notes/DC Dutta Obstetrics 10th Edition_13.txt

Presence  of bleeding  from  the sloughing wound  of cervicovaginal canal should be controlled by hemostatic sutures.  Secondary hemorrhage  following  cesarean section may, at times, require laparotomy. The bleeding from uterine wound can be controlled by hemostatic sutures; may rarely require uterine artery embolization, ligation of the internal iliac arte1y or may end in hysterectomy.
Im Chapter 28: Complications of the Third Stage of Labor



►   Complications of third stage of labor are: (a) PPH, (b) Retained placenta, (c) Shock, (d) Pulmonary embolism, and (e) Inversion of uterus.
►   Obstetric hemorrhage: The major cause of maternal death both in the developed and developing countries. Clinical definition of PPH is more important than the quantitative definition of blood loss >500 ml following birth of the baby.
►   Common causes of PPH are (4Ts): (a) Atonic (80%), (b) Traumatic, (c) Retained tissues, and (d) Coagulopathy.
►   Visual estimation of blood loss is inaccurate. Clinical assessment of maternal health should be done in assessment of PPH.
►   Prediction and prevention of PPH may be possible to some extent, though most cases of PPH have no identifiable risk factor.
►   The 'golden hour' is the time at which resuscitation must be started to ensure best chance of survival. The probability of survival decreases sharply after the first hour, if the patient is not effectively resuscitated.
►   Full management protocol for major PPH (blood loss > 1 L) includes: (a) Communication, (b) Resuscitation, (c) Monitoring and investigations, and (d) Arrest of bleeding.
►   Assessment of Shock Index (SI) and the'rule of 30', is the useful clinical guide to manage the patient.
►   Volume replacement should be quick and balanced. Crystalloid (warmed and isotonic) up to 2 L; colloid up to 1-2 L; cross-matched blood; FFP 4 units for every 6 units of PRBC. Platelets (if count <50 x 109/L) and cryoprecipitate (if fibrinogen <1 g/L).
►   Therapeutic goals is to maintain:• Hemoglobin >8 g/dl • Platelet count >50 x 109/L • Fibrinogen >2 g/L • APTT <1.5 times, the normal • Prothrombin Time (PT) <1.5 times normal.
►   Blood transfusion is as soon as possible. When needed immediate transfusion with group 0, Rh-D negative and K negative is to be done. Routine use of r FVII a is not recommended.
►   Cases with atonic PPH, the following pharmacological agents are most helpful. These are: oxytocin (IV/IM), ergometrine IV/IM; carboprost IM/intramyometrial or misoprostol P/R. Tranexamic acid 1 g IV is given (WHO), when other uterotonics have failed. It is repeated by 30 minutes, if needed.
►   Injection tranexamic acid (0.5-1.0 g), in addition to oxytocin, may be given to a woman with PPH following cesarean delivery (RCOG-2016).
►   The mechanical and conservative surgical measures are: Bimanual uterine compressions, balloon tamponade, hemostatic breast sutures, bilateral ligation of uterine arteries, bilateral ligation of anterior division of internal iliac arteries or selective arterial embolization.
►   Stepwise uterine devascularization and internal iliac artery ligation include successive ligation of: (i) one uterine artery, (ii) both uterine arteries, (iii) low uterine artery (one and both), (iv) one and (v) both utero-ovarian arteries, and (vi) internal iliac artery ligation (Figs. 28.6 and 28.7).
►   Hysterectomy is the last resort in a rare case. However, decision for hysterectomy should not be delayed. A second consultant may be involved in decision-making.
►   lntraoperative cell salvage should be considered for emergency use associated with cesarean section.
►   Multidisciplinary team approach for management of PPH should be made. All staff should receive training in the management of obstetric emergency including PPH.


RETAINED PLACENTA

DEFINITION: The placenta is said to be retained when it is not expelled out even 30 minutes after the birth of the baby (WHO, 15 minutes).
CAUSES: There are three phases involved in the normal expulsion of placenta: (1) Separation through the spongy layer of the decidua; (2) Descent into the lower segment and vagina; (3) Finally its expulsion to outside.
Interference in any of these physiological processes, results in its retention.
■    Placenta completely separated but retained this is due to poor voluntary expulsive efforts.
■    Simple adherent placenta is due to uterine atonicity in cases of grand multipara, overdistension of uterus, prolonged labor and uterine malformation or due to bigger placental surface area. The commonest cause of retention of non-separated placenta is a tonic uterus.
■    Morbid  adherent  placenta-partial  or  rarely, complete.
■  Placenta incarcerated following partial or complete separation  due  to  constriction  ring  (hourglass

contraction),  premature  attempts  to  deliver  the placenta before it is separated.
DIAGNOSIS: The diagnosis of retained placenta is made by an arbitrary time (15 minutes) spent following delivery of the baby. Features of placental separation are assessed (p.  125).  The  hourglass  contraction  or  the  nature  of adherent  placenta  (simple  or  morbid)  can  only  be diagnosed during manual removal.

DANGERS: The risks involved in prolonged retention of placenta are:
(1) Hemorrhage. (2) Shock is due to-(a) blood loss, (b) at times unrelated to blood loss, especially when retained more than one hour. (3) Puerperal sepsis. ( 4) Risk of its recurrence in next pregnancy.
I MANAGEMENT
PERIOD OF WATCHFUL EXPECTANCY
■    During the period of arbitrary time limit of half an hour, the patient is to be watched carefully for evidence of any bleeding, revealed or concealed and to note the signs of separation of placenta.
Chapter 28: Complications of the Third Stage of Labor

■   The bladder should be emptied using a rubber catheter. ■   Any bleeding during the period should be managed as
outlined in third-stage bleeding.
RETAINED PLACENTA:
♦   Separated	♦   Unseparated	♦    Complicated
Placenta is separated and retained-to express the placenta out by controlled cord traction.
Unseparated retained placenta (apparently uncom­ plicated): Manual removal of placenta is to be done under general anesthesia as described earlier.


PLACENTA  ACCRETA  SPECTRUM  (PAS) (Syn: Placenta Adherenta)

It is the rare  disorder of placentation, in which the placental villi are directly anchored to the myometrium partially or completely without any intervening decidua. The  probable  cause is the absence of decidua basalis and  poor  development  of  fibrinoid  layer.  Overall incidence of placenta accreta or its variations is 1 in 800 deliveries.
Risk factors (Box 28.2):
The risk of placenta accreta with placenta previa in an unscarred uterus is about 3%. The risk rises sharply with increasing number of Cesarean Delivery (CD). Placenta previa with one prior CD, the risk of being accreta is about 8%; whereas with two, it is 17%; and it is 40% with prior three and 61% with four or more cesarean sections.
Diagnosis  is  mostly  made  with  USG,  using  gray scale, power Doppler study, 3D images and with MRI.


■   Endometritis.	■   Adenomyosis.
■   Cesarean Delivery (CD).	■   Uterine curettages. ■   Manual Removal of Placenta (MRP).	■   IVF procedures.
■   Uterine Artery Embolization (UAE).	■   Myomectomy. a   Endometrial resection.	■   Chemotherapy.



MRI (added benefits over USG diagnosis of PAS	USG)
■   Loss ofclear zone between the	■   lntraplacental bands placental bed and the myometrium.         (T2-weighted images).
■   Thinning ofmyometrium (<1 mm)	■   Depth of myometrial
■   lntraplacental lacunae.	invasion.
■   Loss of hyperechoic line between	■   Diagnosis of posterior uterine serosa and the bladder.                  placenta previa.
■   Placental bulge and/or exophytic	■   Women with obesity. mass-invading beyond the uterus
to the bladder.
■   Hypervascularity between myometrium and posterior wall of the bladder (Tornado vessels).




Fig. 28.8: Placenta increta.

(Table  28.1):   Unexplained  rise  of  maternal  serum aFP  is  observed  with  placenta  accreta.  Pathological confirmation includes-(a) absence of decidua basalis, (b) absence ofNitabuch's fibrinoid layer (accreta), and (c) varying degree of penetration of the villi into the muscle bundles (increta) (Fig.  28.8) or up to the serosal layer (percreta). Depending on the extent of invasion, grading of  PAS has  been  made  (Ch.  42,  p. 628).  In  advanced cases (G3B), it invades the bladder wall and in G3C it invades the other pelvic organs. Levels of MSAFP is found raised.
The risks include hemorrhage, shock, infection and hysterectomy.
MANAGEMENT:   ♦   Multidisciplinary  team  approach in management is to be done. Delivery   is commonly done in a tertiary care hospital with the facilities of blood banks, interventional radiology and the presence of a pelvic surgeon. Cesarean delivery is done at 34-36 weeks of pregnancy.
In partial placenta accreta (focal) ➔ To remove the placental tissue as much as possible.  Effective uterine contraction and hemostasis are achieved by oxytocic and if necessary, by intrauterine plugging. Sometimes bleeding areas are oversewn. If the uterus fails to contract, an early decision of hysterectomy have to be taken and this is preferable in multiparous women.
♦   In total placenta accreta, hysterectomy is indicated in parous women following cesarean delivery. Patients desiring to  have  a  child,  conservative  attitude  may be taken.  This consists of incising the  uterus  above the placental attachment and clamping and cutting the umbilical cord as close to its base as possible and leaving behind the placenta, which is expected to be autolyzed in due course of time. Appropriate antibiotics should be given. Any attempt of placental separation risks massive hemorrhage and ends in hysterectomy in 100% of cases. Place of interventional radiology: Intraoperative  placement  of  internal  iliac  arterial
Chapter 28: Complications of the Third Stage of Labor

balloons  or  uterine  artery  embolization  is  done. Postoperative therapy with methotrexate has been done for conservation of the uterus.
♦  In a rare case, placenta accreta may invade the bladder (placenta percreta). In that case, it is better to avoid placental  removal.  It  may need hysterectomy and partial cystectomy.
♦  Other options are: Wedge resection of the placental implantation site (partial myomectomy) is done.
■  Complications of uterine conservations are: Secondary hemorrhage, late hysterectomy (58%), fistula for­ mation, sepsis and death.
Follow up: Conservative surgery (uterus sparing) when done successfully, subsequent fertility is not affected. However risks are-recurrent PAS, uterine rupture, PPH and peripartum hysterectomy.

INVERSION OF THE UTERUS

It   is   an   extremely   rare   but   a   life-threatening complication  in  third  stage  in which  the  uterus  is turned inside out partially or completely. The incidence is about 1 in 20,000 deliveries. The obstetric inversion is almost always an acute one and usually complete.
Types  of  uterine  inversion  based  on  time  of occurrence: (A) Acute: Within 24 hours of delivery. (B) Subacute: >24 hours but <4 weeks. (C) Chronic: >4 weeks postpartum.
Incidence is 1 in 2000 to 1 in 2500 deliveries.
VARIETIES (Figs. 28.9A to C)
■  First degree: There is dimpling of the fundus, which still remains above the level of internal os.
■  Second degree: The fundus passes through the cervix but lies inside the vagina.
Third degree (complete): The endometrium with or without the attached placenta is visible outside the vulva. The cervix and part of the vagina may also be involved in the process.
It may occur before or after separation of placenta.
ETIOLOGY: The inversion may be spontaneous or more commonly induced.
Spontaneous  (40%):  This  is  brought  about  by localized atony on the placental site over the fundus



associated with sharp  rise of intra-abdominal pressure as in coughing, sneezing or bearing down effort. Fundal attachment  of  the  placenta  (75%),  short  cord  and placenta accreta, weakness of uterine wall at the placental site are often associated.
Iatrogenic: This is due to the mismanagement of third stage of labor.
■   Pulling the cord when the uterus is atonic, especially when combined with fundal pressure.
■  Fundal pressure  while the  uterus is relaxed-faulty technique in manual removal.
Common risk factors are uterine over enlargement, prolonged labor, fetal macrosomia, uterine malformations, morbid adherent placenta, short umbilical cord, tocolysis and manual removal of placenta. It is more common in women with collagen disease like Ehler-Danlos syndrome.
DANGERS: (I)  Shock  is  extremely  profound  mainly  of neurogenic origin due to-(a) tension on the nerves due to stretching of the infundibulopelvic ligament, (b) pressure on  the  ovaries as  they  are  dragged  with  the  fundus through the cervical ring, and (c) peritoneal irritation.
(2)  Hemorrhage,  especially  after  detachment  of placenta; (3) Pulmonary embolism; ( 4) If left untreated, it may lead to-(a) infection, (b) uterine sloughing, and (c) a chronic one.
DIAGNOSIS: Symptoms: Acute lower abdominal pain with bearing down sensation.
Signs: (I) Varying degrees of shock is a constant feature; (2)  Abdominal  examination-(a)  Cupping  or  dimpling of the  fundal  surface,  (b)  Bimanual  examination  not only helps to confirm the diagnosis but also the degree. In  complete  variety,  a  pear-shaped  mass  protrudes outside the vulva with the broad end pointing downward and  looking  reddish  purple  in  color  (Fig.  28.10), (c) Sonography can confirm the diagnosis  when clinical examination is not clear.
PROGNOSIS:  As  it  is  commonly  met  in  unfavorable surroundings, the prognosis is extremely gloomy. Even if the patient survives, infection, sloughing of the uterus and chronic inversion with ill health may occur.
PREVENTION: Not to employ any method to expel the placenta out when the uterus is relaxed. Pulling the cord


Depressed posterior wall


Partial inversion




rn
Figs. 28.9A to C: Inversion of the uterus: (A) First degree; (B) Second degree; (C) Third degree.
Chapter 28: Complications of the Third Stage of Labor	ID






















Fig. 28.10: Spontaneous acute and complete uterine inversion. Courtesy: Department of Obstetrics and Gynecology, NRS Medical College, Kolkota.

simultaneously with fundal pressure should be avoided. Manual removal should be done in a manner, as it should be (p. 389).
MANAGEMENT: • Call for extra help • Before the shock develops,  urgent manual replacement even without anesthesia, if it is not readily available, is the essence of treatment for a skilled accoucheur.
Principal  steps:  The  patient  is  under  general anesthesia:  (1)  To replace  that  part  first,  which is inverted last  with the placenta attached to the uterus by steady firm pressure exerted by the fingers;  (2)  To apply counter-support by the other hand placed on the

abdomen;  (3) After  replacement,  the  hand  should remain  inside  the uterus until the uterus becomes
contracted by  parenteral  oxytocin  or  PGF2u;   ( 4)
The placenta  is  to be removed manually only after the uterus becomes contracted. The placenta may, however, be removed prior  to replacement-(a) to reduce the bulk which facilitates replacement  or  (h)  if  partially separated   to   minimize  the  blood  loss;  (5)  Usual treatment  of  shock,  including   IV  fluids  and  blood transfusion should be arranged simultaneously.
•  After the shock develops
Principal Steps: (1) The treatment of shock should be instituted with an urgent normal saline infusion and blood transfusion; using wide-bore IV cannula. (2) The inverted fundus  lies on  the palm  of  the  hand  with the fingers placed near the uterocervical junction. When pressure is exerted on the fundus, it gradually returns into the vagina. The vagina is packed with antiseptic roller gauze;  (3) Foot end of the bed is raised; (4) Replacement  of the uterus using hydrostatic method  (O'Sullivan's) under general anesthesia is to be done along with resuscitative measures. Hydrostatic method is quite effective and less shock-producing.
Hydrostatic method: The inverted uterus is replaced into the vagina. Warm sterile fluid (up to 5 liters) is gradually instilled into the vagina through a douche nozzle. The vaginal orifice is blocked by operator's palms supplemented by labial apposition around the palm by an assistant. Alternatively, a silicon cup (vacuum extraction cup) is placed into the vagina. The douche can be placed at a height of about 3 feet above the uterus. The water distends the vagina and the consequent increased intravaginal pressure leads to replacement of the uterus.
•  Subacute stage: (1) To improve the general condition by blood transfusion;  (2)  Antibiotics  are  given  to control sepsis;  (3)  Reposition of the  uterus  either manually or by hydrostatic method may be tried; (4) If fails, reposition may be done by abdominal operation (Haultain's operation).



Injuries to the Birth Canal









❖ Vulva
❖ Perineum
►  Management ❖ Vagina


❖ Cervix
❖ Pelvic Hematoma
❖ Rupture of the Uterus ►  Etiology


►  Pathology ►  Diagnosis
►  Management ❖ Visceral Injuries




Maternal  injuries  following  childbirth  process  are quite common and contribute significantly to maternal morbidity and even to death. Prevention, early detection and prompt and effective management not only minimize the morbidity but prevent many gynecological problems from developing later in life.

VULVA

Lacerations  of  the  vulval  skin  posteriorly  and  the paraurethral tear on the inner aspect of the labia minora are the common sites. Paraurethral tear may be associated with  brisk  hemorrhage  and  should  be  repaired  by interrupted catgut sutures, preferably after introduction of a rubber catheter into the bladder to prevent injury of the urethra.

PERINEUM

While minor injury is quite common, especially during first birth,  gross injury  (third and fourth degree) is invariably a result of mismanaged second stage oflabor. Overall risk is 1 % of all vaginal deliveries (Box 29.1).
CAUSES: Perinea! injury (mainly the third  and fourth degree) results from (i) over-stretching and/or, (ii) rapid stretching of the perineum, especially when the perineum is inelastic (elderly primigravida, perinea! scar).
PREVENTION: Proper conduct in the second  stage  of labor taking due care of the perineum when it is likely to  be  damaged  is  essential.  The  prevention  of  the


■   Big baby (weight  4 kg}.	■   Scar in the perineum 11   Nulliparity.                                                         (perineorrhaphy,
■   Outlet contraction with narrow	episiotomy}
pubic arch.	■   Face to pubis delivery. ■   Shoulder dystocia.	■   Midline episiotomy.
■   Forceps deliverywithoutepisiotomy.    11   Precipitate labor.


perinea! injuries in norm l delivery has been outlined on p. 130. Mediolateral episiotomy (at 60° angle) during crowning is to be used when maneuvers are planned.

I MANAGEMENT
Recent tear should be repaired immediately following the delivery of the placenta. This reduces the chance of infection and minimizes the blood loss. In cases of delay beyond 24 hours, the repair is to be withheld. Antibiotics should be started to prevent infection. The complete tear should be repaired after 3 months if delayed beyond 24 hours. In case of any doubt to grade of 3rd degree tear, it is advisable to classfy to the higher degree rather than lower degree (Box 29.2).
Repair of complete perineal tear:
Step I: Patient is put in lithotomy position. Antiseptic cleaning of the local area is done. Repair may be done with local infiltration of 1 % lignocaine hydrochloride (10-15 mL) or with pudenda! block or preferably under regional or general anesthesia.
Step  II:  Dissection  is  not  required  as  in  an  old complete perinea! tear. (a) The rectal and anal mucosa is first sutured from above downward. No. "3-0" vicryl, on an atraumatic needle with interrupted stitches with knots inside the lumen are used. (b) The rectal muscles,
.
•     t       f1Rf I      ,.	. .
..
RA	•
First degree: Injury to perinea! skin only.
Second  degree:  Injury  to  perineum  involving  perinea!  body (muscles}  but not involving the anal sphincter.
Third degree: Injury to perineum, involving the anal sphincter complex (both external and internal}:
■  3a : <50% of EAS thickness torn. ■  3b: >50% of EAS thickness torn. ■  3c  :  Both EAS and IAS torn.
Fourth degree: Injury to perineum involving the anal sphincter
complex (EAS and IAS} and anal epithelium (Fig. 29.1 }.
Chapter 29: Injuries to the Birth Canal



/	 Rectal mucous membrane


  ""--Perineal body

 

);



nal sphincter nal epithelium



1st	2nd   3rd   4th degree

Fig. 29.1: Diagrammatic representation showing different degrees of perinea! tear.

including the pararectal fascia are  then  sutured by interrupted sutures using the same suture material. (c) The torn ends of the sphincter ani externus (EAS) are then exposed by Allis's tissue forceps. The sphincter is  then  reconstructed and it  is supported by  another layer of interrupted sutures. For repair of EAS either an overlapping or end-to-end approximation method can be used with similar outcome. IAS repair is done by End­ to-End approximation, with 3-0 PDS or 2-0 polyglactin.
Step  III:  Repair  of  perinea!  muscle  is  done  by interrupted  sutures  using  No.  "0"  PDS  or  dexon  or polyglactin {vicryl). Surgical knots are buried under the superficial muscles.
Step IV: The vaginal wall and the perinea! skin are apposed by interrupted sutures with vicryl rapide.
Suture material: For repair of EAS, monofilament sutures such as Polydioxanone (PDS) or polyglactin {vicryl) can be used. Repair of IAS is done with fine suture size such as 3-0 PDS and 2-0 vicryl as they cause less irritation and discomfort.
AFTER  CARE:  The  aftercare  of  the  repaired  perinea! injuries is similar to that following episiotomy. Special care following repair of complete tear-(1) A low
residual  diet consisting of milk,  bread,  egg,  biscuits, fish, sweets,  etc.  is given from third day onward;  (2) Lactulose 8 mL twice daily beginning on the second day
and increasing the dose to 15 mL on the third day is a satisfactory regime to soften the stool; (3) Any one of the broad-spectrum antibiotics (N cefuroxime 1.5 g) is used during the intraoperative and the postoperative period {Figs. 29.2A and B). Metronidazole 400 mg thrice daily is to be continued for 5-7 days to cover the anaerobic contamination of fecal matter. The woman is advised physiotherapy and pelvic floor exercises and she is reviewed  again 6-12 weeks postpartum. In case of persistent incontinence of flatus and feces, endoanal USG and anorectal manometry should be considered to detect any residual defects (20-30%). Consultation with a colorectal surgeon may be needed.



a


Figs. 29.2A and B: Methods of repair of the cervical tear with vertical  mattress suture.

PLAN  FOR  FUTURE  DELIVERY:  All  women  need  to have institutional delivery following repair of obstetric sphincter injury. Vaginal delivery may be allowed in a selected case with or without episiotomy. Women having symptoms  or  with  abnormal  endoanal  USG  and/or manometry should be delivered by elective cesarean birth. Chance of recurrence is 5-7%.

