1. Compressive collapse. Pressure from outside causes compressive collapse e.g. by massive pleural effusion, hemothorax, pneumothorax, intrathoracic tumor, high diaphragm and spinal deformities.
2. Obstructive/absorptive collapse. Obstruction of a bronchus or many bronchioles causes absorption of oxygen in the affected alveoli followed by collapse e.g. by viscid mucus secretions in bronchial asthma, chronic bronchitis, bronchiectasis, bronchial tumors and aspiration of foreign bodies.
3. Contraction collapse. This type occurs due to localised fibrosis in lung causing contraction followed by collapse.
Edematous hemorrhagic syndrome
It is associated with asphyxia when the lung capillaries are overfilled with the blood, vascular permeability increases due to hypoxia.
Diffuse edema and large intra- and extraalveolar hemorrhages develop.
Difficulty of the breathing takes place; the children die because of respiratory insufficiency.
The disease of hyalin membranes often accompanies this condition.
Autopsy demonstrates large lungs with hemorrhages.
Microscopic examination shows intraalveolar pink fluid, hemorrhages.
Respiratory distress syndrome of newborn (RDS)
RDS is one of the most common life threatening complications to confront the newborn infant.
RDS is also known as hyaline membrane disease (HMD), highlighting one of the major pulmonary anatomic findings in this disease.
Lungs are involved, asphyxia develops quickly, and the newborns die within the period of 24 - 36 hours.
It can have many origins, including:
1. Excessive sedation of the mother with consequent depression of respiration in the infant;
2. Brain injury with failure of the central respiratory centers;
3. Feeble respiratory efforts secondary to immaturity of the lungs and sceletal muscles (primary atelectasis);
4. Aspiration during birth of blood clot and amniotic fluid when the amniotic debris (i.e., desquamated keratotic squames, mucus, lanugo hairs, proteinaceous precipitate, and blood) blocks ventilatory function;
5. Asphyxiating coils of umbilical cord about neck of the infant. But more important than all these by an order of magnitude is the idiopathic RDS.
The fundamental defect in RDS is a deficiency of pulmonary surfactant. Surfactant reduces surface tension within the alveoli so that less pressure is required to hold alveoli open, and it maintains alveolar expansion by varying surface tension with alveolar size. It is synthesized by type 2 alveolar cells most abundantly after the 35 week of gestation in the fetus. At birth, the first breath of life requires high inspiratory pressures to expand the lung. With deficiency of surfactant the lungs collapse with each successive breath as it did with the first.
Surfactant synthesis is modulated by a variety of hormones, including cortisol, insulin, prolactin, and thyroxin. The role of glucocorticoids is particularly important. Corticosteroids induce the formation of surfactant lipids and apoproteins in fetal lung. Surfactant synthesis may be suppressed by the infants of diabetic mothers’ compensatory high blood levels of insulin, which counteracts the effects of steroids. This may explain why infants of diabetic mothers have a higher risk of developing RDS.
Morphological features of RDS
Gross examination of the lungs. Although of normal size, they are solid, airless, reddish purple like the liver, and they usually sink in water. Autopsy demonstrates stiff, congested and heavy lungs.
Microscopic examination:
The alveoli are poorly developed, and those that are present are collapsed. The atelectasis results from the clearance of the fluid without its replacement by air.
Interstitial and intraalveolar edema.
In early stage of RDS the necrotic cellular debris is present in the terminal bronchioles and alveolar ducts.
Later, the necrotic material becomes incorporated within pink hyaline membranes that line the respiratory bronchioles, alveolar ducts, and random alveoli, mostly the proximal alveoli.
The membranes are largely made up of fibrinogen and fibrin admixed with cell debris derived chiefly from necrotic alveolar-lining pneumocytes.
In infants who survive more than 48 hours reparative changes are seen in the lungs. The alveolar epithelium proliferates under the surface of the membrane, which may be desquamated into the airspace, where it may undergo partial digestion or phagocytosis by macrophages.
Infants who recover RDS are at increased risk for developing a variety of other complications stiff, as well. Most important among these are patent ductus arteriosus, intraventricular hemorrhage, and necrotizing enterocolitis. Thus, although the high technology of today saves many infants with RDS, it also brings to the surface the exquisite fragility of the immature neonate.
Pneumonia in newborn
Pneumonia of newborns may occur in uterus (in ante- and intranatal periods) as well as after the birth. The etiology is different. The most frequent are coccal pneumonias, klebsiella, and colon bacillus. The disease often develops against the background of amniotic fluid aspiration both infected and not infected.
The most often in newborn the aspiration pneumonia develops.
Aspiration syndrome is the first inspiration done in uterus. Amniotic fluid may be infected or may contain meconium.
The syndrome is due to hypoxia, and is often observed at overmaturation.
