Department of Obstetrics and Gynecology
CLINICAL CASE PRESENTATION
SEPTEMBER 15, 2010
GROUP 2
Ang, Abigail
Ang, Jorge
Ang, Vincent Ryan
Arguelles, Carmen
Arrobio, Rosa Maria
Ascue, Ronald Alvin
Atutubo, Bjorn
Pertinent History and Physical Findings
Patient was admitted due to a bloody mucoid vaginal discharge associated with irregular intrauterine contraction.
It had a single intrauterine fetus without cardiac and somatic activities and with overlapping cranial sutures
Date of Admission: April 23, 2010
LMP: July 21, 2009
AOG: 39 3/7 weeks
(-) fever
(-) dysuria
(-) loose bowel movement
(-) fetal movement
(-) blurring of vision
(-) epigastric pain
(-) headache
(-) nausea/vomiting
(-) edema
Past Medical History
(-) Allergies, asthma, HTN, DM, cardiovascular or lung diseases, thyroid disease (-) previous surgery
Family History
(-) HTN, DM, cardiovascular diseases, cancer, asthma
Social History
Non-smoker, non-alcoholic beverage drinker.
OB History
G4P3 (3003); Present pregnancy, no prenatal check ups
Physical Examination on Admission:
General Survey: Conscious, coherent, ambulatory, not in respiratory distress
Vital Signs: BP: 100/70 HR: 119 bpm
RR: 2o cpm
HEENT: Pale palpebral conjunctivae
Cardiovascular: Tachycardic
Abdomen: Globular, (+) striae gravidaruum and linea nigra, FH: 28 cm, FHT: not appreciated by stethoscope and Doppler.
Leopolds:
I: vertex, unengaged
II: fetal back maternal right
III: breech
Pelvic Exam
Inspection: (+) frank flow of clear amniotic fluid
Internal Exam: Cervix 3 cm dilated, 70% effaced, floating, footling breech, (+) membranes
Extremities:
Full and equal pulses, no cyanosis, (+) grade 1 bipedal edema
Admission Findings:
Anemia: Hemoglobin of 83 mg/dL, Hematocrit of 23% and Platelet count of 120,000
Prolonged Prothrombin and Partial Thromboplastin time
Good uterine contraction (mild to moderate intensity, 2-5 minute intervals, 45-90 second duration) upon oxytocin drip
Persistently tachycardic (HR=110-120 bpm)
Delivery
Partial breech extraction with perineal support to a dead preterm boy
BW – 1000 g
BL – 42 cm
Clear Amniotic fluid
Macerated baby with overlapping of cranial bones
Complete placenta with blunted cotyledons and retroplacental blood clots approximately 500 mL
Patient was tachycardic (120’s-130’s), hypotensive (80/40 mmHg) and still bleeding profusely.
Intra OP findings
Flaccid Uterus and intermittently contracting with bluish discoloration noted on the fundal and lower uterine segment, extending to
the lateral walls and the broad ligaments.
Uterus measures 18 x 10 x 7 cm. On cut section, the anterior myometrium measures 2 cm, the posterior myometrium measures
1.5 cm while the endometrium measures 0.3 cm.
Placental fragments on the posterior wall of the uterine corpus, measuring approximately 4 x 4 x 0.5 cm.
Cervix measures 4 x 4 x 2.5 cm
Patient’s vital signs intraoperatively
BP = 80-110/50-90 mmHg, HR 120-160 bpm, RR 20 cpm, temperature 36.6 – 37.4OC, input vs output – 3000 vs. 280 cc.
Course in the Wards:
On the 1st hospital day, patient’s BP ranged from 120-140/70-100 while HR was 84-100 bpm.
On the 2nd hospital day, patient’s blood pressure remained elevated (140-150/70-100).
Patient was started on Metoprolol 100 mg/tab, 1 tablet twice a day and ferrous sulfate 1 capsule OD.
Symptomatology
Based on the HPI, the patient presented with a bloody mucoid vaginal discharge, more commonly called “bloody show”,
accompanied by uterine contractions, signifying onset of labor. Soon, the patient began having watery vaginal discharge,
probably caused by a leak from, or spontaneous rupture of the bag of water, thus extruding the amniotic fluid. Upon physical
examination, the patient presented with a small fundic height suggesting a small for age fetus since she was in her 39th week
AOG based on LMP. She also presented with Grade 1 bipedal edema, a common finding in term pregnancies.
Baseline laboratory tests revealed that the patient had anemia with low hemoglobin (83 mg/dl), low hematocrit (23%),
and low platelet count of 120,000. These problems were managed by transfusion of packed RBC. Red cell transfusion is
indicated especially when hemoglobin levels are <70-80g/L and when there is a continued and excessive blood loss. The patient
also had prolonged prothrombin and partial thromboplastin time. Based on studies, 25% of women with prolonged retention of a
dead fetus developed coagulopathy. The changes are presumably mediated by thromboplastin from the dead products of
conception. The platelet count tends to decrease in these instances as well.
