Positioning A Baby While Breast Feeding

 

Breastfeeding your baby is always encouraged but at times new mothers find it difficult and face a lot of problems which in the end results in giving up and switching to formula.

Proper positioning the baby is very important for breastfeeding and to prevent problems later on.

How to position a baby while breast feeding  depends on the choice and comfort of both mother and baby. No matter which position is used it is important to make sure that

-         The baby’s whole body is supported

-         Baby’s body is facing and is close to the breast

-         Baby’s neck is straight. (not turned or twisted)

-         Baby approaches the breast and nose is in line with the nipple.

While Breast feeding it is very important that

-Mother is comfortable and relaxed.

She should know and learn how to support the breast while feeding. Baby’s lips should be first touched with the nipple and then wait for the baby to widely open the mouth so that nipple along with areola goes in and baby starts sucking.

Five Possible Positions

1.   Cradle Position: The mother cradles the baby in her arm. The baby should be held close to the mother’s body, with the forearm supporting the baby’ head. For mother’s comfort she may want to support the cradling arm with a pillow or her other arm.

2.   Cross Cradle: The mother cradles the baby in her arm. Her hand is supporting the baby’s head and neck.

3.   Football Hold: The mother is sitting or leaning back and the baby is under her arm with feet pointing back. The mother support the baby’s head and neck with her hand and a pillow may be used to support the baby in this position.

4.   Side lying position: Mother is lying on her side and baby lies on its side facing the mother. Mother supports the baby’s head and neck with her hand or a pillow.

5.   Supine Position: The mother is lying on her back with the baby lying face down on the mother’s chest. Mother’s hand supports the baby’s head on her breast. This position is useful immediately after a c section.

Oppositional Defiant Disorder

Definition: Oppositional defiant disorder (ODD) is a condition in which a child displays an ongoing pattern of uncooperative, hostile, resistant and an annoying behavior towards people in authority. 

In order to be diagnosed the behavior must be present for at least 6 months.

Symptoms: It is difficult to differentiate between a normal but an emotional child with a child with an oppositional defiant disorder. It is not unusual for children to argue, disobey or talk back to their parents, teachers or other adults, but when such a behavior gets too annoying to disrupt the child’s daily life and activities, lasts longer than 6 months and is excessive for the child’s age than it becomes a psychological disorder known as Oppositional defiant disorder. 

ODD is characterized by frequent occurrence of at least four of the following behaviors:

• losing temper
• arguing with adults.
• actively defying or refusing to comply with the request or rules of the adults.
• deliberately doing things that will annoy others
• getting angry
• showing violent behavior.
• blaming others on his/her own mistakes
• being touch and easily annoyed by others.
• unwillingness to compromise.
• Acting aggressive towards peers
• Have academic problems.

Related Mental health issues: A child with oppositional defiant disorder may have associated other mental health issues like anxiety, depression and/or attention deficit hyperactivity disorder. The symptoms of theses conditions may overlap and sometimes it is difficult to diagnose as one particular disorder.

Approach To A New Born With Congenital Heart Disease

A baby may be born with congenital heart disease and may not not present with symptoms in the early few hours of life. 

In order to diagnose the condition following points are summarized below:

1. A Baby With Cyanosis: may have conditions like

• Transposition of Great Arteries (TGA) ,
• Right sided obstruction (Pulmonary atresia, Tricuspid atresia)

2. Presentation with Mild Cyanosis and CCF: include conditions like:

• TAPVC,
• Truncus arteriosus

3. A newborn baby in Shock: may have:

• Hypoplastic left heart syndrome,
• Aortic stenosis

Medical Issues Common In Children With Neurodisability

There are a number of medical problems which are more common in children with disability. These

include:

1. Gastro-esophageal reflux disease (GERD) :Gastro-oesophageal reflux (the non-forceful regurgitation of gastric contents into the esophagus) is more common in children with neuro-developmental problems for a number of reasons. 

Intra-abdominal pressure may be increased for structural reasons such as scoliosis, the lower esophageal sphincter may be functionally immature as a reflection of abnormal muscle tone elsewhere in the body, and difficulties in upright positioning may also exacerbate gastroesophageal reflux.

