Important Topics. (1) Year 4 Paediatrics Notes OmpathStudy

Important Topics. (1) Year 4 · Paediatrics Collection: 4TH YEAR ALL NOTES / PAEDS / OTHER NOTES -- Extra Topics\nobjectives: \n❖ It includes important topics not covered in the lecture\nor the tutorials. this is purely from abu wardah, but it is\nnot enough. read the textbook if possible\n\nDone by: Saud Alrsheed Revised by: Saud Alrsheed Team Leader: Saud Alrsheed\n\n Notes \nImportant \nBook \n\n HEMOLYTIC UREMIC SYNDROME ❖ is a triad of acute renal failure, microangiopathic haemolytic anaemia, and\nthrombocytopenia. Typical HUS is secondary to gastrointestinal infection with\nverocytotoxin-producing E. coli O157:H7, acquired through contact with farm\nanimals or eating uncooked beef, or, less often, Shigella. It follows a prodrome\nof bloody diarrhoea. ❖ The toxin from these organisms enters the gastrointestinal mucosa and\npreferentially localizes to the endothelial cells of the kidney where it causes\nintravascular thrombogenesis. The coagulation cascade is activated and\nclotting is normal (unlike in disseminated intravascular coagulation).\n\n❖ Platelets are consumed in this process and microangiopathic haemolytic\nanaemia (low serum haemoglobin, high serum lactate dehydrogenase) results\nfrom damage to red blood cells as they circulate through the microcirculation,\nwhich is occluded. Other organs such as the brain, pancreas, and heart may\nalso be involved.\n\n❖ With early supportive therapy, including dialysis, the typical\ndiarrhoea-associated HUS usually has a good prognosis, although long-term\nfollow-up is necessary as there may be persistent proteinuria and the\ndevelopment of hypertension and progressive chronic kidney disease. By\ncontrast, atypical HUS has no diarrhoeal prodrome, may be genetic, and may\nrelapse frequently\n\n❖ A monoclonal anti-terminal complement complex antibody, eculizumab, has\ngreatly improved the prognosis of this condition, which previously had a high\nrisk of hypertension, progressive chronic kidney disease and mortality.\nHowever, it is very expensive and the duration of treatment is unknown. \n\n sudden unexpected death in infancy ❖ Deaths that occur suddenly and unexpectedly in infants are termed sudden\nunexpected death in infancy (SUDI). In some, a previously undiagnosed\ncongenital abnormality, e.g. congenital heart disease, will be found at autopsy or\nanother condition, e.g. inborn error of metabolism, is identified. However, in\nmost instances of sudden death in a previously well infant, no cause is identified\neven after a detailed autopsy, and the death is classified as sudden infant death\nsyndrome (SIDS). ❖ There were 200 such deaths in the UK in 2018 (0.3 per 1000 live births). The\npeak age is 2–4 months, but it occurs throughout the first year; 55% are boys,\nand the risk is increased in those who were low birthweight (fivefold) and with\nmothers under 20 years old (fivefold greater than all other age groups). ❖ The vast majority of such deaths, even when occurring more than once in the\nsame family, are due to natural but unexplained causes. Rarely, the death may\nbe due to suffocation, particularly due to unintentional overlying while bed\nsharing, or from non-accidental injury. ❖ The incidence of SIDS has fallen dramatically in the UK since the national ‘Back\nto Sleep’ campaign advising parents to place their infants on their backs to sleep\nrather than previous widely given advice to lay them prone\n\n❖ Further epidemiological studies have identified additional risk factors, and\nadvice to parents to minimize risk of SIDS is summarized in Fig. 6.13. The\nmanagement following the death of an infant from Sudden Infant Death\nSyndrome is outlined in Case History 6.1.\n\n❖ SIDS is the most common cause of death in children aged 1 month to 1 year. The\npeak age for the occurrence of SIDS is 2–4 months. \n\nNEUROLOGICAL ABNORMALITIES \n\n preterm baby ❖ glucocorticoid therapy before preterm delivery accelerates lung maturity and\nsurfactant production. ❖ This has been tested in over 15 randomized trials and markedly reduces the\nincidence of respiratory distress syndrome (relative risk 0.66), intraventricular\nhaemorrhage (relative risk 0.54) and neonatal mortality (relative risk 0.69) in\npreterm infants. ❖ For optimal effect, a completed course needs to be given at least 24 hours\nbefore delivery and within 1–7 days before birth. ❖ Preterm infants are particularly liable to hypothermia, and every effort must be\nmade to keep them warm during resuscitation and stabilization. ❖ Infants of less than 32 weeks’ gestation should, with the exception of the face,\nbe placed into a plastic bag or wrapped in clear plastic sheeting without drying\nto allow the plastic to cling to the skin, and act almost like another layer of skin\nby avoiding evaporative heat loss. A radiant heat source from the resuscitation\ntable and/or thermal mattress can then warm the baby in the bag/wrap. Using\nwarmed humidified respiratory gases may also help. ❖ Excessive tissue ox