After the 3rd stage of labor, the patient started to bleed profusely. Her blood pressure went down to 80/40 mmHg and 70
mmHg palpatory due to continuous blood loss which was approximated at 2 liters. The presentation of tachycardia is due to the
compensatory mechanism of the heart brought about by decreased oxygen circulation caused by the anemia, as well as the
constantly decreasing blood volume.
Metabolic acidosis seen in the patient could have been due to lactic acidosis brought about by poor perfusion to the
muscles. This was particularly seen in the uterus of the patient which presented with a bluish discoloration on the fundal and
lower segments extending to the lateral walls and the broad ligament muscles (Couvelaire's Uterus). The severe anemia could
also have contributed to the metabolic acidosis since there was decreased oxygen in the blood itself.
Diagnosis
ABRUPTIO PLACENTA
Patient presented with profuse vaginal bleeding with irregular contractions several hours before admission, associated
with no fetal movement. It occurred on her third trimester, being her 39th week AOG. With these pertinent symptoms, the most
likely to be considered condition is abruptio placentae. Abruptio placentae is defined as the premature separation of the placenta
from the uterus, usually diagnosed with vaginal bleeding, contractions and fetal distress. It usually poses a significant cause of
third-trimester bleeding associated with both fetal and maternal morbidity and mortality.
Symptoms may include vaginal bleeding, contractions, abdominal tenderness, and decreased fetal movement, in which
the patient had upon complaint. Although the patient did not undergo any prenatal check-ups, the cause may not be clearly
defined. Questioning the patient about cocaine or tobacco abuse, hypertension, alcoholism, or trauma is also crucial. But since
the patient presented with no such risk factors, it puts her to lower risk of having the disease.
Abruptio placentae is a latin word meaning “rending asunder of the placenta”. It denotes a sudden accident, which is a
clinical characteristic of most cases of this complication, and premature separation of normally implanted placenta before delivery
of the fetus. With this definition in mind, abruptio placentae can be differentiated from placenta previa, a condition wherein a
premature separation of the placenta is implanted a distance beyond or over the cervical internal os.
Vaginal bleeding is present in 80% of patients with placental abruptions, and is associated with concealed hemorrhage.
Bleeding usually insinuates itself between the membranes and the uterus, and then escapes through the cervix causing external
hemorrhage. However, there is also concealed hemorrhage, in which the bleeding does not escape externally but is retained
between the detached placenta and the uterus. This usually occurs when there is an effusion of blood behind the placenta
although its margins still remain adherent. The placenta is completely separated, though the membranes retain their attachment
to the uterine wall. Blood gains access to the amniotic cavity as it breaks through these membranes while the fetal head is very
closely applied to the lower uterine segment. This prevents the blood from passing out. Concealed hemorrhage brings about
great maternal hazards, as it causes consumptive coagulopathy in the patient. In this situation, the extent of hemorrhage cannot
be appreciated. Thus, the patient’s prolonged PTT can be due to the coagulopathy producing blood clots retroperitnoeally. If the
bleeding continued, fetal and maternal distress may have developed, and this might have been the cause of fetal death in the
patient. If the bleeding still occurred after the delivery and blood loss cannot be controlled by other means, a hysterectomy may
become necessary. On the other hand, the presence of watery vaginal discharge in the patient indicates clear amniotic fluid,
which may be seen in a partial abruptio placentae. Evidence of placental fragments on the posterior wall of the uterus also
supports a partial type of abruption placentae.
Abruptio placentae occurs when there is bleeding into the decidua basalis, leading to separation of the placenta.
Hematoma formation further separates the placenta from the uterine wall, causing compression of these structures and
compromise of blood supply to the fetus. Retroplacental blood may penetrate through the thickness of the uterine wall into the
peritoneal cavity, a phenomenon known as Couvelaire uterus. The myometrium in this area becomes weakened and may rupture
with increased intrauterine pressure during contractions. Other signs and symptoms include uterine tenderness, back pain, fetal
distress, high frequency contractions, hypertonus, and idiopathic preterm labor.
Furthermore, abruptions are classified according to severity in the following manner:
Grade 0: Asymptomatic and only diagnosed through post partum examination of the placenta.
Grade 1: The mother may have vaginal bleeding with mild uterine tenderness or tetany, but there is no distress of
mother or fetus.
Grade 2: The mother is symptomatic but not in shock. There is some evidence of fetal distress can be found with fetal
heart rate monitoring.
Grade 3: Severe bleeding (which may be occult) leads to maternal shock and fetal death. There may be
maternal disseminated intravascular coagulation. Blood may force its way through the uterine wall into the serosa, a condition
known as Couvelaire uterus.