If the child survives for 3 - 5 hours, small-focal pneumonia develops, in 24 hours it turns into confluent pneumonia.
In massive aspiration, total or disseminated atelectasis of the lungs (primary) may develop as the lungs are filled with aspiration masses and do not spread.
Microscopically, leukocytic and monocytic infiltration of alveolar tissue involving the bronchioles and bronchi are observed. Elements of amniotic fluid are determined in the exudate.
It is considered that intrauterine pneumonia is responsible for the death during the first 1 -3 days of life.
Birth injury
Birth injuries constitute important causes of illness or death in infants as well as in children during the first years of life.
Morbidity associated with birth injury may be acute or the result of later-appearing sequels.
Birth injuries are damage to the fetal tissues and organs with mechanical forces during the delivery. Birth injury should be differentiated from obstetric injury, which occurs when obstetric manipulations are carried out.
Causes of birth injury are due to:
1. The state of the fetus:
a) Embryopathy.
b) Fetopathy.
c) Prematurity (the tissues are easily ruptured) and overmaturity (hypoxia increased vulnerability of the fetus).
2. The state of the maternal passages:
a) Rigidity of the birth canal tissue.
b) Pelvis defects (narrow pelvis, rachitic pelvis, anomalies, tumors, wounds)
c) Tumors of maternal passages
d) Oligoamnios, hydramnion.
3. The state of failure of the delivery’s dynamic:
a) Precipitated delivery.
b) Prolonged delivery.
c) A lot or little of amniotic fluid.
Pathology
Cephalogematoma is produced by an effusion of blood between the pericranium and one of the bones of the head.
It disappears slowly. When infected, it may become a source of purulent meningitis. The most severe intracranial injury is hemorrhage to the meninges and brain substance.
All hemorrhages are divided into
1. Epidural hemorrhages are located between the bones of the skull and the dura mater (inner cephalohematoma).
2. Subdural cephalohematomas occur in rupture of the falciform process and cerebellum tentorium. The blood is accumulated under the dura mater on the brain substance.
3. Subarachnoid cephalohematoma is localized between the arachnoid and pia mater. It occurs in rupture of the falciform process, cerebellum tentorium, veins.
4. Intracerebral cephalohematomas are the hemorrhages to the vascular plexi of the brain, under the ependyma of the lateral ventricles with rupture to the ventricles.
The most frequent course of the death in intracranial injury is rupture of the falciform process and cerebellum tentorium.
Caput succedaneum and cephalhematoma are also so common, even in normal uncomplicated births, that they hardly merit the designation “birth injury”. The first refers to progressive accumulation of the interstitial fluid in the soft tissues of the scalp, giving rise to a usually circular area of edema, congestion, and swelling at the site where the head being to enter the lower uterine canal. Because the fluid accumulates in the subcutaneous tissue, it may extend across the suture lines.
Hematoma of the sternomastoid muscle may follow traction on the head during the birth of the shoulders, or the extraction of the after-coming head.
Visceral hemorrhages: subcapsular hematomas and hemorrhage from spleen, liver, stomach due to fracture.
The most often fractures of the spine (often fatal to the life), fracture of the clavicle, bone’s skull, femoral and humerus bones occurring in large fetuses.
Hemolytic disease of the newborn (HDN) or Erythroblastosis fetalis
Erythroblastosis fetalis is defined as a hemolytic disease in the newborn caused by ABO-group and Rh incompatibility between mother and child.
When the fetus inherits red cells antigenic determinations from the father that are foreign to the mother, a maternal immune reaction may occur, leading to the hemolytic disease in the infant. Basis to such a phenomenon are leakage of fetal red cells into the maternal circulation and, in turn, transplacental passage of the maternal antibodies into the fetus.
Any of the numerous red cell antigenic systems may theoretically be involved, but the major antigens known to induce clinically significant immunologic disease are the ABO and certain of the Rh antigens (Rh negative mother and Rh positive fetus)
The resultant fetal hemolytic reaction may cause mild-to-severe disease in the newborn, or even death.
A hemoliyic disease that may appear during gestation or shortly after delivery.
Classification of erythroblastosis fetalis
1. Congenital hydrops (edematous form) is characterised by edema of skin, subcutaneous fat, meninges and brain substance, there is transudation in the cavities. Microscopically: erythroblastosis in the liver, spleen, lymphatic nodes, and kidneys. Signs of immaturity of organs in mature newborns can be found.
2. Anemia neonatorum (hemolytic anemia) is frequent in immature fetuses. The skin and mucous membranes are pale. Jaundice is absent. Hepatosplenomegaly take place. In the mildest form, the anemia may be only slight, and the child may survive without further complications. More severe hemolysis dives rise to jaundice and other features associated with hemolytic anemias.
