PUERPERIUM COMPLICATION

By:Varsha Sharma

SUBINVOLUTION

 Subinvolution is a medical condition in which after

childbirth, the uterus does not return to its normal
size.

DEFINITION:
When the involution is impaired or retarded it is called
subinvolution. The uterus is the most common organ affected
by subinvolution. As it is the most accessible organ to be
measured per abdomen, the uterine involution is considered
clinically as an index to assess sub involution.

CAUSES
Predisposing factors are
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

Aggravating factors are:

Retained products of conception

Uterine sepsis (endometritis)

Factors that may cause sub involution

Persistent lochia/fresh bleeding

Long labor, anesthesia, full bladder,
difficult delivery, retained placenta,
infection

SYMPTOMS
The condition may be asymptomatic. The
predominant symptoms are:
Abnormal lochial discharge either excessive or
prolonged
Irregular or at times excessive uterine bleeding
Irregular cramp like pain is cases of retained
products or rise of temperature in sepsis

SIGNS

The uterine height is greater than the

normal for the particular day of
puerperium. Normal puerperal uterus
may be displaced by a full bladder or
a loaded rectum. It feels boggy and
softer

MANAGEMENT
Antibiotics in endometritis
Exploration of the uterus in retained products
Ergometrine so often prescribed to enhance
the involution process by reducing the blood
flow of the uterus is of no value in
prophylaxis.

NURSING MANAGEMENT

Encourage early ambulation in postnatal

period
Daily evaluation of fundal height and
documentation.

URINARY
COMPLICATIONS IN
PUERPERIUM

1.
2.
3.
4.

Urinary tract infection

Retention of urine
Incontinence of urine
Suppression of urine

URINARY TRACT INFECTION

Is most common cause of puerperal pyrexia
Incidence 1-5% of all deliveries
The infection may be the consequence of any of the following
Recurrence of previous cystitis or pyelitis
Asymptomatic becomes overt
Infection Contracted for the first time during puerperium is due to
Effect of frequent catheterization either during labor Or in early puerperium to
relieve retention of urine.
Stasis of urine during early puerperium due to lack of bladder tone and less desire to
pass urine

Organisms responsible are:-

E.coliKlebsiella- Proteus- Staph.

Aureus

MANAGEMENT

Antibiotics

RETENTION OF URINE

This is a common complication in early puerperium

CAUSES ARE
Bruising & edema of the bladder neck
Reflex from perineal injury
Unaccustomed position

Treatment of retention of urine:

If simple measure fails to initiate micturation, an
indwelling catheter is to be kept in situ for about 48
hours.
This not only empties the bladder but helps in
regaining the normal bladder tone and sensation of
fullness.
Appropriate urinary antiseptics should be
administered for about 5-7days.

INCONTINENCE OF URINE

This is not a common symptom following birth.

Incontinence may be -

Overflow incontinence
Stress incontinence: Usually manifests in late
puerperium

True incontinence: In the form of genito urinary

fistula usually appears soon following Delivery or within
1st week of puerperium. Stress incontinence is
established by noting the escape of urine through the
urethral opening during stress. The exact nature of
urinary fistula is established by noting the fistula site by
examining the patient in Sims position using Sims
speculum or by three swab test if the fistula is tiny.

NURSING MANAGEMENT
Encourage urination early in the postnatal period.
Encourage to void every 2-4 hrs
Assist the mother to the bathroom or at bed side on bed pan.
Monitor intake and output
Monitor for frequency and volume of urine
If the mother is unable to void catheterize her
Monitor for any signs of infection of urinary tract if, any
report immediately.

John et. Al Vol.181(2) Pages 266273,August 1999,Urinary

incontinence in pregnancy and the puerperium: A prospective study
Objective: Pregnancy and childbirth are commonly thought to be associated with the
development of urinary incontinence and lower urinary tract symptoms. The purpose of this
study was to assess the relationship, if any, between pregnancy and the development of
lower urinary tract symptoms. Study Design: A prospective study of lower urinary tract
symptoms was carried out in a cohort of pregnant women who answered a series of symptom
questionnaires and kept a 24-hour bladder chart on which frequency of urination and volumes
voided were recorded throughout pregnancy and for 8 weeks after birth. Results: A total of
123 women participated in the study. Mean daily urine output (P = .01) and the mean number
of voids per day (P = .01) increased with gestational age and declined after delivery. Episodes
of urinary incontinence peaked in the third trimester and improved after birth (P = .001).
White women had higher mean voided volumes and fewer voiding episodes than did black
women. Ingestion of caffeine was associated with smaller voided volumes and greater
frequency of urination. Conclusion: Pregnancy is associated with an increase in urinary
incontinence. This phenomenon decreases in the puerperium. Pregnancy and childbirth
trauma are important factors in the development of urinary incontinence among women.

