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CBP: Obstetrics
April 30 2009
CASE # 1
• It’s 5 pm on Friday at St Paul’s and you’re going home
early. Just as you hit the metal plate that lets you out of
the unit, your anesthesia R2 catches up to you and tells
you that he just got called for a 26-week pregnant
woman in severe respiratory distress.
• You decide to head down with your resident to take a
look at her before leaving, and realizing you haven’t
seen a pregnant let alone a premenopausal patient
during your three years of internal medicine training,
you pimp your R2 on the physiologic changes seen in
pregnancy:
Question # 1
• Summarize relevant physiologic changes in
pregnancy giving normal values for
important vital signs and relevant lab tests.
(Scot)
Hemodynamic changes in normal pregnancy
Normal pregnancy is characterized by an increase in cardiac output, a reduction in systemic vascular resistance, and a modest decline in mean blood
pressure. These changes are associated with a 10 to 15 beat/min increase in heart rate.
•
Expansion of the plasma volume and an increase in red blood cell mass
begin as early as the fourth week of pregnancy, peak at 28 to 34 weeks of
gestation, and then plateau. Plasma volume expansion exceeds the
increase in red cell volume, leading to "physiologic anemia".
•
The major hemodynamic changes induced by pregnancy include an
increase in cardiac output and reductions in systemic vascular resistance
and systemic blood pressure. Cardiac output peaks a few minutes after
delivery, before gradually returning to prepregnancy levels.
•
Changes in several coagulation factors produce a hypercoagulable state.
•
Labor and delivery is associated with significant hemodynamic changes
due to anxiety, exertion, pain, uterine contractions, uterine involution, and
bleeding. Infection, hemorrhage, and the administration of anesthesia or
analgesia also play a role.
Gastrointestinal
•
Oropharyngeal changes in pregnancy include epulis, gingivitis,
and increased salivation.
•
Gastrointestinal reflux is common in pregnancy because of
decreased lower esophageal sphincter pressure and inhibition
of the adaptive responses of the sphincter.
•
Pregnant women are predisposed to gastric aspiration due to
increased intraabdominal pressure and relaxation of the lower
esophageal sphincter.
•
Abdominal bloating and constipation during pregnancy are
probably caused by hormonal changes that reduce small bowel
and colonic motility.
•
30 to 40 percent of pregnant women are bothered by
hemorrhoids.
Nephrologic
•
Ureteral dilatation during pregnancy results from hormonal effects, external
compression, and intrinsic changes in the ureteral wall. Intermittent vesicoureteral
reflux is also common.
•
Urinary frequency and nocturia are among the most common pregnancy-related
complaints. Urinary incontinence also increases during pregnancy.
•
Glomerular filtration rate (GFR) and renal blood flow rise markedly during pregnancy.
Other renal changes in pregnant women include increased renal size, chronic
respiratory acidosis, mild hyponatremia, and fall in plasma osmolality. Fractional
absorption of glucose, amino acids, and beta microglobulin are decreased. Protein
excretion is increased.
•
The release of vasopressinases from the placenta results in an approximate four-fold
increase rate of vasopressin catabolism, but plasma vasopressin levels remain normal
because of a fourfold rise in the production of vasopressin by the pituitary gland.
Women who have higher than normal vasopressinase levels or decreased vasopressin
reserves may develop gestational diabetes insipidus. The high urine output in this
setting is generally resistant to the administration of vasopressin, but patients
generally remain responsive to desmopressin.
Hematologic
•
Blood Volume increases: magnitude varies according to size, number of pregnancies,
number deliveries, and one or multiple foetuses. Increases in blood volume progress
until term;the average increase in volume at term is 45-50%. Needed for extra blood
flow to the uterus, extra metabolic needs of foetus, and increased perfusion of others
organs, especially kidneys. Also compensate for maternal blood loss at delivery.
•
Red Blood Cells The increase in red blood cell mass is about 33%. Since plasma volume
increases early in pregnancy and faster than red blood cell volume, the hematocrit falls
until the end of the second trimester, when the increase in the red blood cells is
synchronized with the plasma volume increase. The hematocrit then stabilizes or may
increase slightly near term.
•
Iron With the increase in red blood cells, the need for iron for the production of
hemoglobin increases. If supplemental iron is not added to the diet, iron deficiency
anemia will result. Maternal requiriments can reach 5-6mg/d in the latter half of
pregnancy. If iron is not readly available, the fetus uses iron from maternal stores. Thus,
the production of fetal hemoglobin is usually adequate even if the mother is serely iron
deficient. Maternal iron deficiency may cause preterm labour and late spontaneus
abortion.
