Hirschsprung disease, also known as congenital aganglionic megacolon, is a rare congenital disorder that affects the large intestine and causes problems with bowel movements. It is named after the Danish physician Harald Hirschsprung, who described the condition in 1888. In Hirschsprung disease, there is an absence of nerve cells, called ganglion cells, in a segment of the colon.
Ganglion cells are crucial in coordinating the rhythmic contractions that move stool through the intestines. Without these cells, the affected segment of the colon cannot relax and allow stool passage, leading to a blockage or obstruction. The absence of ganglion cells usually occurs in the lower part of the colon, closest to the anus, but it can also affect higher colon segments.
The length of the affected segment can vary, ranging from a small portion to the entire colon. Hirschsprung disease is typically present at birth, although it may not always be diagnosed immediately. Signs and symptoms may vary depending on the severity and length of the affected segment. Newborns with Hirschsprung disease may have difficulty passing stool, leading to constipation.
Epidemiology
Hirschsprung disease is a relatively rare condition, with an estimated incidence of about 1 in 5,000 live births. The prevalence can vary across different populations and ethnic groups. It is more commonly observed in males, with a male-to-female ratio of approximately 4:1. There is some evidence suggesting a genetic component to Hirschsprung disease. Approximately 10-15% of cases have a family history of the condition, indicating a potential hereditary pattern.
In these cases, the disease can be inherited autosomal dominant or recessive, depending on the genetic mutation involved. Certain gene mutations have been associated with Hirschsprung disease, including mutations in the RET, GDNF, EDNRB, and SOX10 genes. Hirschsprung disease can also occur as part of genetic syndromes, such as Down syndrome, Waardenburg syndrome, and others.
The presence of these syndromes increases the likelihood of developing Hirschsprung disease. Geographically, Hirschsprung disease has been reported worldwide, but its prevalence may vary among different populations. Some studies have suggested a higher incidence in specific populations, such as those of Asian or Native American descent, while lower rates have been observed in individuals of African descent.
Anatomy
Pathophysiology
The pathophysiology of Hirschsprung disease involves the absence or deficiency of ganglion cells in the affected segment of the colon. Ganglion cells coordinate the contractions that propel stool through the intestines. In Hirschsprung disease, the lack of ganglion cells causes a functional obstruction in the affected segment. During fetal development, ganglion cells normally migrate from the neural crest to populate the entire colon length.
In Hirschsprung disease, these cells fail to migrate properly, resulting in a segment of the colon lacking ganglion cells. This segment is called the aganglionic or transition zone. Without ganglion cells, the affected segment of the colon cannot relax and undergo the coordinated contractions necessary for normal bowel movements. As a result, stool cannot pass through this segment and becomes trapped, leading to an obstruction. The obstruction causes the colon to dilate proximal to the affected segment, a condition known as megacolon.
The degree of dilation can vary depending on the length and severity of the aganglionic segment. The absence of ganglion cells is thought to be due to genetic factors. Mutations in several genes have been associated with Hirschsprung disease, including the RET, GDNF, EDNRB, and SOX10 genes. These gene mutations disrupt the normal development and migration of ganglion cells during fetal development.
The functional obstruction caused by Hirschsprung disease can lead to various symptoms, including constipation, abdominal distension, vomiting, and poor feeding in newborns. In severe cases, the obstruction can result in enterocolitis, a potentially life-threatening condition characterized by inflammation and infection of the intestines.
Etiology
Genetic Factors: Hirschsprung disease can have a genetic component, and several gene mutations have been identified that are associated with the condition. The RET gene is the most commonly implicated gene, with mutations in RET accounting for most cases. Mutations in other genes, such as GDNF, EDNRB, and SOX10, have also been linked to Hirschsprung disease. These mutations disrupt the normal development and migration of ganglion cells in the colon during fetal development.
Neural Crest Development: During fetal development, the enteric nervous system, which controls the functioning of the digestive tract, originates from a group of cells called the neural crest. Disruptions in the migration or differentiation of neural crest cells can lead to the absence or deficiency of ganglion cells in the colon, resulting in Hirschsprung disease.
