Acute Larynotracheitis (Viral Croup)

Acute laryngotracheitis is the most common cause of acute stridor that is encountered in pediatric practice. It usually occurs in the late fall and winter months, when viral respiratory infections reach their peak incidence. It is more common in boys than in girls, and occurs more often in children between 6 months and 6 years of age who have had an upper respiratory infection for 2 to 3 days before inspiratory stridor develops.

Clinical Features:
Fever usually is present, but the child generally does not appear to be very ill. On cautious examination of the posterior pharynx, the epiglottis may be slightly red and mildly edematous, which is quite different from the gross swelling of acute epiglottitis. The obstruction in acute laryngotracheobronchitis is primarily subglottic in location

Etiology:
Parainfluenza type 1 viruses are the most common cause of viral croups, accounting for up to 65% of the incidents, and parainfluenza type 3, influenza A and B viruses, adenoviruses, respiratory syncytial virus, and echovirus cause most of the rest. Mycoplasma pneumoniae also can produce croup symptoms in older children.

Management:
Most children with croup do not require hospitalization. Treatment at home consists of air humidification, avoidance of agitation, and reduction of fever

If signs of severe obstruction develop, treatment with

Spina Bifida Occulta

This common anomaly consists of a midline defect of the vertebral bodies without protrusion of the spinal cord or meninges. Most individuals are asymptomatic and lack neurologic signs, and the condition is usually of no consequence. In some cases, patches of hair, a lipoma, discoloration of the skin, or a dermal sinus in the midline of the lower back suggests a more significant malformation of the spinal cord .

A spine roentgenogram in simple spina bifida occulta shows a defect in closure of the posterior vertebral arches and laminae, typically involving L5 and S1; there is no abnormality of the meninges, spinal cord, or nerve roots. Spina bifida occulta is occasionally associated with more significant developmental abnormalities of the spinal cord, including syringomyelia, diastematomyelia, and a tethered cord. These are best identified with MRI . Some consider the term spina bifida occulta to denote merely a posterior vertebral body fusion defect. This simple defect does not have an associated spinal cord malformation.
 Other clinically more significant forms are more correctly termed occult spinal dysraphism.
In most of these cases, there are cutaneous manifestations such as a hemangioma, pit, lump, or hairy patch .
A dermoid sinus usually forms a small skin opening, which leads into a narrow duct, sometimes indicated by protruding hairs, a hairy patch, or a vascular nevus. Dermoid sinuses occur in the midline at the site of where meningoceles or encephaloceles may occur: the lumbosacral region or occiput. Dermoid sinus tracts may pass through the dura, acting as a conduit for the spread of infection. Recurrent meningitis of occult origin should prompt careful examination for a small sinus tract in the posterior midline region, including the back of the head. Lower back sinuses are usually above the gluteal fold and are directed cephalad. Tethered spinal cord syndrome may also be an associated problem.

Treatment Options for Duchenne Muscular Dystrophy

There is neither a medical cure for this disease nor a method of slowing its progression. Much can be done to treat complications and to improve the quality of life of affected children.


Cardiac decompensation often responds initially well to digoxin.
Pulmonary infections should be promptly treated. Patients should avoid contact with children who have obvious respiratory or other contagious illnesses. Immunizations for influenza virus and other routine vaccinations are indicated.
Preservation of a good nutritional state is importantBecause sedentary children burn fewer calories than active children and because of depression as an additional factor, these children tend to eat excessively and gain weight. Obesity makes a patient with myopathy even less functional because part of the limited reserve muscle strength is dissipated in lifting the weight of excess subcutaneous adipose tissue. Dietary restrictions with supervision may be needed.
Physiotherapy delays but does not always prevent contractures.

Other treatment of human patients with Duchenne dystrophy involves the use of prednisone, prednisolone, deflazacort, or other steroids. Glucocorticoids decrease the rate of apoptosis or programmed cell death of myotubes during ontogenesis and may decelerate the myofiber necrosis in muscular dystrophy
One protocol gives prednisone (0.75 mg/kg/day) for the first 10 days of each month to avoid

Clinical Manifestations of Hereditary spherocytosis

Hereditary spherocytosis may be a cause of hemolytic disease in the newborn and may present as anemia and hyperbilirubinemia sufficiently severe to require phototherapy or exchange transfusions. Hemolysis may be more prominent in the newborn because hemoglobin F binds 2,3-diphosphoglycerate poorly, and the increased level of free 2,3-diphosphoglycerate destabilizes spectrin-actin-protein 4.1 interactions in the RBC membrane .

The severity of symptoms in infants and children is variable. Some children remain asymptomatic into adulthood, but others may have severe anemia, with pallor, jaundice, fatigue, and exercise intolerance. Severe cases may be marked by expansion of the diploë of the skull and the medullary region of other bones, but to a lesser extent than in thalassemia major.

 After infancy, the spleen is usually enlarged, and pigmentary (bilirubin) gallstones may form as early as age 4–5 yr. At least 50% of unsplenectomized patients ultimately form gallstones, although they may be asymptomatic. Because of the high RBC turnover and heightened erythroid marrow activity, children with hereditary spherocytosis are susceptible to aplastic crisis, primarily as a result of parvovirus infection, and to hypoplastic crises associated with various other infections .

The erythroid marrow failure may result rapidly in profound anemia (hematocrit <10%), high-output heart failure, hypoxia, cardiovascular collapse, and death. White blood cell and platelet counts may also fall .

Clinical features of gasroesophegeal reflux disease

GERD is the most common esophageal disorder in children of all ages. Gastroesophageal reflux (GER) signifies the retrograde movement of gastric contents across the lower esophageal sphincter (LES) into the esophagus. Although occasional episodes of reflux are physiologic, exemplified by the regurgitation of normal infants, the phenomenon becomes pathologic (GERD) in children who have episodes that are more frequent or persistent, and thus produce esophagitis or esophageal symptoms, or in those who have respiratory sequelae.

CLINICAL MANIFESTATIONS.

Most of the common clinical manifestations of esophageal disease can signify the presence of GERD.

Infantile reflux manifests more often with regurgitation (especially postprandially), signs of esophagitis (irritability, arching, choking, gagging, feeding aversion), and resulting failure to thrive; symptoms resolve spontaneously in the majority by 12–24 mo.

Older children, in contrast, may have regurgitation during the preschool years; complaints of abdominal and chest pain supervene in later childhood and adolescence.

Occasional children present with neck contortions (arching, turning of head) designated Sandifer syndrome.

The respiratory presentations are also age dependent: GERD in infants may manifest as obstructive apnea or as stridor or lower airway disease in which reflux complicates primary airway disease such as laryngomalacia or bronchopulmonary dysplasia. Otitis media, sinusitis, lymphoid hyperplasia, hoarseness, vocal cord nodules, and laryngeal edema have all been associated with GERD. In contrast, airway manifestations in older children are more frequently related to asthma or to otolaryngologic disease such as laryngitis or sinusitis.