First line management is postural, with supportive upright seating and sleeping positioners, along with adjustment of feed consistency if required. In addition, pharmacological agents like Proton-pump inhibitors (e.g. omeprazole, lansoprazole, esomeprazole) and H2-receptor antagonists (e.g. ranitidine) are used to alter acid production. Dopamine receptor antagonists (e.g. domperidone) stimulate gastric emptying and small intestinal transit. They also help with GERD by enhancing the tone of the esophageal sphincter. In children with severe symptoms of GORD, surgical intervention such as a Nissen’s fundoplication may be considered.

2. Respiratory complications: Neurological disturbance in children with neurodisability impairs the ability of the child to protect their airway, leading to acute or chronic (‘silent’) aspiration and liability to chemical pneumonitis or secondary infection with anaerobic organisms.

Croup or Viral Laryngotracheobronchitis in Children

Definition 
Croup or viral laryngotracheobronchitis is an acute inflammation of the entire airway, mainly in the glottis and subglottic area, resulting in airway narrowing, obstruction, and voice loss. 

Therefore, it has generally been described as a triad of 

1. hoarse voice, 
2. harsh barking cough, and 
3. inspiratory stridor.

Epidemiology

Typically, the condition affects younger children (6–36 months), with a peak incidence at 2 years of age. It is the most common cause of acute upper airway obstruction in young children; a reported 3% of children experience it before 6 years of age.
Seasonal outbreaks have been described in the fall and winter, although it may occur year round in some areas.
Males are more often affected than females.

Etiology and Pathophysiology
Viral infection is the predominant etiology; parainfluenza (types 1, 2, and 3) is the most common agent. Other common viral agents are respiratory syncytial virus (RSV) and influenza. Less commonly encountered viruses include adenovirus, rhinovirus, enterovirus, and measles virus.
Mycoplasma pneumoniae is one of the few bacterial microorganisms that has been reported as an etiologic agent.

In children, the larynx is very narrow and is comprised by the rigid ring of the cricoid cartilage; therefore, a viral infection causing inflammation of this area leads to airway edema and subsequent obstruction. This obstruction results in the classic symptoms of stridor and cough.

Clinical Presentation

• Croup usually presents initially with a coryzal prodrome (1–4 days).
• Common symptoms include clear rhinorrhea, low-grade temperature, and mild tachypnea followed by barking cough, hoarseness, and stridor.
• Obstructive symptoms occur most commonly at night.
• Severity of airway narrowing may be determined by the presence of stridor at rest, tachypnea, retractions, tracheal tug, cyanosis, and pallor, as well as decreased breath sounds, which indicate critical narrowing.

Treatment Options for Thalassemia Major

Before chronic transfusions are initiated, the diagnosis of Beta-thalassemia should be confirmed and the parents counseled about this lifelong therapy. Initiating transfusion and chelation therapy can be difficult for parents to face early in their child’s life.

If there is the possibility of a bone marrow transplant, the blood should be negative for cytomegalovirus and irradiated.

Blood Transfusion therapy:
Transfusion therapy promotes general health and well-being and avoids the consequences of ineffective erythropoiesis. A transfusion program generally requires monthly transfusions, with the pretransfusion hemoglobin level >9.5 and <10.5 g/dL. In patients with cardiac disease, higher pretransfusion hemoglobin levels may be beneficial. Some blood centers have donor programs that pair donors and recipients, decreasing the exposure to multiple red cell antigens.

Transfusional hemosiderosis causes many of the complications of thalassemia major. Accurate assessment of excessive iron stores is essential to optimal therapy. The serum ferritin level is useful in assessing iron balance trends, but does not accurately predict quantitative iron stores. Undertreatment or overtreatment of presumed excessive iron stores can occur when a patient is managed based on the serum ferritin level alone.

Sudden infant death syndrome

A medical mystery of early infancy, sudden infant death syndrome (SIDS)—commonly called crib death—kills apparently healthy infants, usually between ages 1 month and 1 year, for reasons that remain unexplained, even after an autopsy. Typically, parents put the infant to bed and later find him dead, often with no indications of a struggle or distress of any kind.

