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Etiology and pathogenesis. Diagnostics of puerperal inflammatory diseases. 2. Imaging studies
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ETIOLOGY AND PATHOGENESIS.
The vaginal flora in late pregnancy and at onset of labor includes the following organisms: Doderlein bacillus (60-70%), yeast like fungus with increased prevalence of Candida albicans (25%), Staphylococcus albus and aureus, Streptococcus – anaerobic common, E. coli, M. hominis and Bacteroides group and others. These organisms remain dormant and become harmless during normal delivery conducted in aseptic conditions. Some conditions during labor may lead to penetration and propagation of microbes, namely:
· damage of cervicovaginal mucous membrane during labor, damage of the internal uterine surface, especially in placental site, which transform into an open wound during the 3rd stage of labor,
· the delay of blood clots in the uterine cavity, which are an excellent medium for the growth of microbes.
The pathogenicity of the vaginal flora may be influenced by certain factors, namely the conditions lowering the resistance – general or local, conditions favouring multiplication and increased virulence of microorganisms, introduction of microorganisms from outside, the increased prevalence of organisms resistant to antibiotics and chemotherapy. Pathogens may get into the labor canal from outwards due to lack of asepsis and antisepsis during labor. Mixed infection is the most often type nowadays.
Antepartum and intrapartum factors may facilitate the development of septic process. Antepartum factors include malnutrition and anemia, toxemia of pregnancy, premature rupture of amniotic membranes, chronic illnesses. Intrapartum factors comprise the internal examination during labor, especially after the membrane rupture, injuries of soft tissues, traumatic operative delivery, hemorrhages, retained bits of placental tissue or membranes.
SPREAD OF INFECTION
The following ways of spread of infection are distinguished:
· Direct. The infection of the fibroareolar tissue may occur directly by deep injuries of the genital tract. Such injuries are deep lacerations of the cervix, uterine injuries including cesarean section and vault tear.
· Lymphatic. The infection from the injured site reaches the parametrium through the lymphatic canals.
· Hematogenous. The infection also spreads by blood vessels.
· Mixed. One of the most common types.
Because of low immunity in postpartum period a puerperal septic inflammation is characterized by a high rate of spreading and generalization. On the other hand, there are a lot of atypical forms of infection, which can lead to incorrect diagnosis and treatment.
CLASSIFICATION OF PUERPERAL DISEASES
The classification of puerperal infection is developed by S. Sazonov and A. Bartels.
Various forms of puerperal diseases are regarded as separate stages of a single infectious process.
The first stage: septic infection does not extend beyond the area of the wound (endometritis, puerperal ulcer).
The second stage: the infection spreads beyond the primary focus but it is still localized in the area of the pelvis (metritis, parametritis, metrothrombophlebitis, adnexitis, thrombophlebitis of the pelvic veins, pelvioperitonitis).
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The third stage: the infection spreads out of the pelvic cavity, but is not generalized yet (diffuse peritonitis, progressing thrombophlebitis).
The fourth stage: the infection is generalized (general sepsis).
DIAGNOSTICS OF PUERPERAL INFLAMMATORY DISEASES
1. Laboratory studiesshould include the following:
• Complete blood count (CBC)
• Electrolytes
• Hemocoagulation tests
• Blood protein evaluation
• Blood cultures & sensitivity to antibiotics
• Urinalysis, with cultures and sensitivity tests
• Cervical or uterine cultures
• Wound cultures, if appropriate
• Lactate, if sepsis suspected
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2. Imaging Studies
• Pelvic US may be helpful in detecting retained products of conception, pelvic abscess, or infected hematoma.
• Contrast-enhanced CT or MRI are useful in establishing the diagnosis of septic pelvic thrombosis.
• In some cases, a contrast-enhanced CT examination of the abdomen and pelvis may be helpful if concurrent concern is present for other non-pregnancy–related abdominal/pelvic sources of the infection (eg, appendicitis, colitis).
Puerperal ulcers
These are purulent wounds formed at the site of lacerations and fissures on the perineum, vaginal wall, or uterine cervix. The wound surface is covered with a coat of pus; the adjacent tissues are hyperemic and edematous. The disease usually occurs on the 3-4th postpartum day. The clinical picture is not very significant: more often the patient feels some discomfort and burning in the damaged area; sometimes there may be insignificant elevation of temperature.
Treatment. Bed rest is recomended. Treatment of the wound is performed with a 3% solution of hydrogen peroxide; gauze impregnated with synthomycin emulsion should be placed on the ulcer; ultraviolet treatment of the ulcer is administered. To prevent the spread of infection, uterotonics (mammophizin 1ml intramuscularly, or oxytocin 2. 5 units intravenously) and antibiotics should be given.
