a) Meningocele, diverticulum – like bulging of an arachoid sac filled with clear spinal fluid.
b) Meningomyelocele in which the arachnoidal sac also contains parts of the spinal cord, the cauda equna or the area medullovasculosa (see above), which protrudes because of the accumulation of fluid.
c) Meningomyelycystacele or syrengomyelocele, a combination of meningocele and hydromyelia (ballooning of the spinal cord due to a hydrophic accumulation of the fluid in the central canal).
Anencephally is an absence of the cranial vault (acrania) and of the brain (anencephaly) and a short neck.
Microcephaly is decrease of the brain’s size.
Amyelia, or total aplasia of the spinal cord.
Diplomyelia (Each half of the spinal cord develops separately over many segments).
Diastematomyelia (each half has only one dorsal and one ventral horn with a intervening cystic cavity to represent the central canal).
Arnold-Chiari malformation is a group of different combinations (the full deformity is a herniation of the posterior cerebellum, the medulla and the foramen magnum, with an added sharp curvature of the neuraxix at the cervicomedullary junction).
Congenital stenosis of the aqueduct.
Cyclopia (one eye in the middle of a deformed forehead).
Arrhinencephaly (the olfactory buld and tracts are absent in the mildest form of the disorder).
Agenesis of the corpus callosum is a component of arrhinencephaly.
Hydrocephalus is meant an increased amount of cerebrospinal fluid in the ventriculosubarachnoid pathways of the brain.
II. Errors of migration (Heterotopies, Ectopias)
Status verrucosus is a wart-like appearance of the cortex produced by a disorderly arrangement of the neuroblasts so that fissuration and sulcation are irregular and unpredictable.
Pachygyria is the appearance of large gyri in the cortex due to inadequate differentiation of sulci.
Microgyria (secondary fissures are lacking).
Congenital malformations of the heart
Congenital malformations of the heart represent structural changes that originate during the development of the septa and the rotation of the arterial heart, during the first 3 months of gestation.
Congenital heart defects are the most common forms of heart disease in children. They occur in about 1% of neonates and in 18% of spontaneous aborted and stillborn fetuses.
Most defects manifest themselves within the first year of life, such as large ventricular septal defects and tetralogy of Fallot.
Others, like bicuspid aortic valve, remain silent until middle age, when degenerative changes of the abnormal valve cause stenosis.
Still other defects, like a small ventrical septal defects (VSD) or patent foramen ovale may never cause any difficulty at all.
The most important malformations are:
I. Septal defects
Patent foramen oval (Atrial septal defect).
Ventricular septal defects (Roger’s disease).
Complete absence of the ventricular septum, with or without septal defect (cor bilocular or cor triboculare).
II. Transposition defects
Dextraposition of the aorta (Eisenmenger’s syndrome, tetralogy Fallot).
Dextraposition of the heart.
III. Stenoses
Tricuspid stenosis or atresia.
Pulmonary stenosis.
Mitral stenosis or atresia.
Aortic stenosis or atresia.
Aortic coarctation.
IV. Valvular insufficiency
Congenital tricuspid insufficiency (or Ebstein’s anomaly).
Congenital mitral insufficiency.
V. Persistent fetal vessels
Patent ductus arteriosus (with many congenital cardiac defects).
Anomalies of the pulmonary veins include openings into the superior or inferior vena cava or the coronary sinus.
VI. Combined heart defects
Trialogy of Fallot consists of
Ventricular septal defect.
Stenosis or atresia of the pulmonary outflow tract.
Right ventricular hypertrophy.
Tetralogy of Fallot consists of
Stenosis or atresia of the pulmonary outflow tract.
Ventricular septal defect.
Aorta overriding the right ventricle (aorta dexraposition).
Right ventricular hypertrophy.
Pentalogy of Fallot consists of
Ventricular septal defect.
Stenosis or atresia of the pulmonary outflow tract.
Hypertrophy of the right heart.
Aorta dexraposition.
Defect of interatrial septum.
Classification anomalous development of the heart (by Ebbott)
I. Acyanotic shunt (left-right)
1) Patent ductus arteriosus.
2) Atrial septal defect.
3) Ventricular septal defect (Roger’s disease).
