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OBSTETRIC INJURIES TO

GENITAL TRACT &


OBSTETRIC SHOCK
 OBSTETRIC INJURIES TO GENITAL TRACT
 RUPTURE UTERUS
 IT IS A MOST SERIOUS CONDITION
 It usually occur during labor, rarely during preg.
 Incidence 0.3%.
 Causes:
 -During preg:
 Weak scar
 Previous classical c/s.
 Previous hysterotomy, metroplasty,
myomectomy, perforation.
 Direct trauma to abdomen.
 Congenital abnormality of the uterus
 During labor:
 Obstructed labor.
 Intra uterine manipulation.
 Forcible dilatation of cx.
 Injudicious use of oxytocin.
 Previous weak scar.
 Grand multiparous women
 Pathology:
 -complete rupture
 -incomplete rupture.
 Depending on whether the peritoneal coat is torn or not
 In Britain a weak scar is the commonest cause of rupture
uterus, if the uterus is over distended, scar imperfectly
sutured, sepsis, the placenta implanted over the scar,
when the latest incision is made through the previous
scar.
 c/s in the lower segment may stretch gradually
attenuated avascular fibrosis causing relative
intraperitonial bleeding when the scar give way
 Symptoms and signs:
 Rupture through scar during pregnancy, history of previous
operation, scar on skin, thin abdominal wall, tender sulcus, may
be silent rupture, or severe pain, shock.
 Rupture during labor, dramatic symptoms, not always there is
difficult labor.
 Spontaneous rupture during obstructed labor, signs of
obstruction, exhausted mother, tearing pain, shock, vaginal
bleeding.
 On examination: presenting part high, fetus extruded out of the
uterus, contraction cease.
 Rupture after intra uterine manipulation.
 Extensive cervical laceration.
 Rupture by oxytocic drugs, risk more in multip.
 Direct injury to abdomen
 Prognosis:
 Mortality higher in cases of obstructed labor.
 Fetal death is also more in cases of obstructed
labor than in rupture in previous scar.
 Treatment:
 Recognize disproportion.
 High risk cases deliver at hospital.
 Upper segment scar deliver by c/s
 Improve general condition, blood, I.V fluid,
morphine, operation.
 Repair or hysterectomy. + tubal ligation.
 Antibiotics
 Electrolyte balance.
 LACERATION OF THE CERVIX
 Caused by precipitated labor, forceps
application, rapid delivery of the after coming
head in breech presentation, previous scar in cx.
From previous injury may tear.
 Minor laceration is asymptomatic.
 Deep laceration causes severe he during and
after 3rd stage of labor.
 Treatment:
 Suturing under G.A using interrupted catgut or
vicryl inserted through the whole thickness of its
wall.
 We need sponge forceps to complete our work.
• LACERATION OF THE PERINIUM AND VAGINA
• There are four degrees of this type of injury:
• First degree: it involves only the skin
• Second degree: it involves the perineal body up to the
anal sphincter, but not involving it with a corresponding
vaginal tear.
• Third degree: secondary tear with partial or complete
disruption of the anal sphincter.
• Fourth degree: third degree tear with anal epithelium.
• Extensive tear in the vagina may occur without tear in
the perineum so inspection is important.
• Treatment of first and second degree tears:
• By repair of all lacerations to prevent ay infection.
• If not sutured the possibility of uterovaginal prolapse is
increased.
• Start suturing from apex of the vaginal tear using
continuous or interrupted suture using catgut or dexon
using local anesthesia,G.A,epidural.
• Third and fourth degree tears:
• Experienced obstetric surgeon, theater, G.A, or epidural.
• Early suturing with good results, if delayed the operation
is difficult and incontinence is more also use catgut or
dexon.
• Anal mucosa is 1st repaired with the knot inside the
bowel lumen.
• Anal sphincter with interrupted suture, the rest as in 2nd
degree tear repair.
• After care – daily wash with soap and water, dried, may
need a catheter.
• If bowel motion is –ve by the fourth day, use glycerin
suppositories not oral liquid paraffin.
• If infection occurs we remove the stitches, drain,
antibiotics, bathing until granulation tissue occur then
2ndry suture.
Repair of a second degree
laceration
• A first-degree laceration involves
the fourchet, the perineal skin, and
the vaginal mucous membrane. A
second-degree laceration also
includes the muscles of the perineal
body. The rectal sphincter remains
intact.
