1. Post-partum hemorrhage. 2. Retained placenta. 3. Inversion of the uterus. 4. Obstetric shock. POST PARTUM HEMORRHAGE • Definition : Excessive bleeding during or after the 3rd stage of labor. Excessive means 600ccs or more or an amount which affects the general condition of the patient e.g. anemia or pre-eclampsia (hypovolemia) • Types: 1. Primary post-partum hemorrhage: Bleeding during the 3rd stage of labor or within 24hours of delivery. 2. Secondary post-partum hemorrhage: Bleeding after the 1st day following delivery till the end of puerperium (6 weeks). Primary post-partum hemorrhage • Normal mechanism of hemostasis: After placental separation, contraction of the myometrium (especially the oblique layer) squeeze the blood vessels. This results in showing of circulation allowing for the formation of clots, and occluding the vessels. The average amount of blood loss during episiotomy may be around 100to 200 cc. The average amount of blood loss during cesarean section may be up to 1000 cc. Etiology A. Placental site bleeding: I. Atony : ( abscence contraction) main cause, due to: 1. Prolonged labor, uterine exhaustion. 2. Uterine over distention e.g.: twins, polyhydramnios. 3. Prolonged anesthesia and analgesia ( excessive sedations ). 4. Induction or augmentation. 5. Full bladder or rectum : reflex inhibition of contraction 6. Fibroid : mechanical interference with retraction (squeezing of vessels ) 7. Ante partum hemorrhage. 8. Anemia: hypoxia of myometrium 9. Idiopathic. II. Retained part placenta: Or sometimes the whole placenta, partially or completely separated or a succenturiate lobe. The retained placental tissue acts as a splint preventing myometrial retraction. III. Hypofibrinogenemia :consumption coagulopathy :DIC : coagulation defect 1. Concealed accidental hemorrhage. 2. IUFD. 3. Amniotic fluid embolism . 4. Excessive infusion of plasma substitutes. B. Extra-placental site bleeding: Traumatic post-partum hemorrhage; laceration of perineum, vulva, vagina, cervix or rupture uterus. • Types: - Atonic . - Traumatic. - Mixed. Clinical picture Atonic Traumatic
General General condition and General condition
examination degree of shock may be out and degree of shock of proportion to the amount are in proportion to of revealed bleeding as the amount of blood accumulation inside revealed bleeding the uterus Abdominal Uterus is lax and large, Uterus is examination pressure on the fundus contracted. leads to expulsion of large amounts of blood and blood clots. Dark blood. Bright red blood. Vaginal No laceration laceration examination Treatment I. Prevention : 1. Avoiding predisposing factors e.g.: - Correction of anemia. - Evacuation of bladder, rectum. - Oxytocin, if given for induction or augmentation, should be continued after delivery. - Avoiding excessive anesthesia or analgesia. - Avoiding traumatic delivery. - Avoiding prolonged labor i.e.: CS when indicated. - Proper management of 3rd stage, routine ergotamine and massage. - Examination of birth canal after delivery(4th stage of 2. Careful observation for 1-2 hours after delivery (4th stage of labor) 3. Equipped blood banks should be available in hospitals. II. Correction of shock if present by: 1. Position; elevating the patient’s legs. 2. Morphia. 3. O2 . 4. Warmth. 5. Fluids, plasma. 6. Blood transfusion. 7. Steroids. 8. Antibiotics. III. Treatment of atonic post-partum hemorrhage: A. Before delivery of placenta: 1. Massage. 2. Ergometrine. 3. Brand-Andrews method of if it fail : 4. Manual separation of placenta under anesthesia: Technique of separation: - Anesthesia . - Bladder evacuation . - The right hand follows the cord to the placenta. - The left hand is applied on the abdomen to steady the fundus. - The right hand is then passed to the lower edge of the placenta and a sawing movement from side to side separates the placenta completely. - The placenta is then grasped, delivered and inspected to detect any missing fragment. Potential complication: - Perforation of the uterus. - Sepsis. - Retained placental fragment. - Post-partum hemorrhage. 5. “Crede method”: obsolete in modern obstetrics: - Evacuation of the bladder. - Massage. - The fundus is grasped with four fingers behind and the thumb in front to squeeze the placenta. - The fundus is pushed downwards to expel the placenta. • This method has many disadvantages: - High failure rate: especially in obese patients, rigid abdominal wall and placenta accreta. - A placental fragment may be retained. - May cause shock due to pain . - May cause inversion. - May cause partial separation of placenta, thus increasing post-partum hemorrhage. B. Bleeding after delivery of the placenta: 1. Inspection of placenta and membranes for missing portion. 2. Massage , ergometrine , oxytocin . 3. Manual exploration of the uterus under anesthesia to extract any placental fragments, pieces of membranes or blood clots which may interfere with myometrial contractions and retraction. • If atony persist: 4. Methyl prostaglandin F2 alpha 0.25 mg injected IM following vaginal delivery or intramyometrial following caesarean section. • If atony persists: 5. Bimanual compression under anesthesia. - The closed fist in the anterior fornix and the abdominal hand behind the fundus. - Maintained for a maximum of 30 minutes. - Blood transfusion, ergotamine and oxytocin are given during the procedure. • If atony persist: 6. Bilateral ligation of anterior division of internal iliac artery (through laparotomy) just distal to posterior partial branch. • If bleeding persist: 7. Subtotal hysterectomy (life saving) IV. Bleeding due to hypofibrinogenemia: 1. Fresh blood transfusion. 2. Fibrinogen 4-10 gm IV • if not available : 3. Blood transfusion. 4. Fresh frozen plasma. 5. Antifibrinolytic e.g.: - Epsilon amino caproic acid (EACA) - Trazylol. V. Traumatic post-partum hemorrhage: Treatment according to type e.g.: - Vulval, vaginal, perineal laceration. - Broad ligament hematoma (resulting from rupture uterus or cervical lacerations extending to the lower uterine segment) should be evacuated. Secondary post partum hemorrhage • Etiology : 1. Retained piece of placenta or membranes, blood clots or placental polyp. 2. Infection e.g.: - Infected CS wound. - Infected lacerations. - Infected placental site. 3. Sub mucus fibroid: when it becomes: - Extruded: polyp. - Infected. 4. Choriocarcinoma . 5. Local gynecological lesions e.g.: - Cervical erosion. - Cancer cervix. 6. Puerperal inversion of the uterus. • Treatment : - Blood transfusion if indicated e.g.: severe or persistent bleeding. - Treatment of the cause: 1. Retained parts or placental polyp: - Mild bleeding: ergotamine and antibiotics. - Severe or persistent bleeding: removal of retained parts under anesthesia. 2. Infection : antibiotics. 3.Fibroid: polypectomy. 4. Choriocarcinoma, cancer cervix, inversion: treated accordingly. Retained placenta • Failure of expulsion of placenta for 30 minutes after delivery of the fetus. • Etiology : A. Retained separated placenta: 1. Atony . 2. Contraction ring. 3. Rupture uterus (rare) The placenta passed into the peritoneal cavity. B. Retained non-separated placenta: 1. Atony. 2. Abnormal adhesions either: Simple adhesions or Placenta acreta: deficient decidua basalis, chorionic villi invade deeply, according to depth of invasion may be : - Simple accreta: villi invade the basal layer of decidua and superficial layer of muscles. It may be partial or complete. - Placenta increta: villi invade deep in muscles. - Placenta perceta: villi reach the peritoneal coat. In placenta accreta there is no plane of cleavage. More common with: -Placenta previa. -Implantation over CS scar. • Clinical picture: 1. Bleeding : - Only with placental separation: partial or complete. - Severe bleeding if associated with atony. 2. shock: Even in absence hemorrhage (idiopathic obstetric shock). 3. PV: may diagnose : - Placenta accreta (no plane of cleavage). - Rupture uterus. - Contraction ring. • Treatment : A. In case of atony: 1. Stimulate the uterus to contract by : - Massage . - Ergometrine, then Brand-Andrews maneuver if this fails: 2. Manual removal of placenta. 3. Crede method is not preferred as it has many disadvantages. B. In case of adherent placenta: 1. Simple adhesions: Manual removal of the placenta. 2. Placenta accreta: - Hysterectomy (1st choice) if the patient is very young the following may be attempted. - Cutting the cord and leaving the placenta for autolysis under cover of antibiotics. - Removal of placenta by morcellation (in pieces). - Retroplacental hygroma. C. In case of rupture uterus D. In case of contraction ring: - Deep anesthesia . - Manual removal of the placenta. • Complications: 1. Shock. 2. Post-partum hemorrhage. 3. Puerperal sepsis. 4. Sub involution. - Form a placental polyp. - Develop in choriocarcinoma. 5. Complications of the method used for removal. 6. Complications of anesthesia. Hydrofibrinogenemia Disseminated intravascular coagulopathy (DIC) • Normal level of fibrinogen during pregnancy=400-600mg% • Normal non-pregnant level = 200-400mg% • Etiology : 1. Concealed accidental hemorrhage. 2. Missed abortion: retained more than 4 weeks. 3. Intra-uterine fetal death(IUFD): retained more than 4 weeks. 4. Amniotic fluid embolism. 5. Excessive infusion of low molecular weight Dextran-plasma substitute (rarely used in obstetrics) 6. Septic shock. 7. Injection of intra-amniotic hypertonic saline for induction of abortion (rarely used). • Mechanism : In case of 1,2,3 and 7: - Thromboplasm, thromboplastin- like substances and Fibrinolysins released degenerated tissues or present in the amniotic fluid enter the maternal circulation. - They change prothrombin into thrombin which activates fibrinogen into fibrin leading to formation of wide spread micro thrombi. - Fibrinolysins act on fibrin causing its lysis which results in release of fibrin degradation products (FDPs). In No 5 Dextran can inactivate fibrinogen by forming dextran-fibrinogen compound. In No 6 The toxins produced in septic shock causing releasing of tissue thromboplastin. Finally the patient is left with deficient fibrinogen and other coagulation factors. Signs of incoagulability develop if the level of fibrinogen drops below 100 mg %. • Diagnosis : 1. The condition is suspected in the presence of any etiological factor. 2. Signs of incoagulability, e.g.: persistent bleeding from a vein puncture. 3. Post-partum hemorrhage. 4. Bleeding time and coagulation time are prolonged. Normal bleeding time :1-3 min. Normal coagulation time: 3-8 min. 5. Wiener test: (clot observation test): - 10 CCs of blood are collected in a test tube which is incubated in a water bath (temp 37C) for 1 hour. - Normally, a clot is formed within 10 minutes. - In case of hypofibrinogenemia either : • A clot is not formed within 10 min or • A clot is formed but is dissolved within 1 hour (due to increased fibrinolytic activity). 6. Fibrinogen level in blood : decreased. 7. FDPs in blood: increased. • Treatment : 1. Prevention by proper management and avoidance of predisposing factors. 2. Fresh blood transfusion to replace: - Volume . - RBCs. - Coagulation factors. 3. Fibrinogen : - 4-10 gm I.V. • If not available 4. Fresh frozen plasma. • If not available : 5. Large amount of blood transfusion. 6. Antifibrinolysins : e.g.: - Epsilon Amino Caproic acid (EACA) 4-10 gm. IV. - Trazylol: 50.000-100.000 units IV. • Given if there is evidence of increased fibrinolytic activity in Wiener test or if previous measures fails. 7. Heparin: 5000 U/12hours. If used, it should be only PROPHYLACTIC; in the presence of an etiological factor e.g.: IUFD before development or DIC to prevent stimulation of the coagulation cascade thus, preserving fibrinogen and other coagulation factors. Acute puerperal inversion of the uterus • The uterus is turned inside out, either partially or completely. • Incidence 1: 20.000 (very rare) • Etiology : 1. Induced : (most commonly): - Traction on the cord or: - Pressure on the fundus while the uterus is LAX. 2. spontaneous: - Precipitate labor. - Very short cord. - Straining while the uterus is lax. - Sub mucus fundal fibroid. • Degrees : 1st degree :(cupping) The fundus is depressed but doesn’t pass out side the cervix. 2nd degree : The inverted fundus protrudes through the cervix. 3rd degree: The whole uterus is inverted to appear outside the vulva. - 1st and 2nd degrees: incomplete inversion. - 3rd degree: complete inversion. • Clinical picture: 1. Bleeding: (unless the placenta is completely attached). 2. Shock : due to : - Bleeding . - Traction on peritoneum, shock is out of proportion to amount of bleeding. • Prevention : Avoiding traction on the cord or pressure on the fundus while the uterus is lax. 3. Mass : - At the vulva (3rd degree) or - In the vagina (2nd stage) - The placenta may or may not be attached to it. 4. Sub acute type: (rare): - During the puerperium . - Vaginal bleeding and infected. • Treatment : 1. Correction of shock. 2. Manual reduction under anesthesia . - If the placenta is still attached it is not removed, unless it interferes with reduction. - Massage and ergotamine. 3. Reduction by hydrostatic pressure: The nozzle of a douche is introduced into the vagina, the vulva is closed and the fluid is allowed to escape, its pressure reduces the inverted uterus. 4. Availing repositor in some sub acute cases (rare). Chorionic inversion (very rare) • Etiology: 1. Puerperal . 2. Tumors attached to the fundus ( e.g.: fibroid) • Differential diagnosis: 1. Uterine prolapse: Differentiated from inversion by the presence of external os. 2. Fibroid polyp: Differentiated from inversion by passage of a sound. • Treatment : 1. Puerperal type: surgical repair (abdominal or vaginal). 2. Tumors : treatment of the cause. Shock • Shock is a state of imperfect cellular perfusion ( less than the amount required for normal cellular function and metabolism) • Pathophysiology : 1. Sympathetic stimulation leads to : - Increased cardiac output (tachycardia) is an attempt to restore perfusion . - Arterioral constriction to increase peripheral vascular resistance (PVR). 2. Redistribution of blood with priority to vital organs; brain and heart and diminished perfusion to kidneys (oliguria or anuria), muscles and skin (pallor). 3. Stimulation of the respiratory center (tachypnea). 4. Stimulation of the suprarenals: (cortisol causes salt and water retention and is anti shock). 5. Diminished O2 delivery to the cells leads to a shift to anaerobic metabolism with subsequent accumulation of lactic acid and acidosis. 6. Accumulation of lactic acid leads to paralysis of the precapillary sphincter, pooling and stagnation of blood in the capillaries : “irreversible shock” • Types of shock : 1. Hypovolemic shock: The most important factor is hemorrhage (Hemorrhagic shock) due to various causes ante partum and post-partum hemorrhage. 2. Neurogenic shock: Failure of the autonomic nervous system to maintain peripheral vascular resistance. Occurs in cases of trauma or tissue damage e.g.: - Disturbed ectopic pregnancy. - Concealed accidental hemorrhage. - Rupture uterus. - Acute inversion. - Difficult forceps delivery or beech extraction. - Crede method. N.B.: hypovolaemic and neurogenic shock may be called “surgical shhock” 3. Septic shock: Bacteria circulate in the blood and produce toxins (endotoxins or exotoxins). • These toxins cause the following: - Damage to capillary walls lead to escape of blood outside the vessels with subsequent diminished perfusion (shock). - The same pathology occurs in the capillary circulation of the lungs leading to adult respiratory distress syndrome (ARDS) - Toxins have positive chronotropic effect on the heart, causing marked tachycardia, out of proportion to fever. - Toxins cause hemolysis, with subsequent jaundice and deposition of hemosiderin in renal tubules. - Toxins and fever cause vasodilatation of the skin blood vessels and the patient is flushed. 4. Shock associated with DIC. 5. Other cause of shock : Less relevant to obstetricians include: - Cardiac shock: Failure of the heart to serve as an adequate pump e.g.: acute myocardial infraction. - Anaphylactic shock: Release of large amounts of histamine. • Factors that contribute to development of shock: 1. Anemia . 2. Ante partum hemorrhage. 3. Pre-eclampsia and eclampsia (hypovolemia). 4. Prolonged labor with dehydration and acidosis. • Clinical picture of shock: 1. Hypotension. 2. Rapid weak pulse “Thready pulse”. 3. Hypothermia (except in septic : fever). 4. Pallor: (except in septic shock: fushing ). 5. Tachypnea :especially in hemorrhagic shock, the patient is “air-hunger” 6. Cold sweat: (sympathetic stimulation). 7. Oliguria or anuria. 8. Irritability: especially in hemorrhagic shock due to brain hypoxia. • Treatment of shock: 1. Position : Elevation of the patient’s legs: to increase venous return and cardiac output. 2. Warmth : To minimize metabolic requirements of O2. 2. Morphia :10 mg. IV slowly: - To relieve irritability. - To decrease respiratory rate ( better oxygen). 4. Oxygen administration: To improve O2 delivery to tissues. 5. Fluid replacement: - Crystalloids: e.g.: lactated ringer’s solution, glucose or saline (until blood is available) to maintain blood volume and renal perfusion. - Colloids: • Blood: especially in hemorrhagic and septic shock. • Plasma: especially in neurogenic shock. • Low molecular weight dextran: is NOT given as it interferes with coagulation factors. • Fluid replacement should be monitored by CVP. “central venous pressure” to avoid over transfusion: - Normal 8-13 cm of water. - CVP catheter is inserted into superior vena cava or right atrium . 6. Adrenocortical steroids: in large doses. Mechanism is not fully understood; partly through salt and water retention. 7. Antibiotics : Are especially required in large doses that cover the spectrum in septic shock . • Monitoring of shock: 1. Vital signs, uterine output and central venous pressure (CVP). 2. Surgical interference should be postponed until improvement occurs. • Complications of shock: 1. Death (irreversible shock). 2. Renal failure due to acute cortical necrosis. 3. Sheehan’s syndrome. 4. Complications of blood transfusion. A- Incompatible blood transfusion B- Transmission of disease :AIDS,Hepatitis C- Air embolism D - Rh immunization E- Pyrogenic reaction Thank you Dr. M Hafez