Some infants may have had signs of a cold, but such symptoms are usually absent. SIDS has occurred throughout history, all over the world, and in all climates.

Causes
SIDS is one of the leading causes of infant death. Most of these deaths occur during the winter, in poor families, and among underweight babies and those born to mothers younger than age 20.
Although infants who die from SIDS often appear healthy, research suggests that many may have had undetected abnormalities, such as an immature respiratory system and respiratory dysfunction. In fact, the current thinking is that SIDS may result from an abnormality in the control of ventilation, which causes prolonged apneic periods with profound hypoxemia and serious cardiac arrhythmias.

Risk factors for the infant include 

sleeping on the stomach (up to age 4 months), 

soft bedding in the crib (up to age 1 year), 

premature birth, 

having a history of a sibling who had SIDS, and

being born into poverty. 

Maternal risk factors include 

multiple births, 

smoking or illicit drug use, 

teenage motherhood, 

short intervals between pregnancies, and 

late prenatal care.

Introduction to Hydrocephalus

An excessive accumulation of cerebrospinal fluid (CSF) within the ventricular spaces of the brain, hydrocephalus occurs most commonly in neonates. It can also occur in adults as a result of injury or disease. In infants, hydrocephalus enlarges the head, and in both infants and adults, the resulting compression can damage brain tissue.
With early detection and surgical intervention, the prognosis improves but remains guarded. Even after surgery, such complications as developmental delay, impaired motor function, and vision loss can persist. Without surgery, the prognosis is poor: Mortality may result from increased intracranial pressure (ICP) in people of all ages; infants may also die prematurely of infection and malnutrition.

Causes
Hydrocephalus may result from an obstruction in CSF flow (noncommunicating hydrocephalus) or from faulty absorption of CSF (communicating hydrocephalus).

Noncommunicating hydrocephalus
In noncommunicating hydrocephalus, the obstruction occurs most commonly between the third and fourth ventricles, at the aqueduct of Sylvius, but it can also occur at the outlets of the fourth ventricle (foramina of Luschka and Magendie) or, rarely, at the foramen of Monro.
This obstruction may result from faulty fetal development, infection (syphilis, granulomatous diseases, meningitis), a tumor, a cerebral aneurysm, or a blood clot (after intracranial hemorrhage).

Communicating hydrocephalus
In communicating hydrocephalus, faulty absorption of CSF may result from surgery to repair a myelomeningocele, adhesions between meninges at the base of the brain, or meningeal hemorrhage. Rarely, a tumor in the choroid plexus causes overproduction of CSF, producing hydrocephalus.

Brief Summary of Cerebral Palsy

The most common cause of crippling in children, cerebral palsy is an umbrella term for a group of neuromuscular disorders resulting from prenatal, perinatal, or postnatal central nervous system (CNS) damage. Although nonprogressive, these disorders may become more obvious as an affected infant ages.

Types:
Three major types of cerebral palsy occur—

1. spastic, 
2. athetoid, and 
3. ataxic

—sometimes in mixed forms. Motor impairment may be minimal (sometimes apparent only during physical activities such as running) or severely disabling. Associated defects—such as seizures, speech disorders, and mental retardation—are common.
The prognosis varies. With mild impairment, proper treatment may make a near-normal life possible.

Cerebral palsy is most common in premature infants (anoxia plays the greatest role in contributing to cerebral palsy) and in those who are small for their gestational age. Cerebral palsy is common in whites and is slightly more common in males than in females.

Reye’s syndrome in Children

An acute childhood illness, Reye’s syndrome causes fatty infiltration of the liver with concurrent hyperammonemia, encephalopathy, and increased intracranial pressure (ICP). In addition, fatty infiltration of the kidneys, brain, and myocardium may occur.

Incidence
Reye’s syndrome affects children. It’s most common in patients ages 4 to 12, with a peak incidence at age 6.

