– MedMuv

June 6, 2024

LESSON № 2 (Practical class – 6 hours)

Topics:

1. Infant chronic nutrition disorder.

2. Rickets and its effect on the formation of dental systems.

3. The most common diseases of the respiratory systems in childhood.

Infant chronic nutrition disorder – disorders caused by nutritional imbalance, either overnutrition or undernutrition, occurring in infants ages 0 to 12 months.

Malnutrition is absence of adequate caloric and volume feeding of the child.

There are numerous causes of malnutrition including recurrent bacterial diarrhea, often upper respiratory tract infections, congenital gastrointestinal diseases, diseases of the mother during pregnancy. This state is associated with anergy, infectious complications, high mortality.

Etiology: inadequate feeding, low level of ferments of gastrointestinal tract. Organic factors include congenital heart defects, neurologic lesions, microcephaly, chronic urinary tract infection, gastroesophageal reflux, renal insufficiency, endocrine dysfunction, cystic fibrosis. Malnutrition can also be caused by psychosocial factors, the problem being between the child and primary caregiver, usually the mother. In this situation the lack of physical growth and development is secondary to the lack of emotional and sensory stimulation.

Pathogenesis:

Digestive defects mainly include those conditions in which the enzymes, necessary for digestion are diminished or absent, such as cystic fibrosis, in which pancreatic enzymes are absent; biliary or liver disease, in which bile production is affected, or lactase deficiency, in which there is congenital or secondary lactose intolerance.

Absorptive defects include those conditions in which the intestinal mucosal transport system is impaired. It may be because of primary defect such as celiac disease or gluten enteropathy or secondary to inflammatory disease of the bowel, that results in impaired absorption because bowel motility is accelerated. Anatomic defects such as short bowel syndrome, affect digestion by decreasing the transit time of substances with the digestive juices and affect absorption by compromising the absorptive surface. All this causes leads to maldigestion and malabsorption syndrome, damage of function of all organs and systems of the organism.

Main clinical symptoms are: abdomen pain, regurgitation, periodic vomiting, bad appetite, frequent liquid stool, decreasing or absense of subcutaneous fat. Becides the obvious signs of malnutrition and delayed development, the child seems to have a characteristic posture of “body language”. The child may be unpliable, stiff and rigid. He is uncomforted by unyielding to cuddling and is very slow in smiling or social responding to others. The other extreme is the floppy infant, who is like the rag doll.

Frequently there is a history of difficult feeding, vomiting, sleep disturbances, excessive irritability. Difficulties of infant feeding may include poor appetite, poor suck, crying during feeding, vomiting, hoarding food in the mouth, ruminating after feeding, refuse of liquids and solids, aversion behavior such as turning from food or spitting food. In addition, chronic reduction in caloric intake can lead to appetite depression, which compounds the problem. Another outstanding feature of children with malnutrition is their irregularity in activities of daily living. Some of these children called as “difficult child pattern”. However, another type is the passive, sleepy, lethargic child who does not awake up for feeding.

Other clinical symptoms range from moderate growth failure ( a common occurance in underdeveloped countries ) to more severe conditions such as marasmus and kwashiorcor. The former results from an anadequate intake of a suitable diet; the latter resulrs from a diet with a low protein, energy ratio, frequently with protein of poor biologic quality.

The three stages of protein-energy malnutrition are

marasmus,

kwashiorcor.

marasmic-kwashiorcor

They are compounded by a whole spectrum of nutritional disorders that include deficiences of one or more vitamins, minerals and trace minerals. The three stages of protein-energy malnutrition can be differenciated most clearly on the basis of clinical findings. Intermediate forms known as marasmic-kwashiorcor also are seen. Growth retardation, weight loss, psychic changers, muscular atrophy, pellagroid dermatitis, hair changes, edema, gastrointestinal changers and other abnormalities are present in various combinations.

Marasmus (deficiency in both calorie and protein nutrition)

Marasmus which predominate in infancy, is characterised by severe weight reduction , gross wasting of muscle and subcutaneous tissue, no detectable edema and marked stunting. Marasmus results from inadequate energy intake, impaired absorption of protein, energy, vitamins and minerals. The hair and skin changes and hepatomegaly resulting from fatty infiltration of the liver. The marasmic child, characteristically irritable and apathetic, is the skin and bones portrait of the skeleton.

Kwashiorcor (protein malnutrition predominant)

Kwashiorcor results from either inadequate protein intake , or, more commonly, from acute or chronic infection. It appears predominantly in older infants and younger children. Clinically it is characterised by edema, skin lesions, hair changers, apathy, anorexia, a large fatty liver, and decreased a serum albumine. Weight loos is also usual, without a decrease of energy intake. The edema of kwashiorcor can only partially be explained by the low serum albumine, other contributing factors include increased capillary permeability, increase cortisol, and antidiuretic hormones lewel.

Marasmic – Kwashiorcor (marked protein deficiency and marked calorie insufficiency signs present, sometimes referred to as the most severe form of malnutrition)

Marasmic – Kwashiorcor presents with the clinical findings of both marasmus and kwashiorcor. The child has edema, gross wasting and usually stunted. There may also be mild hair and skin changers and a palpable fatty-infiltrated liver. The child with marasmus-kwashiorcor is one who demonstrated the combined defects of an inadequate intake of nutrients to meet requirements plus superimposed infection.

3. General examination of the patient: patients have asthenic constitution, reduced degree of nourishment, weight loss, the abdomen is great, distended, meteorism, the skin and mucus membranes are dry, turgor of skin is decreased, muscular hypotonia, abdomen is asymmetrical, CNS dysfunktion (retardation of the development).

CLASSIFICATION OF MALNUTRITION

Origin

Stage

Period

Prenatal malnutrition forms

Alimentary factors

Infection factors

Regime breaking, care and upbringing defects

Prenatal factors

Hereditary pathology and congenital development defects

I ( mild)

II (moderate)

III ( severe)

Initial

Progressive

Stabilization

Reconvalecsention (recovery)

Neuropathic

Neurodystrophic

Encephalopathic

Neuroendocrinilogical

MALNUTRITIONAL STAGES

STAGES

WEIGHT DEFICITE

LENTH DEFICITE

CHULITSKA NUTRITIONAL INDEX

10-20%

–

10 – 15

ІІ

20-30%

2-4 sm

0 – 10

ІІІ

More than 30%

7-10 sm

negative

Interpretation

Weight for Height (wasting)

Height for Age (stunting)

Normal

> 90

> 95

Mild

80 – 90

90 – 95

Moderate

70 – 80

85 – 90

Severe

< 70

< 85

Сlinical symptoms of malnutrition I stage – 10-20% weight loss.

The general condition of the patient is satisfactory;

Psychomotorical development is adequate to age;

coefficient weight / length is about 55-60;

proportion index changes;

the index degree of nourishment of Chulitskaya reduces to 10-15;

skin elastisity and turgor moderately reduced also.

Subcutaneous fat on abdomen 0.8-1 sm.

Сlinical symptoms of malnutrition II stage – 20-30% weight loss.

State of moderate severity;

pallorness, dryiness of the skin;

psychomotorical development is reduced;

muskle hypotonia, Decreasing of appetite, vomiting;

coefficient weight / length low than 56;

proportion index changes;

the index degree of nourishment of Chulitskaya reduces to 0-10;

polyhypovitaminosis, anemia, hypo and dysproteinemia;

signs of rickets;

frequent intercurrent infections with poor symptoms.

Decreases immunologic reactivity.

Сlinical symptoms of malnutrition III stage – more than 30% weight loss.

General state of the patient is grave, severe emaciation, cachexia,

subcutaneous fat is absent,

menthal retardation, somnolents,

athrophy of the muscles, temperature of the body is low, regurgitation, vomiting, frequent stools, weight loss more than 30%,

lenght loss – more than 4 sm,

the index degree of nourishement of Chulitskaya is negative,

skin elastisity and turgor are absent, skin and mucus are very dry, great abdomen, breathing is difficult.

Heart beats are quiet, bradycardia, immunologic reactivity paralyses, all systems and organs are impaired – anemia, rickets, bacterial infections.