Layered primary closure of a fourth-degree
obstetric laceration
 VULVAL AND PARAVAGINAL HAEMATOMA
 Divided into two types:
 Supralevator hematoma
 Infralevator hematoma
 Infralevator: includes vulva, perineum, paravaginal,
ischiorectal fossa.
 Supralevator hematoma: it spread upwards and
outwards beneath the broad ligament or partly
downwards to bulge into the wall of the upper vagina and
can track backwards into the retroperitoneal space.
 Incidence: greater than 4 cm in diameter it occurs in
1/1000 deliveries.
 Injury occurs with episiotomy.
 In 20% of cases occur with intact perineum,
 Half of women with genital hematoma have spontaneous
delivery.
 Diagnosis:
 Usually obvious.
 May be missed until shock occurs.
 Symptoms:
 Depend on rate and size of hematoma
 Management:
 Resuscitation, surgical evacuation if hematoma is
larger than 5 cm or if expanding.
 If small and not expanding, observation, ice-packs,
antibiotics, analgesia.
 SUBPERITONEAL HEMATOMA
 Broad ligament hematoma, less common than
genital hematoma.
 It occur in 1 in 20000 deliveries.
 They follow spontaneous vaginal or c/s or
forceps.
 50 % discovered immediately, the other half 24
hrs later
 presentation abdominal pain and hge.
 Management:
 Conservative.
 If unstable homodynamic state do surgical
exploration may need hysterectomy
 FISTULA
 - Due to prolonged pressure of the presenting part in prolonged
labor,
 -Or direct injury during operation, forceps.
 Prolonged pressure causes ischemia then necrosis of anterior
vaginal wall and base of bladder causing vesicovaginal fistula.
 The rectum may also be involved, rectovaginal fistula commonly
caused by complete tear.
 If it is due to pressure necrosis it appears after 8 days when the
slough separate.
 Examination, opening is found.
 Small fistula may heal in the rectum by granulation tissue
healing.
 But for vesicovaginal fistula this is unlikely.
 If direct fistula direct repair.
 If pressure fistula repair 2-3 months later.
• MATERNAL NERVE INJURY DURING LABOR
• -Foot drop from paralysis of dorsiflexor muscles of the
leg may follow delivery.
• In few cases it is due to pressure on lateral popliteal
nerve near the neck of the fibula by a leg support
• -In the majority of cases different type of injury involving
the 4th and 5th lumbar nerve roots.
• -Sudden prolapse of the intervertebral disc during labor,
or pressure on the -----lumbosacral cord by the
presenting part near the pelvic brim.
• The lesion is usually unilateral and it follows difficult
labor.
• -Sensory loss, it follows footdrop and rarely follows
epidural anesthesia.
OBSTETRIC SHOCK
 Shock is a physiologic state characterized by a
significant, systemic reduction in tissue
perfusion, thereby resulting in decreased tissue
oxygen delivery.
 Three broad mechanisms of shock are
recognized:
 Hypovolemic — fall in intravascular volume
 Cardiogenic — fall in cardiac output
 Distributive, most often due to sepsis — fall
in systemic vascular resistance
 Shock may progress through a series of stages
if not successfully treated, culminating in end-
organ damage, irreversible shock, and death.
 Irreversible shock seems to be associated with
pooling of blood in the capillaries and tissues,
leading to a further impairment in tissue
perfusion.
 The ensuing elevation in the capillary hydraulic
pressure favors the movement of fluid out of the
vascular space into the interstitium toxic
products released from injured tissues or from
the local accumulation of neutrophils can
damage the capillary wall.
COMMON FEATURES OF
SHOCK
 Hypotension — Hypotension (systolic BP <90 mmHg) occurs in
most shock patients.
 Cool, clammy skin — In many shock states, regulatory processes
compensate for decreased effective tissue perfusion. Potent
vasoconstrictive mechanisms redirect blood from the periphery to
the vital organs, thus maintaining coronary, cerebral, and splanchnic
perfusion but causing the classic cool, clammy skin of shock.
 Oliguria —
 Other signs of hypovolemia in patients with shock include
tachycardia, orthostatic hypotension, poor skin turgor, absent
axillary sweat, and dry mucous membranes.
Change in mental status —
Metabolic acidosis — Initially, shock
patients may have a respiratory alkalosis.
