Mudaliar

and
Menon’s
Clinical
Obstetric
s
13TH EDITION
 Chapter 49
PUERPERAL
INFECTION
AND OTHER
POSTPARTU
M
COMPLICATI
ONS

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 According to the International Classification
of Diseases, puerperal pyrexia or postpartum
fever is defined as a rise of temperature
greater than 38°C (100.4°F) on any two
occasions in the first 10 days following
childbirth, miscarriage or termination of
pregnancy excluding the first 24 hours.

PUERPE The most common cause of puerperal fever

is puerperal sepsis, which complicates 5–7%
RAL of all deliveries.
PYREXI According to the WHO’s estimates,
puerperal sepsis accounts for 15% of the
A gross maternal mortality and causes at least
75,000 maternal deaths every year, mostly in
developing countries.

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Causes of puerperal pyrexia
Puerperal sepsis
Infection of episiotomy wound, vagina or perineum
Abdominal wound infection following cesarean section
Urinary tract infection
Mastitis, breast abscess
Septic thrombophlebitis
Respiratory complications such as pneumonia, atelectasis
Meningitis following regional anesthesia

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 Risk factors
Pre-existing  Low socioeconomic status
factors  Anemia, malnutrition
 Diabetes, immune compromised state
PUERPE 

Pre-existinggenital infections
Poor hygiene
RAL  BMI >30

SEPSIS Risk factors  Home birth in unhygienic conditions

Puerperal sepsis related to  Prolonged labour
refers to uterine labour and  Prolonged rupture of membranes
delivery  Multiple vaginal examinations
infection following  Operative vaginal delivery
childbirth (puerperal  Trauma to the genital tract
infection).  Cesarean section
 PPH, manual removal of placenta
 Retained placenta and membranes
 Use of fetal scalp electrode
 Droplet infection from caregivers and
attendants

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 Devitalised tissue, trauma and the alkaline
nature of lochia predispose to uterine infection,
which starts as endometritis.
The common routes of spread are the following:
Direct spread along the endometrial surface
Spread along the veins into the pelvic venous
channels
PATHOGENESIS Spread along the lymphatics into the
parametrial tissue
Bloodborne transmission, leading to
septicemia
When the infection spreads to the
bloodstream, septicemia results, leading to
endotoxic shock.

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Grades of Puerperal Sepsis Complications
 Grade I: Infection involving the lower
genital tract and the uterus Salpingo-oophoritis and pelvic cellulitis.
 Grade II: Besides the uterus, the
adnexa are also involved Pelvic abscess
 Grade III: Spread to the entire pelvic
structures with pelvic peritonitis Septicemia
 Grade IV: Spread to the upper
abdomen (general peritonitis) and Septic pelvic thrombophlebitis
septicemia
Delayed complications are chronic
pelvic infection, chronic pelvic pain and
infertility

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 first indication of infection is a rise in temperature
In the early stages of endometritis, there is low-grade
fever, abdominal pain and uterine tenderness and the
lochia is unhealthy.
With deeper and more widespread infection, there is
high-grade fever, rigor and malaise. The uterus is
tender. The lochia is foul-smelling.
SIGNS AND SYMPTOMS In the event of the development of peritonitis or
pelvic abscess formation, the woman looks toxic and
besides fever and rigors, there is abdominal pain and
bloating often associated with diarrhea.
With the release of endotoxin from the gram-
negative organism, the temperature becomes
subnormal, and there is hypotension. The woman
then goes into endotoxic shock. A positive blood
culture will confirm the diagnosis.

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 EXAMINATION
Breast - engorgement and abscess.
The neck - examined for rigidity to rule out meningitis following regional anesthesia.
The throat and chest - examined for infections, especially following general anesthesia.
The lower limbs - examined for thrombophlebitis and deep vein thrombosis.
Suprapubic and renal angle tenderness - rule out urinary tract infection.
On abdominal examination: Signs of wound infection should be looked for. The abdomen
should be palpated for – organomegaly, abdominal distension,guarding and rigidity.
On local examination: Purulent vaginal discharge with infected lacerations in the
perineum; the episiotomy wound may show wound breakdown with necrotic edges.
Pelvic examination: Look for infected vaginal and perineal tears, note the colour of the
lochia and look for subinvolution and tenderness of the uterus and forniceal tenderness.
There may be bilateral adnexal masses.
When there is a pelvic abscess formation, a boggy swelling can be felt through the
posterior fornix, which is well appreciated by rectal examination.

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Evaluatio
n of
puerpera
l pyrexia

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 General measures
Bed rest, adequate fluid intake and control of temperature
with antipyretics and tepid sponging. Urine output should be
monitored.
When the infection is severe or if there is evidence of
peritonitis, intravenous fluid resuscitation is required.
Local wound cleaning should be done.
Antibiotic therapy
Mild infection following a vaginal delivery: Amoxicillin with
MANAGEMENT clavulanic acid with metronidazole, cephalosporins such as
cefotaxime are used by the oral or parenteral route for 7–10
days.
Moderate to severe infection: Parenteral therapy with higher
antibiotics such as a combination of piperacillin/tazobactam.
In MRSA-positive cases, vancomycin may be given.
Severe infection or infection following cesarean section:
clindamycin and gentamicin plus ampicillin.
For moderate to severe infection, parenteral therapy for 48
hours after the temperature has become normal.
When the blood culture is positive, parenteral therapy
should be continued for two weeks.