Hematologic cont’d
•
White Blood Cells Increases from a pre-pregnancy level of 4300-4500/mL to 500012000/mL in the last trimester. Lymphocyte and monocyte numbers stay
essentially the same throughout pregnancy; polymorphonuclear leucocytes are
the primary contributors to the increase.
•
Clotting Factors Marked increases in fibrinogen and factor8. Factors VII, IX, X, and
XII also increased but to a lesser extent.
•
Fibrinolytic activity is depressed during pregnancy and labor, although the precise
mechanism is unknown. The placenta may be partially responsible for this
alteration in fibrinolytic status. Plasminogen levels increase concomitantly with
fibrinogens levels, causing an equilibration of clotting and lysing activity.
•
Coagulation and fibrinolytic systems undergo major alterations during pregnancy.
Understanding these physiologic changes is necessary to manage two of the more
serious problems of pregnancy: haemorrhage and thromboembolic disease, both
caused by disorders in the mechanism of haemostasis.
CASE # 1 (cont’d)
…Walking confidently into the ER with your rediscovered
knowledge of obstetric physiology, you do your best to look
bored and ask the ER doc where your pregnant patient is.
The doc thanks you for coming so quickly, and promptly
tells you that the patient was just brought in by ambulance
with acute onset shortness of breath.
She is on 100% oxygen via non-rebreather, with an O2 sat
of 89%, and a soft blood pressure that’s responded to
boluses so far. You manage to whimper “Is that all?” and
promptly turn to your R2 to pimp him some more:
Question #2
• What’s the differential for shortness of breath
in a pregnant woman? (Naisan)
What’s the differential for shortness of
breath in a pregnant woman?
Crit Care Med 2005; 33[Suppl.]:S248 –S255
CASE # 1 (cont’d)
• The patient looks like she’s tiring, and can barely
answer the nurse’s questions when the doc
interrupts your educational moment and says: “I
was going to intubate her, but since you’re here…
You are a fellow right?”.
• You reassure her that you are in fact a fellow as of
5 days ago and thank her for letting you in on all
the “fun”. You then turn to your R2 and tell him
to get ready to intubate while you go change your
underwear.
Question # 3
• What are the anatomic and physiologic
changes in pregnancy that can make
intubation more challenging? What drugs are
safe for induction? What considerations apply
when mechanically ventilating a pregnant
patient? (Neil)
What are the anatomic and physiologic
changes in pregnancy that can make
intubation more challenging?
• May need smaller Ett 6 or 7
• Peripheral and pulmonary vascular resistance is
decreased so decreased BP and inc PP
• Vena caval compression in supine position
• BVM more difficult
What drugs are safe for induction?
• Little evidence that a single dose of any currently
available IV induction agents is harmful to the
fetus
• Thiopental has most evidence
• Propofol and benzos are ok
• Rocuronium has a longer half life, so adjust dose
(75%)
What considerations apply when
mechanically ventilating a pregnant
• Aim for pCO2 28 – 35 mmHg
• PO2 > 90 mmHg
• Permissive hypercapnea may be harmful to fetus
(animal studies)
• Monitor fetal heart
• May need to allow plateau pressures >30
Case # 1 (cont’d)
• Thanks to your superb supervision, the intubation goes
smoothly without a drop in pressure, and the patient’s
FiO2 comes down to 0.6.
• The CXR shows that the tube is in good position, and
otherwise looks remarkably clean.
• Her vitals are HR 130, BP 100/70, RR 32, PS 18/5, T=
38.2. Her JVP is elevated at 6 cm ASA, she has a loud
P2, and what you think is a right-sided S3. Her lungs
are clear, and her legs look remarkably svelte for a
pregnant woman.
Case # 1 (cont’d)
• Your R2 hands you her EKG and your eyes
immediately focus on leads I and III which
show the following:
Case # 1 (cont’d)
• You look back at the film and notice that her
left PA is prominent and that her left lower
lobe is hyperlucent.
• You smile to yourself suddenly feeling like
House and inform your R1 that this woman
has a PE when you notice him already filling
out a heparin protocol, and think to yourself
“who is this guy?”.
Question # 4
• What factors place the pregnant woman at
higher risk of VTEs? (Scot)
Case # 1 (cont’d)
• You tell your resident that you agree with the
heparin, but that you’re going to have to
actually prove the diagnosis if you’re going to
keep her on it.
Question # 5
• How would you work up a pregnant woman
for PE? Please discuss imaging strategies and
safe levels of radiation exposure in the fetus.
(Neil)
How would you work up a pregnant
woman for PE?
