UNIT X - ABNORMALITIES DURING POSTNATAL PERIOD

ASSESSMENT AND MANAGEMENT OF WOMEN WITH POSTNATAL

COMPLICATIONS
Total: 4 Hours
I. Puerperal sepsis
II. Breast complications
1. Breast engorgement and infection
2. Cracked and retracted nipple
3. Acute mastitis
4. Breast abscess
5. Lactation failure
6. Suppression of lactation
III. Urinary complications
1. Urinary tract infection
2. Retention of urine
3. Incontinence of urine
4. Suppression of urine
IV. Thrombo-embolic disorders
1. Deep vein thrombosis
2. Thrombophlebitis
3. Pulmonary embolism
V. Postpartum haemorrhage
VI. Subinvolution
VII. Psychological complications
1. Postpartum blues
2. Postpartum depression
3. Postpartum psychosis.
 INDEX
PUERPERAL SEPSIS
I. Introduction
II. Definition
III. Incidence
IV. Etiology
V. Riskfactors
a. Antepartum riskfactors
b. Intrapartum riskfactors
VI. Mode of infection
a. Endogenous
b. Autogenous
c. Exogenous
VII. Pathophysiology
VIII. Clinical features
a. Local infection
b. Uterine infection
c. Spreading infection
IX. Diagnostic measures
a. History collection
b. Physical examination
c. Investigations
X. Mangement
a. Medical management
b. Surgical management
c. Nursing Management
XI. Complications
XII. Prevevention
a. Antepartum
b. Intrapartum
c. Postpartum
 PUERPERAL SEPSIS
I. INTRODUCTION
Puerperal sepsis is an infective condition in the mother following chidbirth. Infection of the
reproductive tract is another leading cause of maternal mortality. Theoretically the uetrus is sterile
during pregnancy and until the mebranes rupture. After rupture the pathogens can invade. The risk
of infection is even greater if tissue edema and trauma are present. A puerperal infection is always
potentially serious, because, although it usually begins as only a local infection, it can spread to
involve the peritoneum (peritonitis) or the circulatory system (septicemia).
II. DEFINITION
An infection of the genital tract which occurs as a complication of delivery is termed
puerperal sepsis.
Puerperal sepsis is defined as infection of the genital tract occur at any time between the
onset of rupture of membranes or labour, and the 42nd day following delivery or abortion.
III. INCIDENCE
According to WHO estimates puerperal sepsis accounts for 15% of the 500000 maternal
deaths annually.In low and middle income countries puerperal infections are the sixth leading cause
of disease burden in women during their reproductive years.
IV. ETIOLOGY
• Infection of the episiotomy wound and lacerations of the vagina,vulva or the cervix
• Infection of the placental site by bacteria travelling up from the vagina.(This is commonly
seen in cases of Prolonged labour,after repeated vaginal examination,manual removal of
placenta after retained placenta, rupture of membranes not adequately covered by antibiotics
and sometime in caesarean section).
• Infection of other pelvic organ like ovaries,peritoneum and broad ligament, secondary to
pelvic infection.
 Infections from the anus during delivery or spreading from a sore throat or infected through
the blood
• Infection carried to the patient from doctors, nurses and other visitors.
• Infection can also spread from infected vaginal pads.
Causative Organisms:
• Aerobic:Staphylococcus pyogens,E-coli
• Anaerobic: Anaerobic streptococcus
 Bacteriosides
Cl.welchi,cl tetani
V. RISK FACTORS
Antepartum risk factors:
• History of infection
• History of chronic conditions like diabetes, anemia or poor nutrition, smoking,
obesity
• History of STD/RTI
• Poor immunity
• Sexual intercourse during late pregnancy
Intrapartum risk factors
• Caesarean birth
• Urinary catheterization
• Episiotomy or laceration
• Frequent vaginal examination
• Reatained placenta
• Prolonged rupture of membrane
• Chorioamnionitis
• Traumatic birth due to the use of instrument (forceps, vaccum extraction)
• Use of invasive procedures, such as internal fetal monitoring, fetal scalp sampling
and amnioinfusion.
• Poor sterile technique
VI. MODE OF INFECTION
• Endogenous Origin:
When the organism are present in the genital tract before delivery and become
pathogenic in some conditions. Anaerobic streptococcus is the predominant one.
• Autogenous:
The organism present else where in the body migrate to genital organs either through
blood strain or through droplet infection.
Eg:streptococcus, beta haemolytics, E.coli, Cl.welchi and staphylococcus are thus
migrtaed from sore throat and skin infection
 • Exogenous:
The infection is contracted from some other sources outside the patient. From other
sources the organisms are introduced usually from the doctors or nurses.
The organisms are introduced usually from the respiratory tract of the doctors
or nurse. Eg: E coli,Cl.welchi.
VII. PATHOPHYSIOLOGY
 The primary sites of infection are perineum, vagina, cervix and uterus. The infection is
either localized to the site or spread to distant sites.
 Endometrium (placental implantation site), cervical lacerated wound, vaginal wound or
perineal lacerated wound are the favorable sites for bacterial growth and multiplication due
to the presence of blood clots or dead space.
 The wounds become red, swollen and there is associated seropurulent discharge
 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.
VIII. CLINICAL FEATURES
Three types
1) Local infection
2) Uterine infection
3) Spreading infection
1)Local infection:
 slight rise of temperature,generalised malaise or headache.
o Local wound becomes red and swollen,pus may form due to disruption of the wound.
2)Uterine infection:
Mild:
• Puerperal Pyrexia (It is a rise of temperature reaching 38 degree celcius or 100.4 0 F or
more and lasting for 24hrs or more during the first 3 weeks of puerperium.) with
proportionate rise in pulse rate.
• Lochial discharge becomes offensive (abnormal smell/foul odour of discharge),copious and
often red.
• Uterus is subinvoluted (i.e.less than 2cm/day during the first 8 days after delivery., tender
and softer than usual.
 Severe:
• The onset is acute with high rise of temperature often with chills and rigor,pulse rate is
rapid.
• Lochia may be scanty and odourless.
• Uterus may be subinvoluted, tender and softer.
3)Spreading infection(Extra uterine spread)
• Parametritis(inflammation of the tissue cells of cervix or upper part of the vagina)
• Pelvic peritonitis
• Thrombophlebitis
• Septicemia
Parametritis:
The onset is usually about 7-10th day of puerperium.
• Constant pelvic pain
• Tenderness on either sides on the hypogastrium
• Vaginal examination reveals an unilateral indurated mass pushing the uterus to the
contralateral side
• Rectal examination confirms the induration specially extending along the uterosacral
ligament.
Pelvic peritonitis:
– Pyrexia with increase in pulse rate
– Lower abdominal pain and tenderness. Muscle guard may be absent
– Vaginal examination reveals tenderness on the fornix and with the movement of
cervix.
– Collection of pus in the pouch of douglas is evidenced by swinging temperature,
diarrhoea and a buldging fluctuant mass felt through the posterior fornix.
General peritonitis:
– High fever with rapid pulse
– Generalised abdominal pain,vomiting,abdomen is tender and distended.
– Patient looks very ill and dehydrated.
– Abdomen is tender and distended. Rebound tenderness is often present.
 Thrombophlebitis:
The clinical features of pelvic thrombophlebitis are similar to those of uterine infection or
parametritis.
 There may be swinging temperature continued for a long period with chills and rigor.
 The features of pyaemia are present according to the organs involved. These cases
are fortunately rare with the advent of wide range of antibiotics.
Septicaemia
– There is high rise of temperature associated with rigor
– Pulse rate is usually rapid even after the temperature settles down to normal
– Blood culture is positive
– Symptoms and signs of metastic infection in the lungs,meninges or joints may
appear.
IX. DIAGNOSTIC MEASURES
Objectives
 To locate the site of infection
 To identify the organisms
 To assess the severity of the disease
History:
Antenatal history of anaemia,antepartum haemorrhage, presence of septic foci in teeth and
gums and tonsils, any debilitating disease like haert disease, diabetes, tuberculosis and urinary
tract infection or malaria should be enquired.,
Intranatal history regarding
 Preterm labour
 Duration of rupture of membranes
 Number of internal examination done outside and inside the hospital
 Duration of labour
 Method of delivery
 Nature of intrauterine manipulation
 Any trauma to the genital tract
Clinical examination
 Assess for tachycardia and temperature 380c or more with chills.
 Systematic examination including throat, breast, lungs, heart,liver spleen and legs
  Abdominal examination to note involution of the uterus
 Internal examination to note characteristics of lochia, condition of perineal wound, repaired
or pelvic abscess and bimanual examination to findout any pelvic pathology.
Investigations
Investigations are
 High vaginal and endocervical swabs for culture
 Clean catch mid stream collection of urine for urinalysis sensitivity test.
 Blood for total and differential count of white cells and estimation of haemoglobin
 Blood culture if fever is associated with chills and rigor.
 Pelvic ultrasound to detect any retained bits of conception within the uterus
 CT and MRI: when diagnosis is in doubt or there is pelvic vein thrombosis
 Blood urea 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.
X. MANAGEMENT
Medical Management
The principles are:
 To control the puerperal infection by use of antibiotics.
 To prevent fluid deficit by appropriate fluid and replacement therapy.
Management includes:
 Complete bed rest. Isolation in a seperate room of fever hospital.
 Diet:light diet rich in vitamins and minerals with plenty of fluids.
 Restoration of fluid and electrolyte balance,correction of anemia by oral iron and by blood
transfusion.
 An indwelling catheter is used to relieve any urine retention due to pelvic abscess. It also
help to record urinary output.
 Antibiotics of choice is a comination of cloxacillin and amoxycillin 500mg three times/day
for 5days.
 Paracetamol 500mg orally every 8h for releif of pain.
 Cold fomentation.
 One of these regimen is started till the result of culture and sensitivity
 Antitoxin serum is given in clostridium welchi infection
Surgical Management
 The stitches of the perineal wound may have to be removed to facilitate drainage of pus and
relieve pain. After the infection is controlled, secondary sutures may be given later.
 Incision and drainage of the abscess. In pelvic abscess: posterior colpotomy and drain. In
parametric abscess: incision and drain at the point (usually above the inguinal ligament)
 Manual removal of retained parts if felt during pervaginal examination.
Nursing management
 Assess the vital signs every 2 to 4 hours and record results to monitor progress of infection.
 Encourage fluid intake to promote fluid balance.
 Document intake /output to assess hydartion status.
 Provide oppurtunity to express feelings
 Provide routine post partum care such as regular bathing or sponging, change of vaginal
pads.
 Teach and make use of hand washing techniques to prevent spread of infection.
 Provide support to woman for care.
 Assist with positioning in bed with pillows to promote comfort.
 Offer nonpharmacological pain measures such as backrub to ease aches and discomfort if
desired and enhance effectiveness of analgesics.
XI. COMPLICATIONS
 Chronic Pelvic Inflammatory disease
 Infertility
 Pelvic cellulitis
 Peritonitis
 Severe cellulitis of uterine incision may lead to necrosis and separation.
 Septic shock (Septic shock is diagnosed by the presence of oliguria, hypotension
which is due to septicaemia and haemorrhage).
Management of septic shock
 Rapid crystalloid infusion, 1L in Ist hour followed by IL in next 2h
 Oxygenation
 Antimicrobial therapy
 Antimicrobial prophylaxis
 o Penicillin G,5 million units IV initial dose, then 2.5 million units IV every
4h until delivery.
o Cefazolin, 2g IV initial dose, then 1g IV every 8h until delivery
o Ampicillin, 2g Iv initial dose, then 1g IV every 4h or 2g every 6h until
delivery
o Clindamycin, 900mg IV every 8h until delivery
o Erythromycin, 500 mg IV every 6h until delivery
o Vancomycin, 1gm IV every 12h until delivery.

