Articles by "PEDIATRICS"
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Acute Rheumatic Fever





Is a systemic disease characterized by inflammatory lesions of connective and endothelial tissue :


Acute Rheumatic Fever
Acute Rheumatic Fever


Acute Rheumatic Fever

Etiology :

- The exact pathogens are unknown.

- It is thought to be an autoimmune response to group a beta hemolytic streptococci.

- Most first attacks of rheumatic fever preceded by streptococcal infection of the throat or upper respiratory tract at an interval of several days to several weeks.

Altered physiology :

- The unique pathologic lesion of rheumatic fever is the Aschoff body.

- The basic changes consist of exudative and proliferative inflammatory reactions in the mesenchymal supporting tissues of the heart, joints blood vessels and subcutaneous tissue.

- The inflammatory process involves all layers of the heart.

- The inflammatory may involve the heart valves, most frequent the mitral and/or the aortic valves.

Clinical manifestations :

- The diagnosis is based on a combination of manifestations of the disease.

- The presence of 2 major criteria or 1 major and 2 minor criteria, plus evidence of preceding streptococcal infection are required to establish the diagnosis.

Major manifestations :

1- Carditis: significant murmurs, signs of pericarditis, cardiomegaly or congestive heart failure.

2- Polyarthritis: the affected joints are swollen, tender and red migratory, the large joints are affected.

3- Subcutaneous nodules :
- Firm, painless bodies seen or felt over the extensor surface of certain joints, particularly the elbow, knee and wrists.

- Disappear mostly after 4 months.

- Presence of nodules is an indicator that the heart is involved.

4- Erythema marginatum :
Circinate or annular rash occur on the arms, trunk and legs { never on the face}. evanescent, pink rash, have pale centers and round or wavy margins.

5- Chorea : Purposeless involuntary movement often associated with muscle weakness, incoordination of voluntary movement and emotional instability.

Minor manifestations :

1- Fever.

2- Arthralgia.

3- Prolonged P-R interval in the ECG.

4- Increased E.S.R, leukocytosis, positive C-reactive protein.

5- A history of streptococcal infection, scarlet fever, previous history of rheumatic fever.

Treatment :

1- Bed rest for 2 weeks then gradual ambulation.

2- Cases without cardiac involvement, aspirin only 100 mg/kg/day in 4 hours divided doses . until E.S.R. is normal for 2 weeks.

3- With cardiac involvement aspirin and prednisone.

4- Prevention of rheumatic fever through control of streptococcal infection: procaine penicillin G 1.200.000 units once a month.



READ MORE:


Chickenpox And Diphtheria

Thalassemia major " Cooley's anemia "

Congenital Dislocation Of The Hip CDH



Celiac Disease




Celiac Disease
Celiac Disease


Gluten-induced Enteropathy

Is a mal-absorption disease of the proximal small intestine , that is characterized by abnormal mucosa with permanent intolerance to gluten .

Celiac Disease

Etiology :

1. unknown .
2. genetics .
3. toxic .
4. allergic .

Altered physiology :


Characteristics of the disease include :

- Impaired intestinal absorption .

- Histological abnormalities of small intestine .

- Clinical and histological improvement with gluten-free diet .

- Recurrence of clinical manifestations and histological changes after reintroduction of dietary gluten .

Histological changes :

- Loss of normal villous pattern .

- Obliteration of intervillous spaces .

- Loss of epithelial cell brush border .

These changes result in disaccharide deficiency , inability to absorb fates , fat-soluble vitamins , minerals and some proteins and carbohydrates .

Mal-absorption result from decreased area of absorption .

Clinical manifestations :

- Diagnoses is most commonly made at 6-24 months of age ( it can be made in adult .

- Chronic or recurrent diarrhea ( foul . bulky , and greasy stool ) .

- Anorexia , vomiting , abdominal distention , muscle wasting and hypotonia .

- Steatorrhea .

- Malnutrition .

- Weight loss and dehydration .

- Mood changes ( irritability and nervousness ) .

- Secondary deficiencies such as anemia , hypocalcaemia and hypoproteinemia .

Diagnostic evaluations :

- History and general status .

- Small bowel biopsy .

- D-xylose test ( less than 20-25mg/dl at 60 minute ) .

- Hb level .

- Stool test ( fecal fat excretion ).

- Sweet test ( to rule out cystic fibrosis ) .

- X-ray .