Environmental Factors: While the exact environmental factors contributing to Hirschsprung disease are not well understood, some studies have suggested associations with maternal smoking, maternal drug use, and certain medications taken during pregnancy. These factors may interact with genetic predispositions and contribute to the development of the disease.
Familial and Syndromic Cases: Hirschsprung disease can run in families, indicating a hereditary component. Approximately 10-15% of cases have a positive family history. In these cases, the condition may be inherited in an autosomal dominant or recessive manner, depending on the gene mutation. Hirschsprung disease can also occur as part of genetic syndromes, such as Down syndrome, Waardenburg syndrome, and others.
Genetics
Prognostic Factors
Clinical History
Clinical History
Prenatal History:
In some cases, prenatal ultrasound examinations may reveal signs of Hirschsprung disease, such as dilated loops of the intestines or absent peristalsis (the coordinated movement of the intestines).
Polyhydramnios, an excessive accumulation of amniotic fluid, may be observed in some cases due to impaired fetal swallowing and absorption of amniotic fluid.
Neonatal History:
Delayed passage of meconium: Infants with Hirschsprung disease often experience delayed passage or absence of meconium, the first stool passed by newborns.
Abdominal distension: The abdomen may appear swollen or distended due to the accumulation of stool in the obstructed segment of the colon.
Failure to pass stool: The absence of bowel movements or infrequent, difficult bowel movements may be noted.
Vomiting: Some infants may vomit bile or experience episodes of bilious vomiting.
Poor feeding and weight gain: Difficulties in feeding, inadequate weight gain, and failure to thrive may be observed due to feeding difficulties caused by the obstructed intestines.
Foul-smelling or explosive stools: When partial obstruction is present, stool may accumulate in the dilated portion of the colon and pass through rapidly, leading to explosive, foul-smelling stools.
Postnatal History:
Chronic constipation: As the child ages, chronic constipation may persist despite treatment or surgical intervention.
Recurrent enterocolitis: Enterocolitis, inflammation, and infection of the intestines can occur in individuals with Hirschsprung disease. It may present with symptoms such as fever, abdominal pain, diarrhea, and rectal bleeding.
Growth and developmental issues: In severe or untreated cases, growth, and developmental issues may arise due to ongoing bowel dysfunction and associated complications.
Physical Examination
Physical Examination
The abdomen may appear swollen or distended due to the accumulation of stool and gas in the obstructed segment of the colon. In some cases, a palpable mass may be felt in the rectum, particularly where the aganglionic segment is close to the anus. Upon digital rectal examination, the rectal vault may feel empty or lacking stool, a characteristic finding in Hirschsprung disease.
An important finding in Hirschsprung disease is the lack of relaxation of the anal sphincter during the rectal examination. The anal sphincter fails to relax due to the absence of ganglion cells responsible for coordinating the relaxation. Signs of enterocolitis, such as fever, abdominal tenderness, and foul-smelling explosive diarrhea, may be present.
These signs indicate inflammation and infection of the obstructed intestines. Infants with Hirschsprung disease may exhibit poor feeding, inadequate weight gain, and failure to thrive due to feeding difficulties caused by intestinal obstruction.
Age group
Associated comorbidity
Associated activity
Acuity of presentation
Differential Diagnoses
Differential Diagnoses
Intestinal Obstruction
Anal Stenosis
Laboratory Studies
Imaging Studies
Procedures
Histologic Findings
Staging
Treatment Paradigm
The primary treatment for Hirschsprung disease is surgical intervention. Surgery aims to remove the aganglionic segment of the colon and create a functional connection between the healthy colon and the anus. The specific surgical procedure performed depends on the length and location of the aganglionic segment. The most common surgical techniques include:
Pull-Through Procedure: The most widely used surgical approach is the pull-through procedure. This procedure involves removing the aganglionic portion of the colon and pulling down the healthy section of the colon to the anus. The pulled-through segment is then connected to the anus, allowing stool passage.
Swenson Procedure: The Swenson procedure is a variant of the pull-through procedure. It involves removing the aganglionic segment and pulling the healthy colon down to the anus. The difference is that the Swenson procedure preserves the internal anal sphincter, which helps maintain bowel control.
