Sandbox:Asra
Vomiting
| ❑Assess vital signs ❑Obtain venous access | |||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
| Unstable | Stable | ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
| Stabilize hemodynamics | History and Physical Examination | ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
| Regurgitation | True Vomiting | ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
| Reassurance and follow-up in OPD | Red flag signs ❑ Unstable vital signs ❑ Acidotic breathing ❑ Bile and Blood present in vomiting ❑ Clinical features suggestive of GI obstruction ❑ Inconsolable cry and excessive irritability ❑ Altered sensorium | ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
| Yes | No | ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
| ❑ ICU admission ❑ Stabilise ❑ Investigate for the underlying cause | Fever | ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
| Treat the underlying cause | Present | Absent | |||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
| Infections | ❑ Frequency of vomiting ❑ Effect on oral intake | ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
| Treat the underlying cause | Persistent/Recurrent vomiting Hampering oral intake | Occasional vomiting Not hampering oral intake | |||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
| Antiemetics ❑ Ondansetron ❑ Domeperidone | Observation and Reassurance | ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
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Ewing's sarcoma Microchapters |
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Diagnosis |
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Treatment |
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Case Studies |
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Sandbox:Asra On the Web |
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American Roentgen Ray Society Images of Sandbox:Asra |
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [2];Associate Editor(s)-in-Chief: Suveenkrishna Pothuru, M.B,B.S. [3];Assistant Editor(s)-In-Chief: Michael Maddaleni, B.S., Asra Firdous, M.B.B.S.
Overview
Ewing's sarcoma is the second most common malignant bone neoplasm commonly affecting children and adolescents. It usually affects patients in the second decade of life with a peak incidence around 15 years of age. It comprises 3% of all malignancies in pediatric patients and about 10-15% of childhood bone cancers. The overall incidence of Ewing's sarcoma is approximately estimated at 2.9 cases per million population in the U.S. Ewing's sarcoma is more common in males than females. It is more prevalent in whites than Africans.
Epidemiology and Demographics
- Ewing's Sarcoma is the second most common bone malignancy in children and adolescents.
- 10-15% of childhood bone cancers are Ewing's Sarcoma.
- Ewing's Sarcoma constitutes about 4% of pediatric cancers.
- 200-250 new cases of Ewing's sarcoma are reported each year in the United States.
- Nearly, 60% of the Ewing Sarcoma cases have long-term disease-free survival.
Incidence
- The incidence of Ewing's sarcoma has remained unchanged for 30 years.[1]
- In the United States, the overall incidence of Ewing's sarcoma is 1 cases per million individuals.
- During 1973-2004, the average annual incidence of Ewing's Sarcoma was estimated to be 2.9 cases per million population in the United States.
- The incidence of Ewing's Sarcoma, in the United States, is estimated to be 200-250 cases annually.
Mortality/Morbidity
The overall 5-year survival rate for patients with Ewing's Sarcoma is approximately 70% in primary lesions and 30% in metastatic disease.
Race
- Ewing's Sarcoma is more prevalent in Caucasians than Asians or Hispanics.
- African Americans and Africans are less likely to develop Ewing's Sarcoma.
- The incidence in the Caucasians is 1.5 cases per million population.
- The incidence in the Asians is 0.8 cases per million population.
- The incidence in Africans is 0.2 cases per million population.
Age
- Ewing's Sarcoma commonly affects children and adolescents between 10 and 20 years of age.
- The median age at diagnosis is 15 years
- In patients younger than 5 years, diagnosed in about 0.6 cases per million population.
- In patients aged 10-14 years, diagnosed in about more than 5 cases per million population.
Gender
- Males are more commonly affected than females. The male to female ratio is around 3:2.
Reference
Anemia of Prematurity Symptoms
The majority of patients with Anemia of Prematurity are asymptomatic. In premature infants with severe disease, symptoms are usually vague or non-specific.
