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==Historical Perspective== | ==Historical Perspective== | ||
Hydrops fetalis was first discovered by Dr. John William Ballantyne, a Scottish physician and obstetrician, in 1892. | Hydrops fetalis was first discovered by Dr. John William Ballantyne, a Scottish physician and [[obstetrician]], in 1892. | ||
==Classification== | ==Classification== | ||
Hydrops Fetalis may be classified into two groups based on the presence or absence of rhesus iso-immunization: | Hydrops Fetalis may be classified into two groups based on the presence or absence of [[Rhesus blood group system|rhesus]] iso-immunization: | ||
*'''Immune Hydrops Fetalis''' | *'''[[Rhesus D hemolytic disease of the newborn|Immune Hydrops Fetalis]]''' | ||
*'''Non-Immune Hydrops Fetalis (NIHF)''' | *'''Non-Immune Hydrops Fetalis (NIHF)''' | ||
==Pathophysiology== | ==Pathophysiology== | ||
*It is thought that hydrops fetalis is caused by conditions with either increased rate of fluid transudation from the vascular compartment or decreased lymphatic return to the circulation. | *It is thought that hydrops fetalis is caused by conditions with either increased rate of fluid transudation from the [[vascular]] compartment or decreased [[Lymphatic system|lymphatic]] return to the [[Circulation (physiology)|circulation]]. | ||
*This is shown to be originated from developmental defects in microcirculation and lymphatic system, respectively. | *This is shown to be originated from developmental defects in [[microcirculation]] and [[lymphatic system]], respectively. | ||
*The potential causes may be immune or non-immune, and they often result in anemia and further hypoxia. | *The potential causes may be [[Rhesus D hemolytic disease of the newborn|immune]] or non-immune, and they often result in anemia and further hypoxia. | ||
*The sympathetic system becomes activated due to hypoxia, and it causes blood redistribution with decreased blood flow to the liver and kidneys. | *The sympathetic system becomes activated due to hypoxia, and it causes blood redistribution with decreased blood flow to the liver and kidneys. | ||
*Decreased blood flow to the liver and kidneys, results in decreased albumin, increased ADH, and increased activity of RAAS. | *Decreased blood flow to the liver and kidneys, results in decreased albumin, increased ADH, and increased activity of RAAS. | ||
*Following these changes, the central venous pressure increases, which further results in decreased lymphatic return. | *Following these changes, the central venous pressure increases, which further results in decreased lymphatic return. | ||
*As a result, hydrops fetalis (the accumulation of fluid, or edema, in at least two fetal compartments) | *As a result, hydrops fetalis (the accumulation of fluid, or edema, in at least two fetal compartments) occurs. | ||
*The pathophysiology of non-immune causes also depend on the underlying conditions, include: | *The pathophysiology of non-immune causes also depend on the underlying conditions, include: | ||
**Decreased ventricular filling during diastole (i.e. tachyarrhythmias) | **Decreased ventricular filling during diastole (i.e. tachyarrhythmias) | ||
**Increased central venous pressure due to the increased right heart pressure (i.e. cardiac tumors and subendocardial fibroelastosis) | **Increased central venous pressure due to the increased right heart pressure (i.e. cardiac tumors and subendocardial fibroelastosis) | ||
**Obstruction of lymphatic drainage due to a mass (i.e. cystic hygroma) | **Obstruction of lymphatic drainage due to a mass (i.e. cystic hygroma) | ||
==Causes== | ==Causes== | ||
Hydrops Fetalis is caused by either immune or non-immune conditions. | Hydrops Fetalis is caused by either immune or non-immune conditions. | ||
*'''Immune hydrops fetalis''' | *'''Immune hydrops fetalis''' | ||
**Antibodies may occur due to the exposure of non-self RBC antigens during the previous pregnancy or transfusion. | **Antibodies may occur due to the exposure of non-self RBC antigens during the previous pregnancy or transfusion. | ||
**In the next pregnancy, these antibodies may attack the fetal erythrocytes if the fetus has that antigen. | **In the next pregnancy, these antibodies may attack the fetal erythrocytes if the fetus has that antigen. | ||
**Following the red blood cell destruction, hemolytic disease of the fetus and newborn (HDFN) may occur with a wide range of clinical outcome from only mild anemia to high output heart failure and hydrops fetalis. | **Following the red blood cell destruction, hemolytic disease of the fetus and newborn (HDFN) may occur with a wide range of clinical outcome from only mild anemia to high output heart failure and hydrops fetalis. | ||
***Rh disease is the major cause for immune-mediated hydrops fetalis; however, owing to preventative methods developed in the 1970s, the incidence of Rh disease has markedly declined. | ***Rh disease is the major cause for immune-mediated hydrops fetalis; however, owing to preventative methods developed in the 1970s, the incidence of Rh disease has markedly declined. | ||
***Rh disease can be prevented by administration of anti-D IgG (Rho (D) Immune Globulin) injections to RhD-negative mothers during pregnancy and/or within 72 hours of the delivery. | ***Rh disease can be prevented by administration of anti-D IgG (Rho (D) Immune Globulin) injections to RhD-negative mothers during pregnancy and/or within 72 hours of the delivery. | ||
*'''Non-immune hydrops fetalis (NIHF)''' | *'''Non-immune hydrops fetalis (NIHF)''' | ||