VAGINA

Isolated vaginal tears or lacerations without involvement of the perineum or cervix are not uncommon. These are usually  seen  following  instrumental or  manipulative delivery. In such cases, the tears are extensive and often associated with brisk hemorrhage.
TREATMENT:  Tears  associated with  brisk  hemorrhage require exploration under general anesthesia with a good light. The tears are repaired by interrupted or continuous sutures using chromic catgut No. "0". In case of extensive lacerations,  in  addition  to  sutures,  hemostasis  may be achieved by intravaginal plugging by  roller gauze, soaked with glycerin and acriflavine. The plug should be removed after 24 hours. Selective arterial embolization may also be done if bleeding persists.
COLPORRHEXIS: Tear the vault of the vagina or any of its wall is called colporrhexis. It may be primary where only the vault is involved or secondary when associated with cervical tear (common). It is said to be complete when the peritoneum is opened up.
Treatment: If the tear is limited to the vault close to the cervix, the repair is done from below. If, however, the cervical tear extends high up into the lower segment or major branches of uterine vessels are damaged, laparotomy is to be done simultaneously
-·"ID Chapter 29: Injuries to the Birth Canal
with resuscitative measures. Evacuation ofhematoma and arterial ligation may be needed.


CERVICAL INJURY

Minor degree of cervical tear ( <0.5 cm) is invariable during first delivery and requires no treatment. Extensive cervical tear is rare. It is the commonest cause of traumatic postpartum hemorrhage. Left lateral tear is the most common.
CAUSES
11    Iatrogenic: Attempted forceps or ventouse delivery or breech extraction through incompletely dilated cervix.
11    Rigid  cervix:  This   may  be  congenital  or  more commonly following scar from previous operations on the cervix like amputation, conization or presence of a lesion like carcinoma cervix.
11    Strong uterine contractions as in precipitate labor or extremely vascular cervix as in placenta previa.
11    Detachment: Detachment of the cervix may be annular which involved the entire circumference of the cervix. This  occurs  following  prolonged  labor  in  primary cervical dystocia.  It may, however,  involve only the anterior lip when it is nipped between the head and the symphysis pubis in association with the sacral os. In both varieties, the bleeding is minimal and healing occurs through epithelialization.
Rarely  cervical  tears  extend upwards to reach the lower uterine segment and involve the uterine artery and its major branches.  Severe laceration may cause broad ligament hematoma.
DIAGNOSIS:  Excessive vaginal bleeding immediately following delivery in presence of a hard and contracted uterus-raises the suspicion of a traumatic bleeding. Exploration of the uterovaginal canal under good light not only confirms the diagnosis but also helps to know the extent of the tear.
COMPLICATIONS:
Early-(1)  Deep  cervical  tears  involving  the  major vessels  lead  to  severe  postpartum  hemorrhage;  (2) Broad  ligament  hematoma;  (3)  Pelvic  cellulitis;  ( 4) Thrombophlebitis.
Late-(!)  Ectropion;  (2)  Cervical incompetence with midtrimester abortion.

TREATMENT: Only deep cervical tear (>l cm) associated with bleeding should be repaired soon after delivery of the placenta.  Repair should be done under general anesthesia, in lithotomy position with a good light (Fig. 29.3). The prerequisites are-Sims'  posterior  vaginal speculum,  vaginal wall retractors,  at least two sponge­ holding forceps and an assistant.
Procedures: The anterior and posterior margins of the torn cervix are grasped by the sponge-holding forceps.
Instead of giving traction to the forceps, it is better to














Fig. 29.3: Vulval hematoma following spontaneous delivery.

push down the fundus gently by an assistant. This makes the tear more accessible for effective suturing. The apex is to be identified first and the first vertical mattress suture is placed just above the apex using polyglactin (vicryl) or chromic catgut No. "O" taking whole thickness of the cervix. The bleeding stops immediately. The rest of the tear is repaired by similar mattress sutures. Mattress suture is preferable as it prevents rolling in of the edges. A helpful guide for proper exposure in such a case is to start suture at the proximal end and using the suture for traction, more distal tear area is exposed until the apex is in view and is repaired. The cervical tears extending to the lower segment or vault with broad ligament hematoma are managed as outlined in ruptured uterus (p. 390).

PELVIC HEMATOMA

DEFINITION: Collection of blood anywhere in the area between the pelvic peritoneum and the perineal skin is called pelvic hematoma.
Vulvar  hematoma  m y  be  due  to  injury  to  the pudendal artery, Inferior Rectal Artery, or Perinea! arteries. Paravaginal hematomas are due to the injury of descending branch of uterine artery.
ANATOMICAL TYPES: Depending upon the location of the hematoma, whether below or above the levator ani, it is termed as:
♦    Infralevator hematoma-common ♦  Supralevator hematoma-rare
INFRALEVATOR HEMATOMA
The commonest one is the vulval hematoma.
Etiology:  (I)  Improper  hemostasis  during  repair of vaginal or perinea! tears or episiotomy wound-(a) Failure of suturing the apex of the tear, (b) Failure to obliterate  the  dead  space  while suturing  the  vaginal walls;  (2) Rupture of paravaginal venous plexus either spontaneously or following instrumental delivery.
Chapter 29: Injuries to the Birth Canal	ll .

Symptoms: (1) Persistent, severe pain on the vulvar or perinea! region;  (2) There may be rectal tenesmus or bearing down efforts when extension occurs to the ischiorectal fossa. There may be even retention of urine.
Signs: (I) Variable degrees of hypovolemia shock may be evident; (2) Local examination reveals a tense swelling at the vulva which becomes dusky and purple in color and tender to touch (Fig. 29.3).
n·eatment: A small hematoma (<5 cm) may be treated conservatively with cold compress.  Larger hematomas should  be  explored  in  the  operation  theater  under general anesthesia. Simultaneous resuscitative measures are to be taken. The blood clots are to be scooped out and the bleeding points are to be secured. Usually, a generalized oozing surface is visible. The dead space is to be obliterated by deep mattress sutures and a closed suction drain may be kept in that place for 24 hours. A Foley catheter is inserted till the tissue edema subsides. Prophylactic antibiotic are to be administered.
SUPRALEVATOR  HEMATOMA:  Causes:  (1)  Extension of  cervical  laceration  or  primary  colporrhexis  (vault rupture); (2) Lower uterine segment rupture (Fig. 29.4); (3) Spontaneous rupture of paravaginal venous plexus adjacent to the vault.
Diagnosis: The diagnosis is usually  late  as pain is not of a  conspicuous  nature and so also the vaginal bleeding. Unexplained shock with features of internal hemorrhage following delivery raises the suspicion. Abdominal  examination  reveals  a  swelling  above  the inguinal ligament pushing the uterus to the contralateral side.  Vaginal examination reveals-(a) occlusion of the vaginal canal by a bulge or (b) a boggy swelling felt





Peritoneum

Obturator
fascia
..
.
-
.... .. _--------------.
..
_
_
-
-






lnfrafascial


through the fornix.  Rectal examination corroborates the presence of the boggy mass. It may extend between the leaves of  the broad ligament. This is detected on abdominal palpation only. Imaging with USG or CT is useful. Ultrasonography or CT may be needed for exact localization of the hematoma.
Management:  Usual  treatment  of  shock  is  to  be instituted and  arrangement is  made for laparotomy. The anterior leaf of the broad ligament peritoneum is incised and the blood clot is scooped out. The bleeding points, if visible, are to be secured and ligated. Random blind sutures should not be placed to prevent ureteric damage. If the oozing continues,  one may have to tie
the anterior division of the internal iliac artery. Selective arterial  (uterine)  embolization  may  be  done  as  an alternative. The presence of associated rupture uterus may modify the treatment as mentioned later in this chapter.
!li
'
i: 	..
-t
-   ':

RUPTURE OF THE UTERUS

DEFINITION:  Disruption in the continuity	•!]
of  the  all uterine  layers  ( endometrium,       '.	'I
myometrium and serosa) any time beyond	·	.  :i 20  weeks of  pregnancy is  called  rupture   !li
of the uterus. Small rupture to the wall of the uterus in early months is called perforation either instrumental or perforating hydatidiform mole. Rupture of a rudimentary pregnant horn has got a special clinical entity and is grouped in ectopic pregnancy.
INCIDENCE:  The  prevalence  widely  varies  from  1  in 2,000 to 1 in 200 deliveries. There is a significant change in the etiology of rupture uterus. Currently there is decline in multiparity, traumatic rupture due to internal podalic version





Round ligament
 -----<;,-- Superior and inferior fascia of levator ani
muscle

Supralevator
hematoma
IM/1--- Obturator internus

---



lnfralevator
hematoma


Superior and inferior
fascia of urogenital diaphragm


Fig. 29.4: (Al Schematic diagram showing normal disposition of pelvic muscles, fascia and the spaces; (Bl Supralevator hematoma; (Cl lnfralevator hematoma (small).
l9 Chapter 29: Injuries to the Birth Canal

and breech extraction, difficult forceps delive1y, obstructed labor, fetal abnormality (hydrocephalus). On the other hand there is rise in cesarean delivery, myomectomy, operative hysteroscopy,  uterine  curettage  and  perforation (most common instrument causing perforation is suction cannula: 50%. The anterior uterine wall is most  commonly  injured:  40%),  sequential  use  of prostaglandins and oxytocin for induction of labor and abdominal trauma are the important ones.

I ETIOLOGY

The causes of rupture of the uterus are broadly divided into (Flowchart 29.1):
♦  Spontaneous rupture ♦    Scar rupture
♦   Iatrogenic rupture
SPONTANEOUS
During pregnancy: It is indeed rare for an apparently uninjured uterus to give way during pregnancy. The causes are:  (1) Previous damage to the uterine  walls following dilatation and curettage operation or manual removal of placenta; (2) Rarely in grand multiparae due to thin uterine walls; (3) Congenital malformation of the uterus (bicornuate variety) is a rare possibility; (4) In Couvelaire uterus.
Spontaneous rupture during pregnancy is usually complete,  involves the upper  segment  and  usually occurs in later months of pregnancy. On rare occasion, spontaneous rupture may occur even in early months. During  labor:  Spontaneous  rupture  which  occurs predominantly in an otherwise intact uterus during labor is due to:
♦   Obstructive rupture:  This  is  the end  result  of an
obstructed labor. It is less common these days.


♦   Nonobstructive rupture: Grand multiparae are usually affected.  Weakening  of  the  walls  due  to  repeated previous births is the responsible factor.
OTHER CASES ARE: Cases with repair of previous uterine rupture, prior vigorus curettage (Ch. 23, p. 315).
SCAR RUPTURE: With the liberal use of primary cesarean section,  scar  rupture  constitutes  significantly  to  the overall incidence of uterine rupture. The incidence of lower segment scar rupture is about 1-2%, while that following classical one is 5-10 times higher. Uterine scar  following hysterotomy  behaves  like  that  of  a classical scar and is of high risk.
During pregnancy: Classical cesarean or hysterotomy scar  is  likely  to  give  way  during  later  months  of pregnancy. The weakening of such scar is due to the stretching. Lower segment scar rarely ruptures during pregnancy.
During  labor:  The  classical   or  hysterotomy  scar or cornual resection  for ectopic pregnancy is  more vulnerable to rupture during labor. Although rare, lower segment scar predominantly ruptures during labor.
IATROGENIC OR TRAUMATIC
During pregnancy: (1) Injudicious administration of oxytocin;  (2)  Use  of  prostaglandins  for  induction  of abortion or labor; (3) Forcible external version, especially under general anesthesia; ( 4) Trauma: Fall or blow on the abdomen.
During  labor:   (1)   Internal  podalic   version;   (2) Destructive operation; (3) Manual removal of placenta; ( 4) Application of forceps or breech extraction through incompletely dilated cervix;  (5) Injudicious administra­ tion of oxytocin for augmentation of labor.


Flowchart 29.1: Scheme showing etiology of ruptured uterus.
I
I

Ruptured uterus
I During p;egnancy I	!	Durin1 labor

Spontaneous	Iatrogenic	Spontaneous	Iatrogenic
I
I
l	l	l


Intact uterus	Scarred uterus	Traumatic	Oxytocics	Traumatic	Oxytocics
!
l
• Multiparae.	♦CS scar.	• External cephalic	♦ Oxytocin.	■ Difficult forceps delivery.  ■ Oxytocin.
■ Prostaglandins.
■ Internal version.
version.
♦ Congenital n	• Hysterotomy scar.	♦ Fall or blow.	• Prosta­s.	■ Manual removal of
glandin
malformatio
• Previous manual
placenta.
of uterus.	removal.	• Motor vehicle accident.
• Vigorous uterine	♦ Metroplasty.	♦ Internal podalic version	----'--- 
!
 --
uterus
curettage.
(rare).
!
Scarred uterus
♦Trauma (blunt/sharp).
lntac
♦ Repair of previous	\	■ CS or hysterotomy scar.
uterine repture.
♦	♦
Non-obstructive	Obstructive	■ Repair of previous rupture uterus.
Myomectomy scar.
■
■
Following obstructed labor.
■ Grand multipara.
■ Congenital malformation of uterus.   ■ Pelvic tumor.	■ Cornual resection of ectopic pregnancy.
■ Metroplasty.
■ Rudimentary horn pregnancy.


I PATHOLOGY
TYPES: Pathologically,  it is customary to distinguish between complete and incomplete rupture depending on whether the peritoneal coat is involved or not. So far from the treatment point of view, it matters little. In incomplete rupture, the peritoneum remains intact.
Incomplete rupture usually results from rupture of the lower segment scar (Fig. 29.5) or extension of a cervical tear into the lower segment with formation of a broad ligament hematoma. Complete rupture usually occurs following disruption of the scar in upper segment. It may also be due to spontaneous rupture of both obstructive and nonobstructive type.
SITES:  Spontaneous  nonobstructive  rupture  usually involves the upper segment and often involves the fundus. Whereas, in obstmctive type, the mpture involves the ante­ rior lower segment transversely and often extends upward along the lateral uterine wall. The margins are ragged and necrosed (Fig. 29.7). On occasion, the posterior wall may be involved due to friction with the sacral promontory.
Not infrequently, the tear extends downward to involve the cervix and the vaginal wall (colporrhexis). The bladder may be involved, at times. Rupture over the previous scar is almost always located at the site of the scar. The margins of the ruptured cesarean scar are usually clean and look fibrosed (Fig. 29.6). The rent over the lower segment scar may extend to one or both the sides to involve the major branches of uterine vessels.
The morbid pathology of traumatic rupture following destructive operation or internal version is almost similar to that met in spontaneous obstructive variety. This may, at times, be indistinguishable (Fig. 29. 7).
















Fig. 29.5: lntraoperative photograph of cesarean delivery. Lower segment of the uterus is shown using the Doyen's retractor. Scar dehiscence is seen as there is: disruption of almost entire length of the scar (see arrow). Amniotic membrane is seen bulging out and it is intact. Bleeding is almost absent or minimal.

Chapter 29: Injuries to the Birth Canal    ID Dehiscence and scar rupture
Scar dehiscence (intact uterine serosa)-(a) disruption of part of scar and not the entire length, (b) fetal membranes remain intact (Table 29.1), (c) bleeding is almost nil or minimal (Fig. 29.5).
Scar rupture-(a) disruption of the entire length of the scar, (b) complete separation of all the uterine layers including serosa,  (c) rupture of the membranes with, (d) varying amount of bleeding from the margins or from




















Fig. 29.6: Lower segment scar rupture (arrow). The margins are found clean and scarred. There is omental adhesion on the upper segment. Total hysterectomy was done.
(Courtesy: Museum, Department of Obstetrics and Gynecology, NRSMCH, Kolkata)


















Fig. 29.7: Rupture of uterus following obstructed labor. Rupture extends  along  the  lateral  border  of the  uterus.  Margins  are irregular, bruised and necrosed. Total hysterectomy has been done.
Im Chapter 29: Injuries to the Birth Canal

its extension,  (e)  uterine cavity and peritoneal cavity become continuous.
FETUS AND PLACENTA: In incomplete rupture, both the fetus and placenta remain inside the uterine cavity or part of the fetus may occupy in between the layers of broad ligament. In complete rupture, the fetus with or without the placenta usually escapes out of the uterus. The uterus remains contracted. Blood loss is not much unless major vessels are affected.
PROGNOSIS:  Fetal  prognosis  depends  upon  the degree of placental separation, severity of hemorrhage and   hypovolemia.   Lower   segment   scar  rupture gives a comparatively better prognosis. But, rupture following  obstructed  labor  either  spontaneous  or due to instrumentation causes maternal mortality of about 20%  or  more.  The  major  causes  of  death are hemorrhage, shock and sepsis. Late sequelae include intestinal obstruction  and scar rupture in subsequent pregnancies.
I DIAGNOSIS
Obstetrician should be conscious of the entity for an early diagnosis.
During Pregnancy: ♦    Scar rupture
♦    Spontaneous rupture ♦    Iatrogenic rupture
Scar rupture: Classical or hysterotomy-the patient complains of a dull abdominal pain over the scar area with slight vaginal bleeding. There is varying degrees of tenderness on uterine palpation. FHS may be irregular or absent. CTG tracings reveal variable or late deceleration (most consistent finding).  The features may not  be always  dramatic in  nature  (silent  phase).  Sooner  or later, the rupture becomes complete. There is a sense of something giving way accompanied by acute abdominal pain and collapse. The diagnosis is self-evident (Ch. 23, p. 315, VBAC).
Spontaneous rupture  in uninjured  uterus:  The rupture is usually confined to the high parous women. The onset is usually acute but, sometimes, insidious. In acute types, the patient has acute abdominal pain with fainting attacks and may collapse.  The diagnosis is established by the presence of features of hypovolemia, shock, acute tenderness  on  abdominal  examination,  palpation  of superficial fetal  parts,  if the  rupture is  complete  and absence  of fetal heart  rate.  However,  with insidious onset, the diagnosis is often confused with concealed placental abruption or rectus sheath hematoma.
Rupture following fall,  blow or external  version or use of oxytocics: There  is  the  history of such an accident followed by acute pain abdomen and slight vaginal bleeding.  Rapid pulse and tender uterus raise the  suspicion  of  rupture.  The  confirmation  is  done


by  laparotomy.  This  is  too  often  confused  with accidental hemorrhage.
During labor:
♦    Scar rupture
♦    Spontaneous obstructive rupture
♦   Spontaneous nonobstructive rupture ♦    Iatrogenic rupture
Scar rupture: Classical or hysterotomy scar rupture­ the  features  are  the   same  as  those  occur  during pregnancy. The onset is usually acute.
Lower segment scar rupture: The onset is insidious. There is no classical feature of lower segment scar rupture (p. 402). The confirmation is by laparotomy. It is called "silent rupture''.
Spontaneous obstructive  rupture:  This  type  of spontaneous rupture has got a distinct premonitory phase prior to rupture.
Phase of rupture: (1) There is a sense of something giving  way  at  the  height  of  uterine  contraction; (2) The constant pain is changed to dull aching pain with  cessation  of  uterine  contractions;  (3)  General examination reveals features of exhaustion and shock; (4) Abdominal examination reveals-(i) superficial fetal parts, (ii) absence ofFHS, (iii) absence of uterine contour, and (iv) two separate swellings, one contracted uterus and the other-fetal ovoid; (5) Vaginal examination reveals­ (i)  recession  of  the  presenting part,  and (ii) varying degrees of bleeding.
Spontaneous nonobstructive rupture: This  is rare and solely confined to high parous women. The patient at the height of uterine contraction is suddenly seized with an agonizing bursting pain followed by a relief, with cessation of contractions. The diagnostic features of the catastrophe are-presence of shock, evidences of internal hemorrhage,  tenderness  over  the  uterus  and  varying amount of vaginal bleeding.
Rupture following manipulative or instrumental delivery: Sudden deterioration of the general condition of the patient

Table 29.1: Differentiation'of Ute;ine Scar'Dehiscenc  and Rupture.
Scar dehiscence (Fig. 29.5)	Scar rupture (Fig. 29.6) ■  Occult scar separation (no pain).  • Suprapubic pain.
■  Often diagnosed at laparotomy.  •  Bleeding PN, tachycardia .
•
■  Serous coat: Intact.	Disrupted; clinically diagnosed. ■  Muscle layer partly separated.    •  Disruption of all the layers
of the uterus. II    Hemorrhage from the margins   • lntraperitoneal
absent/minimal.	hemorrhage++.
■  Fetal health-often not            • FHR abnormality: Bradycar-affected.                                           dia, prolonged deceleration
(CTG).
•
t .
Fetal mortality
11      Maternal health not affected.	•  Maternal morbidity and maternity
tt.


with varying amount of vaginal bleeding following manipulative or instrumental delivery raises the suspicion. Shortening of the cord immediately following a difficult vaginal delivery is pathognomonic of uterine rupture, the placenta being extruded out into the abdominal cavity, through the rent in the uterus.

I MANAGEMENT

PROPHYLAXIS: The following guidelines  are helpful to prevent or to detect at the earliest the diagnosis of rupture uterus:

Chapter 29: Injuries to the Birth Canal	ID Flowchart 29.2: Management of scar dehiscence
and rupture uterus.

Management of Scar Dehiscence and Uterine Rupture


Urgent resuscitation and laparotomy. • IV crytalloids • Blood transfusion
• Injection ceftriaxone IV• Catheterization


Laparotomy



•   The  at-risk  mothers,  likely  to  rupture,  should  have mandatory hospital delivery. These are-(a) Contracted pelvis,   (b)   Previous  history  of  CD,  hysterotomy  or myomectomy, (c) Uncorrected transverse lie, (d) High parity.
•   General anesthesia should not be used to give undue force in external version.
•   Undue delay in the progress of labor in a multipara with previous uneventful delivery should be viewed with concern and the cause should be sought for.
•   Judicious selection  of cases  with  previous history of cesarean sections for vaginal delivery (VBAC).
•   Judicious selection of cases for oxytocin infusion either for induction or augmentation oflabor.
•   There is no place of internal podalic version in singleton fetus in present-day obstetrics.
•   Attempted forceps delivery or breech extraction through incompletely dilated cervix should be avoided.
•   Destructive vaginal operations should be performed by skilled personnel and exploration of the uterus should be done as a routine following delivery.
•   Manual removal in morbid adherent placenta-should be done by a senior person.