Malnourished children are clearly more susceptible to infection. The consequent interaction of infection with malnutrition is one of the major factors of the increased morbidity and mortality. Many authors demonstrated that nutritional deficiency was associated with 60,9% of the death from infectious diseases. Diarrhea and measles were the diseases with the greatest morbidity and mortality in which malnutrition was the main factor. The mechanism by which infection leads to a malnourished child include a) anorexia; b) replacement of solid foods with a low-energy, low-protein diet; c) decreased nutrient absorption resulting from diarrhea and intestinal parasites; d) increased urinary losses of nitrogen, potassium, magnesium, zinc, phosphate, sulfur and vitamins A, C, B2. Increased urinary nitrogen excretion results from an increased mobilisation of amino asids from peripheral muscle for gluconeogenesis in the liver with a deamination and exretion of nitrogen in the form of the urea. Without an increased dietary intake, to compensate for losses, a kwashiorcor-like syndrome results. Despite the mobilisation of aminoasids from peripheral muscle, there is also the decrease in whole blood amino acids after the exposure to an infectious agent. An increased synthesis of acute-phase reactants, including haptoglobin, C-reactive protein, a-antitrypsin, a2-macroglobulin, also occurs.

Diagnosis

I. Damage of growth and development of the child

II. peripheral blood : leukocytosis with a prepoderanse ofneutrophils electrolyte losses acidosis, hyponatremia, hypoalbuminemia polyhipovitaminoses, anemia, low level of ferments, low level of T-, B-lymphocytes and immunoglobulines .

III. Stool examination for blood, leukocytes, pH, fat, reducing sugars or parasites;

IV.Culture of stool, urine and blood.

Children with protein-energy malnutrition may have either hypochromic microcytic or normochromic normocytic anemia, which is the result of defective hemoglobine synthesis. Infection also affects the endocrine system. Changes in hormone levels occur simultaneously with infection and precede the changes in amino acids.

During diarrhea, it is significant loss of potassium and magnesium in the stools, leadind to a decrease in serum electrolytes. There is also urinary loss of electrolytes as a result of increased muscle breakdown. Iron absorption and methabolism are also affected by infection. Infections such as malaria and typhoid may cause increased hemolysis and resultant acute hemolytic anemia.

Treatment

Nutritional Management

FEEDING

1 PERIOD – period of making toleranse to food

MALNUTRITION OF 1 STAGE

1 DAY – 1/2 – 2/3 of day volume of food

2 DAY – 2/3 – 3/4 of day volume of food

3 DAY – full volume of food

MALNUTRITION OF 2 STAGE

1 week – 1/2 of day volume of food

2 week – 2/3 of day volume of food

3 week – full volume of food

MALNUTRITION OF 3 STAGE

1 week – 1/3 of day volume of food

2 week – 1/2 of day volume of food

3 week – ¾ of day volume of food

4 week – full volume of food

PARENTERAL FEEDING

AMINOASIDS

POLIAMIN, ALVESIN, LEVAMIL

PROTEIN GIDROLIZATES

INFEZOL – 20/ ml/kg in 10% glucose (1:1) temperature 20°-30° C with 1 IU

insuline to 5 gr. of glucose – 5-8-10 drops/minute – 5-8 days

MEDICAMENTAL THERAPY

1. FERMENTS

FESTAL, PANCREATIN, DIGESTIN

2. BACTERIAL DRUGS

HILAC, BIFIDUM – BACTERIN, BIFI-FORMA, LINECS

3. STIMULATOR THERAPY

APILAC, METILURACIL, PENTOKSID

4. VITAMINS

AEVIT, B,C, P

5. HORMONE THERAPY

NEROBOL – 0,1 MG/KG/DAY

RETABOLIL – 1 MG/KG/DAY

6. SYMTOMATIC TREATMENT

FERUM-LEK – 1 MG/KG/DAY INTRAMUSCULAR

PER OS – 5 MG/KG/DAY ACTIFERIN (DROPS)

7. ANTIOCSIDANT THERAPY

TOCOFEROL ACETATI – 3-5 MG/KG/DAY

Indigestion is due to over feeding, wrong feeding, over excitement, overheating, chilling too much of milk

The first symptoms of indigestion are “nervousness,” irritability, bad breath, bloated bowels, coated tongue, cold feet, constipation, colic, hives, sleeplessness, grinding of the teeth in sleep, drooling. Babies are always irritable and cry easily when they have indigestion. There will be undigested curds in the stools and often foul stools.

Belching or burping or eructing is normal phenomena to expel the gas from the stomach which is caused by swallowing air or gas. The usual cause of belching is distended stomach due to swallowed air or gas. The distension of stomach leads to abdominal discomfort. The belching expels the air and relieves the symptoms. Burping the infants during bottle or breast feeding is very important to expel the air from the stomach which has been swallowed during feeding.

During and after each feeding, take time to burp your baby. But don’t stop there. Your baby may need to burp between feedings as well.

Symptoms of indigestion in infants

· Excessive cry.

· Irritability

· Bloated bowels

· Constipation

· Bad breath

Causes of indigestion in infants

· Excessive play

· Excitement, excessive anger, anxiety, fear.

· Overindulgence

· Overfeeding

· Eating between meals.

Excessive feeding of sugar content food, undiluted juices may increase the formation of gas.

Treatment of indigestion

· It is advised to burp the child after the feeding and also in between the feeding.

· Avoid overfeeding of the child. Maintain regular feeding time and the amount of milk taken.

· Medications like simethicone are helpful in expelling the gas.

· Anti-colic’s can be given for pain.

Teething does not cause indigestion, but indigestion may result in difficulties in teething. There can be no doubt that teething, which is normally a painless and unnoticed process, can be very painful in sickly babies. The gums may become inflamed and painful, the baby will cry and fret and its digestion will be upset still more, but the basic cause of the indigestion, which is the forerunner of painful teething is enervation.

What can be done about indigestion? Remove the cause. How? Stop the overfeeding. Cease overexciting the baby. Discontinue feeding it between meals and at night. Cease feeding starch and other foods which it is not physiologically equipped to handle. Give it less juice. Stop over-bathing it. Dress it more warmly or less warmly, as required. Do not permit it to overplay. Give due attention to its afternoon sleep. Give up the drugging.

Mothers want to know what they should do immediately, when the baby has indigestion. The care required is simple. Put the baby to bed with something warm at its feet. Let it rest and keep quiet until it is normal. Often within twenty-four hours the baby will be able to eat. If baby wakes up smiling, in good humor and with a sweet breath, it is ready to be fed. But, if it wakes up crying and irritable, with pungent breath and white lines (lines of stomach irritation) around the mouth and nose, complaining of discomfort, the fast should be prolonged for another twenty-four hours. Indeed this program should be continued until the baby is normal, even if it takes several days. Mothers are usually in a hurry to feed and by feeding prematurely, they prolong the indigestion. Give the body an opportunity to get rid of the surplus food, toxemia, and to restore functioning power.

When baby is ready to resume feeding, the food should be a little fruit juice—orange juice, fresh tomato juice, or other fresh fruit juice in season (I have used watermelon juice, canteloupe juice, papaya juice, peach juice, apricot juice, plum juice, pear juice, apple juice, etc.) which may be given every three hours. If the baby goes through this first day of feeding comfortably and rests well through the night, the next day regular feeding may be resumed, giving but about one-third what had been previously given. In one or two days, if the baby continues to do well, the amount may be increased to half the amount the baby had been in the habit of eating. After another day or two a full diet may be resumed. By a full diet, I do not mean the diet conventionally fed to babies, nor do I mean a return to the prior overfeeding and feeding between meals.

Until the baby is two years old it needs and should have no other food but milk and fruit juices. The best food in the world for the baby is its own mother’s milk. There is no adequate substitute for mother’s milk. Baby is physiologically unequipped to chew and digest starches before the age of two years and starch foods should not be given before that age. Indeed, baby is not equipped to chew solid foods until it has a mouth full of teeth and, normally, a full set of deciduous teeth is developed at 24 months.

Mothers and others who care for children, whether under or over two years of age, should be able to recognize the symptoms that precede, accompany, and follow indigestion, constipation, gas, distention of the bowels, excessive urination, a gradual growing state of dissatisfaction, white curds in the stools of milk-feeding babies, hard stools, etc. It should be known that white curds in the stools indicate that the baby is getting more milk than it can digest. It is being overfed. Mothers should not wait until the child is pronouncedly sick before doing something about this. Cut down the milk one-half and continue this feeding program until the bowels are moving regularly and the stools show a normal consistency.

When the baby is obviously taking in adequate amounts of milk and there are still curds in the stools, it means indigestion. The indigestion must be remedied before more milk is given. Unfortunately, our love of feeding and fondness for “butter balls” causes us to want to overstuff babies at all times. If a baby is not gaining weight or if it is losing weight, we tend to become frantic and fly to extremes.

During the hot months, constipation often fluctuates with diarrhea. The diarrhea is the means of expelling the accumulation in the bowels. Some children will have both vomiting and diarrhea. The care in these cases should be the same as that previously described. Put the baby to bed, stop all food, and keep him/her warm. No food is to be given until all indications of diarrhea are gone. If there is pain in the abdomen, hot application to the abdomen may be used for relief.