XII. PREVENTION:
Puerperal sepsis is to a great extent preventable. Privided certain measures are undertaken
before, during and following labour .
 Antenatal
 Improvement of general condition
 Treatment of septic cocci
 Abstinence from sexual intercourse in the last two months.
 Care about personal hygeine:bathing in dirty water to be avoided.
 Avoiding contact with people having infection
 Avoiding unnecessary vaginal examinations and douches in the later months.
 Improvement of nutritional status of the pregnant women.
 Intrapartum
 Staff attending on labour should be free of infections
 Full surgical asepsis to be taken while conducting delivery
 Women having respiratory tract infection or skin infection should be admitted in
single room or seperate ward.
 Membranes should be kept intact as long as possible and vaginal examination should
be restricted to minimum.
 Prophylactic use of antibiotic at the time of caesarean section has significantly
reduced the incidence of wound infection, UTI and other serious infection
Eg:Ceftriaxone 1gm IV immediately after cord clamping and a second dose
  Traumatic vaginal delivery and intrauterine manipulation should be preferably
avoided. If required should be done using fresh gloves with liberal use of strong
antiseptic solution.
 Excessive blood loss during delivery should be replaced promptly by transfusion to
improve the general body resistance.
 Prophylactic antibiotic must be administered in cases of premature rupture of
membranes, prolonged labor or following traumatic delivery.
 Postpartum
 Take aseptic precautions while dressing the perineal wound.
 Restriction of the visitor in the postpartum ward.
 Mothers to be instructed to use sterile sanitary pads and to change them frequently
 Vulva and perineum to be cleaned with mild antiseptic solution following urination
and defecation.
 Infected mothers and babies are to be isolated.
 Too many visitors restricted, sterilized sanitary pads are to be used , infected babies
and mothers should be in isolated room.
 To keep the floor of the in-patient ward dust free by frequent mopping.
 BREAST COMPLICATIONS
Several common problems that may arise during the breast feeding period. This includes
 Breast engorgement
 Acute mastitis
 Breast abscess
 Cracked and retracted nipple
 Lactation failure
BREAST ENGORGEMENT
INDEX
I. Introduction
II. Meaning
III. Incidence
IV. Etiology
V. Pathophysiology
VI. Clinical features
VII. Diagnostic measures
i. History collection
ii. Physical examination
VIII. Management
i. Medical management
ii. Nursing management
IX. Complications
X. Prevention
BREAST ENGORGEMENT (Stagnation of milk)
I. INTRODUCTION
The three basic components of breast engorgement are congestion/vascularization,
accumulation of milk and edema caused by the congestion and obstruction of lymphatic
drainage.
Breast engorgement is a condition which occur due to
  Excessive production of milk
 Obstruction in the outflow of milk
 Poor removal of milk by baby, that is decreased intake of milk from breast.

II. MEANING
Breast engorgement means painful overfilling of breasts with milk. This occur usually by an
imbalance between milk supply and infant demand.
Breast engorgement occurs in the mammary glands due to expansion and presssure exerted
by the synthesis and storage of breast milk.
It usually occurs on the 3rd or 4th day of the post partum period when the milk production in the
breast rises.
III. INCIDENCE
IV. ETIOLOGY
 Late initiation of breast feeding
 Infrequent feeding
 Restriction on duration and frequency of breast feeding
 Use of complementary foods
 Babies with poor suck
 Incorrect techniques
 Use of pacifiers.
V. PATHOPHYSIOLOGY
On 2nd to 6th day following births of baby, the extra blood and lymph fluids travelling to the
breast to prepare the breast for milk production.
The breast of the mother become larger, heavier and a little tender when milk production is
increased.
This fullness starts decreasing within first few weeks after the birth, when the baby starts taking
feed regularly.
But if the baby has not been taking feed often or long enough / when suddenly stop breast
feeding, then fullness develop causing breast engorgement.
VI. CLINICAL FEATURES
1) Both breasts are
 Swollen
  Warm
 Tender
 Shiny
 Firm
 Painful breast
2) Nipples become
 Edematous
 Hard areola
 Flushed
 Flattened out nipples
3) Veins over breast:
 Prominent
 Engorged
4) Low grade fever (100 F)or 37.8C due to overfilling of breasts with milk
5) General malaise- ill feeling of health with loss of appetite, general weakness, fatigue and
chills
6) Swollen and tender lymph nodes in armpits due to congestion and obstruction of lymphatic
drainage.
7) Pain on feeding to baby due to accumulation of milk and edema.

VII. DIAGNOSTIC MEASURES:

It is diagnosed only based on symptoms.
History collection: Includes the history of feeding pattern, parity,health condition of the
baby
Physical Examination:
 Assess for breast tenderness, engorged veins, lymph nodes in armpits
 Check the vital signs.
VIII. MANAGEMENT
Medical Management
 Support the breast with a binder or brassier
  Manual expression of any remaining milk after each feed. 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.
 Administer ibuprofen to reduce pain and swelling.
 Warm compresses and massage before feeding can help drain the milk
 If it still feel uncomfortable after nursing apply a cold compress to reduce swelling,
edema and pain. Use a frozen wet towel, a cold pack or a bag of frozen vegetables.
Apply it to the breast for 15 minutes at a time every hour as needed. To prevent
damage to the skin, place a thin cloth between breast and the cold pack.
 The baby should be put to the breast regularly at frequent intervals
Nursing management
 Check the temperature
 Palpate the breast to assess tenderness and firmness
 Advise to take warm shower or apply warm moist compress to breast
 Supervise the mother at time of breast feeding to make sure that the baby is positioned
and latched on correctly.
 Ask the mother to give the feed to baby from both the breasts for unrestricted amount
of time.
IX. COMPLICATIONS
 Sore and cracked nipple
 Blocked milk ducts
 mastitis
X. PREVENTION
 Initiate breast feeding early and unrestricted
 Exclusive feeding on demand
 Feed the baby in correct position and make sure that the baby is latching on and
feeding well.
 When breasts are hard and overfilled, let out (express) milk enough to soften nipples
before putting the baby to the breast.
 Empty one breast completely before going to the other side.
 MASTITIS
I. INTRODUCTION
II. MEANING
III. INCIDENCE
IV. CAUSATIVE ORGANISMS
V. RISK FACTORS
VI. MODE OF INFECTION
VII. PATHOLOGY
VIII. CLINICAL FEATURES
IX. DIAGNOSTIC MEASURES
a. History collection
b. Physical examination
c. Investigations
X. MANAGEMENT
a. Medical management
b. Nursing Management
XI. COMPLICATIONS
XII. PREVENTION

MASTITIS
I. INTRODUCTION
Mastitis is inflammation of the breast tissue usually unilateral after the milk flow is
established.It is caused by streptococcal or staphylococcal invasion of the breast tissue through
cracks or fissures around the nipple. It usually occurs in the second and third weeks after
delivery, and very rarely, after the twelfth week. Mastitis usually is unilateral, but it may be
bilateral as well.
II. MEANING
 Mastitis is an infection of milk ducts (laciferous ducts) of the breast tissue of the
breast. It occurs most frequently during the time of breast feeding by cross infection from
baby to mother.
III. INCIDENCE
2-5% in lactating women, most within first 6 weeks of breast feeding or during weaning
and less than 1 per cent in nonlactating women.
IV. CAUSATIVE ORGANISMS
 Staphylococcus aureus
 S.epidermidis and streptococci
V. RISK FACTORS
1) Milk stasis
 Failure to change infant position to allow emptying of all lobes
 Failure to alternate breast feedings
 Poor suck
 Poor let down
2) Actions that promote access/multiplication of bacteria
 Poor hand washing technique
 Improper breast hygeine
 Failure to air dry breasts after breast feeding
 Use of plastic lined breast pads that trap moisture against nipple
3) Breast/ nipple trauma
 Incorrect positioning for breast feeding
 Poor latch on
 Failure to rotate position on nipple
 Incorrect or aggressive pumping technique
 Cracked nipples
4) Obstruction of ducts
 Restrictive clothing
 Constricting bra
5) Change in number of feeding/ Failure to empty breasts
 Attempted weaning
 Missed feeding
 Prolonged sleeping of infant,inckuding sleeping through the night
  Favoring side of nipple soreness
6) Lowered maternal defenses
 Fatigue
 Stress
 Poor diet
VI. MODE OF INFECTION
There are two different types of mastitis depending upon the site of infection.
1) Infective- It includes cellulitis and primary mammary adenitis.
2) Non infective: It may be due to milk stasis. Feeding from the affected breast solves the
problem.
VII. PATHOLOGY
Infective
a) Staph aureus (from baby’s mouth)

Enters through cracked nipples

Involve parenchymal tissue of breast

Cellulitis
b) Staph aureus (from baby’s mouth)

Enters milk producing ducts (lactiferous ducts)

Flow of milk is blocked

Mammary adenitis
Non infective
Intraductal pressure rises due to milk stasis with consequent flattening of alveolar cells and
development of spaces between the cells
Some components (mainly immunoproteins and sodium) cross from plasma into milk and
from milk into the interstitial tissue (especially cytokines)through this space inducing an
inflammatory response
The accumulated milk, the inflammatory response, and the resulting tissue damage facilitate
the establishment of the infection.
VIII. CLINICAL FEATURES
Symptoms
 Generalized malaise and head ache
 Severe pain in one quadrant of the breast.
Signs
 High fever (1020F or more) with chills
 Presence of a wedge shaped swelling on the breast with its apex at the nipple. The overlying
skin is red, hot and flushed and feels tense and tender.
 Axillary lymph nodes are enlarged
 Presence of toxic features.
 Sodium and chloride levels are elevated in the milk where as lactose levels are low, which
makes the milk taste saltier and may be rejected by the infant.
IX. DIAGNOSTIC MEASURES
History collection: Includes the history of breast engorgement, cracked nipple,
infections, congenital anomalies of the baby like cleft palate, short frenulum.
Physical examination:
o Includes the breast examination: Assess for pain and swelling over the breast. The
overlying skin is red, hot, flushed and feels tender.
o Check the temperature
Investigations
 Whenever possible, it is recommended to count cells and colonies in the milk for a more
accurate diagnosis.
 A sample with more than 106 leukocytes and over 103bacteria per ml of milk indicates
infection
 More than 106 leukocytes and less than 103 bacteria per ml indicates non-infectious
inflammation
 Less than 106 leukocytes and less than 103 bacteria per ml represents only milk stasis.
 Milk culture: to determine the infectious agent. If milk culture is not viable as a routine
prectice, it should be performed in the situations like lack of response to antibiotic
therapy, recurrent mastitis and in severe cases.
  After washing the breast in running water and carefully washing the hands with soap and
water, the milk should be expressed, not letting the nipple touch the collection vial,
which should have been sterilized. The first 3 to 5 ml of milk should be disregarded.
X. MANAGEMENT
Principle:
 To stabilise the condition and treat appropriately
 To prevent complications such as breast abscess.
Medical Management
 Proper treatment is indicated other wise breast abscess will develop.
 Bed rest foe at least 24 hour
 Increased fluid intake (at least 2-2.5 L/day)
 Stop lactations from the affected breast and breast is emptied manually or by an electric
pump. When the acute phase is over breast feed can be resumed.
 Support the breast over a pad of cotton.
 Antibiotic therapy: A sample of milk is sent for culture and sensitivity the antibiotic started.
 Flucloxacillin 500mg / 6 hours orally is started. Erythromycin is an alternative to patients
who are allergic to pencillin.It is continued for atleast 7 days.
 Bromocriptine (Parlodel) 2.5mg orally for 14 days to suppress lactation.
 Analgesics (Ibuprofen), antipyretics are given.
 Use breast pump or hand expressing the milk. Moving fresh milk through the breast will
help clear out the infection.
Nursing Management
 Check the vital signs
 Give breast care.
 Manually express the milk, if breast is engorged to relieve engorgement.
 Provide adequate knowledge on mastitis and its prevention and care.
 Emotional support.Mastitis can be frustrating, can cause anxiety, and can make a woman
feel very sick.
XI. COMPLICATIONS
 Breast abscess
 Breast lump
 Nipple discharge
XII. PREVENTION
 Maintain the hygeinic measures.
 Reduce the amount of bacteria in the environment (clean housing and bedding)
 Milk flow is maintained by breast feeding the infant. This prevents proliferation
of staphylococcus in the stagnant milk. The ingested staphylococcus will be
digested without any harm.
 Provide early management of breast engorgement,plugged ducts and cracked
nipple.