Pathophysiology

Incidence of Reye’s syndrome usually rises during influenza outbreaks and is linked to aspirin use. It almost always follows within 1 to 3 days of an acute viral infection, such as an upper respiratory tract infection, type B influenza, or varicella (chickenpox).
With Reye’s syndrome, damaged hepatic mitochondria disrupt the urea cycle, which normally changes ammonia to urea for its excretion from the body. This results in hyperammonemia, hypoglycemia, and an increase in serum short-chain fatty acids, leading to encephalopathy.Simultaneously, fatty infiltration is found in renal tubular cells, neuronal tissue, and muscle tissue, including the heart.

Signs and symptoms
Reye’s syndrome develops in five stages, but the severity of the child’s signs and symptoms varies with the degree of encephalopathy and cerebral edema. Infants may have atypical presentation.
After the initial viral infection, a brief recovery period follows when the child doesn’t seem seriously ill. A few days later, he develops intractable vomiting, lethargy, rapidly changing mental status (mild to severe agitation, confusion, irritability, delirium), hyperactive reflexes, and rising blood pressure, respiratory rate, and pulse rate.
Reye’s syndrome may progress to coma. As the coma deepens, seizures develop, followed by decreased tendon reflexes and, commonly, respiratory failure.
Increased ICP, a serious complication, results from cerebral edema. Such edema may develop as a result of acidosis, increased cerebral metabolic rate, or an impaired autoregulatory mechanism.

Neonatal Resuscitation Procedure

Initial Steps
Prevent hypothermia—place infant on preheated radiant warmer, dry infant, then rewrap in warm, dry blankets. Polyethylene (food grade) bags may help maintain body temperature of very-low-birth weight infants.

Position—place the infant in a supine position with the head slightly extended (“sniffing position”); a small roll placed under the shoulders may be helpful.

Airway—if there are copious secretions compromising the airway, suction the mouth first and then the nose using either a suction bulb or 8F or 10F suction catheter; avoid prolonged and deep suctioning. Negative pressure should not exceed 100 mm Hg.

Tactile stimulation—if the infant remains apneic after drying, positioning, and suctioning, further tactile stimulation is unlikely to help; brief, gentle back rubbing or flicking the soles of feet, may be tried, but these efforts should not delay onset of positive-pressure ventilation.

Oxygen Administration
Free-flow 100% oxygen (at least 5 L/min) should be provided to any infant who has central cyanosis, pending further intervention(s). If positive-pressure ventilation (PPV) is begun, 100% supplemental oxygen is recommended. To reduce potential harm from excessive tissue oxygenation in preterm infants, the use of an oxygen blender and pulse oximetry is recommended in order to titrate supplemental oxygen delivery, maintaining oyxgen saturations between 90% and 95%. In any infant, if the heart rate does not respond by increasing to >100 beats per minute, 100% oxygen should be given.

Bag/Mask Ventilation
Indications—apnea or gasping; heart rate less than 100 beats per minute; central cyanosis despite free-flow oxygen.

Technique—proper mask size and shape, tight seal between mask and face, proper head position, clear airway, and adequate inflation pressure, ventilation rate of 40 to 60 breaths per minute. If ventilation pressure is being monitored, PPV with an initial inflation pressure of 20 cm H2O may be effective, but ?30 to 40 cm H2O may be required in some term babies without spontaneous ventilation.

Assessment—increasing heart rate is the primary sign of effective ventilation. Also look for improving color, spontaneous respirations, and improving muscle tone. If the heart rate is not improving, chest wall movement should be assessed and sufficient ventilating pressure should be used to move the chest wall with each breath.

Gastric decompression—if bag/mask ventilation is prolonged, an 8F orogastric tube should be inserted, aspirated, and left open as a vent to prevent gastric distension.

Special note: Flow-controlled pressure-limited mechanical devices (e.g., T-piece resuscitators) are recognized as an acceptable method of administering positive-pressure ventilation during newborn resuscitation; however, self-inflating and flow-inflating bags remain the preferred method for prolonged resuscitation.

Laboratory Workup For Children Who Present With Extremity Pain

Laboratory studies are unnecessary for most extremity pain. However, if the history and physical examination do not lead to a definitive diagnosis, if they raise suspicion of a systemic or an infectious disease, or if the pain persists longer than anticipated, then screening laboratory
tests are in order.

