OBSTETRIC INJURIES TO GENITAL TRACT

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OBSTETRIC INJURIES TO GENITAL TRACT OBSTETRIC
SHOCK

• Dr Samar Sarsam

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• 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

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• 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

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• 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

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• 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.

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• 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.

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• 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,epidura
  l.

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• 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.

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Repair of a second degree laceration
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• 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.

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Layered primary closure of a fourth-degree
obstetric laceration
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• 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.

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• 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.

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• 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

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• 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.

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• 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.

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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

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• 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.

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COMMON FEATURES OF SHOCK

• Hypotension Hypotension (systolic BP lt90 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.

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• 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.

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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.

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• Causes
• 1-Concealed hge any bleeding as in episiotomy,
  vaginal hematoma, rupture uterus with out obvious
  external bleeding leads to obstetric shock.
• 2-Uterine inversionhas 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

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• 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.

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• 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.

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• 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.

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• 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

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• 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 .

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• 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

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• 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 .

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• 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.

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• 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.

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• 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.

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• 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

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• COMPLICATIONS Acute respiratory distress
  syndrome occurs as part of septic shock.
• PROGNOSIS Septic shock is a morbid event with
  high lethality