BREAST ABSCESS
INDEX
I. INTRODUCTION
II. DEFINITION
III. INCIDENCE
IV. ETIOLOGY
V. PATHOLOGY
VI. CLINICAL FEATURES
VII. DIAGNOSTIC MEASURES
a. History collection
b. Physical examination
c. Investigations
VIII. MANAGEMENT
a. Medical management
b. Surgical management
c. Nursing Management
IX. COMPLICATIONS
X. PREVENTION

BREAST ABSCESS
I. INTRODUCTION
 Breast abscess is caused by untreated mastitis or results from late or inefficient treatment.
Improper emptying of the breast affected by mastitis, which often occurs when feeding is
discontinued on that breast, favors the development of breast abscess.
II. DEFINITION
Breast abscess is a condition in which there is inflammation and infection with a collection
of pus within the breast tissue.
III. INCIDENCE
It affects 5 to 10% of women with mastitis.
IV. ETIOLOGY
 Bacterial infection:Staphylococcus or streptococcus, E coli, Salmonella
 Cracked nipples
V. PATHOPHYSIOLOGY
Breast abscess is caused by a bacterial infection. The most common type of bacteria
involved are staphylococcus aureus
Mastitis, invades the fatty tissue of the breast and leads to swelling and pressure on the milk
ducts.

Collection of pus within soft tissues (abscess).

An abscess contains bacteria, acute inflammatory cells, protein exudate and necrotic tissue,
it is surrounded by granulation tissue.
VI. CLINICAL FEATURES
 Fever: Fever accompanied by severe chills and rigor. Body temperature may be very
high, even upto 1050F.
 Abscess on the breast.
Since the breast abscess occurs predominantly in one of the glandular system (each
breast has 20 glandular system)one part of the breast show red , hard tender area. The
area is indurated and thicken, the surrounding skin is red and shiny. If the abscess is
not treated immediately there is breakdown of tissues involves in the abscess. There is
collection of pus under the skin and the area becomes soft and fluctuent.Pus draining
from nipples.
 Severe pain
 Occur on movement of the entire breast
 The axillary lymph node may also get inflamed red and tender.
VII. DIAGNOSTIC MEASURES
History collection:Includes the present history of mastitis, feeding pattern,infections
Physical examination:
 Breast examination: Floating sensation at breast on palpation. Red , hard tender area
over the breast.
 Check the temperature: Temperature is very high, even upto 1050F.
 Assess for any evidence of breast engorgement, cracked or fissure in the nipple.
Investigation
 Count cells and colonies in the milk for accurate diagnosis
 Milk culture to determine the infectious agent
 Ultrasonography: helps to confirm the disease and also indicating the best site for
incision or aspiration.
VIII. MANAGEMENT
Medical management
 Antibiotic such as pencillin and analgesics are given to control pain and inflammation
 The breast should be supported with proper brassiers.
 The milk on the affected site should be drained out by a breast pump
 Breast feeding :should be stopped on the affected side till the condition is cured.however
feeding may be continued on the healthy side. Feeding can be restarted on the affected side
after healing of the abscess.
 Clean vaginal pads:must be used and changed frequently to prevent spread of infection.
Surgical management
Surgical drainage or aspiration:
 The pus of the abscess is drained out by a deep radical incision parallel to the
lactiferous duct. The incision should be made very carefully so that the lobular
systems are not touched.
 Repeated aspirations have the advantage of being less painful and less multilating
than incision and drainage and can be performed under local anaesthesia.
Nursing mangement
 Maintain cleanliness and personal hygeine of both mother and newborn
  Application of heat to affected breast if suppuration is present.
 Use comfort measures such as breast support, tight binder or brassier.
IX. COMPLICATIONS
 Extensive abscesses may need large resections wich result in breast deformities and
functional involvement.
 Breast cancer
X. PREVENTION
Any measure that prevents the development of mastitis will consequently prevent breast
abscess.

CRACKED NIPPLE
INDEX
I. INTRODUCTION
II. MEANING
III. PREVALENCE
IV. ETIOLOGY
V. PATHOPHYSIOLOGY
VI. CLINICAL FEATURES
VII. MANAGEMENT
a. Medical management
b. Nursing Management
c. Home remedies
VIII. COMPLICATIONS
IX. PREVENTION
CRACKED NIPPLE
I. INTRODUCTION
Cracked nipple is a condition that can occur in breast feeding women as a result of a number
of possible causes. Developing a cracked nipple can result in soreness, dryness or irritation to or
bleeding of, one or both nipples during breast feeding.
II. MEANING
Cracked nipple means loss of surface epithelium with the formation of raw area in the nipple or
fissure situated at the tip or base of the nipple. Due to this the nipples become painful.
 III. PREVALENCE
The prevalence of cracked nipple is 32% in the first 30 days postpartum.
IV. ETIOLOGY
 Lack of cleanliness and dryness of the nipple.
 Vigorous sucking of a hungry baby in deficient lactating breast.
 Leaving the baby too long at the breast.
 Repeated taking and leaving the nipple by the baby to breath if its nose is obstructed
by the breast.
 Monilial infection:fungal infection-candida
 Retracted nipples
 Poor hygeine resulting in formation of crust over the nipple
 Excessive use of soap makes the nipples macerated and prone to fissuring
V. PATHOPHYSIOLOGY
Poor positioning, improper latch, poorly graspable nipples, infant facial abnormalities or
loss of moisture barrier.

Improper and vigorous sucking

Nipples become irritated, sore or even cracked due to friction.

VI. CLINICAL FEATURES
 Soreness and pain at site of fissures
 Fissure if infected, the infection spread deeper resulting mastitis.
VII. MANAGEMENT
a) Medical Management
 Proper breast care and cleanliness to prevent crust formation.
 Rest:Baby should not put on the affected breast till healing occurs while it is emptied
manually. Gradual going back to the breast is recommneded to prevent recurrence.
 Hot fomentation
 Panthenol oinment or liquid paraffin applied locally
 Application of tincture benzoin after feeding.
 Purified lanonin along with the mother’s milk can be applied 3-4 times a day.
 Keep the nipple dry.
  Expose the nipples to air.
 Persistence of nipple fissure needs biopsy
 Miconazole lotion is applied over the nipple as well as the babys mouth if there is oral
thrush. If it fails to heal rest is given to the affected nipple.
 Nipple shield can be used. The persistence of a nipple ulcer in spite of therapy mentioned,
needs biopsy to exclude malignancy.
b) Nursing Management
 Advice the mother to breastfeed from the uninjured side first
 Experiment with different breast feeding positions to determine which is most
comfortable.
 If breast feeding is too painful, express milk from the injured side to reduce the risk of
mastitis and to maintain supply.
c) Home Remedies
 Apply the warm coconut oil on the nipples and massage gently.
 Apply the aloe vera leaf gel on the affected areas and allow it to dry on its own. Clean the
area with lukewarm water and pat dry with a soft towel.
 Apply the paste of basil leaves on the nipples and allow it to air dry. Then wash off the paste
before feeding the baby.
 Wrap a few ice cubes in a thin towel.Place the towel on the affected area.
 A mixture of honey and olive oil can soften and moisturized damaged nipples.
 Cabbage leaves acts as a cold compress, which helps to reduce the pain and swelling over
the breast.
VIII. COMPLICATIONS
 Mastitis
 Breast engorgement
 Breast abscess
 Failure of lactation.
IX. PREVENTION
 Proper feeding techniques
 Avoid soap and harsh washing or drying of the breasts and nipples. This can cause
dryness and cracking.
 Rubbing a little breast milk on the nipple after feeding to protect it.
  Keeping the nipples dry to prevent cracking and infection.
 Oil massage to the nipples during the last trimesters.
 Local cleanliness during pregnancy and puerperium before and after each breast
feeding prevent crust formation over the nipple.
RETRACTED NIPPLE
XI. INTRODUCTION
It is commonly met in primigravida. It is usually acquired. Babies are able to attach to the
breast correctly are able to suck adequatley. In difficult cases, manual expression of milk
can initiate lactation. Gradually breast tissue becomes soft and more protactile, so that
feeding is posssible.
XII. MEANING
It is a condition in which the nipple is pulled inward into the breast instead of
pointing outward.
XIII. MANAGEMENT
 Retracted nipple can be pulled out sufficiently.
The nozzle end of a 10ml disposable syringe is cut off. The piston is introduced into
the nozzle from the cut end. The smooth end is put to the breast, and the piston is pulled
gently, and the nipple protrudes into the syringe. It is held in that position for one minute,
and then the piston is released. The procedure should be done just before each feed for the
first few days.
LACTATION FAILURE(Inadeuate milk production)
I. INTRODUCTION
II. MEANING
III. CAUSES
a) Maternal:Physiological and social causes
b) Breast feeding related
c) Biological causes
d) Drugs causing suppression of lactation
e) Neonatal causes
IV. CLINICAL MANIFESTATIONS
 Symptoms
 Signs
 V. APPROACH TO MOTHER WITH LACTATION FAILURE
VI. MANAGEMENT
a) Antenatal
b) Puerperium
VII. PREVENTION

LACTATION FAILURE
I. INTRODUCTION
Lactation failure is a condition where the mother is either able to achieve full lactation but
an extrinsic factor has interfered with the process or one or more factors results in failure to
attain an adequate milk production.
II. MEANING
Lactation failure or deficiency, also known as agalactia or agalactorrhea, as well as
hypogalactia or hypogalactorrhea, is a medical condition in which lactation is insufficient or
fails completely due to an inadequency of breast milk production and or a failure of the milk
let down reflex in response to suckling following childbirth.
III. INCIDENCE
Lactation failure will occur in about 4 percentage of cases.
IV. CAUSES
a) Maternal: Psychological and social causes
 Infrequent sucking
 Insufficient milk
 Refusal by baby
 Illness of the mother
 Maternal employment
 Dislike for breast feeding
 Previous unsuccessful breast feeding experience
 Lack of confidence
 Worry, stress
b) Maternal:Breastfeeding related
 Delayed rest
 Fixed schedule feeding
  Infrequent feeds
 Poor attachment
 Bottle/pacifier
c) Maternal: Biological causes
 Sore and cracked nipple
 Inverted nipple
 Engorged breast
 Mastitis and abscess
 Burn/scarring
 Breast surgery
 Insufficient glandular tissue
 Retained placenta
 Endocrinopathies:thyroid,pituitary,ovarian dysfunction
 Chronic maternal illness:DM,SLE,HTN
 Physical disability
 Psychiatric disorder
d) Drugs causing suppression of lactation
 Calcitonin
 Diuretics:Loop,Thiazide
 Dopamine receptor agonist:Bromocriptine,Cabergoline
 Levodopa
 Contraceptives
 Pyridoxine
 Tamoxifen
e) Neonatal Causes
 Neonatal illness: early maternal/infant separation interferes with initiation of lactation
 Neonatal disorders associated with poor suck (cleft lip, cleft palate, short frenulum)
 Neonatal asphyxia, preterm birth, Down’s syndrome
 The wrong perception by the mother leads to the introduction of complementary feeding
which negatively affects milk production.
V. CLINICAL MANIFESTATIONS
 Symptoms
 Infant is not satisfied after feeds, cries a lot
 Take very long feeds
 Improper weight gain
 Infrequent bowel movement-small in amount, dry and hard.
Signs
 Weight loss greater than 10% of the birth weight
 Not regaining birth weight upto two weeks of life
 No urinary output for 24hrs
 Absence of yellow stools in the first week
 Clinical signs of dehydration
VI. APPROACH TO MOTHER WITH LACTAION FAILURE
History + Clinical Examination
No disease
True Lactational failure or not
Yes No Counsel
Check for position, attachment,suckling, night feeds and frequency
No problem
Plan for establishment of relactation
VII. MANAGEMENT
For maintanence of effective lactation in an otherwise healthy individual the following
guidelines are helpful.
 Antenatal
 To counsel the mother regarding the advantages of nursing for baby with breast milk.
 To take care of any breast abnormality specially a retracted nipple and to maintain
adequate breast hygiene specially in the last two months of pregnancy.
 Puerperium
 To encourage adequate fluid intake
 To nurse the baby regularly
 Painful local lesion is to be treated to prevent development of nursing phobia.
  Metoclopromide, intranasal oxytocin and sulpride (selective dopamine antagonist)
have been focused to increase milk production. They act by stimulating prolactin
secretion. Metoclopromide given in a dose of 10mg the daily is found helpful.
VIII. PREVENTION
 Medicated and interventional labor should be avoided as far as possible. It interferes
with instinctive rooting behavior to locate and latch onto the breast.
 Initiate breast feeding as soon as possible after complete delivery of placenta
It will cause early breast stimulation and intiates early lactation
 Proper positioning, attachment, latching on supervised.
 Counselling regarding diet of mother
 Frequency on demand usually 2-3 hourly including night feeds
 Mothers should be explained that it takes time for proper milk formation