Soave Procedure: The Soave procedure is another variant of the pull-through procedure. It involves removing the aganglionic segment and replacing it with a segment of a healthy colon obtained from the inside layer of the colon. This procedure helps preserve the colon’s outer muscular layer, contributing to better bowel function.
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Hirschsprung disease, also known as congenital aganglionic megacolon, is a rare congenital disorder that affects the large intestine and causes problems with bowel movements. It is named after the Danish physician Harald Hirschsprung, who described the condition in 1888. In Hirschsprung disease, there is an absence of nerve cells, called ganglion cells, in a segment of the colon.
Ganglion cells are crucial in coordinating the rhythmic contractions that move stool through the intestines. Without these cells, the affected segment of the colon cannot relax and allow stool passage, leading to a blockage or obstruction. The absence of ganglion cells usually occurs in the lower part of the colon, closest to the anus, but it can also affect higher colon segments.
The length of the affected segment can vary, ranging from a small portion to the entire colon. Hirschsprung disease is typically present at birth, although it may not always be diagnosed immediately. Signs and symptoms may vary depending on the severity and length of the affected segment. Newborns with Hirschsprung disease may have difficulty passing stool, leading to constipation.
Hirschsprung disease is a relatively rare condition, with an estimated incidence of about 1 in 5,000 live births. The prevalence can vary across different populations and ethnic groups. It is more commonly observed in males, with a male-to-female ratio of approximately 4:1. There is some evidence suggesting a genetic component to Hirschsprung disease. Approximately 10-15% of cases have a family history of the condition, indicating a potential hereditary pattern.
In these cases, the disease can be inherited autosomal dominant or recessive, depending on the genetic mutation involved. Certain gene mutations have been associated with Hirschsprung disease, including mutations in the RET, GDNF, EDNRB, and SOX10 genes. Hirschsprung disease can also occur as part of genetic syndromes, such as Down syndrome, Waardenburg syndrome, and others.
The presence of these syndromes increases the likelihood of developing Hirschsprung disease. Geographically, Hirschsprung disease has been reported worldwide, but its prevalence may vary among different populations. Some studies have suggested a higher incidence in specific populations, such as those of Asian or Native American descent, while lower rates have been observed in individuals of African descent.
The pathophysiology of Hirschsprung disease involves the absence or deficiency of ganglion cells in the affected segment of the colon. Ganglion cells coordinate the contractions that propel stool through the intestines. In Hirschsprung disease, the lack of ganglion cells causes a functional obstruction in the affected segment. During fetal development, ganglion cells normally migrate from the neural crest to populate the entire colon length.
In Hirschsprung disease, these cells fail to migrate properly, resulting in a segment of the colon lacking ganglion cells. This segment is called the aganglionic or transition zone. Without ganglion cells, the affected segment of the colon cannot relax and undergo the coordinated contractions necessary for normal bowel movements. As a result, stool cannot pass through this segment and becomes trapped, leading to an obstruction. The obstruction causes the colon to dilate proximal to the affected segment, a condition known as megacolon.
The degree of dilation can vary depending on the length and severity of the aganglionic segment. The absence of ganglion cells is thought to be due to genetic factors. Mutations in several genes have been associated with Hirschsprung disease, including the RET, GDNF, EDNRB, and SOX10 genes. These gene mutations disrupt the normal development and migration of ganglion cells during fetal development.
The functional obstruction caused by Hirschsprung disease can lead to various symptoms, including constipation, abdominal distension, vomiting, and poor feeding in newborns. In severe cases, the obstruction can result in enterocolitis, a potentially life-threatening condition characterized by inflammation and infection of the intestines.
Genetic Factors: Hirschsprung disease can have a genetic component, and several gene mutations have been identified that are associated with the condition. The RET gene is the most commonly implicated gene, with mutations in RET accounting for most cases. Mutations in other genes, such as GDNF, EDNRB, and SOX10, have also been linked to Hirschsprung disease. These mutations disrupt the normal development and migration of ganglion cells in the colon during fetal development.
Neural Crest Development: During fetal development, the enteric nervous system, which controls the functioning of the digestive tract, originates from a group of cells called the neural crest. Disruptions in the migration or differentiation of neural crest cells can lead to the absence or deficiency of ganglion cells in the colon, resulting in Hirschsprung disease.
