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Malformations and Deformations: 1. Cleft lip, gross 2. Lateral cleft lip, gross 3. Facial abnormalities, gross 4. Hands with abnormal crease, gross 5. Omphalocele, gross 6. Gastroschisis, gross 7. Limb-body wall complex, gross 8. Limb-body wall complex, gross 9. Alobar holoprosencephaly, gross 10. Semilobar holoprosencephaly, gross 11. Holoprosencephaly, gross 12. Hydranencephaly, gross 13. Syndactyly, hand and foot, gross 14. Syndactyly, hand, gross 15. Bowel atresia, gross 16. Duodenal atresia, gross 17. Colonic atresia, gross 18. Tracheo-esophageal fistula and atresia, gross 19. Sirenomelia, gross 20. Intrauterine fetal demise, external features, gross 21. Recessive polycystic kidney disease, gross 22. Diaphragmatic hernia, gross 23. Diaphragmatic hernia, gross 24. Renal agenesis, gross 25. 'Potter facies' from oligohydramnios, gross 26. 'Potter facies' and 'glove-like' hand from oligohydramnios, gross
27. Normal chest cavity, gross 28. Pulmonary hypoplasia, gross 29. Pulmonary hypoplasia, microscopic 30. Varus deformities, feet, gross 31. 'Rocker bottom' foot, gross 32. Clenched hand, gross 33. Hydrops fetalis, gross Abnormalities of Twinning: 34. Siamese twins (craniothoracopagus), gross 35. Siamese twins (thoracopagus ), gross 36. Acardius acephalus (chorangiopagus parasiticus), gross 37. Acardius anceps (chorangiopagus parasiticus), gross 38. Twin-twin transfusion syndrome, gross Neural Tube Defects: 39. Meningomyelocele, gross 40. Meningomyelocele, gross 41. Anencephaly, gross 42. Anencephaly, gross 43. Anencephaly, gross 44. Iniencephaly, gross 45. Rachischisis, gross 46. Iniencephaly, encephalocele, rachischisis, gross 47. Exencephaly, gross Pediatric Neoplasia: 48. Nasopharyngeal teratoma, congenital, gross 49. Teratoma, congenital, low power microscopic 50. Lymphangioma, congenital, gross 51. Lymphangioma, congenital, medium power microscopic 52. Lymphangioma, congenital, medium power microscopic 53. Hemangioma, congenital, gross 54. Wilms tumor, gross
55. Wilms tumor, medium power microscopic 56. Neuroblastoma, gross 57. Neuroblastoma, medium power microscopic 58. Rhabdomyosarcoma, low power microscopic 59. Rhabdomyosarcoma, medium power microscopic Congenital Infections: 60. Congenital syphilis, gumma in heart, gross 61. Spirochetes (Treponema pallidum), microscopic 62. Cytomegalovirus, congenital, kidney, microscopic 63. Parvovirus, congenital, spleen, microscopic 64. Congenital pneumonia, microscopic Complications of Prematurity: 65. Hyaline membrane disease, lung, microscopic 66. Bronchopulmonary dysplasia, lung, microscopic 67. Germinal matrix, brain, normal and with hemorrhage, low power 68. 69. 70. 71. 72.
microscopic Intraventricular hemorrhage, gross Intraventricular hemorrhage, severe, gross Kernicterus, brain, gross Neonatal necrotizing enterocolitis (NEC), gross Neonatal necrotizing enterocolitis (NEC) and normal bowel, low power microscopic
73. Pyloric stenosis, gross 74. Meconium ileus, gross 75. Meconium ileus with peritonitis, gross 76. Hirschsprung disease, gross 77. Pneumatosis intestinalis, microscopic 78. Normal skin with hair, gross 79. Accessory spleens, gross 80. Postmaturity with prominent fingernails, gross
medium power microscopic 86. low power microscopic 84. gross 82. Thymus with macrophages. Subgaleal hemorrhage. gross 83. gross 85.81. Maceration. high power microscopic . Meconium aspiration. Meconium aspiration. Fetal chest with thymus.