TREATMENT: • Resuscitation	• Laparntomy
Depending upon the state of the clinical condition, either resuscitation is to be done followed by laparotomy or in acute conditions, resuscitation and laparotomy are to be done simultaneously.
LAPAROTOMY: Any of the three procedures (Flowchart 29.2) may be adopted following laparntomy:
♦   Hysterectomy:  Hysterectomy  is  the  surgery  for ruptured uterus unless there is sufficient reason to   preserve  it.   This  is   especially  indicated  in spontaneous obstructive rupture.  It is preferable to perform a quick subtotal hysterectomy, rather than total hysterectomy (Read more  Dutta's  Clinics in Obstetrics, Ch.  53).  Risk of injury to the ureters  or bladder is thereby reduced. It takes less time.
•  However, if the condition permits and/or there is colporrhexis, a total hysterectomy may be done.
♦   Repair: This is mostly applicable to a case with scar rupture where the margins are clean (Table 29.1). Repair is done by excision of the fibrous tissue at the margins. Remote prognosis during future pregnancy is very much unfavorable because of high risk of scar rupture.


Spontaneous	Scar rupture/
obstructive rupture	scar dehiscence

• Hysterectomy (sub-total)	Delivery ➔ Repair of the scar preferred.	± bilateral tubal ligation
OR
• Total hysterectomy.	Hysterectomy.


♦    Repair and sterilization: This  is  mostly  done in patients with a clean cut scar rupture having desired number of children.
To tackle a broad ligament hematoma-To open up the anterior leaf of the broad ligament ➔ Scoop out the blood clot ➔ Secure the bleeding points ➔ Replaced by ligature, taking care not to injure the ureter. Failing to secure the bleeding points ➔ To tie the anterior division of the internal iliac artery.

VISCERAL INJURIES

BLADDER: Causes: Obstetrical injury to the bladder may be due to:
(A)  Traumatic:  (1)  Instrumental  vaginal  delivery such  as  destructive  operations  or  forceps  delivery especially with Kielland; (2) Abdominal operation such as hysterectomy for rupture uterus or cesarean section. (B) Sloughing fistula: It results from prolonged compression effect on the bladder between the head and symphysis pubis in obstructed labor.
Diagnosis: (A) Traumatic-(})  Urine-dribbles  out soon following the operative delivery. Blood-stained urine following cesarean section or hysterectomy is suggestive of bladder injury; (2) Margins are clean cut with oozing surfaces. (B) Sloughing fistula-(}) History of prolonged labor; (2) Dribbling of urine occurs after varying interval following delivery (5-7 days); (3) Margins devitalized and necrosed.
Management:  Traumatic fistula: Immediate local repair is preferable, if the local tissues are healthy.
In unfavorable condition, a self-retaining catheter is introduced and to be kept for 10-14 days or even longer. Urinary antiseptics are prescribed. In a small size fistula, there may be spontaneous closure of the fistula. If it fails, repair is to be done after 3 months.
-· Im Chapter 29: Injuries to the Birth Canal
Sloughingfistula: Repair should not be attempted as the conditions are not ideal (vide supra), instead, a self­ retaining catheter is placed as outlined above. Repair is to be done after 3 months.
RECTUM: Rectal injury, other than that involved along with complete perinea! tear is rare in obstetrics. This is because, the middle-third of the rectum is protected by the curved sacral hollow and the upper third is protected by the peritoneal lining. Prolonged compression of the




rectum by the head in midpelvic contraction with a flat sacrum predisposes to ischemic necrosis of the anterior rectal wall and results in rectovaginal fistula. The repair in such cases should be postponed for at least 3 months.
URETHRA: Urethral injury may be traumatic resulting from instrumental delivery or during pubiotomy; may be ischemic sloughing, the mechanism of which is similar to that of bladder necrosis. The principles in management are similar to those of bladder injmy.



-:fi•MIH
►  Fourth degree perinea I (complete) tear involves tear of the posterior vaginal wall, perinea! body, anal sphincter complex with tear of the anal or rectal mucosa. Recent tear can be repaired immediately.
►  Pelvic hematoma is commonly due to vulvar hematoma (infralevator). Large vulval hematoma should be explored in the operation theater.
►  Rupture of uterus may be-(i) spontaneous, (ii) scar rupture or (iii) iatrogenic. Rupture of uterus may occur either during pregnancy or during labor. Diagnosis is difficult. One should be conscious of the entity.
►  Management of rupture uterus is resuscitation and laparotomy. Subtotal hysterectomy is commonly done. Repair may be done in cases where margins are clean. Repair and sterilization is done when the woman has completed her family.
►  Obstetric emergencies are often very frightening though rare.
►  Obstetric emergency drill training should be regularly practiced by the labor ward team to face such emergencies.
►  Rupture uterus, cord prolapse, PPH, shoulder dystocia, eclampsia, inversion uterus are some of the many obstetric emergencies. All these need prompt and appropriate management.
►  All the staff should receive training in the management of obstetric emergency.
►  Debriefing and to discuss the events in respect of rupture uterus and hemorrhage and hysterectomy should be done with the woman and the family members.

Abnormalities of the
Puerperium


CHAPTER



CHAPTER OUTLINE
❖  Puerperal Pyrexia ❖ Puerperal Sepsis
►  Pathology
►  Clinical Features
►  Investigations of Puerperal Pyrexia
► Treatment


❖ Subim:iolution
❖ Urinary Complications in Puerperium ❖  Breast Complications
❖ Puerperal Venous Thrombosis ❖ Pulmonary Embolism
►  Prophylaxis and Management ❖ Obstetric Palsies


❖ Puerperal Emergencies
❖  Psychiatric Disorders during Puerperium
❖ Psychological Response to Perinatal Deaths and Management




PUERPERAL PYREXIA
DEFINITION: A rise of temperature reaching   !l	  !l
g
!l
l
100.4°F (38°C) or more (measured orally) on	ii';.Cj two separate occasions and 24 hours apart           (excluding first 24 hours) within first 10 days           following delivery is called puerperal pyrexia. In some countries, postabortal fever is also included.
The pathology and prevention of childbirth fever (puerperal - pyrexia) are best known from the works of Ignaz Semmelweis,
working in Vienna in the nineteenth century. He faced dificulties
to establish his doctrine. Unfortunately, he died of an infection on his right hand that he contracted during an operation.

PUERPERAL SEPSIS (Syn: Puerperal Infection)
DEFINITION: An infection of the genital tract which occurs as a complication of delivery is termed puerperal sepsis. Puerperal pyrexia is considered to be due to genital tract infection unless proved otherwise (Box 30.1).
There has been marked decline in puerperal sepsis during the past few years due to: (1) improved obstetric care; (2) availability of wider range of antibiotics.
Puerperal sepsis is commonly due to-(i) endome­ tritis,  (ii) endomyometritis, or  (iii) endoparametritis


■    Puerperal sepsis (genital tract infection).
11   Urinary tract infections: Cystitis, pyelonephritis. 11   Mastitis, breast abscess.
■   Wound infections: CS or episiotomy.
11   Pulmonary infections: Atelectasis, pneumonia. 11   Septic pelvic thrombophlebitis.
■   A recrudescence of malaria or pulmonary tuberculosis. ■   Others: Pharyngitis, gastroenteritis.

or a combination of all these when it is called pelvic cellulitis.
Vaginal flora: The vaginal flora in late pregnancy and at the onset of labor consists of the  following organisms:

(1)   Doderlein's   bacillus   (60-70%);   (2)   Candida albicans (25%); (3) Staphylococcus albus or aureus; (4) Streptococcus-anaerobic common;  beta-hemolytic rare;  (5) Escherichia coli and Bacteroides group;  (6) Clostridium welchii on occasion.

These organisms  remain dormant and are harmless during normal delivery conducted in aseptic condition.
PREDISPOSING FACTORS OF  PUERPERAL SEPSIS: The pathogenicity of the vaginal flora may be influenced by  certain  factors:  (1)  The  cervicovaginal  mucous membrane is damaged even in normal delivery; (2) The uterine surface (the placental site), is converted into an open wound by the cleavage of the decidua which takes place during the third stage of labor; and (3) The blood clots present at the placental site are excellent media for the growth of the bacteria.
Antepartum risk factors: (1) Anemia;  (2) Preterm labor;  (3)  Premature rupture of the membranes;  ( 4) Prolonged  rupture  of  membrane  (,: 18  hours);  (5) Diabetes; (6) Immunocompromised (HIV).
Intrapartum  risk factors:  (1)  Repeated  vaginal examinations;  (2)  Traumatic  vaginal  delivery;  (3) Hemorrhage-antepartum or postpartum; (4) Retained bits of placental tissue or membranes;  (5)  Prolonged labor; (6) Obstructed labor; (7) Cesarean delivery; (8) Dehydration and ketoacidosis during labor.
Due to the factors mentioned above, the organisms (Box 30.2) gain foothold either in the traumatized tissues
r----

·ID Chapter 30: Abnormalities of the Puerperium


11    Aerobic:
• Group A, beta hemolytic Streptococcus: Toxic shock syndrome; necrotizing fasciitis in episiotomy or CS wound.
• Group B, beta hemolytic Streptococcus: Neonatal septicemia, respiratory  disease  and  meningitis,  Methicillin-Resistant, S.  aureus  (MRSA)-severe  infection  (cellulitis),  Methicillin­ Sensitive S. aureus (MSSA).
• Gram-negative: E coil, Klebsiella, Proteus, Pseudomonas.
o  Gram variable: Gardnerel/a vaginitis. o  Others: Chlamydia, Mycop/asma.
• Anaerobes: Cocci: Peptostreptococcus; Peptococcus.
■   Others: Bacteroides (Fragi/es, Bivims, Fusobacteria, Mobiluncus, Clostridia).



lacerated  wound are the favorable  sites  for  bacterial growth and multiplication. The devitalized tissue, blood clots, foreign body (retained cotton swabs}, and surgical trauma favor polymicrobial  growth,  proliferation and spread  of  infection.  This  ultimately  leads  to  metritis, parametritis and/ or cellulitis.
Uterus: Endomyometritis-the incidence varies from 1 % to 3% following vaginal delivery and about 10% following cesarean delivery. It is commonly polymicrobial. The decidua, especially over the placental site, is primarily affected. The risk factors for endometritis are mentioned before.
The necrosed decidua sloughs off. The discharge is offensive. A zone of leukocytic barrier prevents the infection to the deeper myometrium. Severe infection is rare nowadays.

Most of the infections in the genital tract are polymicrobial with a mixture of aerobic and anaerobic organisms.

of the uterovaginal canal or in the raw decidua left behind or in the blood clots, especially at the placental site.
MODE OF INFECTION: Puerperal sepsis is essentially a wound infection.  Placental site  (being a raw surface), lacerations of the genital tract or cesarean section wounds may be infected in the following ways:
11   Sources of infection: ♦ Endogenous where organisms are  present  in  the  genital  tract  before  delivery. Anaerobic   Streptococcus   is   the   predominant pathogen.  ♦  Autogenous  where  organisms present elsewhere  (skin,  throat) in the  body and migrate to the genital organs by  bloodstream or  by the patient herself.   Beta-hemolytic   Streptococcus,  E.   coli, Staphylococcus are important.  ♦   Exogenous  where infection  is  contracted  from  sources  outside  the patient (from hospital or attendants). Beta-hemolytic Streptococcus, Staphylococcus and E. coli are important.
II PATHOLOGY

The primary sites of infection are:  (1)  Perineum; (2) Vagina;  (3)  Cervix;  (4)  Uterus. The infection is either localized to the site or spreads to distant sites. The lacerations on the perineum,  vagina and the cervix are often infected by the organisms due to the presence of  blood clots or  dead  space.  The  wounds  become red,   swollen  and  there  is  associated  seropurulent discharge.  There  may  be  disruption  of  the  wound  if repaired before control of infection. Diabetes,  obesity, immunocompromised state (HIV) are the other high­ risk factors for wound infection.
I PATHOGENESIS

Endogenous	Bacterial colonization
Bacterial infection	(aerobic, anaerobic
Exogenous	and others)

Endometrium  (placental  implantation  site),  cervical lacerated wound, vaginal wound (episiotomy) or perinea!

SPREAD OF INFECTION
■  Pelvic cellulitis (parametritis) is due to spread of infection to the pelvic cellular tissues by direct or by lymphatic or hematogenous routes. The infection causes exudation and formation of an indurated mass usually c'onfined to one side of the uterus. The uterus in that case is pushed to the contralateral side.
II   Peritonitis is common following  infection (metritis) after cesarean delivery. There may be necrosis of uterine incision wound  and  dehiscence.  Patient  presents  with  bowel distension and a dynamic ileus.
11   Salpingitis may be interstitial (due to lymphatic spread) or perisalpingitis (following pelvic peritonitis). Endosalpingitis (tubal mucosa) is uncommon.
11   Pelvic  abscess following pelvic peritonitis  may  be  due to spread of infection. Rarely,  there  may be generalized peritonitis. With a dynamic ileus pelvic abscess has become rare (<l %) with the use of antibiotics. A suppurative wound infection takes 7-10 days to develop.
11   Septic Pelvic Thrombophlebitis (SPT)-may involve the ovarian veins,  uterine veins,  pelvic veins and rarely,  the inferior vena cava. Formation of thrombus in deep pelvic veins are due to the result of hypercoagulable  state  in pregnancy. Once infected, these release septic microemboli that effect the lungs or kidneys. Imaging studies USG, CT or MRI can diagnose larger thrombus. A negative result does not rule out SPT. SPT is a diagnosis of exclusion. The clinical features of pelvic thrombophlebitis are similar to those of uterine infection or parametritis. There may be swinging temperature continued for a longer period with chills and rigor. Persistent fever despite the use of antibiotics is due to SPT. Anticoagulation with heparin or enoxaparin is started. LMWH at a dose of 1 mg/kg/every 12 hours is commonly started. APTT of 1.5 to 2.0 times the normal is maintained. Antibiotics are continued until the patient is a febrile for 24-48 hours.
■   Septicemia and septic shock-may be due to hemolytic streptococci  (streptococcal  toxic  shock  syndrome)  or anaerobic streptococci. Septicemia may cause lung abscess, meningitis, pericarditis, endocarditis or multiorgan failure. Death occurs in about 30% of cases.
I CLINICAL FEATURES 11   Local infection
11    Uterine infection
11    Spreading infection


LOCAL  INFECTION  (WOUND  INFECTION):  (I)  There is slight rise  of temperature,  generalized malaise  or headache; (2) The local wound becomes red and swollen; (3) Pus may form which leads to disruption of the wound. When severe (acute), there is high rise of temperature with chills and rigor.
UTERINE INFECTION
Mild: (I) There is rise in temperature (>100.4°F} and pulse rate (>90); (2) Lochial discharge becomes offensive and  copious;  (3)  The  uterus  is  subinvoluted  and tender.
Severe:  (I)  The  onset  is  acute  with  high· rise  of temperature, often with chills and rigor; (2) Pulse rate is rapid, out of proportion to temperature; (3) Often there is breathlessness, coughs, abdominal pain and dysuria; (4) Lochia may be scanty and odorless; (5) Uterus may be subinvoluted, tender and softer. There may be associated wound infection (perineum, episiotomy wound or the cervix}.
SPREADING  INFECTION  (EXTRAUTERINE  SPREAD)  is evident  by  presence  of  pelvic  tenderness  (pelvic peritonitis), pelvic cellulitis with tenderness on the fornix (parametritis), bulging fluctuant mass in the pouch of Douglas (pelvic abscess). Rare presentations are: abdominal tenderness (general peritonitis}, pelvic thrombophlebitis or septicemia or even septic shock.
Parametrial phlegmon: Rarely parametritis (parametrial cellulitis) occurs following cesarean delivery. lnduration develops within the layers of broad ligament (phlegmon). The cellulitis may spread along the natural planes of the broad ligament cleavage. This may spread to the pelvic side wall, rectovaginal septum and around the cervix. It takes longer time (7-10 days) to resolve with the use of broad-spectrum antibiotics. Suppuration of a parametrial phlegmon is rare. The abscess may manifest as a fluctuant mass in the POD or as psoas abscess or may point above the inguinal ligament. Drainage of abscess may be done by culdocentesis or percutaneous drainage under CT guidance.
Toxic shock syndrome is often manifested by fever, headache, nausea, vomiting, diarrhea and erythematous skin rash. Major organ dysfunction (renal failure, hepatic dysfunction,  DIC) have  been  observed.  Etiologically staphylococcal exotoxin (Staphylococcus aureus) has been found to activate T cells to create a "Cytokine storm''. Maternal mortality is high unless promptly treated. Supportive therapy and antibiotics are used to prevent the capillary endothelial injury.
Septicemia: (I) There is high rise of temperature usually associated with rigor. Pulse rate is usually rapid even after the temperature settles down to normal; (2) Blood culture is positive, (3) Symptoms and signs of metastatic infection in the lungs, meninges or joints may appear.
Bacteremia, endotoxic or septic shock is due to release of bacterial endotoxin (lipopolysaccharide) causing circulatory inadequacy and tissue hypoperfusion. It is manifested by hypotension, oliguria and adult respiratory distress syn­ drome.

Chapter 30: Abnormalities of the Puerperium	- .
II INVESTIGATIONS OF PUERPERAL PYREXIA

The underlying principles in investigations are: (I) To locate the site of infection; (2) To identify the organisms; (3) To assess the severity of the disease.
A  case  of  puerperal  pyrexia is  considered to  be due to genital sepsis unless proved  otherwise.  The investigations should also be directed  to find  out any extragenital source of infection to account for the fever as well.
History: Antenatal, intranatal and postnatal history of any high-risk factor for infection like anemia, prolonged rupture of membranes or prolonged labor are to be taken.
Clinical  examination  includes  thorough  general, physical and systemic examinations. Abdominal and pelvic examinations are done to note the involution of genital organs and locate the specific site of infection. Legs should be examined for thrombophlebitis or thrombosis.
Investigations  include:  (I)   High   vaginal   and
endocervical swabs for culture in aerobic and anaerobic media  and  sensitivity  test  to  antibiotics;  (2)  "Clean catch" midstream specimen of urine for analysis and culture including sensitivity test; (3) Blood for total and differential white  cell  count,  hemoglobin  estimation and  lactate  measurement.  A  low platelet  count  may indicate septicemia or DIC. Thick blood film should be examined for malarial parasites; (4) Blood culture, if fever is associated with chills and rigor. Other specific investigations as per the clinical condition are needed; (5) Serum urea, creatinine and electrolytes may be done in a selected case to have a baseline record in the event that renal failure develops later in the course of the disease or laparotomy is needed. (6) Pelvic ultrasound is helpful­ (i) to detect any retained bits of conception within the uterus, (ii) to locate any abscess within the pelvis, (iii) to collect samples (pus or fluid} from the pelvis for culture and sensitivity, and (iv) for color flow Doppler study to detect venous thrombosis. Use of CT and MRI is needed, especially when diagnosis is in doubt or there is pelvic vein thrombosis; (7) Chest X-ray (CXR) should be taken in cases with suspected pulmonary Koch's lesion and also to detect any lung pathology like collapse and atelectasis (following inhalation anesthesia).

I PROPHYLAXIS
Puerperal sepsis is to a great extent preventable provided certain  measures  are undertaken before,  during,  and following labor.
Antenatal  prophylaxis  includes  improvement  of nutritional  status  (to  raise  hemoglobin  level}  of  the pregnant woman and eradication of any septic focus (skin, throat, tonsils} in the body.
Intranatal  prophylaxis includes-(a)  Full surgical asepsis  during  delivery,  (b)  Screening for  Group  B
· i	-   Chapter 30: Abnormalities of the Puerperium


Streptococcus in a high-risk patient.  Prophylactic  use of  antibiotic  is  not  recommended  as  a  routine,  (c) Prophylactic use of antibiotic at the time  of cesarean section has significantly reduced the incidence of wound infection, endometritis, urinary tract infection and other serious infections.
Postpartum prophylaxis includes aseptic precautions for at least 1 week, following delivery until the open wounds in the uterus, perineum and vagina are healed up. Too many visitors are restricted. Sterilized sanitary pads are to be used. Infected babies and mothers should be in isolated room.
I TREATMENT

General care: (i) Isolation of the patient is preferred, especially when hemolytic Streptococcus is obtained on culture, (ii) Adequate fluid and calorie are maintained by intravenous infusion (N), (iii} Anemia is corrected by oral iron or if needed by blood transfusion, (iv) An indwelling catheter is used to relieve any urine retention due to pelvic abscess. It also helps to record urinary output, (v) A chart is maintained by recording pulse,  respiration, temperature,  lochial discharge,  and  fluid  intake  and output, (vi) Antibiotics: Ideal antibiotic regimen should depend on the culture and sensitivity report. Pending the report, empirical therapy with gentamicin (2 mg/kg IV loading dose, followed by 1.5 mg/kg IV every 8 hours) and clindamycin (900 mg IV every 8 hours) should be started. Metronidazole 0.5 g N is given at 8 hours interval to control the anaerobic group. The treatment is continued
until the infection is controlled for at least 7-10 days.
CHOICE  OF  ANTIBIOTIC  REGIMENS:  Severe  sepsis. A  combination  of  either  piperacillin-tazobactam  or carbapenem plus clindamycin has broadest range of antimicrobial coverage. Women with MRSA infection should be treated with vancomycin or teicoplanin.
Surgical treatment: There is little role of major surgery in the treatment of puerperal sepsis.
11    Perineal wound-management of episiotomy wound
infection and dehiscence. •  Antibiotics-Iv.
•  Removal of sutures and wound dressing.
•  Wound debridement-under analgesia/anesthesia. •  Repeated sitz bath.
•  Wound  dressing  and  debridement  till  healthy granulation tissue develops.
•   Secondary wound repair with nonabsorbable suture. •  Removal of sutures after 10-12 days.
a   Retained uterine products with a diameter of 3 cm or less may be disregarded and left alone. Otherwise, surgical  evacuation after antibiotic coverage for 24 hours should be done to avoid the risk of septicemia. Cases with septic pelvic thrombophlebitis are treated with N heparin for 7-10 days.