Environmental Factors: While the exact environmental factors contributing to Hirschsprung disease are not well understood, some studies have suggested associations with maternal smoking, maternal drug use, and certain medications taken during pregnancy. These factors may interact with genetic predispositions and contribute to the development of the disease.
Familial and Syndromic Cases: Hirschsprung disease can run in families, indicating a hereditary component. Approximately 10-15% of cases have a positive family history. In these cases, the condition may be inherited in an autosomal dominant or recessive manner, depending on the gene mutation. Hirschsprung disease can also occur as part of genetic syndromes, such as Down syndrome, Waardenburg syndrome, and others.
Clinical History
Prenatal History:
In some cases, prenatal ultrasound examinations may reveal signs of Hirschsprung disease, such as dilated loops of the intestines or absent peristalsis (the coordinated movement of the intestines).
Polyhydramnios, an excessive accumulation of amniotic fluid, may be observed in some cases due to impaired fetal swallowing and absorption of amniotic fluid.
Neonatal History:
Delayed passage of meconium: Infants with Hirschsprung disease often experience delayed passage or absence of meconium, the first stool passed by newborns.
Abdominal distension: The abdomen may appear swollen or distended due to the accumulation of stool in the obstructed segment of the colon.
Failure to pass stool: The absence of bowel movements or infrequent, difficult bowel movements may be noted.
Vomiting: Some infants may vomit bile or experience episodes of bilious vomiting.
Poor feeding and weight gain: Difficulties in feeding, inadequate weight gain, and failure to thrive may be observed due to feeding difficulties caused by the obstructed intestines.
Foul-smelling or explosive stools: When partial obstruction is present, stool may accumulate in the dilated portion of the colon and pass through rapidly, leading to explosive, foul-smelling stools.
Postnatal History:
Chronic constipation: As the child ages, chronic constipation may persist despite treatment or surgical intervention.
Recurrent enterocolitis: Enterocolitis, inflammation, and infection of the intestines can occur in individuals with Hirschsprung disease. It may present with symptoms such as fever, abdominal pain, diarrhea, and rectal bleeding.
Growth and developmental issues: In severe or untreated cases, growth, and developmental issues may arise due to ongoing bowel dysfunction and associated complications.
Physical Examination
The abdomen may appear swollen or distended due to the accumulation of stool and gas in the obstructed segment of the colon. In some cases, a palpable mass may be felt in the rectum, particularly where the aganglionic segment is close to the anus. Upon digital rectal examination, the rectal vault may feel empty or lacking stool, a characteristic finding in Hirschsprung disease.
An important finding in Hirschsprung disease is the lack of relaxation of the anal sphincter during the rectal examination. The anal sphincter fails to relax due to the absence of ganglion cells responsible for coordinating the relaxation. Signs of enterocolitis, such as fever, abdominal tenderness, and foul-smelling explosive diarrhea, may be present.
These signs indicate inflammation and infection of the obstructed intestines. Infants with Hirschsprung disease may exhibit poor feeding, inadequate weight gain, and failure to thrive due to feeding difficulties caused by intestinal obstruction.
Differential Diagnoses
Intestinal Obstruction
Anal Stenosis
The primary treatment for Hirschsprung disease is surgical intervention. Surgery aims to remove the aganglionic segment of the colon and create a functional connection between the healthy colon and the anus. The specific surgical procedure performed depends on the length and location of the aganglionic segment. The most common surgical techniques include:
Pull-Through Procedure: The most widely used surgical approach is the pull-through procedure. This procedure involves removing the aganglionic portion of the colon and pulling down the healthy section of the colon to the anus. The pulled-through segment is then connected to the anus, allowing stool passage.
Swenson Procedure: The Swenson procedure is a variant of the pull-through procedure. It involves removing the aganglionic segment and pulling the healthy colon down to the anus. The difference is that the Swenson procedure preserves the internal anal sphincter, which helps maintain bowel control.