SUPPRESSION OF LACTATION
I. INTRODUCTION
This becomes necessary if the baby is born dead or dies in the neonatal period or when the
patient does not like to breast feed her baby or if breast feeding is contraindicated. This can be
affective either by using hormones or by mechanical means.
II. INDICATIONS
 Breast cancer due to need for treatment
 Mother on anticancer drugs or other teratogenic drugs
 Mother on IV drug abuse
 HIV positive mother if she can afford formula feeds
 Galactosaemia
 Active pulmonary tuberculosis
 Puerperal psychosis
III. DRUGS
 Combination of testosterone and estrogen preparation Mixogen 2 ampules
intramuscularly.The risk of using oestrogenic preparations in puerperium includes
thromboembolic manifestation or late postpartum blood loss.
 Bromocriptine (dopamine agonist that inhibits prolactin), 2.5 mg 1 tab daily for 10-14 days
may be given. Cabergoline, pyridoxine all are effective.
 Non pharmacological methods are the use of tight binding to the breasts and jasmine
flowers. Probably jasmine have an effect like the dopamine agonists, centrally mediated
through the olfactory hypothalamic hypophyseal pathway, there by inhibiting prolactin
release from the pituitary.
URINARY COMPLICATIONS
URINARY TRACT INFECTION
INDEX
I. INTRODUCTION
II. MEANING
III. INCIDENCE
IV. ETIOLOGY
V. PATHOPHYSIOLOGY
VI. CLINICAL FEATURES
VII. DIAGNOSTIC MEASURES
a. History collection
b. Physical examination
c. Investigations
VIII. MANAGEMENT
a. Medical management
b. Nursing Management
IX. COMPLICATIONS
X. PREVENTION
RETENTION OF URINE
INCONTINENCE OF URINE
SUPPRESSION OF URINE

URINARY TRACT INFECTION

XIV. INTRODUCTION
 During pregnancy, when stasis of urine occur, this led to the formation of reservoir of
organism. Even trauma during labour or inadequate vulval hygiene causes the infection of
urinary tract. It is a common problem among women.
XV. MEANING
UTI means infection of any part of the urinary tract, especially the urethra or bladder
(cystitis) or the kidney( pyelonephritis). It is one of the common causes of puerperal pyrexia.
XVI. INCIDENCE
Incidence of UTI in pregnant women is one in 5 women
XVII. ETIOLOGY
 Recuurence of previous cystitis or pyelitis
 Asymptomatic bacteriuria becomes overt
 Infection contracted for the first time during puerperium is due to effect of frequent
catheterization either during labour or in early puerperium due to lack of bladder tone
and less desire to pass urine.
 Trauma following instrumental delivery and prolonged labour.
 Inadequate perineal hygiene
 Inadequate asepsis technique.
 Causative organisms:
The organism responsible are E.coli, Klebsiella, proteus and staphylococcus aureus.
XVIII. PATHOPHYSIOLOGY
Causative organism
Due to stasis of urine
From traumatic area due Enters urinary tract through
to not maintaining asepsis urinary meatus/bladder

Inadequate vulval hygiene Causes an ascending infection

Mostly occur during puerpeium
If recurrent infections

Chronic pyelonephritis
XIX. CLINICAL FEATURES
 Spiking temperature with chills
 Costovertebral angle pain
  Suprapubic discomfort
 Frequent and often painful micturition
 Nausea and vomiting
 In severe UTI blood can be seen in urine.
XX. DIAGNOSTIC MEASURES
History collection: Includes the history related to mode of delivery, duration of
labour,retention of urine, pain on micturition, previous history of UTI
Assess the knowledge of woman related to urinary tract infection and its complications
Physical examination:
 Assess the perineal area/vulval areas to assess hygienic conditions
 Check the vital signs to assess the fever, whether having or not.
 Assess for the pain and discomfort at the suprapubic region.
Investigations
 Examination of an uncontaminated midstream clean catch sample for urinalysis.
 Culture and antibiotic sensitivity test.
XXI. MANAGEMENT
Medical Mangement
 High fluid intake (>2 litres per day)
 Adequate drainage of urine
 Appropriate antibiotics such as ampicillin (500mg qid), amoxicillin- clavulinic
acid (375 mg tid), Cephalexin (500mg qid) and nitro furantoin (100mg qid). A
course of 10-14 days will cure 70-100%. Single dose therapy is also suggested.
 Orally administer potassium citrate mixture.(10-20mEq with each meal.
 Urinary analgesics such as phenazo-pyridine hydrochloride (pyridium), 100gm
PO.
Nursing Management
 Encouraging the woman to void spontaneously and helping her to use toilet.
 Provide privacy, assist her to be in the normal position for voiding.
 The woman should be medicated for whatever pain may be having before attempting
to void because pain may cause reflex spasm of the urethra.
 Perineal icepacks applied after birth may reduce edema, which may interfere with
voiding.
  Pouring warm water over perineum and having the woman void in a sitz bath is also
effective
 Catheterization can be done under aseptic conditions.
 If symptoms of UTI occur, report to the physician and urine culture can be used.
XXII. COMPLICATIONS
 Acute pyelonephritis
 Premature labour
 Low birth weight baby
 Increased newborn mortality.
 Persistent bacteriurea.
XXIII. PREVENTION
 Keep the perineal area dry and clean
 Avoid bubble bath.
 Encourage fluid intake especially water.
 Acidify the urine with juices such as cranberry juice.
 Not to allow retention of urine, void frequently.
 Wear cotton underpants
 Wash the perineal area after each void.
 Change the perineal pad frequently.

RETENTION OF URINE
There is a common complication in early puerperium. The causes are
 Bruising and edema of the bladder neck.
 Reflux from the perineal injury
 Unaccustomed position
TREATMENT
If simple measures fails to initiate micturition, an indwelling catheter is to be kept in situ for
about 48hrs. It also help in regaining the normal bladder tone and sense of fullness.
INCONTINENCE OF URINE
This is not a common symptom following birth. The incontinence may be
 Overflow incontinence: following retention of urine should first be excluded before
proceeding to differentiate between either two
  Stress incontinence (due to uterine stress) usually manifest in late puerperium
 True incontinence: in the form of genitourinary fistula usually appears soon following
delivery or within first week of puerperium.
SUPPRESSION OF URINE
If 24hrs urine excretion is less than 400ml or less, suppression of urine is diagnosed, the
cause is sought to be for and appropriate management is instituted.
NURSING MANAGEMENT
1) Providing comfort
 Providing comfort measure is important (relieve pain and burning on urination,
prevent urinary statsis by emptying the bladder frequently).
 Urinary statsis is good medium for organism growth further compounding her
risk for infection. Therefore assist the women with comfort measures such as
running warm water over the perineum or using a sitz bath when voiding
 Administer analgesics such as acetaminophen(Tylenol) as ordered. A urinary
analgesic pyridium is effective.
2) Promote adequate hydrations
 Encourage the women to drink atleast 3000ml of fluid a day.
 Suggest her to drink one glass per hour to ensure adequate intake and to keep a
record of her inatke
 Advise the woman to drink fluids that make the urine acidic, destroys organism
growth. Fluids such as cranberry, plum, apricot juices are examples.
 Tell the women to avoid carbonated beverages because they increase the
alkalinity of urine which promote organism of growth.
 If woman has pyelonephritis expect to administer fluids intravenously in addition
to oral fluid to ensure adequate hydration.
3) Provide patient teaching
 Regarding the compliance with therapy instruct women to complete the full drug
regimen which can range from 5 to 10 days.
 Breast feeding should be continued based on the particular antibiotic she is
taking.

THROMBO EMBOLIC DISORDERS

 INDEX
I. INTRODUCTION
II. MEANING
III. INCIDENCE
A. PUERPERAL VENOUS THROMBOSIS
I. INTRODUCTION
II. DEFINITION
III. INCIDENCE
IV. ETIOLOGY
V. RISKFACTORS
VI. PATHOPHYSIOLOGY
VII. TYPES OF THROMBOSIS depending upon the veins affected
a) Superficial vein thrombosis
b) Deep vein thrombosis
VIII. CLINICAL MANIFESTATIONS
Superficial vein thrombosis
Deep vein thrombosis
IX. DIAGNOSTIC MEASURES
a. History collection
b. Physical examination
c. Investigations
X. MANAGEMENT
a. Medical management
b. Nursing Management
XI. COMPLICATIONS
XII. PREVENTION
a) Antepartum measures
b) Intrapartum measures
c) Post partum measures