■   Pelvic abscess should be drained by colpotomy under ultrasound guidance.
■  Wound  dehiscence:  Dehiscence   of   episiotomy or  abdominal  wound  following  cesarean  section is  managed  by  scrubbing  the  wound  twice  daily, debridement of all necrotic tissue and then closing the  wound  with  secondary  suture.  Appropriate antimicrobials   are   used   following   culture   and sensitivity.
11    Laparotomy has got limited indications: Maintenance of electrolyte  balance  by intravenous  fluids along with appropriate antibiotic therapy usually controls the peritonitis. However, in unresponsive peritonitis, laparotomy   is   indicated.   Even   if   no   palpable pathology is found, drainage of pus may be effective. Hysterectomy is indicated in cases with rupture or perforation,  having multiple abscesses,  gangrenous uterus   or   gas   gangrene   infection.    Ruptured tuboovarian abscess should be removed.
11    Necrotizing  fasciitis  (Fig.  30.1)  is  rare  but  fatal complication of wound infection (abdominal, perinea!, vaginal),  involving muscle and fascia. Risk factors are diabetes, obesity and hypertension. Infection is caused by Group A beta-hemolytic Streptococcus and  often  it  is  polymicrobial.  Tissue  necrosis  is the  significant   pathology.   Treatment  includes: Rehydration,  wound  scrubbing,  debridement of all necrotic tissues, and use of high-dose broad-spectrum (N) antibiotics.
Indications of intensive  care  unit  management: (1)  Hypotension;  (2)  Oliguria;  (3)  Raised  serum creatinine;  (4) Raised serum lactate ('.4 mmol/L);  (5) Thrombocytopenia; (6) ARDS; (7) Hypothermia.
11    Management   of   bacteremic   or   septic   shock includes-fluid and electrolyte balance (to monitor CVP),  respiratory  supports  (to  maintain  arterial P02   and PC02},   circulatory support (dopamine  or
















Fig. 30.1:  Necrotizing fasciitis involving the skin, subcutaneous tissues, rectus sheath and the muscles (myofasciitis) in a cesarean section wound.
 


Chapter 30: Abnormalities of the Puerperium	IIIL· w


dobutamine),  infection control (intensive antibiotic therapy, surgical removal of septic foci) and specific management (as hemodialysis for renal failure).

SUBINVOLUTION

DEFINITION:  When  the  involution  is  impaired  or retarded, it is called subinvolution. The uterus is the most common organ affected in subinvolution. As it is the most accessible organ to be measured per abdomen, the uterine involution is considered clinically as an index to assess subinvolution.
CAUSES: Predisposing factors are-(1)  Grand multi­ parity;  (2)  Overdistension of  uterus  as in twins  and hydramnios; (3) Maternal ill-health; (4) Cesarean section; (5)  Prolapse of the uterus;  (6)  Retroversion after the uterus becomes pelvic organ; (7) Uterine fibroid.
Aggravating factors are:  (1)  Retained products of conception; (2) Uterine sepsis (endometritis).
SYMPTOMS:  The  condition  may  be  asymptomatic. The predominant symptoms are: (1) abnormal lochial discharge, either excessive or prolonged; (2) irregular or at times, excessive uterine bleeding; (3) irregular cramp-like pain in cases of retained products or rise of temperature in sepsis.
SIGNS: (1) The uterine height is greater than the normal for the particular day of puerperium. Normal puerperal uterus may be displaced by a full bladder or a loaded rectum. It feels boggy and softer; (2) Presence of features responsible for subinvolution may be evident.
MANAGEMENT: Mere size of the uterus is not important and  provided  there  is  absence  of  features,  such  as excessive lochia or irregular bleeding or sepsis, the size of the uterus can be safely ignored. Appropriate therapy is to be instituted only when subinvolution is found to be a mere sign of some local pathology: (1) Antibiotics in endometritis; (2) Exploration of the uterus in retained products;   (3)   Pessary  in  prolapse  or  retroversion. Methergine, so often prescribed to enhance the involution process, is of little value in prophylaxis.

URINARY COMPLICATIONS IN PUERPERIUM

URINARY TRACT INFECTION: It is one of the common causes of puerperal pyrexia, the incidence being 1-5% of all deliveries. The infection may be the consequence of any of the following: (1) Recurrence of previous cystitis or  pyelitis;  (2)  Asymptomatic  bacteriuria  becomes overt;  (3)  Infection  contracted  for  the  first  time during puerperium is due to-(a)  effect of frequent catheterization, either during labor or in early puerperium to relieve retention of urine, (b) stasis of urine during early puerperium due to lack of bladder tone and less desire to pass urine.

The organisms responsible are-E.  coli, Klebsiella, Proteus and S. aureus. The clinical features, diagnosis and management have been described.
RETENTION OF URINE: This is a common complication in early puerperium. The causes are-(1) Bruising and edema of the bladder neck;  (2)  Reflex  pain from the perinea! injury; (3) Unaccustomed position.
Postpartum Urinary Retention (PUR) is common after childbirth, depending on the type of delivery. Risk factors for PUR include: Epidural analgesia, prolonged first  or  second stage of labor,  instrumental  delivery, episiotomy, primiparous women, physiological changes such as increased progesterone levels.
Treatment:  If simple  measure  fails  to  initiate micturition within 6 hours of delivery, an indwelling catheter is to be kept in situ for about 48 hours. This not only empties the bladder but helps in regaining the  normal bladder tone  and  sensation  of fullness. Following removal of catheter, the amount of residual urine is to be measured. If it is found to be more than 100 mL, continuous drainage is resumed. Appropriate urinary antiseptics should be administered for about 5-7 days.
INCONTINENCE  OF  URINE:  This  is  not  a  common symptom following birth.  The incontinence may be: (I) overflow incontinence; (2) stress incontinence; (3) true incontinence.  Overflow incontinence following retention  of  urine  should  first  be  excluded  before proceeding to differentiate between the other two. Stress incontinence usually manifests in late puerperium, whereas true incontinence in the form of genitourinary fistula  usually  appears  soon  following  delivery  or within first week of puerperium. Diagnosis of stress incontinence is  established by noting the escape of urine through the urethral opening during stress. The exact nature of urinary fistula is established by noting the fistula site by examining the patient in Sims' position, using Sims' speculum or by three-swab test, if the fistula is tiny.
SUPPRESSION  OF  URINE:  One  should  differentiate suppression from retention of urine. If the 24 hours urine excretion is less than 400 mL or less, suppression of urine (oliguria) is diagnosed; the cause is to be sought for and appropriate management is instituted.

Physiological changes in pregnancy.
Change	Clinical effects
50-60% increase in renal blood flow and	Increased urinary glomerular filtration rate.	frequency
Dilatation of urinary collecting system and	Increased risk of UTI ureters.
Bladder and urethra elevated and stretched     Urinary incontinence with reduced tone and sensation.	and retention.
·fl Chapter 30: Abnormalities of the Puerperium

Physiological changes in the puerperium.
Change	Clinical effects
Fluid shift from extravascular space to	Increased urinary intravascular space, renin-angiotensin-	output alodesterone system activity (Ch. 5, p. 46).
Bladder wall becomes edematous, hyperemic;	Urinary retention compression of urethra, reduced bladder tone
and sensation.
Atony of pelvic floor muscles	 Urinary incontinence
Dilatation of urinary collecting system and	Increased risk of ureters secondary to smooth muscle relaxation    UTI.
or compression of ureters by enlarged uterus

BREAST COMPLICATIONS

The common breast complications in puerperium are: (1) Breast engorgement; (2) Cracked and retracted nipple leading to difficulty in breastfeeding; (3)  Mastitis and breast abscess; (4) Lactation failure. Breast engorgement and infection are responsible for puerperal pyrexia.
I BREAST ENGORGEMENT

Cause: Breast engorgement is due to exaggerated normal venous and lymphatic engorgement of the breasts which precedes lactation. This, in turn, prevents escape of milk from the lacteal system. The primiparous patient and the patient with inelastic breasts are likely to be involved.
Onset: It usually manifests  after  the milk secretion starts (third or fourth day postpartum).
Symptoms  include:  (a)   Considerable  pain   and feeling of tenseness or heaviness in both the breasts; (b) Generalized malaise or even transient rise of temperature; and (c) Painful breastfeeding.
Prevention includes: (i)  To  avoid prelacteal feeds, (ii) To initiate breastfeeding early and unrestricted, {iii) Exclusive  breastfeeding  on  demand,  {iv)  Feeding  in correct position, (v) Correct latch on.
TI·eatment: (1) To support the breasts with a binder or brassiere; (2) Frequent suckling; (3) Manual expression of any remaining milk after each feed; (4) To administer analgesics for pain; (5) The baby should be put to the breast regularly at frequent intervals; (6) In a severe case, gentle use of a breast pump may be  helpful.  This will reduce the tension in the breast without causing excess milk production.
I CRACKED AND RETRACTED NIPPLE

Cracked nipple: The nipple may become painful due to-(1) Loss of surface epithelium with the formation of a raw area on the nipple; or (2) Due to a fissure situated either at the tip or the base of the nipple.  These  two conditions  frequently  coexist  and  are  referred  to  as cracked  nipple.  It is  caused  by-(a)  unclean hygiene

resulting in formation of a crust over the nipple,  (b) retracted nipple, and (c) trauma from baby's mouth due to incorrect attachment to the breast, (d) infection with Candida albicans and S. aureus is often present. The condition may remain asymptomatic but becomes painful when  the  infant  sucks.  When infected,  the  infection may  spread  to  the  deeper  tissue  producing  mastitis. Prophylaxis includes local cleanliness during pregnancy and in the puerperium before and after each breastfeeding to prevent crust  formation over the nipple.  Treatment: Correct  attachment (latch on) will provide immediate relief from  pain  and rapid healing.  Fresh  human milk and saliva have got healing properties.  Purified lanolin with the mother's milk is applied three or four times a day to hasten healing. When it is severe, mother should use a breast pump and the infant is fed with the expressed milk.  Inflamed nipple and areola may be  due to thrush also.  Miconazole lotion is applied over the nipple as well as in  the baby's mouth if there  is oral  thrush.  If it fails to  heal  up,  rest  is  given  to  the  affected  nipple  using  a breast pump while the nipples heal.  Nipple shields (thin latex) can be used. The persistence of a nipple ulcer,  in spite  of therapy mentioned,  needs  biopsy to exclude malignancy.
Retracted and flat nipple:  It is commonly  met in primigravidae.  It is usually acquired.  Babies are able to  attach to  the  breast correctly  and  are  able  to  suck adequately. In difficult cases, manual expression of milk can initiate lactation.  Gradually, breast tissue becomes soft and more protractile, so that feeding is possible.
I ACUTE MASTITIS

The  incidence of  mastitis  is 2-20%  in  lactating  and less  than  1 %  in non-lactating  women.  The common organisms involved are S. aureus (MRSA), Staphylococcus epidermidis and Streptococcus viridans. Risk factors for mastitis are poor nursing, maternal fatigue and cracked nipple.
Mode of infection: There are two different types of  mastitis  depending  upon  the  site  of  infection. (1)  Infection  that involves  the  breast parenchymal tissues leading to cellulitis. The lacteal system remains unaffected;   (2)  Infection  gains  access  through  the lactiferous  duct  leading  to  development  of  primary mammary adenitis. The source of organisms is the infant's nose and throat.
Noninfective  mastitis  may  be  due  to  milk  stasis (plugged duct). Feeding from the affected breast solves the problem.
Onset: In superficial cellulitis, the onset is acute during first 2-4 weeks postpartum. However, acute mastitis may occur even several weeks after the delivery.
Clinical   features:   Symptoms    include-(a)
Generalized malaise and headache, nausea, vomiting,
Chapter 30: Abnormalities of the Puerperium    11

(b) Fever (>38.5°C or more) with chills, (c) Severe pain and tender swelling in one quadrant of the breast and {d) Indurated. Signs include-{a) Presence of toxic features, and {b) Presence of a swelling on the breast. The overlying skin is red, hot and flushed and feels tense and tender.
Diagnosis: Microscopic examination of breast milk, showing leukocytes more than 106 /mL and bacterial count more than 103 /mL, supports the diagnosis of mastitis.
Complications: Due to variable destruction of breast tissues, it leads to the formation of a breast abscess.
PROPHYLAXIS: Thorough handwashing before each feed, cleaning the nipples  before  and  after  each  feed,  and keeping them dry, reduce the nosocomial infection rates.
Management:   (a)   Breast  support,   (b)  Plenty  of oral fluids,  (c)  Breastfeeding is continued  with  good attachment. Nursing is initiated on the uninfected side first to establish let down, (d) The infected side is emptied manually with each feed, (e) Dicloxacillin (penicillinase­ resistant penicillin) is the drug of choice. A dose of 500 mg every 6 hours orally is started till the sensitivity report available. Erythromycin or clindamycin is an alternative to  patients  who  are  allergic  to  penicillin.  Antibiotic therapy  is  continued  for  10-14  days,  (f)  Analgesics (ibuprofen) are given for pain, (g) Milk flow is maintained by breastfeeding the infant.  This  prevents proliferation of  Staphylococcus  in  the  stagnant  milk.  The  ingested Staphylococcus will be digested without any harm.
BREAST ENGORGEMENT: Bilateral generalized tenderness of breasts is seen on 2 to 4 days postpartum. Low grade fever is often associated. It is due to interstitial edema or accumulation of excess of milk. It is treated with worm compress followed by expression (by hand or pump) of milk. Continued breast feeding is helpful.
BREAST ABSCESS: Features are-(1)  Flushed breasts not  responding  to  antibiotics  promptly;  (2)  Brawny edema of the overlying skin; (3) Marked tenderness with fluctuation; (4) Swinging temperature.
Breast abscess is to be drained under general anesthesia by a deep radial incision extending from near the areolar margin to prevent injury of the lactiferous ducts. Incision perpendicular to the lactiferous ducts increases the risk of fistula formation and ductal occlusion. Finger exploration is done to break up the walls of the loculi. The cavity is loosely packed with gauze which should be replaced after 24 hours by a smaller pack. The procedure is continued till it heals up. The abscess can also be drained by serial percutaneous needle aspiration under ultrasound guidance.
Breastfeeding is continued in the uninvolved side. The infected breast is mechanically pumped every 2 hours and with eve1y let down. Recurrence risk is about 10%. Once cellulitis has resolved, breastfeeding from the involved side may be resumed.
Antibiotics to be continued depending upon the culture report of pus.
Breast pain may be due to engorgement,  infection ( C.  albicans), nipple trauma, clogged milk, mastitis or occasionally with latching on or let down reflex.


Management: Appropriate nursing technique,  posi­ tioning and breast care can reduce pain significantly when it is due to nipple trauma, engorgement or mastitis. Use of miconazole oral lotion or gel to both the nipples and into infant's mouth thrice daily for 2 weeks is helpful.
INADEQUATE MILK PRODUCTION: The normal volume of milk produced at the end offirst postpartum week is 550 mL/ day. By 2-3 weeks it is increased fom 80 about 800 mL/day. Production peaks at 1.5-2.0 L/day. The causes of inadequate milk production are: (1) Infrequent suckling; (2)  Depression  or  anxiety state  in  the  puerperium; (3)  Reluctance  or apprehension to nursing;  (4)  Ill­ development of the nipples; (5) Painful breast lesion; (6) Endogenous suppression of prolactin (retained placental bits); {7) Prolactin inhibition (ergot preparations diuretics, pyridoxine);  (8)  Previous  breast  surgery;  (9)  Insulin resistance; (10) High androgen levels.
r
Treatment: For maintenance of effective lactation in an otherwise healthy individual, the following guidelines are helpful.
+   Antenatal:  (1) To counsel the mother regarding the advantages of nursing her baby with breast milk; (2) To take care of any breast abnormality, especially a retracted nipple  and to  maintain  adequate  breast hygiene, since 36 weeks of pregnancy.
+   Puerperium: (1) To encourage adequate fluid intake; (2)  To  nurse  the  baby  regularly;  (3)  Painful  local lesion is to be treated; ( 4) Metoclopramide, intranasal oxytocin and sulpiride (selective dopamine antagonist) have been found to increase milk production. They act by stimulating prolactin  secretion.  Metoclopramide given in a dose of 10 mg thrice daily is found helpful.

PUERPERAL VENOUS THROMBOSIS (VT) AND PULMONARY EMBOLISM (PE)
Approximately 80% of VTEs in pregnancy are due to DVT and 20% are PE. Pregnant women 4-5 times are more likely to have VTE. About 50% of all DVT and VTEs occur in antepartum period.
Basic pathology for venous thrombosis are-(i) Vascular stasis, (ii) Hypercoagulability of blood (pregnancy), and (iii) Vascular endothelial trauma (Virchow's triad 1856). Other pregnancy­ specific risk factors are as mentioned below:
Venous thromboembolic diseases include:
♦   Deep vein thrombosis (iiiofemoral-70% ).
♦   Thrombophlebitis (superficial and deep veins). ♦   Pulmonary embolus (PE).
Pathophysiology: (1) In a normal pregnancy there is rise in concentration of coagulation factors I, II, VII, VIII, IX, X, XII (20-100%). Plasma fibrinolytic inhibitors are produced by the placenta and the level of protein S is markedly (40%) decreased; (2) Alteration in blood constituents-increased number of young platelets and their adhesiveness; (3) Venous stasis is increased due to compression of gravid uterus to the inferior vena cava and iliac veins. This stasis causes damage to endothelial cells.
Thrombophilias are hypercoagulable states in pregnancy that increase the risk of venous thrombosis. It may be inherited
······II Chapter 30: Abnormalities of the Puerperium

or acquired. Inherited thrombophilias are the genetic conditions associated with the deficiencies of antithrombin III, protein C, protein S and prothrombin gene mutation. Others are factor V Leiden mutation and hyperhomocysteinemia. Acquired thrombophilias are due to the presence lupus anticoagulant and antiphospholipid antibodies.
Risk factors for  VTE-(1)  High  l'isk: Previous VTE, thrombophilia; (2) Intermediate risk: (a) Heart disease, (b) SLE, (c) Surgical procedures (LSCS); (3) Low risk: Presence of less than three from any of these risk factors mentioned: (a) age >35 years, (b) Obesity (BMI >35), (c) Parity  3, (d) Immobility, (e)
Dehydration, (f) Hyperemesis, (g) Multiple pregnancy.
Note: Low risk factors more than  three make the patient as intermediate risk.
DEEP VEIN THROMBOSIS: Diagnosis: Clinical diagnosis is unreliable. In majority, it remains asymptomatic.
Symptoms include pain in the calf muscles, tenderness, edema legs and rise in skin temperature. On examination asymmetric leg edema ( difference in circumference between the affected and the normal leg more than 2 cm) is significant (Fig. 30.2). A positive Roman's sign-pain in the calf on dorsiflexion of the foot may be present ( <15%).
Investigations: The following biophysical tests are employed to confirm the diagnosis:
1.  Venous duplex imaging, including compression.
2.  Ultrasound, color and spectral Doppler sonography is the gold standard and the noninvasive diagnostic method.
3.  MRI is done when iliac vein thrombosis is suspected and compression USG results are negative or equivocal. It has sensitivity of 100% and specitivity of99%.
4.  D-dimer test is sensitive but nonspecific for DVT.
5 .  Doppler ultrasound to detect the changes in the velocity of blood flow in the femoral vein by noting the alteration of the characteristic  "whoosh"  sound  which is audible from a patent's vein. Venous Ultrasonography (VUS): It is done by placing the transducer over the femoral vein and then gradually it is moved to the great saphenous vein, the popliteal vein and to its branches with the deep veins of the calf.
















Fig. 30.2: Deep vein thrombosis of the lower limb (right) showing massive edema of both the legs and the  thighs.  Compression ultrasonography was positive.


6.  Magnetic Resonance Imaging (MRI) is found superior to VUS and equivalent to contrast venography in the diagnosis ofDVT. MRI is helpful to detect thrombosis in pelvic, iliac or femoral veins. The sensitivity and specificity of MRI in the diagnosis ofDVT are 100% and the accuracy is 99%.
7.  D-dimer assays: D-dimer is a product of degradation of fibrin by plasmin. Testing for D-dimer is not preformed for acute episode ofVTE in pregnancy.
SEPTIC PELVIC THROMBOPHLEBITIS (SPT): Postpartum thrombophlebitis  originates in the  thrombosed  veins at the placental site by organisms such  as  anaerobic streptococci or Bacteroides fragilis). When localized in the pelvis, it is called pelvic thrombophlebitis. There is no specific clinical feature of pelvic thrombophlebitis, but it should be suspected in cases where the pyrexia continues for more than a week in spite of antibiotic therapy. It is a diagnosis of exclusion.
Extrapelvic spread: (1) Through the right ovarian vein into inferior vena cava and thence to the lungs; (2) Through the left ovarian vein to the left renal vein and thence to the left kidney; (3) Retrograde extension to iliofemoral veins to produce the clinicopathological entity of "phlegmasia alba dolens" or white leg. It is rare these days.
Clinical features: (1) It usually develops on the second week of puerperium; (2) Mild pyrexia is common prior to the dramatic local manifestations. At times, the fever may be high with chills and rigor; (3) Evidences of constitutional disturbances such as headache, malaise and rising pulse rate or features of toxemia may be present; ( 4) The affected leg is swollen, painful, white and cold. The pain is due to arterial spasm as a result of irritation from  the nearby thrombosed vein;  (5)  Blood count shows polymorphonuclear leukocytosis. The diagnosis may be made by venous ultrasound, Computed Tomography (CT) scan or by Magnetic Resonance Imaging (MRI).

PROPHYLAXIS AND MANAGEMENT FOR VENOUS THROMBOEMBOLISM (VTE) IN PREGNANCY AND PUERPERIUM

Preventive measui-es include:
■   Prevention of trauma, sepsis, anemia in pregnancy and labor. Dehydration during delivery should be avoided.
■  Use  of  elastic  compression  stocking  and  intermittent pneumatic compression devices during surgery.
■  Leg exercises, early ambulation are encouraged following operative delivery.
Women at risk of venous thromboembolism during pregnancy have been grouped into different categories depending on the presence ofriskfactors (see above). Thromboprophylaxis to such a woman depends on the specific risk factor and the category.
(1) A low-riskwoman has no personal or family history ofVTE and is heterozygous for factor V Leiden mutation. Such a woman needs no thromboprophylaxis, early mobilization and adequate hydration to be maintained. (2) A high-risk woman (prothombin gene mutation) needs Low-Molecular-Weight Heparin (LMWH) prophylaxis throughout pregnancy and postpartum 6 weeks. (3) Intermediate risk women with three or more risk factors are considered for antenatal prophylaxis with LMWH up to 7 days of puerperium.