Endometritis
It is an inflammation of endometrium after delivery. The case when the adjacent muscular fibres are involved into the inflammatory process is named metroendometritis.
Two forms of puerperal endometritis are usually distinguished:
· a classic form;
· an atypical form.
A classicform of puerperal endometritis usually starts from the 3rd–4th day after labor. The temperature elevates up to 38-39º C, the pulse rate accelerates accordingly, the appetite worsens and sleep deranges. Fever may also occur and it means growth of infection. Palpation of the low abdomen reveals painful, enlarged uterus, sometimes without clear borders. Vaginal discharges (lochia) are turbid, with traces of blood in the pus and a foul smell. Contraction of the cervical os may lead to remaining of contents in the uterine cavity called lochiometra. It is attended with pyrexia and worsening of the general condition of the patient.
Vaginal examination: the uterus does not correspond to the date of puerperal period in size (it is enlarged), softened, painful on palpation. The cervical canal is open for one or more fingers. Cervical discharges are rich in volume, purulent or sanguineous, with unpleasant smell.
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An atypical form. The onset of the process is later than in a classic form – after the 7-9th day. The main sign of this form is subinvolution of the uterus.
Treatment should be very intensive. Bed rest and intensive care are recommended. Antibiotic therapy includes: ampicillin 0. 5-1g 4-6 times daily (or cephazoline 0. 5-1 g every 6-8 hours) intramuscularly or intravenously; uterotonics (methylergometrine 1 ml intramuscularly or intravenously), desensitizing therapy, sedative therapy, vitamins, antipyretic drugs. Infusional therapy is very effective for these patients: a 5% glucose solution, physiological saline solution, frozen plasma, 10% albumin solution.
In case of retained bits of placenta tissue or membranes the instrumental curettage of the uterine cavity should be done in combination with complex therapy. In severe cases the intrauterine lavage should be applied.
Parametritis
It is an inflammation of parametrial tissues spreading through the genital soft tissues. Parametritis begins on the 10th or 12th day of puerperium. The first signs are chill and high temperature (39-40º C), pulse is accelerated and the lower abdominal pain develops. The disfunction of adjacent organs may occur due to their involving into the inflammatory process (frequent micturition, painful urination and defecation). An infiltrate can be palpated by side of the uterus during vaginal examination. The infiltrate is first soft but later becomes firm. It reaches the lateral pelvic wall to displace the uterus towards the opposite side. The clinical symptoms of parametritis are varied. Temperature, pains in the lower abdomen irradiating to the loin and thighs, the development of abscess accompanied by chill, high remittent temperature, a severe general condition are characteristic. If the abscess is not opened surgically it may open spontaneously (into the vagina or the bladder). The treament is the following: bed rest, antiinflammatory drugs, antibiotics, desensitizing therapy, intravenous infusions of saline solutions, frozen plasma, hemodes. The abscess is opened through the posterior fornix of the vagina (posterior colpotomy) or through the abdominal wall.
Adnexitis
Puerperal inflammation of the uterine appendages (tubes, ovaries) is termed adnexitis or salpingo-oophoritis. The disease begins on the 10th or 14th day of puerperium. The symptoms are as follows: elevated temperature, worsening of the general condition, intensive pain in the lower abdomen, urinary disfunction, painful defecation, constipation. At the beginnig of the process the abdomen is tense, sharply painful on palpation. The Shchotkin-Blumberg symptom may be possible. The vaginal examination reveals painful enlarged tubes and ovaries (on one or both sides), which mobility is limited due to commissures formed between the adnexa and adjacent organs. The treatment is bed rest, antibiotic and anti-inflammatory therapy, infusional therapy, sedatives, desensitizing drugs. Surgical treatment if indicated.
Pelvioperitonitis
It is an inflammation of the pelvic peritoneum. Puerperal pelvioperitonitis may occur due to septic inflammation or due to gonorrhea. The disease begins on the 15th–25th day of puerperium. The disease is manifested by chill, high temperature (39-40º C), sharp pain in the lower abdomen. The onset of the disease is marked by nausea, vomiting, tense abdominal muscles, positive Shchotkin-Blumberg symptom. The pulse is accelerated, general condition is bad, appetite is lost, sleep is deranged.
If pathogenetic therapy is given these symptoms subside, the infiltrate in the small pelvis is localized and resolved gradually. Commissures between the organs of the pelvic cavity remain after the patient’s recovery and lead to chronic pelvic pains. Principles of treatment are the same.