THROMBO EMBOLIC DISORDERS

I. INTRODUCTION
 Most thrombo embolic disorders developed during postpartum and result from vascular trauma
during delivery. Cesarean delivery also increases risk. The thromboembolic disorders are a common
cause of death in pregnant women.
II. MEANING
Thrombo-embolic disorders are the vascular occlusive processes which includes venous
thrombosis, thrombo-phlebitis and pulmonary embolism.
III. INCIDENCE
The incidence of venous thrombotic episode is 0.78:1000 during pregnancy, 10 times that
reported in non pregnant women. The incidence is 3.5-fold higher in the puerperium,i.e,2.5:1000
compared to that during pregnancy.
A. PUERPERAL VENOUS THROMBOSIS
I. INTRODUCTION
Thrombosis of the leg veins and pelvic veins is a common complication in puerperium,
especially in the Western countries. The prevelance is however low in Asian and African countries.
II. DEFINITION
Venous thrombosis refers to formation of a blood clot (thrombus formation) at an area of
impeded blood flow in a superficial or deep vein.
Thrombosis in the deep vein develops secondary to the superfical vein thrombosis. Ileofemoral
vein is affected. Clinically, it may remain asymptomatic in majority of cases. DVT is more serious,
occurs most commonly in post partum women between post partum days10 to 20.
III. INCIDENCE
The incidence of venous thrombo embolism in pregnancy is approximately five times the
incidence in non pregnant patients. That is 0.7 to 1.2 per 10000 pregnancies. This risk increases to
approximately 20 times in the post partum period.
IV. ETIOLOGY
Three major causes of thrombo-embolic disease, often referred to as Virchow’s triad, are
hyper-coagulability of blood, venous stasis, injury to the epithelium of the blood vessel.
1) During pregnancy, there is rise in blood coagulation factors,number of young platelets and
adhesiveness. There is increased hypercoagulability of the blood.
2) Venous stasis is increased due to compression of gravid uterus on the inferior vena cava and
iliac veins. This predisposes to damage of endothelial cells, there by increasing risk for
coagulation in the blood vessels of lower body organs
3) Infection, pelvic cellulitis cause inflammation of the venous walls to which the thrombus
may get easily attached
4) Trauma to the venous wall: Pelvic walls are traumatized due to the pressure of the head and
that in the leg veins due to pressure of stirrup while in lithotomy position.
5) Other high risk factors are: Advanced age and multiparity, obesity, anemia, heart disease,
trauma or injury to venous wall are predisposing factors of venous thrombosis in
puerperium.
V. RISK FACTORS
 Advanced age and parity
 Operative delivery
 Obesity
 Anaemia
 Heart disease
 Infection-pelvic cellulitis
 Trauma to the venous wall
 Immobility
 Smoking
 Poor deep vein thrombosis or pulmonary embolism
VI. PATHOPHYSIOLOGY
 In a normal pregnancy there is rise in concentration of coagulation factors I, II, VII,
VIII, IX, X, XII.
 Plasma fibrinolytic inhibitors are produced by the placenta and the level of protein S
is markedly (40%) decreased.
 Alteration in blood constitutes – increased number of young platelets and their
adhesiveness.
 Venous stasis is increased due to compression of gravid uterus to the inferior vena
cava and iliac veins. This stasis causes damage to the endothelial cells.
 Thrombophilias: are hypercoagulable states in pregnancy that increase the risk of
venous thrombosis.It may be inherited or acquired. Inhereted thrombophilias are the
genetic conditions associated with the deficiencies of antithrombin III, Protein C and
Protein S. Others are factor V Leiden mutation and hyperhomocysteinemia.
 Acquired thrombophilias are due to the presence lupus anticoagulant and
antiphospholipid antibodies.
VII. TYPES OF THROMBOSIS
Depending upon the veins affected, there are two types”
a) Superficial vein thrombosis
b) Deep vein thrombosis
a) Superficial vein thrombosis
It affects the superficial veins of the legs.Mainly affects the varicose vein. Mostly occur in
women who are overweight or have high parity. It spread upward to involve long saphenous
vein and to femoral vein.
b) Deep vein thrombosis
It is the thrombosis of deep vein of the calf, thigh or pelvis.Usually manifests during first
two weeks after delivery. It can develop as a primary condition or secondarily as an extension
of superficial venous thrombosis.
VIII. CLINICAL MANIFESTATIONS
Superficial vein thrombosis
 Pain and tenderness in the affected area
 Rise in temperature (more than 380c)
 Tachycardia
 Skin over affected area is reddened
Deep vein thrombosis
 Pain in the calf muscle
 oedema and rise in temperature (more than 380c)
 difference in circumference of both the normal and the affected leg is found.
 On examination: there is calf tenderness on deep pressure and a positive Homan’s
sign-pain in the calf on dorsiflexion of the foot may be present. A difference of
circumference of the calf or thigh of 2cm or more at identical sites on the legs should be
regarded as significant.
IX. DIAGNOSTIC MEASURES
History Collection: Includes the obstetrical history of parity, mode of delivery, medical
history of anemia, heart diseases, thrombophilias and pelvic cellulitis.
Physical examination:
  Assess the Homan’s sign
 Assess the body temperature
 Assess for the oedema on the legs.
Investigations
The following biophysical test are employed to confirm the diagnosis.
1) Doppler ultrasound test is done to detect the changes in the blood flow in the femoral
vein by noting the alteration of the characteristic ‘ ‘Whoosh’’sound which is audible from a
patent vein.
Venous ultrasonography is done by placing the transducer over the femoral vein and then
gradualy it is moved to the great saphenous vein , the popliteal vein and to its branches with
the deep veins of the calf.
Doppler USG: the most accurate ultrasound criteria for diagnosis of venous thrombosis is
a) Soft tissue mass within the venous lumen
b) Noncompressibility of the venous lumen in a transverse plane under gentle probe
pressure. The overall sensitivity and specificity of the VUS using duplex and colour flow
doppler is at 90-100 percent for proximal vein thrombosis.
2) Venography is done to find out filling defect in the lumen of the vein. It is done by
injecting non-ionic water soluble radioopaque dye to note the filling defect in the venous
lumen is a reliable method, if carefully interpreted. Venogram is restricted in pregnancy, due
to the risk of radiation and contrast allergy. It can be performed when needed using pelvic
and abdominal shield with lead aprons.
3) Fibrinogen scanning
4) Magnetic resonance Imaging( MRI): is found superior to VUS and equvalent to
contrast venography in the diagnosis of DVT. The sensitivity and specifity of MRI in the
diagnosis of DVT is 100% and the accuracy is 96%.
X. MANAGEMENT
Medical management
 Anticoagulant therapy: Heparin 15,000 units followed by 10,000 units 4-6 hourly for
four to six injections when the blood coagulation is likely to be depressed to the
therapeutic level. Heparin is continued for 7-10 days or even longer if thrombosis is
severe. Prolongation of Activated Thromboplastin Time (APTT) to 1.5-2.5 times
indicate effective and safe anticoagulation. Serum heparin level should be of 0.1 to 0.2
 u/ml. Low molecular weight heparin (LMWH), can be used safely in pregnancy.
Enoxaparin 40mg daily is given. It does not cross the placenta. Fondaparinux, a
synthetic pentasaccharide can inhibit factor Xa but not thrombin. It has limited
transplacental passage. It can be used in cases with heparin induced thrombocytopenia or
heparin allergics.
 A drug of coumarin series-warfarin is commonly used orally with an overlap of atleast
three days with heparin. The intial daily single dose of 7mg for 2 days is adequate for
induction. Subsequent maintenance dose is depends upon international normalised ratio
(INR) which should be within the range of 2.0-3.0. the daily maintenance dose of
warfarin is usually 5 to 9 mg to be taken at the same time each day. The anticoagulant
therapy should continue till all evidences of he disease have disappeared which generally
take 3-6 months. The anticoagulant should not prevent the mother from breast feeding.
 Bed rest: Restriction of movement until the clotting time has shown signs of
improvement
 Analgesics are given to relieve pain in the affected area and sedative to ensure sleep.
 After about a week, on subsiding pain slight movement can be started but in case of
suspected DVT, the patient is not allowed to walk about.
Nursing Management
 Assess for the signs and symptoms of thrombo embolic disorders.
 Encourage for early ambulation even after a normal delivery in low-risk patients
 Maintain hydration
 Encourage the patients to wear compression stockings at all times except when they
are removed for skin care or bathing.
 Provide the mechanical prophylaxis includes measures such as physiotherapy and
exercises, use of compression stockings, foot pumps na dintermittent pneumatic
compression devices.
 Helps the patients to perform active and passive exercises to the lower extrimities.
 Health education
XI. COMPLICATIONS
 Pulmonary embolism
 Septic embolization
XII. PREVENTION
Prevention for venous thromboembolism in pregnancy and puerperium is done by adopting
the following measures:
a) Antepartum measures
 Advise the woman to avoid sedentary life style and to exercise as much as possible
 Recoomend plenty of water to avoid dehydration
 Advise to quit smoking
 Teach to avoid prolonged standing or sitting in one position or sitting with legs
crossed.
 Encourage elevation of legs when sitting
 Teach to avoid tight-knee hose or other constrictive garments
 Encourage to take frequent breaks during long car trips to walk around, thereby
preventing prolonged venous statsis.
 Prevention of trauma, sepsis,anaemia during pregnancy.
b) Intrapartum measures
 Early ambulation in early labour and following operative delivery are encouraged.
Later encourage leg ecercises.
 Ensure correct positioning in stirrups that minimizes pressure on the popliteal area.
 Pad the stirrups
 Use anti-embolism stockings for women who are at risk for DVT.
c) Post partum measures
 Encourage early ambulation
 Encourage fluids to avoid dehydration
 Use anti-embolism stockings with those at risk. Pneumatic compression stockings
may be ordered after cesarean birth until ambulation starts.
 Encourage elevation of legs while sitting.
 Administration of anticoagulant therapy is done for prophylactic measures. The
patient can continue feeding from breasts.
 Avoiding the use of oestrogens for suppression of lactation.
 A high risk women is one who has previous VTE in present pregnancy or
antithrombin III deficiency such women needs low molecular weight heparin
prophylaxis through out the pregnancy and postpartum 6 weeks. Women with
antithrombin III deficiency can be treated with antithrombin III concentration
prophylactically.
 B. THRMBOPHLEBITIS
INDEX
I. INTRODUCTION
II. DEFINITION
III. INCIDENCE
IV. ETIOLOGY
V. PATHOPHYSIOLOGY
VI. CLINICAL MANIFESTATIONS
VII. DIAGNOSTIC MEASURES
a. History collection
b. Physical examination
c. Investigations
VIII. MANAGEMENT
a. Medical management
b. Nursing Management
IX. COMPLICATIONS
X. PREVENTION

THRMBOPHLEBITIS
I. INTRODUCTION
Postpartum thrombophlebitis orginates into the thrombosed veins at the placental site by
organism such as anaerobic streptococci or bacteriosides. Pelvic thrmbophlebitis is a condition
which occur when the condition is localised in the pelvis.
II. MEANING
When thrombus is formed in response to inflammation in the vein wall, it is termed as
thrombophlebitis.
Thrombophlebitis is the inflammation of a vein with blood clot formation, inside the vein at
the site of inflammation. Thrombophlebitis is also known as phlebitis and phlebothrombosis.
There can be extra pelvic spread which is ,
1. Through the right ovarian vein into the inferior venacava and then to the lungs
2. Through the left ovarian vein to the left renal vein and then to the left kidney.
 3. Retrograde extension to ileofemoral vein to produce the clinicopathological entity of
phlegmasia alba dolens or white leg. The femoral vein may be directly affected from
adjacent cellulitis.
III. INCIDENCE:
Only one in every 3,000 women will develop septic pelvic vein thrombophlebitis
after delivery of their baby.
IV. RISKFACTORS
 Cesarean delivery
 Pelvic infection, such as endometritis or pelvic inflammatory disease
 Uterine fibroids.
 Miscarriage or abortion
 Gynecological diseases.
V. PATHOPHYSIOLOGY
 Blood clot forms in the veins because of blood not moving the way it should
through the leg veins (long-term bed rest such as after a major illness or surgery).
Varicose veins can lead to thrombophlebitis. This allows blood to pool in the
vessel instead of flowing straight through in one direction.
 Clots lodged in veins near the surface of the skin.
 These blocked veins can lead to infection. They can even lead to tissue damage
from the loss of healthy circulation.
 When the deep veins are involved, a piece of the clot can break off and enter the
blood stream. It can travel far from the site where it formed and cause major
problems. If the clot reaches the lungs and blocks circulation there, it can lead to
death.
VI. CLINICAL FEATURES
1. It is usually develops on the second week of puerperium
2. Mild pyrexia (38.40F) is common at times with chills and rigor.
3. Head ache, malaise and raising 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 nearly thromosed veins.
5. Polymorpho nuclear leukocytosis is evident from the blood count. Signs of toxaemia
are visible.
VII. DIAGNOSTIC MEASURES
 a) History Collection: Includes any history of infection by streptococcus or bacteriosides.
b) Physical Examination:
 Check the vital signs.
 Observation of swollen,painful,white and cold leg.
 Assess for chills, malaise and headache.
c) Investigations:
 Venous ultrasound: to visualize the thrombosed vein and to assess the extent of
infection.
 CT SCAN or by MRI to assess the thromosed vein and areas of inflammation.
 A trial of heparin therapy to be considered. When the symptoms improve with heparin
therapy, diagnosis is confirmed.
VIII. MANAGEMENT
Medical Management
 Bed rest with foot end raised above the heart level
 Analgesics to relieve pain in the infected area and sedatives to ensure sleep
 Antibiotics
 Anticoagulant therapy i.e. Heparin therapy is started and continued for 7-10 days or more.
The dose depends upon the estimation of clotting time which should done daily. Heparin
15,000 units followed by 10,000 units 4-6 hourly for four to six injections when the blood
coagulation is likely to be depressed to the therapeutic level. It is followed by warfarin
(oral). The dose of warfarin is adjusted by estimating prothrombin time of blood. The intial
daily single dose of 7mg for 2 days is adequate for induction. The daily maintenance dose of
warfarin is usually 5 to 9 mg to be taken at the same time each day.
NURSING MANAGEMENT
IX. PREVENTION Same as of thrombosis
X. COMPLICATIONS
 Septic pelvic thrombophlebitis
 Septic embolization
 Pulmonaryabscesses