SUPPRESSION OF URINE

If the 24 hrs urine

excretion is less than
400ml or less

BREAST
COMPLICATIONS

1 Breast engorgement
2 Cracked and retracted nipple leading
to difficulty in breast feeding
3 Mastitis and breast abscess
4 Lactation failure.

Breast Engorgement
Engorgement is defined as an uncomfortable swelling of the breast associated

with increased milk secretion and usually occurs from the second to fourth day
post natal.
There may be lymphatic and vascular congestion and possible interstitial
edema, causing swelling and tenderness. This exacerbates the tension of milk in
the ducts and may cause stasis of the milk, resulting in inability of the milk to
flow. This swelling and hardness may make it difficult for the baby to attach to
the nipple and problems can be further aggravated by nipple soreness.
the primiparous patient and the patient with inelastic breasts are likely to be
involved .
Engorgement is an indication that the baby is not in step with the stage of
lactation .

 ONSET : it usually manifests after the milk sectretion starts

(2rd to 4th day postpartum )

SYMPTOMS
Considerable pain and feeling of tenseness or heaviness in the
both breasts.
Generalized malaise
Rise of temperature
Painful breast feeding

PREVENTION
Avoid prelacteal feeds
Initiate breast feeding early and
unrestricted
Exclusive breast feeding on demand
Feeding in correct position.

MANAGEMENT OF BREAST ENGORGEMENT

1. Administer analgesics to relieve pain
2. The baby should be put to breast at regular
intervals
3. Manual expression of any remaining milk after each
feed
4. In severe cases the breasts are emptied by
expressing them manually or by a breast pump.
5. Elevate the breasts by supporting brassieres.

CRACKED AND RETRACTED

NIPPLE

Cracked nipple:

The nipple may become painful due to Loss of

surface epithelium the formation of a raw
area on the nipple. Due to a fissure situated
either at the tip or base of the nipple

It is caused by

Unclean hygiene resulting in formation of a crust

over the nipple
Retracted nipple
Trauma from babys mouth due to incorrect
attachment to the breast.
The condition may be asymptomatic but becomes
painful when the infant sucks.

PROPHYLAXIS
Includes

Local cleanliness during pregnancy

&puerperium before and after each
breast feeding to prevent crust
formation over the nipple .

TREATMENT
Correct attachment will provide immediate relief from pain and rapid healing.
Purified Lanolin with mothers milk is applied 3 or 4 times a day to hasten healing
when it is severe mother should use a breast pump and infant is fed the expressed
milk.

Inflamed nipple areola may be due to thrush also

Miconazole lotion is applied over the nipple as well as in the babys mouth if there is
oral thrush.
If it fails to heal up, rest is given to the affected nipple using a breast pump while
the nipples heal.
The persistence of a nipple ulcer in spite of therapy mentioned, needs biopsy to
exclude malignancy.

RETRACTED AND FLAT NIPPLE

It is commonly met in primigravidae.
It is usually acquired.
Babies are able to attach to the breast correctly and
are able to suck adequately. In difficult cases, manual
expression of milk can initiate lactation.
Gradually breast tissue becomes soft and more
protractile, so that feeding is possible.

MASTITIS

 Mastitis is defined as inflammation

of the mammary gland.
INCIDENCE
2-5% in lactating and less than 1% in
non lactating women.

TWO TYPES
Mammary cellulitis : inflammation of the connective
tissue between lobes in the breast
Mammary adentitis: infection in the lobes and ducts of
the breast

ETIOLOGY

Milk stasis and cracked nipples, which contribute to

the influx of skin flora, are theunderlying factors
associated with the development of mastitis.
Mastitis is also associated with primiparity,
incomplete emptying of the breast, and improper
nursing technique.

The most common causative organisms include

Staphylococcus aureus
Staphylococcus epidermidis,
saprophyticus,
Streptococcus viridans,
E coli.

MODE OF INFECTION

There are two types of mastitis depending upon the site of

infection
1. Infection that involves the breast parenchyma tissues
leading to cellulitis. The lacteal system remains unaffected.
2.Infection gains access through the lactiferous duct leading to
development of primary mammary adenitis.
Non Infective Mastitis may be due to milk stasis. Feeding from
the affected breast solves the problem

ONSET

The onset is acute during late first

week of puerperium. Where as in
mammary adenitis, the onset is
insidious and usually occurs near the
end of the first week.