The primary cause of placental abruption is unknown, but there are associated risk conditions like increased age and
parity, pre-eclampsia, chronic hypertension, preterm ruptured membranes, cigarette smoking, thrombophilia, cocaine use, prior
abruption, and uterine leiomyoma. Race and ethnicity is also important, as it is more common in Caucasians and African
American than Asians or Latin Americans. There was also a study stating that increased risk occurs in patients younger than 20
years and those older than 35 years. Among the risk factors stated above, the most commonly associated condition is
hypertension which includes pre-eclampsia, gestational hypertension or chronic hypertension. With regards to the patient, the
only probable cause of the disease would be hypertension, as what was noted during her course in the wards. Other medical
conditions that may increase the risk for abruptio placenta include an abnormally shaped uterus, asthma or a lung infection, blood
clotting disorders, infection in your uterus or placenta, lack of nutrition and vitamins and too much or too little fluid in the uterus.
Abruptio placentae is also the most common cause of intrauterine fetal demise. The early separation of the placenta
from the uterus also detaches the fetus’s source of nourishment, leading to too much blood loss from the mother and to fetal
ischemia, thereby causing it to be in distress and resulting to death. In this case, a breech extraction is indicated.
Tests for further evaluation include the following: fetal heart monitoring, CBC, blood and Rh typing, PT/PTT, Serum
fibrinogen and fibrin-split products (the most sensitive indicator) and transabdominal or pelvic ultrasonography. Patient’s CBC
revealed anemia, with low hematocrit and platelets. The diagnosis of abruptio placenta can be confirmed if ultrasound shows a
clot behind the placenta; a complete blood count shows decreased hemoglobin, hematocrit, and platelets; a bleeding tendency is
found with clotting tests such as a prothrombin time; or if the baby's heart rate or rhythm is abnormal or absent.
In addition, the patient had consumptive coagulopathy as a complication, or DIC (disseminated intravascular
coagulopathy), which places abruptio placenta as the most common cause. In DIC, there will be thrombocytopenia, prolongation
of prothrombin time and activated partial thromboplastin time, a low fibrinogen concentration and increased levels of fibrin
degradation products. The major mechanism is almost certainly the induction of coagulation intravascularly and to a lesser
degree, retroplacentally. Supposedly, thromboplastin from deciduas and placenta entered the maternal circulation and incited
intravascular coagulation. This resulted to hypofibrinogenemia- less than 150 mg/dL of plasma along with elevated levels of
fibrinogen, fibrin degradation products, D-dimer, and variable decreases in other coagulation factors found in about 30% of
women with abruption placenta severe enough to kill the fetus. An important consequence is the activation of plasminogen to
plasmin, which lyses fibrin microemboli, thereby maintaining patency of the microcirculation. When the abruption placenta is
severe enough to kill the fetus, there is most likely more than 100 ug/ml of fibrinogen-fibrin degradation products in the maternal
serum. Other complications of this condition include shock, renal failure and couvelaire’s uterus.
Couvelaire’s uterus or so called uteroplacental apoplexy is another common complication in abruption placenta. This
occurs when there is a widespread extravasation of blood into the uterine musculature and beneath the uterine serosa. It is also
seen beneath the tubal serosa, in the connective tissue of the broad ligaments, in the ovaries and as well as free peritoneal
cavity.
Treatment of abruptio placentae is designed to assess, control, and restore the amount of blood lost; to deliver a viable
infant; and to prevent coagulation disorders. Immediate measures for abruptio placenta include starting IV. Infusion of appropriate
fluids (lactated Ringer's solution) to prevent hypovolemia; placing a central venous line and urinary catheter to monitor fluid
status; drawing a blood sample for Hb level and hematocrit determination, coagulation studies, and typing and crossmatching;
initiating external electronic fetal monitoring; and monitoring maternal vital signs and vaginal bleeding.
Methergine® (methylergonovine maleate) is a semi-synthetic ergot alkaloid used for the prevention and control of
postpartum hemorrhage and for routine management after delivery of the placenta and postpartum atony.
ACCESSORY LOBE
The intermittent uterine relaxation and subsequent bleeding could be due to the presence of retained placental
fragments obtained on post-partum curettage. But even after the curettage, the patient continued to bleed. Post-hysterectomy
specimen still revealed placental fragments inside the uterus which could have accounted for the continuous bleeding. The
placenta was said to have been easily delivered after two minutes and was noted to be complete with blunted cotyledons. The
placental fragments found post-operatively could have been from an accessory lobe. It should be noted that ruling in or out of the
presence of an accessory lobe can be done upon proper assessment of the placenta after delivery. Post-partum curettage is
always indicated even though the placenta that was spontaneously extracted is complete.
In addition to this, uterine atony and hemorrhage is also likely to occur after delivery if oxytocin was used to initiate or
augment the labor.
References:
Fauci A.S. et al. (2008). Harrison’s Principle of Internal Medicine 17th Edition Volume 1. McGraw-Hill Companies, Inc
Cunningham F.G.et al. (2005) Williams Obstetrics 22nd Edition. Mc Graw-Hill Companies, Inc.
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