C. PULMONARY EMBOLISM
INDEX
 I. INTRODUCTION
II. DEFINITION
III. INCIDENCE
IV. RISKFACTORS
V. PATHOPHYSIOLOGY
VI. CLINICAL MANIFESTATIONS
a) Minor pulmonary embolism
b) Major pulmonary embolism
VII. DIAGNOSTIC MEASURES
a) History collection
b) Physical examination
c) Investigations
VIII. MANAGEMENT
a) Medical management
b) Surgical management
c) Nursing mangement
IX. COMPLICATIONS
X. PREVENTION

PULMONARY EMBOLISM

I. INTRODUCTION
Pulmonary embolism is the leading cause of maternal deaths in many centres specially in the
developed countries after the sharp decline of maternal mortaity due to haemorrhage, hypetension
and sepsis. While deep venous thrombosis in the leg or in the pelvis is most likely the cause of
pulmonary embolism, but in about 80-90%, it occur without any previous clinical manifestations of
deep vein thrombosis.
II. DEFINITION
Whenever there is venous thrombosis in legs or pelvis, the thrombus (clot) breaks away
from the vessel and enters the systemic circulation. When it reaches in pulmonary artery, it causes
obstruction due to smaller lumen, then the condition known as pulmonary embolism.
III. INCIDENCE
 The incidence of pulmonary embolism in the united states is estimated to be one case per 1000
persons per year.
IV. RISKFACTORS
 Caesarean section
 Obesity
 High parity
 Immobility
 Trauma to legs
 Smoking
V. PATHOPHYSIOLOGY
A piece of blood clot becomes detached from the thrombus in the veins of the pelvis or lower limbs
Travel through inferior vena cava to the right side of the heart and via the pulmonary artey to the
lungs.
It causes an obstruction as soon as it reaches a vessel with a lumen smaller than it impairing
circulation to the particular area.
Obstructing the pulmonary blood flow to one or both sides.
VI. CLINICAL MANIFESTATIONS
The clinical features depends on the size of the embolus and on the preceding health status of
the patient.
a) In case of minor pulmonary embolism:
 Chest pain, dyspnoea, hemoptysis
 Tachycardia
b) Major pulmonary embolism:
 Dyspnoea
 Hypotension
 Pyrexia
 Cyanosis
 Distension of jugular vein
 The patient turns pale, dyspnoeic, perspires, hypotensive and distressed. Collapse,
respiratory failure and cardiac arrest ,may follow.
  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 vaginal
inhibition.
VII. DIAGNOSTIC MEASURES
a) History Collection: History of deep vein thrombosis in the legs or pelvis
b) Physical Examination:
 Assess for rise in temperature, pulse and respiration and fall in blood pressure.
 Assess the breathing pattern
 Observe for chest pain, dyspnea
 Observe for oedema on the legs and homan’s sign.
c) Investigations
 Chest X ray shows diminished vascular supply in the areas of infarction, elevation of dome
of diaphragm and often pleural effusion. It is useful to rule out pneumonia, pulmonary
infiltrates and atlectasis
 ECG: tachycardia, right axis shift, non specific ST change
 Pulmonary angiography: Tge trest confirms the diagnosis
 Altered blood gas analysis: Raised alveolar oxygen partial pressure and arterial,oxygen
partial pressure due to hyperventilation occurs. PO2 >85 mm Hg on room air is reassuring
but doesnot rule out PE. Oxygen saturation <95% on room air needs further investigation
 D-Dimer: A negative D-Dimer value may rule out the diagnosis of PE.
 Doppler’s ultrasound: Shows positive result, therefore anticoagulant therapy is indicated.
 Lung scans: Perfusion scan will detect areas fo diminished blood flow where as a reduction
in perfusion with maintenance of ventilation indicates pulmonary embolism
 MRI: can be used in pregnancy as the risk of ionising radiation is absent
 Pulmonary angiography: is accurate to the diagnosis but has got high risks of complications
 Spiral Computed Tomographic Pulmonary Angiography( Spiral CT): Using an IV contyrast
is now the preferred screening and diagnostic modality for PE
 Magnetic Resonance Angiography(MRA) with IV gadolinium: MRA has got semsitivity of
100% and specificity of 95% in the diagnosis of PE.

VIII. MANAGEMENT
a) Medical Management
 Resuscitation: Cardiac massage, oxygen therapy and intravenous heparin bolus dose of 5000
Iu and morphine 15mg (IV) are started. Heparin remains tghe main stay of therapy for VTE.
Heparin therapy is to be continued up to 40,000 IU per day so as to maintain the clotting
time to over 12 minute for the first 48 hours. Heparinlevel is maintained at 0.2 to 0.4
units/ml or activated partial thromboplastin time (APTT) about twice the normal.
 Administration of oxygen in fowler’s position.
 IV fluid supplementation
 Blood pressure is to be maintained by dopamine/ adrenaline drip.
 Tachycardia is conteracted by digitalis
 Thromboembolytic therapy with streptokinase
 Digitalisation to counteract tachycardia
 Pain may be relieved with intravenous administration of Morphine.
 Fibrinolytic agents: streptokinase produce rapid reduction of pulmonary embolism
b) Surgical Management
 Recurrent attacks of pulmonary embolism necessitate surgical treatment like
embolectomy,Venous thrombectomy, placement of caval filter or ligation of inferior vena cava
and ovarian veins, depending upon the severity or extent of embolus or the findings of
pulmonary angiography.
 Venacaval filters are used for patient with pulmonary embolism or anticoagulant therapy is
failed. Venacava may be completely ligated by teflon clips.
c) Nursing Management
 Assess for the signs and symptoms of thrombo embolic disorders.
 Encourage for early ambulation even after a normal delivery in low-risk patients
 Maintain hydration
 Encourage the patients to wear compression stockings at all times except when they are
removed for skin care or bathing.
 Provide the mechanical prophylaxis includes measures such as physiotherapy and exercises,
use of compression stockings, foot pumps na dintermittent pneumatic compression devices.
 Helps the patients to perform active and passive exercises to the lower extrimities.
 Health education
IX. COMPLICATIONS
 Pulmonary hypertension: Large number of clots obstruct blood flow in the vessels of
lungs.
  Heart damage
X. PREVENTION
 Preventing pulmonary embolism focuses on lowering risk factors associated with the
disease.
 It begins with preventing deep vein thrombosis.
 Use compression stockings to prevent DVT
 Early and regular ambulation
 Active leg exercises to avoid venous stasis

POST PARTUM HAEMORRHAGE

INDEX
I. INTRODUCTION
II. DEFINITION
III. INCIDENCE
IV. RISKFACTORS
V. TYPES
a) Depending on the amount of blood loss
b) Depending on the time of occurence
i) Primary PPH
ii) Secondary PPH
VI. ETIOLOGY
a) Primary PPH
a. Third stage haemorrhage
b. True PPH
b) Secondary PPH
VII. CLINICAL MANIFESTATIONS
VIII. DIAGNOSIS
a) History collection
b) Clinical examination
c) Investigations
IX. MANAGEMENT
a. Management of third stage haemorrhage
 b. Management of True PPH
c. Management of Secondary PPH
d. Nursing management
X. COMPLICATIONS
XI. PREVENTION
a) Antenatal
b) Intranatal

POSTPARTUM HAEMORRHAGE

I. INTRODUCTION
The third stage of labour starts after the delivery of the fetus and ends at the delivery of the
palcenta and membranes. Of all the stages of labour, third stage is the most crucial one for the
mother. PPH is one of the most common obstetric complications and one of the major causes of
maternal mortality.
II. DEFINITION
Any amount of bleeding from or into the genital tract following delivery of the baby
upto the end of puerperium which adversely affects the general condition of the patient
evidenced by rise in pulse rate and fall in blood pressure is called PPH.
PPH: Exceeding 500ml after vaginal delivery
Exceeding 1000ml after Cs
Exceeding 1500ml after Cs with hysterectomy.
III. INCIDENCE
PPH is the leading cause of maternal mortality worldwide with a prevalence rate of
approximately 6%. In Africa and Asia, where most maternal deaths occur, PPH accounts
for more than 30% of all maternal deaths.
IV. RISKFACTORS
 Conditions that distend the uterus beyond average capacity: Mulptiple
gestations,hydramnios, a large baby and presence of uterine myomas
 Conditions that could have caused cervical or uterine lacerations: A woman who
underwent operative birth or rapid birth develop lacerations that would cause
bleeding.
  Conditions with varied placental site attachement.
V. TYPES
a) Depending on the amount of blood loss
1) Minor <1L
2) Major>1L
3) Severe>2L
b) Depending on the time of occurence of bleeding
1) Primary PPH
2) Secondary PPH
1) Primary PPH
Haemorrhage occurs within 24hrs following the birth of the baby. In the majority of
haemorrhage occurs within 24hrs following delivery.
Two types
• Third stage haemorrhage:bleeding occurs before expulsion of placenta
• True PPH:Bleeding occurs subsequent to expulsion of placenta
2) Secondary PPH
• Haemorrhage occurs beyond 24 hours and within puerperium also called delayed or late
puerperal haemorrhage.
• Bleeding usually occurs between 5th to 14th day of delivery.
VI. ETIOLOGY
a) Primary PPH
1) Atonic
2) Traumatic
3)Mixed
4)Blood coagulopathy
1) Atonic uterus: Failure of uterus to contract and retract following the delivery. Condition
which often interefer with retraction of the uterus as a whole and of placental site.
• Grand multipara:Inadequate retraction and frequent adherent placenta contribute to
it.Associated anemia may also probably play a role.
• Over distension of the uterus: as in multiple preganacy,hydramnios and large baby.
Imperfect retraction and a large placental site are responsible for excessive bleeding.
• Malnutrition and anaemia: Even slight amount of blood loss may develop clinical
manifestation of PPH
• APH
• Prolonged labour:Poor retraction,infection,dehydration and analgesic drugs used during
labour.
• Anaesthesia:depth of anaesthesia and anaesthetic agents (ether, halothane or cyclopropane)
which causes atonicity.
• Initiation or augmentation of delivery by oxytocin:post delivery uterine atonicity is likely
unless the oxytocin is continued for atleast one hour following delivery.
• Persistent uterine distention:retention of partially seperated placenta or bits of placenta or
blood clots interfere with effective retraction.
• Malformation of the uterus: Implantation of the placenta in the uterine septum of a septate
utreus or in the cornual region of a bicornuate uterus may cause excessive bleeding.
• Uterine fibroid:causes imperfect retraction mechanically.
• Mismanaged third stage of labour: This includes
• Too rapid delivery of the baby preventing uterine wall to adapt to the diminishing
contents
• Premature attempt to deliver the placenta before it is separated.
• Kneading and fiddling the uterus
• Pulling the cord. All these produce irregular uterine contractions leading to partial
seperation of placenta and haemorrhage.
• Manual seperation of the placenta increases blood loss during caesarean delivery.
• Constriction ring: Hour glass contraction formed in the upper segment across the
partially seperated placenta or at the junction of the upper and lower segment with the fully
seperated placenta trapped in the upper segment may produce excessive bleeding.
• Precipitate labour: In rapid delivery seperation of the placenta occurs following the
birth of the baby. Bleeding continues before the onset of uterine retraction.
2) Traumatic
Trauma to the genital tract usually occurs following operative delivery, even after
sponatneous delivery. Blood loss from the episiotomy wound is often underestimated. Blood
loss in caessarean section amounting to 800-1000ml is most often ignored. Trauma involves the
cervix, vagina,perineum, para-urethral region, rupture of the uterus.
3)Mixed
 Combination of atonic and traumatic causes.
4)Blood coagulopathy (acquired or congenital)
Condition where such disorder may occur are abruptio placenta, jaundice, pergnancy,
thrombocytopenic purpura, HELLP syndrome or in IUD.
b)Secondary PPH
 retained bits of cotylidon or membranes
 Infection and separation of slough over a deep cervico vaginal laceration
 Endometritis and subinvolution of placental site.
 Secondary haemorrhage from Cs section occurs between 10-14 days
 Withdrawal bleeding following estrogen therapy
 Other causes are chorion epithelioma occurs usually beyond 4 weeks of delivery, carcinoma
cervix, placental polyp, infected fibroid or fibroid polyp and puerperal inversion of uterus.
VII. CLINICAL MANIFESTATIONS
 Heavy vaginal bleeding: more than 500ml in a normal vaginal delivery and more than
1000ml in a cesarean section.
 Tense and rigid uterus
 Anemia
 Hypotension
 Tachycardia
VIII. DIAGNOSIS
a) History Collection:History of Parity, duration of labour, operative delivery, uterine fibroid,
malformation of uterus and anemia.
b) Clinical Examination
– Bleeding may be in bright red and of varying amount
– Internal examination reveals evidence of sepsis,subinvolution of the uterus.
– Uterus is flabby and becomes hard on massaging.
c) Investigations
– Ultrasonography is useful in detecting the bits of placenta inside the uterine cavity.
– Blood test: Low hemoglobin
IX. MANAGEMENT
a) Management of third stage bleeding
Principles:
– To empty the uterus of its contents and to make its contract
– To replace the blood
– To ensure haemostasis in traumatic bleeding
Steps of management
– Placental site bleeding
– Traumatic bleeding
1)Placental site Bleeding
– To palpate the fundus and uterus to make it hard.:Massage is done by placing four
fingers behined the uterus and thumb infront of bleeding continues after the uterus becomes
hard, suggests the presence of genital tract injury
– Ergometrine 0.25mg or methergin 0.2mg is given intravenously
– To start dextrose saline drip and arrange for blood transfusion if necessary.
– To catheterize the bladder, if it is found to be full.
– Sedation may be given with morphine 15mg intramuscularly
2) Management of Traumatic bleeding
– The uterovaginal canal is to be explored under GA after the placenta is expelled and
haemostatic sutures are placed on the offending sites.
Principles
 To diagnose the cause of bleeding, atonic or traumatic
 To take prompt and effective measure to control bleeding
 To correct hypovolemia.
b) Management of true PPH
Scheme of management of true PPH
 Immediate measures
 Call for extra help
 Commence IV line witha wide bore cannula
 Send blood for cross matching and ask for 2
units of blood
 Rapidly infuse normal saline 2 litres till blood
is available.