II. Cyanotic shunt (Right-left)
1) Tetralogy of Fallot.
2) Eisenmenger’s complex (variant of the tetralogy of Fallot).
3) Transposition of great vessels.
III. No shunt
1) Coarctation of the aorta.
2) Aortic stenosis.
Examplies of some heart defects
Patent ductus arteriosus (PDA)
Before birth the ductus arteriosus (DA) is the only route by which blood in the right ventricle (RV) can reach the systemic circulation.
The DA is located superior to the bifurcation of the pulmonary arteries and enters the aorta just distal to the left subclavian artery. It is invested with spirals of smooth muscle, which contract at birth in response to high tension (coming from the newly aerated lungs). Within a day or two, the DA is usually functionally closed.
Not infrequently and often in premature infants, the DA fails to close, hence a PDA. With the drop in pulmonary arterial pressure, which occurs following lung inflation after birth, blood shunts from the aorta across the PDA and into the main pulmonary artery.
The RV responds to increased flow and pressure with either dilatation (congestive heart failure) or hypertrophy.
If pulmonary resistance exceeds systemic resistance (due to hypoplastic lungs, for instance), blood is shunted right-to-left and cyanosis may ensue.
Atrial septal defects (ASD)
The most common ASD is a secundum ASD or ASD II. A secundum ASD means that the ASD is reminiscent of the ostium secundum i.e., the ostium secundum is not covered over. An ASD II may form in any of four ways:
1. Deficient formation of septum primum.
2. Deficient formation of septum secundum.
3. Combination of both.
4. Dilation of the atria, thereby pulling septum primum and septum secundum apart.
After birth, the blood shunts from left to right atrium. This shunt may be large if the septal defect is large.
In atrial septal defects, the pulmonary artery pressure falls to normal or near normal levels soon after birth. However, the resulting atrophy of the right ventricle makes this chamber more distensible than the left ventricle.
With a sizable atrial defect, pressures in the two atria are similar and the right ventricle fills more easily than the left.
Consequently, not only does the vena caval blood enter the right ventricle but also much of the pulmonary venous blood from the left atrium enters the right ventricle as well.
Pulmonary blood flow is greatly increased while oxyhemoglobin saturation in the systemic arterial system is normal.
The pulmonary arterial bed responds to this “over circulation” with smooth muscle hyperplasia and hypertrophy.
If the septal defect is operatively closed at this stage, the pulmonary arterial muscle will atrophy and a normal circulatory pattern will be established. If a large defect is not closed in time, diastolic overloading of the right ventricle continues and both the right ventricle and atrium dilate and hypertrophy.
Left ventricular output is usually near normal so that these infants develop normally.
Over the course of several decades, pulmonary vascular obstruction takes place within the pulmonary arterial bed.
This progressively narrowed bed offers greater and greater resistance to pulmonary blood flow. Resistance in the pulmonary arterial bed may eventually equal or exceed that in the systemic bed.
When this occurs, shunts are reversed and cyanosis appears or becomes more prominent.
If the normal cardiac anatomy is now restored through surgery, such patients will develop right-sided cardiac failure since the right ventricle is incapable of forcing all of the caval blood through the restricted pulmonary vascular bed.
Ventricular septal defects (VSD)
These are the most common of the cardiac defects. The ventricles are separated by the growth of the muscular septum and by the growth and fusion of the endocardial cushions near the atria. VSD’s can be located near the atrioventricular valves or nearer to the apex (i.e. tip) of the heart.
Before birth, VSD’s are of little consequence since the pulmonary arterial pressure is equal to the systemic pressure and thus, most of the blood enters the systemic circulation.
After birth, VSD’s may be of little consequence if they are small. But, if they are large, they allow significant left-to-right shunting, since now (after birth) the pulmonary (right) pressure is lower than the systemic (left) pressure.
Thus, the pulmonary vascular bed is faced with abnormally high pressures, as is the RV. The pulmonary vessels become thicker by undergoing smooth muscle hyperplasia/hypertrophy.
The RV may also hypertrophy. These changes reflect the presence of pulmonary hypertension.
Because of this left-to-right shunting, pulmonary blood flow may be greatly increased, leading to pulmonary congestion, edema, hemorrhage, pneumonia and congestive heart failure.
