Macroscopic appearance:
Pictures
Premature 24-week gestation newborn child with birth weight
of 690 g. The baby survived only for a few minutes. Premature
rupture of membranes was complicated by prolapse of upper
right extremity.
Immaturity, 24-week, Macro, autopsy (73857)Immaturity, 24-week, Macro, autopsy (73858)
Premature infant born at 31 week's gestation. The baby died
of necrotising enterocolitis which is a frequent complication
of immaturity.
Immaturity, 31-week, Macro, autopsy (73859)
Premature twin infant born at 33 week's gestation. Birth weight
was 1200 g. This twin had serious congenital heart defect.
Immaturity, 33-week, Macro, autopsy (73860)
Hypotrophia, immaturity (25-week):
Immaturity, hypotrophy (25th week), Macro, autopsy (74411)
Clinical signs:
Early complications in virtually all body systems occur as a result of difficulties in maintaining homeostasis
A preterm infant has difficulties with fetal to neonatal transition and maintaining homeostasis i.e. temperature control, euglycemia, fluid and electrolyte balance. Preterm infants usually exhibit significant jaundice and profound anemia. Full enteral nutrition is a problem even in healthy a near-term infant.
Internal organs immaturity
Introduction:
Preterm infant is susceptible to heat loss and hypothermia immediately after birth.
Etiology:
Introduction:
80% of extremely preterm infants develop significant jaundice requiring treatment. There is a risk of kernicterus.
Etiology:
Introduction:
Preterm infants compared to the term ones have proportionally more fluid in the extracellular compartment than in the intracellular and are thus susceptible to free water loss. Postnatal weight loss is up to 15 – 20% of birthweight compared to 10% in term infants. Disturbances of fluid balance contribute to intraventricular hemorrhage and patent ductus arteriosus. Nonoliguric hyperkalemia, hyponatremia or hypernatremia are frequent problems.
Etiology:
Introduction:
Defined as a cessation of respiratory activity for more than 20 seconds with bradycardia and/or cyanosis.
Etiology:
Usually ceases by 37 weeks of postmenstrual age, but may persist for several weeks beyond term in some ELBW infants.
Episodes of apnea may be induced by hypoxia, sepsis, hypoglycemia, temperature disturbances or neurologic lesions.
Introduction:
Physiologic anemia is seen between 2nd and 3rd month of life in term infants. In preterm infants anemia occurs earlier and is more severe than in term babies.
Etiology:
Introduction:
Also known as respiratory distress syndrome (RDS). The incidence is inversely proportional to gestational age.
Etiology:
Deficiency of pulmonary surfactant.
Vicious cycle: Decreased alveolar surfactant — lungs collapse at end expiration with each breath — increasing difficulty in breathing — exhaustion — atelectases (airless areas) — hypoxemia — endothelial and epitethelial damage: hyaline membrane formation — profound hypoxemia, hypercarbia and acidosis — progressive atelectases, abundant hyaline membranes.
Surfactant
Clinical signs:
Macroscopic appearance:
Histology:
Pictures
Hyaline membrane disease:
Hyaline membranes, newborn, HE 40x (72311)
RDS, 27-week, 6th day after delivery, twin B:
Respiratory distress syndrome, 27-week, HE 60x (74597)
Introduction:
NEC is more prevalent in premature infants but can be also observed in near-term or term infants. In preterm infants the incidence is inversely related to gestational age.
Etiology:
The etiology is controversial, several factors have been suggested as being important:
NEC in premature infants
The average age of onset in preterm babies is he second ane third week of life. NEC is associated with enteral feeding, but not with birth asphyxia. Higher incidence of NEC is reported in patent ductus arteriosus.
NEC in term infants
Term infants develop NEC soon after birth in babies who have not been fed yet. The likely initiating event is an ischemic insult to the gut often following birth asphyxia.
