6. http://www.emedicinehealth.com/epiglottitis/article_em.htm
Epiglottitis is an infection which attacks epiglotits and supraglotis structure, makes acute airway obstruction and cause death if not treated. Acute epiglottis an emergency so that the diagnosis should be established as quickly as possible, but must be done quickly and precisely in order to reduce mortality. The situation that is potentially deadly and dramatic this usually occurs in
children aged 2-7 years, peak incidence occurs at age 3.5 years.b. Etiology
Epiglotitis almost always caused by Hemophilus influenza type B. Other causes are S. aureus, S. pneumonia, C.albicans, viruses and trauma.
c. Clinical manifestations
Epiglotitis marked by a sudden high fever and severe sore throat, shortness of breath, followed by symptoms of progressive airway obstruction quickly, can deteriorate into total obstruction of breathing and death.In younger children initially good general condition, often appear either before sleep but then wake up at night with high fever, afoni, protruding tongue, accompanied by severe breathing (respiratory disstres) moderate or severe stridor with inspiration.
Older children, initially complained of sore throat and dysphagia, the patient prefers a sitting position, body bent forward with his mouth open and neck extension. Respiratory crisis can occur within minutes or start 3-4 days after the occurrence of rhinitis. Inconvenience or substernal chest pain under the front there and could often compounded by coughing. When the condition getting worse, patients may be disturbed by the sound of whistling during respiration (may ronkhi), chest pain, and sometimes by shortness of breath.
d. Diagnosis
The diagnosis is based on the discovery of a large epiglottis, swollen and red cherries, with checks or direct laryngoscopy. On radiological examination showed picture thumb sign.
Thumb Signe. Treatment
Provision of oxygen
Provision of weight adjusted intravenous fluids and hydration status
Provision of Salin Sulfate inhalation
Intubation or tracheostomy
Antibiotics
Antibiotics given intravenously in the form of third-generation cephalosporins (cefotaxim or ceftriaxone), sefotaxim (50-100 mg / kg / day in three divided doses) for 7-10 days and free child fever two days, while ceftriaxone (50-100 mg / kg / day) can be given a single dose for 5 days.
References
1. http://www.waent.org
2. http://www.virtualpediatrichospital.org
3. http://emedicine.medscape.com
4. http://www.drugs.com/cg/acute-epiglottitis-in-children.html
5. http://www.privatehealthcare.co.uk/diseases/ear-nose-throat/epiglottitis-children
6. http://www.emedicinehealth.com/epiglottitis/article_em.htm
Acute Otitis Media in Children
a. Definition
Otitis media is an acute inflammation of the middle ear which associated with effusion and a buildup of fluid in the middle ear. Usually, interference occurs the middle ear aeration is caused by a disturbed function of eustachius duct.
b. Etiology
In most cases, Acute otitis media caused by a virus, but it is difficult to distinguish between viral or bacterial etiology based on clinical presentation and examination using otoskop only. Acute otitis media is usually exacerbated by upper respiratory infections caused by viruses that cause edema in the eustachius fallopian. This resulted in an accumulation of fluid and mucous which then is infected by bacteria. The most common pathogens infecting the children are Streptococcus pneumoniae, Haemophilus influenzae, Moraxella catarrhalis. Bacteria are involved in different chronic infection with acute otitis media, where P. aeruginosa, Proteus species, Staphylococcus aureus, and the combined anaerobic become real.
c. Risk factors
Men
Age under 2 years
White, American Indian
The first attack usually under 6 months
S. Infection Pneumonia.
Acute Otitis Media
d. Clinical manifestations
Classic symptoms include pain, fever, malaise, and sometimes in addition to head pain, ear pain, especially in children can occur anorexia and sometimes nausea and vomiting. Fever may be high but may also not found in 30% of cases. All or part of the tympanic membrane is typically become red and prominent, and blood vessels in the tympanic membrane and stalk malleolus dilates and becomes prominent. It is best diagnosed using pneumatic otoskop. If otoskop not available, should be suspected of an acute otitis media if there is discharge coming out of the ear for less than two weeks, or there is a sudden ear pain, persisten.
e. Diagnosis
Examination of the tympanic membrane showed a reduced movement, convex, reddish and turbid, it can also be found that purulent secretions.
f. Treatment
Oral amoxicillin 40 mg / kg / day, three times a day for 10 days
The second option can be given a combination of erythromycin 50 mg / kg / day with sulphonamides 100 mg / kg / day or sulfiksoksazol 150 mg / kg / day four times a day.
Supportive therapy: analgesics, antipyretics, decongestants.
Patients with severe ear pain conducted miringotomi
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