After a long time, pulmonary pressure may equal or even exceed systemic resistance. In the latter situation, blood shunts from right-to-left, resulting in cyanosis.
Common atrioventricular canal (CAVC)
In this cardiac malformation, the endocardial cushions fail to separate the atrioventricular canal into right and left sides.
Because the atrioventricular valves (mitral and tricuspid) are also formed by the endocardial cushions, they are malformed as well.
Thus, blood from the right atrium (RA) and the left atrium (LA) enters into a common, undivided atrioventrical (AV) canal above the incompletely divided RV and left ventricle (LV). Much mixing of blood occurs.
This defect is commonly associated with Down’s syndrome (Trisomy 21).
Transposition of the great arteries (TGA)
This is a fairly common defect and it is important to recognize it early since surgical correction is possible and successful.
It is thought to be due to abnormal development of the conal muscle beneath the two semilunar valves.
In this defect the aorta arises from the right ventricle and the pulmonary artery arises from the left ventricle. In utero, this defect causes no trouble, since venous blood (from the placenta) is oxygenated.
After birth, however, the pulmonary and systemic circulations are disconnected.
Venous blood enters the RA, then the RV and then out the aorta. Pulmonary venous blood enters the LA, then the LV and then out the pulmonary arteries back to the lungs.
Survival is dependent on any kind of mixing of oxygenated and unoxygenated blood whether through an ASD, a VSD or a patent ductus arteriosus.
Whatever mixing of the two systems there is, it is usually inadequate and these neonates have marked cyanosis.
If the communication between the two circulations is adequate for oxygenation, then problems of cardiac failure and pulmonary hypertension will inevitably develop.
Combined heart defects:
Tetralogy of Fallot
It was Etienne-Louis Arthur Fallot in 1888 who well described this form of cyanotic heart disease. Fallot did not actually coin the term, “tetralogy of Fallot”. He used the term la maladie bleu, i.e., the blue disease. It was Maude E. Abbott who first used this term tetralogy of Fallot in 1924.
What comprises tetralogy of Fallot?
1. Stenosis or atresia of the pulmonary outflow tract.
2. Ventricular septal defect.
3. Aorta overriding the right ventricle.
4. Right ventricular hypertrophy.
Actually, the basic abnormality is underdevelopment of the subpulmonary cone of muscle (conus), resulting in stenosis/atresia of the pulmonary outflow tract.
This underdevelopment of the conus results in malaligament of a band of muscle (the parietal band) that lies beneath the pulmonic valve.
In tetralogy, this band of muscle shifts anteriorly, superiorly and to the left, which obstructs the pulmonary outflow tract. This opens up a “hole” in the interventricular septum (hence a VSD).
With this leftward shift, the aorta is “looking down into” the RV (hence an “overriding” aorta).
Finally, with the narrowed pulmonary outflow tract, there is obstruction (hence right ventricular hypertrophy).
The VSD also contributes to right ventricular hypertrophy.
So, in essence, Fallot’s congenital anomaly could be called “monology of Fallot” with the single underlying abnormality being an underdeveloped conus resulting in a stenotic or atretic pulmonary outflow tract. The other three abnormalities are a result of this one abnormality.
The degree of cyanosis depends on the degree of pulmonary outflow obstruction. This obstruction can be at the level of the pulmonic valve or in the right ventricle just beneath the pulmonic valve.
The right ventricle hypertrophies, in response to the increased resistance and because of the large VSD. With severe right ventricular outflow obstruction, right to-left shunt occurs across the VSD and the patient suffers from severe cyanosis.
Surgical repair is now highly effective; complete repair usually being done within the first two years of life.
Despite the nearly unbelievable variety of cardiac malformations that are possible, the net result of these abnormalities can be reduced to a mercifully short list of clinical signs and symptoms.
Congenital anomalies of the kidneys and the lower urinary tract
Agenesis.
Hypoplasia.
Displacement.
Polycystic kidney disease.
Horseshoe kidney.
Accessory (Additional) kidneys.
Reduplication of the urachus.
Congenital anomalies of the genital system
I. Male
Phimosis.
Hipospadias and epispadias.
Cryptorchidism.
II. Female
Septate uterus.