Pelvic Thrombophlebitis
Puerperal thrombophlebitis is an inflammation of veins of pelvic wall, which spreads from the genitalia. Thrombophlebitis of the uterine veins (metrothrombophlebitis) develops from metroendometritis. The symptoms in general are similar to those at endometritis. But pain is more significant, irradiating to the loin and legs. On vaginal examination the inflamed veins may be palpated as enlarged, painful, with tight cords on the lateral side of the uterus. Pelvic thrombophlebitis usually has similar symptoms: nagging, persistent pains in the lower abdomen, elevated temperature and pulse rate, enlarged painful uterus. On vaginal examination one can palpate the inflamed veins on the lateral side of the pelvis, enlarged, painful and hardened. The treatment is the same; spasmolytics and anticoagulative therapy should be added. The examination of blood clotting must be done every day to prevent thromboembolism.
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Puerperal Progressing Thrombophlebitis
It is an inflammation which occurs in puerperium, extending to the external and internal iliac and femoral veins and then giving rise to obstruction to the venous return to the limb.
Clinical features. Usually during the second week after delivery shivering attack or actual rigor occurs or the temperature rises up to 39-40º C and is quickly followed by clinical evidence of femoral thrombosis, the vein becoming hard and tender, and the whole leg swells and becomes painful. In case of superficial thrombophlebitis the overlying skin looks red. In case of deep venous thrombosis the leg becomes enlarged, edematous, and painful. The pulse rate is absent in the area of ankles.
Treatment. The patient is prescribed bed rest with the foot end of the bed raised above the heart level. Pain in the affected area may be relieved with analgetics and antipyretics (baralgin, indometacin); appropriate antibiotics are to be administered. Anticoagulants should be also administered: heparin 15, 000 units intravenously followed by 10. 000 units, 4 to 6 hourly when the blood is likely to be depressed to the therapeutic levels. Breast feeding should be arrested during the period of therapy. Reopoliglukin 400 ml intravenously droppingly, trental 5 mg /kg/body weight are necessary. In case of high risk of embolism surgical treatment is indicated.
Puerperal Peritonitis
Obstetrical peritonitis is one of the severest and most dangerous situations in clinical practice. Commonly the incidence of puerperal peritonitis is 1-4. 5%. The rate of maternal lethality due to peritonitis is 10-35%.
Most often the source of infection is the uterus (chorioamnionitis in labor, postpartum endometritis, endometritis after cesarean section, rupture of uterine sutures after cesarean section). There are a lot of contents in the uterine cavity after delivery and cesarean section: blood clots, elements of decidual membrane, elements of placental tissue; all these suggest a growth medium for microbes. Blood supply of the uterus, which is increased in pregnancy, facilitates the development of infectious process in the puerperal uterus (puerperal wound). The infectious–inflammatory development in this case happens against lowering immunity, general weakening of maternal organism after delivery, etc.
Thus uterus is an entry of infection in puerperal period.
Infectious agents: the most common type is mixed infection nowadays: Coli-bacillus, blue pus bacillus, staphylococcus, Bacillus proteus are of primary significance in development of puerperal peritonitis. Endogenous opportunistic infectious agents, which are resistant to antibiotics, take part in the development of the process. Anaerobic-aerobic colonies acquire greater significance in development and occurrence of puerperal peritonitis, as well as hospital infections.
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Pathogenesis of Obstetrical Peritonitis
The following ways of contamination are distinguished:
· the most common type is ingress of contamination (of infectious agents) into the abdominal cavity during operation (cesarean section);
· spread of microbes from the uterine cavity due to its rupture or perforation;
· contamination through the tube canals.
· hematogenic way of contamination.
The main factors of development of peritonitis are:
· congestive hyperemia of peritoneum;
· hyperpermeability of blood vessels of the peritoneum;
· transudation.
While entering the abdominal cavity, the causative agents provoke reflex irritation of peritoneal receptors resulting in hyperemia of peritoneum and hyperpermeability of blood vessels of the peritoneum.
Plenty of fluids, albumins, electrolytes are lost because of transudation through the increased permeability of the intestinal walls. Due to leukocyte migration the exudation becomes purulent, due to fibrin production the adhesive processes develop, the intestinal motility decreases, and paralytic (adynamic) ileus develops. It is followed by production of toxic agents and metabolites (kinins, histamine), while the level of serotonin decreases in this process, which is a mediator of excitation of intestinal muscles.
Thus, due to paralytic condition the intestinal loops become overdistended, the intestinal walls become more permeable for fluids, microbes, toxins. Due to loss of albumin into intestinal space hypoproteinemia develops. The level of total protein decreases to 50-45 g/l, which is a threatening prognostic symptom. The colloid-oncotic pressure decreases, hypovolemia and hemoconcentration, DIC syndrome, thrombosis, multiple organ failure develop and death occurs.
