Rotavirus Infection in Children

Diarrhea is a leading cause of childhood mortality in the world, accounting for 5–10 million deaths per year. In early childhood, the single most important cause of severe dehydrating diarrhea is rotavirus infection.

Epidemiology:
Rotaviruses, which are in the Reoviridae family, cause disease in virtually all mammals and birds. The virus is a wheel-like, triple-shelled icosahedron containing 11 segments of double-stranded RNA. The diameter of the particles by electron microscopy is approximately 80 nm. Rotaviruses are classified by serogroup (A, B, C, D, E, F, and G) and subgroup (I or II).
Occasional human outbreaks of group C rotavirus are reported. The other serogroups infect only nonhumans.
Rotavirus infection is most common in winter months in temperate climates. In the United States, the annual winter peak spreads from west to east
Disease tends to be most severe in patients 3–24 mo of age, although 25% of the cases of severe disease occur after 2 yr of age, with serologic evidence of infection developing in virtually all children by 4–5 yr of age. Infants younger than 3 mo are relatively protected by transplacental antibody and possibly breast-feeding. Infections in neonates and in adults in close contact with infected children are generally asymptomatic

Clinical Features:
Rotavirus infection typically begins after an incubation period of <48 hr (range 1–7 days) with mild to

Clinical Manifestations of Measles

Measles is a serious infection characterized by high fever, an enanthem, cough, coryza, conjunctivitis, and a prominent exanthem.

After an incubation period of 8–12 days, the prodromal phase begins with a mild fever followed by the onset of conjunctivitis with photophobia, coryza, a prominent cough and increasing fever.

The enanthem, Koplik spots, is the pathognomonic sign of measles and appears 1 to 4 days prior to the onset of the rash . They first appear as discrete red lesions with bluish white spots in the center on the inner aspects of the cheeks at the level of the premolars. They may spread to involve the lips, hard palate, and gingiva. They also may occur in conjunctival folds and in the vaginal mucosa. Koplik spots have been reported in 50–70% of measles cases but probably occur in the great majority.

Symptoms increase in intensity for 2–4 days until the 1st day of the rash.

The rash begins around the forehead (around the hairline), behind the ears, and on the upper neck as a red maculopapular eruption. It then spreads downward to the torso and extremities, reaching the palms and soles in up to 50% of cases. The exanthem frequently becomes confluent on the face and upper trunk

With the onset of the rash, symptoms begin to subside and the rash fades over about 7 days in the same progression as it evolved, often leaving a fine desquamation of skin in its wake.

Of the major symptoms of measles, the cough lasts the longest, often up to 10 days. In more severe cases, generalized lymphadenopathy may be present, with cervical and occipital lymph nodes especially prominent.

Approach to the Neonate With Poor Feeding

Clinical Presentation and Physical Examination

• A term infant does not feed by mouth.
• Examine the infant. Is he or she ill or well appearing?

Diagnosis and Treatment

• In an ill-appearing infant, evaluate for sepsis, respiratory distress, and congestive heart failure. Appropriate evaluation depending on signs and symptoms would be then indicated.
  
  
• In a well-appearing infant, consider whether he or she is (has):
  • Borderline preterm? Telltale signs include thin red skin, poorly developed breast tissue, undescended testes or poorly developed scrotal rugae (prominent labia minora), and few creases on the anterior third of the feet. A detailed Ballard score would also be helpful
  • Not feeding because he or she has never fed so far or may be very young (only a few hours old) and not learned how to feed. Tincture of time is all that may be required.
  • Very sleepy from just being a normal infant or from maternal magnesium sulphate or narcotics? Cold? Hypoglycemic? All these are easily reversible and require observation.
  • Anatomical barriers to feeding (cleft palate, small chin)?
  • Topical infection (oral thrush)? Tongue tie is not a cause of

Aplastic Crises In Sickle Cell Anemia

Because sickle cell anemia is a congenital hemolytic anemia, there is ongoing red cell destruction, which must be supported by endogenous erythropoiesis manifest as reticulocytosis. Any concurrent illness that suppresses endogenous erythropoiesis will result in reticulocytopenia and a decrease in hemoglobin level and hematocrit.

Acute aplastic crises are characterized by a decrease in the level of hemoglobin of >3.0 g per dL in the setting of reticulocytopenia.

Causes :
These crises often occur in association with an infection that leads to transient bone marrow suppression; human parvovirus B19, the etiologic agent of erythema infectiosum (fifth disease), is notorious for causing this complication.

Management:
Patients should be given supportive red cell transfusions when they have hemodynamic instability, which may present with tachycardia, tachypnea, postural hypotension, and unstable blood pressure. Symptomatic anemia, indicative of the need for transfusion, includes dyspnea, dizziness, excessive fatigue, and difficulty in concentrating. Clinical management depends on the degree of anemia and cardiovascular compromise. Aggressive transfusions should be avoided, because transfusion to levels much above the patient's baseline hematocrit may suppress endogenous erythropoiesis further

Acute Splenic Sequestration Crises In Sickle Cell Anemia

Acute splenic sequestration is the sudden pooling of blood in the spleen resulting in anemia, which may be life threatening. This type of crisis occurs most often in young children between 10 and 27 months of age in whom autoinfarction of the spleens has not yet happened.
The cause of this syndrome is unclear; it may be seen in the setting of concurrent bacterial or viral infection.

Diagnostic criteria
The diagnostic criteria for acute splenic sequestration include an acutely enlarging spleen, a decrease in hemoglobin level of at least 2 g per dL below baseline, thrombocytopenia often with a platelet count <100,000 per mm,³ leukopenia, and evidence of bone marrow compensation with reticulocytosis.

In its most severe form, acute splenic sequestration results in life-threatening anemia, hypovolemia, and shock. Decreases in the levels of hemoglobin <4 g per dL are associated with 35% mortality rates. It is estimated that as much as 50% of the patient's red cells can be sequestered in the spleen. Approximately 50% of patients who survive an episode of acute splenic sequestration will experience a recurrence.

Mangement
Emergency management is aimed at restoring circulatory blood volume and hemodynamic stability. Although