Soave Procedure: The Soave procedure is another variant of the pull-through procedure. It involves removing the aganglionic segment and replacing it with a segment of a healthy colon obtained from the inside layer of the colon. This procedure helps preserve the colon’s outer muscular layer, contributing to better bowel function.
medtigo
Hirschsprung Disease
Updated :
July 2, 2023
Hirschsprung disease, also known as congenital aganglionic megacolon, is a rare congenital disorder that affects the large intestine and causes problems with bowel movements. It is named after the Danish physician Harald Hirschsprung, who described the condition in 1888. In Hirschsprung disease, there is an absence of nerve cells, called ganglion cells, in a segment of the colon.
Ganglion cells are crucial in coordinating the rhythmic contractions that move stool through the intestines. Without these cells, the affected segment of the colon cannot relax and allow stool passage, leading to a blockage or obstruction. The absence of ganglion cells usually occurs in the lower part of the colon, closest to the anus, but it can also affect higher colon segments.
The length of the affected segment can vary, ranging from a small portion to the entire colon. Hirschsprung disease is typically present at birth, although it may not always be diagnosed immediately. Signs and symptoms may vary depending on the severity and length of the affected segment. Newborns with Hirschsprung disease may have difficulty passing stool, leading to constipation.
Hirschsprung disease is a relatively rare condition, with an estimated incidence of about 1 in 5,000 live births. The prevalence can vary across different populations and ethnic groups. It is more commonly observed in males, with a male-to-female ratio of approximately 4:1. There is some evidence suggesting a genetic component to Hirschsprung disease. Approximately 10-15% of cases have a family history of the condition, indicating a potential hereditary pattern.
In these cases, the disease can be inherited autosomal dominant or recessive, depending on the genetic mutation involved. Certain gene mutations have been associated with Hirschsprung disease, including mutations in the RET, GDNF, EDNRB, and SOX10 genes. Hirschsprung disease can also occur as part of genetic syndromes, such as Down syndrome, Waardenburg syndrome, and others.
The presence of these syndromes increases the likelihood of developing Hirschsprung disease. Geographically, Hirschsprung disease has been reported worldwide, but its prevalence may vary among different populations. Some studies have suggested a higher incidence in specific populations, such as those of Asian or Native American descent, while lower rates have been observed in individuals of African descent.
The pathophysiology of Hirschsprung disease involves the absence or deficiency of ganglion cells in the affected segment of the colon. Ganglion cells coordinate the contractions that propel stool through the intestines. In Hirschsprung disease, the lack of ganglion cells causes a functional obstruction in the affected segment. During fetal development, ganglion cells normally migrate from the neural crest to populate the entire colon length.
In Hirschsprung disease, these cells fail to migrate properly, resulting in a segment of the colon lacking ganglion cells. This segment is called the aganglionic or transition zone. Without ganglion cells, the affected segment of the colon cannot relax and undergo the coordinated contractions necessary for normal bowel movements. As a result, stool cannot pass through this segment and becomes trapped, leading to an obstruction. The obstruction causes the colon to dilate proximal to the affected segment, a condition known as megacolon.
The degree of dilation can vary depending on the length and severity of the aganglionic segment. The absence of ganglion cells is thought to be due to genetic factors. Mutations in several genes have been associated with Hirschsprung disease, including the RET, GDNF, EDNRB, and SOX10 genes. These gene mutations disrupt the normal development and migration of ganglion cells during fetal development.
The functional obstruction caused by Hirschsprung disease can lead to various symptoms, including constipation, abdominal distension, vomiting, and poor feeding in newborns. In severe cases, the obstruction can result in enterocolitis, a potentially life-threatening condition characterized by inflammation and infection of the intestines.
Genetic Factors: Hirschsprung disease can have a genetic component, and several gene mutations have been identified that are associated with the condition. The RET gene is the most commonly implicated gene, with mutations in RET accounting for most cases. Mutations in other genes, such as GDNF, EDNRB, and SOX10, have also been linked to Hirschsprung disease. These mutations disrupt the normal development and migration of ganglion cells in the colon during fetal development.
Neural Crest Development: During fetal development, the enteric nervous system, which controls the functioning of the digestive tract, originates from a group of cells called the neural crest. Disruptions in the migration or differentiation of neural crest cells can lead to the absence or deficiency of ganglion cells in the colon, resulting in Hirschsprung disease.