Treatment :

- Lifelong gluten free diet .

- Adequate caloric intake .

- Supplemental vitamins .

- Decreased fat intake .

Treatment of celiac crisis :-

1. Restore fluid and electrolyte balance .

2. Parenteral hyperalimination .

3. Steroids .



READ MORE:


Measles and German Measles

Esophageal Atresia with Tracheoesophageal Fistula

Hirschsprung's Disease ( Congenital A ganglionic Megecolon )


Hirschsprung's Disease ( Congenital A ganglionic Megecolon )




Is congenital anomaly that results in mechanical obstruction from inadequate motility of part of the intestine .


Congenital A ganglionic Megecolon
Hirschsprung's Disease

Hirschsprung's Disease

Etiology :

- Arrest in embryological development affecting the migration of parasympathetic nerves of the intestine ( prior to the 12th week of gestation ) .

- Unknown cause .

- May be familial .

Clinical manifestations : { vary depending on degree of involved bowel } .

- Appearing at birth or within first weeks of life .

- Failure to pass meconium within 24- 48 hours after birth .

- Vomiting ( bile-stained or fecal ) .

- Abdominal distention .

- Reluctance to ingest fluids .

- Overflow – type diarrhea .

Older children :

- History may reveal obstipation at birth .

- Abdominal distention .

- Constipation ( relieved temporary with enema ) .

- Ribbon like , foul - smelling stool .

- Inadequate weight again .

- Fecal masses may be palpable .


Complications :


- Prior to surgery : Enterocolitis ( major cause of death ) , water intoxication ( enemas ) , perforation .

- Post-op : Enterocolitis , leak of anastomosis , pelvic abscess .

- Colostomy : hemorrhage , shock , and infection .

- Diagnostic evaluations :

- Rectal examination : no fecal material .

- Barium enema : narrow intestine proximal to anus , dilated intestine proximal to narrow segment .

- Rectal biopsy : absence or reduced number of ganglion nerve cells .

Treatment :

- Initially : colostomy or ileostomy to decompress the intestine rest normal bowel .

- Definitive surgery : abdominal pull- through , at 9-12 months or 7-10 kg body wt. .



READ MORE:


Acute Rheumatic Fever

Measles and German Measles

Esophageal Atresia with Tracheoesophageal Fistula


Measles and German Measles



Measles and German Measles
Measles and German Measles


Measles ( Rubeola )



Agent : rubeola measles virus .

Source : respiratory secretions, blood and urine of infected person .

Transmission : by direct contact with infected person .

Passive immunity : birth to 1 year of age if mother is immune prior to pregnancy .

Incubation period : 5-15 days .

Common age : school age in spring .

Period of communicability : 4 days before to 5 days after rash appear .

Clinical manifestations :

- Catarrhal stage : fever, malaise, cough, conjunctivitis, koplik's spots .

- Rash : Appear 2-4 days after onset of catarrhal stages begins in face and gradually spread downward .

Treatment :

- Vitamin A supplement .

- Bed rest .

- Antipyretics .

- Antibiotics to prevent secondary bacterial infections .

- Calamine lotion to minimize itching .


Rubella ( German measles )


Agent : rubella virus .

Source : respiratory secretions, blood and urine of infected person .

Transmission : by direct and indirect contact with infected person .

Incubation period : 14-21 days .

Period of communicability : 7 days before to 5 days after rashes appear .

Clinical manifestations :

- catarrhal stage : headache , anorexia , low grade fever , sore throat , conjunctivitis and malaise for 1-5 days and subside1 day after appearance of rashes .

- rash : firstly in face then down ward to neck , arms , trunk and legs and disappear the same way by the 2nd or 3rd day .

Treatment :


no treatment necessary other than antipyretics and analgesics .

complications : greatest danger is teratogenic effect on fetus ( cataract , CHD , and deafness )




READ MORE:

Acute Rheumatic Fever

Thalassemia major " Cooley's anemia "

Esophageal Atresia with Tracheoesophageal Fistula


Esophageal Atresia with Tracheoesophageal Fistula





Is malformation caused by failure of the esophagus to develop a continues passage , the esophagus may or not form a connection with the trachea .



Esophageal Atresia with Tracheoesophageal Fistula
Esophageal Atresia with Tracheoesophageal Fistula

Esophageal Atresia

Altered physiology :

Failure of septal development between trachea and esophagus , during the 4th week of gestation .