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MASTITIS AND BREAST ABSCESS
Mastitis is an inflammatory condition of the breast that usually occurs
during the first six weeks postpartum but can occur at any time during
lactation.
Risk factors for mastitis include maternal age above 30 years, sore and
cracked nipples and a history of mastitis in the previous pregnancy.
Breast engorgement, blocked lactiferous ducts and milk stasis also
contribute to the development of mastitis.
Etiology
Staphylococcus aureus
Methicillin-resistant Staphylococcus aureus
Escherichia coli and Haemophilus influenzae

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Puerperal mastitis presents with acute-onset
maternal fever (100.4°F or higher), chills, myalgia,
malaise and breast tenderness with associated
erythema.
Mastitis is most commonly unilateral.
CLINICA
On examination of the breast, the erythema is
segmental, usually in the upper, outer quadrant, with L
variable degrees of induration and tenderness.
If a palpable, fluctuant mass is felt, breast abscess
FEATUR
should be suspected and confirmed by an
ultrasound.
ES
Culture of the breast milk - recurrent mastitis.

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TREATMENT
Early antibiotic therapy, regular emptying of the breasts and local
comfort measures
Dicloxacillin, amoxicillin or first-generation cephalosporins
Erythromycin and vancomycin for women who have a penicillin allergy
Given for 10–14 days
Women who wean or decrease feeding during an episode of mastitis
have a higher risk of developing a breast abscess
Analgesics - ibuprofen or acetaminophen
Increased fluid intake and adequate nutrition
Either cold or warm compresses may be used for pain relief

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Breast abscess can develop when there is a delay in initiating antibiotic treatment or
inadequate emptying of the breast in the presence of mastitis.
When in doubt, USG of the breast can be taken.
During incision and drainage, all loculation should be opened, and biopsy of the abscess
wall should be considered to rule out rare cases of carcinoma. The pus should be sent for
culture and sensitivity.
Antibiotic therapy should be continued.
In abscesses involving the parenchyma - the incisions should radiate outwards from the
nipple so as to open up any pockets or lobules that are distended with the suppurating
material.
The resulting cavity should be loosely packed with gauze, which should be removed after
24 hours.
If there is an abscess behind the areola, it is best opened towards the lower and outer
quadrant and also at any spot where the pus points.

BREAST
ABSCESS
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 THROMBOPHELEBITIS
Inflammation and infection may involve the venous channels of
the pelvis or the lower limbs, leading to thrombus formation.

Septic pelvic thrombophlebitis

Bacterial infection usually begins at the placental site -
VENOUS myometrial venous thrombosis – spread to the ovarian veins -
COMPLICATIONS IN extend to the inferior vena cava or the left renal vein.
THE PUERPERIUM The clinical manifestation - persistent high fever with chills
despite antibiotic therapy and abdominal pain.
Diagnosis: CT or MRI imaging.
The addition of heparin to the antimicrobial therapy may
improve the outcome.

Superficial vein thrombophlebitis of the lower limb

Refers to thrombus formation in a superficial vein of the leg
and inflammation in the tissue surrounding the vein.
It is infective in origin.

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 Clinical features
Superficial thrombophlebitis is characterised by pain,
Etiology
 Anaerobic streptococci tenderness, induration and/or erythema in a superficial
 Risk factors - anemia, vein.
varicose veins and There is often a palpable cord with warmth and erythema,
thrombophilic disorders. which suggests the presence of a thrombus.
 The infection occurs by
direct spread from Fever with rigors.
adjacent cellulitis or
retrograde spread from SVT most often occurs in the saphenous vein of the lower
pelvic thrombophlebitis. limbs, and its tributaries; rarely, the femoral vein may be
 Embolism is uncommon. affected.
Often, there is secondary arterial spasm leading to pallor
and coldness in the swollen leg. This condition is sometimes
called phlegmasia alba dolens. The symptoms subside with
antibiotic and anticoagulant (heparin) treatment.
If the collateral veins are also involved, the leg is
congested and edematous. This condition is called
phlegmasia cerulia dolens.

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VTE includes deep vein thrombosis (DVT) and pulmonary embolism (PE).

During normal pregnancy, the concentrations of the clotting factors fibrinogenVII and
VIII and von Willebrand IX, X and XII are all increased, resulting in a hypercoagulable
state.

Mechanical obstruction produced by the growing uterus compromises venous outflow

and subsequently increases the susceptibility of pregnant and postpartum women to
developing thromboembolisms.

Risk of VTE increases by 5-fold in pregnant women and to ≥20-fold in the puerperium
and until 12 weeks postpartum.