. You must note the presence of any anomalies. The anomaly seen in this photograph. The presence of one anomaly suggests that additional anomalies may be present. a large bilateral cleft lip. as well as detail size and gestational age. is not so subtle. Call a clinical geneticist for consultation. but some anomalies are. including internal anomalies such as congenital cardiac defects that may be life-threatening.Examination of a stillborn fetus or neonate should consist of a careful and detailed physical examination.
and a karyotype revealed 47. XY. the constellation of anomalies suggested a possible chromosomal anomaly.Here is a lateral cleft in a child with multiple congenital anomalies. . In this case. +18 (trisomy 18).
. with micrognathia.The facial features shown in the 3rd trimester fetus above and the 2nd trimester fetus below are typical for trisomy 18 (e. The face is small in proportion to the head. XY. . 47. +18).g.
There is an abnormal transverse crease across the palm of each hand seen here. Together with the single flexion crease on the 5th digit, this is quite typical for trisomy 21 (e.g., 47, XX, +21).
Here is a ventral abdominal wall defect. This defect involves the region of the umbilical cord, so this is an omphalocele. Note that there is a thin membrane covering the herniated abdominal contents (loops of bowel can be seen under the membrane). This defect would have to be repaired over a period of time. Since the bowel has mainly developed outside of the abdominal cavity, it is malrotated and the cavity is not properly formed (too small).
stomach. This is a gastroschisis. . and liver are herniated outside the abdominal cavity.This is large lateral abdominal wall defect does not involve the umbilical cord and is not covered by a membrane. Much of the bowel.
Not seen here are craniofacial clefts and defects that can also occur with LBW complex.This is a gastroschisis in association with a limb-body wall (LBW) complex. . Seen here in association with LBW complex are reductions of the extremities. particularly the left upper extremity. and scoliosis. This complex is sometimes called "amnionic band syndrome" but such bands may only be present in half of cases of LBW complex.
The bands. may arise from early embryonic disruption with formation of adhesions and subsequent abnormal formation and loss of structures such as extremities and abdominal wall.This is limb-body wall (LBW) complex with constricting amnionic bands. as well as the other defects. .
Hence. This condition may be associated with trisomy 13. The "alobar" form of holoprosencephaly is shown here in which there a single large ventricle. because there is no attempt to form separate cerebral hemispheres. etc) accompanying this condition. cleft palate. there are usually midline facial defects (cleft lip. . often accompanied by the failure of fetal facial midline structures to form properly. cyclopia. It may rarely occur in association with maternal diabetes mellitus.This is holoprosencephaly.
with maternal diabetes mellitus. Holoprosencephaly can be associated with chromosomal anomalies (such as trisomy 13). and can be seen sporadically. . because there is a small cleft representing an attempt to separate the hemispheres.The skull is opened here to reveal the "semilobar" form of holoprosencephaly. There is no gyral pattern here because this stillborn fetus was under 20 weeks gestation. Holoprosencephaly is a grave condition with little or no brain function.
Here is a cross section though a brain with holoprosencephaly. Toward the base of the brain are the fused thalami typical of this process. revealing a single ventricle. .
.This is hydranencephaly. because an intrauterine vascular accident involving the brain led to lack of blood flow and subsequent loss of cerebral tissue. The brain is essentially a bag of water.
Most of these syndromes do not have a specific genetic defect yet defined. Below. Seen above are the digits of the hand fused together.Syndactyly represents fusion of two or more digits. partially fused digits. It can be an isolated finding or part of syndromes that define patterns of anomalies. the foot has rudimentary. . though some do.
. This particular pattern can be seen with triploidy (69 chromosomes).Here is an example of syndactyly in which the 3rd and 4th fingers are fused into one large digit.