Rickets

Rickets is a disorder involving softening and weakening of the bones (of children) primarily caused by lack of Vitamin D, or lack of calcium or phosphate. It is a general disease of the children’s organism characterised by deep damage of all types of metabolism, especially mineral metabolism, damaging of different organs and systems, inadequate or delayed mineralisation of bones and an excess of osteoid.

Etiology: A lack of vitamin D may arise because of

1) Insufficient endogenous synthesis;

2) A primary deficiency state due to a dietary lack of the nutrient;

3) Secondary deficiency caused by malapsorption of the lipid-soluble vitamin D (diseases of pancreas, billiard tract, intestinal diseases).

1. Lack of sunshine due to:

• 1) Lack of outdoor activities

• 2) Lack of ultraviolet light in fall and winter

• 3) Too much cloud, dust, vapour and smoke

2. Improper feeding:

1) Inadequate intake of Vitamin D

• Breast milk 0-10IU/100ml

• Cow’s milk 0.3-4IU/100ml

• Egg yolk 25IU/average yolk

• Herring 1500IU/100g

2) Improper Ca and P ratio

3. Fast growth, increased requirement (relative deficiency)

4. Diseases and drug:

• Liver diseases, renal diseases

• Gastrointestinal diseases

• Antiepileptic

• Glucocorticosteroid

Pathogenesis:

A deficiency of vitamin D induces not only abnormal serum levels of calcium and phosphate, but also secondary hyperparathyroidism and skeletal morphologic changers. It is now clear that vitamin D itself is not active in calcium metabolism. It must first conversion to its active metabolite, 1-Alfa-, 25 – dihydroxyvitamin D3 which is essence constitutes a hormone since it is formed in the kidney and acts on distant target organs.

Clinical Symptoms

· Bone pain or tenderness (arms, legs, spine, pelvis)

· Increased tendency toward bone fractures

· Fever, especially at night

Restlessness, especially at night weakness

· Decreased muscle tone (loss of muscle strength)

· Decreased muscle development

· Muscle cramps

· Impaired growth (short stature and slow growth)

Skeletal deformities:

· Bow legs

Forward projection of the breastbone (pigeon chest)

· “Bumps” in the rib cage (rachitic rosary)

Asymmetrical or odd-shaped skull

Spine deformities (spine curves abnormally, including scoliosis or kyphosis)

Pelvic deformities

Dental deformities:

· Delayed formation of teeth

· Defects in the structure of teeth, holes in the enamel

· Painful teeth, aching aggravated by sweets, or by cold/hot food or drinks

· Increased incidence of cavities in the teeth (dental caries)

Diagnostic signs and tests

· Serum calcium and serum phosphorus may be low.

· Serum alkaline phosphatase may be high.

· Arterial blood gases may reveal metabolic acidosis.

· Bone X-rays may show decalcification or changes in the shape or structure of the bones.

TREATMENT

1 STAGE VITAMINE D3– 2000 IU 1 TIME\DAY 30 DAYS

2 STAGE VITAMINE D3– 3500 IU 1 TIME\DAY 40 DAYS

3 STAGE VITAMINE D3– 5000 IU 1 TIME\DAY 45 DAYS

THEN PROFILACTIC DOSE – 500 IU TILL THE END OF THE SECOND YEAR OF LIFE

SPECIFIC POSTNATAL PROFILACTIC

HEALHU BABY – 500 IU TILL THE END OF THE SECOND YEAR OF LIFE

PREMATURE BABY – FROM THE 10-14 DAYS OF LIFE

1 STAGE OF PREMATURING VITAMINE D3– 500 IU 1 TIME\DAY 6 MONTHS

2 STAGE OF PREMATURING VITAMINE D3- 1000 IU 1 TIME\DAY 6 MONTHS

3 STAGE OF PREMATURING VITAMINE D3– 2000 IU 1 TIME\DAY 6 MONTHS

THEN PROFILACTIC DOSE – 2000 IU DURING 30 DAYS 2-3 TIME \YEAR WITH INTERVALES 3-4 MONTHS TILL 3-D YEAR OF LIFEAYTILL THE END OF THE SECOND YEAR OF LIFE

SPASMOPHILIA

Spasmophilia (children’s tetany) – disease, in the basis of which disturbances of mineral metabolism (decrease of concentration of ionized calcium in a blood) lies. It is characterized heightened nervous-muscle exiting and predilection to tonic and clonic cramps of separate groups of muscles, in particular larynxes, legs and arms. The spasmophilia sometimes shows by rare, but most dangerous form- eklampsia. Such condition very dangerous, as during cramps can be an apnoea or stopping of heartbeating. Therefore knowledge of clinic, treatment, preventive maintenance of spasmophilia are very important, in particular, by granting of first help.

Etiology:

hypovitaminosis D, hypoparathyreoidism.

Pathogenesis:

decrease of Ca, increase of an alkaline reserve of a blood and K with P.

Clinical picture:

Disposition to the cramps children of the 4-18-24 months with the richets.

There are latent and manifest forms.

Latent tetany: sign Еrba, Hvostek, Trussо, Maslov.

а) Hvostek sign — (also Weiss sign) is one of the signs of tetany. It refers to an abnormal reaction to the stimulation of the facial nerve. When the facial nerve is tapped at the angle of the jaw (i.e. masseter muscle), the facial muscles on the same side of the face will contract momentarily (typically a twitch of the nose or lips) because of hypocalcemia (ie from hypoparathyroidism, pseudohypoparathyroidism, hypovitaminosis D) with resultant hyperexcitability of nerves.;

b) Trousseau sign — To elicit the sign, a blood pressure cuff is placed around the arm and inflated to a pressure greater than the systolic blood pressure and held in place for 3 minutes. This will occlude the brachial artery. In the absence of blood flow, the patient’s hypocalcemia and subsequent neuromuscular irritability will induce spasm of the muscles of the hand and forearm. Sign is also known as main d’accoucheur (French for “hand of the obstetrician”) because it supposedly resembles the position of an obstetrician’s hand in delivering a baby.

c) Maslov sign — the deposition of a mild nyxis in a skin of the child with a spasmophilia predetermines an apnoea at the altitude of inhalation, for the healthy child such boring predetermines acceleration and recess of breathing;

d) Еrb Sign — a boring of a mediaerve in a ulnar crimp by a galvanic current call reduction in case of current intensity, smaller than 5 sm (in the norm — more than 5 sm).

The manifestative form: laryngospasm, spastic stricture of arms and legs, eklampsia.

Laboratory symptoms: decrease of a level of calcium and magnesium; decrease of Ca, increase of an alkaline reserve of a blood and K with P.

Treatment

I. First aid.

1. At a laryngospasm to create the dominant locus of excitation in a brain (to clap on cheeks, to wash by cold water, to click the radical of tongue).

2. At cramps – Seduxenum (0,5 % solution, 0,1 mg/kg), and simultaneously to enter a gluconate of calcium (10 % solution, 0,5-1,0 ml / kg).

ІІ.

1. Correction of a feed (limitation of the cow milk, increase of a quota of vegetables and fruit).

2. Compensation of an acidosis (5-10 % of ammonium chloride on 1 tea spoon 5-6 times per day.

3. Drugs of calcium (10 % solution of calcium of a gluconate at the rate of 50-55 mgг/кг/day; 1 ml of solution contains 36 mg of calcium).

4. After normalization of a level of calcium in a blood – treatment by vitamin D3 (2000-5000 МО 30-45 days depending on a degree of gravity of a rickets).

Vitamins A, Е, B for age doses.

The most common diseases of the respiratory systems in childhood.

Rhinitis in Children

Rhinitis is defined as having 2 of the listed symptoms for > 1 hour /day for > 2 weeks:

1. Blockage

2. Running (including post nasal drip)

3. Sneezing

Rhinitis in toddlers is frequently due to upper respiratory tract infections

Normal children have 6 to 8 episodes per year

Often allergic and is then frequently associated with other atopic manifestations such as eczema

A persistent unilateral purulent discharge may indicate a foreign body

Treatment

Avoidance of allergens which can be:

Perennial – house dust miles, cats, dogs

Seasonal – tree and grass pollen, mould spores

Drug Treatment (should always be combined with allergen avoidance measures where possible). See also Lothian Joint Formulary

Age < 2, nasal saline drops or sprays can help to clear the nose before eating

Age < 4, Sodium Cromoglicate, 1 spray, 2 – 4 times daily

Age > 4, Fluticasone, 1 spray, once daily

Age > 2, oral therapy with various antihistamine sugar free syrups

Do NOT use decongestants

Adenoidectomy/Adenotonslllectomy

Considered in children and adults with persistent or recurrent dirty nasal discharge, nasal blockage, nasal speech and snoring

Surgery should only be considered if the symptoms are upsetting to the child

Untreated symptoms will simply settle by the age of 8-10 years

Pharyngitis

Pharyngitis is also called sore throat. It is an inflammation (swelling) or infection of the tissues and structures in your cild’s pharynx (throat). The symptoms of pharyngitis may be mild or severe.