However, as shock progresses, a
metabolic acidosis develops, reflecting
decreased clearance of lactate by the
liver, kidneys, and skeletal muscle. If
shock progresses to produce circulatory
failure and tissue hypoxia, lactate
production is increased due to anaerobic
metabolism and can worsen acidemia.
Obstetrical shock
 It does not differ from surgical shock; it
results from depression of many
functions.
 Inadequate perfusion, oxygen
depletion, accumulation of metabolites.
 Hypotension without significant external
bleeding may develop in an obstetric
patient.
 Causes:
 1-Concealed hge: any bleeding as in episiotomy, vaginal
hematoma, rupture uterus with out obvious external bleeding leads
to obstetric shock.
 2-Uterine inversion:has been discussed
 3-Amniotic fluid embolism
 4-septic shock
 Diagnosis:
 History
 Examination
 Manual exploration
 If no cause is found think of coagulopathy.
 Management:
 Resuscitation
 Oxytocic drugs
 Removal and treatment of the cause
 Amniotic fluid embolism:
 This condition occurs when amniotic fluid enters the
maternal circulation.
 It causes cardio respiratory compromise as well as
coagulation defect which is often severe.
 Incidence and etiology:
 1 in 30000 pregnancies.
 Associated with rupture membranes
 Rapid labor
 Vaginal delivery and c/s
 Mechanism: access of amniotic fluid at higher pressure
than usual into the maternal circulation through a defect
some where near the placental site.
 It is unpredictable and catastrophic consequences: acute
cardiopulmonary embarrassment, coagulation failure.
 Symptoms:
 -Sudden onset of severe chest discomfort.
 -Difficult breathing
 -Pallor
 -Cyanosis
 -Cardiovascular collapse
 Signs:
 -Venous congestion with raised JVP.
 -Output failure with tachycardia, hypotension, and peripheral
vasoconstriction.
 -Hge, coagulation failure, petechial skin hge.
 -Bleeding at puncture site, vaginal bleeding.
 -Coagulopathic signs may be the presenting features with out
other symptoms.
 Investigations:
 -no time for investigations
 -30 % will die in the first hr.
 -suspicion when cardio respiratory collapse during
labor or soon after delivery.
 -diagnosis only confirmed at postmortem , by finding
pulmonary vasculature packed with amniotic debris
and trophoblast or aspirating blood from the
pulmonary artery and examine for trophoblastic
tissue.
 -coagulation profile requested
 Differential diagnosis:
 Thromboembolism.
 Management:
 -Artificial ventilation
 -Cardio pulmonary resuscitation
 -Circulatory support
 -I.V dopamine, steroids may be useful
 -Correct acidosis
 -Treat coagulopathy
 -If the patient survive taken to the intensive care, anticoagulant,
antifibrinolytics.
 -fetus is unlikely to survive.
 -after stabilizing the maternal condition vaginal delivery is
preferable.
 Prognosis:
 Maternal mortality 90%
 Prevention by avoiding excessive uterine contraction with
oxytocin
 VENOUS THROMBOEMBOLISM
 IT IS A LEADING CAUSE OF MATERNAL DEATH
 It occurs in 0.3% of pregnancies.
 SEPTIC SHOCK:
 Septic shock refers to a constellation of infection-
mediated clinical findings marked by impaired
vascular integrity resulting in inadequate tissue
oxygenation and circulatory failure. Cellular hypoxia,
organ dysfunction, and death ensue if the course of
this process is left unaltered .
 sepsis remains an important cause of maternal
mortality in obstetrics, along with thromboembolism,
hemorrhage, and hypertension .
 PREGNANCY AND SEPTIC SHOCK — Pregnancy is
traditionally considered an immunocompromised state.
 Incidence — The incidence of bacteremia is approximately 8 to
10 percent in obstetric patients with clinical evidence of local
infection. These patients rarely progress to more significant
complications, such as septic shock.
 Etiology —
 Post-cesarean delivery endometritis
 Endometritis following vaginal delivery
 Urinary tract infections
 Septic abortion
 Intra amniotic infection
 Necrotizing fasciitis
 Toxic shock syndrome
 Predisposing factors:
 include prolonged premature rupture of membranes, cerclage in the
presence of ruptured membranes, retained products of conception,
pregnancy with a retained intrauterine contraceptive device, and
instrumentation of the genitourinary tract.