Double uterus with double cervix.
Congenital anomalies of the gastrointestinal tract
Agenesis (esophagus, intestinum).
Atresia.
Fistulous tract of the esophagus with the trachea or main stem bronchi.
Stenosis.
Megaesophagus.
Diaphragmatic Hernias.
Pyloric stenosis.
Meckel’s Diverticulum.
Megacolon (dilation of bowel) in Hirschprung’s disease. Hirschsprung’s disease results from a failure of migration of neuroblasts that form the myenteric plexus. In all patients, ganglioncells are absent in the region of the anorectal junction. The result is intestinal obstruction in affected neonates. The incidence is 1 per 5000 live births.
Congenital Cystic liver disease.
Agenesis, hypoplasia, hyperplasia, total reduplication of the qallbladder.
Ectopia of the pancreas.
Congenital anomalies in the face (8th to 10th week of the embryonal period)
1. Lateral facial clefts:
a) Cheiloschisis or cleft lip (limited to the upper lip).
b) Gnathoschisis (extend to the maxilla).
c) Palatoschisis (extend to the hard palate).
2. Median facial clefts may also be limited to the upper lip, maxilla, or palate. The nose is troguently flat due to the aplasia of the vomer.
3. Oblique facial clefts extend from the upper lip to the corner of the eye.
Congenital malformations of the bone-cartilage system
Hondrodysplasias is characterized by the shortening and thickening of the legs.
Achondroplasia is a derangement in epiphyseal cartilaginous growth resulting in dwarfism.
Hondrodysplasia of fetus (lethal micromelia):
a) Chondrodysplasia.
b) Increase of the head.
c) Open mouth.
d) Saddle-like nose.
e) Thickening of the tongue.
f) Short neck.
g) Hypoplasia of the thorax and lungs.
h) Thickening of vertebra.
Sirenomelia. The term comes from “siren” or “mermaid” because of the characteristic fusion of the lower extremities that results from a failure of normal vascular supply from the lower aorta in utero.
Aplasia (Amelia) of legs.
Phocomelia is underdevelopment of the proximal parts of legs, when the foot and arm growth from trunk.
Polyductyly is a malformation consisting of supernumerary finger development.
Syndactyly is partial or complete fusion of several fingers.
Defects of placental development
Placental hypoplasia (normal mass is 0.5 - 0.7 kg), placenta/fetus ratio is 1/5 -1/7. When the mass of the placenta decreases, fetus hypoplasia develops.
Defects of placenta localization are marginal and central placenta presentation in respect to internal uterus orifice. This develops as a result of Mastopathy, its causes are unknown, and it presents a risk of placenta detachment during the delivery and intranatal death of the fetus.
Defects of placenta detachment are placenta adhesion (caused by deep implantation of blastocyst). The placenta does not detach after the delivery. Hemorrhage may occur.
Placenta abruption. This occurs at extragenital and genital maternal pathology. It may result in intranatal fetus asphyxia.
Umbilical cord defects (its normal length is 0.5 - 0.7 m). If the length is less than 0.5 m, the cord is short, more than 0.7 in it is long.
Disturbance of the umbilical cord attachment to the placenta:
1. Central and eccentric are normal types of attachment.
2. Membranous is pathological one, when the umbilical cord is attached to the membranes, its vessels may be compressed with the parts of the fetus and amniotic fluid, which may cause their rupture, ante-, and intranatal fetus death may occur.
Amnion development defects: - hydramnion (2000 ml and more), oligoamnios (500 ml and less).
Fetopathy
Fetopathy is characterised by the combination of the impairment of tissue morphogenesis and reactive processes.
In early period the impairment of tissue morphogenesis predominates.
In late period the reactive processes such as the disturbance of the blood circulation, degenerations, necrosis, inflammation, presence of immune reactions, compensative and adaptative processes, regeneration.
Fetopathies may be infectious and non-infectious.
Infectious fetopathies
Infectious fetopathies can be connected with the influence of viruses and bacterium.
Inflammation in placenta takes place.
Pathologic morphology of fetopaties:
a) Necrosis of parenhymatous organs and brain (rubella, cytomegaly, chickenpox, toxoplasmolis).
b) Formation of granulomas (syphilis, tuberculosis).
c) Hemorrhagic syndrome.
d) Immune reactions.
e) Hepato- and splenomegaly.
f) Jaundice.