Causes of pharyngitis

Viral pharyngitis: Pharyngitis in children is usually caused by a virus, such as cold or flu viruses. Pharyngitis is common in adolescents with an illness called infectious mononucleosis (mono). Mono is caused by the Epstein-Barr virus.

Bacterial pharyngitis: Pharyngitis may be caused by bacteria. The most common bacteria that cause pharyngitis is group A streptococcus (strep throat). Adolescents who are sexually active can get a sore throat from gonorrhea or other sexually shared bacteria.

Pharyngitis can spread when an infected person coughs or sneezes. Pharyngitis can also be spread if the person shares food and drinks. A carrier can also spread pharyngitis. A carrier is a person who has the bacteria in his throat but does not have symptoms. Germs are easily spread in schools, daycare centers, work, and at home. Some germs that cause pharyngitis may be passed between adolescents who are sexually active.

Signs and symptoms of pharyngitis

– Cough

– Hoarseness

– Runny or stuffy nose

– Irritated, watery eyes

– Diarrhea

– A rash on his body or in his mouth

– Your child may have any of the following with bacterial pharyngitis:

– Sudden pain in his throat, and pain when he swallows

– Fever and headache

– Red, swollen throat and bad breath

– Whitish-yellow patches on the back of his throat

– Nausea (sick to his stomach), vomiting (throwing up), and stomach pain

– Tender, swollen lumps on the sides of his neck

– Rash that looks like a sunburn with little bumps

How is pharyngitis diagnosed?

Signs and symptoms: child’s caregiver will look into your child’s throat and feel the sides of his neck and jaw. The signs and symptoms that your child has may help show whether he has an infection.

Tests: child’s caregiver may do a throat culture. A cotton swab is rubbed against the back of your child’s throat. This test may show if bacteria are causing your child’s sore throat and the type of bacteria that are causing it.

Pharyngitis usually gets better without treatment within a few days. With treatment, your child may feel better faster. He may be able to return to school more quickly. Treatment may help prevent the spread of infection to others. It may also decrease your child’s risk of heart or kidney problems as a result of the infection. Your child may need any of the following:

Medicines:

Ibuprofen or acetaminophen: Ibuprofen and acetaminophen are over-the-counter medicines that are given to decrease pain and fever. Ask your child’s caregiver what medicine to give your child, and how much and how often to give it. Do not give aspirin to children under 18 years of age. Child may develop a very serious illness called Reye syndrome if he takes aspirin when he is ill. Read medicine labels to see if your child’s medicine has aspirin in it.

Antibiotics: child may need to take antibiotics if bacteria are the cause of his pharyngitis. Follow caregivers’ instructions carefully. Make sure your child finishes all the doses of antibiotics. Your child is still contagious (can infect others) for 24 hours after he starts to take the antibiotics. If other family members have symptoms of pharyngitis, they may also need to be treated.

Steroids: Steroid medicine may be given to reduce swelling in your child’s throat.

Surgery: If child often gets pharyngitis with symptoms such as fever and pain, he may need his tonsils removed. Tonsils are tissues on both sides of your child’s throat that contain cells to fight infection. Your child may have pharyngitis less often after his tonsils are removed.

What are the risks of pharyngitis?

If child takes antibiotics, he may have side effects, such as nausea or diarrhea. He also may have an allergic reaction to the medicine. Frequent antibiotic use may decrease how well the medicine can fight infection. Your child may still get throat infections even if he has surgery to take out his tonsils.

If child has a bacterial infection and does not take antibiotics, the infection may get worse. It may spread to his ears, sinuses, and other body areas. Your child may have problems breathing or swallowing. Without treatment, pharyngitis may lead to more serious illnesses, such as peritonsillar abscess or meningitis. Your child may get rheumatic fever, which can lead to problems with his heart or joints. The infection may spread to his neck veins and lungs. Ask your child’s caregiver for more information about these risks.

How can I help care for my child with pharyngitis at home?

Rest: Have your child rest as much as possible.

Increase liquids: Give your child liquids so that he does not get dehydrated. Give him liquids that are easy to swallow and will soothe his throat.

Sore throat relief: If your child is 12 years or older, give him throat lozenges or hard candy to help decrease his throat pain. If your child can gargle, give him one-quarter of a teaspoon of salt mixed in 1 cup of warm water to gargle.

Add humidity: Your child may breathe more easily after he breathes in mist or steam. You may want to use a steam or cool mist vaporizer in your child’s room. Ask caregivers how often and what to use to clean the device. You may run a hot water shower to make steam in the bathroom. Close the bathroom door and sit with your child near the shower as he breathes in the steam. Do not put your child in the hot shower.

How can I help prevent the spread of pharyngitis?

Wash your hands and your child’s hands often. Keep your child away from other people while he is still contagious. Ask your child’s caregiver how long your child is contagious. If your child is taking antibiotics, he should not share food or drinks until he has taken all the doses of antibiotics. Do not let your child share toys or pacifiers. Wash these items with soap and hot water.

When should my child return to school or daycare?

If your child has started antibiotics, ask his caregiver when he may return to school or daycare. If your child is not on antibiotics, his symptoms such as fever or sore throat may go away on their own. When his symptoms go away, your child may return to daycare or school.

Laryngitis

Laryngitis is swelling and irritation (inflammation) of the voice box (larynx) that is usually associated with hoarseness or loss of voice.

Causes

The voice box (larynx) is located at the top of the airway to the lungs (trachea). The larynx contains the vocal cords. When the vocal cords become inflamed or infected, they swell. This can cause hoarseness, and may sometimes block the airway.

The most common form of laryngitis is an infection caused by a virus. It may also be caused by:

· Allergies

· Bacterial infection

· Bronchitis

· Common cold

· Flu

· Injury

· Irritants and chemicals

· Pneumonia

Laryngitis often occurs with an upper respiratory infection.

Several forms of laryngitis occur in children that can lead to dangerous or fatal respiratory blockage. These forms include:

Croup

Epiglottitis

Symptoms

Ø Fever

Ø Hoarseness

Ø Swollen lymph nodes or glands in the neck

Exams and Tests

A physical examination can determine whether hoarseness is caused by a respiratory tract infection.

Patients with lasting hoarseness (especially smokers) will need to see an ear, nose, and throat doctor (otolaryngologist) for tests of the throat and upper airway.

Treatment

Because most common laryngitis is caused by a virus, antibiotics may not help. Your health care provider will make this decision.

Resting your voice helps by reducing inflammation of the vocal cords. A humidifier may soothe the scratchy feeling that comes with laryngitis. Decongestants and painkillers may relieve the symptoms of an upper respiratory infection, if you have one.

Outlook (Prognosis)

Laryngitis that is not caused by a serious condition should get better.

Possible Complications

Rarely, severe respiratory distress may develop. This will require medical attention.

When to Contact a Medical Professional

Call your health care provider if:

A small child who is not teething has difficulty breathing, swallowing, or is drooling

A child less than 3 months old has hoarseness

Hoarseness has lasted for more than 1 week in a child, or 2 weeks in an adult

Prevention

Try to avoid people who have upper respiratory infections during cold and flu season.

Wash your hands regularly.

Avoid crowded places.

Stenosing laryngitis

Stenosing laryngitis – acute inflammatory process in a larynx, quite often grasping a trachea and bronchuses.

It is observed, as a rule, in an initial stage of acute respiratory virus infections as display of the disease, but can be and result of connection of the bacteriemic factor and then the stenosing laryngitis is surveyed as complication of acute respiratory virus infections. Especially often it arises at children with an allergic and exudative catarral diathesis and proceeds more hardly at early age, quite often has wavy current. The inflammation and an edema of a mucosa at rather narrow lumen of a larynx at children cause difficulty of the respiration, amplifying a reflex spastic stricture.

Clinical picture. The stenosing laryngitis arises was quite often acutely, mainly at night. At a part of children it is preceded with signs of a usual (not stenosing) laryngitis (dry, especially barking tussis, small hoarseness of a voice). Gravity of a stenosing laryngitis is defined by a degree of a stenosis and a respiratory failure.

