Oral Candidiasis In Children

Oral thrush, or oral pseudomembranous candidiasis, is a superficial mucous membrane infection that affects approximately 2–5% of normal newborns. Infants acquire Candida from their mothers at delivery and remain colonized.

Thrush may develop as early as 7–10 days of age. The use of antibiotics, especially in the 1st year of life, may lead to recurrent or persistent thrush. The plaques of thrush invade the mucosa superficially and may be found on the lips, buccal mucosa, tongue, and palate. Removal of plaques from these surfaces may cause mild punctate areas of bleeding, which helps to confirm the diagnosis.

Thrush may be asymptomatic or may cause pain, fussiness, and decreased feeding. It is uncommon after 12 months of age but may occur in older children treated with antibiotics. Persistent or recurrent thrush with no obvious predisposing reason, such as recent antibiotic treatment, warrants investigation of an underlying condition such as diabetes mellitus or immunodeficiency, especially vertically transmitted HIV infection.

Treatment:
Treatment of mild cases may not be necessary.

Treatment of Kawasaki Disease

Patients with acute Kawasaki disease should be treated with intravenous immunoglobulin (IVIG) and high-dose aspirin as soon as possible after diagnosis and, ideally, within 10 days of disease onset.

The mechanism of action of IVIG in Kawasaki disease is unknown, but treatment should result in rapid defervescence and resolution of clinical signs of illness in 85–90% of patients. With therapy, the CRP normalizes much more quickly than the ESR, which will often increase immediately after IVIG therapy. IVIG reduces the prevalence of coronary disease from 20–25% in children treated with aspirin alone to 2–4% in those treated with IVIG and aspirin within the 1st 10 days of illness. Consideration should even be given to treatment of patients diagnosed after the 10th illness day if fever has persisted, because the anti-inflammatory effect may be helpful, although the effect of such therapy on the risk of developing coronary aneurysms is unknown. The dose of aspirin is decreased from anti-inflammatory to antithrombotic doses (3–5 mg/kg/day as a single dose) on the 14th illness day or after the patient has been afebrile for at least 3–4 days. Aspirin is continued for its antithrombotic effect until 6–8 wk after onset, when the ESR has normalized in patients that have not developed abnormalities detected by echocardiography.

Cleft lip and Cleft palate

Cleft lip and cleft palate—an opening in the lip or palate—may occur separately or in combination. These deformities originate in the 2nd month of pregnancy, when the front and sides of the face and the palatine shelves fuse imperfectly. Cleft deformities usually occur unilaterally or bilaterally, rarely midline. Only the lip may be involved, or the defect may extend into the upper jaw or nasal cavity.
Cleft lip and cleft palate occur in twice as many males as females; isolated cleft palate is more common in females.

Causes
Cleft lip or palate can occur as part of another chromosomal or Mendelian abnormality (more than 150 have been identified); however, exposure to teratogens during fetal development or a combination of genetic and environmental factors may also produce these defects.
Cleft lip with or without cleft palate occurs in about 1 in 1,000 births among Whites; the incidence is higher among Asians (1.7 in 1,000) and Native Americans (more than 3.6 in 1,000) but lower among Blacks (1 in 2,500). A positive family history is a risk factor for cleft defects.

Signs and symptoms
Congenital defects of the face usually occur in the upper lip. They range from a simple notch to a complete cleft from the lip edge through the floor of the nostril, on either side of the midline, but rarely along the midline itself.

Clubfoot deformity in Children

The most common congenital disorder of the lower extremities, clubfoot, or talipes, is marked primarily by a deformed talus and shortened Achilles tendon, which give the foot a characteristic clublike appearance. In talipes equinovarus, the foot points downward (equinus) and turns inward (varus), and the front of the foot curls toward the heel (forefoot adduction).
Clubfoot, which has an incidence of about 1 per 1,000 live births, usually occurs bilaterally and is twice as common in boys as it is in girls. It may be associated with other birth defects, such as myelomeningocele, spina bifida, and arthrogryposis. Clubfoot is correctable with prompt treatment.

Causes
A combination of genetic and environmental factors in utero appears to cause clubfoot. Heredity is a definite factor in some cases, although the mechanism of transmission is undetermined. If a child is born with clubfoot, his sibling has a 1 in 35 chance of being born with the same anomaly. Children of a parent with clubfoot have 1 chance in 10.
In children without a family history of clubfoot, this anomaly seems linked to arrested development during the 9th and 10th weeks of embryonic life, when the feet are formed. Researchers also suspect muscle abnormalities, leading to variations in length and tendon insertions, as possible causes of clubfoot.

Signs and symptoms
Talipes equinovarus varies in severity. Deformity may be so extreme that the toes touch the inside of the ankle, or it may be only vaguely apparent.
In every case, the talus is deformed, the Achilles tendon shortened, and the calcaneus somewhat shortened and flattened. Depending on the degree of the varus deformity, the calf muscles are shortened and underdeveloped, with soft-tissue contractures at the site of the deformity. The foot is tight in its deformed position and resists manual efforts to push it back into normal position.
Clubfoot is painless, except in older, arthritic patients. In older children, clubfoot may be secondary to paralysis, poliomyelitis, or cerebral palsy, in which case treatment must include management of the underlying disease.

Pediatric Aphthous Ulcers

Commonly termed canker sores, aphthous ulcers, or aphthous stomatitis, have been the focus of study and research for many years, although the exact etiology of the lesions has yet to be identified. Categorized as an idiopathic disease, aphthous ulcers are frequently misdiagnosed, treated incorrectly, or simply ignored.

Causes
Precipitating factors include trauma, salivary gland dysfunction, stress, genetic predisposition, local infections, nutritional deficiencies, GI disorders, systemic disorders, food allergy or hypersensitivity, hormonal fluctuations, and chemical exposure.