To feel the uterus by abdominal palpation

Uterus atonic Uterus hard and contracted
(traumatic)
 Massage the uterus to make it hard
 Inj.methergin 0.2mg IV
 To add oxytocin 10 units in 500ml of normal Exploration
saline at the rate of 40 drops per minute.
 To examine the expelled placenta
 To catherterize the bladder. Haemostatic sutures on the tear sites.

Uterus remains atonic

 Exploration of the uterus
 Blood transfusion
 To continue oxytocin drip
Uterus atonic
 15 methyl PGF2 α250µg IM/ intramyometra
 Or
 Misoprostol 1000µg per rectum.
Uterus atonic

Uterine tamponade
 Bimanual compression
 Tight intrauterine packing under anaesthesia
 Insertion of a sengstaken blakemore tube and inflation
Uterus atonic

Surgical methods
 Ligation of uterine artery and utero-ovarian
 anastomatic vessels unilateral or bilateral
 Ligation of anterior diversion of
  internal iliac artery (unilateral or bilateral)
 B.Lynch brace sutures
 Angiographic arterial embolisation with gelatin sponge
Hysterectomy (rarely)

c) Management of secondary postpartum haemorrhage

Principles
 To assess amount of blood loss and to replace the lost blood
 To find out the cause and to take appropriate steps to rectify it.
Supportive therapy:
 Blood transfusion
 To administer ergometrine 0.5mg IM,if the bleeding is uterine in origin.
 To administer antibiotics as routine
Conservative :
If the bleeding is slight and no apparent cause is detected, a careful watch for a period of 24
hrs or so is done in the hospital.
Active treatment:
As the commonest cause is due to retained bits of cotyledon or memebranes, it is
preferable to
– Explore the uterus urgently under GA
– Gentle curettage is done by using flushing curette
– Ergometrine 0.5mg is given IM
– The materials removed are to be sent for histological examination
– Presence of bleeding from the sloughing wound of cervico vaginal canal should be
controlled by haemostatic sutures
– Secondary haemorrhage following Cs section may require laparotomy
– Bleeding from uterine wound can be controlled by haemostatic sutures may rarely
require ligation of internal iliac artery or may end in hysterectomy.
d) Nursing Management
 Assess the amount of bleeding, vital signs, signs of shock
  Place the woman in a side lying position to make sure that no blood is pooling
underneath her
 Save all perineal pads used during bleeding and weigh them to determine the amount of
blood loss
 Assess lochia frequently.
X. COMPLICATIONS
 Blood loss
 Shock
 Death due to blood loss
 Septicemia

XI. PREVENTION
PPH cannot always be prevented.
a) Antenatal
• Improvement of health status of the patient and to keep the haemoglobin level normal
(>10gm/dl)
• High risk patients who are likely to develop post partum haemorrhage (such as twins,
hydramnios,grand multipara, APH, severe anaemia) are to be screened and delivered in a well
equipped hospital.
• Blood grouping should be done for all women so that no time is wasted during emergency.
b) Intranatal
• Slow delivery of the baby is done : Baby should be pushed out by the retracted
uterus and not to be pulled out.
• Expert obstetric anaesthetist is needed when the delivery is conducted under general
anaesthesia. Local or epidural anesthesua is preferable in forceps, ventouse or breech delivery.
• During caesarean section spontaneous seperation and delivery of the placenta
reduces blood loss
• Active management of the third stage specially of the at risk patients should be a
routine.
• Temptation of fiddling or kneeding with the uterus or pulling the cord should be
avoided.
• Examination of the placenta and membranes should be routine so as to detect at the
earliest any nursing part.
• In all cases of the induced or accelerated labour by oxytocin, the infusion should be
continued for atleast one hour after delivery.
• Exploration of the utero vaginal canal for evidence of trauma following difficult
labour or instrumental delivery.
• To observe the patient for about two hours after the delivery and if the uterus remain
hard and contracted only then she should be sent to the ward.
All said and done, it is the intelligent anticipation, skilled supervision, prompt detection
and effective institution of therapy that can prevent an otherwise normal care from undergoing a
disastrous consequences.

SUBINVOLUTION OF UTERUS
INDEX
I. INTRODUCTION
II. MEANING
III. INCIDENCE
IV. CAUSES
a) Predisposing factors
b) Aggravating factors
V. PATHOPHYSIOLOGY
VI. CLINICAL MANIFESTATIONS
a) Symptoms
b) Signs
VII. DIAGNOSIS
a) History collection
b) Physical examination
c) Investigations
VIII. MANAGEMENT
a) Medical management
b) Nursing management
IX. COMPLICATIONS
 X. PREVENTION
SUBINVOLUTION OF UTERUS
I.INTRODUCTION
Subinvolution is the failure of the uterus to return to a nonpregnant state . The uetrus is 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.
II. MEANING
Subinvolution is a medical condition in which after childbirth, the uterus does not return to its
normal size.
When the involution is impaired or retarded it is called subinvolution.
III INCIDENCE
The incidence is one per 2500 deliveries. The incidence has increased 10 fold in the past 50
years.
IV. CAUSES
a) Predisposing factors
 Grand multiparity
 Over distension of uterus as in twins and hydramnios
 Maternal ill health
 Caesarean section
 Prolapse of the uterus
 Retroversion after the uterus becomes pelvic organ
 Uterine fibroid
b) Aggravating factors
 Retained products of conception
 Uterine sepsis
V. PATHOPHYSIOLOGY
After birth with the uterine contractions, the uterus has to shrink back down to its pre-
pregnancy shape and size.

These contractions are the postpartum cramps (afterbirth pains) usually over within the
first day or 2 days after giving birth.
 Uterus continues to contract after this. If the process happens too slowly, the uterus
remains enlarged.

Subinvolution.

VI. CLINICAL MANIFESTATIONS

The condition may be asymptomatic
The predominant symptom
 Abnormal lochia discharge either excessive or prolonged
 Irregular or at times excessive uterine bleeding
 Irregular cramp like pain in cases of retained products or rise of temperature in
sepsis.
Signs:
 The uterine height is greater than the normal for the particulars
 Normal puerperal uterus may be displaced by a full bladder or a loaded rectum,it feels
boggy and softer
 Presence of features responsible for subinvolution may be evident.
VII. DIAGNOSIS
a) History collection: Assess the history of prolapsed uterus, fibroid, multiple gestation and
the history of any uterine infection.
b) Physical examination: Abnormal lochial discharge, fatigue and backpain.
Bimanual examination:uterus is larger and softer than normal
Internal examination shows massive bleeding and evidence of sepsis
c) Ultrasonography:detects the bits of placenta inside the uterine cavity.
VIII. MANAGEMENT
a) Medical management:
 Exploration of the uterus in retained products
 Methergine 0.2mg PO q4 x 24hrs.
 Antibiotics in endometritis: T.Cindamycin 900mg,Inj. Gentamicin 1.5mg/Kg, Inj.Ampicillin
sulbactam (1.5gm)
 Pessary in prolapse or rectoversion (plastic or metal ring shaped device inserted to vagina to
support a prolapsed uterus.
 b) Nursing management
 Daily evaluation of fundal height to document involution.
 Check the vital signs
 Check the amount of bleeding
 Provide psychological support to the patient
 Assess the level of pain and take the adequate measures to reduce the abdominal
pain.
IX. COMPLICATIONS
 Continuous bleeding lead to shock
 Infections of the reproductive tract.