Distinguish four degrees of a stenosis.

A stenosis of 1 degree – short-term difficulty of respiration or more long, but weakly expressed; attacks of the complicated respiration arise seldom, respiratiooisy, the hoarse voice, barking tussis, the small cyanosis, slightly expressed retraction of pliable places of a thorax, basically in epigastriums. The respiratory failure is absent.

The stenosis of 2 degrees is characterized by duration (till 5 day), disturbance of the general condition of the child which becomes restless, amplifies barking, rasping tussis, often arise attacks of the complicated respiration, being accompanied by retraction of all pliable places of a thorax; respiratiooisy, heard on distance. The stenosis can бытьпостоянным-or have wavy character. The respiratory failure is moderately expressed. Sharp deterioration of the general condition is characteristic, the expressed paleness, a cyanosis of labiums, extremities are marked.

Stenosis of 3 degrees – appreciable and constant difficulty of respiration with retraction of all pliable places of a thorax (a bulbar fossa, supraclavicular and subclavial spaces, epigastric area). The sweating, sharp anxiety of the child (the patient twitches in bed) are observed, respiration in lungs is weakened. Attributes of a cardiovascular failure and an accrueing anoxemia – paleness, an adynamia are marked. The respiratory failure is sharply expressed.

A stenosis of 4 degrees – a stage of an asphyxia.

Croup

Croup is a type of laryngitis in children, and is associated with a seal-bark cough and difficulty inhaling air caused by swelling of the voice box (larynx) and windpipe (trachea). Croup is usually the result of a virus, but can also be caused by allergies, bacteria, or inhaled irritants. Croup is most common in children ages six months to three years, although children can get croup at any age. Croup is common during the months of October through March. Most cases today are not serious, but severe cases might require hospitalization.

Symptoms of croup are a very hoarse, deep, seal-bark-type cough appearing after several days of cold symptoms that is usually worse at night. As croup continues, a child may have labored breathing, a high-pitched squawking or crowing noise on inhalation, and a low fever. Croup is usually worst the first two or three nights, resolving in a week or so. Vaccines for measles, Haemophilus influenzae(Hib), and diphtheria protect children against the more dangerous forms of croup.

First Aid for Croup

Moist and cold air helps reduce the swelling of the airways. This can be done at home in the following way:

Turn the hot water on in the shower or tub of a bathroom and shut the door.

Once the bathroom is steamy, take your child into the bathroom and sit with him for fifteen to twenty minutes with the door closed.

You may also take your child, dressed warmly, out into the cold night air.

Your child should sit straight up or stand to breathe more easily. The steam treatment may help, but it doesn’t cure the cough completely, so you may need to repeat this routine throughout the night each time your child wakes up coughing. You can also:

Use a cool-mist humidifier in your child’s room. (Humidifiers need to be cleaned daily with a bleach-and-water solution to prevent the growth of mold or bacteria.)

Make sure your child is well hydrated with fluids.

Give the appropriate dose of acetaminophen or ibuprofen for fever. Never give your child aspirin, and don’t give cough medicine either; it won’t help the swelling in the throat, and it can make it more difficult to cough up mucus.

If your child is not getting any relief with steam and cold air, call your doctor for possible oral steroids to reduce swelling and help her breathe more easily. Severe cases of croup can lead to serious breathing difficulties, so call your doctor for advice if you think your child has croup. Labored breathing at rest, separate from a coughing fit, may indicate a serious, potentially life-threatening swelling in the throat. If your child is struggling for breath and drooling, and her lips or skin are turning blue, call 911 immediately.

First aid for children:

ACUTE BRONCHITIS

Acute inflammation of the bronchial mucosa, usually associated with inflammation of the trachea i.e. tracheobronchitis.

Etiology  Mainly viral in origin as common cold viruses, influenza, measles. 

Bacteria as Bordetella pertussis, and hemophilus influenza.

Predisposing factors : 

Recurrent upper respiratory tract infection. 

Ø Allergy 

Ø Rickets 

Ø Malnutrition 

Ø Dust, other chemical and physical irritants as smoking.

Pathology : 

The tracheobronchial mucosa is red and swollen, sometimes with hemorrhagic spots. It is covered by tenacious mucus, at times it is purulent.

Clinical picture:

Cough is the most constant symptom, starts dry and then becomes productive.

· Rhonchi is the most important sign, may be associated with non consonating crepitations due to secretions.

· Fever of mild degree, if present.

· The course of the disease takes about 10-15 days, but in young infants may be long.

· X-ray chest sometimes show increased bronchial markings.

Treatment:

General:

antipyretics, and good fluid intake.

Specific mainly viral, no antibiotics.

FOREIGN BODY ASPIRATION

The changes produced by foreign bodies depend upon : their nature, location and the degree of obstruction of the air passages. Sequelae of foreign body aspiration :

1. The foreign body may be expelled immediately by reflex cough.

2. Laryngeal obstruction

a. If large F.B. ===> complete obstruction and suffocation.

b. If small F.B. ==> manifestations of laryngeal obstruction : as hoarseness of voice, croupy cough, aphonia and stridor.

The F.B, may produce inflammatory reaction with resulting increase in the degree of laryngeal obstruction which may prove fatal if not early managed

3. Tracheal foreign body: cough, dyspnea and cyanosis may occur.

The characteristic signs arc audible slap and palpable thud.

4. Bronchial foreign body :  Most often the F.B. is aspirated into the right lung. There is usually an immediate episode of choking, gagging, and paroxysmal coughing.  After the initial symptoms, which may have been forgotten, there is often symptom free period which may last for hours, days or weeks.  Bronchial foreign body produces obstruction (partial or complete) with or without inflammation.

The clinical effects include:

A. Obstructive hyperinflatation leading to wheezy chest:

B. This occurs if the foreign body produces partial obstruction of the bronchi. The patient presents as a case similar to bronchial asthma.

Lack of response to bronchodilatros may help in differentiation from asthma.

B. Complete obstruction: This leads to collapse of a lobe or a part of a lobe depending on the obstructed bronchus. Local signs include diminished movements, diminished air entry and dullness of the affected lobe.

C. If inflammation occurs due to secondary bacterial infection or if the foreign body is of plant origin e.g. a peanut, this may result in: pneumonia, lung abscess, empyema, or bronchiectasis.

Diagnosis of foreign body inhalation:

1. History : in some cases, the history may be evident. Absence of history is not against the possibility.

2. Physical examination : foreign body inhalation may present by any chest manifestation e.g. stridor, wheezy chest, pneumonia, lung abscess,… etc. Foreign body inhalation should be put in mind in any chest case with chronic or recurrent chest infection, wheezy chest not responding to treatment or unexplained lung collapse.

3. Investigations.

A. Laryngeal obstruction: Laryngoscopy, opaque F.B. is clearly demonstrated by lateral X-ray on the neck.

B. Tracheal foreign body : by plain x-ray chest or bronchoscope.

C. Bronchial F.B. :  Plain x-ray chest: if the F.B. is radio-opaque. 

Fluoroscopy : the affected lung is hyperinflated during expiration, the diaphragm is flattened, while the heart and mediastinum shift towards the healthy side. 

Bronchoscopy: helps in visualization and removal of F.B.

Treatment:

1. Laryngeal F.B. : laryngoscopy and removal of the F.B. under direct vision. In severe life threatening cases, tracheostomy may be life saving at first.

2. Tracheal and bronchial F.B.: bronchoscopy and removal under direct vision. Antibiotics are used for infections.

Broncho-obstructive syndrome is the collective term including a symptom-complex of specificly outlined clinical implications of disturbance of bronchial passableness, having in the basis narrowing or an occlusion of respiratory tracts.

Clinically expressed syndrome of respiratory obstruction often enough meets at children, especially early age.

Occurrence and its development are influenced by various factors and, first of all, a respiratory virus infection contamination.

To number of viruses most often causing an obstructive syndrome carry a respiratory syncytial virus (about 50 %), then a parainfluenza virus, a pneumonia mycoplasma, is rarer – viruses of a flu and an adenovirus. In development of bronchial obstruction the certain role is played by the age features inherent to children of first three years of life. Bronchuses at small children have smaller diameter, than at adults. The narrowness of bronchuses and all respiratory apparatus considerably enlarge aerodynamic resistance. So, the edema mucous bronchuses of all on 1 mm causes rising of resistance to an air flow in a trachea more than on 50 %.

For children of early age the pliability of cartilages of the bronchial tract, an insufficient rigidity of osteal structure of the thorax, freely reacting an indrawing of compliant places on resistance rising in pneumatic pathes, and also features of position and a diaphragm constitution are characteristic.