Types :

1- Type (A) : 8% blind at each end of the esophagus , widely separated with connection to the trachea.

2- Type (B) : rare , proximal segment of esophagus opens into trachea , distal end is blind .

3- Type (C) : 80-90% , proximal esophagus segment terminates in a blind pouch , and the distal segment is connected to the trachea or primary bronchus by a short fistula at or near the bifurcation .

4- Type (D) : rare , both upper and lower esophagus segment connected to the trachea .

5- Type (E) : 5% , fistula without atresia .

- Child is unable to swallow effectively .

- Saliva or formula accumulate in upper esophagus pouch and is aspirated .

- Reguratiation of gastric acid.

- Abdominal distention may lead to respiratory distress.

Clinical manifestation :

- Appear soon after birth , excessive amount of secretions , constant drooling , intermittent cyanosis , abdominal distention , choking fluids retune through nose and mouth through feeding process.

- Inability to pass catheter through nose or mouth.

Diagnostic evaluation :

- Recognize infants risk " premature + polyhdramnios ".

- Observe symptoms.

- Inability to pass 10 -12 stiff catheter.

- X-ray (chest and abdomen ) gas in stomach , tip of the catheter in blind pouch.

Complications and associated problems :

- pneumonitis ( salivary or gastric acid reflex ) , congenital heart disease , imperforated anus , prematurity.

Treatment :

- Propping infant at 30-degree angle to prevent reflux of gastric content.

- Suctioning.

- Supportive I.V fluids , antibiotic , respiratory support.

- Surgery.




READ MORE:


Acute Rheumatic Fever

Thalassemia major " Cooley's anemia "

Congenital Dislocation Of The Hip CDH



Thalassemia major " Cooley's anaemia "



Cooley's anemia
Thalassemia major " Cooley's anemia "


- Beta-thalassemia refers to inherit the group of blood disorders characterized by a reduction or absence of the beta chain of globulin in haemoglobin syntheses.

- Haemoglobin b-thalassemia is the most severe of the b-thalassemia syntheses and is known as thalassemia major or cooleys anaemia.

Etiology :

- Genetically determined inherited disease.

- The autosomal recessive pattern of inheritance.

Incidence :

- Most prevalent in the Mediterranean, Middle East, India, Pakistan, Southeast, Asia and Africa.

Prognosis :

- No known cure.

- often fatal in late childhood or early adolescent.

Preventive measures :

- Parents of a child with thalassemia should be tested for the trait and referred for genetic counselling.

- Prenatal diagnosis terminates pregnancy .

Clinical manifestations :

- Insidious onset at the end of the 1st year of the life.

- Pallor, poor feeding, protuberant abdomen due to hepatosplenomegaly, headache, bone pain, exercise intolerance and easy fatigability and growth retardation.

Complications :

1. Splenomegaly and hepatomegaly due to extramedullary hemopoiesis and rapid destruction of RBCs. coagulation abnormalities.
2. Growth and endocrine complications :
- Growth retardation.
- Diabetes in older children due to iron deposition in the pancreas.
- Adrenal and pituitary dysfunction. 
3. skeletal complication :
- Maxillary hypertrophy. 
- Broad ribs. 
- Skeletal osteoporosis. 
4. Cardiac complication : 
- Arrhythmia, pericarditis, congestive heart failure " the usual cause of death of thalassemics ".
5. Skin :
- Brownish discolouration due to iron deposition. 
- Jaundice.

Treatment :

- Frequent and regular blood transfusion to maintain haemoglobin level above 9-10 gm/ dl.

- Packed RBCs usually used.

- Iron chelating agent to reduce the toxic side effects of excess iron " hemosiderosis ".

- E.g. deferoxamine: desferal.

- Folic acid.

- Splenectomy in huge hypersplenism.

- Bone marrow transplantation.



READ MORE:


Chickenpox And Diphtheria

Polyhydramnios And Oligohydramnios

Congenital Dislocation Of The Hip CDH


Congenital Dislocation Of The Hip CDH






Refers to a malposition of the femur in the acetabulum. the head of the femur is usually dislocated postero-superiorly. dislocation may be either partial or complete and may be either unilateral or bilateral.


Congenital Dislocation Of The Hip CDH
Congenital Dislocation Of The Hip CDH


Aetiology:

1. Unknown.

2. Possible causes :
- abnormal development of the joint caused by fatal position or genetic factors.

- Hormonal factors.