- Common symptoms of Anemia of Prematurity include
- Tachycardia
- Tachypnea
- Decreased activity or lethargy
- Difficulty feeding
- Pallor
- Less common symptoms of Anemia of Prematurity include
- Poor weight gain despite adequate calorie intake
- Breathing difficulties
- Metabolic acidosis due to increased lactic acid production from anaerobic metabolism in the cells
- Heart murmurs
Pathophysiology of Anemia of Prematurity
The pathogenesis of anemia of prematurity is multifactorial. Anemia of prematurity is the result of a combination of decreased erythropoietin production, increased erythropoietin metabolism, deficient iron stores, decreased RBC lifespan, and blood loss during phlebotomy.[2][3]
Physiological anemia in newborns
Normally, all the newborns experience a fall in the haemoglobin concentration during the first few weeks of life. Healthy, fullterm infants usually develop anemia around 10-12 weeks of life after birth. Hemoglobin concentration never falls below 10 g/dl in healthy infants. Physiological anemia is well tolerated by and does not require any therapy.[3]
- After birth, an embryo transitions from a hypoxic state in-utero to an infant in a relatively hyperoxic environment
- This transition leads to an increase in blood oxygen and tissue oxygen concentration in newborns
- Increased oxygen concentration inhibits erythropoietin production and eventually stops erythropoiesis
- Due to the rapid growth and disproportionate RBC production, hemoglobin levels fall gradually in infants
- The drop in hemoglobin concentration continues until the tissue hypoxia develops which usually takes around 6-12weeks after birth
- Tissue hypoxia activates the oxygen sensors present in the kidney and liver to stimulate the erythropoietin and red blood cells production
- Fullterm newborns have enough iron stores for erythropoiesis until 20 weeks of life
- Infants have a shorter RBC lifespan and increased erythropoietin metabolism when compared to adults[4]
Pathological Anemia of Prematurity
In preterm infants, multiple physiological factors exaggerate and combine to result in pathological anemia. Hemoglobin levels drop rapidly to less than 10 g/dl around 4-6 weeks after birth. Infants with 1-1.5 kg of birthweight have hemoglobin levels around 8 g/dl, whereas infants with birthweight less than 1 kg have hemoglobin levels around 7 g/dl or less. The profound decrease in hemoglobin levels in premature infants produce abnormal signs and symptoms and require a blood transfusion. [3]
- Iron transport from mother to infants and a greater proportion of fetal erythropoiesis occur during the third trimester. So, infants born prematurely have deficient iron stores required for the red blood cells production
- Blood loss during phlebotomy is the major contributor of anemia of prematurity
- Majority of preterm infants are sick and critically ill that require frequent blood sampling for various laboratory investigations needed for their clinical monitoring. The average amount of blood loss during sampling ranges from 0.8-3.1 ml/kg/day, a significant amount that requires replacement
- Preterm infants are at increased risk of nosocomial infections that lead to oxidative hemolysis
- In premature infants, liver is the major site of erythropoiesis. Liver EPO is less sensitive to anemia and tissue hypoxia[5]
- Preterm infants have deficient Vitamin E, Vitamin B12, Folic acid stores required for red blood cells production
- A combination of blood loss, decreased erythropoietin production, deficient iron stores, increased erythropoietin metabolism, shortened RBC lifespan contribute to the development of anemia of prematurity
Vomiting
| ❑Assess vital signs ❑Obtain venous access | |||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
| Unstable | Stable | ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
| Stabilize hemodynamics | History and Physical Examination | ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
| Regurgitation | True Vomiting | ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
| Reassurance and follow-up in OPD | Red flag signs ❑ Unstable vital signs ❑ Acidotic breathing ❑ Bile and Blood present in vomiting ❑ Clinical features suggestive of GI obstruction ❑ Inconsolable cry and excessive irritability ❑ Altered sensorium | ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
| Yes | No | ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
| ❑ ICU admission ❑ Stabilise ❑ Investigate for the underlying cause | Fever | ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
| Treat the underlying cause | Present | Absent | |||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
| Infections | ❑ Frequency of vomiting ❑ Effect on oral intake | ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
| Treat the underlying cause | Persistent/Recurrent vomiting Hampering oral intake | Occasional vomiting Not hampering oral intake | |||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
| Antiemetics ❑ Ondansetron ❑ Domeperidone | Observation and Reassurance | ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
- ↑ Ewing's sarcoma. National cancer institute.http://www.cancer.gov/types/bone/hp/ewing-treatment-pdq#section/_1
- ↑ Stockman JA, Graeber JE, Clark DA, McClellan K, Garcia JF, Kavey RE (1984). "Anemia of prematurity: determinants of the erythropoietin response". J Pediatr. 105 (5): 786–92. doi:10.1016/s0022-3476(84)80308-x. PMID 6502312.
- ↑ 3.0 3.1 3.2 Strauss RG (2010). "Anaemia of prematurity: pathophysiology and treatment". Blood Rev. 24 (6): 221–5. doi:10.1016/j.blre.2010.08.001. PMC 2981681. PMID 20817366.
- ↑ Widness JA, Veng-Pedersen P, Peters C, Pereira LM, Schmidt RL, Lowe LS (1996). "Erythropoietin pharmacokinetics in premature infants: developmental, nonlinearity, and treatment effects". J Appl Physiol (1985). 80 (1): 140–8. doi:10.1152/jappl.1996.80.1.140. PMID 8847295.
- ↑ Dame C, Fahnenstich H, Freitag P, Hofmann D, Abdul-Nour T, Bartmann P; et al. (1998). "Erythropoietin mRNA expression in human fetal and neonatal tissue". Blood. 92 (9): 3218–25. PMID 9787158.