A basic evaluation should include

• a complete blood cell count (CBC),
• a sedimentation rate, 
• a C-reactive protein, and 
• a sickle cell preparation or
• hemoglobin electrophoresis when indicated. 

Appropriate serologies should be considered if features of the physical examination are consistent with rheumatologic disease.

•  An elevated sedimentation rate raises suspicion of an infectious or inflammatory disorder or, occasionally, of a neoplasm.
• A CBC may reveal anemia or may suggest an infectious disease. 
• With leukemia, the white blood cell (WBC) count varies, but immature forms may be present in the differential WBC count or thrombocytopenia may be present. 
• A creatine phosphokinase determination is occasionally indicated if muscular pain or weakness is suspected.

Imaging

Radiologic studies are often unnecessary in evaluating limb pain. However, because of the plasticity of children’s bones, traumatic injury that would ordinarily cause only a sprain in an adult is more likely to result in a greenstick or buckle fracture in a child. 

The presence of point tenderness or gross deformity in an extremity or pain on motion of the involved limb increases the likelihood of fracture. 

In an effort to minimize the use of radiographic studies after traumatic injury to the knee and ankle, The Ottawa Criteria have been developed for use in adults. These criteria have also now been validated for use in children older than 5 years. 

Summary of Autistic disorders

A severe, pervasive developmental disorder, autistic disorder is marked by unresponsiveness to social contact, gross deficits in intelligence and language development, ritualistic and compulsive behaviors, restricted capacity for developmentally appropriate activities and interests, and bizarre responses to the environment. Autistic disorder may be complicated by epileptic seizures, depression and, during periods of stress, catatonic phenomena.

Age of Presentation
Autism usually becomes apparent before the child reaches age 30 months, but in some children, the actual onset is difficult to determine. Occasionally, autistic disorder isn’t recognized until the child enters school. It affects three to four times more boys than girls, usually the firstborn boy. The prognosis is poor; most patients require a structured environment throughout life.

Causes
Autistic disorder is thought to result from a combination of psychological, physiologic, and sociological factors. The parents of an autistic child may appear distant and unaffectionate. However, because autistic children are unresponsive or respond with rigid, screaming resistance to touch and attention, parental remoteness may be merely a frustrated, helpless reaction to this disorder, not its cause.
Some autistic children show abnormal but nonspecific EEG findings that suggest brain dysfunction, possibly resulting from trauma, disease, or a structural abnormality. Autistic disorder also has been associated with maternal rubella, untreated phenylketonuria, tuberous sclerosis, anoxia during birth, encephalitis, infantile spasms, and fragile syndrome X.

Signs and symptoms
Typical features of infantile autistic disorder include unresponsiveness to people, language impairment, lack of imaginative play, bizarre behavior patterns, and abnormal reactions to sensory stimuli.

Approach To A Child Presenting With Extremity Pain - History And Physical Examination

Introduction:
Extremity pain is a common complaint in primary care pediatric practice. Up to 16% of school-aged children report at least 1 episode of activity-limiting extremity pain annually.
There is some evidence that extremity pain is more common in obese children Overall, approximately 6% of pediatric office visits are related to extremity pain. Fortunately, most of these visits involve
pain caused by minor trauma, overuse syndromes, and normal skeletal growth variants.
Occasionally, however, limb pain is the presenting complaint of a systemic illness, a neoplasm, an infectious process, a nutritional derangement, a specific orthopedic disorder, or a rheumatologic disease.
The challenge for the physician is to determine when the pain is significant without exposing the child to excessive diagnostic studies and without delaying treatment or referral. For the most part, this determination is based on the history and physical examination alone.

History
A thorough history from patients and parents often reveals the cause of extremity pain in children.

• Pain described as aching or cramping is likely to be muscular in origin.
• Bone pain is often described as deep.
• Nerve pain as burning, tingling, or numbness.
• Referred pain is common in children; thus, although usually helpful, the location of pain may be deceiving. 
• Migrating extremity pain is less likely to occur after trauma and is more typical of systemic illnesses such as leukemia, acute rheumatic fever, disseminated gonorrhea, and arthralgia or arthritis associated with inflammatory bowel disease. 