Environmental Factors: While the exact environmental factors contributing to Hirschsprung disease are not well understood, some studies have suggested associations with maternal smoking, maternal drug use, and certain medications taken during pregnancy. These factors may interact with genetic predispositions and contribute to the development of the disease.
Familial and Syndromic Cases: Hirschsprung disease can run in families, indicating a hereditary component. Approximately 10-15% of cases have a positive family history. In these cases, the condition may be inherited in an autosomal dominant or recessive manner, depending on the gene mutation. Hirschsprung disease can also occur as part of genetic syndromes, such as Down syndrome, Waardenburg syndrome, and others.
Clinical History
Prenatal History:
In some cases, prenatal ultrasound examinations may reveal signs of Hirschsprung disease, such as dilated loops of the intestines or absent peristalsis (the coordinated movement of the intestines).
Polyhydramnios, an excessive accumulation of amniotic fluid, may be observed in some cases due to impaired fetal swallowing and absorption of amniotic fluid.
Neonatal History:
Delayed passage of meconium: Infants with Hirschsprung disease often experience delayed passage or absence of meconium, the first stool passed by newborns.
Abdominal distension: The abdomen may appear swollen or distended due to the accumulation of stool in the obstructed segment of the colon.
Failure to pass stool: The absence of bowel movements or infrequent, difficult bowel movements may be noted.
Vomiting: Some infants may vomit bile or experience episodes of bilious vomiting.
Poor feeding and weight gain: Difficulties in feeding, inadequate weight gain, and failure to thrive may be observed due to feeding difficulties caused by the obstructed intestines.
Foul-smelling or explosive stools: When partial obstruction is present, stool may accumulate in the dilated portion of the colon and pass through rapidly, leading to explosive, foul-smelling stools.
Postnatal History:
Chronic constipation: As the child ages, chronic constipation may persist despite treatment or surgical intervention.
Recurrent enterocolitis: Enterocolitis, inflammation, and infection of the intestines can occur in individuals with Hirschsprung disease. It may present with symptoms such as fever, abdominal pain, diarrhea, and rectal bleeding.
Growth and developmental issues: In severe or untreated cases, growth, and developmental issues may arise due to ongoing bowel dysfunction and associated complications.
Physical Examination
The abdomen may appear swollen or distended due to the accumulation of stool and gas in the obstructed segment of the colon. In some cases, a palpable mass may be felt in the rectum, particularly where the aganglionic segment is close to the anus. Upon digital rectal examination, the rectal vault may feel empty or lacking stool, a characteristic finding in Hirschsprung disease.
An important finding in Hirschsprung disease is the lack of relaxation of the anal sphincter during the rectal examination. The anal sphincter fails to relax due to the absence of ganglion cells responsible for coordinating the relaxation. Signs of enterocolitis, such as fever, abdominal tenderness, and foul-smelling explosive diarrhea, may be present.
These signs indicate inflammation and infection of the obstructed intestines. Infants with Hirschsprung disease may exhibit poor feeding, inadequate weight gain, and failure to thrive due to feeding difficulties caused by intestinal obstruction.
Differential Diagnoses
Intestinal Obstruction
Anal Stenosis
The primary treatment for Hirschsprung disease is surgical intervention. Surgery aims to remove the aganglionic segment of the colon and create a functional connection between the healthy colon and the anus. The specific surgical procedure performed depends on the length and location of the aganglionic segment. The most common surgical techniques include:
Pull-Through Procedure: The most widely used surgical approach is the pull-through procedure. This procedure involves removing the aganglionic portion of the colon and pulling down the healthy section of the colon to the anus. The pulled-through segment is then connected to the anus, allowing stool passage.
Swenson Procedure: The Swenson procedure is a variant of the pull-through procedure. It involves removing the aganglionic segment and pulling the healthy colon down to the anus. The difference is that the Swenson procedure preserves the internal anal sphincter, which helps maintain bowel control.
Soave Procedure: The Soave procedure is another variant of the pull-through procedure. It involves removing the aganglionic segment and replacing it with a segment of a healthy colon obtained from the inside layer of the colon. This procedure helps preserve the colon’s outer muscular layer, contributing to better bowel function.
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