• 5 x increased prevalence in pregnant vs. non-pregnant state
• Clinical symptoms
– Less specific in preg
– Dyspnea, tachypnea, tachycardia, leg sewlling are normal
• ECG
– cannot rely on usual picture
– Preg will show LAD and tachy normally
• D-dimer not useful
• CT vs VQ
IV Contrast Dye
• Class B drug
– animal reproduction studies have not
demonstrated a fetal risk, but there are no
controlled studies in pregnant women and they
should be used only after assessing the potential
risk/benefit
Take Home
• The American College of Obstetricians and
Gynecologists published the following policy
statement: “Women should be counseled that
x-ray exposure from a single diagnostic
procedure does not result in harmful fetal
effects. Specifically, exposure to less than 5
rad [50 mGy] has not been associated with an
increase in fetal anomalies or pregnancy loss.”
Case # 1 (cont’d)
• The patient comes up to the unit looking
stable, when she suddenly drops her BP to 70
systolic and a her FiO2 requirements go back
up to 1.0.
• You quickly throw an echo probe on her chest
and notice a dilated RV with septal shift, and
wonder if you have any more clean underwear
in your gym bag.
Question # 6
• What’s the treatment for PE in a pregnant
patient? Can thrombolytics be used (if so
when)? When should a filter be considered?
(Naisan)
What’s the treatment for PE in a pregnant
patient?
• Incidence of venous thromboembolism is
estimated at 0.76 to 1.72 per 1000
pregnancies,
• 4 times as great as the risk in the nonpregnant population.
Initial Treatment
• Treatment with LMW heparin or
unfractionated heparin is recommended until
the diagnosis is ruled out by objective testing
Heparin
• Neither unfractionated heparin nor LMWH
crosses the placenta,
• advantages of LMWH
– include a reduced risk of bleeding,
– Predictable pharmacokinetics allowing weightbased dosing without the need for monitoring,
– reduced risk of HIT
– and heparin-induced osteoporotic fractures
Heparin
• a twice-daily weight-based regimen has been
recommended due to increased renal
excretion
Fondaparinux
• A synthetic pentasaccharide and direct
inhibitor of factor Xa,
• Suggests that it may be a safe alternative
• Passes the placental barrier in vivo, resulting
in low but measurable anti–factor Xa activity
Anticoagulant therapy during
labor and delivery
• Advised that once they are in established
labor, no further heparin should be taken
• Patients commonly are switched to
subcutaneous unfractionated heparin for the
last few weeks of pregnancy,
• The pharmacokinetics and pharmacodynamics
of subcutaneous unfractionated heparin are
unpredictable during the 3rd trimester,
• Meticulous monitoring of the aPTT with
dosage adjustment as needed
Post Partum
• Treatment with low-molecular-weight heparin
may be resumed within 12 hours after
delivery in the absence of persistent bleeding.
• Should wait >24 hrs if had epidural or poorly
controlled bleeding
Duration of Tx
• LMWH or warfarin is recommended
• For at least 6 weeks post partum and for a
total of at least 6 month
Thrombolytics
• Experience with thrombolytic therapy in
pregnancy is limited,
• Due to its large molecular size (72000 kd) rt-PA
does not cross the placenta.
• Concern that thrombolytic therapy will lead to
placental abruption, but this complication has
not been reported
Maternal Complications
• Complication rates of thrombolytic therapy in
pregnant patients are not higher than in the
large randomized trials on stroke, myocardial
infarction and pulmonary embolism
• Comparing case reports though
• J Thromb Thrombolysis 21(3), 271–276, 2006.
Post Partum
• Thrombolytic therapy within 10 days after
cesarean section or delivery is
contraindicated,
• But successful thrombolysis has been reported
within 1 hour after vaginal delivery and within
12 hours after cesarean section
• ajem.2005.12.003
IVC Filters
• VC filter insertion may be considered in
pregnant patients who have contraindications
to anticoagulation or develop extensive VTE
shortly before delivery (within 2 weeks).
Retrievable filters should be considered (grade
C, level IV)
• Guidelines for the use of Vena Cava Filters; British
Journal of Haematology, 2006, 134, 590–595
Case # 2
• The patient improves rapidly following thrombolysis. Your watch says 9
pm, and the 5 missed calls on your phone tell you you’ve missed dinner. As
you walk by the ER on your way out, the emergency physician accosts and
says: “You’re not going to believe it hot shot, but I’ve got another one for
you”.
• She walks you over to an incredibly pregnant-looking patient on BiPAP and
gives you the story “32 year old G1P0A0, 38 weeks in, has a 48h history of
headache and now comes in with shortness of breath. Oh yeah, and her
BP is 210/120”.
• Having just reviewed the differential for shortness of breath in the
pregnant patient, you decide to examine the patient yourself and note
that she has bilateral crackles, a mildly elevated JVP, 3+ pitting edema in
her legs, and you manage to elicit a knee jerk by lightly tapping her
patellar tendon with your finger.