 - The mode of onset, variability, duration, and frequency of pain also help in determining its cause.  -  - Activities associated with worsening or relief of pain can also lead to a diagnosis.
 - Similarly, color change associated with extremity pain may indicate inflammation (faint red), infection (intense red), or autonomic dysfunction (pallor, cyanosis, and erythema).
 - Stiffness, especially with clinical evidence of arthritis not associated with trauma, should prompt concern about a rheumatologic process.

A history specific to trauma associated with extremity pain can be helpful. If the physical findings of trauma are greater than would be expected from the history, then physical abuse must be considered.

The child’s general health history completes the picture of extremity pain. For example, the differential diagnosis changes with age.

• Toxic synovitis of the hip is a common diagnosis in a child younger than 10 years; 
• a slipped capital femoral epiphysis is more likely in an overweight adolescent.

As a screen for systemic disease, all systems should be reviewed briefly. Particular attention should be paid to a history of fever, recent weight loss, sweating, rashes, and gastrointestinal symptoms.

A history of recent medications is important and might reveal a serum sickness–like illness. Even a short course of systemic steroids can cause aseptic necrosis of the hip or can result in demineralization of bone.

Immunizations, particularly for rubella, may cause joint or extremity pain, and a history of exposure to viral illness might explain myalgia or arthralgia.

The patient’s family history may reveal a tendency toward autoimmune disease or recent exposure to infectious diseases. The family history is particularly helpful in identifying hemoglobinopathies.

Juvenile Rheumatoid Arthritis

Affecting children younger than age 16, juvenile rheumatoid arthritis (JRA), also known as juvenile chronic arthritis, is an immune-mediated inflammatory disorder of the connective tissues characterized by joint swelling and pain or tenderness. It may also involve such organs as the skin, heart, lungs, liver, spleen, and eyes, producing extra-articular signs and symptoms.
JRA has three major types: systemic (Still’s disease or acute febrile type), polyarticular, and pauciarticular. Depending on the type, this disease can occur as early as age 6 weeks—although rarely before 6 months—with peaks of onset between ages 1 and 3 and 8 and 12. It’s considered the major chronic rheumatic disorder of childhood; overall incidence is twice as high in girls, with variation among the types.

Causes
JRA is thought to be an autoimmune disorder. Research has linked causation to genetic and immune factors. Viral or bacterial (particularly streptococcal) infection, trauma, and emotional stress have been identified as precipitating factors.

Signs and symptoms
Signs and symptoms vary with the type of JRA.

Systemic JRA
Affecting boys and girls almost equally, systemic JRA accounts for 20% to 30% of cases. Affected children may have mild, transient arthritis or frank poly-arthritis associated with fever and rash.
Fever in systemic JRA occurs suddenly and spikes to 103° F (39.4° C) or higher once or twice daily, usually in the late afternoon, then rapidly returns to normal or subnormal. (This sawtooth, or intermittent spiking, fever pattern helps differentiate JRA from other inflammatory disorders.) When fever spikes, an evanescent rheumatoid rash typically appears, consisting of small, pale or salmon pink macules, most commonly on the trunk and proximal extremities and occasionally on the face, palms, and soles.
Massaging or applying heat intensifies this rash, which is usually most conspicuous where the skin has been rubbed or subjected to pressure, such as that from underclothing.
Other signs and symptoms of systemic JRA include hepatosplenomegaly, lymphadenopathy, pleuritis, pericarditis, myocarditis, and nonspecific abdominal pain.

Approach To Dysuria In Children

Introduction
Dysuria is any discomfort with urination but particularly refers to pain or burning during urination. Generally stemming from irritation of the bladder or urethra, it is a commonly reported sensation that affects men, women, and children alike.

Although dysuria can be caused by any condition associated with inflammation, irritation, or obstruction of the urinary tract, in children and adolescents it most commonly accompanies urinary tract infections (UTIs), urethritis, and chemical or traumatic irritation. Identifying the underlying
cause of dysuria requires a detailed history, a careful physical examination, and a focused laboratory evaluation as needed.