Classification of Peritonitis
It is subdivided into:
· local peritonitis (pelvioperitonitis)
· diffuse peritonitis
Acute Diffuse Puerperal Peritonitis
It may occur after natural way of delivery, after obstetrical operations (application of forceps, etc), and after cesarean section.
After natural way of delivery peritonitis develops due to spread of infection from the uterine cavity by lymphatic vessels and through fallopian tubes.
The disease occurs a few days after delivery, but it may also appear on the 1-2nd day of puerperal period.
Clinical features. The following stages of obstetric peritonitis are usually distinguished:
· a reactive phase
· a toxic phase
· a terminal phase
The first phase (first 24 hours) is manifested by absence of metabolic failure; general condition is not bad but enteroparesis just starts. Signs of inflammation may be found in blood tests.
A toxic phase (24-72 hours) is manifested by elevated intoxication, worsening of general condition, development of severe metabolic changes, increase of enteroparesis.
A terminal phase (> 72 hours) is manifested by deep changes in the central nervous system, very severe general condition, the function of abdominal organs being deeply changed.
The typical clinical signs are increased body temperature up to 39-40˚ C, shivering, hyperemia of the face, a dry, coated tongue. In severe cases, due to decreased immune reactivity of maternal organism the body temperature may be normal. One should pay attention to the difference between axillary and rectal temperature (in the rectum the temperature is 1. 5-3˚ C higher than in axillary cavity). The pulse rate is elevated but often there is no correspondence with the elevation of temperature (“scissors” symptom-Vreden’s symptom). The pulse is rapid, weak and soft on palpation, arrhythmia is not rare. The arterial blood pressure decreases. Respiration is quickened (tachypnea). At the beginning the upper abdomen takes part in respiration, then discontinues. Nausea, vomiting, tympanism appear.
It is of significance that Shchotkin-Blumberg symptom and muscle tension (defance musculorum) are not typical of diffuse obstetric peritonitis, because of overdistension of abdominal muscles due to pregnancy. The intestinal peristalsis is slowed at first, and then it stops at all. Passage of gases is arrested; stool retention is typical of these patients. There is moderate tympanitis in the upper parts of the abdomen, and weakening of percussion sound in the lower abdomen on percussion.
On vaginal examination one can find protrusion of posterior vaginal fornix, flattening of lateral fornices, the cervical canal gapes, discharges are bloodish. Vaginal examination is painful. In puncture of Duglas pouch a serous effusion may be taken.
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Significance: at intensive therapy the clinical course of peritonitis may be wave-like. A temporary effect of treatment may be evaluated as a good result, and if the treatment is discontinued, the recurrent worsening of general condition happens. Intensification of intoxication, suppression of host defenses will increase probability of maternal death.
But usually in obstetrical practice peritonitis is masked by atypical clinical course that makes this disease more dangerous.
As to peritonitis after cesarean section, it may develop in three forms:
1. The first form – an early form. It develops at the end of the 1st or at the beginning of the 2nd day after the operation. It means that the peritoneum was infected during the operation.
2. The second form is middle depending on the term of development. This form occurs in term of 3-4 days after cesarean section. Usually it develops because of enteroparesis in post-operative period.
3. The third form is late – it occurs in term of 7-9 days after the operation; usually the main reason of this form is incompetent surgical suture.
Treatment. Treatment of diffuse peritonitis is surgical. The earlier diagnostics and surgical treatment are – the better prognosis and outcome are. Sometimes it is necessary to administer a conservative treatment for 6-7 hours to prepare the patient for operation. This treatment includes antibiotics, anti-inflammatory, anti-histamine therapy, infusion therapy, which can lead to stabilization of the heart condition, arterial blood pressure, to prevention of maternal death during the operation. The volume of operation is extirpation of the uterus, treatment and drainage of the abdominal cavity.
A bacteriological examination of the cervcal discharge and a secret, contained in the Douglas pouch (which is obtained by puncture the posterior fornix of the vagina or during the surgical operation) is indicated for patients with acute pelvic peritonitis. The culture of the pathogens and sensitivity to antibiotics would be determined. The data obtained in this case is the background for the choice of effective antibiotic therapy of the patient. Antibiotic therapy usually should be started before the operation, continued during and after operation.
An intensive therapy of diffused inflammation should be continued in post-operative period.
Common principles of choice of antibacterial medications are:
1. Pathogen is unclear - use gentamicin + metronidazole, which is effective for E. coli and anaerobic bacteria.
2. When the bacterial culture and drug susceptibility test results are detected - the choice should be based on drug sensitivity test results.