**Currently, with the decreased prevelance of Rh disease, non-immune causes are responsible for up to 90% of cases. | **Currently, with the decreased prevelance of Rh disease, non-immune causes are responsible for up to 90% of cases. | ||
**The most common causes of non-immune hydrops fetalis are hematologic diseases, and chromosomal abnormalities, followed by lymphatic anomalies, and cardiovascular diseases. Causes of NIHF include: | **The most common causes of non-immune hydrops fetalis are hematologic diseases, and chromosomal abnormalities, followed by lymphatic anomalies, and cardiovascular diseases. Causes of NIHF include: | ||
***Structural cardiac malformations (especially hypoplastic left heart, endocardial cushion defect) | ***Structural cardiac malformations (especially hypoplastic left heart, endocardial cushion defect) | ||
***Arrhythmias | ***Arrhythmias | ||
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==Epidemiology and Demographics== | ==Epidemiology and Demographics== | ||
*In developed countries, the incidence of non-immune hydrops fetalis (NIHF) is 25-79 per 100.000 live born infants worldwide. | *In developed countries, the incidence of non-immune hydrops fetalis (NIHF) is 25-79 per 100.000 live born infants worldwide. | ||
*The median gestational age (GA) at diagnosis of NIHF is 23 weeks. | *The median gestational age (GA) at diagnosis of NIHF is 23 weeks. | ||
*Gestational age is predictive of mortality, as preterm infants with this condition are more likely to die. | *Gestational age is predictive of mortality, as preterm infants with this condition are more likely to die. | ||
*The case-fatality rate of NIHF is ranged from 43.2% to 78.2%. | *The case-fatality rate of NIHF is ranged from 43.2% to 78.2%. | ||
==Risk Factors== | ==Risk Factors== | ||
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==References== | ==References== | ||
<br /> | <br /> | ||
<references /> |
Revision as of 10:33, 24 April 2021
Hydrops Fetalis
Overview
Historical Perspective
Hydrops fetalis was first discovered by Dr. John William Ballantyne, a Scottish physician and obstetrician, in 1892.
Classification
Hydrops Fetalis may be classified into two groups based on the presence or absence of rhesus iso-immunization:
- Immune Hydrops Fetalis
- Non-Immune Hydrops Fetalis (NIHF)
Pathophysiology
- It is thought that hydrops fetalis is caused by conditions with either increased rate of fluid transudation from the vascular compartment or decreased lymphatic return to the circulation.
- This is shown to be originated from developmental defects in microcirculation and lymphatic system, respectively.
- The potential causes may be immune or non-immune, and they often result in anemia and further hypoxia.
- The sympathetic system becomes activated due to hypoxia, and it causes blood redistribution with decreased blood flow to the liver and kidneys.
- Decreased blood flow to the liver and kidneys, results in decreased albumin, increased ADH, and increased activity of RAAS.
- Following these changes, the central venous pressure increases, which further results in decreased lymphatic return.
- As a result, hydrops fetalis (the accumulation of fluid, or edema, in at least two fetal compartments) occurs.
- The pathophysiology of non-immune causes also depend on the underlying conditions, include:
- Decreased ventricular filling during diastole (i.e. tachyarrhythmias)
- Increased central venous pressure due to the increased right heart pressure (i.e. cardiac tumors and subendocardial fibroelastosis)
- Obstruction of lymphatic drainage due to a mass (i.e. cystic hygroma)
Causes
Hydrops Fetalis is caused by either immune or non-immune conditions.
- Immune hydrops fetalis
- Antibodies may occur due to the exposure of non-self RBC antigens during the previous pregnancy or transfusion.
- In the next pregnancy, these antibodies may attack the fetal erythrocytes if the fetus has that antigen.
- Following the red blood cell destruction, hemolytic disease of the fetus and newborn (HDFN) may occur with a wide range of clinical outcome from only mild anemia to high output heart failure and hydrops fetalis.
- Rh disease is the major cause for immune-mediated hydrops fetalis; however, owing to preventative methods developed in the 1970s, the incidence of Rh disease has markedly declined.
- Rh disease can be prevented by administration of anti-D IgG (Rho (D) Immune Globulin) injections to RhD-negative mothers during pregnancy and/or within 72 hours of the delivery.
- Non-immune hydrops fetalis (NIHF)
- Currently, with the decreased prevelance of Rh disease, non-immune causes are responsible for up to 90% of cases.
- The most common causes of non-immune hydrops fetalis are hematologic diseases, and chromosomal abnormalities, followed by lymphatic anomalies, and cardiovascular diseases. Causes of NIHF include:
- Structural cardiac malformations (especially hypoplastic left heart, endocardial cushion defect)
- Arrhythmias
- Congenital lymphatic dysplasia
- Chromosomal abnormalities (Turner Syndrome, trisomy 13, trisomy 18, trisomy 21)
- Alpha-thalassemia
- Fetomaternal transfusion
- Infections (Parvo-B19, CMV, Adenovirus, Enterovirus)
- Twin to twin transfusion syndrome (both donor and recipient fetus)
- Congenital cystic adenomatoid malformation
- Diaphragmatic hernia
- Extrapulmonary sequestration
- Hydrothorax
- Chylothorax
- Noonan Syndrome
- Urethral Obstruction
- Prune belly syndrome
- Lysosomal storage disease
- Vascular tumors
- Teratoma
- Leukemia
- Hepatic tumors
- Neuroblastoma
- Meconium peritonitis
- Gastrointestinal obstructions
Epidemiology and Demographics
- In developed countries, the incidence of non-immune hydrops fetalis (NIHF) is 25-79 per 100.000 live born infants worldwide.
- The median gestational age (GA) at diagnosis of NIHF is 23 weeks.
- Gestational age is predictive of mortality, as preterm infants with this condition are more likely to die.
- The case-fatality rate of NIHF is ranged from 43.2% to 78.2%.
Risk Factors
References