- Environmental factors such as breech delivery.

Incidence: more common in females than in males.


Clinical manifestations :

- May not be observed until 1-2 month of age.

- Asymmetry of gluteal folds with deeper creases apparent on the affected side.

- Limited ability to abduct the hip when the infant is lying on his back with his knee and hips flexed to 90 degrees.

- Trendelenburg's sign: pelvis drops on the normal side if the child stands on his abnormal leg.

- Leg length inequality with unilateral complete dislocation.

- Delayed walking.

- Limp, waddling gait with bilateral dislocation.


Treatment :

- Varies with age and extent of the defect.

- Early stages: reduction with gentle manipulation, splinting the hip in abduction by means of double or triple diapers.

- Later stages: preliminary traction, closed or open reduction with immobilization in a hip Spica cast.


Care of child in spica cast :

- Prepare the child for application of the cast.

- Observe for complications resulting from the pressure of the cast, discolouration or cyanosis, impaired movement, loss of sensation, oedema, temperature changes or absent pedal pulses.

- Provide good skin care, inspect skin for a sign of irritation, bathing if possible and good skin massaging.

- Prevent the skin around the edges of the cast from being excoriated.

- Prevent urine and faeces from soiling the cast.

- Plans for short periods of muscle exercise every day.

- Have the child breath deeply at intervals.

- Turn the child every 2 hours.



READ MORE:


Chickenpox And Diphtheria

Laryngitis And Laryngeal Cancer

Polyhydramnios And Oligohydramnios



Chickenpox And Diphtheria 



Chickenpox ( Varicella )


varicella
Chickenpox ( varicella )



Agent: Varicella Zoster.

Source: secretion of the respiratory tract, to a lesser degree skin lesion.

Most common age: 2-8 years.

Transmission: direct contact, droplet spread and contaminated objects.

Incubation period: 2-3 weeks.

Period of communicability: 1 day prior to the first lesion to the last vesicle is dried.

Clinical manifestations :

- Slight fever, malaise, anorexia.

- Rash highly pruritic begins as macule rapidly progress to papule and then vesicles surrounded by the erythematous base breaks easily and form crusts in the face and proximal extremities.

- Irritability.


Treatment :

- Anti-viral ( acyclovir ).

- Varicella zoster immunoglobulin.

- Antihistamine.

- Skin care.

Complication :

- Secondary bacterial infections . ( abscess , cellulites ).

- Encephalitis , due to viremia.



Diphtheria 



Diphtheria
Diphtheria


Agent: corynabacterium diphtheria.

Source: discharge from the mucous membrane of nose, nasopharynx, skin and other lesions of infected person and carriers.

Transmission: direct contact, droplet spread by sneezing or coughing and contaminated object.

Incubation period: 2-5 days.

Period of communicability: 2-4 weeks.

Incidence: increase in winter and autumn.

Diagnostic test: culture from nose and throat.


Clinical manifestations :

 vary according to the anatomic location of pseudo-membrane.

1. Nasal: common cold and discharge, low-grade fever whitish-grey membrane on nasal septum, epistaxis.

2. Tonsillar/pharyngeal: white or grey membrane on tonsils, uvula and soft palate, low-grade fever, anorexia, general malaise.

3. laryngeal: potential airway obstruction, fever, cough and respiratory difficulty.

4. Non-respiratory: eye ear and rarely skin.

Treatment :

Anti-toxin for diphtheria.



READ MORE:


Pleurisy and Peural Effusion

Laryngitis And Laryngeal Cancer

Polyhydramnios And Oligohydramnios


Breastfeeding




Breastfeeding
Breastfeeding


Advantages of Breastfeeding:


For infant:

1. Promote emotional security and infant-mother bonding.

2. Immunological protection.

3. Fewer problems with colic than bottle-fed infants.

4. Fewer problems with digestion and constipation.

5. Ready any time.

6. Promotes facial and muscular development.

7. Fresh and free of contamination.

8. Human milk is probably sufficient and balanced.

For mother:

1. Help returns rapidly to the pre-pregnant state.

2. It is the most economical method of feeding, it is not free milk ( mother need high protein and high caloric diet).

3. May help space pregnancies.

4. A relaxing experience that is both physically and emotionally enjoyable.

5. Lactated women have the lowest risk for breast cancer.

6. Breastfeeding also may offer protection against obesity and atherosclerosis for mother.

Contraindication to breastfeeding:

1. Serious debilitating maternal disease such as hearts disease or Advanced cancer.

2. Galactosemia in the infant.

3. Hepatitis B and TB in mother.

4. Human immune deficiency virus.

Note:- Mastitis is no contraindication.