This is atresia of the bowel. since the swallowing and absorption of amniotic fluid by the fetus is impaired. like many anomalies. often happens along with other anomalies.The meconium-filled bowel ends in a blind pouch. . Such a defect. Bowel atresias are accompanied by polyhydramnios.
. liver. Interestingly. few cases of Down syndrome have duodenal atresia. half of all duodenal atresias occur with Down syndrome.There is a point of marked narrowing indicative of congenital duodenal atresia depicted here. although conversely. By ultrasound. there is a "double bubble" sign from duodenal enlargement proximal to the atresia accompanying the normal stomach bubble. and gallbladder are seen here as well. The normal esophagus.
The right testis and the left testis are cryptorchid. and the term "multiple congenital anomalies" applies. .This is a colonic atresia accompanied by additional anomalies. The presence of one anomaly suggests that others are present as well. and there is absence of the penis. including a persistent cloaca that resulted from failure of the urogenital septum to form.
. The esophageal atresia is present in the mid-esophagus. The tracheoesophageal fistula is located below the carina.This is a tracheo-esophageal fistula with esophageal atresia.
The term comes from "siren" or "mermaid" because of the characteristic fusion of the lower extremities that results from a failure in the development of a normal vascular supply to lower extremities from the lower aorta in utero. .This is sirenomelia.
It was idiopathic in this case. it is very important that pregnant mothers be advised that drugs (including cigarette smoking and alcohol consumption) may have profound effects on the fetus.The first thing to notice is the features of intrauterine fetal demise: skin slippage and reddening. but in the 1950's the drug thalidomide was responsible for many cases when pregnant women took it. Thus. These features are those of maceration and not trauma or birth defect. known as phocomelia. . Note the shortened lower extremities.
This is an example of autosomal recessive polycystic kidney disease (ARPKD). .The two enormous masses beneath the liver are cystic kidneys.
Below the stomach is a dark spleen (at the white arrow). the diaphragmatic dome is missing on the left. which has been displaced by the stomach. The white arrow overlies the left lobe of liver which is extending upward. allowing herniation of the abdominal contents into the chest cavity. The metal probe in the photograph is behind the left lung. .In this case.
most are associated with multiple anomalies. . Though diaphragmatic hernia may occur as an isolated defect that is potentially repairable. The herniating liver has become tilted vertically. Incursion of abdominal contents into the chest cavity will result in pulmonary hypoplasia.A diaphragmatic hernia on the left allows herniation of bowel into the left chest cavity. and often with chromosomal abnormalities.
diminished lung development. and this renal agenesis will result in oligohydramnios. and pulmonary hypoplasia. because amniotic fluid is mainly derived from fetal urine.Agenesis refers to the absence of formation of a body part in embryogenesis. The oligohydramnios leads to deformations such as a constricted chest. Here the kidneys are absent from the retroperitoneum. .
This is an example of a deformation sequence in which an anomaly (here the lack of normal kidneys) leads to lack of fetal urine output with resultant oligohydramnios that causes deformation through constraint.This baby demonstrates the typical "Potter's facies" with prominent infraorbital folds resulting from oligohydramnios in utero. .
like a loose glove. The umbilical cord may be short. Oligohydramnios restricts fetal movement.Seen in the right panel is the characteristic facial appearance with oligohydramnios. with prominent infraorbital creases and a flattened nose. . In the left panel the hand appears to have excessive skin folds.
Note the prominent pink thymus above the heart in the mediastinum. Note the size of the heart in relation to the lungs and chest cavity. . The diaphragmatic leaves are intact. The liver is normally quite large in neonates in relation to other organs.This is the normal appearance of the chest cavity in a neonate.
but in utero the constriction from diminished amnionic fluid would have decreased the chest cavity size. Note the extremely small lungs in this case on each side of the heart in the middle of the chest.The most serious consequence of oligohydramnios is pulmonary hypoplasia. The chest cavity is opened here at autopsy and the lung appear small in comparison to chest size. .