CLINICAL FEATURES

Generalized

malaise and headache

Fever, chills
Myalgias,
Erythema, warmth, swelling, and breast tenderness.
Presence of toxic features
Presence of 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.

MORBIDITY AND MORTALITY

Neglected, resistant, or recurrent infections can lead to the development of

an abscess, requiring parenteral antibiotics and surgical drainage.
Abscess development complicates 5-11% of the cases of postpartum mastitis
and should be suspected when antibiotic therapy fails. Mastitis and breast
abscess also increase the risk of viral transmission from mother to infant.
The diagnosis of mastitis is solely based on the clinical picture.
Physical examination focus on vital signs, review of systems, and a complete
examination to look for other sources of infection. Typical findings include
an area of the breast that is warm, red, and tender. When the exam reveals
a tender, hard, possibly fluctuant mass with overlying erythema, a breast
abscess should be considered.

DIAGNOSIS

No laboratory tests are required. Expressed milk

can be sent for analysis, but the accuracy and
reliability of these results are controversial and aid
little in the diagnosis and treatment of mastitis

TREATMENT
Prophylaxis:
Encourage mother to wash her hands before each feed
Encourage to clean the nipples before and after each feed Reduce the nosocomial infection rates.
Curative management
Provide breast support
Encourage to take plenty of oral fluids
Encourage the mother to continue the breast feeding with good attachment
Nursing is established first on the unaffected side to establish let down.
The infected side is emptied manually with each feed
Flucloxacillin (pencillin) is the drug of choice. Erythromycin is the alternative drug of choice who are allergic
to penicillin.
Antibiotic therapy is continued for at least 7 days
Analgesics are given for pain

BREAST ABSCESS

Features are
Flushed breasts not responding to antibiotics
promptly
Browny edema of the overlying skin
Marked tenderness with fluctuation
Swinging temperature.

MANAGEMENT

Drain the abscess under general anesthesia

Encourage the breast feeding on the unaffected
side.
The infected breast is pumped every 2 hrs and
with every let down
Once cellulites is resolved breast feeding from
the involved side may be resumed.

BREAST PAIN

Candida albicans is a common

cause of breast pain

Risk factors
Diabetes mellitus
Oral thrush of infant

TREATMENT
Use of Miconazole oral lotion or gel into both the
nipples after each feed and into the infants mouth
thrice daily for 2 weeks.

LACTATION FAILURE : (INADEQUATE MILK PRODUCTION)

CAUSES are
Infrequent suckling
Depression or anxiety state in the puerperium
Reluctance or apprehension to nursing
Ill development of nipples
Painful breast lesion
Endogenous suppression of Prolactin (retained placental bits)
Prolactin inhibition

TREATMENT
Antenatal:
Council the mother regarding the advantages of nursing her baby with breast milk
Take care of any breast abnormality specially a retracted nipple and to maintain
adequate breast hygiene especially in the last 2 months of pregnancy.

Puerperium:
Encourage adequate fluid intake
Nurse the baby regularly
Treat the painful local lesions
Metaclopromide and sulpride have been found to increase milk production.

NURSING DIAGNOSIS
Altered comfort (pain) related to infection and
inflammation in the breast
Anxiety related to clients inability to continue breast
feeding
Altered parenting related to clients inability to
continue breast feeding.
Knowledge deficit related to care of the breast, breast
feeding techniques.

PLANNING AND INTERVENTIONS

Explain about the breast care and breast feeding
techniques
Instruct the mother on the signs and symptoms of
infection and need for prompt treatment.
Inspect nipples for any cracks and soreness
Provide warm applications
Administer antibiotics

PUERPERAL VENOUS
THROMBOSIS

 Thrombosis of the leg veins is one of the common and

important complications in puerperium especially in the
western countries
Venous thrombo- embolic diseases include
Deep vein thrombosis
Thrombophlebitis
Septic pelvic thrombophlebitis
Pulmonary embolus

ETIOPATHOGENESIS

Alteration in blood constituents

Venous stasis is increased due to compression of gravid uterus to the inferior vena cava
and iliac veins. This stasis causes damage to cells
Thrombophilias are hypercoagulable states in pregnancy that increase the risk of venous
thrombosis. It may be inherited or acquired. Inherited Thrombophilias are the genetic
conditions associated with the deficiencies of anti antithrombin III, Protein C, and
protein S. Others are factor V Leidenmutation
Acquired are due to the presence lupus anticoagulant and antiphospholipid antibodies.
Other acquired risk factors for thrombosis are (a) Advanced age and parity, (b) Operative
delivery (10 times more), (c) Obesity, (d) Anemia. (C)Heart disease, (f) Infection-pelvic
cellulites. (g) Trauma to the venous wall.