Clinical signs:
Treatment: antibiotics, nothing per os, surgery (resectin of the affected portion of the bowel, ileostomy)
Complications
Macroscopic appearance:
Pictures
Premature infant with birth weight 450 g. Preterm elective delivery at 25 week's
gestation because of eclampsia in the mother. The infant died 6 weeks later from
necrotizing enterocolitis with shock. Patent ductus arteriosus was one of the risk
factors.
Necrotizing enterocolitis, Macro, autopsy (73845)Necrotizing enterocolitis, Macro, autopsy (73846)Necrotizing enterocolitis, Macro, autopsy (73847)Necrotizing enterocolitis, Macro, autopsy (73848)
Necrotizing enterocolitis in slightly premature neonate with
severe birth asphyxia (pH a. umbilicalis 6.7). Elective delivery
because of eclampsia in the mother at 33 weeks, birth weight
1600 g. NEC affecting a short segment of terminal ileum with
perforation occured as early as the third day of life.
Necrotizing enterocolitis, Macro, autopsy (73853)Necrotizing enterocolitis, Macro, autopsy (73854)
Necrotizing enterocolitis in premature infant born at
31 w.g. with birth weight 1380 g, twin A. NEC was the cause
of death at the age of 7 days.
Necrotizing enterocolitis, Macro, autopsy (73842)Necrotizing enterocolitis, Macro, autopsy (73843)Necrotizing enterocolitis, Macro, autopsy (73844)
Necrotizing enterocolitis in premature infant born at 31 weeks
with birth weight 1490 g, (twins). Necrotizing encterocolitis
developed at the age of 3 weeks. Detail of the intestine:
Necrotizing enterocolitis, Macro, autopsy (73849)Necrotizing enterocolitis, Macro, autopsy (73850)Necrotizing enterocolitis, Macro, autopsy (73852)Necrotizing enterocolitis, Macro, autopsy (73851)
Necrotizing enterocolitis with perforation and peritonitis in premature infant
born at 25 week's gestation. NEC developed at the age of 3 weeks.
Necrotizing enterocolitis, Macro, autopsy (73855)Necrotizing enterocolitis, Macro, autopsy (73856)
Necrotizing enterocolitis:
Necrotizing enterocolitis, Macro, autopsy (74405)Necrotizing enterocolitis, Macro, autopsy (74406)Necrotizing enterocolitis, Macro, autopsy (74407)
Histology:
Hemorhagic necrosis of the mucosal layer which may extend to transmural necrosis. Inflammatory reaction is present only in slowly developing NEC.
Introduction:
Germinal matrix consists of primitive neuroectodermal cells lying between the ependyma and nc. caudatus. Primitive neurons and later glial cells are generated in the zone and migrate out to their final position. The germinal zone is programmed to melt away after 32 to 34 weeks. Hemorrhage into the germinal matrix with spread of blood to the lateral ventricles is characteristic of premature infants less than 32 weeks gestation. There is strong correlation of IVH and mechanical ventilation, barotrauma, severe HMD, hypoxia, hypercapnia, patent ductus arteriosus, rapid volume expansion in the first days and intrauterine growth retardation. The incidence and severity are inversely related to gestational age.
Etiology:
The pathogenesis is multifactorial. The final hypothesis is that damage from factors listed below especially hypoxia and transient rises of arterial pressure lead to rupture of fragile capillaries in the periventricular germinal matrix which is the origin of germinal matrix hemorrhage. This deletorious effect is even accentuated by the cerebral vasodilation caused by the hypercapnia and hypoxia with RDS.
Classification:
Clinical signs:
Death is the result of increased intracranial pressure, hernation and depression of function of the vital medullary centers.
Macroscopic appearance:
Subependymal hematoma over the nc. caudatus, may be bilateral or mutiple.
Intraventricular hemorrage follows the rupture of subependymal hematoma with spread through the ventricular system — to the opposite lateral ventricle, third ventricle, aqueduct, fourth ventricle and subarachnoid space of the cisterna magna.
