Puerperal Mastitis. Treatment. Management of “non-reassuring fetal status.”

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.

Management of “non-reassuring fetal status.” Standart protocol of treatment includes:

- Indication for admitting to the hospital are BPP is - 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 30^th 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

Management in labor
- Avoid supine position of mother
- To arrest augmentation of labor pains with Oxitocin
- In case of intrapartum fetal distress:
- To make VE and evaluate obstetrical situation:
- In the 1st stage of labor cesarean section is indicated
- In the 2nd stage – forceps delivery/ vacuum delivery/ extraction of the fetus by podalic end (in breech presentation).

Intrauterine growth retardation (syn: dysmaturity, small-for-gestational-age-infant, iugr). Any infant whose weight is below the 10th percentile for gestational age is named a small-for-gestational age infant.

Etiology. An infant may be small at birth because of genetic factors. Nongenetic factors that can retard intrauterine growth are usually not apparent before 32 to 34 wk gestation and include placental insufficiency that often results from maternal disease involving the small blood vessels (as in preeclampsia, primary hypertension, renal disease, longstanding diabetes); placental involution accompanying postmaturity; infectious agents, such as cytomegalovirus, rubella virus, virus of toxoplasmosis.

An infant may also be small for gestational age if the mother is a narcotic addict, or a heavy user of alcohol, or to a lesser degree, if she smoked cigarettes during pregnancy.

The syndrome of intrauterine growth retardation (IGR) can be encountered in two forms:

· symmetric - (incidence is 10-30%) - develops from the early terms of pregnancy and is characterized by proportional lag of body mass and length of fetus. Reasons are various: intrauterine infections, chromosomal anomalies, inadequate nutrition of mother, genetic syndromes, mother’s harmful habits, radiation, medicinal therapy, hypoxic diseases in mother (heart diseases of dark blue type, severe asthma);

· asymmetric - (incidence is 70-90%) is characterized by lag of body mass at normal length of fetus (hypotrophy) with delay in development of some organs (liver, other parenchymatous organs). It is more common in the III trimester of pregnancy on a background of pregnancy complications (EPH-complex, multiple pregnancy, defects of development of placenta, bleeding in the III trimester of regnancy) and extragenital diseases.

Degrees of IGR at Pregnancy. I degree - lag in development of fetus up to 2 weeks.

II degree - lag in development of fetus up to 2-4 weeks.

III degree - lag in development of fetus over 4 weeks (irreversible changes and intrauterine fetal death are possible).

At IGR the delay or absence of uterus growth (disparity to gestational age of fetus) and absence of increase of body mass of pregnant are originally marked, then symptoms of chronic intrauterine fetal hypoxia occur. The delay of development of fetus may be accompanied by symptoms of threatened interruption of pregnancy. The first signs of IGR can appear in 18-19 or 24-26 wk. By 28-29 wk of pregnancy the delay of fetus development, as a rule, is symmetric, i.e. deficit of body mass and length of the fetus is available. This type of intrauterine growth retardation is less favourable.

The onset of syndrome in 32 weeks of pregnancy is more typical of asymmetric form.

If there is only a mass deficit at full-term newborn, it means that a factor causing retardation of fetal growth affected during the last 2-3 months of pregnancy.

After delivery of fetus the type of intrauterine growth retardation of the fetus is determined by a clinical picture for making a prognosis of the course of early neonatal period.

A Hypotrophic Type, or Asymmetric Form of IGR. At 1^st degree thinning of subcutaneous fat, decline of turgor of tissues occur.

At 2^nd degree the skin of a child is dry, pale, with peeling and chaps, the subcutaneous fat is thin. The course of neonatal period is usually complicated by asphyxia, metabolic disturbances. Early neurological disorders such as syndrome of hyperexcitability or suppression of the central nervous system come to light.

At 3rd degree of asymmetric form of IGR the skin is wrinkled, folded, dry, pale, with chaps. The subcutaneous fat is absent, muscular mass is diminished. In early neonatal period there is usually a hemorrhagic syndrome, anemias, neurological, cardiac, infectious complications.

A Hypoplastic Type, or Symmetric Form of IGR. Children at this variant of IGR look proportionally built but little. The degree of IGR is determined by deficit of body length and circumference of head in relation to term of pregnancy. In early neonatal period hypoglycemia, hyperbilirubinemia, infectious complications are common.

A Dysontogenetic Type. This type is encountered at combination of delay of IGR with vices of development. The state of children at this variant is determined by presence of hereditary diseases and vices of development.

Management of IUGR. Despite numerous approaches to managing IGR, there are no effective treatments to improve the growth pattern of a fetus. The universally available therapeutic option that shows improvement in outcome includes the antenatal administration of steroids in preterm pregnancies and delivery at an institution with a neonatal care unit that is able to deal with the management complexities of the growth?restricted neonate. Antenatal steroids should be given to any growth?restricted fetus whose delivery is expected before 34?weeks' gestation.

Betamethasone (given as a combination of betamethasone sodium phosphate and betamethasone acetate), is administered as two doses of 12mg given intramuscularly, 24 hours apart. Dexamethasone sodium phosphate is administered as four doses of 6mg given intramuscularly, 12 hours apart. As there are no effective treatments to reverse fetal growth restriction, prenatal management is aimed primarily at determining the ideal timing and mode of delivery.

This assessment must be individualised, depending on several variables: gestational age of the fetus, maternal health, severity of growth restriction and fetal well?being.At term

Prognosis. Perinatal asphyxia is the most serious potential complication for infants with IGR because of placental insufficiency, and if it can be avoided, a neurologic prognosis is quite favourable for these infants. Infants with IGR due to genetic factors, congenital infections, or maternal drug abuse often have a worse prognosis, which depends on specific diagnosis.