Clinical History
The younger the child, the less precise is the complaint of painful urination. Other symptoms, such as pruritus or pain in the genital or perineal area, may be more noticeable while the child is voiding and not distracted. Although dysuria may be the only complaint, it is more often accompanied by associated symptoms.

Regardless of the child’s age, dividing the associated symptoms into either specific urinary symptoms or nonspecific symptoms is helpful.

Symptoms specific to the urinary tract include

• hematuria, 
• discharge, 
• malodorous urine, 
• frequency, 
• urgency, 
• refusal to void, 
• new-onset nocturnal enuresis, and 
• daytime incontinence. 

The physician should inquire about exposure to detergents, perfumed soaps, bubble baths, or ointments and about the type of underwear fabric, any of which can irritate the mucosal lining of the urethra or bladder.

A thorough history of the timing of toilet training, last occurrence of daytime accidents, nocturnal enuresis, withholding maneuvers, and constipation can help elucidate a diagnosis of dysfunctional elimination syndrome.The lack of a history of trauma may not be accurate because children often do not recall it or, in the case of masturbation or sexual abuse, may deliberately deny it.

To judge the possibility of a sexually transmitted infection, adolescents should be asked about sexual activity and safety practices.

A family history of nephrolithiasis should focus attention on hypercalciuria as a cause for dysuria, and a more detailed dietary history should be elicited, including intake of salt, dairy products, and vitamins.

Symptoms outside the urinary tract, such as conjunctival injection, oral and genital ulcers, arthralgia, or a generalized rash, could suggest a systemic inflammatory condition, such as Stevens-Johnson syndrome, Reiter syndrome, or Behçet disease.

A history of fever suggests an infectious condition such as pyelonephritis, appendicitis, or pelvic inflammatory disease.

Necrotizing Enterocolitis

Neonatal necrotizing enterocolitis (NEC) is a clinical condition characterized by an initial mucosal intestinal injury that may progress to transmural bowel necrosis. Although NEC is common, its cause is unknown. NEC is the leading surgical emergency in neonates in North America.
Infectious complications associated with bowel necrosis include bacterial peritonitis, systemic sepsis, and intra-abdominal abscess formation.

Causes
NEC usually occurs in premature neonates (less than 34 weeks’ gestation) and those of low birth weight (less than 5 lb [2.3 kg]). NEC is occurring in more neonates, possibly because of the higher incidence and survival of premature and low-birth-weight neonates.

Possible risk factorsNEC can develop when the infant suffers perinatal hypoxemia due to shunting of blood from the gut to more vital organs. Subsequent mucosal ischemia provides an ideal medium for bacterial growth. Hypertonic formula may increase bacterial activity because—unlike maternal breast milk—it doesn’t provide protective immunity and because it contributes to the production of hydrogen gas. As the bowel swells and its integrity breaks down, gas-forming bacteria invade damaged areas, producing free air in the intestinal wall. This may result in fatal perforation and peritonitis.

Signs And Symptoms

• Any infant who has suffered from perinatal hypoxemia has the potential for developing NEC. 
• A distended (especially tense or rigid) abdomen, with gastric retention, is the earliest and most common sign of oncoming NEC, usually appearing from 1 to 10 days after birth.
• Other signs and symptoms include increasing residual gastric contents (which may contain bile), bilious vomitus, and occult or gross blood in stools. One-fourth of patients have bloody diarrhea. 
• A red or shiny, taut abdomen may indicate peritonitis.
• Nonspecific signs and symptoms include thermal instability, lethargy, metabolic acidosis, jaundice, and disseminated intravascular coagulation (DIC). 
• The major complication is perforation, which requires surgery.
• Recurrence of NEC and mechanical and functional abnormalities of the intestine, especially stricture, are the usual cause of residual intestinal malfunction in any infant who survives acute NEC. They may develop as late as 3 months postoperatively.

Severe Combined Immunodeficiency Disease

Both cell-mediated (T-cell) and humoral (B-cell) immunity are deficient or absent in severe combined immunodeficiency disease (SCID). This results in susceptibility to infection from all classes of microorganisms during infancy.