3. Against the backround of the first choice of antibiotics - determine whether antibiotic to be replaced. If the general effect is good - do not replace; if medication is not effective - it should be replaced dependant on results of sensitivity test, use the stronger medication with higher doses
Puerperal Mastitis
Unless proper precautions are observed during suckling, the breast may become infected by bacteria which gain access to it through superficial skincracks, or through the ducts which open upon the nipple. The lactating breast is particularly prone to infection by staphylococcus pyogenes and infections by pneumococcus and other pyogenic bacteria are rare. It is often difficult to determine the cause of infection. As, however, about 50 percent of nursing mothers are “carriers” of staphylococcus pyogenes in nasopharynx, the surface of the breast may be frequently contaminated by their fingers and clothing. Alternatively infection may be derived from the baby's nose. A 'cracked nipple' presents a site of entry for infective agents, then a direct spread of infection may result in the formation of a sub-areolar abscess. Infection may also spread by way of the milk ducts with or without an initial lesion of the nipple thus causing a deeper abscess in the breast tissue. Minor disorders of lactation predispose to infection. The 'engorged breast' frequently seen when the milk first comes in on the third or fourth day of puerperium occasianally becomes infected in a patient who is debilitated by some medical disorder or as the result of pregnancy toxaemia or complicated labour. More frequently infection complicates a 'flushed breast' which is due to a blocked mammary duct and is most frequently seen about or ten days after delivery. Local pain or a tender swelling in one quadrant of the breast is the first sign of this condition but usually, in addition, the patient has a temperature of 39°C by Celsius and higher and the skin over the affected part of the breast soon develops a marked hyperaemic flush. The condition often subsides so rapidly with treatment that it is difficult to believe that it is due to a primary infection. More probably the duct is blocked in the first instance by swelling of its walls and coagulation of milk in its lumen resulting from damage inflicted by the infant when suckling; pyrexia and general malaise may be the result of absorption of protein from the milk under tension in the blocked lobule. Secondary infection is however likely to develop as bacteria rapidly multiply in the stagnant milk if they once gain access to it.
The onset of true infective mastitis, a condition most commonly seen some weeks after delivery, is attended by a rapid rise in temperature, headache and other signs of general malaise and by severe pain in the affected breast, an acutely tender swelling develops in the breast and a wedge-shaped area of skin flushing appears over it, the apex being towards the nipple. Suppuration may be accompanied by rigors and the common local signs are softening of the inflamed area, redness and edema of the skin and fluctuation if the abscess is superficial. A sub-areolar abscess may rupture on to the surface or in to a large milk duct, leading to discharge of pus from the nipple. Sometimes both breasts may be affected but seldom simultaneously, the second breast probably becoming infected from the first through sucking.
Any patient who has signs of infective mastitis must be isolated until she is proved to be free from infection. Her baby should be kept with her and be tended by her as far as possible to reduce the risk of spreading the infection.
Treatment. Prophylaxis of mastitis consists in proper management of breasts during pregnancy and puerperal period. In brief, they should be washed thoroughly twice a day but the nippels should not be scrubbed. Flattened nipples should be drawn out and an elevating supporting brassiere, a size or two larger than normally should be worn. When the breasts are considerably engorged as the milk comes in, a single tablet of ethinyl oestradiol 0. 25 mg (and perhaps repeated in 6 hours) may be given with reasonable safety at this early stage to prevent the condition from progressing, especially if it is practical to put the child to the breast as well. Local heat in the form of an electric hot pad is very comforting. If, owing to the death of the child or any other reason, the mother does not suckle, the breasts should be thoroughly washed and a firm, uplifting breast binder should be applied over a protective layer of sterile cotton wool. It is not often necessary to restrict the patient’s fluid intake. If local or generalized tender swelling of the breasts persists for more than twenty four hours and is associated with pyrexia an intramucular injection of methicillin (cebexin) should be given, 1 g every six hours. When there is evidence of infective mastitis the following measures should be taken:
· The breast should be completely tested by supporting it firmly with an uplift breast-binder and by the cessation of suckling from it, the milk being gently pressed out at feeding times and discarded.
· A course of methicillin injections (1 g every 6 hours) should be maintained.
· Dry heat should be applied locally by means of an electrtc pad. Suppurating areas must be drained by one or more incisions radiating from the nipple. After four or five day's penicillin therapy cultures from the wounds are often sterile and then it is possible, if they are large and gaping, to dose them by secondary suture, thereby shortening the period of convalescence, but if this is done penicillin therapy should be continued for at least a further week. It is unwise to continue, or to attempt the resumption of breast-feeding from a breast which has not been shown to be free of infection.