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RISK FACTORS
Pre-existing New-onset
 Previous VTE  Hyperemesis, dehydration
 Congenital thrombophilia with  Severeinfection—puerperal sepsis,
antithrombin deficiency, protein C pyelonephritis
orprotein S deficiency, factor V Leiden  Prolonged immobility after delivery
mutation  Pre-eclampsia
 Acquired thrombophilia—APLA  Prolonged labour
 Age >35 years  Postpartum hemorrhage
 BMI >30
 Gross varicose veins
 Anemia
 Paraplegia
 Sickle cell disease, polycythemia or
nephrotic syndrome

Prevention
•LMWH as prophylaxis and treatment of DVT and PE
•Inj. Enoxaparin 40–60 mg daily
•Inj. Dalteparin (Fragmin) 5,000–6,000 units daily depending on the woman’s weight

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 DVT begins in the deep veins of the calf or soles of the
feet and extends upwards.
If it remains undiagnosed and untreated, 15–24% of
these patients will develop pulmonary embolism, which
is fatal.
Clinical features
Leg pain and swelling (usually unilateral), tenderness
on palpation and lower abdominal pain often on the left
side.
DEEP VEIN
Sharp dorsiflexion of the foot elicits pain in the calf.
THROMBOSIS This is termed Homans’ sign.
(DVT) There may be a slight rise in temperature and pulse
rate, with no obvious cause, usually on the 7–10th day
of the puerperium.
Diagnosis
Compression duplex ultrasound is the primary
diagnostic test for DVT.
When iliac vein thrombosis is suspected, Doppler
ultrasound of the iliac vein and magnetic resonance
venography should be carried out.
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Symptoms
 Unexplained collapse or respiratory distress in the puerperal
period
 Dyspnea, chest pain, hemoptysis, cough, pink and frothy
sputum and collapse.
 In massive embolisms, death occurs within a few minutes.
Laboratory investigations
 Electrocardiogram (ECG) and a chest X-ray (CXR).
 Ventilation/perfusion (V/Q) lung scan
 Computerised tomography pulmonary angiogram (CTPA)
 Blood gas analysis and echocardiogram are other helpful
investigations. PULMONA
Management
 Graduated elastic compression stocking to reduce the RY
edema EMBOLIS
 Mobilisation and antibiotics
 Temporary inferior vena cava filter in the peripartum period M (PE)
for women with iliac vein VTE to reduce the risk of PE
 Anticoagulant therapy
 Therapeutic doses of subcutaneous LMWH should be
employed during the remainder of the pregnancy and for at
least 6 weeks postnatally with a loading dose of 80 units/kg,
followed by a continuous intravenous infusion of 18
units/kg/hour
 APTT level at 1.5–2.5 times the average laboratory control
value
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 Postpartum mothers are vulnerable to psychological
disturbances.
Nearly 85% of women experience some type of mood
disturbance.
10–15% of women develop more significant symptoms of
depression or anxiety.
PUERPER Postpartum psychiatric illness is typically divided into three
AL classes, which are as follows:
PSYCHIAT 1. Postpartum blues
RIC 2. Postpartum depression

MORBIDI 3. Postpartum psychosis

TY The mood changes and psychiatric morbidity following delivery

have been attributed to abrupt changes in cortisol, oxytocin,
endorphins, thyroxine, progesterone and estrogen levels.
The sudden decrease in estrogen in the postpartum period
triggers a hypersensitivity of certain dopamine receptors, which
may be responsible for the severe mood disturbance.

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 Risk is due to the hypercoagulable state of pregnancy.
Contributing factors: Infection, cesarean section,
obesity, prolonged bed rest, anemia,
pre-eclampsia/eclampsia and dehydration in the
postpartum period.
Commonly, the superior sagittal and transverse
CEREBRAL VENOUS AND sinuses are affected.
SINUS THROMBOSIS
This condition is associated with headache, seizures,
(CVT) visual disturbances, altered consciousness and focal
neurological findings such as hemiparesis or aphasia.
CT scan remains the first imaging modality.
Treatment: anticonvulsants, anti-edema measures
and anticoagulants

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 POSTPARTUM PITUITARY NECROSIS OR SHEEHAN SYNDROME

Clinical Features
The first symptom is failure to lactate.
The patient is apathetic with prominent asthenia and
lethargy; hypothyroidism, decreased insulin tolerance and
frequent attacks of hypoglycemia develop.
 Rare condition - necrosis of the Adrenal cortical failure: loss of pubic and axillary hair,
anterior pituitary following decrease in skin pigmentation and decreased sweating.
hemorrhagic shock due to PPH/APH. Deficiency of pituitary erythropoietin, anemia.
 The degree of ischemic necrosis is
Pituitary cachexia: Weight loss and atrophy of breast and
proportional to the amount of blood
loss, sludging and thrombosis of the genital organs, even death can occur due to severe
hypotension and hypoglycemia.
vessels supplying the anterior
pituitary.
 Manifests as decreased Evaluation
gonadotrophic activity, decreased Thyroid and adrenal function.
corticotrophic activity, decreased
thyrotrophic activity and decreased
somatotrophic hormones. Management
Maintenance dose of thyroxine, corticosteroids and HRT.
Exogenous pulsatile GnRH if pregnancy is desired.
Medical alert bracelet to alert physicians as to the need
for additional corticosteroids at times of stress.

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