Considerably burden flow a broncho-obstructive syndrome at children structural features of a bronchial side, such as a considerable quantity of the goblet cells mucifying and raised viscosity of a bronchial secret, bound to high level of sialine acid can.

Doubtless influence on functional disturbances of a respiratory organs at the small child

such factors, as longer sleep render also, the frequent crying, primary stay on a back in the first months of life.

The early children’s age is characterised by imperfection of immunologic mechanisms: interferon formation in the top respiratory tracts, a serumal immunoglobulin is considerably lowered And, a secretory immunoglobulin And, functional activity of T-system of immunodefence is lowered also. The majority of explorers influence of factors of a premorbidal background on development a broncho-obstructive syndrome admits. These are toxicoses of the pregnant women, the complicated labours, a hypoxia in sorts, a prematurity, the burdened allergological anamnesis, a hyperreactivity of bronchuses, a rachitis, a dystrophia, a thymus hyperplasia, a perinatal encephalopathy, the early artificial feeding, the tolerated respiratory disease at the age of 6-12 months.

Among factors of environment which can lead to development of an obstructive syndrome, especially the great value is given to passive smoking in monogynopaedium. Under the influence of a tobacco smoke there is a hypertrophy of bronchial mucous glands, the mucociliary clearance is broken, slime progression is slowed down. Passive smoking promotes a destruction of an epithelium of bronchuses. The tobacco smoke is an inhibitor of a chemotaxis of neutrophils. At long influence the tobacco smoke influences immune system, reduces activity of T lymphocytes, oppresses synthesis of antibodies of the basic classes, suscitates synthesis of immunoglobulins E, raises activity of a vagus nerve. Especially vulnerable in this plan children of 1st year of life are considered.

Certain influence renders also an alcoholism of parents. It is proved, that alcohol reduces rate of deducing of pathogenic microbes, causes an atony of bronchuses, development of protective inflammatory reaction inhibits.

Other important unfavorable factor is contamination of surrounding atmosphere by industrial gases: ammonia, chlorine, various acids, sulphurus gas, Carboneum oxide, ozone, phosgene, etc., an inorganic dust (coal, quartz, cement, etc.) an organic dust (cottonous).

In occurrence of bronchial obstruction various mechanisms – such as lay:

a dystonia

a hypertrophy of a muscular tissue

a hypercrinia

a dyscrinism

mucociliary clearance disturbance

an edema

inflammatory infiltration

a hyperplasia and a mucosa metaplasia

a prelum, an obturation and deformation of bronchuses

defects of aboriginal and system immunodefence, defects macrophage systems

On the basis of literature data it is possible to secure the following bunches of diseases accompanied by a syndrome of bronchial obstruction:

Diseases of a respiratory organs:

Infectious-inflammatory diseases (a bronchitis, a bronchiolitis, a pneumonia)

Allergic diseases (an asthmatic bronchitis, a bronchial asthma)

Bronchopulmonary dysplasia

Developmental anomalies of bronchopulmonary system

Tumours of a trachea and bronchuses

Foreign bodys of a trachea, bronchuses, an esophagus

Diseases of an aspiration genesis (or an aspiration obstructive bronchitis) – a gastroesophageal reflux, a tracheoesophageal fistula, developmental anomalies of a gastrointestinal tract, a phrenic hernia.

Diseases of cardiovascular system of the congenital and got character (a hypertensia of a small circle of a circulation, anomaly of pots, congenital not rheumatic cardites, etc.).

Diseases of the central and peripheric excitatory system.

Hereditary anomalies of an exchange.

The congenital and got immunodeficient conditions.

Rare diseases

Other conditions:

Traumas and combustions

Venenatings

Influences of various physical and chemical environmental factors

Prelum of a trachea and bronchuses out of a pulmonary parentage

From the practical point of view, depending on etiological pathogenetic mechanisms excrete 4 variants of a broncho-obstructive syndrome

Ø infectious, educing as a result of virus and (or) a bacteriemic inflammation in bronchuses and bronchioles

Ø allergic, educing owing to a spastic stricture and an allergic inflammation of bronchial structures with prevalence of the spastic phenomena over the inflammatory

Ø obturation, observed at a foreign body aspiration, at a prelum of bronchuses

Ø hemodynamic, arising at a heart failure on is left ventricular type

In pediatric practice most often there are first two clinico-pathogenetic variants of a broncho-obstructive syndrome.

On flow the broncho-obstructive syndrome can be acute, fixing, recurring and is continuous – recurring (in case of a bronchopulmonary dysplasia, a bronchiolitis, etc.).

On expression of obstruction it is possible to secure:

Ø easy degree of obstruction (1 degree)

Ø moderately severe (2 degree)

Ø serious (3 degree)

BRONCHIAL ASTHMA

Definition: Paroxysmal attacks of cough, dyspnea, and wheezes caused by generalized obstruction of the airways due to bronchial hyper-reactivity to a variety of stimuli and associated with a high degree of reversibility of the obstruction either spontaneously or after treatment.

A characteristic finding in asthmatics is the bronchial hyper-reactivity which is a condition resulting in increased bronchial responses (i.e. branchial obstaiction) following a stimulus that does not cause such a response iormal individuals.

The degree of bronchial hyper-reactivity varies from patient to patient and trie severity of the disease depends on the degree of hyper-reactivity. The following stimuli trigger the bronchial hyper-reactivity in astlimatics and thus result in bronchial obstruction.

Allergens as house dust, pollens, danders and certain food in atopic patients.

· Exposure to strong odours and irritant fumes such as sulfur dioxide, tobacco smoke, cooking odours, air pollutants in cities etc. 

· Viral infections as respiratory syncytial virus, adenovirus and rhinovirus. 

· Rapid changes in the environmental temperature or barometric pressure.  Muscular exercise. 

· Emotional disturbances.

Etiology :

Many factors contribute to the etiology of bronchial asthma. These factors are present in varying proportions in different individuals.

1. Autonomic factors

-adrenergic receptors might be present

Cough receptors of bronchial mucosa have a lower threshold for being stimulated causing a reflex broncho-constriction through the vagus.

2. Biochemical factors Imbalance between chemical substances which cause broncho-dilatation (e.g. endogenous catecholamines and prostaglandins E 2 ) and those which cause broncho-constriction (e.g. histamine, leukotrienes).

3. Immunologic factors An Ig E mediated allergic response could be responsible. Allergens bridge the sensitized mast cells in the bronchial mucosa leading to their degranulation with release of mediators.

4. Infectious factors Viral infection stimulates the afferent vagal receptors or mediates an IgE response to the infection (as to respiratory syncytial virus).

5. Other factors As endocrinal, psychologic and hereditary factors play a role Pathophysiology: Release of mediators from the mast cells is situeted by immunologic (as IgE mediated mechanism) or non immunologic.

1. Early phase Where preformed mediators inside mast cells as histamine and eosinophil chemotactic factor bronchospasm + edema and increased mucus secretion.

2. Late phase Newly formed mediators like prostaglandins and leukotrienes ==> accumulation of inflammatory cells especially eosinophils which release major basic protein which are injurious to the bronchi al mucosa. This means that obstruction of bronchial airways is produced by :

a. Spasm of the smooth muscle.

b. Edema of the mucosa.

c. Congestion and infiltration of the bronchial walls by inflammatory cells as eosinophils, neutrophils.

d. Intraluminal exudation of mucus, shedded epithelial cells and inflammatory cells. It is evident that bronchial asthma is an inflammatory reaction of the bronchial tree.

The obstruction of the airways produces increased airway resistance to the air flow with premature closure of the bronchi in expiration. These will lead to the following :

1. Air trapping and hyperinflation of the lung alveoli.

2. Disturbed gaseous exchange will result in : Hypoxia, hypercapnia, and low pH.

3. Cardiovascular changes in the form of pulmonary hypertension, right ventricular strain and decreased left ventricular filling may occur.

Clinical Manifestations :

1 Asthma may have its onset at any age : 50% of patients usually start to suffer before 2 years and 80- 90% have their attacks before 4-5 years.

2. Paroxysms of cough, dyspnea and wheezes that vary in severity between different patients. The paroxysms may occur at a certain time of the year (e.g. in winter or spring) or may occur at any time (i.e. not seasonal).

3. The onset of the attack may be acute (e.g. after exposure to irritants as cold air, irritant fumes or exposure to allergens in atopic children). The onset may be insidious (e.g. following viral infection).

4. During the attack, the patient may suffer, from tightness of the chest, irritability (due to hypoxia), abdominal pain (due to the use of the diaphragm and abdominal muscles especially during cough) Cyanosis is present in severe cases.