Self Test
1. Puerperal endometritis is:
A. the 1st stage of puerperal septic diseases
B. the 2nd stage of puerperal septic diseases
C. the 3rd stage of puerperal septic diseases
2. Which of the forms of puerperal endometritis is most common nowadays?
A. classic form
B. atypical form
3. Diffuse peritonitis is
A. the 1st stage of puerperal septic diseases
B. the 2nd stage of puerperal septic diseases
C. 3rd stage of puerperal septic diseases
4. The treatment of peritonitis should be:
A. nonsurgical
B. surgical
5. What is the volume of operation in patients with peritonitis after cesarean section?
A. extirpation of the uterus, treatment and drainage of the abdominal cavity
B. amputation of the uterus, treatment and drainage of the abdominal cavity
C. laparotomy and treatment and drainage of the abdominal cavity
6. Shchotkin-Blumberg symptom is:
A. atypical of diffuse obstetric peritonitis
B. typical of diffuse obstetric peritonitis
7. Metrothrombophlebitis is:
A. thrombophlebitis of the uterine veins
B. thrombophlebitis of veins of the pelvic wall
C. thrombophlebitis of deep femoral vein
D. superficial vein of the shank
8. The onset of puerperal mastitis is attended by all the following except for:
A. rapid elevation of temperature
B. headache
C. general malaise
D. severe pain in the affected breast
E. purulent discharge from vagina
9. Antibiotic therapy in case of puerperal mastitis is:
A. indicated
B. contraindicated
10. Removing the source of infection (uterus, adnexa) in general sepsis should be performed:
A. just at making the diagnosis of sepsis
B. after stabilization of hemodynamics
CHAPTER 35. PERINATOLOGY. CONCEPTION OF A FETOPLACENTAL SYSTEM
Birth of a viable healthy child is the basic end of normally flowing pregnancy. All activity of organism of mother during pregnancy is directed at providing the normal development of fetus. The normal development of fetus is determined by permanent coordination of functions of two organisms, i. e. of mother and fetus. Coordination of functions of mother’s and fetus’ organisms is realized by a special functional system “mother-fetus”. Another name of this system is fetoplacental or complex. Thus, the fetoplacental system consists of two functional subsystems:
· functional hemodynamic system of maternal organism, furnishing circulation of the fetus (delivery of necessary nutritives, biologically active substances, elimination of products of metabolism, etc. );
· endocrine functional system of the fetus, which activity is directed at maintenance of its homeostasis.
A placenta is the main connective link between a mother and fetus. Before the formation of placenta the communications between a maternal and fetal organisms are unaccomplished. In the fetoplacental system the placenta, both for mother and fetus, is the main bilateral humoral communication channel between mother and her fetus. On one hand, the placenta reliably divides antigenic different organisms of mother and fetus; on the other hand, it serves as a connective link providing an active exchange between them. The role of placenta is extraordinarily great both at physiological course of pregnancy and at unfavorable terms of intrauterine development of fetus related to complications of pregnancy and birth, as well as to diseases of mother and fetus.
The functions of placenta are varied. Through the placenta the nutrition and interchange of gases of the fetus, the selection of products of metabolism are carried out, forming the hormonal and immune status of the fetus. In the process of pregnancy the placenta replaces the failing functions of blood-brain barrier to the fetus, protecting its nerve centres and the whole organism from effect of toxic factors. Of no small importance is the role of amniotic fluid and fetal membranes in realization of these functions, which together with placenta form a single complex. The placenta is an endocrine gland synthesizing hormones with participation of maternal and fetal predecessors. The placenta cooperating with organs and tissues of the fetus promotes the formation of the fetal adaptive reactions.
The placenta not only connects two different antigenic organisms (mother’ and fetus’), but also disconnects them. It is presented by two systems of blood circulation separated from each other by a placental membrane, or “placental barrier”. It is through a placenta barrier that the processes of exchange between a mother and fetus take place.
In interrelation between the organisms of mother and fetus the paraplacental exchange which takes place through the amniotic fluid and extraplacental fetal membranes is of particular significance. The transition of water, electrolytes, products of metabolism of mother and fetus are carried out through membranes. There is an active transport of sodium in amniotic membranes.
From certain stages of its developmenrt, the fetus joins in adjusting both its own and maternal homeostais. Special part in that is taken by the endocrine system of the fetus. So, a special role of adrenal glands of the fetus in metabolism of estrogens during pregnancy is well known. From androgenic hormones, acting from fetus, the synthesis of estrogens is carried out in placenta.
Thus, estrogens are products of a single fetoplacental system. To the action of estrogens many biochemical processes taking place in myometrium are related, e. g. growth, increase of ribonudeic acid and actomyosin synthesis, strengthening of synthesis and activity of enzyme systems participating in these processes, rise of power exchange, accumulation of glycogen, adenosine triphosphate (ATP), etc).
