VIRAL CROUP

Def.: heterogeneous group of mainly acute and infectious upper airway obstruction processes that are characterized by a barking like or brassy cough and may be associated with hoarseness, inspiratory stridor, and respiratory distress.

It is acute laryngotracheitis, Laryngotracheobronchitis!

Incidence:

·       The most common form of acute upper respiratory obstruction.

·       Affect about 15% of children.

·       It is most common between 6 m΄ and 6 years of age, with a peak prevalence in the 2^nd year of life, rare over the age of 10 years.

·       Boys > girls.

·       Season; a peak in autumn and winter is associated with parainfluenza virus but can occur throughout the year.

·       Croup is uncommon < 6 months of life.

·       Rarely lasts more than 10 to 14 days.

·       Approximately 15% of patients have a strong FHx of croup.

ETIOLOGY:

·       Parainfluenza viruses type 1 , 2 and 3 (account for ≈75% of cases(

·       Other viruses including RSV, adenovirus, influenza, and measles: Influenza has been associated with more severe cases.

Pathogenesis:

·       After inhalation of the virus, the cells of the local respiratory epithelium become infected.

·       There is marked edema of the lamina propria, submucosa, and adventitia accompanied by cellular infiltration with histiocytes, lymphocytes, plasma cells, and PNLs.

·       The infant’s glottis and subglottic region are normally narrow, and a small ↓ in diameter → large ↑ in airway resistance & ↓ in airflow.

Clinical Signs and Symptoms of Refeeding Syndrome.

Clinical Signs and Symptoms of Refeeding Syndrome

References  

1. Fuentebella, J., & Kerner, J. A. (2009). Refeeding Syndrome. Pediatric Clinics of North America, 56(5), 1201–1210. doi:10.1016/j.pcl.2009.06.006.
2. Jason M. Nagata and Andrea K. Garber, refeeding syndrome, Nelson 22th ed 2024, Vol 1, ch 63.

 

 

Pathogenesis of refeeding syndrome.

Pathogenesis of refeeding syndrome

 How does refeeding syndrome develop?

Prolonged fasting:

During prolonged fasting, hormonal and metabolic changes are aimed at preventing protein and muscle breakdown.

Muscle and other tissues decrease their use of ketone bodies and use fatty acids as the main energy source. This results in an increase in blood levels of ketone bodies, stimulating the brain to switch from glucose to ketone bodies as its main energy source.

The liver decreases its rate of gluconeogenesis, thus preserving muscle protein. During the period of prolonged starvation, several intracellular minerals become severely depleted. However, serum concentrations of these minerals (including phosphate) may remain normal. This is because these minerals are mainly in the intracellular compartment, which contracts during starvation. In addition, there is a reduction in renal excretion.

Refeeding:

During refeeding, glycaemia leads to increased insulin and decreased secretion of glucagon. Insulin stimulates glycogen, fat, and protein synthesis. This process requires minerals such as phosphate and magnesium and cofactors such as thiamine. Insulin stimulates the absorption of potassium into the cells through the sodium-potassium ATPase symporter, which also transports glucose into the cells. Magnesium and phosphate are also taken up into the cells. Water follows by osmosis. These processes result in a decrease in the serum levels of phosphate, potassium, and magnesium, all of which are already depleted.

The clinical features of the refeeding syndrome occur as a result of the functional deficits of these electrolytes and the rapid change in basal metabolic rate.