DEEP VEIN THROMBOSIS

Diagnosis:
Clinical diagnosis is unreliable. In majority it remains asymptomatic.

Symptoms include
Pain in the calf muscles,
Edema legs
Rise in skin temperature.
On examination a symmetric leg edema (difference in circumference between the
affected and the normal leg more than 1cm) is significant.
A positive homans sign pain in the calf on dorsiflexion of the foot may be present.

INVESTIGATIONS

The following biophysical tests are employed to

confirm the diagnosis:
1. Doppler ultrasound to detect changes in the
velocity of blood flow in the femoral vein.
2. Venography by injecting non-ionic water soluble
radio-opaque dye to note the filling defect in the
venous lumen

PELVIC THROMBOPHLEBITIS
Postpartum thrombophlebitis originates in the thrombosed veins at
the placental site by organisms such as anaerobic Streptococci or
Bacteroides (fragilis).
When localized in the pelvis, it is called pelvic thrombophlebitis
There is no specific clinical feature of pelvic thrombophlebitis, but it
should be suspected in cases where PYREXIA continues for more than
a week inspite of antibiotic therapy

 Extra pelvic spread:

Through the right ovarian vein into inferior vena cava and then to the lungs.Through
the left ovarian vein to the left renal vein and then to the left kidney.Retrograde
extension to ilio-femoral veins to produce the clinico-pathological entity of "
phlegmasia alba dolens" or white leg
Phlegmasia alba dolens(Syn : White leg) :
It is a clinico-pathological condition usually caused by retrograde extension of pelvic
thrombophlebitis to involve the ilio-femoral vein. The femoral vein may be directly
affected from adjacent cellulitis. The condition is seldom met now-a-days.

CLINICAL FEATURES
(1) It usually develops on the second week of puerperium.
(2) Mild pyrexia At times the fever may be high with chills and
rigor.
(3) Evidences of constitutional disturbances such as headache,
malaise, and rising pulse rate.
(4) The affected leg swollen, painful, white and cold. The pain is
due to arterial spasm as a result of irritation from the nearby
thrombosed vein.
(5) Blood count shows polymorph nuclear leucocytosis.

DIAGNOSIS

may be made by ultrasound,

computed tomography (CT) scan
or by magnetic resonance
imaging (MRI)

PROPHYLAXIS FOR VENOUS THROMBOEMBOLISM in PREGNANCY AND

PUERPERIUM

Preventive measures include:

Prevention of trauma, sepsis, anemia in pregnancy

and labor. Dehydration during delivery should be
avoided
Use of elastic compression stocking and intermittent
pneumatic compression devices during surgery.
Leg exercises, early ambulation are encouraged
following operative delivery.

 Women at risk of venous thromboembolism during pregnancy have been grouped into
different categories depending on the presence of risk factors. Thrombo prophylaxis
to such a woman depends on the specific risk factor and the category
(1) A low risk woman has no personal or family history of VTE and are heterozygous
for factor V Leiden mutation. Such a woman needs no thrombo prophylaxis. (2) A high
risk woman is one who has previous VTE or VTE in present pregnancy, or
Antithrombin-in deficiency. Such a woman needs low molecular weight heparin
prophylaxis throughout pregnancy and post partum 6weeks. Women with
antithrombin-III deficiency can be treated with antithrombin-III concentrate
prophylacticaly

MANAGEMENT
(1)The patient is put to bed rest with the foot end raised above
the heart level.
(2) Pain on the affected area may be relieved with analgesics.
(3) Appropriate antibiotics are to be administered.
(4) Anticoagulants

 Heparin is continued for at least 7 to 10 days or even longer. if thrombosis is severe.

Prolongation of activated partial thromboplastin time (APTT) to 1.5-2.5times indicates
effective and safe anti coagulation.Low molecular weight heparin (LMWH), can be used
safely in pregnancy.
Enoxaparin 40 mg daily is given. It does not cross the placenta,
(b) A drug of coumarin series warfarin is commonly used orally with an overlap of at
leastthree days with heparin. The initial daily single dose of 7 mg for 2 days is adequate
for induction. Subsequent maintenance dose depends upon international normalized
ratio(1NR) 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 be continued till all evidences of the disease have
disappeared which generally take 3-6 months. Neither anticoagulant should prevent the
mother from breast-feeding.