At least three types of SCID exist: 

1. reticular dysgenesis, the most severe type, in which the hematopoietic stem cell fails to differentiate into lymphocytes and granulocytes; 
2. Swiss-type agammaglobulinemia, in which the hematopoietic stem cell fails to differentiate into lymphocytes alone; and 
3. enzyme deficiency, such as adenosine deaminase (ADA) deficiency, in which  the buildup of toxic products in the lymphoid tissue causes damage and subsequent dysfunction.

SCID affects more males than females; its estimated incidence is 1 in every 100,000 to 500,000 births. Most untreated patients die from infection within 1 year of birth.

Causes
SCID is usually transmitted as an autosomal recessive trait, although it may be X-linked. In most cases, the genetic defect seems associated with failure of the stem cell to differentiate into T and B lymphocytes.
Many molecular defects, such as mutation of the kinase ZAP-70, can cause SCID. X-linked SCID results from a mutation of a subunit of the interleukin-2 (IL-2), IL-4, and IL-7 receptors. Less commonly, it results from an enzyme deficiency.

Signs and symptoms
An extreme susceptibility to infection becomes obvious in the infant with SCID in the first months of life. The infant fails to thrive and develops chronic otitis, sepsis, watery diarrhea (associated with Salmonella or Escherichia coli), recurrent pulmonary infections (usually caused by Pseudomonas, cytomegalo-virus, or Pneumocystis carinii), persistent oral candidiasis (sometimes with esophageal erosions), and possibly fatal viral infections (such as chickenpox).
P. carinii pneumonia usually strikes a severely immunodeficient infant in the first 3 to 5 weeks of life. Onset is typically insidious, with gradually worsening cough, low-grade fever, tachypnea, and respiratory distress. A chest X-ray characteristically shows bilateral pulmonary infiltrates.

Attention deficit hyperactivity disorder

The patient with attention deficit hyperactivity disorder (ADHD) has difficulty focusing his attention or engaging in quiet, passive activities, or both. Although the disorder is present at birth, diagnosis before age 4 or 5 is difficult unless the child shows severe symptoms. Some patients, though, aren’t diagnosed until adulthood. Males are three times more likely to be affected than females.

Causes
ADHD is commonly thought to be a physiologic brain disorder with a familial tendency. Some studies indicate that it may result from disturbances in neurotransmitter levels in the brain.

Signs and symptoms
Typically, the patient is characterized as someone who fidgets and daydreams. Other descriptive terms include inattentive and lazy. Although the patient may be highly intelligent, his school or work performance patterns are sporadic, and he may jump from one partly completed project, thought, or task to another. Some patients have an attention deficit without hyperactivity; they’re less likely to be diagnosed and treated.
In a younger child, signs and symptoms include an inability to wait in line, remain seated, wait his turn, or concentrate on one activity until it’s completed. An older child or an adult may be described as impulsive and easily distracted by irrelevant thoughts, sounds, or sights. He may also be characterized as emotionally labile or inattentive. His disorganization becomes apparent when he has difficulty meeting deadlines and keeping track of school or work tools and materials.

Diagnosis
Commonly, the child with ADHD is referred for evaluation by the school. Diagnosis of this disorder

Treatment For Cystic Fibrosis

Cystic fibrosis is a genetic disorder that is inherited in an autosomal recessive pattern and is characterized by a defective transport of chloride and sodium across the epithelium that causes thick, sticky mucus to build up in the lungs, digestive tract, and other areas of the body. It is one of the most common chronic lung diseases in children and young adults.

Some of the treatment options are discussed briefly here:

1. Physiotherapy
Daily chest percussion and physiotherapy with postural drainage reduces respiratory exacerbations

3. Antibiotics
Early high dose , broad spectrum , long duration (minimum 2-3 weeks) antibiotics helps minimize lung damage in infective exacerbations. Oral or intravenous fluroquinolones combined with nebulized antibiotic is often the initial choice; resistance and chronic carriage needs intravenous combinations. Prophylactic antibiotics are also increasingly used.

3. Bronchodilators
These are helpful for symptomatic relief.

4. DNase- alpha mucolytics
These are administered as areosol spray. Mechanism of action is that it interferes with sputum neutrophil DNA, helping to liquefy sputum and encourage expectoration, thus helps in reducing cough.