Successful process of breastfeeding:

1. An initial feeding opportunity as soon as after delivery as possible and at least 2-3 hours thereafter.

2. Mother must wash her hands before feeding her infant.

3. The mother must be comfortable in order to relax this assist the letdown sensation.

4. The mother may either sit or lie down while she nurses her baby.

5. Mother must put the infant in a semi setting position through feeding time.

6. Mother must sure that infant has both areola and nipple in his mouth.

7. Mother must help her infant by gently milking her breast while holding it by opposite hand (3rd, 4th, 5th fingers holding the breast from down, areola and nipple between 2nd and 3rd fingers with thump above breast body).

8. Mother must sure that infant nasal pathway is open.

9. Mother must alternate breast each feeding to promote milk production in both breasts.

10. Mother must observe her infant for full time during feeding.

11. Scheduling breastfeeding every two to four hours and feeding on demand.

12. Mother must burp her infant after each meal correctly.

13. Lying infant on his right side after the meal or on his abdomen.



READ MORE:

Diarrhea

Nephrotic Syndrome

Acute Glomerulonephritis





Acute Glomerulonephritis





Acute Glomerulonephritis
Acute Glomerulonephritis


Acute Glomerulonephritis

Refers to inflammation of the kidneys caused by an antigen-antibody reaction following an infection in some part of the body. it is a predominantly a disease of childhood and is the most common type of nephritis in children.

Aetiology:

It is a sequel of group A beta-hemolytic streptococcal infection.

Incidence: most common in preschool and early school age groups 5-10 years rare in children under 3 years of age.

Altered physiology:

- The organism responsible for nephritis contain antigens similar to those of the basement membrane of the renal glomeruli.

- Antibodies produced to fight the invading organism also react against the glomerular tissue, forming an immune complex become trapped in the glomerular loop and cause an inflammatory reaction in the affected glomeruli.

Clinical manifestation:

- Onset usually 1-3 weeks after the initial streptococcal infection.

- Urinary changes: hematuria, urine may be bloody, smoky or brown in colour, oliguria.

- Oedema: usually mild, often manifested by periorbital oedema in the morning oedema may appear only as rapid weight gain.

- Hypertension: present in 60-70% of patients. severe hypertension may develop rapidly over a period of few hours, therefore frequent measurement of the blood pressure must be made in the first few days of the disease.

- Malaise, headache, low-grade fever, anorexia and vomiting.

Diagnostic evaluation:

1- urinalysis:

- Specific gravity usually high, gross hematuria.

- Mild to moderate proteinuria.

- Decreased urinary output.

2- blood:

- Urea and Creatinine often mildly to moderately elevated.

- ESR is elevated.

- ASOT is usually elevated.

- Renal function is normal in 50 % of patients.

Complications:

1- hypertensive encephalopathy.

2- congestive heart failure.

3- uremia.

4- anaemia.

Treatment:

1- Hospitalization and daily weight, urine output, urinalysis and more frequent measuring of blood pressure.

2- Bed rest during the acute phase.

3- Dietary restriction: fluid amount should be equal to 24 hours urinary output salt restriction, low potassium diet, low protein diet.

4- Drug therapy: 10 days penicillin and hydralazine to treat hypertension.



READ MORE:


Diarrhea

Imperforate Anus

Nephrotic Syndrome


Diarrhea




Diarrhea
Diarrhea




Acute diarrhea ( gastroenteritis): is an inflammation of the stomach and intestines caused by various bacterial, viral and parasitic pathogens.

Diarrhea: increase frequency, fluidity and volume of faeces.

As why diarrheal disorders are serious during infancy? this is because dehydrated much more quickly than adults.




Aetiology:

Acute and infectious factors:

- Bacterial such as E.coli, salmonella, Shigella and Vibro cholera.

- Viral such as Rotavirus and Adeovirus .

- Fungal such as candida enteritis.

- Parasitic such as Giardia Lamblia.

- Normal flora after ingestion of antibiotic.

- Non-infectious factors.

- Allergy to certain foods.

- Metabolic disorders ( celiac disease ).

- Overfeeding.

- The unsuitable formula for age.

- Environmental factors.