Clinical Presentation
The diagnosis of aphthous ulcers (canker sores) is primarily clinical. Patients typically describe a prodromal stage of a burning or pricking sensation of the oral mucosa 1-2 days before the ulcer appears.

Aphthous ulcers occur on areas of the mouth in which the mucosa is nonkeratinized and loosely attached, particularly the buccal mucosa, the labial mucosa, the floor of the mouth, the ventral surface of the tongue, and the soft palate. Ulcers may appear as single or multiple lesions, and they are easily distinguished from primary or secondary viral infections, bacterial infections (eg, necrotizing ulcerative gingivitis), dermatologic conditions (lichen planus, cicatricial pemphigoid, pemphigus), and traumatic injuries (contusions, lacerations, burns) by the healthy appearance of adjacent tissues and the lack of distinguishing systemic features.

Introduction to Colic

Colic is commonly described as a behavioral syndrome characterized by excessive, paroxysmal crying. Colic is most likely to occur in the evenings, and it occurs without any identifiable cause. During episodes of colic, an otherwise healthy neonate or infant aged 2 weeks to 4 months is difficult to console. They stiffen, draw up their legs, and pass flatus. Colic is one of the common reasons parents seek the advice of a pediatrician or family practitioner during their child’s first 3 months of life.

Definition
The most widely used definition of colic is based on the amount of crying (i.e, paroxysms of crying lasting >3 hours, occurring >3 days in any week for 3 weeks).

Causes
Colic is a poorly understood phenomenon. It is equally likely to occur in both breastfed and formula-fed infants. Although potential adverse sequelae have been described, the disorder is generally believed to be self-limited and benign. Different feeding practices and crying may result in large amounts of air entering the gastric lumen, which suggests that excessive aerophagia may be associated with colic. Colonic fermentation is the second proposed source of excessive intestinal gas in infants. However, no experimental evidence supports either theory.

Epidemiology

• Colic affects 10-30% of infants worldwide.
• This condition is encountered in male and female infants with equal frequency.
• The colic syndrome is commonly observed in neonates and infants aged 2 weeks to 4 months.

Introduction to Rickets

Introduction

Rickets is a disease of growing bone that is unique to children and adolescents. It is caused by a deficiency or impaired metabolism of vitamin D, magnesium, phosphorus or calcium. It leads to softening and weakening of the bones.

Rickets is among the most frequent childhood diseases in many developing countries. The predominant cause is a vitamin D deficiency, but lack of adequate calcium in the diet may also lead to rickets .

Types of Rickets
Different types have been described and may include:

• Nutritional Rickets
• Vitamin D Resistant Rickets
• Vitamin D Dependent Rickets
•  - Type I
•  - Type II
• Congenital Rickets

Pathophysiology
Vitamin D deficiency rickets occurs when the metabolites of vitamin D are deficient. Less commonly, a dietary deficiency of calcium or phosphorus may also produce rickets. Vitamin D-3 (cholecalciferol) is formed in the skin from a derivative of cholesterol under the stimulus of ultraviolet-B light. It is converted into the active metabolite calcitriol after final hydroxylation in the kidney. Calcitriol acts to regulate the body’s calcium metabolism by the following mechanisms:

(1) it promotes absorption of calcium and phosphorus from the intestine; 

(2) it increases reabsorption of phosphate in the kidney; and, 

(3) it acts on bone to release calcium and phosphate. Calcitriol may also directly facilitate calcification. These actions result in an increase in the concentrations of calcium and phosphorus in extracellular fluid.

Failure to Thrive – Differential Diagnosis

A child may present with failure to thrive and not gaining appropriate weight for his age. There are a number of different factors responsible for it and a doctor should consider the following differentials in his mind.

Inadequate Intake
May result from a swallowing problem, formula mixing error, lack of access to formula or other foods due to limited finances, inappropriate substitution of other liquids ( eg juices ) for formula or neglect.

Excessive losses due to Diarrhea
Consider infectious agents ( bacterial, giardia ), HIV, cystic fibrosis or inflammation due to food allergies.

Increased Needs
It may be due to hyper metabolic states or disease that cause increased work of breathing. Consider cystic fibrosis, hyperthyroidism and cardiac disease.

Fever Of Unknown Origin – Differential Diagnosis

Definition: Fever of unknown origin is defined as a fever in which patient has a temperature of more than 101F (38.3 C ) on most of the days for at least 3 weeks duration of a single illness and the diagnosis is unclear despite 1 week of intense inpatient investigations.

The list of potential etiologies of FUO is vast but following can be considered:

1. Infection
In almost all reviews of FUO in pediatric patients , infection is the largest category. It is important to recognize uncommon manifestations of common disorders. About half of the localized infections involve the respiratory tract and a careful history and x-ray can confirm the diagnosis. Other locations that are sources of prolonged fever include urinary tract, bone and CNS. Look for clues to more generalized infections like epstein-barr virus , enteric fever, cat-scratch disease etc in which there may be evidence of multiple organ involvement.

2. Collagen or Connective tissue Disease
Juvenile rheumatoid arthritis may present with a long duration of fever before a diagnosis is established. Additional causes include Kawasaki disease, SLE, rheumatic fever and other vasculitic syndromes. Some of these diseases may produce additional physical findings but some patients have only atypical presentations with only a few manifestations of the disorder.

3. Neoplasia
Most common in this group are lymphoreticular malignancies ( e.g lymphoma. leukemia ). If there are any joint symptoms , there may at times be confused with JRA. Neuroblastomas and occasionally other sarcomas may also sometimes present with fever as the only major symptom.