The main infectious fetopathies are cytomegaly and congenital toxoplasmosis.
Cytomegaly
Cytomegaly (from cytos - cell and megaios - large) is a virus infection involving salivary glands. The disease is characterized by formation of giant cells with intranuclear inclusions.
Generalized form of infection develops in the newborns. DNA-containing virus enters the organism of the fetus from the mother through the placenta.
Generalized infection in children is characterized by central nervous system (CNS) involvement, which is not observed in acquired cytomegaly. Encephalitis with formation of cytomegalic cells, perivascular infiltration and calcinosis foci in the subependymal zone are observed in children. These phenomena cause hydrocephalia.
Cytomegalic cells contain intranuclear formation resembling “owl’s eye”. They can be found in the lungs, kidneys, liver, intestine, pancreas, adrenal gland, and thymus.
Hemorrhages and necroses can also be observed in these organs.
The disease lasts several days (sometimes weeks). It ends with death caused by damage to vitally important organs.
Congenital toxoplasmosis
Congenital toxoplasmosis is a disease caused by toxoplasma. It develops as a result of hematogenic transfer from the mother’s organism.
Toxoplasma is a protozoic microorganism from tripanosomid family. The source of human infection is dogs and cats. The fetuses are infected through the maternal placenta.
During teratogenic termination period, embryopathy incompatible with life occurs.
Early period is characterised by microcephalia of brain, porencephalia with gliosis (consolidation of the remained brain tissue) and calcinosis. Microscopic examination demonstrates cysts filled with granular spheres.
Late period occurs the foci of necrosis, and calcinosis in the brain, pseudocysts and free parasites, encephalitis in the whole brain, meningopathy, ependymatitis, and hydrocephalus. Productive necrotic rhinitis and uveitis in the retina. Generalized form: besides GNS involvement there is hepato- and splenomegaly, jaundice, ulcers of the intestine, myocarditis, interstitial pneumonia. Microscopic examination demonstrates erythroblastosis in the liver and spleen, necrosis, calcinosis and lymphohistiocytic infiltration in the liver, myocardium, kidneys, cholestearosis in the liver.
Outcome: death of fetuses and newborns or complication (paralysis, mental retardation, hemorrhage).
Noninfectious fetopathies
The main noninfectious fetopathies are hemolytic disease of the newborn, fetal mucoviscidosis, fibroelastosis of myocardium and diabetic fetopathy.
Early fetopaties occur by the isolated congenital defects (pylorostenosis, megacolon, megaloureter, agenesia, cystosis) and systemic congenital defects of the bone and muscular tissues, skin.
Diabetic fetopathy
Diabetic fetopathy is the disease of the fetus due to maternal prediabetes and diabetes.
As a rule, the body mass is 4 - 6 kg.
The skin is purple cyanotic with small point hemorrhages, the neck is short, and the face as well as the soft tissues of the back and chest are swollen.
The signs of immaturity are observed in the mature fetus.
Hepatomegaly and cardiomegaly can be seen.
Microscopic examination demonstrates hypertrophy of islets of Langerhars, increased amount of B-cells, fat degeneration of the liver, glycogen accumulation in the tubular epithelium in the kidneys, hydropic degeneration of the myocardium.
During the delivery of the child with fetopathy, hypoxia due to placenta vascular sclerosis and disturbance of placental circulation may occur.
Hyaline membrane disease may develop because synthesis of surfactant is disturbed due to disturbed lipid exchange (lipoproteid).
The death is caused by antenatal and intranatal asphyxia, respiratory insufficiency, birth injury, and hypoglycemia after birth stress.
Cystic fibrosis (Fetal mucoviscidosis)
A disorder of exocrine glands, affecting both mucus-secreting and eccrine sweat glands throughout the body, leading to viscid mucinous secretions and obstructive disease in lungs, pancreas, liver.
A simple autosomal recessive syndrome; heterozygotes are unaffected.
The mutant gene may code for abnormal protein that affects chloride transport channels across epithelial membranes.
General morphologic feature: obstruction by viscous mucoid secretions.