- The rise of atmospheric temperature.

- Poor sanitation.

- Exposure to cold drafts.

- Low socio-economical status.


- Clinical manifestations:

Stool:

- Greenish to yellow-green in colour.

- Loose and fluid in consistency.

- May contain pus, mucus or blood.

- Frequency various from 2 to 20 time.

- Fever, anorexia, vomiting, rapid respiration, irritability and general weakness.


Dehydration:

- Poor skin turgor, and dry mucous membrane.

- Decreased urinary output.

- Sunken eyes and anterior fontanel.

- Rapid pulse, low blood pressure.

- Dry mouth, thirst.

- Loss of weight.


Complications:

- Dehydration.

- Acidosis.

- Electrolyte imbalance.

- Infection.


Diagnostic evaluation:

- Health history.

- General physical appearance.


Laboratory studies :

- Serum electrolytes .

- Arterial blood gases analysis.

- CBC ( high HCT ) .

- Urine and stool analysis and culture.

Treatment:

- Prevention.

- Breastfeeding. 

- Health education for mothers.

- Enteric isolation precautions to prevent the spread of infection.

- Maintain hydration.

- Supportive care.


Oral Rehydration Solution:

 - Indication for all cases of dehydration as long as the child strong to drink.


Drug treatment:

- Symptomatic antidiarrheal drugs are usually not recommended.

- Anti-emetic drugs are not indicated.

- Antibiotic in the treatment of diarrhea.



READ MORE:


Intussusception

Imperforate Anus

Nephrotic Syndrome



Nephrotic Syndrome



Is a clinical state characterized by an increased permeability of the glomerular membrane to protein, which results in massive urinary protein loss?


Nephrotic Syndrome
Nephrotic Syndrome


Aetiology:


the syndrome may be classified as :

1- Primary: idiopathic nephrotic syndrome.

2- Secondary: resulting from D.M, syphilis, AGN, or other conditions.

3- many observers think that nephrotic syndrome is an autoimmune disease.

Altered physiology:

For the unknown reason, the glomerular membrane usually impermeable to large proteins.

Protein especially albumin leaks through the membrane and lost in the urine.

Plasma proteins decrease as proteinuria increase.

The colloidal osmotic pressure reduced to result in oedema.

There is increased susceptibility to infection because of decreased gamma globulin.

The symptoms complex characterized by oedema, marked proteinuria, hypoalbuminemia and hypercholesterolemia.

Clinical manifestation:

Oedema, weight gain, puffiness of the face and abdominal swelling.

Respiratory difficulty ( pleural effusion).

Diarrhea, anorexia, malabsorption.

Extreme skin pallor, muscle wasting.

Irritability, easily fatigued, lethargic.

Decreased urinary output.

Normal or decreased blood pressure.

Susceptibility to infection.

Diagnostic evaluation:

1- urinalysis: oliguria, proteinuria.

2- kidney function test, usually normal.

3- blood:
Reduced total serum protein. normal ( 6.5 -8 g/dl).
Reduced serum albumin . normal ( 3.5-4.5g/dl ).
High serum cholesterol . normal ( 180-250 mg/dl ).

Management:

1- Rest: should be kept in bed during periods of severe oedema.

2- Prevention and treatment of infection.

3- Diet
- Appropriate for child age.

- Ample intake of proteins.

Increase the intake of calcium and vitamin D.

Restriction of fluid intake if oedema is progressive.

4 - Drugs:

Diuretics.

Prednisone.

Human albumin.



READ MORE:


Intussusception

Imperforate Anus

Myocarditis And Pericarditis

Imperforate Anus





Imperforate Anus
Imperforate Anus


Imperforate Anus

Is a congenital malformation in which the rectum has no outside opening.


Aetiology:

Abnormal embryological development of the anus " 8th wks. "

Cause:

Unknown ( associated with other congenital anomalies).

Types:

1- low imperforate anus: the rectum has descended below the pubococcygeal line ( puborectalis muscle), the internal and external sphincters are present and well developed with normal function and there is no connection with the genitourinary tract.

2- High Imperforated Anus: the rectum ends above the puborectalis muscle. this is usually associated with genitourinary tract ( fistula ) rectourethral (male), or rectovaginal ( female).

Complications:

Rectal stenosis.

Separation of the anastomosis.

Ureteral injury.

UTI.

Rectal fistulas.

Clinical manifestations:

- Is usually discovered immediately after birth ( within several hours).