Pictures
Intraventricular hemorrhage, 1st grade:
Intraventricular hemorrhage, 1st grade, Macro, autopsy (74397)
Intraventricular hemorrhage, 3rd grade:
Intraventricular hemorrhage, 3rd grade, Macro, autopsy (74398)
Intraventricular hemorrhage in premature 27-week at 2 days of
age in a newborn child who also suffered from severe respiratory
distress syndrome. The birth weight was 990 g.
Intraventricular hematoma, Macro, autopsy (73828)Intraventricular hematoma, Macro, autopsy (73829)
Intraventricular hemorrhage in extremely premature 24-week
neonate, twin B. Birth weight was 780 g. Hemorrhage in lateral
ventricles is assymetric, almost unilateral. Hematoma is
readily seen in subarachoid cisterna magna. Death occured at
the age of 6 days.
Intraventricular hematoma, Macro, autopsy (73826)Intraventricular hematoma, Macro, autopsy (73827)
Periventricular hemorrhagic infarction in premature twin infant
born at 29 weeks with birth weight 1150 g. The baby suffered
from birth asphyxia (Apgar score 1-3-6) and respiratory
distress syndrome.
Hemorhagic infarction, periventricular leucomalacia, Macro, autopsy (73792)Hemorhagic infarction, periventricular leucomalacia, Macro, autopsy (73793)Hemorhagic infarction, periventricular leucomalacia, Macro, autopsy (73794)Hemorhagic infarction, periventricular leucomalacia, Macro, autopsy (73795)Hemorhagic infarction, periventricular leucomalacia, Macro, autopsy (73796)Hemorhagic infarction, periventricular leucomalacia, Macro, autopsy (73797)
Periventricular hemorrhage in the right occipital lobe with
spread of hemorrhage in the ventricle system. Premature birth
at 36 weeks with birth asphyxia.
Intraventricular hematoma, Macro, autopsy (73830)
Intraventricular hemorrhage:
Intraventricular hemorrhage, Macro, autopsy (74399)
Introduction:
Periventricular leukomalacia means infarction of the periventricular white matter.
The periventricular area is particularly vulnerable to hypoxic-ischemic injury because of high metabolic rate and watershed blood supply (boundary between the ventriculopetal and ventriculofugal arteries within the brain, the latter are poorly developed in premature infants) The lesion is common in preterm infants, 28 – 32 weeks is the highest incidence.
Etiology:
Clinical signs:
Macroscopic appearance:
Pictures
Cystic periventricular leucomalacia in 6-weeks old infant. Elective premature
delivery at 32 weeks because of severe hydrops universalis. The cause of hydrops
was not found. Sepsis occured during the stay in the neonatal intesive care unit
and the baby died of protracted septic shock.
Periventricular leucomalatia, Macro, autopsy (73866)Periventricular leucomalatia, Macro, autopsy (73867)Periventricular leucomalatia, Macro, autopsy (73868)Periventricular leucomalatia, Macro, autopsy (73869)Periventricular leucomalatia, Macro, autopsy (73870)
Introduction:
Clinically significant PDA is quite frequent in very sick preterm infants with RDS, prolonged hypoxia and acidosis.
Etiology:
Clinical signs:
Introduction:
The combination of prematurity and medical intervention results in several pathological consequences mainly complications of assisted ventilation, complications related to vascular cannulation and blood sampling, nosocomial infections. High concentration of oxygen administered for prolonged periods causes retinopathy of prematurity and bronchopumonary dysplasia.
Clinical signs:
Pictures
Larynx perforation caused by endotracheal intubation in premature neonate
weighing 970 g.
Perforation of the larynx, Macro, autopsy (73861)Perforation of the larynx, Macro, autopsy (73862)
Introduction:
Occurs predominantly in preterm infants with severe RDS requiring mechanical ventilation, the ventilation pressures must be high enough to prevent alveolar collapse in this situation. Ventilated term infants with severe meconium inhalation are also at risk of air leak.