3. Icterus gravis (severe jaundice of the newborn) is evident by the end of the first day. The disease develops quickly. The most serious threat in this disease is central nervous system damage known as kernicterus. In jaundiced infants, the unconjugated bilirubin appears to be particularly toxic to the brain tissue. The brain is enlarged and edematous and, when sectioned, is found to have a bright yellow pigmentation (kernicterus). The cells stain by yellow color. The liver and spleen are enlarged; they have the signs of erythroblastosis and hemosiderosis. There are bilirubin infarcts in the kidneys.
Histologically in all forms, the diagnosis of erythroblastosis depends on the identification of abnormally increased erythropoetic activity in the infant. The red cells series in the marrow is hyperactive and extramedullary hematopoesis is almost invariably present in the liver, spleen, and possibly other tissues, such as lymph nodes, kidneys, lungs, and even in the heart.
In early massive immunization of the mother, early fetopathy develops. The fetus dies before the birth, on the 5th - 7th month of gestation.
When the mother’s immunization is later and more moderate, the child is born alive with one of the forms of HDN.
In children who survived HDN, defects of CNS development (including complete idiopathy) may occur in future.
Sudden infant death syndrome (SIDS)
Included here since some cases of SIDS may be related to congenital cardiac disorders. Defined as sudden and unexpected death in a previously basically well infant, when the cause of death cannot be explained even after autopsy.
Probably a multifactorial entity or common end point of diverse derangements.
Ninety per cent of SIDS deaths occur in the first 6 months of life, most between the ages of 2 and 4 months. The deaths occur without a struggle during the night after a period of sleep.
Often there are minor antecedent respiratory tract infections.
Causes of death are unknown. Among innumerable hypotheses, those favored are:
- Cardiac arrhythmias.
- Disturbed regulation of respiration, “the apnea hypothesis”.
- Inherited disorders of fat oxidation.
- Unsuspected intestinal infection with Clostrium botulinum.
- Defective regulation of body temperature with resultant acute malignant hyperthermia.
Morphology
A variety of changes of uncertain significance.
Abnormalities in the myocardial conduction system have been observed, not always present and of diverse nature.
Subtle medial thickening of small pulmonary arteries and brain-stem gliosis suggests chronic hypoxia.
Right ventricular hypertrophy may be secondary to pulmonary vascular changes or a primary anomaly.
Also seen are retention of fetal hemoglobin, extramedullary.
INFECTIOUS DISEASES
Infectious diseases are those caused by infectious agents (viruses, bacteria, fungi). Protozoa and helminths cause invasive diseases. Infectious diseases have a number of common features.
Clinical-morphological characteristics of infectious diseases
Each infectious disease has its own causative agent, which can be isolated from the blood or excreted materials of the patient.
In infectious, one can observe formation of a primary infectious complex consisting of a primary affect, lymphangitis and lymphadenitis.
The route of the infection from the primary focus or complex may be lymphogenic, hematogenic, intracanalicular, and perineural, contact.
Each infectious disease is characterized by local changes in the portal of entry of infectious agent.
A number of common changes (rash, vasculitis, hyperplastic processes in the lymphatic nodes, spleen, bone marrow, inflammatory processes in the interstitial tissue and degenerative changes in the parenchymatous organs) are observed in infectious diseases.
Infectious diseases are chiefly cyclic. The course of the infectious disease is divided into incubative and prodromal periods and the period of main manifestations of the disease (phases of increase of the signs, climax and extinction).
Infections can be either exogenic or endogenic.
Infectious diseases are classified according to a number of signs.
Biological classification:
Anthroponoses - infectious diseases typical only for people.
Antropozoonoses - infectious diseases that can develop both in people and animals.
Biocenoses - a group of anthroponoses and anthropozoonoses transmitted through the bites of insects, which become the place of causative agent multiplying.
According to the etiology they are divided into
Viral.
Rickettsiosis.
Bacterial.
Fungal.
Protozoal.
Parasitogenic.
Classification according to the mechanism of transmission:
Intestinal.
Respiratory.
Blood (transmissive) transmitted by blood-sucking insects.
Infections of the external integument, {subcutaneous fat and muscles).
Infections with different mechanisms of transmission.
According to the duration there are
Acute.
Chronic.
Latent.
VIRAL DISEASES
Respiratory disorders are caused by a wide variety of viruses, of different families, species, and serotypes. These include:
Orthomyxoviruses (influenza A, B, and C – RNA virus).
Paramyxoviruses (respiratory syncytial virus, parainfluenza viruses, measles virus, mumps virus)
Adenoviruses.
Herpesviruses (varicella-zoster virus).
Cytomegalovirus.
Herpes simplex virus (HSV).
Picornaviruses (rhinoviruses, echoviruses, and coxsackieviruses).
Human respiratory coronaviruses.
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