Thus, the fetoplacental system is the unique system incorporated by the common, biologically important function of saving a man, as a biological kind. A difficult mechanism of adjusting of this system provides cooperation between the organism of mother and fetus, directed at an ultimate goal - birth of healthy posterity. The disfunction of fetoplacental system, the so-called fetoplacental insufficiency, results in development of different pathological states of fetus (intrauterine fetal hypoxia, asphyxia, intrauterine growth retardation).
Intrauterine fetal distress
The diminished oxygenation of the fetus results in a complex of metabolic complications up to intrauterine fetal death termed intrauterine distress (also known as fetal hypoxia).
Incidence. The incidence of fetal distress is 4-6%.
Classification
Hypoxia of the fetus usually develops as a result of altered transport of oxygen through the placenta and/or disturbed utilization of oxygen.
Depending on pathogenesis, the following types of fetal hypoxia are distinguished:
· hypoxic hypoxia means a low level of oxygen in blood (for example, due to low level of oxygen in the air);
· circulatory hypoxia means microcirculatory disturbances, which lead to hypoxygenation of tissues, while the level of oxygen in blood is normal;
· anemic hypoxia means a low level of erythrocytes or hemoglobin, etc.;
· tissue hypoxia which develops in cases of disturbed condition of cells; they can not utilize oxygen.
· a mixed form which is more common.
Depending on clinical course, acute and chronic fetal distress is distinguished.
Etiology
The etiological factors of chronic form are:
· maternal diseases, which lead to maternal hypoxia (heart diseases, diabetes mellitus, anemia, pulmonary diseases, intoxications, infections), occupational hazards;
· complications of pregnancy (preeclampsia and eclampsia syndrome, postmaturity, polyhydramnios);
· fetal diseases (hemolytic disease, generalized intrauterine infection of the fetus, germinal developmental defects).
A chronic form of intrauterine distress develops during pregnancy, has a prolonged course and may lead to fetal hypotrophy, dismaturity, intrauterine fetal death, asphyxia neonatorum.
The etiology of acute form of fetal distress may be placental abruption, placenta previa, compression of the umbilical cord, inadequate blood perfusion on the placenta. Insufficient amount of oxygen is delivered to the fetus in convulsive contractions of the uterus. Hypoxia may develop due to disorders in the cerebral blood circulation which results from prolonged pressure of the birth canal on the fetal head.
An acute form of intrauterine distress more often develops during labor (due to abnormalities of labor pains, cord compression, etc. ) and rarely during pregnancy (uterine rupture, placental abruption).
Pathogenesis of intrauterine fetal distress
The diminished transplacental diffusion of oxygen leads to fetal hypoxemia, while the following processes develop as a result:
· increased intensity of placental circulation;
· increased production of catecholamines, renin, vasopressin, glucocorticoids;
· increased tonus of the vessels, decreased volume of vascular rate, blood deposition in the liver of the fetus;
· prevalent blood supply of the brain, heart, adrenal glands, diminished oxygenation of the lungs, kidneys, gastrointestinal system of the fetus;
· changing the heart function.
Clinical Picture
The main clinical features of fetal distress are disturbances of the fetal heart sounds, changing of intrauterine fetal mobility and amniotic fluid. The symptoms depend on significance of oxygen insufficiency.
Three stages of intrauterine fetal hypoxia may be distinguished:
· The first is initial, or developing distress. It is characterized by tachycardia > 160 beats per minute (bpm), the fetal heart sounds become loud and sonorous, fetal mobility is increased.
· The second stage is progressive distress. It is characterized by bradycardia up to 110–100 bpm, the fetal heart sounds become dull, arrhythmia occurs in this stage, and fetal mobility decreases.
· The third stage is a severe intrauterine distress of the fetus. It is characterized by a progressive bradycardia (the rate of the fetal heart sounds is less than 100 bpm), progressive arrhythmia and dullness of heart sounds; fetal mobility is decreased or absent.
The diagnosis is based on:
· previous anamnesis (conditions of life, nutrition, medical diseases, the course of pregnancy, complications, if any, and treatment);
· character of intrauterine fetal movements;
· auscultation of the fetal heart sounds;
· fetal heart rate monitoring (cardiotocography);
· ultrasound examination (biophysical profile);
· Doppler investigation
· other investigations: amnioscopy, amniocentesis and biochemical examination of amniotic fluid.
Interrogation of the patient, as well as external palpation and auscultation help to suggest intrauterine fetal hypoxia, while the fetal heart rate monitoring and ultrasound examination help to determine the stage of hypoxia and management.
The Fetal Heart Rate Monitoring
Either an external device (cardiotocography, ultrasound Doppler principle) or an internal electrode attached to the fetal scalp is used to monitor the fetal heart rate in conjunction with uterine contractions.
Three aspects are to be noted when assessing cardiotocography: basal fetal heart rate, beat-to-beat variation, any transient changes of fetal heart rate in relation to uterine contractions.