Etiology:
Alveolar over-distension and rupture results in entry of air into the perivascular, peribronchial and subpleural connective tissue.
Macroscopic appearance:
Pictures
Acute pulmonary intersticial emphysema in premature neonate:
Acute interstitial emphysema, Macro, autopsy (73781)Acute interstitial emphysema, Macro, autopsy (73780)
Acute pulmonary intersticial emphysema in premature newborn:
Intersticial emphysema, Macro, autopsy (74396)
Chronic pulmonary intersticial emphysema in a single lung lobe. The baby was delivered
prematurely at 26 weeks and survived for 7 weeks. Pnemothorax was another complication
of barotrauma which occured earlier after birth.
Chronic interstitial emphysema, Macro, autopsy (73787)Chronic interstitial emphysema, Macro, autopsy (73788)Chronic interstitial emphysema, Macro, autopsy (73789)Chronic interstitial emphysema, Macro, autopsy (73790)
Chronic interstitial emphysema, immature newborn:
Intersticial emphysema, Macro, autopsy (74419)Intersticial emphysema, Macro, autopsy (74420)Intersticial emphysema, Macro, autopsy (74421)
Histology:
In chronic emphysema irregular cysts are seen composed of thin to thick fibrous connective tissue wall partially lined by multinucleated foreign body giant cells. The intervening lung parenchyma is collapsed.
Introduction:
BPD is a chronic lung disease that occurs in infants who received respiratory support with mechanical ventilation and prolonged oxygenation. It is seen in babies recovering form respiratory distress syndrome, sepsis or prolonged apnea and most babies who develop BPD nowadays have birthweights below 1000 g. BPD is defined as receiving supplemental oxygen or ventilatory support at 36 weeks of postmenstrual age.
Clinical signs:
Etiology:
Macroscopic appearance:
Classic BPD
Originally described in 1967 as severe lung injury caused by oxygen toxicity and barotrauma with prolonged aggresive ventilation in the treatment of RDS. Its etiopathogenesis was abnormal reparative process in response to injury and inflammation. There was a progress from an acute exsudative phase of acinar injury to reparative and chronic fibroproliferative phase. The histopathologic findings originally reported were airway epithelial lesions, smooth muscular hyperplasia, extensive peribronchiolar and instersticial fibrosis, focal hemorrhage, areas of overdistension and atelectasis and hypertensive vascular disease.
New BPD
In recent years with gentler ventilation techniques, antental glucocoricoid therapy and surfactant therapy the histologic changes seen in infants differ.New BPD is characterised by decrease in alveolar number (enlarged simplified alveoli), abnormal microvasculature and intersticium with less prominent celularity and fibroproliferation. The current view is that new BPD is caused by interruption of normal developemental pathways for terminal maturation and alveolarization of lungs of very preterm infants. The maximum rate of accretion of alveoli is seen in a period from 25 weeks to 4 months after birth.
Pictures
Classic bronchopulmonary dysplasia in infant aged
3 months. Premature birth at 29 weeks with birth weight
970 g. The baby was dependent on ventilatory support from birth.
Premature rupture of membranes which occured at 23 week's
gestation was a significant risk factor as well as several
episodes of sepsis. Death from pneumonia.
Bronchopulmonary dysplasia, Macro, autopsy (73786)
Bronchopulmonary dysplasia in 11-week old infant. Premature
birth at 26 weeks with birth weight 1100 g. The baby suffered
from early onset neonatal sepsis, (Streptococcus agalactiae),
RDS, repeated episodes of late sepsis and was operated on
necrotizing enterocolitis. Death due to massive intracranial
hemorrhage.
Bronchopulmonary dysplasia, Macro, autopsy (73785)
Bronchopulmonary dysplasia:
Bronchopulmonary dysplasia, Macro, autopsy (74363)
Introduction:
First described in 1940 and termed retrolental fibroplasia. The incidence of ROP is inversely proportional to gestational age. ROP probably develops in genetically susceptible infants.