This results in insufficient gas exchange from respiration following birth. in this premature baby with pulmonary hypoplasia from oligohydramnios. only tubular bronchioles incapable of significant gas exchange.Microscopic examination of the lung reveals no alveolar development. .
The feet are turned inward. .Deformation from constraint with oligohydramnios in utero can result in the appearance of the club feet (varus deformity) seen here.
. Such an anomaly may suggest a chromosomal abnormality such as trisomy 18.This is the appearance of a "rocker bottom" foot with a prominent calcaneus and rounded bottom.
.These are clenched hands resulting from camptodactyly (fingers bent over) and clinodactyly (fingers inclined to one side or the other). This particular appearance is very suggestive of trisomy 18.
. is not common when Rh immune globulin is employed in cases of potential Rh incompatibility. There are many causes for fetal hydrops. and congenital anomalies. congestive failure (from anemia or cardiac abnormalities).Generalized edema from fluid collection in the soft tissues results in hydrops fetalis. The most common are "non-immune" types that include infections. from maternal antibody formed against fetal red blood cells. Immune hydrops.
and the hearts and gastrointestinal tracts are fused as well. or twins joined at the head and chest. The location and amount of fusion can vary. The popular term is "siamese" twins. There is only one brain.This is an uncommon complication of monozygous twinning in which there is fusion of the twins. . The scientific term applicable in the case shown here is craniothoracopagus.
This is an example of thoracopagus. Note the large omphalocele in the lower abdomen shared by these monozygous twins. These twins shared a heart and liver and several other organs were partially fused. Attempts at separation of such twins can either be viewed as heroic new technology or expensive futility. The survival rate with significant fusion of organs is essentially nil.
This is another abnormality of twinning in which one fetus is essentially a poorly formed blob attached to, or separate from, a complete fetus. This condition is called acardius-acephalus because there is typically no heart or brain in the "blob" twin. The photograph here reveals an acardiac twin that consists mainly of just lower extremities. Such a non-viable twin can be surgically removed.
This is a more complete acardiac twin in which actual body regions are present. There were few poorly formed internal organs present. Nonetheless, it is non-viable.
. there is diminished blood flow to one twin (the "donor") and increased blood flow to the other twin (the "recipient"). then a twin-twin transfusion syndrome can develop. The pale appearing donor is smaller and may die for lack of sufficient blood flow. In this condition.If there is a vascular connection across a monochorionic twin placenta. the larger plethoric recipient may die from congestive heart failure. More commonly.
with failure of the vertebral body to completely form.Neural tube defects are are one of the more common congenital anomalies to occur. Such defects result from improper embryonic neural tube closure. Here is a large meningomyelocele in which the defect is large enough to allow meninges and a portion of spinal cord to protrude through the defect. . Such defects can be suggested by an elevated maternal serum alphafetoprotein (MSAFP). but the defect is not open. can include a meningocele. Open neural tube defects with lack of a skin covering. in which meninges protrude through the defect. The most minimal defect is called spina bifida.
This is a fetus from a termination of pregnancy via dilation and extraction. . Note the large neural tube defect in the lower back. which is done in the second trimester.
Note that this fetus died in utero-there are signs of maceration. with skin slippage and reddening.This is anencephaly. The brain cannot form properly when exposed to amniotic fluid. This condition occurs when there is failure of formation of the fetal cranial vault. .
Supplementing the maternal diet with folate prior to and during pregnancy can reduce the incidence of neural tube defects. .Note the absence of the cranial vault in this fetus with anencephaly.
Note the low set external ear. .The eyes appear proptotic with anencephaly because of the lack of the skull.
. The head is tilted back.This is a slight variation of a neural tube defect known as iniencephaly in which there is lack of proper formation of occipital bones with a short neck and defect of the upper cord.
.A severe rachischisis is shown here in a fetus that also has iniencephaly.