- No anal opening.

- Thermometer can't be inserted into the rectum.

- The absence of meconium.

- Green-tinged urine, ( if fistula present).

- Progressive abdominal distention.

Diagnostic evaluation:

- Visual examination.

- General examination for associated anomalies.

- Urine examination ( stool in urine ).

- Sonography.

- Wangensteen-Rice X-ray: ( upside down position ), useful after 24hrs.

Treatment:

- Low: decompression of bowel, dilation of fistula, then definitive repair by angioplasty.

- High: colostomy for decompression, then definitive repair by pull-through surgery when infant one year or about 10 kg weight).

Pre-op and post-op care:
- high risk for injury related to the inability to evacuate rectum, surgery.

- Altered nutrition ( less than body requirements ) related to the inability to feed.

- Altered family processes related to the care of a child with a physical defect, hospitalization.



READ MORE:


Intussusception

Cleft lip And Cleft palate

Myocarditis And Pericarditis




Intussusception




Intussusception
Intussusception 

Intussusception

Is an invagination or telescoping of a portion of the intestine into another, resulting in obstruction beyond the defect.

Aetiology:

Not usually known, may be due to increase motility of intestine.

Possible causes:

Polyps or cysts in the bowel, malrotation, acute enteritis, abdominal, injuries, abdominal surgery, cystic fibrosis, celiac disease.

Altered physiology:

Intestine become curved, sausage-like blood supply is cut off bowel begins to swell haemorrhage may occur and complete obstruction may occur necrosis of involved segment.

Classification:

Iileocecal ( most common ) , colocolic , ileoileo .

Clinical manifestations:

- ( 4-10 months ) is the most common age.

- Onset is sudden, paroxysmal abdominal pain.

- Current jelly-like stool, blood and mucus present in stool ( following rectal exam).

- Vomiting.

- Abdominal distention.

- Sausage-like mass palatable in the abdomen.

- Dehydration.

- Fever.

- Shock.

Diagnostic evaluation:

- History.

- General appearance.

- X-Ray abdomen: reveals staircase pattern.

- Barium enema: the coil-like appearance of the bowel.

Treatment:

- Hydrostatic reduction with the barium enema.

- Surgical reduction, resection if the bowel is gangrenous.

Patient problems:

- Altered comfort level ( pain ) related to invagination of the bowel.

- Alteration in fluid and electrolyte balance related to vomiting.

- Respiratory distress related to abdominal distention.

- Parental anxiety related to the suddenness of the child's illness, hospitalization, surgery, the lake of Understanding of the condition.

- N.G. tube may be inserted to prevent vomiting and aspiration.


READ MORE:


Cleft lip And Cleft palate

Myocarditis And Pericarditis



Cleft Lip and Cleft Palate



 Cleft lip And Cleft palate
 Cleft lip And Cleft palate



Cleft Lip:

Is a malformation resulting from the failure of the maxillary and median nasal processes to fuse during embryonic development?

Cleft Palate:

Is a midline fissure of palate resulting from the failure of the two sides to fuse during embryonic development.

Aetiology:

Unknown cause.

The hereditary factor may be due to mutant genes, chromosomal abnormalities or teratogens.

Altered Physiology:

Cleft lip:

Varies from a notch in the lip to complete separation of the lip may be unilateral or bilateral.

Cleft palate:

- Cleft of uvula, soft palate.

- Cleft of both soft and hard palate through the roof of the mouth.

- Unilateral or bilateral.

- Failure of mesodermal masses of lateral palatine processes accrues between the 7th and 12th week of gestation.


Cleft palate and lip combined:

Submucous cleft:

Muscles aren’t joined, not recognized until child talks, can't be seen at birth.

Associated problems and complication:

- Eating ( suction can't be creating for sucking, food retunes through the nose ).

- Nasal speech, lack of dental appearance, otitis media and hearing loss.

- Pierre Robin syndrome.

Clinical manifestation:

- Physical appearances of cleft lip and palate, incompletely formed lip.

- Opening in the roof of the mouth felt with examiners fingers on the palate.

Treatment:

- Management is focused on the closure of the cleft, prevention of complications, maintaining normal growth and development.

- The cleft lip is repaired before palate.

- The cleft lip: immediate repair or at 6-12 weeks of age.

- The cleft palate repair was done between 6 months and 5 years.


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Placenta Previa

Abruptio Placentae