 Microbiology — The principal etiologic agents of septic shock are
endotoxin producing aerobic Gram-negative bacilli, Gram-positive
bacteria and mixed or fungal infections. Anaerobic organisms (eg,
Bacteroides species, Fusobacterium, Peptostreptococci,
Clostridium) are usually involved in mixed infections.
 Prolonged hospitalization and use of broad spectrum antibiotics
increase the risk of infection with resistant gram negative organisms
and Pseudomonas sp. Anaerobes are part of the normal
genitourinary and gastrointestinal flora, but may become pathogens
when the normal mechanisms limiting their growth are altered.
Antibiotics, decreased local vascular supply, foreign body material,
and tissue trauma all favor anaerobic infection .
 CLINICAL MANIFESTATIONS — The severity of the clinical
presentation of sepsis is determined by the vigor of the host
inflammatory response, rather than the virulence of the inciting
infection
 Early symptoms — Initial symptoms of sepsis may include
malaise, nausea, vomiting, and, occasionally, profuse diarrhea.
Bacteremia is typically manifested by shaking chills, a sudden
rise in temperature, tachycardia, and warm extremities.
Reductions in cerebral blood flow may cause abrupt alterations in
mental status. Tachypnea or dyspnea result from a direct effect
of endotoxin on the respiratory center and may immediately
precede the clinical development of acute respiratory distress
syndrome (ARDS).
 Early in the course of shock blood pressure may actually be
normal due to peripheral vasoconstriction; perfusion is
disproportionately diverted from the renal and splanchnic
circulations to maintain central blood pressure. The diagnosis of
septic shock is often overlooked before hypotension occurs,
although the woman may appear critically ill.
 Late symptoms — Cold extremities, oliguria,
and peripheral cyanosis are late manifestations
in untreated and poorly responding cases.
Myocardial depression becomes a prominent
feature of prolonged septic shock, with marked
reductions in cardiac output and systemic
vascular resistance. Overt evidence of
prolonged cellular hypoxia and dysfunction
include profound metabolic acidosis, electrolyte
imbalances, and disseminated intravascular
coagulation (DIC). If these symptoms are left
unabated, rapid progression to irreversible
shock is the rule.
 DIAGNOSIS — A careful physical examination and selected
imaging studies are important in excluding uncommon sources.
 The microbiological evaluation should include specimens from blood
(at least two sets of blood cultures), urine, sputum, wound (in post-
operative patients), and endometrium.
 Both ultrasound and computed tomography (CT) imaging are helpful
in searching for an intra abdominal abscess, retained products of
conception, microabscesses in the myometrium, and septic pelvic
vein thrombophlebitis.
 Laboratory findings —
 The white blood cell count may be depressed at first; however, a
marked leukocytosis usually becomes evident.
 A transient increase in blood glucose concentration due to
catecholamine release and tissue underutilization is replaced by
hypoglycemia when a reduction in gluconeogenesis subsequently
occurs from hepatic dysfunction.
 decreased platelet count, decreased fibrinogen concentration,
elevated fibrin split products, and an elevated thrombin time.
 Initial arterial blood gases may show a transient respiratory alkalosis
from tachypnea, but metabolic acidosis develops as the lactic acid
concentration increases from tissue hypoxia.
 Management:
 In pregnant women, priorities should first be directed toward
maternal well-being, in spite of potential deleterious effects on
the fetus. Improvements in the maternal status should have
positive effects on the fetal condition since fetal compromise
primarily results from maternal cardiovascular decompensation.
 Volume expansion —
 Vasoactive drug therapy —Dopamine is commonly used.
 Oxygenation —
 Antimicrobial therapy —
 Empiric therapy in the septic patient should cover a wide variety
of both aerobic and anaerobic Gram-negative and Gram-positive
bacteria. A common antibiotic regimen is ampicillin (2 grams Q 4
hours), gentamicin (1.5 mg/kg Q 8 hours for patients with normal
renal function), and clindamycin (900 mg Q 8 hours) or
metronidazole (15 mg/kg initially then 7.5 mg/kg Q 6 to 8 hours).
 Surgery —
 COMPLICATIONS — Acute
respiratory distress syndrome occurs
as part of septic shock.
 PROGNOSIS — Septic shock is a
morbid event with high lethality

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