This fetus also has a retroflexed head from iniencephaly. The encephalocele extends down to partially cover a rachischisis on the back. .Seen protruding from the back of the head is a large encephalocele that merges with the scalp above.
but a brain is present. Such an event is very rare.This form of neural tube defect is known as exencephaly. The cranial vault is not completely present. because it was not completely exposed to amniotic fluid. which results from early amnion disruption. . It may be part of craniofacial clefts associated with the limb-body wall complex.
Shown here is a large nasopharyngeal teratoma that is protruding from the oral cavity. .Congenital and pediatric neoplasms are uncommon. One type that can occur is a teratoma.
and a colonic gland (endoderm) at the right.The microscopic appearance of a teratoma is seen here. . or child. cartilage (mesoderm) at the bottom left center. infant. can become a large mass that has severe consequences for a small fetus. The three embryologic germ layers are represented by skin (ectoderm) at the top. though benign from a microscopic standpoint. This neoplasm.
. This congenital neoplasm turned out to be a lymphangioma.There is a large mass involving the left upper arm and left chest of this fetus.
with large lymphatic spaces lined by a thin endothelium. . The adjacent stroma has lymphoid nodules. Lymphangiomas in the pediatric age range tend to involve head. neck.Here is the microscopic appearance of the lymphangioma at medium power. and chest.
such lesions tend to be poorly circumscribed and extend widely into surrounding soft tissues. However. the histologically benign nature of the lymphangioma is apparent.At high magnification. making their surgical removal difficult. There are enlarged lymphatic spaces lined by a thin endothelium. .
.Beneath the skin surface at the left are many dilated vascular channels filled with many red blood cells. This is a neoplasm known as a hemangioma.
About a fourth of cases are associated with hypertension. . Over 90% of Wilms tumors are diagnosed during the first 6 years of life.This lobulated tan-white mass involving the kidney of a child is a Wilms tumor. It manifests most often as an abdominal mass.
. Wilms tumor is associated with mutations involving the WT1 tumor suppressor gene on chromosome 11. with primitive glomeruloid structures and a cellular stroma.Wilms tumor microscopically resembles the primitive nephrogenic zone of the fetal kidney. This neoplasm is very treatable with an excellent prognosis and >80% cure rate overall.
This is the gross appearance of a neuroblastoma arising in the right adrenal gland. and 75% of cases are diagnosed in children less than 4 years old. . It is the most common pediatric malignancy in infancy. These tumors most often present as an abdominal or mediastinal mass.
Histologic variations. neuroblastoma is a "small round blue cell" tumor. as well as staging and cytogenetic characteristics help to determine the prognosis.Microscopically. .
The alveolar variant is shown here. This malignant neoplasm has skeletal muscle derivation. . These neoplasms occur most frequently in the head and neck area.A rare neoplasm that appears most commonly in the first decade of life is the rhabdomyosarcoma. as well as the genitourinary tract.
This alveolar rhabdomyosarcoma is composed of primitive round blue cells (rhabdomyoblasts) arranged in nests with spaces and surrounded by a fibrous stroma. A variant of this neoplasm seen in the genital tract is the sarcoma botryoides. .
Syphilis can be acquired in utero in the third trimester.S.This is an example of a granulomatous process known as a "gumma" in a case of congenital syphilis. The gumma shown here is located in the heart of a fetus. Congenital syphilis is increasing in incidence in the U. .
These are Treponema pallidum organisms and are the causative agents for syphilis. .Spirochetes are seen here.
The inclusions may appear in the urine of a liveborn infant with CMV. .Here within the tubular epithelium of a fetal kidney can be seen many large violet intranuclear inclusions characteristic cof congenital cytomegalovirus (CMV) infection.
but pregnant women can pass the virus to the fetus. or "fifth" disease. the illness often goes unnoticed. In adults. produces a mild illness in children. where it may produce marked fetal anemia and hydrops in some cases. Parvovirus. .The large pink inclusion in the erythroid precursor seen here in fetal spleen is evidence for parvovirus infection. marked by a "slapped cheek" facial rash.