Pancreas: plugging and dilatation of ducts, atrophy of acini, and progressive fibrosis.
Liver: bile ducts plugged by mucus with biliary obstruction and fibrosis.
Lung: Obstruction and secondary infection of air passages, hyperplasia and hypertrophy of mucus-secreting cells.
Salivary glands: progressive dilatation of ducts, squamous metaplasia, glandular atrophy, and fibrosis.
Intestinum: obstruction by mucus (meconium ileus)
Endocardial Fibroelastosis
Primary myocardial metabolic/enzymic defect and congenital malformations take place.
It is characterized by focal to diffuse, cartilage-like fibroelastic thickening of the myocardium, cardiomegaly due to hypertrophy of left ventricle.
Death can be due to acute cardiac insufficiency in first days of life or due to chronic cardiac decompensation at connection (intercurrent) of the others diseases (pneumonia).
Alcogolic syndrome of fetus
Alcogolic syndrome of fetus occurs by signs of embryofetopathy.
Prematurity, small weight of fetus.
Tight forehead, flat bridge.
Narrow palpebral fissures.
Hyperthelorism, ptosis, epicanthus.
Cleft palate, short fingers.
Malformations of the heart, kidney, hip-joint.
Small cerebellum.
Decreased pulmonary surfactant.
Frequent mental retardation.
PERINATAL PATHOLOGY
Perinatal period means the period before and after the delivery, begining from the 22th week of gestation (196th day) to the 1st week of extrauterine life.
Perinatal period and the respective pathology and mortality is divided into
1. Antenatal period (from the 22nd week of gestation to the delivery).
2. Intranatal period (during the delivery) begins in the moment of the delivery until the birth.
3. Postnatal (neonatal) period (from birth to 7th day after birth).
In the 22nd week of gestation the fetus must have the weight more than 500 g and the length of the body – 25-30 cm. This fetus can live a life of independence.
Delivery of a smaller fetus and until the end of 22 week of the gestation is called abortion.
Stillborn is fetus without breathing and palpitation in the moment of the delivery.
Liveborn is infant with signs of the breathing and palpitation.
Perinatal mortality is stillborn and infant mortality within the first 7 days of the life.
Causes and morphological features of prematurity and overmaturity of newborns
Features of the prematurity
1. Premature infant is defined as those when the term of gestation is until 37 week.
2. Body weight is less then 500 gramms.
3. Body length is less then 25 cm.
4. Lanugo hair on the face.
5. Underdeveloped nails.
6. Soft lobe of the ear.
7. In girls the labia minora and clitoris are not covered by labia majora.
8. In boys the testes are not descended, scrotum isn’t wrinkled.
9. Soft cranial bones.
10. Beclard’s nucleus of the distal femoral epiphysis is absent (in mature children it is 5 - 7 mm).
Microscopic examination of the organs in premature fetus allows determining the degree of prematurity:
1. Embryonic glomeruli are noted in the superficial layer of the cortical substance of the kidneys.
2. Erythroblastosis foci are observed in the kidneys and liver.
3. Thickening of interalveolar septa in the lungs.
4. Sprout zone in the brain is widened.
Main causes of the prematurity:
1. Diseases of the genital tract of the pregnant women.
2. Placental insufficiency.
3. Early agein of placenta.
4. Placental infections.
5. Acute and chronic infections of the pregnant women.
6. Severe toxicosis of pregnancy (nephropathy, eclampsia).
7. Rh antigens incompatibility.
Features of the overmaturity
1. Overmaturity infant is defined as termination from the 41st week of gestation and later.
2. Epidermis is dry, peeling, macerated, yellow or yellow-greenish color.
3. Very dense cranial bones.
4. Dense long lobe of the auricle.
5. Long nails.
6. General hypotrophy of fetus.
7. Decreased amount of amniotic fluid.
8. Amniotic fluid, umbilical cord, amniotic membranes are usually staining with meconium (yellow-greenish color) as the fetus experiences intrauterine hypoxia.
9. Beclard’s nucleus has 8 mm and more).
10. Signs of the placenta’s agening (placental infarction, petrification of the placenta).
Main cause of the overmaturity is late prime-gravide.