Management: (1) The patient is put to bedrest with the foot end raised above the heart level. (2) Pain on the affected area may be relieved with analgesics. (3) Appropriate antibiotics are to be administered. (4) Anticoagulants-Ca) Weight adjusted LMWH is used for the treatment ofVTE. Advantages of LMWH are: Less bleeding complications, less thrombocytopenia and osteoporosis, longer plasma half-life and more predictable dosed response. Monitoring of LMWH is peak plasma anti-factor Xa activity. Use of LMWH for the prevention and treatment ofVTE in pregnancy is recommended. (b)  Heparin 15,000 units are administered intravenously, followed by  10,000  units  4-6 hourly for 4-6 injections when the blood coagulation is likely to be depressed to the therapeutic level. Risk of major bleeding withUFH is about 2%.
Heparin is continued for at least 7-10 days or even longer if thrombosis is severe. Prolongation of activated partial thromboplastin time  (APTT)  to  1.5-2.5  times  indicates  effective  and  safe anticoagulation. Serum heparin level should be of 0.1-0.2U/mL.
(c) A drug of coumarin series-warfarin is commonly used orally with an overlap of at least 3 days with heparin. The initial daily single dose of 7 mg for 2 days is adequate for induction. Subsequent maintenance dose depends upon international normalized ratio (INR) which should be within the range of 2.0-3.0. The daily maintenance dose of warfarin is usually 5-9 mg, to be taken at the same time each day. The anticoagulant therapy should be continued till all evidences of the disease have disappeared which generally  take  3-6 months.  The anticoagulant (warfarin, LMWH or unfractionated heparin) is safe for breastfeeding. (5) As soon as the pain subsides, gentle movement is allowed on bed by the end of first week. High quality elastic stockings are fitted on the affected leg before mobilization. (6) Inferior vena cava filters are used for patients with recurrent pulmonary  embolism  or  where  anticoagulant therapy  is contraindicated.Vena cava may be completely ligated by teflon clips. (7) Fibrinolytic agents like streptokinase produce rapid resolution of pulmonary emboli. (8)  Venous thrombectomy is needed for massive iliofemoral vein thrombosis or for massive pulmonary embolus.
ii PULMONARY EMBOLISM (PE)

Pulmonary Embolism (PE) is the lead cause of maternal deaths (20%) in  many parts of the world. The clinical features depend on the size of the embolus and on the preceding  health  status  of the patient.  The classical symptoms of massive pulmonary embolism are sudden collapse with acute chest pain  and air hunger. Death usually occurs within short time from shock and vagal inhibition.
The important signs and symptoms of pulmonary embolism are: Sudden tachypnea (>20 breaths/min), dyspnea, pleuritic chest pain, cough, tachycardia (>100 bpm), hemoptysis and rise in temperature more than 37°C.
DIAGNOSIS:
♦   X-ray of the chest shows diminished vascular marking in areas of infarction, elevation of the dome of the diaphragm and often pleural effusion. I t is useful to rule out pneumonia, pulmonary infiltrates and atelectasis.
♦   ECG: ECG is abnormal in 41 % of women with acute PE. The most common abnormalities are: Twave inversion (21%);

Chapter 30: Abnormalities of the Puerperium

Sl Q3 T3 pattern (15%) and right bundle branch block (18% during pregnancy and 4.2% in the puerperium). ABG analysis is of limited diagnostic value.
♦   Arterial blood gas: PO2  more than 85 mm Hg on room air is reassuring but does not rule out PE. More than 50% of
pregnant women with a documented PE have a  normal alveolar-arterial gradient.
♦   D-Dimer:  A  negative  D -dimer  value  may  rule  out  the diagnosis of PE. It has a high negative predictive value.
♦   Doppler ultrasound can identify a DVT. When the test is positive for DVT, anticoagulation therapy should be started.
♦   Lung scans(ventilation/perfusion scan orV/Q scan): Perfusion scan  will detect  areas  of diminished blood flow whereas a  reduction  in perfusion with  maintenance  of  ventilation indicates pulmonary embolism. V/Q scanning is the method of choice for patients with suspected PE and with normal chest radiograph. High probabilityV/Q scan suggests PE.
♦   Magnetic Resonance  Imaging  (MRI)   can  be  used  in pregnancy as the risk of ionizing radiation is absent.
♦   Pulmonary  angiography  is  the  gold  standard  to  the diagnosis but has got high risks of complications. Mortality rate is 0.5% and overall complication rate is 3%.
♦   Computed Tomographic (pulmonary) Angiography (CTA) is  the  recommended  imaging  in  pregnant women  with suspected PE. The CTA is cost effective and has lower dose radiation effect to the fetus than a V/Q scan. Multidetector CTA allows visualization of finer pulmonary vascular detail. It has higher diagnostic accuracy.
Radiation exposure: Two-view chest radiograph is <0.001 rad V/Q scan-fetal radiation is 0.064-0.08 rads compared with CTA (0.0003-0.0131 rad). Pulmonary angiography provides about 0.2 to 0.4 rad with femoral approach and <0.05 rad with brachia! approach.
In V/Q and CTPA, the absolute risk is very small. The radiation dose to the fetus at any stage of pregnancy: CXR: Less than 0.01 mSv(millisievert); CTPA: 0.1 mGy(milligray);V/Q Scanning: 0.5 mCy (milligray)
♦   Magnetic  Resonance   Angiography   (MRA)   with  IV gadolinium: It has got sensitivity of 100% and specificity of 95% in the diagnosis of PE.
Management: Prophylaxis (as mentioned on p. 414).
Active treatment includes:  (1) Resuscitation-cardiac massage, oxygen therapy, intravenous heparin (UFH) bolus dose of 10,000 IU and morphine 15 mg (IV) are started. Heparin remains the mainstay of therapy for VTE. Therapeutic doses of LMWH [enoxaparin 1 mg/kg subcutaneous (SC) twice daily] may be used. Antifactor Xa levels of 0.6-1U /mL are to be maintained. Heparin therapy (IV) should be continued for 5-10 days until patient improves clinically. Thereafter, it is changed to SC injections. Anticoagulation may need to be continued for 6 weeks to 6 months depending upon the case. Heparin level is maintained at 0.2-0.4 U/mL or the Activated Partial Thromboplastin Time (APTT) about twice the normal (1.5-2.5 times). (2) IV fluid support is continued and blood pressure is maintained, if needed by dopamine or adrenaline. (3) Tachycardia is counteracted by digitalis. (4) Recurrent attacks of pulmonary embolism necessitate surgical treatment like embolectomy, placement of inferior caval filter or ligation of inferior vena cava and ovarian veins. Surgical treatment
is done following pulmonary angiography.
Chapter 30: Abnormalities of the Puerperium

Indications of inferior vena cava filters are: (a) absolute contraindication to medical anticoagulation, {b) failure of anticoagulation, (c) heparin-induced thrombocytopenia, {d) allergy to UFH or LWH.
Contraindications of heparin therapy are:
♦   Women with active antenatal or postpartum bleeding. ♦   Risk of major hemorrhage (placenta previa).
♦   Coagulopathy.	•   Thrombocytopenia. ♦   Allergic to UFH or LWH.
Contraception for women with a history of VTE: Due to thrombogenic potential of estrogenic-containing contraception, progestin only or nonhormonal methods are recommended.
Natural family planning, condoms, POP, LNG-IUCD, copper IUD, tubectomy are the options.

OBSTETRIC PALSIES
(Syn: Postpartum Traumatic Neuritis)

The commonest form of obstetric palsy encountered in puerperium is foot drop. It is usually unilateral and appears shortly after delivery or during first day postpartum or so. It is thought to be due to stretching of the lumbosacral trunk by the prolapsed intervertebral disk between L5 and SI. Backward rotation of the sacrum during labor may also be a contributing factor. Direct pressure either by the fetal head or by forceps blade on the lumbosacral cord or sacral plexus as a causative factor is no longer tenable.
The condition is usually mild and may pass unnoticed unless there is disability. Neurological examination reveals lower motor neuron type of lesion with flaccidity and wasting of the muscles. Post-traumatic neuropathies: In some cases, there may be foot drops. This is due to the injury oflumbosacral trunk, sciatic nerve or common peroneal nerve. The common peroneal nerve may compressed when the legs are placed in stirrups for a long time. Management of the damaged lumbosacral nerve roots is the same as that of the prolapsed intervertebral disk in consultation with an orthopedist.



abruptio placentae, mismatched  blood transfusion or eclampsia; (8) Decreased milk supply.
(c) Delayed: (1) Secondary postpartum hemorrhage; (2)   Thromboembolic   manifestation-pulmonary embolism; (3) Septic thrombophlebitis; (4) Psychosis; (5) Postpartum cardiomyopathy;  (6) Postpartum hemolytic uremic syndrome.
Sudden postpartum collapse is a life threatening event. It may be due to (Table 30.1):
■  Hemorrhagic or	11      Non-hemorrhagic conditions.

I CHORIOAMNIONITIS

It is the infection of amniotic fluid, amnionitic membranes with or without infection of the fetus. It is seen in term pregnancy  (2-5%). It is more common with preterm delivery and/or PROM. The infection  may  be  evident clinically or may remain sub-clinical.
The common organisms are: Prevotella specis, E. Coli, anerobes, bacteroides, group B streptococci.
Risk factors are: Long duration of rupture of membranes, multiple vaginal examination, pre-existing infections in the genital tract.
Diagnosis: Clinical presentation: ■  Rise in maternal temperature
11    Tachycardia: Both maternal and fetal, 11    Uterine tenderness and
11    Vaginal leakage of amniotic fluid-thick and turbid.
Investigations: Commonly done are: (A) Complete hemo­ gram (polymorphonuclear leukocytosis);  (B) Amniotic fluid  (obtained  following  abdominal  amniocentesis)

Table 30.1: Common causes of sudden postpartum collapse.



Paraplegia due to epidural hematoma or abscess (arachnoiditis) following regional anesthesia is extremely rare.
During labor: Lateral femoral cutaneous nerve neuropathies are also common. Nerve injuries with transverse cesarean incision include the iliohypogastric or the ilioinguinal nerves. Injury leads to loss of sensation over the area supplied.


Obstetric complications.



Medical

11      Massive postpartum hemorrhage. 11      Amniotic fluid embolism.
11     Acute inversion of the uterus. 11      Septic shock.
11     Severe pre-eclampsia and eclampsia.
•   Cardiac:




PUERPERAL EMERGENCIES

There are many acute complications that may occur during the puerperium. The majority of the alarming complications, however,  arise immediately following delivery.  The  late complications are relatively less risky. The acute complications are:
(a)  Immediate: (1)  Postpartum hemorrhage,  (2) Shock-hypovolemic, endotoxic or idiopathic, (3) Post­ partum eclampsia, ( 4) Pulmonary embolism- liquor amnii or air, (5) Inversion of the uterus.
(b) Early (within one week): (1) Acute retention of urine; (2) Urinary tract infection; (3) Puerperal sepsis; ( 4) Breast engorgement; (5) Mastitis and breast abscess; (6) Pulmonary infection (atelectasis); (7) Anuria following

disorders in	11      Myocardial infarction. pregnancy.	11     Cardiomyopathy.
11      Cardiac arrhythmias.
11      Pulmonary: ■   Embolism.
■  Acute respiratory failure (pulmonary edema).
Neurological.	■  Cerebral hemorrhages.
■   Cerebral venous thrombosis. Metabolic	• Hypo-/hyperglycemia. disorders.                     Hypo-/hyperkalemia.
•
Anesthetic	■  High spinal (diaphragmatic paralysis). causes:	■  Mendelson's syndrome.
■   Intravenous use of local anesthetic drug.
Anaphylaxis.	■   Drug toxicity.
Read more Dutta's Clinics in Obstetrics, Ch. 38
Chapter 30: Abnormalities of the Puerperium    -
Table 30.2: Complications of chorioamnionitis.	Complications of chorioamnionitis: Table 30.2.

Maternal



Fetal/neonatal (5-10%):


■   Febrile morbidity due to infections (10%); ■  Operative interventions (CD);  ■  Wound infection; ■  Dysfunctional labor; ■   Pelvic abscess (rare); ■   Sepsis
■    Bacteremia;   ■    Sepsis;   ■    Pneumonia; ■   Meningitis; ■   Respiratory distress syndrome; ■   lntraventricular hemorrhage;  ■   Necrotizing enterocolitis; ■   IUFD; ■   Mortality (1-4%)


Management:  Combination of ampicillin (2 g every 6 hours) and gentamicin 3 mg/kg eve1y 8 hours for 5-7 days is given. For anaerobic coverage either Clindamycin or Metronidozole is administered.
Neonatal  prognosis:  Short  term  outcomes:  Broncho pulmonary  dysplasia,   sepsis  and  intraventricular hemorrhage are more with preterm neonate.



• Gram stain and culture to slow organisms, and growth of pathogens (gold standard); (C) Amniotic fluid glucose <10-15 mg/dL; (D) Amniotic fluid IL-6 > 7.9 ng/mL; (F) Amniotic fluid leukocyte esterase >1 + reaction (Table 22.1).

Long-term outcomes: RDS, periventricular leukomalacia and  cerebral  palsy.  Fetal  inflammatory  response syndrome (SIRS) is mainly due to excess production of cytokines.



MENTAL HEALTH AND PSYCHIATRIC DISORDERS DURING PREGNANCY AND PUERPERIUM


In the first 3 months after delivery, the incidence of mental illness is high. Overall incidence is about 15-20%.
HIGH-RISK  FACTORS  FOR  POSTPARTUM  DEPRESSIVE DISORDERS (PPDD)
♦   Past history: Psychiatric illness, puerperal psychiatric illness.
♦   Family  history:  Major psychiatric illness,  marital conflict, poor social situation.
♦   Present pregnancy: Young age,  cesarean delivery, difficult labor, neonatal complications.
♦    Others: Unmet expectations (fetal loss).
♦   Postpartum   Depression   (PPD)   most   common complication of child birth.
Others:  Unmet  expectations  (fetal  loss,  financial problems).
Diagnostic criteria for PPD: Depressed mood, sleep changes  (insomnia),  lack  of energy,  loss of interest, hopelessness,  guilt.  May change to Major Depressive Disorder (MDD) (Edinburgh Postnatal Depression Scale score ::13).
Pharmacotherapy is indicated if depression is moderate to severe (suicidal ideation). Selective Serotonin Reuptake Inhibitors (SSRls) are preferred in such a case.
■  Bipolar  Affective Disorders (BPAD): It is a severe mood disorder characterized by periods of depression and periods of abnormally elevated  mood. Genetic involvement is stronger in BPAD than MDD. Patients with confirmed or suspected BPAD should be referred to a psychiatrist for evolution.
■  Perinatal Mood and Anxiety Disorders (PMADs) are highly prevalent during pregnancy and postpartum period.
Treatment: SSRI and Cognitive Behavioral Therapy. Gabapentin can offer immediate relief.


■   Obsessive-Compulsive Disorder ( OCD) in pregnancy and puerperium
•  OCD is not uncommon in pregnancy and postpartum period.
•  Obsessions are repetitive, intrusive,  less wanted thoughts and can be directed toward the fetus or the infant. Thoughts may be the fear of loss or death, fear of infections. Patient recognizes obsessions as irrational but unable to control them. Delusion is a false belief but the patient firmly believes it is true, despite the evidence to the contrary.
Treatment: Patient should be referred to psychiatrist evaluation. In such a situation temporary separation and nursing supervision are needed.
Pregnancy and puerperium in a woman with primary psychiatric disorders
11    Women with psychiatric  disorders  are  at  elevated risks of Cesarean Delivery (CD), placental abruption, preterm delivery,  PPROM, hemorrhage, FGR,  fetal distress and even fetal death.
■  For most medications plasma level will drop by 50% during pregnancy and will rise in puerperium. Dose adjustment is needed in pregnancy and puerperium.
■  Transfer  of  all  psychotropic  medications  occurs through the placenta and the breast milk. Physicians must be conversant of the drug dose information with the latest version of recommendations and monitoring the women with serum level of the drug when needed.
Commonly used drugs are:
•  SSRI: Escitalopram; sertraline, fluoxetine.
•  Tricyclic antidepressants: Amitriptyline, imipra-mine, duloxetine.
•  Antipsychotics: Olanzapine, lithium, carbamazepine.
Treatment: Psychotherapy is the preferred treatment option for mild to moderate episodes of anxiety or
Chapter 30: Abnormalities of the Puerperium

depression. Antidepressant medication is started when the episode is considered severe.
■  Electroconvulsive Therapy (ECT) for ve1y severe cases of depression, or mixed states.
■  Psychological:  Psychotherapy including Congenic Behavioral   Therapy   (CBT)   and   Interpersonal Psychotherapy (IPT) is for Mild/Moderate Perinatal Mood and Anxiety (PMAD).

PSYCHOLOGICAL RESPONSE TO PERINATAL DEATHS AND MANAGEMENT

Most perinatal events are joyful. But when a fetal or neonatal death occurs, special attention must be given



to the grieving patient and her family. Perinatal grieving may also be due to unexpected hysterectomy, birth of a malformed or critically ill infant. Prolonged separation from  a  critically  ill  newborn  can  also  provoke  grief reaction.  Physician,  nurse  and  attending  staff  must understand the patient's reaction. The common maternal somatic symptoms are: insomnia, fatigue and  sighing respirations, feeling of guilt, hostility and anger.
Management of perinatal grieving: Facilitating the grieving process with consolation, support and sympathy is important. Others are: supporting the couple in seeing or holding or taking photographs of the infant; autopsy requests, planning investigations, follow-up visit and plan for subsequent pregnancy.





►  The common causes of puerperal pyrexia are: (i) Puerperal sepsis, (ii) Urinary tract infection, (iii) Mastitis, (iv) Infection of the cesarean section wound, (v) Pulmonary infection, (vi) Septic thrombophlebitis, (vii) Recrudescence of malaria, tuberculosis or (viii) Unknown.
►  The common causes of puerperal sepsis are the infections in the genital tract. This includes: (i) Endometritis, (ii) Endomyometritis, or (iii) Episiotomy wound infection.
►  Pathogens commonly responsible for female genital infections are: (A) Aero bes (gram-positive-streptococci and staphylococci, gram­ negative-E. coli, Klebsiel/a or gram-variable-Gardnere//a). (B) Anaerobes (peptostreptococci, Fusobacterium, Clostridium) and (C) Others (Mycoplasma, Chlamydia).
►  Common causes of subinvolution are: (a) Excess enlargement of the uterus (twins), (b) Anemia, (c) Retained bits of tissues, (d) Endometritis.
►  Common breast complications in the puerperium are: (a) Breast engorgement, (b) Cracked and retracted nipple, (c) Mastitis and breast abscess.
►  Puerperal emergencies are often immediate (third-stage complications). There may be some complications that are relatively delayed but acute and alarming. These are-(i) Mastitis and breast abscess, (ii) thromboembolism, (iii) Psychiatric disorders, and (iv) Postpartum cardiomyopathy.
►  Workup for Women with Suspected Pulmonary Em bolus
►  D-dimer, CXR, VUS, V/Q scan, CTPA are to be done depending upon individual woman's signs and symptoms. Woman with positive observation in VUS, CXR, V/Q scan and CTPA need therapy. Anticoagulation is started in the absence of contraindications.
►  Risk factors for VTE are: (a) Previous VTE, (b) Heart disease, (c) SLE, (d) Surgical procedure (LSCS), (e) Obesity, (f) Immobility.
►  Thromboprophylaxis against VTE for women with intermediate-risk and high-risk factors are: LMWH throughout pregnancy and postpartum 7 days to 6 weeks, respectively.


The Term Newborn Infant








CHAPTER OUTLINE
❖ Physical Features of the Newborn ❖ Immediate Care of the Newborn


❖ Infant Feeding
►  Breastfeeding


► Artificial Feeding
►  Childhood Immunization Program




DEFINITION: A healthy infant born at term  (between 38 weeks and 42 weeks) should have an average birth weight for the country ( usually  exceeds 2,500 g),  cries immediately  following birth,  establishes independent rhythmic respiration and quickly adapts to the changed environment.
The  weight  is  variable  from  country  to  country but  usually  exceeds  2,500  g.  In  India,  the  weight varies between 2.7 kg and 3.1 kg with a mean of 2.9 kg (Fig. 31.1). The length (crown to foot) is 50-52 cm. The length is a more reliable criterion of gestational age than the weight. Occipitofrontal circumference measures about 32-37 cm and the biparietal diameter measures about 9.5 cm.

PHYSICAL FEATURES OF THE NEWBORN
The newborn must be examined thoroughly within 24 hours of birth. Before the actual examination, the important maternal and perinatal history should be reviewed. Maternal history ( age, parity, medical disorders, etc.), pregnancy problems-present


and past (drugs, IUFD, pre-eclampsia, IUGR, prematurity), labor and delivery history (duration, anesthesia, duration of PROM, Apgar score) should be obtained. Assessment of gestational age is done (Table 31.1).
A.  Examination of vital signs:
a.  Temperature is recorded and the site (e.g., rectal, oral or axillary) is mentioned.
b. Respiration: Normal,  30-60  breaths/min.  May need screening with pulse oximetry (>95% and :;3% difference between right hand and foot).
c. Pulse: Normal, 100-160 beats per min (bpm) and when asleep, it is around 70-80 bpm.
d. Blood pressure: Normal range 45-60/25-40 mm Hg. BP is directly related to gestational age and birth weight of the infant.
B. General examination:
1. Skin color: It is the single most important parameter of cardiorespiratory function.
a.  Pallor may be due to anemia, birth asphyxia, or shock.



















Fig. 31.1: A healthy term baby weighing 3.3 kg.
[l Chapte, 31 ,The Teem Newbom Infant
Table 31.1: Assessment of gestational age at birth.

Character
Sole creases


<36weeks
1-2 transverse creases on anterior 1 /3rd of sole.


37-3Bweeks
Multiple creases on anterior 2/3rd of sole.


>39weeks
Entire sole covered with creases.

Breast nodule   2mm.	4mm.	7mm.