. Seen here is a congenital pneumonia with many neutrophils filling immature bronchioles.One of the most common forms of perinatal congenital infection arises from bacterial agents that ascend the birth canal and may be seen in association with premature rupture of membranes (PROM) and acute chorioamnionitis.
.This is hyaline membrane disease due to prematurity and lack of surfactant production from type II pneumonocytes within the immature lung. Note the thick pink membranes lining the alveolar spaces.
there is interstitial fibrosis and inadequate alveolar development for good pulmonary function.A later complication of prematurity should the baby survive the immediate neonatal period. Respiratory distress can continue for months to years. during which time mechanical ventilation was necessary. . is bronchopulmonary dysplasia (BPD). With BPD.
The dense layer of small dark blue cells seen here below the ependyma of the lateral ventricle is the germinal matrix. . If severe and if survival occurs. mainly between 22 and 30 weeks gestation. the hemorrhage may organize and lead to obstructive hydrocephalus. The germinal matrix is a highly cellular and highly vascularized region from which cells migrate out during brain development. A germinal matrix hemorrhage is shown below. This area is highly vulnerable to birth injury and changes in blood pressure following birth.
including difficulty regulating blood pressure.This coronal section of a premature neonatal brain shows intraventricular hemorrhage (IVH) extending from a germinal matrix hemorrhage. Such hemorrhages can be devastating. . Such hemorrhages occur from a variety of factors that afflict neonates.
and extending down the third ventricle and out into the subarachnoid space. . extending into brain parenchyma.Intraventricular hemorrhage (IVH) can be minimal. The prognosis is grim. but can also be severe as shown here with blood filling and distending all of the lateral ventricles.
MD. There is a coronal section of medulla on the left and cerebral hemisphere on the right demonstrating kernicterus in deep grey matter of hemisphere and brain stem. [Image contributed by Jeannette J. low birth weight. Increased unconjugated bilirubin. and increased bilirubin levels.The yellow staining in the brain of a neonate is known as kernicterus. Kernicterus is more likely to occur with prematurity. Townsend. is toxic to the brain tissue. which accounts for the kernicterus. University of Utah] .
MD. [Image contributed by Ted Pysher. Seen at autopsy here is a dark red appearance to the small intestine of a premature neonate.A complication of prematurity and low birth weight is neonatal necrotizing enterocolitis (NEC) in which ischemia results in focal to confluent areas of bowel necrosis. most often in the terminal ileum. University of Utah] .
beginning in the mucosa and extending to involve the muscular wall.The clinical manifestations of neonatal necrotizing enterocolitis (NEC) in premature neonates include abdominal distension. Compared to normal bowel at the left. . with the potential for perforation. ileus. and bloody stool at several days of age. bowel involved by NEC at the right shows hemorrhagic necrosis.
Males are affected more than females. . and contain the enzyme heme oxygenase-2 which generates carbon monoxide (CO) as a neurotransmitter to cause relaxation in adjacent smooth muscle cells. The overall incidence is approximately 3 per 1000 livebirths.This is pyloric stenosis. Note the prominent hypertrophied muscle with elongation and narrowing of the pylorus at the gastric outlet on the left. The lack of ICCs in pyloric stenosis results in deficient CO production leading to motility dysfunction. Pyloric stenosis is uncommon. but is a cause for "projectile" vomiting in an infant about 3 to 6 weeks of age. The "pacemaker" interstitial cells of Cajal (ICC) regulate motility.
and little or no meconium is passed per rectum. the abnormal pancreatic secretions lead to inspissated meconium that produces intestinal obstruction. The dilated coils of ileum are opened here to reveal the inspissated green meconium (which may also be tarry or gritty). University of Utah] . In cystic fibrosis. MD. [Image contributed by Ted Pysher.Meconium ileus is most often seen in the first few days of life in neonates with cystic fibrosis. while the unopened colon at the upper left and the appendix at the lower left beyond the ileocecal valve are not dilated. but can rarely occur in infants with a normal pancreas.
which produces a chemical peritonitis. Another complication of meconium ileus is volvulus. Calcifications in the spilled meconium may be seen radiographically.Meconium peritonitis shown here as a greenish exudate overlying the serosal surfaces of the peritoneal cavity can complicate meconium ileus in utero. The bowel ruptures and leaks meconium. MD. University of Utah] . particularly in fetuses with cystic fibrosis. [Image contributed by Ted Pysher.