Etiology:
Classification:
Staging of ROP
Clinical signs:
Clinical signs:
Complicacions related to vascular cannulation
Insertion of both umbilical arterial catheter and umbilical venous catheter is routinely performed after birth or several days after in the neonate. Umbilical venous catheter is preferred when immediate vascular access is required. Cannulation of umbilical vein has more frequent complications. Catheters are also insterted into subclavian vein. With use of vascular cannulation there is a general risk of accidental dislogement, hemorrhage, endothelial trauma and associated thrombosis, thrombemboli and infection by bacteria and fungi colonizing the lines. Otherwise a small trombus adherent to the tip of the catheter is quite common as well as small mural thrombi.
More serious complications are:
Pictures
Gangrene of the finger, immaturity, the child died at age 6 weeks:
Dry gangrene of the finger, Macro, autopsy (74438)Dry gangrene of the finger, Macro, autopsy (74439)
Introduction:
Disturbance of liver function and cholestatic jaundice are well recognized complications of prolonged paranteral nutrition. The TPN-associated cholestasis is related to the duration of treatment and correlated inversely with the gestational age and birth weight.
Etiology:
Macroscopic appearance:
Dark green liver.
Pictures
Hepatic damage with prolonged total parenteral nutrition in premature infant born
at 25 week's gestation with birth weight 800g. The baby underwent an operation for
necrotizing enterocolitis for the first time at the age of 10 days. The baby died
from complications of NEC at 33 days of age. Note the icteric skin and dark green
liver.
Intrahepatic cholestasis, Macro, autopsy (73831)Intrahepatic cholestasis, Macro, autopsy (73832)
Histology:
Introduction:
All forms of handling and especially invasive procedures put the ill preterm infant at risk of acquiring infection from endogenous hospital flora (nosocomial). The less mature or more severely ill the infant is, the greater is the hazard of infection.
Etiology:
Colonization of skin, lower gastrointestinal tract, nose and throat is a normal neonatal event.
Abnormal colonization occurs more frequently in premature infants or infants admitted to neonatal intestive care units. Overt infection may develope depending on the state of maturity of the infant, the level of colonization and virulence of the organism. The infection may be introduced into vessels, airways or body cavities via catheters, endotracheal tubes, drainage tubes etc.
Clinical signs:
Nosocomial sepsis and meningitis are important causes of mortality and long-term morbidity. Multiresistent bacteria are dangerous.
Introduction:
Viablity is the point at which the fetus becomes viable, that is potentionally able to live outside the mothers womb albeit with artificial aid. The age of viability appears to be between 23 and 24 weeks of gestation corresponding to fetal lung developement, the respiratory system is probably the last to achieve functional maturity. 24 weeks of gestation finished (24 + 0) is the lower limit of vialibity in the Czech republic since 1994.
Introduction:
Survivability correlates with gestational age in infants who are appropriately grown. Babies born in singleton preganancies are more likely to survive than babies from multiple pregnancies.
50% of babies born at 24 weeks of gestation survive the neonatal period.
70% of babies born at 25 and 90% of babies born at 27 – 28 weeks survive the neonatal period
Neonatal mortality rate improves rapidly with each extra gestational week achieved at delivery. Neonatal mortality rate at 33 weeks is very low comparable to low mortality rate of babies born at term.
Introduction:
Babies born at the lower limit of viability have 25% chance of normal life without severe handicap.
Clinical signs:
Gestational age (weeks) | Children survivnig with severe handicap (%) |
23 – 24 | 60 – 70 |
25 – 26 | 50 |
27 – 29 | 10 – 30 |
30 a více | Pod 1% |
Birth weight | Survivors with severe handicap (%) |
Under 750 g | 30 and more |
750 – 1000 g | 15 – 20 |
1000 – 1500 g | 5 – 7 |
1500 – 2500 g | 1 |