On examination :

General:

· The patient is dyspneic, the respiration is rapid with prolonged expiration.

· Acting alae nasi. use of accessory muscles of respiration, irritability, sweating and cyanosis in severe cases are present.

Local.

Inspection: Barrel-shaped chest with decreased movements and intercostal retractions.

Palpation . Decreased tactile vocal fremitus, central mediastinum (unless lung collapse or pneumothorax are present), palpable rhonchi.

Percussion : Hyper-resonance with encroachment on the cardiac and hepatic dullness.

Auscultation : 

Ø Decreased air entry on both sides. 

Ø Vesicular breathing with prolonged expiration.

Ø Decreased vocal resonance. 

Ø Wheezes mainly expiratory, and in severe cases are also inspiratory. Non consonating crepitations due to excess mucus secretion in the bronchi may be heard.

In severe attacks, wheezes may be absent and heard after giving a bronchodilator.

At the end of the attack, the patient usually has a productive cough of thick white sputum. In between the attacks, the child may be completely free of symptoms and has no evidence of pulmonary disease on examination.

Asthmatic patients can be divided into two main groups : Atopic and non atopic Atopic patients have : positive family history of asthma, or hay fever or eczema, eosinophilia in the blood and secretions (sputum and nasal secretions), ‘increased levels of serum IgE, positive skin test against certain allergens, and the patient may show other manifestations of allergy as eczema. Non atopic patients do not have these criteria. Complications:

1. Massive collapse of the lung.

2. Pneumothorax, pneumomediastinum, and even surgical emphysema.

3. Pulmonary infections and later on bronchiectasis.

4. Respiratory failure.

Diagnosis of bronchial asthma :

– History  Recurrent attacks of cough, dyspnea and wheezes. 

– History of other allergic conditions in the same patient as allergic conjunctivitis, atopic dermatitis. 

– Family history of allergic diseases as eczema, asthma ect. 

– History of precipitation of the attack after exposure to certain conditions as house dust, smoke, muscular exercise, viral upper respiratory tract infections.

–  Each patient should be asked for the details of onset, course, precipitating factors, frequency of attacks, his condition in between the attacks, and how does the attack end.

2. Physical exemination : to exclude other causes of wheezy chest as heart failure.

3. Investigations

1. Complete blood picture : Eosinophilia (the absolute eosinophil count is more than-400/mm 3 ). In atopic patients the eosinophils are present also in bronchial secretions, sputum and nasal secretions.

2. Serum IgE is elevated in atopic children. Specific IgE by RAST (radio-allergo–sorbant test) helps in detecting the antigen to which the patient is sensitive.

3. X-ray chest

– Changes during the attack include : hyperinflation (transverse ribs and descent of diaphragmatic cupolae) ± Scattered opacities due to scattered atelectatic areas.

– The X-ray helps in exclusion of other causes of wheezy chest as T.B. and to detect complications of asthma as pneumothorax.

4. Allergic skin tests: to detect the allergen.

5. Bronchial hyperreactivity testing (or bronchial challenge test):

A small diluted dose of histamine or methacholine is given by inhalation.

If normal ===> no reaction.

If has bronchial hyperreactivity ===> broncho-constriction.

6. Assessment of pulmonary function :

Useful in assessing the severity of airway obstruction before treatment and to demonstrate the reversibility of this obstruction with therapy. This is done by using a hand held spirometer to measure the Peak Expiratory Flow Rate (PEFR) = greatest flow obtained on forced expiration after complete inspiration to total lung capacity.

7. Measurement of blood gases and p.H during severe attacks and status asthmaticus. Differential Diagnosis bronchial asthma In early months of life :

recurrent wheezy chest is caused by :

1. GIT anomalies as H-type of tracheoesophageal fistula (choking with feeding, treatment is surgical).

2. Gastroesophageal reflux : wheezes usually disappears by treatment the reflux.

3. Congenital vascular ring: ring of vessels around the lower part of trachea and esophagus (present with stridor and wheezes, diagnosed by angiography, treatment is surgical).

4. Congenital lobar emphysema : hyperinflation in one lobe, treatment is surgical

5. Left to right shunt (VSD, ASD, PDA) due to blood flow to lung.

In older children causes include

Foreign body inhalation

Sudden onset of gagging and chocking(rnay be forgotten) then a symptom free period occurs then obstruction of the bronchus ===> hyperinflation ===> cough and recurrent wheezes.

Diagnosis : 

– X-ray : Unilateral hyperinflation and if radio-opaque it will appears. 

– Bronchoscopy

Enlarged hilar lymph nodes . commonest cause is T.B. 

+ve (positive) tuberculin test. 

X-ray : hilar lymph nodes. 

+ve (positive) family history may be present. 

Treatment:

• Antituberculous drugs.

• No response to bronchodilator.

Immune deficiency diseases

Present with repeated attacks of chest infection associated with wheezes

Cystic fibrosis of pancreas (Mucoviscidosis)

Involves multiple systems associated with abnormal secretions ==-=> obstruction of bronchi ===> wheezes associated with decreased pancreatic secretions, decreased bile secretion and ! end with liver cirrhosis.

Acute bronchiolitis Viral type of pneumonia due to respiratory syncytial virus, parainfluenza or adenovirus ===>inflammatory reaction of bronchioles ===> obstruction ==> hyperinflation of lung alveoli but 

» Single attack, usually not recurrent. 

» It occurs in the first 2 years (mostly 6 months). 

» Same physical signs as asthma  No family history of allergies.  No eosinophilia or increased serum lgE. 

» Minimal or no response to bronchodilators.

TREATMENT OF BRONCHIAL ASTHMA

I. Treatment of the acute attack :

Treatment depends on the severity of the attack which is classified into mild, moderate or severe as follows:

Classification of Acute Attacks of Asthma According to Severity

1. Treatment of mild attack

Give inhaled short acting beta-2 agonist (e.g. salbutamol) by 

» Metered dose inhaler ± spacer (2-4 puffs at 20 minutes interval for 3 times). 

» or Nebulizer (Salbutamol dose —- 0.15 mg/kg or 0.03 ml/kg every 20 minutes for up to 3 doses). The dose is diluted in 3-4 ml saline.

2. Treatment of moderate attack 

As in mild attack, the patient is given 3 doses of the β2 agonist in the first hour, then one inhalation every 2-3 hours + prednisolone 2 mg/kg/day orally in a single daily dose for 3 days.

N.B. If inhaled β2 agonist is not available, epinephrine 1/1000 concentration (1 mg/ml) is given at a dose of 0.01 mg/kg up to 0.3 mg every 20 minutes for 3 doses. 3. Treatment of severe attacks

a. Oxygen by mask or nasal prongs

b. Bronchodilator: 

» Inhaled short acting β2 -agonist as salbutamol is given 0.03 ml/kg/dose every 20 inutes for 3 doses then every 1-2 hours till improvement. The dose of salbutamol is . diluted in 3-4 ml of saline. O 2 instead of air is connected to the nebulizer. If salbutamol not available, epinephrine can be used as mentioned before).

c. Insert I.V. cannula and give : 

» Dextrose 5% + saline (ratio 4:1). fluids are very important to correct the dehydration usually present and to help expectoration. 

» Hydrocortisone : 4 mg/kg/6 hours for 1 st day then 2 mg/kg/6 hours thereafter. Start oral prednisolone as the condition improves (2 mg/kg/day for 3-5 days).

» Aminophylline 5 mg/kg/dose can be repeated every 6 hours. Improvement is expected in 6-12 hours. The IV line can be removed by 24 hours.

4. Treatment of Status Asthmaticus Status asthtnaticus is defined as the acute attack in which the patient continues to have significant respiratory distress despite administration of sympathomimetic drugs and aminophylline. The management is as follows :

1. The patient should be admitted to hospital preferably to an intensive care unit.

2. Monitoring the patient for :

a. Clinical parameters: cyanosis, respiratory rate, heart rate, blood pressure, consciousness, intercostal and suprasternal retractions as well as the air entry.

b. Laboratory data : PaO2, PaCO2 pH, serum electrolytes.

c. Cardiac monitoring since hypoxemia and acid base disturbance predisposes to cardiac arrhythmias and potentiates the cardiotoxic drugs (theophylline).

3. Humidified oxygen is given by mask or nasal prongs at concentration 40% and flow rate 2-31 per minute to maintain PaO 2 of 70-90 mmHg.

4. IV fluids to prevent dehydration and help expectoration. Glucose saline is usually given and KC1 is added after micturition to prevent hypokalemia produced by β2 stimulants.

5. Bronchodilator aerosols initiated in the emergency room is continued and aminophylline 5 mg/kg IV is given slowly every 6 hours.