Scalp hair Ear lobe
Testes and scrotum


Fine, wooly, fuzzy. No cartilage.
Testes partially descended, scrotum small and few rugae.


Fine, wooly, fuzzy.
Moderate amount of cartilage. -


Coarse, silky.
Stiff earlobe, thick cartilage.
Testes fully descended, scrotum normal size, prominent rugae.



b. Cyanosis:
♦   Cental cyanosis (bluish skin, including the tongue and lips) is caused by low oxygen saturation. It may be due to congenital heart or lung disease. Desaturation of hemoglobin should be >3-5 g/dL.
r
♦  Peripheral cyanosis (bluish skin with pink lips and tongue) may be due to drugs (nitrates or nitrites) or hereditary. It is often associated with
methemoglobinemia (hemoglobin oxidizes from ferrous to ferric form).
♦  Acrocyanosis (bluish hands and feet only) may be normal immediately following birth. It may be due to cold stress.
c. Plethora  is  commonly  seen  in  infants  with polycythemia. It may be seen in an overheated or over­ oxygenated infant. Hematocrit value may be done.
d.  Jaundice: Bilirubin level >5 mg/ dL.
e.  Extensive  bruising  may  be due to difficult  or traumatic delivery.
2.  Skin rashes:
a. Milia seen on the nose, cheeks and forehead are due to plugged sweat glands.
b.  Mongolian spots are bluish, often large, commonly seen on the back, buttocks or thighs. Usually present in Blacks and Asians (90%).  They disappear by 4 years of age.
c.  Erythema toxicum: These are papular lesions with an erythematous base. Commonly seen after 48 hours of birth. They resolve spontaneously.
d. Diaper rash usually the skinfolds are involved. It appears as erythematous plaques and the edges are well demarcated. It is a form of irritant contact dermatitis. It may be infected with Candida albicans.
3.  Head: Fontanels:
a.  Large fontanels are associated with hypothyroi­ dism, osteogenesis imperfecta or chromosomal anomalies (Down syndrome). Bulging fontanel may be due to increased intracranial pressure, meningitis or hydrocephalus. Depressed fontanels are seen with dehydration. A small fontanel may be  due  to  hyperthyroidism,  microcephaly  or craniosynostosis.
b.  Caput succedaneum should be differentiated from cephalhematoma.

c. Molding  seen  with  prolonged  labor.  Usually molding subsides within 5 days.
d.  Cephalhematoma   is   due   to   subperiosteal hemorrhage resulting from a traumatic delivery. It never extends beyond the suture line.  X-ray and CT scans should be taken to exclude skull fracture. Hematocrit and bilirubin levels should be estimated. Aspiration of hematoma is rarely needed as they often resolve in 4-6 weeks of time.
e.  Raised intracranial pressure is diagnosed by the following signs: (i) Bulging anterior fontanel; (ii) Separation of suture lines; (iii) Paralysis of upward gaze; (iv) Prominent veins of the scalp.
Craniosynostosis is the premature closure of one or more of sutures of the skull.  On palpation, a bony ridge is felt over the suture line and the cranial bones cannot be moved. X-ray studies of the skull should be done.
4.  Neck: It is checked for movements, goiter, thyroglossal cysts, sternomastoid hematoma (sternomastoid tumor) or short neck, webbed neck (Turner's syndrome).
5.  Face and mouth: Face is looked for hypertelorism (eyes widely separated) or low-set ears (trisomy 9, 18, triploidy) or facial nerve injury. Mouth is checked for clefts (palate, lips), natal teeth, lingual frenulum (tongue tie), macroglossia (Beckwith syndrome) or oral thrush. Thrush is treated with nystatin suspension.
6.  Eyes are examined for congenital cataract, Brushfield's spots in the iris (Down's syndrome) or subconjunctival hemorrhage (traumatic delivery) and conjunctivitis.
7. Chest is examined for any asymmetry (tension pneumothorax), tachypnea, grunting, intercostal retractions (respiratory distress), pectus excavatum and the breath sounds. The newborn's breasts may be enlarged (normal 1 cm in diameter) due to maternal estrogen. The white discharge from nipple is common known as "Witch's milk''.
8.  Heart is examined for rate (normal 120-160 bpm), rhythm, the quality of heart sounds and presence of any murmur. Murmurs may be associated with VSD, PDA, ASD, transposition of great vessels, tetralogy of Fallot, coarctation of aorta and others. Fetal echocardiography at 18-20 weeks of gestation can make the antenatal diagnosis in utero. Fetal cardiac intervention in utero is a new and promising method of treatment.
Chapter 31:TheTerm Newborn Infant     ID

9. Abdomen is examined for any defect, e.g., omphalocele, hepatomegaly (sepsis), splenomegaly (CMV, rubella infection) or any other mass. A scaphoid abdomen may be due to diaphragmatic hernia.
10.  Umbilicus is examined for any discharge, redness or infection. A greenish-yellow colored cord suggests meconium staining (fetal distress). Single umbilical arte,y (more in twin births) indicates genetic (trisomy 18) and congenital anomalies (40%), and FGR.
11. Genitalia should be examined carefully before gender assignment. Male is examined for penis (normal >2 cm), testes within the scrotum, any hydrocele or hypospadias. Prepuce is normally long and phimosis is present. Female is examined for any clitorial enlargement (maternal drug), fused labia with clitorial enlargement (adrenal hyperplasia). Blood-stained vaginal discharge may be due to maternal estrogen withdrawal. Normally labia majora cover the labia minora and clitoris.
12. Anus and rectum are checked to rule out imperforation and their position. Meconium should be passed within 48 hours of birth.
13. Extremities, spine and joints are examined for syndactyly (fusion of digits), polydactyly, Simian crease (Down's syndrome), talipes equinovarus, hip dislocation ( Ortolani and Barlow maneuvers).
14. Nervous system is examined for any irritability, abno­ rmal muscle tone, reflexes, cranial and peripheral nerves (Erb's paralysi). Neurological development is dependent on gestational age. The reflexes including Moro reflex are present at birth.
15.  Hematological findings: Blood volume soon after birth is about 80 mL/kg body weight if immediate cord clamping is carried out. RBC-6-8 million/cu mm, Hb%-18-20 g%, WBC-10,000-17,000/cu mm, platelets-3,50,000/cu mm, nucleated red cells 500/ cu mm, sedimentation rate is elevated. Clotting power may be poor because of deficient vitamin K which is necessary for the production of prothrombin from the liver. Reticulocyte count ranges from 3% to 7%. In a healthy term infant, hemoglobin values reach a nadir of 11 g/dL at 8-12 weeks of birth. This is known as physiological anemia of infancy. In preterm infants, the decline (7-9 g/dL) is more at 4-8 weeks.
REFLEX BEHAVIORS:
(A) Muscle tone: Hypotonia (floppiness) or hypertonia (increased resistance) is examined.
(B) Reflexes:
1.  Rooting reflex: Stroke the corner of the cheek with a finger and the infant will turn in that direction and open her mouth.
2.  Glabellar reflex: To tap gently over the forehead and the eyes will blink.
3.  Grasp reflex (palmar grasp): Place a finger in the open palm of the infant's hand and the infant will grasp the finger.

4.  Moro reflex:  The  infant is supported from  behind the upper back with one hand and then the baby is allowed to drop back  l cm but not on the mattress. The baby will symmetrically abduct, extend the arms and fingers. This is followed by flexion and adduction of the arms. Asymmetry may signify a fractured clavicle, hemiparesis or brachia! plexus injury. An absent Moro reflex may signify CNS pathology.
5.  Sucking and swallowing reflexes: A  normal infant starts sucking when something (nipple and the areola) touches the palate. Baby swallows when the mouth is filled with milk.
(C) Gestational age (Table 31.1)

IMMEDIATE CARE OF THE NEWBORN
♦   Care at birth	♦  Care in nursery CARE AT BIRTH: This has already been described on p. 131.
CARE IN NURSERY:
Admission in nurse1y: All healthy newborns are kept in the delive1y room with their mother to promote immediate breastfeeding and early bonding. Common indications for admission of the newborn in the nursery are: prematurity, respiratory distress, poor perfusion or presence of pallor or
cyanosis, malformation and need for 02 therapy.
Routine  nursery  care:  The  newborn  is  examined systematically and assessment of the gestational age is done.
Infant's weight, Pronto-occipital Circumference (FOC) and length are recorded. On these bases, the newborn is classified as Average for Gestational Age (AGA), Small for Gestational Age (SGA) or Large for Gestational Age (LGA).
The newborn must be kept under a neutral thermal condition. This is defined as the external temperature range where metabolic rate and oxygen consumption are at minimum. The normal skin temperature in the neonate  is  36.0-36.5°C  (96.8-97.7°F).  Normal  core (rectal) temperature is 36.5-37.5°C (97.7-99.5°F). Axillary temperature may be 0.5-l.0°C lower.
Mechanisms  of heat  loss  are:  (i)  Radiation,  (ii) Conduction from the infant to the surface in direct contact, (iii) Convection from the infant to the surrounding area, and (iv) Evaporation of water from the skin.
Consequences of excessive heat loss: (i) Compensatmy heat  production  through  increase  in  metabolic  rate, (ii) Insufficient oxygen supply ➔ Hypoxia ➔ Anaerobic metabolism, (iii) Hypoglycemia, (iv) Metabolic acidosis, (v) Apnea; and (vi) Pulmona1y hypertension.
Consequences  of hypothermia  are:   (a)  DIC,  (b) Pulmonary hemorrhage, (c) Shock, (d) IVH, (e) Increased mortality.
The measures to prevent heat loss are: (i) Place the baby under a preheated (36.5°C) radiant warmer (servo­ control) immediately following delivery,  (ii)  Dry baby
L ··ID Chapter 31:TheTerm Newborn Infant

immediately  after  birth,  (iii)  Cover  baby  (including the head) with a pre-warm towel, (iv) Put baby close to mother's breast (Kangaroo mother care), (v) Wrap the mother and baby together,  and  (vi)  Commence early breastfeeding.
Kangaroo Mother Care (KMC) is the care for preterm and LBW infants. It includes:
a. Kangaroo position: Skin-to-skin contact between the mother and the infant in a vertical position.
b. Kangaroo nutrition: Exclusive breastfeeding.
c.  Kangaroo discharge and follow-up:  Early discharge from neonatal unit.
Benefits: Protects the baby against cold stress and hypothalamia and it increases milk production in mothers for exclusive breastfeeding.

DAILY OBSERVATION AND CARE
Rooming-in: Soon after birth, if mother is fit, baby is kept in a cot by the bedside of mother. This establishes mother-child relationship. Mother also learns the art of baby care.
Baby bath: Routine bath is delayed until the baby is able to maintain the body temperature and has started breastfeeding. The excess vernix,  blood or meconium are wiped off from the skin using sterile moist swabs and then make the skin dry by using a soft towel. The water for baby bath should be at body temperature (>97.5°F} and a separate bathtub should be earmarked for each baby.
Umbilical cord care: It is kept exposed to air and allowed to dry to promote early detachment. Topical antiseptics or antibiotics such as triple dye or neosporin powder may be applied to reduce bacterial colonization.
Routine medications: A single intramuscular dose
of 0.5-1 mg of vitamin K1  (phytonadione) is given to all newborns within 6 hours of birth. This prevents vitamin K
deficient bleeding.
Eyes are  kept clean  with  cotton wool soaked with sterile normal saline as a prophylaxis against ophthalmia neonatorum (Chlamydia,  Gonococcus). Erythromycin ointment (0.5%) bilaterally in the conjunctiva! sac or tetracycline (1%} ointment may be used.
Immunization and vaccines: Hepatitis B vaccine is given at birth. Other vaccine information is given to the parents.
Screening of the newborn: Commonly done screen­ ing  tests  are:  (A)  Glucose  screening  and  detecting hypoglycemia, especially for infants of diabetic mothers, SGA and LGA infants; (B) Bilirubin screening; (C) Other metabolic screen depending on need (e.g., galactosemia).
Assessment of vital signs: Respiratory rate, heart rate, axillaiy temperature are recorded eve1y 6-8 hours in the baby's chart. Each of urine and stool output is recorded. Most  of  the  newborns pass  urine  by  24 hours  and meconium by 48 hours of life. Daily weights are recorded.


Weight loss in excess of 7% is often due to inadequate calorie intake.
Feedings: The frequency, duration and volume of each feed is important for newborn's growth and development. The infant  should be put to breast as soon as possible after delive1y in the delive1y room. Feeding is allowed on demand (demand feeding). Usually, it is 8-12 times per day.
Discharge: Each infant is evaluated carefully to decide the optimal time of discharge. Considering  the huge number of institutional deliveries in a developing country set up, early discharge of mother and infant may be done to avoid overcrowding in the postnatal ward and in the nurse1y.
The  following infants  may  be  discharged  by 48 hours  of  age:  Vaginal  delivery,  gestational  age  >38 weeks, singleton birth, birth weight-AGA, normal vital signs, passed urine and stool, initial immunization done, successful feedings and normal on physical examination.
Follow-up: Follow-up ofnewborns should be organized depending upon the risks of feeding problems, infections, hyperbilirubinemia  or  other  issues.  During  follow-up, the newborn is assessed for weight, hydration, infection and   for   any  new  problem.   Parental  education  and immunization schedule are discussed.
INFANT  GROWTH  ASSESSMENT:  Serial measurement of weight,  length and head circumference  allow for evaluation of infant growth.
WEIGHT: There is weight loss of 7-10% in the first week of life. Weight gain generally begins by the second week. Average daily weight gain is 20-30 g/day. The infant should be weighed daily.
LENGTH: Normal weekly length gain is 0.8-1.0 cm for first 8-12 weeks.
HEAD CIRCUMFERENCE: Intrauterine growth is 0.5-0.8 cm/week.

INFANT FEEDING
The rate of growth of the infants during the first 6 months of life is greater and faster than any other period of life. Its weight is doubled by the age of 5 months and tripled by the end of one year. Keeping this in mind, the baby should be nursed adequately (both quantitatively and qualitatively) which allows easy digestion and absorption.
NUTRITIONAL REQUIREMENTS IN THE NEONATE
■  The infant should get sufficient fluid: Fluid intake should be 150-175 mL/kg body weight per day.
■  The  infant should  get  adequate  calorie:  A  term healthy  infant  needs  100-110  kcal/kg   of  body weight per day. Low birth weight infant needs about 105-130 kcal/kg/day. Each  30 mL  (1 oz)  of breast milk gives  20 calories. Calorie needs are primarily dependent on oxygen consumption.


■   The food should have a balanced composition of protein  (2-4  g/kg/ day),  fat  ( 4-6  g/kg/ day),  carbo­ hydrate (10-15 g/kg/day), minerals and vitamins and it should be easily digestible.
TYPES OF FEEDING:
♦  Breastfeeding	♦  Artificial feeding
I BREASTFEEDING
The two vital considerations for the infants in tropical
countries are breastfeeding and avoidance of infection. Artificial feeding may be required in a ve1y rare situation, but where the mothers have an inadequate knowledge of the technical details of artificial feeding, gastroenteritis and malnutrition of the neonates are inevitable consequences. All the babies, regardless of the type of delive1y, should be given early and exclusive breastfeeding up to 6 months of age. Exclusive  breastfeeding means giving nothing orally other than colostrum and breast milk. Medicines and vitamins are allowed.
Breastfeeding  is  the  "Gold  standard"  for  infant feeding. There are several areas of biological superiority of breastfeeding and breast milk over artificial (formula) milk. Obstetricians and midwives should educate the mother  during  prenatal  and  postnatal  care  for  the usefulness of breastfeeding.
BABY-FRIENDLY  HOSPITAL  INITIATIVE:  Baby-friendly hospital   initiative   with   ten   steps   to   successful breastfeeding (WHO/UNICEF 1992: Protecting, promoting and supporting breastfeeding).

These are: (i) There must be a written breastfeeding policy;  (ii)  All healthcare  staff  must  be  trained  to implement this policy; (iii) All pregnant women must be  informed  about  the  benefits  of  breastfeeding; (iv) Mothers should be helped to initiate breastfeeding within half an hour of birth; (v) Mothers are shown the best way to breastfeed; (vi) Unless medically indicated, the newborn  should  be  given no food or drink other than  breast  milk;  (vii)  To  practice  'rooming-in'  by allowing  mothers and babies to  remain together 24 hours a day; (viii) To encourage demand breastfeeding; (ix) No artificial  teats to babies should be given;  and (x) Breastfeeding support  groups are established and mothers are referred to them on discharge.

A baby-friendly hospital should  also provide other preventive  health  cares,  e.g.,  infant  immunization, rehydration salts against diarrheal dehydration and child's growth and development surveillance.
ADVANTAGES OF BREASTFEEDING
A. Composition: Breast milk is an ideal food with easy digestion and low osmotic load.
♦   Carbohydrate: Mainly lactose, stimulates growth of intestinal flora, produces organic acids needed for synthesis of vitamin B.

Chapter 31:TheTerm Newborn Infant

♦   Fat:  Smaller  fat  globules,  better emulsified  and digested.
♦   Protein: Rich in lactalbumin and lactoglobulin, less in casein.
♦   Minerals: Low osmotic load (K+, Ca2+, Na+, c1-), less burden on the kidney.
B. Protection against infection and deficiency states:
1. Vitamin D promotes bone growth, protects the baby against rickets
2.  Leukocytes, lactoperoxidase prevent growth of infective agents
3. Lysozyme, lactoferrin, interferon protect against infection
4.  Long-chain  omega-3  fatty  acids  essential  for neurological development
5.  Immunoglobulins IgA (secretory), IgM, IgG protect against infection
6.  Supply of nutrients and vitamins.
C. Breast milk is a readily available food to the newborn at body temperature and without any cost.
D. Breastfeeding acts as a natural contraception to the mother. Criteria  for  LAM  inculde:  ■  Continuous amenorrhea;  ■  Exclusive  breastfeeding;  ■  Night nursing.
E. Additional advantages are: (i) It has laxative action; (ii)  No  risk  of  allergy;  (iii)  Psychological  benefit of  mother-child  bonding;  (iv)  Helps  involution  of the  uterus;  and  (v)  Lessens  the  incidence  of  sore buttocks, gastrointestinal infection and atopic eczema. The  incidence  of  scurvy  and  rickets  is  significantly reduced.
Long-term risks of exclusive artificial (bottle) feeding: (a) Type I diabetes;  (b) Sudden infant death;  (c) Adult type 2 diabetes; (d) Childhood obesity; (e) Adult obesity; (f)  Crohn's disease;  (g)  Ulcerative colitis;  (h) Atopic dermatitis; and (i) Reduced Intelligence Quotient (IQ).

PREPARATIONS FOR BREASTFEEDING: • Counseling for the need of early feeding ( <l hour of birth),  • Frequent feeds  (>10/day),  •  No  supplemental  feeding,  unless medically indicated. •  To  educate  appropriate  way  to get the baby good latch on to the breast with comfortable position.  •  Massaging  the  breasts,  expression  of  the colostrum  and  maintenance  of  cleanliness  should  be carried out during the last four weeks of pregnancy.

MANAGEMENT  OF  BREASTFEEDING:  The   modern practice is to reduce nipple cleansing to a minimum and to wash the breasts once daily. A clean, soft, supporting brassiere should be worn. The mother should wash her hands prior to feeding. Mother and the baby should be in a  comfortable  position  during  feeding  (Fig.  31.3). Frequent feedings, 8-12 feeds/24 hours are encouraged.
First feed: In the absence of anatomical or medical complications,  a  healthy  baby  is  put  to  the  breast
L.. Chapte,31,TheTe,m Newborn lofaot
t	· .
.
I
!


I  I









Figs. 31.2A and B: Technique of breastfeeding: (A) Poor attachment; (Bl Good attachment.


immediately or at most <l hour following normal delivery. Following cesarean delive1y, a period of 4-6 hours may be sufficient for the mother to feed her baby.
Milk transfer: Milk transfer to infant is a physiological process. It starts with good latch on. The nipple is tilted slightly downward using a "C-hold". The milk is extracted by the infant not by negative pressure but by a peristaltic action from the tip of the tongue to the base. The latent period  between  latch  on  to  milk  ejection  is  about  2 minutes. Nearly 90% of the milk is obtained in the first 5 minutes. The calorie-rich hind milk is obtained at the end part of suckling.
Frequency of feeding:
♦  Time schedule: During the first 24 hours, the mother should  feed  the  baby  at  an  interval of 2-3  hours. Gradually, the regularity becomes established at 3-4 hours pattern by the end of first week. Baby should be fed more on demand.
♦  Demand feeding: The baby is put to the breast as soon as the baby becomes hungry. There is no restriction of the number of feeds and duration of suckling time.
Duration of feed: The initial feeding should last for 5-10 minutes at each breast. This helps to condition the letdown reflex. Thereafter, the time spent is gradually increased. Baby is fed from one breast completely so that baby gets both the foremilk and the hind milk. Then the baby is put to the other breast if required. Hind milk is richer in fat and supplies more calories and satiety to the infant. The next feed should start with the other breast.
Night feed: In the initial period, a night feed is required to avoid long interval between feeds of over 5 hours. It not only eliminates excessive filling and hardening of the breasts but also quietest and ensures sound sleep for the baby. However, as the days progress, the baby becomes satisfied with the rhythmic 3-4 hourly feeding.
Amount of food: The average requirement of milk is about 60 mL/kg/24 hours on the first day, 100 mL/kg/24 hours on the third day and is increased to 150 mL/kg/24 hours on the  10th day. However, the baby can take as much as required.
Technique: The mother and the baby should be in a comfortable position. Feeding in the sitting position, the


mother holds the baby in an inclined upright position on her lap; the baby's head on her forearm on the same side close to her breasts, the neck is slightly extended. Good attachment means the infant's mouth is wide open and chin touches the breast (Figs. 31.2A and B). The mother should guide the nipple and areola into the baby's mouth for effective milk transfer. The milk transfer to the infant begins with good latch on and by a peristaltic action of the tip of the tongue to the base. The proper position for milk transfer is chest-to-chest contact of the infant and mother. The infant's ear, shoulder and hip are in one line (Fig. 31.3). Baby sucks the areola (lactiferous sinuses)  and  the  nipple  holding  between  the  tongue and  the palate.  Feeding in lateral position following cesarean delivery or with painful perineum is carried out by placing the baby along her side between the trunk and the arm.
When  latching  on,   the  neonate  should  take  as much of the areola as possible into its mouth. "C-hold" (Fig. 31.3) showed four fingers are placed below for cupping and supporting the weight of the breast. The thumb is placed above and 1-2 cm away from the areolar edge. This position points the nipple downward. Thumb should  not  retract  the  areola  away  from  the  mouth.
