 (5) As soon as the pain subsides, gentle movement is allowed on bed by the end of
first week.
High quality elastic stockings are fitted on the affected leg before mobilization.
(6) Vena cava fillers are used for patients with recurrent pulmonary embolism or
where anticoagulant therapy is contraindicated.
(7) Fibrinolytic agents like streptokinase produce rapid resolution of pulmonary
emboli.
(8) Venous thrombectomy is needed for massive illio femoral vein thrombosis or for
massive pulmonary embolus.

Torben Vol120( 4),2007, Pp 505509

Maternal smoking, obesity, and risk of venous thromboembolism during pregnancy and
the puerperium: A population-based nested case-control study
Background
Smoking and obesity are associated with adverse pregnancy outcomes. The aim of the present study was to
examine the association between smoking, obesity (BMI>30), and risk for venous thromboembolism (VTE) during
pregnancy and the puerperium.
Materials and methods
In a population-based case-control study nested within a Danish cohort of 71,729 women, we identified 129 cases
with VTE in pregnancy or the puerperium, and 258 pregnant non-VTE controls. We obtained data from medical
records regarding current smoking status, BMI, and other covariates, and computed the odds ratios (OR) for VTE
as a measure of relative risk.
Results
Smoking and obesity were associated with increased risk of VTE during pregnancy and the puerperium (adjusted
OR 2.7 (95% CI: 1.5, 4.9) and 5.3 (95% CI: 2.1, 13.5), respectively). Obesity appeared to be associated with a
higher risk of pulmonary embolism (adjusted OR: 14.9 (95% CI: 3.0, 74.8) than of deep venous thrombosis
(adjusted OR: 4.4, 95% CI: 1.6, 11.9).
Conclusion

PULMONARY
EMBOLISM

Pulmonary embolism is the leading cause of maternal deaths in

many centresespecially in the developed countries after the
sharp decline of maternal mortality due to hemorrhage,
hypertension and sepsis.
While deep venous thrombosis in the leg or in the pelvis is
most likely the cause of pulmonary embolism, but in about 8090%, it occurs without any previous clinical manifestations of
deep vein thrombosis.

 The predisposing factors are those already mentioned in venous

thrombosis
The clinical features depend on the size of the embolus and
on the preceding health status of the patient.
The classic symptoms of massive pulmonary embolism are
Sudden collapse with acute chest pain and air hunger. Death
usually occurs with inshort time from shock and vagal
inhibition.

The important signs and symptoms of

pulmonary embolism are:
Tachypnoea,
dyspnoea,
pleuritic chest pain,
cough,
tachycardia,
haemoptysis rise in temperature > 37c.

DIAGNOSIS
: X-ray of the chest shows diminished vascular marking in areas of infarction,elevation of the
dome of the diaphragm and often pleural effusion. It is useful to ruleout pneumonia and
atelectasis.
ECG : tachycardia, right axis shift.
ARterial blood gas : POa > 85 mm Hg on room air is reassuring but does not ruleout PE. Oxygen
saturation < 95% on room air needs further investigation.
Doppler ultrasound
can identify a DVT. When the test is positive for DVT, anticoagulation therapy should be started.
Lung scans : (Ventilation /Perfusion scan) Perfusion scan will detect areas of diminished blood
flow whereas a reduction in perfusion with maintenance of ventilation indicates pulmonary
embolism. Magnetic Resonance Imaging (MRI) can be used in pregnancy as the risk of ionizing
radiation is absent.
Pulmonary angiography: is considered to be the most accuratemethod of diagnosis.

MANAGEMENT
Prophylaxis (as mentioned in venous thromboembolism)
Active treatment includes:
(1)Resuscitation : cardiac massage, oxygen therapy, intravenous heparin bolus dose of 5,000 IU and morphine
15 mg (I.V.) are started. Heparin therapy is to be continued upto 40,000 IU per day so as to maintain the
clotting time to over 12minutes for the first 48 hours. Heparin level is maintained at 0.2 to 0.4 units/ml or the
activated partial thromboplastin time (APTT) about twice the normal.
(2) I.V. fluid support is continued and blood pressure is maintained if needed bydopamine or adrenaline.
(3)Thrombolytic therapy
Streptokinase with a loading dose of 600,000 IU can be given and continued with 100,000 IU per hour. It does
not cross the placentawhen used during pregnancy.
(4) Tachycardia is counteracted by digitalis
.(5) Recurrent attacks of pulmonary embolism necessitate surgical treatment like embolectomy, placement of
vena caval filter or ligation of inferior vena cava andovarian veins.
Surgical treatment is done following pulmonary arteriography.