6. Corticosteroids : hydrocortisone 4 mg/kg every 4-6 hours. Corticosteroids improve the efficiency of β2 stimulants and decrease airway obstruction by their anti-inflammatory action.

7. Mechanical ventilation is indicated for those children who fail to respond to the previous measures. The usual indications are significant hypoxia (PaO 2 less than 60 mmHg) and hypercapnia (PaCO 2 more than 65 mmHg).

Treatment in between the attacks (long term management or day to day management)

1. General: 

» Try to find out the precipitating factors especially in atopic patients (by history and skin allergy tests) and avoid exposure to them. 

» Avoid exposure to dust, smoke, perfumes, animals, sudden change of environmental temperature etc. 

» Proper treatment of respiratory infections. 

» Hyposensitization therapy may be attempted.

2. Drugs

» The recent trend in asthma therapy is to follow the stepwise approach depending on the soverity of asthma.

Classification of Asthma Severity (See the following table) N.B. Patients at any level of severity can have mild, moderate or severe exacerbations. Some patients with intermittent asthma experience severe and life-threatening exacerbations separated by long periods of normal lung function and no symptoms.

PNEUMONIAS

Definition : Inflammation of the lung parenchyma

1. Anatomical classification :

A. Lobar pneumonia: The consolidation involves all or part of the lobe

B. Bronchopneumonia: The consolidation involves scattered lobules.

C. Interstitial pneumonia: As in viral pneumonia where inflammatory infiltrate involves mainly interstitial tissue between alveoli.

2. Etiological classification :

A. Bacterial:

» Gram +ve : Streptococcus pneumoniae (Pneumococcus), Staphylococcus, Streptococcus pyogenus.

» Gram –ve: Hemophilus influenza, Klebsiella pneumoniae, Pseudomonas, Mycobacterium tuberculosis.

B. Viral : Respiratory Syncytial virus, Parainfluenza, adenovirus, Influenza virus.

C. Fungal :as Histoplasma, Candida albicans.

D. Others : Mycoplasma pneumoniae and Pneumocystis carinii

E. Aspiration Pneumonia : Aspiration of foreign body, lipoid substance, hydrocarbons as Kerosene. Aspiration of amniotic fluid, foreign body, lipoid substance.

F: Loeffler’s Syndrome.

G: Hypostatic pneumonia.

Predisposing factors of pneumonia (causes of recurrent or unresolved pneumonia):

1. Immune deficiency.

2. Foreign body.

3. Increased pulmonary blood flow (as in large left to right shunt e.g. large VSD).

4. Cystic fibrosis.

5. Congenital anomalies (as cleft palate, tracheoesophageal fistula, congenital lung anomalies, and immotile cilia syndrome).

LOBAR PNEUMONIA

Etiology:

1. Most common cause is streptococcus pneumoniae (pneumococcus).

2. Less commonly, hemophilus influenza.

PNEUMOCOCCAL PNEUMONIA

Streptococcal pneumoniae (pneumococcus) is the most common bacterial pathogen causing pneumonia, accounting for over 90% of childhood bacterial pneumonia.

Epidemiology : 

» Common in winter and early spring. 

» The incidence is highest between 3-8 y of age. 

» Infection is more common through asymptomatic carriers.

Pathology :

Pneumococcal organisms are aspirated into the periphery of the lung from the upper airway or nasopharynx. One or more lobes or parts of lobes are involved.

The involved lobe undergoes the following changes:

1. Congestion : Alveoli are filled with edema fluid and organisms.

2. Red Hepatization : Alveoli contain polymorphs, RBCs, fibrin+edema and organisms.

3. Grey Hepatization : characterized by deposition of fibrin over the pleural surfaces Phagocytosis starts inside the alveoli which are now filled with polymorphs and fibrin.

4. Resolution : the neutropliils degenerate, the fibrin threads and remaining bacteria are digested and removed by phagocytes., In untreated cases a clinical crisis occurs about the 7th day of illness and resolution and reexpansion require additional 1-3 weeks. Antibiotics given in the first days of illness interrupt the course, and the previous stages are not seen.

Clinical Manifestations : The clinical picture of pneumococcal pneumonia in the older child is similar to that of adult, but in infants it is more variable. The onset of pneumonia in both infants and children is usually preceded by a mild upper respiratory tract infection for some days.

In Children : The onset of disease is by a shaking chills followed by high fever. This is accompanied by drwosiness with intermittent restlessness, a dry irritating cough and rapid shallow respirations. The child may prefer to lie on the affected side to minimize pleuritic pain.

Chest Examination : The affected lobe shows the following signs :

In Stage of Congestion :  Impaired note on percussion, decreased tactile vocal fremitus, diminished breath sounds and fine crepitations. 

In Stage of consolidation: Signs of consolidation are present.

Inspection : limited movements of the affected part and intercostal retractions.

Palpation : Increased tactile vocal fremitus.

Percussion : Dullness.

Auscultation : Diminished breath sounds, bronchial breathing, and increased vocal resonance.

In Stage of Resolution : Bronchial breathing disappears and crepitations appear. The initial dry cough becomes productive of blood tinged sputum.

In Infants : The pathology is lobular consolidation (not lobar consolidation) i.e. scattered patches of consolidation in the affected part but bronchi are free.

The clinical picture is characterized by the following:

1. After the initial upper respiratory disease, there is sudden rise of temperature with restlessness and respiratory distress manifested by : 

» Working alae nasi,expiratory grunting and inverted breathing (Triad of pneumonia).  Fast and shallow breathing (Fast breathing means respiratory rate = 60/minute or more in infants less than 2 months, 50/minute in infants 2-12 months and 40/minute or more in children 1 -5 years). 

» Dyspnea and often cyanosis in severe cases.

2. Signs of consolidation are usually not apparent (lesions are patchy in distribution)

3. Dullness if present may denote complicating empyema.

4.Chest findings : decrease movement, decrease breath sounds with consonating crepitations on affected side. No bronchial breathing.

5.Gastrointestinal disturbances are common, marked abdominal distension may occur due paralytic ileus. In children, right lower lobar pneumonia may be associted with abdominal pain in the lower right quadrant simulating acute appendicitis.

6. Neck stiffness is usually found with involvement of the upper lobe

Laboratory Findings:

1. Leucocytosis with predominance of polymorphonuclears.

2. The organism can be isolated from nasopharynx, secretions obtained from deep coughing, gentle tracheal aspiration, from blood or from pleural fluid.

3. Detection of bacterial antigen in blood,urine or pleural fluid by immuno-electrophoresis.

X-Ray Chest:  May appear earlier and disappear later than the clinical findings. The characteristic finding is homogenous opacity in the area of one or more lobes.  A small amount of pleural collection may be seen denoting pleural reaction.  Empyema may be detected in complicated cases. Persistence of X-Ray findings beyond few weeks (unresolved pneumonia) denotes underlying foreign body or immune deficiency.

Right side focal pneumonia

Right side lobar pneumonia

Lobar pneumonia

Left side focal pneumonia

Complications:

1. Local: empyema and lung abscess.

2. Metastatic complications : as meningitis, pericarditis… etc. These complications are not commoow with the use of antibiotics.

Treatment:

» General:

Oxygen administration to patients with significant respiratory distress; it should be given before the patient is cyanotic. Oxygen is the best sedative for hypoxic irritable patients.

Antipyretics may be needed.

Proper intake of fluids and diet.

» Specific:

The drug of choice is penicillin since most pneumococci are sensitive to it.

In infants and young children, IM penicillin G in a dosage of 50,000 units/kg/day.

In older children a single IM injection of procaine penicillin 400,000 units daily. Treatment is given for 7-10 days in uncomplicated cases. If the patient is sensitive to penicillin ==> erythromycin, chloramphenicol or cephalosporin provide effective alternative therapy.

Bibliography

а) Basic

1. Janette B. Benson. Diseases and Disorders in Infancy and Early Childhood / Janette B. Benson Marshall M. Haith. – Academic Press, 2009 – 424 p.

2. Maureen R. Nelson. Pediatrics / Maureen R. Nelson. – NY: Demos Medical Publishing, 2010. – 259 p.

3. Vicky R. Bowden. Pediatric Nursing Procedures / Vicky R. Bowden, Cindy Smith Greenberg. – Philadelphia: Lippincott Williams & Wilkins, 2011. – 822 p.

4. Ruth McGillis Bindler. Clinical skills manual for pediatric nursing: caring for children / Ruth McGillis Bindler, Ruth C. McGillis Bindler, Jane Ball. – Pearson/Prentice Hall, 2008. -181 p.