I
Fig. 31.3: Technique of breastfeeding-proper way of holding the baby. C-hold with good latch-on.
Chapter 31:TheTerm Newborn Infant    -    -


Normally, breast is washed with clean water and allowed to air dry.
Breaking the wind (Burping): All  babies  swallow varied amount of air during sucking. To break up the wind, the baby should be held upright against the chest and the back is gently patted till the baby belches out the air. It is better to break up the wind in the middle of sucking so as to make the stomach empty,  enabling the baby to take more food and at the end of sucking to prevent hiccough and abdominal colic.
FACTORS FOR  SUCCESSFUL LACTATION:  {i)  Positioning (Fig.  31.3),  {ii)  Attachment  to  breast  (Fig.  31.2),  {iii) Nursing technique (to avoid breast pain,  nipple trauma, incomplete  emptying),  and  (iv)  A  rotation  of  positions is helpful  to  reduce focal  pressure on the nipple  and to ensure complete emptying. To break the suction, a finger is inserted between the baby's lips and the breast.  Other­ wise it can injure nipple by forceful disengagement.
DIFFICULTIES  IN  BREASTFEEDING  AND  THE  MANAGEMENT: At  times,  breastfeeding  poses  some  problems  and  if  it  is not promptly detected and rectified,  it may lead  to  adverse consequences.
The causes may be classified as those: •   Due to mother    ♦   Due to infant
Due to mother:
- Reluctance or dislike to breastfeeding-careful listening to mother and intelligent counseling can solve the problem.
- Infant's attachment to breast (Fig. 31.2)-when poor,  it leads to quick shallow sucks instead of slow and deep. Areola remains outside  the  lips.  This  causes nipple pain.  Skilled support from healthcare provider can improve the technique of breastfeeding. Prelacteal feeds (e.g., honey, milk) inhibit lactation process and should be avoided.
- Anxiety and stress,  previous  history of failed lactation or elderly primipara-the mother fails to relax during feeding and  as  such,  the  baby refuses  to  suck.  Reassurance  and practical support is helpful.
- Following operative delivery such as cesarean section  or following prolonged and exhaustive labor often there is a delay. So mother should be helped to feed the baby in a comfortable position as early as possible.
- Milk   secretion   is   inadequate-unrestricted   feeding, well-positioned  infant,  practical  and  emotional  support to   mother-all   are   important.   Dopamine   antagonist (metoclopramide) may be useful.

Table 31.2: Contraindications to breastfeeding.
Temporary

- Breast ailments such  as  engorgement  of  breast,  cracked nipple, depressed nipple and mastitis need treatment. Previous breast surge1y and circumareolar incision have unsuccessful breastfeeding. Loss of breast sensation may be the cause.
Due to infant:
- Low birth weight baby: The baby is too small or feeble to suck.
- Temporary illness such as respirato1y tract infection, nasal obstruction due to congestion, lethargy due to jaundice and oral thrush. All these conditions lead to imperfect suckling and are managed appropriately.
- Overdistension of the stomach with swallowed air: The problem can be overcome by breaking the wind of the baby several times during feeding.
- Congenital malformation such as cleft palate needs surgical correction.

CONTRAINDICATIONS OF BREASTFEEDING (Table 31.2): Contraindications are very few (Table 31.2). In cases of temporary contraindications, the baby should be put to the breasts as soon as the condition permits. HIV -positive mothers are counseled as regard the risks and benefits. She is helped to make an informed choice.

DRUGS  AND  BREASTFEEDING:  Most  drugs  taken  by the  mother  appear  in  the  breast  milk.  Fortunately, drug  level  in  the  breastfed  infant  ranges  from  0.001 to  5%  of  the  therapeutic  doses.  The  infant  tolerates the  drug  without  any  toxicity.  Very  few  drugs  are absolutely contraindicated. These are: anticancer drugs, chloramphenicol,  radioactive materials, phenylbutazone and atropine. Some drugs are used with caution:
■   Nitrofurantoin: Not given to babies less than 8 days due to hemolysis.
■   Codeine: Maternal side effects, like cyanosis,  brady increases prolactin. Cause drowsiness in babies.
■  Metronidazole: Metronidazole alters breast milk taste. Increased oral or rectal colonization with candida.
■   Fluoxetine: Colicky pain and drowsiness.
■   Levetiracetam: Levels needs to be monitored.

MATERNAL NUTRITION  DURING  LACTATION: A  healthy mother while breastfeeding will produce about 500-900 mL breast milk  per  day.  This  will  give her  baby  about 75 kcal/dL. This requires additional 750 kcal/day for the mother. This amount is either to be supplemented

'  '

Permanent



Maternal




Neonatal


1. Acute puerperal illness.
2. Acute breast complications such as cracked nipples, mastitis or breast abscess.
3. Herpes simplex lesion of the breast.
4. Breast reduction/augmentation surgery.
1. Very low birth weight baby (expressed milk). 2. Asphyxia and intracranial stress.
3. Acute illness.


1. Chronic medical illness such as decompensated organic heart lesion, active untreated pulmonary tuberculosis.
2. Puerperal psychosis.
3. Mother having high doses of antiepileptic, antithyroid, antipsychotic or anticancer drugs.
1. Severe degree of cleft palate. 2. Galactosemia.
II Chapter 31: The Term Newborn Infant

through her diet or is made up from her body stores. A store of 5 kg of fat throughout pregnancy is adequate to make up the nutritional deficit.
The daily allowances of nutrients recommended for a lactating woman is given in Table 10. l. There is additional need (increased by 50%) of folic acid, iron, calcium and protein during pregnancy. Mother should drink at least 1 extra liter of fluid per day to make up the fluid loss through  milk. Bone  mineral  density  decreases  in  the breastfed women and it returns to normal after 12 months of stoppage of breastfeeding.

ASSESSMENT OF WELLBEING OF THE INFANT:
1. General condition-the baby is happy, sleeps between feeds and at night, does not vomit and passes urine at least six times in 24 hours;
2. Good vigor which is manifested by movements of the limbs and cry;
3. Infant has stopped losing weight;
4. Has yellow seedy stools and no more meconium stools; and
5.  Expected level of weight curve.

UNDERFEEDING:  It is commonly seen in artificially fed babies.  The  features  are:  (1)  Failure  of  the  infant  to gain weight as per schedule, evidenced from the weight curve; (2) The infant appears dissatisfied with the feeds evidenced by cry in between feeds, and at night, disturbing the sleep; (3) The baby has constipation; (4) The urina1y output  (normally  >6  times)  becomes  scanty  and  high colored; and (5) Test feeding is the only reliable method of diagnosis (vide infra).
Management:  The  deficient  amount  of  milk should be substituted by artificial milk. The required deficit of 24 hours as calculated from test feeding is to be divided by the number of feeds to be given in 24 hours. The amount of deficit for each feed, so calculated, should be given after each feed. As soon as sufficient milk comes to the breast, the supplementary feed is withdrawn.

CARE OF THE BREASTS: Daily washing of the breasts with clean water is essential. The nipple should be cleaned with clean water before and after each feed. Brassieres are to be worn for support and comfort.

FEEDING DIFFICULTIES DUE TO NIPPLE ABNORMALITIES Breast  engorgement  usually  occurs   on   day  3-5 postpartum. There is copious milk production. Breasts are swollen and hard. There is dificulty to latch on for the infant. Treatment options are: (i) Gentle hand expression of milk to make the breasts soft so that the infant can latch on;  (ii) Application of moist  heat  and  cold compress to  relieve  edema;  (iii)  Gentle  breast  massage  during feeding or milk expression; and (iv) Pain relief to reduce inflammation (ibuprofen).

Long nipples may cause poor feeding due to improper latch on to the nipple without the areola. Mother has to help the baby to draw the areola also.
Short nipples usually cause no problem. Mother is reassured.
Inverted and flat nipples attachment to the breasts is possible and babies are able to feed adequately. In difficult cases, lactation is initiated by expression. Baby is then attached to breast as breast tissue becomes soft and protractile gradually. It can be corrected by suction with a syringe or breast pump.
Expression of breast milk or artificial removal of breast milk is not generally needed where breastfeeding is normal. The indications of expressing breast milk are: (i) Where
the baby is separated from the mother due to prematurity or illness; (ii) Where there are dificulties in breastfeeding as in attaching the baby to the breast, e.g., cleft palate; (iii) When the mother is separated from the baby because of work; and (iv) Colostrum should always be expressed and given to the babies if they cannot suck properly.
Methods of milk expression: (a) Breast milk expression is needed when mother and her baby are separated for a longer period (6-8 hours). The breast is massaged in a spiral fashion starting at the top and moving towards the  areola. It is done in a comfortable  environment. Mechanical, or electric breast pump is of help when breast feeding appears to be difficult or impossible. Breast pump may be helpful for flat or inverted nipples. It increases the level of prolactin that helps to maintain lactation for longer period. It can be practiced anywhere and costs nothing, (b) Breast pumps may be electrical or manual.
Donor breast milk: Historically, it has been used for centuries. Currently, its use is limited. Transmission of infection (HIV, CMV, hepatitis B, TB) is the concern for its safety. If the donor breast milk or milk banks are used, donor screening, pasteurization of milk and parental counseling are recommended.
Breast milk can be stored frozen at - 20°C for up to 6
months,  refrigerated at <4°C for 96 hours and at room temperature ( <25°C) for 4 hours. Fresh, unrefrigerated milk can be used within 4 hours of expression. Frozen milk should be thawed in a waterless warmer or in a container of tepid (not hot) water. Microwave thawing should not be done.
METHODS OF INITIATION OF LACTATION: The following methods  may  be  employed  with  varying  success  to establish lactation after it has been temporarily withheld.
For  the  baby:  (I)  To  discontinue  bottle  feedings; (2) To put the baby to the breast at frequent intervals; (3) Baby should suck in a well-attached manner.
For the mothers: (I) To encourage plenty of fluid (1 L extra) and milk intake; (2) Drugs like metoclopramide or oxytocin (nasal spray) are of help.
Chapter 31: The Term Newborn Infant     ID· Table 31.3: Composition of human and cow milk.


Human
Cow milk

Lactose (g/100 mL) 7
4.5


Fat (g/100 mL) 3.5
3.5


Protein (g/100 mL) 1.2
3.4


Sodium (mmo//L)	Water 7                                  89
22	88


Calories (kcal/100 mL) 75
67



I FORMULA MILK
When the infant is fed by any preparation other than human milk, it is called formula feeding. As artificial feeding is commonly accomplished by using a bottle, it is often called as bottle feeding. But an artificial feeding can be given without a bottle.
Indications
- Contraindications to breastfeeding either temporary or permanent (mentioned earlier).
- Changing  lifestyle of  women or pressurised under changed socioeconomic conditions (expressed breast milk may be an alternative).
FOOD   USED:   There  is  no  perfect  substitute  for  breast milk. Most formula milk products use cow milk or soyabean constituents  as  a  substrate.   Minerals,   vitamins,   proteins, carbohydrates and  fats are added to pasteurized bovine milk for the nutritional needs. Palm or coconut based oils are added to  make  artificial  formula  milk  appear  creamy.  Compared  to human milk, formula milk has major differences in the validity of proteins, carbohydrates,  minerals, vitamins and fats.  Breast milk promotes optimal somatic growth, cognitive development and metabolic need.
Composition: The principal compositions of the breast milk and the cow milk are given in Table 31.3.
Qualitative differences between human and cow milk: The sugar in both is lactose. Breast milk is sweeter due to its high lactose  concentration.  The fat globules in cow milk are coarser and hence difficult to digest. The caseinogen (protein) in cow milk causes indigestion. Sodium content in cow milk is about four times higher.
Humanization of cow milk: It is indeed impossible to change the composition of the cow milk to that of human milk, no matter how the amounts of protein, fat, carbohydrate and minerals are altered. As such, so called humanization of the cow milk is an inappropriate usage.
•   Quantitative  changes in  the  constituents  can  be done by dilution  followed  by addition.  One  part of milk is added to one part of water. To bring about readjustment, about 4% of sugar and 2% of fat are to be added to the diluted cow milk. The sugar can be added as cane sugar or glucose in the proportion of a quarter of teaspoonful to each ounce of milk. The fat is added as cream (30-60%). However, in the tropical countries, addition of cream may be omitted.
•   The qualitative alteration is principally directed to change in the caseinogen to make it easily digestible by boiling.


Sterilization: Sterilization of the milk should be done by boiling followed by rapid cooling or pasteurized by heating to 160°F (73°C) for 20 minutes followed by rapid cooling.
Container: Babies may be fed either by spoon from the bowl (katori) or by feeding bottle. It is easy to clean the former. The feeding bottle and the teat should be cleaned prior to and after each feeding. The rubber teat and the bottle should be boiled after each feeding. Spoon feeding is always preferred to bottle  feeding to avoid nipple confusion.
PRINCIPLES TO FOLLOW IN BOTTLE FEEDING
♦    The baby is to be held in comfortable position during feeding.
•   The hole of the teat should be of such size that 20-30 drops of milk are suckled by the baby per minute.
♦    Burping of the baby should be done in the middle and at the end of each feed.
♦    Not more than 20 minutes should be spent for each feed.
•   All utensils, including the bottle and teat are to be cleaned before and after each feed and to be sterilized by boiling.
SUCCESSFUL FEEDING: The  most satisfactory guide to successful feeding is the regular weight gain of the baby after 10 days which should be at the rate of 25-30 grams per  day up to  3 months.  If the baby  fails  to attain the weight gain evidenced by  weekly  weighing  or appears unsatisfied, the feeding is to be increased until the baby gains weight. Figure 31.4 shows the normal weight chart.

12 11
10	,-
/
9
8	Overweight - lJonlilal  "'    7                            ,,v	_--
-
 
,--
--
v
Ol
.S
:c   6
/
    5	I/V
/
/
3     ,.	Underwei@ht
2
1
0 0   1     2    3    4     5    6     7     8     9   10   11 12 Months
Fig. 31.4: Normal weight chart.
ID Chapter 31:TheTerm Newborn Infant

WEANING: It is the process during which the baby gets accustomed to food other than its mother's milk. This period extends from 6th month to  1  year. The infant requires-110-125 calories/kg body weight per day and its fluid requirement is about 150-175 mL/kg body weight per day. During the period of 3-4 months, the baby may weigh  as  much  as  5-5.5  kg  and  as  such,  its  demand is  more.  The  breast  milk  cannot  supply  the  necessary baby's need and as such  additional foods are required by  6 months of age.  Semisolid  foods  such  as rice,  dal, boiled fish, egg are gradually incorporated in the tropical countries. These also prevent the baby from becoming anemic.   Breastfeeding   supports  the   development  of neurological and immunological system up to 4-6 years of  age.  The  dangers  of  the  weaning  period  are:  (a) Nutritional  disturbances,  (b)  Weaning  diarrhea  due  to altered  composition  of  the  food  or  contaminated  with
[· :   ' , ,. , ,.	'. . . ....  ..	c<,o •	.	.., ...	··•,: At birth               :   BCG, OPV, Hepatitis B· 1 (BD).
"•Ja 11i.t.1•
.
.
..  ...
_
•
•
•
6 weeks	:   DTwP/DTaP-1, IPV-1, Hib-1, Hep B-2, Rotavirus-1, PCV-1.
•
10 weeks	:   DTwP/DTaP-2, IPV-2, Hib-2, Hep B-3, Rotavirus-2, PCV-2.
•
14 weeks	:   DTwP/DTaP-3, IPV-3, Hib-3, Hep B-4, Rotavirus-3, PCV-3.
•  6 months                Influenza (IIV)-1. 7 months            :   Influenza (IIV)-2.
•
•
•
•
6-9 months	:   Typhoid conjugate vaccine. 9 months	:   MMR-1
12 months	:    Hepatitis A

pathogens, and ( c) Psychological trauma to the baby when weaning is abrupt.

CHILDHOOD IMMUNIZATION PROGRAM (BOX 31.1)

Vaccines for high-risk children (under special circum­ stances)
1. Influenza vaccine
2. Meningococcal vaccine
3.  Japanese encephalitis vaccine 4.  Cholera vaccine
5.  Rabies vaccine
6. Yellow fever vaccine
7. Pneumococcal Polysaccharide Vaccine (PPSV 23)


•  BCG	 Bacillus Calmette-	•  DTwP:   Diphtheria, Tetanus, Guerin .                                                Whole cell Pertussis.
•  Hep B:   Hepatitis B	•  IPV	Injectable Polio •  DTaP	Diphtheria, Tetanus,                         Vaccine.
Acellular Pertussis.	•  B,	Booster 1
•  Hib	Haemophilus	•  B2	Booster 2
influenzae type B.	•  Td	Tetanus, low dose •  MMR	Measles, Mumps,                                Diphtheria.
Rubella.	•  PCV	Pneumococcal
•  TdaP	Tetanus, low dose	Conjugate Vaccine.
Diphtheria, low dose    •  RV	Rotavirus Vaccine.
Acellular Pertussis.
•  OPV	 Oral Poliovirus Vaccine.


Comments: BCG: before discharge; OPV: as soon as possible after birth; Hep B should be administered within 24 hours of birth; DTwP or DTaP may be administered in primary immunization; IPV: 6-10-14 weeks is the recommended schedule. If IPV, as part of a hexavalent combination vaccine, is unaffordable, the infant should be sent to a government facility for primary immunization as per UIP schedule; RV1: 2-dose schedule, all other rotavirus brands: 3-dose schedule. An additional 4th dose of Hep B vaccine is safe and is permitted as a component of a combination vaccine. Uniform dose of 0.5 ml for DCGI approved brands. To be repeated every year, in pre-monsoon period, till 5 year of age. As of available date, there is no recommendation for a booster dose. Single dose for live attenuated vaccine.

'£i1-mm
►  Assessment of gestational age of a newborn at birth is done by careful clinical examination of: ear lobe, breast nodule, sole creases, scalp hair, and genitalia.
►   Baby-friendly hospital initiative with ten steps is aimed to successful breastfeeding.
►  Breastfeeding is the 'Gold standard' for infant feeding. Advantages to the newborn (better growth and neurodevelopment, less allergy, protection against infection) are many.
►  Advantages of breastfeeding to the mother are: faster postpartum involution, less insulin resistance, less diabetes mellitus, less breast cancer, better infant-mother bonding and less cost.
►  Contact with the breast within half to one hour of birth increases duration of breastfeeding.
►  Correct position of nursing the infant and correct latch on are essential for efficient milk transfer. It also reduces breast pain and nipple injury.
►   Childhood immunization is done according to IAP recommendations.
►   Exclusive breastfeeding provides contraceptive protection in 98% of women up to 6 months after delivery.


Low Birth Weight Baby








.   CHAPTER OUTLINE
❖ Preterm Baby
►  Complications of a Preterm Neonate


►  Management
►  Care of a Preterm Neonate


❖ Fetal Growth Restriction (FGR) ►  Management




Failure of a fetus to reach the optimum growth potential makes pregnancy a high risk one. Survival outcome of an infant depends both on the gestational age and birth weight. Fetal Growth Restriction (FGR) is the second leading cause of perinatal mortality next to prematurity. Overall perinatal mortality rates of FGR is as high as 120 per 1000 for all cases of FGR. Optimal fetal growth and development depends on: (A) Transfer of nutrients like glucose, amino acids and free fatty acids and (B) Oxygen delivery by the placental circulation for utilization of the nutrients.
Normal fetal growth involves sequential phases of cellular hyperplasia, hyperplasia and hypertrophy and finally cell hypertrophy.
Fetal growth  dynamics  when  lead to  reduced cell number, cell size or the both, IUGR is the outcome.
Growth has been classified by absolute birth weight {Fig. 32. I).
■   Low Birth Weight {LBW): •  Very Low Birth Weight {VLBW);	• Extremely Low Birth {ELBW).

WEIGHT PERCENTILES
4600 "'•"",----,,-,----,,---,---,,-,-., Large for 4400 ·	: gestational 4200 ·.                                                                                                              age

3800
· 1
3600+r--t-t-++---t-t-++-+-t-+-z	Appropriate
for
3400
:t--t-t
-
++-+
-
t-t
-
++   +
-
1ff:-
-
3200t-t--!-t-+-+-+-!-t-+-t-+,,-f-	gestational
3000t----t-++-+-!-t-+--t.	age






t"-t-+-1-t-+-+-+--t-+-+-;1 Small for +--+-+-1-+-!--+-+-1-+-!-+--l-l  gestational
Term	age

0 313	6 37 383940 41 42 43
Gestational age (week)
Fig. 32.1: Graph showing-correlation of birth weight and gestational age in percentile.

■   Macrosomia
Currently birth weight has been classified in terms of small for gestational age (Table 32.1).
• Very Small for Gestational Age (VSGA).
• Small for Gestational Age (SGA). • Average Gestational Age (AGA). • Large for Gestational Age (LGA).
■   Preterm: Preterm Birth (PTB) is defined as the one when birth occurs before completion of 37 menstrual weeks of gestation regardless of birth weight. The growth potential may be normal and appropriate for the gestational period (10th to 90th percentile).
■  Small for Gestational Age {SGA): About 70% of infants with a birth weight below the 10th percentile are found normally grown. They are constitutionally small and not at any increased risk for adverse outcome. They present at the end of the normal spectrum for growth. The remaining 30% are truly growth restricted. These neonates are at increased risk for perinatal morbidity and mortality. The percentile cut-off values to define IUGR is a matter of debate.
The identification of these two distinct clinical entities is  important  from both  prognostic and management points of view.