Multiple genetic mutations have been found. Infants with the disease may have alternating diarrhea and constipation. Hirschsprung disease is thought to result from mutation of susceptible genes interacting with environmental and other factors. Colonic perforation may occur. but about half of familial cases and 15% of sporadic cases are associated with RET gene mutations that inactivate RET receptor kinase activity. It has a 4:1 . Hirschsprung disease results from an absence of ganglion cells in both submucosal and myenteric plexuses and can occur in either a segment of colon (short segment disease) or the entire colon (long segment disease). resulting in variable penetrance. The aganglionic segment becomes narrowed. Mucosal damage and secondary infection may follow. with fever and diarrhea. while children mainly have constipation.Shown here is dilation of bowel (megacolon) proximal to the affected region of narrowing at the lower left center in sigmoid colon. Affected newborns may develop focal inflammation at the point of obstruction. Treatment consists of surgical correction with resection of the aganglionic segment. The incidence of Hirschsprung disease is 1 in 5000 livebirths. RET promotes survival and growth of neurites and provides direction to migrating neural crest cells. with proximal dilation. causing obstruction.
while the rarer long segment disease predominates in females.male to female predominance. . Short segment disease is more common in males.
.Pneumatosis intestinalis is a rare finding in which gas-filled cysts appear in submucosa. as in this case. The gas may dissect into submucosa or may be generated by bacteria. It may complicate necrotizing enterocolitis.
The skin is soft and the hair is fine in a normal newborn. as seen here. .
.The accessory spleens seen here at the hilum of the normal-sized spleen are not uncommon and by themselves have no significance.
There are few changes indicative of postmaturity (gestation beyond 42 weeks). Here are long fingernails that can be seen with postmaturity. .
Seen here is one of the earliest changes (within half a day) which is slippage of the skin. the skin becomes reddened. . As this process advances.Death of the fetus in utero is accompanied by changes of maceration.
and liver are seen here as well. diaphragm. The thymus is a large structure with the important job of developing the cell-mediated immune system with T-cells. . heart. The right lung.The normal fetal chest at term is shown here.
Note the "starry sky" appearances here from increased macrophages. One of the earliest changes seen is an increase in cortical macrophages.Stress from a variety of illnesses in the fetus and neonate may be manifested with thymic involution. typical in 1 to 2 days following the onset of illness. .
The neonatal scalp is reflected at autopsy to reveal dark red blood beneath the galea aponeurotica (dense connective tissue of scalp) and over the cranium. This is subgaleal hemorrhage and it is fairly common during the birth process. .
Rugby ball shaped balls of meconium as well as numerous "squames" from fetal skin are seen here. . Fetal distress also leads to reflex gasping efforts by the baby. A clue to this occurrence is greenish staining of fetal skin or fetal surface of the placenta. with the result that the meconium in the amniotic cavity is aspirated into the lungs. typically when there is fetal distress with loss of anal sphincter tone and passage of meconium into amniotic fluid. The worst consequence of meconium spillage is meconium aspiration into the lungs.Meconium spillage is a complication seen at or near term.
small rounded balls of meconium are seen in an alveolus. Meconium is an irritant that leads to respiratory distress. At birth. tracheal suction and lung lavage may be useful to help remove the meconium. . along with flattened "squames" or desquamated fetal skin cells that are found in the amnionic fluid.In this case of meconium aspiration.
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