Overmaturity may lead to antenatal and intranatal death of the fetus due to hypoxia.
The most important diseases of perinatal period
Asphyxia (anoxia)
Asphyxia means lack of oxygen and excess of carbon dioxide in the blood suppling.
Asphyxia may be
1. Antenatal asphyxia is called the intrauterine asphyxia of the fetus (fetal asphyxia) and arises during pregnancy.
2. Intranatal asphyxia (asphyxia neonatorum) arises during delivery.
3. Postnatal asphyxia (asphyxia neonatorum) is called asphyxia of the newborn and arises after delivery in result of illnesses of newborn.
Causes of asphyxia
I. Causes of antenatal asphyxia associated with maternal factors resulting in decreased placental blood flow and placental insufficiency, such as:
Maternal cardiovascular diseases.
Late toxemia of the pregnancy.
Chronic renal and pulmonary diseases of the mother.
Endocrine diseases (diabetes mellitus, thyreotoxicosis).
Accidental hemorrhage.
Severe infections of the mother.
Social causes (narcomania, alcohol, heavy cigarette smoking).
II. Causes of intranatal asphyxia associated with defects of the placenta and complications of the delivery:
Pretermed placental separation.
Placental abruption.
Placenta previa.
Prolaps of the umbilical cord.
Cord knots.
Multiple gestations.
Complications of the delivery: weakness of the delivery processes, fetus breech presentation, disproportion between the fetus’ head and delivery tract of mother (narrow pelvis, large fetus), rupture the short umbilical cord, umbilical cord winding round the neck of fetus.
III. Causes of postnatal asphyxia associated with disturbance of the breathing.
As a rule, postnatal asphyxia is a continuation (or consequence) of intranatal asphyxia.
When during the delivery CNS (including respiratory center) is damaged or under the influence of intrauterine hypoxia, the fetus makes the first inspiration intrauterinally (carbon dioxide stimulates the respiratory center) and amniotic content is aspirated. In this case the alveoli cannot spread after the delivery; postnatal asphyxia develops.
Brain trauma or edema with suppression of the respiratory center.
A birth injury of the spinal cord and central nervous system.
Infections of newborn.
Aspiration pneumonia.
Background: progressive fetal asphyxia.
Besides, fetal factors import for all types of asphyxia, because they lead to an inadequate supply of nutrients from the mother, to inadequate of the delivery and may lead to birth injury. Prominent among such fetal conditions are chromosomal disorders, congenital anomalies, and congenital infections.
The main clinical-morphological syndromes of asphyxia
Hemorrhagic syndrome: petechial hemorrhage in brain, adrenal glands, serous membranes and mucosa, congestion, dark fluid blood in the heart chambers, development of syndrome’s disseminated intravascular coagulopathy on the other hand, resulting in fibrin thrombi in the microcirculatory vesells.
Edematous syndrome in inner organs and cavities.
Degenerative changes in the liver, kidneys, myocardium, brain.
Aspiration of amniotic fluid containing skin epithelium, lanugo, meconium.
If such children survive, the disturbance of the psychomotor development and cardiosclerosis may develop.
Pneumopathies
Pneumopathies are noninflammatory pulmonary diseases, which lead to asphyxia of newborn. They occur as a rule in preterm children. There is atelectasis, development of the hyaline membranes, edematous-hemorragic syndrome.
Atelectasis
Atelectasis in the newborn or primary atelectasis is defined as incomplete expansion of a lung or part of a lung.
Stillborn infants have total atelectasis, while the newborn infants with weak respiratory action develop incomplete expansion of the lungs and clinical atelectasis.
The common causes are prematurity, cerebral birth injury, CNS (central nervous system) malformations and intrauterine hypoxia.
Macroscopicall appearance of atelectasis:
Large plural space.
Small and collapsed lungs against vertebral column and are of cyanotic color.
Slitlike air spaces.
Heart and great vessels fully exposed.
Microscopic examination demonstrates collapsed alveoli.
While pulmonary collapse or primary atelectasis is the term used for reduction in lung size of a previously expanded and well-aerated lungs.
Secondary atelectasis in children and adults may occur from various causes such as compression, obstruction, contraction and lack of pulmonary surfactant. Collapse may be of the following 3 types:
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