INCIDENCE:  The  incidence  of  low  birth  weight  is generally highest in those countries where the mean birth weight is low and  as such  varies from about

Table 32.1: Fetal growth classifications.
Fetal growth classification based on birth weight
ELBW	VLBW	LBW	Macrosomia <1000g	<1500 g	<2500 g	>4000g Fetal growth according to birth weight percentile
VSGA	SGA	AGA	LGA
<3rd	<10th	Between 10th	>90th percentile	percentile	and 90th	percentile
percentile
r-·= I
£	i-	Chapter 32: Low Birth Weight Baby
5-40% of live births. In India,  about one third of the infants weigh less than 2500 g. The factors influencing the low birth weight of the baby, apart from the preterm birth period, are socioeconomic status and intrauterine environment.  Ethnic  background and genetic control are also important. Thus, it is logical to correlate birth weight  and  gestational  age  with  risks  of  neonatal morbidity and mortality of the individual countries or population groups.


PRETERM BABY
(Syn: Prematurity, Premature Baby)

DEFINITION: A baby born before 37 completed weeks of  gestation  calculating  from  the  first  day  of last menstrual period  is  arbitrarily defined  as preterm baby. Babies born before 37 completed weeks usually weigh 2,500 g or less. However, in less than 5%, the babies may weigh more than 2,500 g even when born before 37 completed weeks.  Preterm baby's weight corresponds to average weight (above 10th percentile) for its gestational age.
INCIDENCE: Preterm baby constitutes two-thirds of low birth weight babies. The incidence of low birth weight baby is about 30-40% in the low resource countries, as such the incidence of preterm baby is about 20-25%. In the high resource settings the incidence of preterm baby is less than 10%.














Fig. 32.2: Neonatal intensive care unit management of a preterm newborn weighing 1.1 kg.
Courtesy: Neonatal Care Unit-NRS Medical College and Hospital, Kolkata.


Plasma	Biological	Placental    Mater-



ETIOLOGY: Discussed in preterm labor (Ch. 22).

Antenatal
corticosteroids


half-life
(minutes)


half-life
(hours)


transfer (%)


nal: fetal
ratio



MANIFESTATIONS OF PREMATURITY: The clinical mani­ festations differ with the degree of prematurity.
Anatomical: The weight is 2,500 g or less and the length is usually less than 44 cm. The head and abdomen are relatively large; the skull bones are soft with wide sutures and posterior fontanel. The head circumference disproportionately exceeds that of the chest (Normally, the head circumference is greater than the chest circumference at birth and the difference is about 1.5 cm). Pinnae of ears are soft and flat. The eyes are kept closed {Fig. 32.2).
The skin is thin, red and shiny, due to lack of subcutaneous fat and covered by plentiful lanugo and vernix caseosa. Muscle tone is poor. Plantar deep creases are not visible before 34 weeks. The testicles are undescended; the labia minora are exposed because the labia majora are not in contact. There is a tendency of herniation. The nails are not grown right up to the finger tips (Table 31.1, p. 420).

I COMPLICATIONS OF A PRETERM NEONATE
More preterm the infant is, higher the risk of disabili­ ties. Risk stratification of preterm infants according to gestational  age are:  <30  weeks-severe risk:  between 30-32 weeks moderate risks and 33-34 weeks mild risks. Administration of antenatal corticosteroids ( <34 weeks) magnesium  sulfate  ( <32  weeks)  showed  improved outcome.


Dexamethasone    200-300	 Long-acting   50	2:1 (36-54)
Betamethasone	300+	 Long-acting   33	3:1 (36-54)

Preterm infants are at risk of many complications due  to immaturity of  various  organs  and  also  for the  cause  of  preterm  birth.  Late  preterm  infants {born between 34 and 37 weeks) though they appear equivalent to term infants, they have some short-term difficulties.
■   Asphyxia: The babies are often asphyxiated because of anatomical and functional immaturity. Even minor degree of anoxia may produce subserosal hemorrhages, especially in the heart, lungs and liver. In addition, it may produce intense congestion of the choroid plexus leading to Intraventricular Hemorrhage (IVH).
■   Hypothermia: A low birth weight baby has reduced subcutaneous  as  well  as  brown  fat  and  increased surface area. Very often the newborn fails to maintain the thermoneutral range of temperature.
■   Pulmonary  syndrome  (23%):  This  includes:  (a) Pulmonary edema;  {b) Intra-alveolar hemorrhage; (c) Idiopathic Respiratory Distress Syndrome (RDS); {d) Bronchopulmonary dysplasia. The first two are
Chapter 32: Low Birth Weight Baby

the effects of hypoxia; RDS is one of the major causes	■   Apnea and Sudden Infant Death Syndrome (SIDS) is of death in  preterm  babies  born  before 34  weeks.          due to immaturity of the autonomic nervous system. The deficient lung surfactant is the principal factor           The risks of bradycardia, apnea and SIDS are increased.
responsible  for  pulmonary  atelectasis  leading  to	■   Retinopathy of prematurity is a multifactorial disorder hypoxia and acidosis. Surfactant therapy is effective in          of the retina caused by abnormal neovascularization. reducing RDS.                                                                                        It is an important cause of blindness for the children
■   Development of the respiratory tract begins on day 22	under  6  years.  The  cause  is mostly  related to  the and continues to form the trachea, lungs, bronchi, and	liberal administration of high concentration of oxygen alveoli. It has five stages: Emb,yonic, Pseudoglandular,	above 40% for a prolonged period (1-2 days) following Canalicular, Saccular, and Alveolar stage: • Embryonic	birth. Persistent hypoxia is an important cause. The stage: 3-6 weeks;• Pseudoglandular stage: 5-17 weeks;	blindness is  due to  the  formation  of an  opaque •  Canalicular stage:  16-25  weeks; •  Saccular stage:  24	membrane behind the lens.
weeks to birth;• Alveolar stage: 36 weeks onwards.	■   Length of hospital stay: Increased length of hospital 11     Cerebral  hemorrhage:  The  causes  are:  Soft  skull          stay, especially for the neonates who are early preterm
bones allow dangerous degree of moulding leading to	( <32 weeks).
subarachnoid hemorrhage. The severity of hemorrhage
PROGNOSIS:
The chance of survival is directly related
is   assessed   by   neuroimaging   studies,   Cranial     to the birth weight. A baby weighing more than 1500 g limited to germinal matrix; Grade-2: Intraventricular     is most likely (95%) to survive. With intensive neonatal hemorrhage; Grade-3: Hemorrhage with ventricular     is to the extent of 80%. With gestational age <23 weeks, mortality is >97%. The deaths are due to complications
Ultrasound (CUS) or MRI. Grade-I: Hemorrhage is
care, the survival rate of the baby weighing 751-1000 g
dilatation and Grade-4: Parenchymal damage. The
lesions with degeneration  and  cystic  changes  are
known as Periventricular Leukomalacia (PVL). This	as mentioned (Table 32.2). Most of the deaths {two­ correlates with cerebral palsy.
thirds) occur within 48 hours.
11     Hypoglycemia (blood glucose <40 mg/dL) is observed	LONG-TERM  PROGNOSIS: Major handicaps (cerebral
in about 15% of infants due to lack of glycogen stores     palsy),  hearing  loss,  chronic  lung  disease  and  poor in the liver. Cold stress, hyperinsulinemia and poor     growth are observed. Infants <2500 g are more likely to
feeding, are the other causes.	suffer Attention Deficit Hyperactivity Disorder (ADHD)
{Table 32.2).
1.   J/ea,:t.Jailu,:e-lt-may-be-precipitated-by-asphy.xia-wit,--------	--------------- 
rapid development of pulmonary edema,  which,  in
turn, impairs pulmonary aeration. There may be patent       Table 32.2: Complications of low birth weight infants. ductus arteriosus.                                                                              System               Early                                  Longterm

11     Oliguria, anuria: As the immature kidneys are unable to handle water, solute and acid loads. Normal urine output on D-2 is 1-2 mL/kg/h. After that it increases to 3.0-5.0 mL/kg/hr.
■   Infection: As the transfer of protective immunoglob­ ulins from the mother to a preterm baby is less, the incidence of infection is increased by 3-10 folds.
■  Jaundice:  Because   of  hepatic  immaturity,   the bilirubin  produced  by  the  excessive  hemolysis cannot be conjugated adequately. This leads to rise in unconjugated bilirubin which is responsible for exaggerated physiological jaundice.
■   Patent Ductus Arteriosus (PDA): Persistent PDA is inversely related to gestational age. Incidence of PDA is about 70% in infants with  birth weight <1000 g. Overhydration should be avoided.
11    Dehydration and acidemia due to immature renal function may occur abruptly.
■   Anemia:  Lack  of  stored  iron,  hypofunction  of  the bone marrow and excessive hemolysis all contribute to anemia. Blood transfusion is often needed in LBW
infants.

■   Cardiac



• Pulmonary


•  Renal



• Endocrino-logical

■   CNS




■   Eye


+  Cardiogenic shock. +  Hypotension.
+  PDA
+  Pulmonary hypertension.
+  RDS +  HMD
+  Pulmonary hemorrhage.
+  Acute tubular necrosis.
+  Electrolyte imbalance.
+  Oliguria
+ Adrenal hemorrhage. + Cortisol deficiency.
+ Hypoglycemia.
IVH, Germinal Matrix Hemorrhage (GMH), PVL.


Retinopathy of prematurity.


+  Pulmonary hypertension.
+  Hypertension in adult life.

+  Chronic lung disease. ♦  BPD


+  Hypertension in adult life.



+  Increased insulin resistance.
+  Diabetes.
+  CP
+  Epilepsy.
+  Neurodevelopmental delay.
+  ADHD.
+  Blindness +  Myopia
+  Strabismus
=ID Chapter 32: Low Birth Weight Baby
Very Preterm  (VPT)  babies  (born  before 32 weeks of gestational age) have special medical needs. These neonates run the higher risks of morbidities and mortality. Many of these neonates are saved with advanced neonatal care. An increased risk for long-term complications are: neurodevelopmental impairment, cerebral palsy, learning disabilities, visual and hearing impairments and attention deficit  disorders.  Furthermore  these  infants  revealed reduced cognition and motor performances.
I MANAGEMENT
♦   Prevention of prematurity.
♦   Management of preterm labor. ♦    Care of preterm neonate.
The prevention of prematurity and the management of preterm labor have been discussed (p. 302).

L _! RE OF A PRETERM   ---------	--IMMEDIATE MANAGEMENT FOLLOWING BIRTH
NEONATE
--
♦    Delayed Cord Clamping (DCC) by at least 60 seconds.
♦    The cord length is kept long (about 8-10 cm) in case exchange transfusion is required.
♦   The air passage should be cleared of mucus promptly and gently using a mucus sucker.
♦    Adequate oxygenation through mask or nasal catheter in concentration not exceeding 35%.
♦   The baby should be  wrapped,  including head  in a  sterile warm  towel  (normal temperature  36.5-37.50C). Hypothermia and its sequelae: Hypoxia➔ Hypoglycemia➔ Anaerobic metabolism➔ Metabolic acidosis.
♦    Aqueous  solution  of  vitamin  K  I  mg  is  to  be injected  intramuscularly  to  prevent  hemorrhagic manifestations.
INTENSIVE   CARE   PROTOCOL:   Preterm  babies   are functionally immature and 'special care' is needed for their survival. Those requiring 'special care' are judged by:  (i)  Inability to suckle  the  breast and to swallow, (ii) Incapacity to regulate the temperature within limited range from 96-99°F (35.6-37 .2°C}, (iii) Inability to control the cardiorespiratory function without cyanotic attacks.
The principles of special care are:
- Delayed cord clamping  (DCC) by  60 seconds has significant reduction in mortality for preterm infants.
- To   maintain   a   relatively   stable   thermoneutral condition-keep delivery room warm, wrap the baby with a warm towel (plastic wrap), keep LBW neonate with mother-skin-to-sldn contact (Kangaro care).
- Adequate humidification to counterbalance increased insensible water loss.
- Oxygen therapy and respiratory support. - To prevent infection.
- To maintain nutrition and close monitoring.



To maintain body temperature: As the premature babies are extremely thermolabile, they can easily develop hyperpyrexia or
hypothermia. The axillary temperature should be between36.0°C
and36.5°C.
The ELBW babies are best placed in prewarmed double­ walled incubators  where temperature and humidity can be better stabilized. Alternatively,  the baby could be managed under radiant warmer with protective plastic covers. The skin temperature should be maintained at36-36.5°C with surrounding humidity 80%.
Slow warming should be done for infants who become hypothermic.
Fluid, electrolyte balance and nutrition: Initially IV fluid dextrose solution is used to maintain blood glucose levels of >45-50 mg/dL. ELBW infants need more energy to protect against growth immaturity, hypothermia,  anemia and infection. Daily requirement is 110-120 Kcal/kg/day. Parenteral Nutrition (PN) is needed in infants weighing <1500 g at birth. PN using a standard solution is given at the rate of 60 mL/kg/ day. It provides proteins, lipids and carbohydrates.
Respira tory support: Oxygen concentration  is adjusted so as to keep saturation level of 90-95% for all babies <32 weeks.  Many infants may need initial sup­ port with either Positive Pressure Ventilation (PPV} or Continuous Positive Airway Pressure  (CPAP). The early use of CPAP with surfactant therapy in extremely preterm infants ( <32 weeks} reduces the risk of Bronchopulmo­ nary Dysplasia (BPD), atelectasis or death.
Indications of mechanical ventilation and surfactant
therapy are:  (a) Rise in 02  need even after maximal
pressure (>8 cm H2O} with CPAP and (b) recurrent apnea. Surfactant therapy:  For infants with RDS who are
ventilated with mean ailways pressure of at least 7 cm H2O and have an inspired oxygen concentration (FiO2} of >0.35.
The first dose is given as soon as possible after birth and intubation. However, CPAP is the initial therapy.
Caffeine citrate is used as prophylaxis, soon after
admission. Early (<2 days) caffeine therapy is associated with better neurodevelopmental outcome in infants born <30 weeks gestation.
Desirable level of arterial blood gas values should be:
(i) PaO2  55-65 mm Hg, (ii) PaCO2  35-45 mm Hg, and
(iii) pH 7.35-7.45 and pulse oximeter reading should be 90-95% oxygen saturation.
Hyperbilirubinemia:  Serum  bilirubin  should  be maintained <10 mg/dL. Infant may need phototherapy or exchange transfusion.
Ifection: The main sites of infection are respiratory tract, gastrointestinal tract, skin and the umbilicus. The incidence is as high as 70% in VLBW infants ( <1000 g).
Group B Streptococcus (GBS) is a common pathogen. In India, multidrug resistant, Acinetobacter baumannii and  Klebsiella  has  fatality  rate  of  59%.  Prophylactic antibiotic (ampicillin and amikacin) are commonly used pending culture results.
Chapter 32: Low Birth Weight Baby    Im

The common antibiotics used are ampicillin 100 mg/ kg per day and amikacin 10-15 mg/kg per day to be given intravenously in two divided doses for 5-7 days. GBS is an important pathogen.
Nutrition: Preterm infants are often unable to suck and swallow. Enteral feeding may be possible depending on gestation age and vigor. Babies may require gavage feeding or parenteral nutrition. Human milk is the first choice  of nutrition  for  all  low  birth  weight  babies. Colostrum,  foremilk,  hindmilk and preterm milk help faster growth of the baby.
Commencement:  Early  feeding  within  ½-1  hour of  birth is  now  widely  recommended.  It  eliminates hypoglycemia, lowers serum bilirubin and neurological sequelae.
Intervals: Depending upon the birth weight, the interval of feeding ranges from hourly in extreme prematurity to 3 hourly feeds in babies born after 36 weeks.
Methods: The methods used depend on the size and vigor of the infant and his ability to suck and swallow. Thus, while a LBW infant with vigor can be put to the breast right from the beginning, the smaller one should be fed by any of the following methods:
♦   Tube (Gavage)
♦    Pipette, dropper, katori and spoon ♦   Bottle
♦    Intravenous
General guidelines are to start intravenous fluids to a baby weighing <1200 g ( <30 weeks) and gradually to initiate tube (gavage) feeding after 1-3 days and spoon after 2-4 weeks and thereafter breastfeeding after some more time. Baby weighing 1200-1800 g (30-34 weeks) may be started with tube feeding and gradually to move onto spoon and breastfeeding. Whereas babies weighing >1800 g (>34 weeks) generally have no dificulty to start with breastfeeding.
II   Tube or Gavage: A fine polythene tube of  about  0.5 mm internal diameter is used. It should be passed through the nose down to esophagus. Expressed breast milk is started with a small volume and is gradually built up. It may be safely continued for about 7 days. Calculated amount of fluid is delivered with a syringe by gravitation (gavage feeding).
II  Pipette, droppe,;  katori and spoon: This is used where the baby can swallow but fails to suck.
II  Bottle: It is used when the baby can suck and swallow but cannot manage to express the milk out from the breast.
■  Intravenous fluid therapy: Neonates within the incubator or under radiant heaters have 10% increased fluid requirement to counterbalance the increased insensible water loss.
Fluid  requirement varies from  60-80 mL/kg/day of  10% dextrose water or breast milk 10-20 mL/kg/day on first day and to increase by 15 mL/kg/day. Amount should be 10% more, if phototherapy is used. Monitoring of fluid is done by measuring

body weight, urine output, its specific gravity and serum sodium level.
Calorie requirement: It is a paradox that the premature
infants require more  calories  than  their mature counterpart because of relatively greater loss of heat from the body swface. The calorie intake of 60 calories per kg per day on 7th day is to be stepped up gradually to 100 on 14th day and about 120-150 on 21st day.
Food volume: To meet the calorie requirements, the amount of  milk  to  be  given  is  slowly  but  progressively  increased. Requirement on 1st day is 80 mL/kg. Gradually increased by 15 mL/kg/day to reach 200 mL/kg/day by 8th to 10th day. This is expected to be achieved by 2 weeks.
Additional  supplements:  All  premature  babies  should receive additional supplement of vitamins and minerals which should be started after 2 weeks. The daily requirement consists of vitamin A 2500 IU, vitamin D 400 JU, vitamin C 50 mg, folic
acid 65  1g and vitamin B1  0.5 mg. Supplementation of calcium and phosphate are also essential. In addition, iron supplement
should be given in the second or third week. A liquid preparation containing 2-4 mg/kg/day of elemental iron is given in two divided doses. Intravenous gamma globulin therapy (400 mg/kg/ dose) may be given to prevent infections in selected cases. For ve1y low birth weight ( <1200 g) babies parenteral nutrition with amino acids and lipids along with dextrose and multivitamins are  given. The  single  most  important  factor  is high standard of nursing.
FAVORABLE SIGNS OF  PROGRESS: The following  are the favorable signs: (1) The color of the skin remains pink all the time; (2)  Smooth and regular breathing; (3)  Increasing vigor evidenced by-(a) movements of the limbs, and (b) cry;  ( 4)  Progressive gain in weight. Baby loses 1-2% weight every day for the first 5-7 days. Thereafter, baby gains 1-1.5% of birth weight daily. Baby regains birth weight by 10-14 days.
WHEN  TO  DISCHARGE?  The  premature babies  are discharged:  (1)  When  they  attain  sufficient weight; (2)  Attain  good  vigor;  (3)  Able  to  suckle  the  breast successfully.
ADVICES ON DISCHARGE: If possible, the supervision is to be continued at home by public health nurses or health visitors. Parental education is given for care of the baby at home. The following advices are given on discharge:
- Advice about feeding schedule.
- Prescribe  a  suitable  multivitamin  and  oral  iron preparation as mentioned earlier.
- To attend the well-baby clinic for subsequent check-up, immunization and guidance.
FOLLOW-UP  VISIT:  Assessment  is  done  for  infant's general health, weight, hydration and degree of jaundice. Immunization schedule is verified. Any new problem needs to be identified. Pattern of feeding and its adequacy are explored. Screening test, if any, to be done. Guidance for infant care is given to the mother.
ml Chapter 32: Low Birth Weight Baby

FETAL GROWTH RESTRICTION (FGR) Syn: Intrauterine Growth Restriction (IUGR),
chronic placental insufficiency DEFINITION: FGR is a syndrome where fetus  @. !]
  •f 
 --.!j
fails to reach its growth potential due to several underlying disorders related to maternal, fetal
l
or placental. Small for Gestational Age (SGA)  !J:\ .,.ii is defined as an estimated fetal weight below the 10th per­ centile for the gestational age. ■  Fetal Growth Restriction (FGR) is defined on a combination of measures of fetal
size percentile and Doppler abnormalities. FGR may be with early onset (<32 weeks) or late onset (z:32 weeks). Growth restriction can occur in preterm, term or post­ term babies. Fetal weight estimation: Hadlock (based on HC, AC and FL) equation is used.
INCIDENCE: FGR comprises about one-third of low birth weight babies. In high income group countries, its overall incidence is about 2-8%. The incidence among the term babies is about 5% and that among the post-term babies is about 15%.
NOMENCLATURE:  SGA fetuses constitute 70% of the babies with birth weight <10th centile. These fetuses fulfill the growth potential and are not growth restricted. They are constitutionally small but otherwise normal. They have no increased obstetric or neonatal risks. They grow parallel to  the  lower  centile  throughout  the  pregnancy.  These babies are small due to constitutional reasons and said as 'small mother small baby'. On the other hand, early onset of pathological cessation of growth may produce a baby with typical features ofFGR. Sonographic Estimated Fetal Weight (SEFW) is determined (population specific) and the cut off value <10 percentile is more appropriate to define the FGR. This group (30%) is of higher perinatal risk.
TYPES: Based on the clinical evaluation and ultrasound examination, the small fetuses are divided into:
1.  Fetuses who are small and healthy. The birth weight is less  than  10th  centile  for  their gestational  age. They are small for gestational age. They have normal


Table 32.3: Features of early onset and late onset growth restricted fetuses.
Early onset: 20%	Late onset: 80%
Uniformly small	 Head larger than abdomen.
Pondera! index (birth weight/Crown-heel	Low length3)-normal.
HC:AC and	Elevated. FL: AC ratios-normal.
Etiology:	Chronic placental ■  Genetic syndromes (5%), aneuploidy,	insufficiency-
triploidy, trisomy 13, 18.	extrinsic to fetus,
■  Infection-intrinsic to fetus.	constilunally small. ■  Early onset severe hypertension.
Definition for fetal growth restriction
Early-onset FGR (<32 weeks)	Late-onset FGR (!:32 weeks)
■  EFW or AC <3rd percentile.	•  EFW or AC <3rd percentile OR                                 OR
UA with AREDV.	■   !:2 of the following three OR                                 criteria: