S A B Xu
Upcoming SlideShare
Loading in...5
×
 

S A B Xu

on

  • 2,860 views

 

Statistics

Views

Total Views
2,860
Slideshare-icon Views on SlideShare
2,855
Embed Views
5

Actions

Likes
1
Downloads
127
Comments
0

1 Embed 5

http://www.slideshare.net 5

Accessibility

Categories

Upload Details

Uploaded via as Microsoft PowerPoint

Usage Rights

© All Rights Reserved

Report content

Flagged as inappropriate Flag as inappropriate
Flag as inappropriate

Select your reason for flagging this presentation as inappropriate.

Cancel
  • Full Name Full Name Comment goes here.
    Are you sure you want to
    Your message goes here
    Processing…
Post Comment
Edit your comment

    S A B Xu S A B Xu Presentation Transcript

    • Early Pregnancy Complications
      • Spontaneous abortion
      • Ectopic pregnancy
    • Spontaneous Abortion
    • Definition of abortion
      • Before 20 weeks gestation
        • Based on LMP
      • Or delivery of fetus
        • Weight less than 500 grams
    • Etiology of spontaneous abortion
      • 50% of SA during the first 12 weeks with abnormal karyotype (Aneuploidy)
      • Abnormal development noted in majority of cases
      • Incomplete cervix cause of second trimester loss
    • Etiology of spontaneous abortion
      • Maternal factors
        • Systemic disease
        • Uterine defects
        • Immunologic disorders
        • Malnutrition
      • Toxic factors
      • Trauma
    • Abortion classification
      • Threatened abortion
      • Inevitable abortion
      • Incomplete abortion
      • Complete abortion
      • Missed abortion
      • Septic abortion
      • Recurrent abortion
    • Threatened abortion
      • Bleeding during early pregnancy
      • Prognosis worse with pain or cramping
      • Rule out other course of bleeding
        • Cervical lesions
        • Polyps
        • Implantation bleeding
    • Management of threatened abortion
      • Serial hCG
      • Serial progesterone
      • Vaginal sonograms
      • Pelvic rest
      • Bed rest
    • Inevitable abortion
      • Certain to occur
      • Rupture of membranes
      • Cervical dilation
    • Management of inevitable or incomplete abortion
      • Evacuation of the uterus by suction D and C
      • Prognosis is excellent if the retained tissue is promptly and completely evacuated.
    • ECTOPIC PREGNANCY
    • Yanwen Xu , M.D., PhD The First Affiliated Hospital of Sun Yat-sen University ECTOPIC PREGNANCY
    •  
      • Definition:
      • A fertilized ovum implants in an area other than the endometrial lining of the uterus.
    • Sites of ectopic pregnancies
    •  
    •  
    •  
    •  
    •  
    • Residual uterus pregnancy Uterus
    • Tubal ectopic pregnancy
    • Etiology
      • Tubal factor
        • Ovarian factors
          • Other factors
              • IUD
    • Time of Rupture
      • Rupture is usually spontaneous
        • Isthmic pregnancies 6-8 week’s gestation
        • Ampullary pregnancies 8-12 week’s gestation
        • Interstitial pregnancies 12-16 weeks’s gestation
    • Pathology
      • Little or no decidual reaction and minimal defense against the permeating trophoblast in the ectopic implantation sites.
      • A hematoma in the subserosal space enlarges as pregnancy progress.
      • Bleeding is of uterine origin and is caused by endometrial involution and decidual sloughing.
      • The Arias-Stella reaction in endometrium is non specific.
    •   Clinical findings
      •     Three major symptoms :
          • Amenorrhea
            • Pain
              • Vaginal bleeding
    • Clinical findings
      • Dizziness, lightheadedness, and/or syncope is present in one-third to one-half cases.
    • Signs
      • General condition
      • Abdominal examination
        • Diffuse or localized abdominal tenderness
      • PV :
        • A unilateral adnexal mass
        • Adnexal and/or cervical motion tenderness
        • Uterus may undergo typical changes of pregnancy
    • Laboratory findings
      • Hematocrit
        • Depending on the degree of intraabdominal bleeding
      • White blood count
      • Pregnancy tests
        • The β -HCG is positive.
        • Two-thirds of ectopic pregnancy have abnormal serial titers.
      • Ultrasound
      • Culdocentesis
    • Normal Pregnancy Ectopic Pregnancy
    • Culdocentesis
    • Culdocentesis
      • Nonclotting blood shows intra-abdominal bleeding.
      • If the blood clots, it is likely from a punctured vessel in the vaginal wall.
      • If culdocentesis is positive, laparoscopy or laparotomy should be performed immediately .
      • A negatively result may rule out a ruptured or leaking ectopic but not an intact one.
    • Differential Diagnosis
      • Abortion
      • Acute salpingitis
      • Hemorrhagic corpus luteum
      • Acute appendicitis
      • Ovarian cyst torsion
    • Treatment
      • Expectant management
        • The β -HCG titers are low (<200 mIU/mL) or decreasing.
        • The risk of rupture is low.
      • Surgical treatment
        • Conservative surgery in the hemodynamically stable patient with an ampullary pregnancy.
        • Laparoscopy is preferred over laparotomy in stable pregnancy.
    • Treatment in hemodynamically unstable patients----Salpingectomy
    • Treatment
      • Interstitial pregnancies require a corneal wedge resection, with uterine reconstruction and sometimes salpingectomy on the affected side.
      • Cervical ectopics with methotrexate or hysterectomy.
      • Ovarian pregnancy requires oophorectomy and sometimes salpingectomy on the affected side.
      • Abdominal pregnancy involves delivery of the fetus with ligation of the umbilical cord. The placenta is left.
    • Medical management
      • ① Small (<3cm)
      • ② Intact
      • ③ Extr-auterine gestation with no
      • fetal heart motion
      • MTX or 5-FU
    • Pre-eclampsia & eclampsia Yanwen Xu , M.D., PhD The First Affiliated Hospital of Sun Yat-sen University
    • Patient history
      • 謝 x 芳, 30 y/o F
      • Chief complain: Twin pregnancy at 32+ gestational weeks with elevated BP and vaginal watery discharge since 8/8 12:00am
      • Past history:denied any systemic disease, such as HTN, DM, CAD, pulmonary dx
      • Allergy history:denied
      • Drug use history:denied
      • OP and anesthesiology history:denied
    • Present pregnancy history and menstrual history
      • G1P0, got this pregnancy by ET
      • LMP:94-12-26, EDC:95-10-12
      • Routine pregnancy exam. no abnormality was told such as GDM, PIH before 8/2
    • Symptom and sign
      • 8/2 8/3 8/4 8/5 8/6 8/7 8/8
      Epiphora Proteinuria Abdominal edema at lower abdomen Fetal movement decrease in right side Dyspnea, orthopnea Insomnia, urinary frequency BP:136/80 BP:210/100
    • Events at 8/8
      • 12am 4pm 5pm 18am
      watery discharge BP : 210/100mmHg BT:1’30”, CT:1’40” WBC:8.4x10 3 /ul RBC:3.19x10 6 /ul Hb : 10g/dl , Hct:29% Plt : 9.7K/μL O2, adalate, trandate(5mg) refer to ER BT:37.6 HR:129 BP:198/118 SpO2:100% RR:27/min Admission to 5FD BT:37.6 HR:120 BP:181/102 RR:22/min 5:40pm BP:161/104 HR:110 SaO2:100% MgSO4:10ml/hr
      • 6pm 6:30 6:40
      接獲通知,前往探視 送入 DR O2 mask 3L, SaO2:93% room air, SaO2:97%  70%  97% BP:232/148 , HR:105 dyspnea could not lie down , edema , difficult in breathing , cough with frothy sputum Induction Etomidate:20mg laryngoscopy Trandate:15mg LMA Cisatracurium:10mg laryngoscopy ENT standby 備 fiber ASA VE
      • 6:40 7:00 8:00
      Maintenance Sevoflurane:0.2-0.3MAC add N 2 O Lasix:40mg Morphine:10mg midazolam:5mg bicarbonate:5amp ventilation: volume control ,PEEP:8 cmH 2 O suction 6:42 Operation 6:47 twin A F 1510g , 1  7 twin B F 1698g , 4  8 7:45 finish, IV:150ml blood loss:200ml On A-line ABG :7.05/77.3/162/21.5/-9.4/12.3/37/98.4/193/5.2/144/4.4/112.8/1.03 Endo:6.5mm fix 21cm
    •  
    • Lab data 8/8 pre OP
      • WBC:11.55 K/uL
      • RBC:3.75M/uL
      • Hb:11.1 g/dL
      • HCT:34.4%
      • PLT:107K/uL
      • PT:11sec
      • PTT:29.5sec
      • INR:0.93
    • Lab data
      • AST:36U/l
      • ALT:18U/l
      • CRP:0.52mg/dl
      • Alb:2.67g/dL
      • D-Bil:0.1mg/dl
      • Na:140mmole/l
      • K:3.5mmole/l
      • Cl:110mmole/l
      • Mg:0.74mmole/l
      • BUN:6.4mg/dl
      • Cre:0.8mg/dl
      • FDP:53.2ug/mL
      • D-Dimer:2978
      • Random urine:
      • Sp.Gr.:1.01
      • pH:5.5
      • protein:1+ (70mg/dL)
      • Glu.:-
    • Definitions - pre-eclampsia
      • Persistent hypertension from gestation 20 th week onwards defined by either :
        • Diastolic bp >90 Torr
        • Systolic bp >140 Torr
        • Or relative increase diastolic bp >15 Torr or systolic bp>25 Torr
      • Proteinuria > 0.3g in 24 hours
      • Generalised oedema (mainly lower extremities, hands)
    • Definition of Eclampsia
      • One or more convulsion , not caused by other cerebral condition, in a patient with pre-eclampsia
    • Definition of severe pre-eclampsia
      • Features of pre-eclampsia plus one the following :
        • Systolic bp > 160 Torr
        • Diastolic bp >110 Torr
        • Proteinuria > 2 g per 24 hours
        • Cerebral or visual disturbances
        • Oliguria ≤ 500ml per 24 hours
        • Epigastric pain
        • Pulmonary oedema
        • Haemolysis, elevated liver enzymes and low platalet syndrome = HELP syndrome
    • Mild and severe preeclampsia <100000 >100000/mm 3 Platelet count Yes No HELLP Yes No cynosis Yes No Pulmonary edema Yes No RUQ pain Yes No Epigastric pain Yes No Visual disturbances Yes No headache <500 >500ml/24hr Urine output >=5 3+or4+ <5g/24hr 1+or2+ Urinary protein >=110 <110mmHg DAP >=160 <160mmHg SAP severe mild
    • Epidemiology
      • Incidence pre-eclampsia 6 % all pregnancies
      • Incidence eclampsia 2-5 in 1000 deliveries
      • PEE is associated with 1.8 % maternal mortality and 7 % fetal/ neonatal mortality
    • Pathogenesis
      • Factors predisposing
        • Increase Oxygen demand states e.g.
          • Multiple pregancies
          • Fetal macrosomia
        • Decrease Oxygen transfer
          • Maternal anemia, High altitude (Tibet,Nepal,Peru)
          • Microvascular di s ease e.g. Hypertension, Diabetes, collagen disease , smoking
          • Abnormal placentation
        • Genetic e.g. Angiotensin gene
        • Immune mechanism e.g. antiphospholipid syndrome
    • Pathogenesis
      • Primary defect involves abnormal migration of extravillous trophoblast in placenta
          • Myometrial vessels retain musculoelastic architecture instead of being converted into sinusoidal vessels( as occurs in normal pregnancy)
          • Defect occurs with the inhibition of second wave of migration i.e. in second trimester
          • Consequence of this defect includes
            • Hypoperfusion and hypoxia of placenta endothelial cells
            • Change in ratio of vasopressor substances tromboxane prostacyclin ratio by endothelium causing vasospasm
    • Faulty placentation Genetic, immunologic, inflammatory factors Maternal vascular disease Excessive trophoblast Reduced uteroplacental perfusion Endothelial activation Capillary leak hemoconcentration edema proteinuria Vasospasm Activation of coagulation thrombocytopenia Vasoactive agents: Prostaglandins nitric oxide endothelins Noxious agents: Cytokines Lipid peroxidases oliguria HTN seizures abruption liver ischemia
    • Pathophysiology - cerebral
      • Cerebral involvement include
        • Eclamptic convulsions – principal sequlae
        • pathogenesis may be due to:
          • Focal cerebral vasospasm and hypoperfusion causing abnormal electrical activity with hypertension occurring as secondary response – most likely explanation
          • Hypertension causes breakdown in cerebral autoregulation, leading to overdistension of vessels and extravasation of fluid
        • Visual disturbances i.e. cortical blindness (rare)
        • Cerebral haemorrhage
    • Pathophysiology - circulation
      • Circulation
        • Uteroplacental vascular resistance increases with decrease in blood flow , leading to placental ischaemia and fetal growth retardation
        • Systemic circulation – 2 models
          • Traditional model – occurs in 80% pre-eclampsia with picture of
            • Decreased plasma volume
            • Vasoconstriction
          • and therefore hypoperfusion of placenta and kidney
          • Hyperdynamic model – high CO with compensatory vasodilation
    • Pathophysiology - renal
      • Renal involvement occurs in 2 stages:
        • Impairment of tubular function occurs early – reflected by development of hyperuricaemia .
          • Serum uric acid levels are a sensitive marker of progression and risk
        • Glomerular filtration impaired later in disease – reflected by proteinuria > 0.5g in 24 hours or in severe pre-eclampsia > 2 g in 24 hours
        • Acute renal failure (rare) due to:
          • Acute tubular necrosis (more common and reversible)
          • Acute cortical necrosis (permanent)
    • Pathophysiology – Blood
      • Platelets
        • usually associated with thrombocytopaenia ( < 100,000/mm 3 ) and increase in mean platelet volume
          • Immune mediated
        • Increase platelet activation
          • Possibly due to endothelial activation or intrinsic changes in platelets
    • Pathophysiology – blood
      • Coagulation cascade activated to greater extent than normal pregnancy
        • Increase factor VIII consumption
        • Increase thrombin activity
        • All leads to heightened risk of thrombosis
      • Anticoagulant protein levels decreased
        • Decreased antithrombin III
        • Decreased protein C and S
      • Fibrinolytic system – conflicting results
    • Pathophysiology – liver
      • Liver complications consists of:
        • Impaired liver function tests due to vasoconstriction of hepatic bed causing
          • Periportal fibrin deposition
          • Hepatocellular necrosis
        • Hepatic infarction and rupture – worst but rare condition
        • HELLP syndrome-hemolytic anemia, elevated liver enzymes, and low platelet count
    • Pathophysiology – HELLP syndrome
      • Constellation of laboratory findings in pre-eclampsia
        • H aemolysis - seen on peripheral blood smear and bilirubin levels > 1.2mg/dL
        • E levated L iver enzymes – serum aspartate aminotransferase (AST) levels > 70 U/L
        • L ow P latelets < 100,000/mm 3
      • Pathogenesis uncertain but may be due to vasospasm
    • Pathophysiology –pulmonary system
      • Pulmonary edema occur with severe pre-eclampsia or eclampsia.
        • Excessive fluid administration
        • Delayed mobilization of extravascular fluid
        • Decreased plasma colloid oncotic pressure from proteinuria
        • Decreased hepatic synthesis of albumin
      • Hypertension
      • Proteinuria
        • An indicator of fetal jeopardy
      • Edema
        • Weight gain >2 lb/wk or a sudden weight gain over 1 to 2 days
      Clinical Findings
    • Symptoms
      • Headache
      • Oedema
      • Visual disturbance
      • Focal neurology, fits, anxiety, amnesia
      • Abdo pain
      • Decreased urine output
      • None
      Multisystem disease with varying clinical presentations.
    • Signs
      • Hypertension
      • Tachycardia and tachypnoea
      • Creps or wheeze on auscultation
      • Neurological deficit
      • Hyperreflexia
      • Petechiae, intracranial haemorrhage
      • Generalised oedema
      • Small uterus for dates
    • Complications
      • Early delivery and fetal complications due to prematurity.
      • Chronic uteroplacental insufficiency increases the risk of IUGR and oligohydraminos.
      • Abruptio placentae
    • Treatment-mild preeclampsia
      • Maternal treatment should include:
        • Bed rest
        • Serial or continuous blood pressure monitoring
        • Urinanalysis for proteinuria – quantification for degree of severity
        • Blood test include
          • B P + platelet count and morphology
          • Haemocoagulation system
          • Uric acid, creatinin for renal function
          • Serum uric acid – useful early and for progression
          • Hepatic enzymes (AST,ALT, GMT)
        • Fluid balance – urine output, CVP, Sa02 etc
        • ECG , medical Management Consulting ( neurologists, internists)
    • Assessment of fetal status
      • Fetal monitoring:
        • Regular fetal HR monitoring NST – for acceleration, loss of variability or decelerations
        • Fetal ultrasound may be useful for fetal size and morphology, amniotic fluid volume estimation , placenta maturation
        • Amniocentesis to determine the L:S ratio
        • Corticosteriods to accelerate fetal lung maturity
          • If delivery may occur in the next 2-7 days
    • Treatment-severe preeclampsia
      • Goals of management:
        • Prevention of convulsions
        • Control of blood pressure
        • Maintain placental perfusion with delivery timed appropriately
    • Management – Anticonvulsant therapy
      • Magnesium sulphate : anticonvulsant of choice
        • Action by :
          • antagonism of calcium and hence decreased systemic and cerebral vasospasm
          • Increase release of PGI 2 by vascular endothelium
        • Other effects in parturient include:
          • Tocolysis
          • Decreased cathecholamine release
          • Mild antihypertensive
          • Increases renal and uterine blood flow
    • Management – anticonvulsant therapy
      • Magnesium continued
        • Renally excreted – so reduce dose in renal failure
        • Therapeutic level 4.8-8.4mg/dL ; must monitor for toxicity
        • Repeated seizures despite therapeutic levels need to consider others
      • Monitoring during MgSO 4 treatment
        • Deep tendon reflex
        • Urine output at least 100mL during the preceding 4 hours
        • Respirations 12/min
        • 10mL of 10% calcium chloride or calcium gluconate
    • Management – Anticonvulsant therapy
      • Diazepam : effective especially if needed acutely but causes fetal/ neonatal complications
        • Adverse effect
          • depression of muscle tone and breath centre
          • Competing with bilirubin for albumin bingding, predisposing the infant to kernicterus
    • Management of eclamptic seizures
      • Airway protection
      • Maintain oxygenation (O2 inhalation via mask)
      • Control of seizures
        • Continued convulsions may indicate other cerebral pathology
        • Management may involve treatment cerebral oedema (CS)
      • Delivery of fetus when mother is in stable condition, even in some situation SC is needed acutely
    • Management – Antihypertensive therapy
      • Treatment required when :
        • Diastolic bp > 110 mmHg
        • The goal is to bring Bp into 90-100 mmHg
      • Hydralazine : agent of choice
        • Causes direct arteriolar vasodilation
        • Improves renal and uteroplacental blood flow
      • Labetalol : nonselective beta blocker
        • causes rapid decrease in arterial bp without compromising uteroplacental flow
        • May cross placenta but fetal complications rare
    • Management – Antihypertensive therapy
      • Nifedipine : causes direct relaxation of arteriolar smooth muscle
        • Maintains uterine perfusion
        • Can cause uterine muscle relaxation – increase risk of post partum haemorrhage
        • Contra-indicated with use of Mg
      • Sodium nitroprusside : hypertensive emergencies
      • Nitroglycerin : useful especially when pulmonary oedema complicates situation
    • Management – Antihypertensive therapy
      • Unsuitable therapies :
        • α - Methyldopa – slow onset
        • Clonidine – rebound hypertension on cessation
        • B-blockers – risk of hepatotoxicity, decrease uteroplacental perfusion, fetal complications
        • ACE-Inhibitors – contraindicated in pre-delivery because of intrauterine death, oliguria, renal failure in mum and neonate
        • Diuretics –avoid - because deplete intravascular volume
    • Conclusion
      • Pre-eclampsia due to a primary disturbance of placental vasculature is leading to increase systemic vascular resistance and bears a potential for multiorgan disturbances / failure secondary to vasospasm.
      • Mainstay of management is early diagnosis, prevention of hypertension and seizures.
      • Severe pre-eclampsia requires intensive management and the ultimate cure being delivery of fetus.
      • Eclamptic seizures and pulmonary oedema often occur in the post-partum period (strict patient control after delivery) .
    • Maternal Mortality - Obstetrical Hemorrhage - 4(4%) D.I.C. 9(10%) Couvelaire uterus 17(16%) Abruptio placenta 7(7%) Placenta previa 66(63%) Uterine atony Patients (n=103) Indication
    • Placenta Previa
    • The placenta provides the fetus with oxygen and nutrients and takes away waste such as carbon dioxide via the umbilical cord.
      • Definition    
        • Placenta previa is a condition that may occur during pregnancy when the placenta implants in the lower part of the uterus and obstructs the cervical opening to the vagina (birth canal).
    • Incidence
      • The incidence of placenta previa is approximately 1 out of 200 births.
      • Increases with each pregnancy , and it is estimated that the incidence in women who have had 6 or more previous deliveries may be as high as 1 in 20 births.
      • Doubled in multiple pregnancy (such as twins and triplets).
      • Risk factors
        • Multiparity (previous deliveries)
        • Multiple pregnancy
        • Previous myomectomy (removal of uterine fibroids through an incision in the uterus)
        • A previous C-section (if the scar is low and close to the vaginal cervix region).
    • Etiology
      • Endometrium factors:
        • a scarred endometrium (lining of the uterus)
        • Curretage for several times
        • an abnormal uterus
      • Placental factors
        • Large
        • Abnormal formation of the placenta (succenturiate lobe or placenta diffusa).
      • Development retardation of fertilized egg
    • Mechanisms of bleeding
      • Mechanical separation of the placenta from its implantation site
      • Placentitis
      • Rupture of poorly supported venous lakes in the deciduas basalis
    • Classification
      • Total placenta previa
      • The internal cervical os is covered completely by placenta
      • Partial placenta previa
      • The internal os is partially covered by placenta
      • Marginal placenta previa
      • The edge of the placenta is at the margin of the intenal os.
    • classification
    • Clinical findings
      • Symptoms    
        • Spotting during the first and second trimesters
        • Sudden, painless, and profuse vaginal bleeding in pregnancy during the third trimester (usually after 28 weeks)
        • --Bleeding may not occur until after labor starts in some cases
        • --Anemia, shock
      • Signs
        • The uterus is usually soft, relaxed and nontender.
        • The infant position is oblique ( // ) or transverse ( == ) in about 15% of cases.
        • Fetal distress is not usually present unless vaginal blood loss has been heavy enough to induce maternal shock , placenta abruptio , or a cord accident occurs.
        • No vaginal and rectal examination 
    • Accessory examinations
      • Ultrasonography:
        • Accuracy 95%
        • 34 th week
      • Postpartum examination of placenta and membrane
        • 7cm
      • Differential diagnosis
        • Placental abruption
        • vagina bleeding with pain, tenderness of uterus.
        • Vascular previa
        • Abnormality of cervix
        • cervical erosion or polyp or cancer
    • Complications    
      • Maternal complications
        • major hemorrhage, shock , and death.
        • Implanted placenta
        • Anemia and infection
      • Fetal complications
        • Prematurity (infant is less than 36 weeks gestation) is responsible for about 60% of infant deaths secondary to placenta previa.
        • Fetal blood loss or hemorrhage may occur because of the placenta tearing away from the uterine wall during labor. It may also occur with entry into the uterus during a C-section delivery.
    • Treatment
      • The course of expectant treatment depends on
        • The amount of abnormal uterine bleeding
        • Whether the fetus is developed enough to survive outside the uterus
        • The amount of placenta over the cervix
        • The position of the fetus
        • The parity (number of previous births) for the mother
        • The presence or absence of labor.
    • Treatment
      • Early in pregnancy, transfusions may be given to replace maternal blood loss .
      • Medications may be given to prevent premature labor, prolonging pregnancy to at least 36 weeks.
      • Beyond 36 weeks, the benefits of additional infant maturity have to be weighed against the potential for major hemorrhage.
    • Treatment
      • In selecting the optimum time for delivery, tests of fetal lung maturation are invaluable adjuvants.
      • Cesarean section is the method for delivery. It has proven to be the most important factor in reducing maternal and infant death rates.
    • Expectations (prognosis)
      • The maternal prognosis (probable outcome) is excellent when managed appropriately.
        • This is done by hospitalizing those at risk who are exhibiting signs and symptoms, and by performing C-section delivery.
    • ABRUPTIO PLACENTAE
    • Definition
      • Abruptio Placentae( placental abruption):
      • premature separation of the normally implanted placenta from the uterine wall.
      • Incidence :
        • 1/77-89 deliveries
        • Severe form (resulting in fetal death)1/500-750
    • Classification
      • Concealed separation : no vaginal bleeding
      • Apparent separation : vaginal bleeding will be
      • Mixed separation : vaginal bleeding will be apparent
    •  
    • Classification
      • Concealed form (20%)
        • Detachment of the placenta may be complete
        • Complications are often severe. About 10% with DIC.
      • External form (80%)
        • Placenta detachment is more likely to be incomplete
        • Complications are fewer and less severe.
    • Etiology
      • Mechanism: hemorrhage into the decidua basalis, leading to premature placental separation and further bleeding.
      • Associated factors:
      • Maternal hypertension
      • Sudden decompression of the uterus
      • Maternal age and multiparity
      • trauma
    • Pathophysiology and pathology
      • Local vascular injury that results in vascular rupture into the decidua basalis, bleeding, and hematoma formation.
        • Preeclampsia-eclampsia, chronic hypertension, DM, chronic renal disease
      • An abrupt rise in uterine venous pressure transmitted to the intervillous space.
        • Vasodilatation secondary to shock, compensatory hypertension and the paralytic vasodilation of conduction anesthesia.
    • Pathophysiology and pathology
      • Uteroplacental apoplexy
        • Extensive intramyometrial bleeding, resulting in a purplish and copper-colored, ecchymotic, indurated organ that all but loses its contractile power because of disruption of muscle bundles.
    • Pathophysiology and pathology
      • Coagulation abnormalities
      • Hypofibrinogenemia
      • Increaseing levels of fibrin degradation products
      • decreasing platelet count
      • Increasing prothrombin time and partial thromboplastin time
      • Decreasing other serum clotting factors
    • Diagnosis
      • Classic clinical presentation :
      • vaginal bleeding 80%
      • Tender uterus 2/3
      • Uterine contractions 1/3
      • Fetal distress 50%
      • Ultrasonography:
      • Placental examination
      • The extent of placental abruption of the maternal surface of the placenta on which a clot is detect at the time of delivery.
      • Complication
      • DIC
      • Shock
      • Amniotic fluid embolism
      • Acute renal dysfunction
    • Management
      • Maintain hemodynamic stabilization ( Transfusion therapy)
      • Crystalloid transfusion
      • Whole blood therapy
      • Component therapy
      • Correct coagulation status
      • Delivery
      • When the fetus is mature, vaginal delivery is preferable unless there is evidence of fetal distress or hemodynamic instability.
      • When the fetus is not mature and placental abruption is limited, observation with close monitoring of both fetal and maternal status.
    • Delivery
      • Cesarean section is indicated :
        • Fetus exhibits persistent evidence of distress.
        • Situation is not favorable for rapid delivery.
        • Uncontrollable hemorrhage
        • A rapid expanding uterus with hemorrhage.
        • Uterine apoplexy
    • Thank you for your attention!