The basal fetal heart rate is a rate per minute in between uterine contractions. It normally varies between 120 and 160 beats per minute. Base line bradycardia is defined as a rate of less than 120 beats per minute. Base line tachycardia is defined as a base line fetal heart rate of over 160 beats per minute. In either variety, association of some other abnormality requires further investigation.
Beat-to-beat variation is probably the most reliable index of intrauterine fetal status. Beat-to-beat variations are estimated as physiological at amplitude of changes from beat to beat 10-25 b/min. Pathological beat-to-beat variation means that amplitude of changes from beat to beat is less than 5 beats per minute.
Now-a-days, it is recommended that the term fetal distress should be replaced with “non-reassuring fetal status. ”
Alteration of Fetal Heart Rate in Relation to Uterine Contractions
Acceleration pattern: a rise of fetal heart rate which coincides with the uterine contraction is of little significance.
Deceleration pattern: a slowing-down of fetal heart rate which concides with the uterine contractions. Three basic types of deceleration are observed and are called early, late and variable. In early deceleration (type I Dips), the fetal heart rate begins to slow at the beginning of uterine contraction; nadir of deceleration (the lowest point of the fetal heart rate) coincides with the apex of the uterine contraction and the fetal heart rate returns to normal before the contraction passes off. Early deceleration is physiological. It is regarded as being due to head compression and can be prevented by atropine. In late deceleration (type II Dips), the fetal heart rate begins to slow after the onset of contraction; nadir of deceleration occurs after the apex of the contraction and fetal heart rate returns to normal after the contraction passes off, but before the next uterine contraction. This is suggestive of chronic fetal hypoxia. Variable deceleration includes all other patterns of temporary slowing of fetal heart rate which are not necessarily related to uterine contractions. It is thought to indicate cord compression and may disappear with the change in position of the patient. Thus, normal tracking would show a base line rate of 120-160 beats/min with a base line variation of more than 5 beats/min. There is no episode of bradycardia even with Braxton-Hicks contractions. If there is late and variable deceleration of the fetal heart rate in response to uterine contractions, it indicates fetal hypoxia.
A basic ultrasound examination may be used to identify fetal presentation, fetal cardiac activity, localization of the placenta, determination of amniotic fluid adequacy, etc. The biophysical profile (BPP) is a method of ultrasound fetal assessment that includes the following: amniotic fluid volume, fetal tone, fetal movement, fetal breathing, nonstress test. A score of 2 (normal) to 0 (abnormal) is assigned to each component. Summary score of 8-10 is normal fetal condition, 6 is equivocal, 4 –fetal hypoxia, 0-2 score means a severe fetal distress demanding urgent cesarean section.
Doppler investigation represents the blood flow (microcirculation) in the fetal part of placenta (fetal blood supply and oxygenation).
Signs of intrauterine fetal distress in Doppler investigation are:
· failure of blood stream in uterine artery (mother’s blood flow to the placenta)
· failure of blood stream in placenta.
· failure of blood stream in uterine artery and in umbilical artery.
Amnioscopy
Transvaginal amnioscopy may be used to identify meconium staining of amniotic fluid. The colour of the fluid becomes dark-green, it may be associated with maternal hypertension, prolonged pregnancy, suspected fetal growth retardation, fetal distress, etc. It is less used nowadays.
Management of “non-reassuring fetal status. ”
Standart protocol of treatment includes:
· Indication for admitting to the hospital are BPP is < 6, recurring 7-8 score; diastolic blood stream in umbilical arteries is slow.
· Electronic fetal monitoring should be restarted in theatre and maintained as long as possible.
· Investigation to determine the type and reasons of fetal distress.
· Oxygen inhalations.
Administration of supplemental oxygen to the mother results in improved fetal oxygenation, assuming that placental exchange is adequate and umbilical cord circulation is unobstructed.
· Maternal position.
The left lateral positioning releases vena caval compression by the gravid uterus, which allows the increased venous return, increased cardiac output, increased BP, and therefore improved uterine blood flow.
Before the 30th week of pregnancy treatment of concomitant disease is indicated: treatment of maternal anemia, hypertensive syndromes, heart diseases, premature uterine contractions, excessive uterine contractions, etc.
· Medicamental treatment
· Tocolysis terbutaline 0. 25 mg subcutaneous (0. 5 ml from a 1ml ampoule). alternatively for immediate action Glyceryl trinitrate (GTN) sublingual spray, 2 puffs initially, repeat after 1 minute until contractions stop, maximum 3 doses
· Repeated investigation is indicated to determine the effect of treatment. In case of non-effective treatment urgent delivery (abdominal or vaginal) is indicated.
· Management after the 30th week – the most appropriative is urgent cesarean section
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