X. PREVENTION
 Adequate breastfeeding releases the oxytocin that triggers uterine contractions.
 Adequately check whether the placenta is expelled completely or not.
 Provide appropriate antibiotics and reduce the risk of infection.
 Ensure safe hygienic method of delivery
PSYCHOLOGICAL COMPLICATIONS
In the first three months after delivery the incidence of mental illness is high. Three
psychiatric disorders may arise in the post partum period.
1. Post partum blues
2. Post partum depression
3. Post partum psychosis
High risk factors for post partum mental illness
 Past history: Psychiatric illness
 Family history:major psychiatric illness, mental conflict
 Present pregnancy: Caesarean delivery, difficult labour, neonatal complications
 Others: Unmet expect
PUERPERIAL BLUES
INDEX
I. INTRODUCTION
II. MEANING
III. INCIDENCE
 IV. CAUSES
V. PATHOPHYSIOLOGY
VI. CLINICAL MANIFESTATIONS
VII. MANAGEMENT

I. INTRODUCTION
Post partum blue is a transient condition that 75-80% of mothers could experience
shortly after childbirthg witha wide variety of symptoms which generally involve mood
lability, tearfulness and some mild anxiety and depressive symptoms.
II. MEANING
It is a transient state of mental illness observed 4-5 days after delivery and it last for few
days.
III. INCIDENCE
75-80% of mothers could experience shortly after child birth.
IV. CAUSES
Exact cause is unknown
Hormonal changes
V. PATHOPHYSIOLOGY
 After the placenta is delivered, the placental hormones shuts down causing radical changes
in hormone levels.
 Symptoms occurs due to withdrawal from the high pregnancy levels of estrogen,
progesterone and endorphins.
 Combined with the shift in hormone levels in the physical, mental and emotional exhaustion
as well as sleep deprivation typical of parenting a newborn.
VI. CLINICAL MANIFESTATIONS
 Depression
 Anxiety
 Fearfulness
 Insomnia
 Helplessness
 Negative feeling towards infant
 No specific metabolic or endocrine abnormalities have been detected. But lowered
tryptophan level is observed. It suggests altered neuro transmitter function.
VII. MANAGEMENT
Reassurance and psychological support by the family members.
POSTPARTUM DEPRESSION
INDEX
I. INTRODUCTION
II. MEANING
III. DEFINITION
IV. INCIDENCE
V. RISKFACTORS
VI. ETIOLOGY
VII. PATHOPHYSIOLOGY
VIII. CLINICAL MANIFESTATIONS
a) Emotional
b) Behavioral
c) Cognition
IX. MANAGEMENT
a) Medical management
b) Nursing mangement
X. COMPLICATIONS

POSTPARTUM DEPRESSION

I. INTRODUCTION
Postpartum depression is a type of mood disorder associated with childbirth. It is more
gradual in onset over the first 4-6 months following delivery or abortion.
II. MEANING
It is a severe form of depression or elation occuring in the first few weeks after the
baby is born.
III. DEFINITION
 A feeling of sadness that occurs for more than a year after the postpartum period and
interferes with the normal functions of the mother is called postpartum depression.
IV. INCIDENCE
It is observed in 10-20% of mothers.
V. RISKFACTORS
 Prior episode of postpartum depression
 Bipolar disorder
 Family history of depression
 Psychological stress
 Complications of childbirth
 Lack of family support
 Drug use disorder
 Stressful life events experienced during pregnancy.
 Maternity blues
 Previous stillbirth or miscarriage
 Cigarette smoking
 Low self esteem
 Low social support
 Poor marital relationship or single marital status
 Unplanned or unwanted pregnancy
 Elevated prolactin levels
 Oxytocin depletion
VI. ETIOLOGY
 The cause of puerperal depression is unclear. It is a biological including the hormonal
changes that occur following childbirth . Changes in the hypothalamo-pituitory adrenal
axis may be a cause.
 Women with a history of manic depression have the greater risk.
 Women which have caesarean section or still birth.
VII. PATHOPHYSIOLOGY
An anticlimactic feeling is experienced by the woman after birth.
Hormonal changes in estrogen, progesterone and gonadotropin-releasing hormone rises
and falls.
VIII. CLINICAL MANIFESTATIONS
a) Emotional
 Persistent sadness, anxiousness or empty mood
 Severe mood swings
 Frustration, irritability, restlessness, anger
 Feeling of hopelessness or helplessness
 Guilt, shame, worthlessness
 Low self esteem
 Inability to be comforted
 Trouble bonding with the baby
b) Behavioral
 Lack of interest or pleasure in usual activities
 Low or no energy
 Low libido
 Changes in apetite
 Fatigue, decreased energy and motivation
 Poor self care
 Social withdrawal
 Insomina or excessive sleep
c) Cognition
 Diminished ability to make decisions and think clearly
 Lack of concentration and poor memory.
 Worry about harming self, baby or partner.
Risk of recurrence is high (50-100%) in subsequent pregnancies.
IX. MANAGEMENT
a) Medical management
 Fluoxetine or paroxetine (serotonin uptake inhibitors), 20mg once a day is effective
and has fewer side effects.
 General supportive measures like reassurance and psychological support are essential
 If no prompt response with medication, psychiatric consultation is needed.
 Psychotherapy.
  Cognitive behavioral therapy: reduces the negative parenting behavior scores and
lower rates of anxiety, stress and depression.
b) Nursing Management
 Assess the woman’s psychological health even before the delivery
 Assess her history of illnesses to determine if she needs any counseling prior to
her delivery to avoid postpartum depression.
 Assist the woman in planning for her daily activities, such as her nutrition
program, exercise and sleep.
 Encourage the woman to keep in touch with her social circlke as they can also
serve as her support system.
 Advise the woman to take some time for herself every day so she can have a
break from her regular baby care.
X. COMPLICATIONS
 Postpartum psychosis
 Psychiatric emergency
 Bipolar disorder.
POST PARTUM PSYCHOSIS (SCHIZOPHRENIA)
INDEX
I. INTRODUCTION
II. MEANING
III. INCIDENCE
IV. RISKFACTORS
V. CLINICAL MANIFESTATIONS
VI. MANAGEMENT
Medical management
Nursing management
VII. PREVENTION OF POSTPARTUM PSYCHIATRIC DISORDER

POST PARTUM PSYCHOSIS (SCHIZOPHRENIA)

I. INTRODUCTION
 Postpartum psychosis typically occurs around the time of delivery and affects less than 1%
of women. The cause is unknown. It begins suddenly in the first two weeks after childbirth.
II. MEANING
Postpartum psychosis is a rare psychiatric emergency in which symptoms of high mood and
racing thoughts (mania), depression, severe confusion, hallucinations and delusions.
III. INCIDENCE
Observed in about one in 500 to 1000 mothers commonly seen in women with past history
of psychosis or with a positive family history.
IV. RISKFACTORS
 Family history of postpartum psychosis have high risk, about 25-50% of women
in this group will have postpartum psychosis, around 37% of women with bipolar
disorder have a severe postpartum episode.
 For a woman with no history of mental illness who has a close relative ( a mother
or sister) who had postpartum psychosis, the risk is about 3%.
 Genetic factors: Mutations in chromosome 16
 Autoimmune thyroid dysfunction
 Other factors: Pregnancy and delivery complications, caesarean section, sex of
the baby, length of the pregnancy.
V. CLINICAL MANIFESTATIONS
 The symptoms vary and can change quickly
 Onset is relatively sudden usaully within 4 days of delivery. The most severe
symptoms last from 2 to 12 weeks, and recovery takes 6 months to a year.
 Manifested by fear, restlessness,confusion followed by hallucination,delusion and
disorientation (usually manic or depressive).
 Suicidal, infanticidal impulses may be present. In the case temporary separation and
nursing supervision is needed.
 Risk of recurrence in the subsequent pregnancy is 20-25% and there is increased risk
of psychotic illness outside pregnancy also.
VI. MANAGEMENT
a) Medical Management
 Psychiatrist must be consulted urgently
 Admission is needed
 Chlorpromazine 150mg stat and 50-150mg three times a day is started.
 Sublingual oestrdiol (1mg thrice daily) results in significant improvement.
 Electroconvulsive therapy is considered if not responded to drugs. Lithium is
indicated in mania depressive psychosis( in that case breast feeding is contraindicated).
b) Nursing Mnangement
 Help parents understand the lifestyle changes and role demands
 Provide realistic information
 Dispel myths about the perfect mother or the perfect newborn
 Educate about the possibility of postpartum blues
 Educate about the symprtoms of poatpartum depression
VII. PREVENTION OF POSTPARTUM PSYCHIATRIC DISORDERS
 Help parents understand the lifestyle changes and role demands.
 Provide realistic information
 Anticipatory guidance
 Dispel myths about the perfect mother or the perfect newborn.
 Educate about the possibilty of postpartum blues.
 Educate about the symptoms of postpartum depression.

NURSING DIAGNOSIS (ABNORMAL PUERPERIUM)

PPH
1. Fluid volume deficit related to excessive vaginal bleeding as manifested by
decreased blood pressure.
2. Acute pain(abdomen) related to infection process/ subinvolution/retention of
clots/LSCS as evidenced by verbalization.
3. Anxiety related to disease condition as evidenced by asking doubts.
BREAST COMPLICATIONS
4. Insufficient breast milk secretion related to stress/ hormonal changes/ inadequate
intake of food as evidenceed by baby frequently cry
5. Ineffective breast feeding pattern related to breast complication as evidenced by
verbalization/observation
6. Imabalanced nutritional status less than body requirement related to loss of apetite/
infections/ stress process as evidenced by verbalization
 7. Disturbed sleep pattern related to hospitalization/ disease condition as evidenced by
verbalization.
PUERPERAL INFECTION
1. Risk for spread of infection related to entry of micro-organisms
 Review prenatal, intranatal and postnatal records
 Maintain strict handwashing policy for staff, client and visitors
 Provide for and instruct client in proper disposal of contaminated
dressings, perineal pads and disposable draw sheets
 Implement isolation setup if indicated
 Demonstrate and encourage correct perineal cleaning after voiding and
defecation and frequent changing of perineal pads.
 Demonstrate proper fundal massage. Review importance and timing of
procedure.
 Monitor temperature, pulse and respiration,note presence of chills or
reports of anorexia or malaise.
 Observe and record other signs of infection such as fowl smelling, lochia
or drainage, subinvolution of the uterus, extreme uterine tenderness and
edema.
 Monitor parenteral fluid intake, stress the need for atleast 2000ml of fluid
per day. Note urine output, degree of hydration and presence of nausea,
vomiting or diarrhoea.
 Encourage semi fowlers position
 Promote early ambulation balance with adequate rest
 Administer antibiotics as indicated.
2. Imbalanced nutrition less than body requirement related to infections
 Encourage choice of foods, high in protein, iron and vitamin C when oral
intake is permitted.
 Promote intake atleast 2000ml/day of juices, soups and other nutrition
fluids.
 Encourage adequate rest and sleep.
 Administer parenteral fluid nutrition as indicated
 Administer iron preparation and or vitamins as indicated.
3. Acute pain related to infection process
  Assess nature of discomfort or pain
 Provide instruction regarding and assist with maintenance of hygiene and
warmth.
 Change clients position frequently provide comfort measures eg:
backrubs, linen changes.
 Instruct client in relaxation techniques. Provide diversional activities such
as radio, television or reading if appropriate.
 Administer analgesics or antipyretics.
URINARY COMPLICATIONS
 Altered urinary elimination related to urinary tract infection
 Hyperthermia related to increased metabolic rate, due to illness or trauma.
Nursing Intervention
 Review the lab tests.
 Determine the patient’s previous pattern of elimination
 Palpate the bladder to assess retention.
 Encourage fluid intake to maintain renal function and prevent infection.
 Keep the perinela/vulval area clean and dry to reduce the risk of infection.
 Monitor the vital signs.
 Encourage the woman to void frequently and to empty the bladder completely with
each voiding.
 Advice the woman to wear cotton underpants.
 Wash the perineal area after each voiding
Teach the woman about UTI, its prevention and about complications.
THROMBOEMBOLIC DISORDERS
 Impaired peripheral tissue perfusion related to venous stasis
 Check the vital signs
 Assess for and report he signs and symptoms of diminished tissue perfusion
(decreased blood pressure, restlessness, confusion, cool extremities,
diminished or absent peripheral pulses, slow capillary refill, edema and
oliguria)
 Administer oxygen
 Monitor the peripheral pulses
  Impaired cardio pulmonary tissue perfusion related to pulmonary embolism secondary to
dislodgement of deep vein thrombus
 Check the vitak signs
 Monitor the oxygen saturation
 Monitor the cardiac output
 Administer oxygen via nasal prone / mask
 Risk for fluid volume deficit related to blood loss secondary to over heparinization.
 Assess the client’s hydration status
 Maintain intake/output chart
 Encourage to take plenty of fluids
 Watch for haemorrhage
PSYCHOLOGICAL COMPLICATIONS
 Ineffective individual coping related to postpartum depression
 Risk for altered p[arenting related to postpartal mental illness
 Risk for violence against self (suicide), newborn and other children related to depression.