Question 7
• What are the risk factors and diagnostic
criteria for mild vs severe pre-eclampsia?
What are possible complications? What lab
tests would you order? (Yoan)
Dx
Preeclampsia
Severe
PEclampsia
HELLP
Acute fatty liver
-HTN
-Proteinuria (>2+ or 300/d)
•Sustained sBP >160
•Sustained dBP>110
•Pulmonary oedema
•Proteinuria >5 g/24 h
•Oliguria <500 mL/24 h
•Persistent headaches
or scotomata
•Persistent RUQ or
epigastric pain
•Plt <100 000/mm3
•I/U growth restriction
<10th percentile
-Smear: Schistocytes
-Bili > 20
-ALT > 3x
LDH > 600
Plt < 100 000
3rd trimester
Hyperbili
Hypoglyc
Hyperammoniemia
DDx PreEclampsia-AFL-HELLP
Patients
-Nullipara
-non White
-Low social status
-early 20s
-White
-Multipara
-> 35yo
Delivery
-Bishop score, Gest age,
Complications
-DIC
-ARF
-Liver Failure
-Liver rupture
-ICH
-Cardiac Arrest
-Aspiration
-Pulm edema
-Postpartum
Hemorrhage
-Liver rupture
-DIC
-ARF
-Pulm edema
-Carotid thrombosis
-CVA
Recurrence
2%
3-27%
Labs
CXR, LFTs, Urine dipstick,
proteins 24h, fetal U/S, CBC
Creat + LFTs q6, then
daily post delivery
Evolution
Polyuria =
resolution
Resolve 96h post
delivery (majority)
Indicated (urgent)
Vag or C/S
±steroids 6-12 dex q 6h
Death 10-15%
Fetal death 15-66%
Hypoglyc 50%
Coagulopathy 50%
Renal failure
Encephalopathy
Pancreatitis
Severe PreEclampsia
Risk factors for preeclamspia
• Extremes of age
(<18 or > 35)
• Diabetes
• Chronic hypertension
• Nulliparous
• Chronic renal failure
• Multifetal gestation
• Fetal hydrops
• High BMI
Lab investigations
• CBC, blood smear
• Electrolytes + Creatinine
• LDH, uric acid
• Urinalysis + 24h urine
protein
• Coags, fibrinogen
• TSH
• Liver enzymes + direct
bilirubin
• Fetal assessment
Case # 2 (cont’d)
• You ask for the usual lab tests, and the urine
dip shows 3+ protein confirming your
suspicion.
• The platelets come back at 95, the ALT 120,
and her hemoglobin, LDH, bilirubin are all
within normal limits.
Question # 8
• How do you treat severe preeclampsia? What
antihypertensives are
indicated/contraindicated? What are
indications for delivery? (Todd)
How do you treat severe
preeclampsia?
• Ask the superstar R2; he seems to know
everything else so far.
• He might say something along the lines of:
– Maintain maternal organ function.
• Including BP management.
– Manage seizures.
– Monitor fetus.
– Evaluate for delivery.
Blood Pressure Control
• Cerebrovascular accident is a major cause of
maternal death in preeclampsia.
– Including hemorrhagic stroke.
• BP target < 160/110
– No prospective data to support this.
– Beta blockers (labetalol 10-20 mg IV q 20 min, to maximum
bolus dose of 80 mg and cumulative dose of 300 mg.)
• 1-2 mg/min infusion may be used.
– Hydralazine 5-10 mg IV q 20 min.
• Maternal hypotension more common with this agent.
What NOT to use…
• ACE inhibitors/ARBs: teratogenic at all stages of pregnancy.
• Nitroprusside: risk of cyanide toxicity, thus a last-resort agent,
used for less than 4 hours’ duration.
• Nifedipine/nicardipine (IV): less evidence for these, but may be
useful for refractory HTN.
–
J Hypertens. 2005 Dec;23(12):2319-26, Intensive Care Med. 2002 Sep;28(9):1281-6. Epub
2002 Jul 26, Obstet Gynecol. 1994 Sep;84(3):354-9.
• L-argininge (no evidence) Obstet Gynecol. 2006 Apr;107(4):886-95.
• Plasma volume expansion
BJOG. 2005 Oct;112(10):1358-68
Seizure control
• Most eclamptic seizures are self-limited (< 5 min), but there is
no truly safe duration of seizure.
– They recur in approximately 10% of eclamptic women.
• Magnesium sulfate 2g IV, repeated q 15 min to maximum 6g*
– Obtain serum Mg level after 1st dose in patients receiving prophylaxis
with magnesium sulfate (please refer to Dr. Mclean’s slides).
– Mechanism of anticonvulsant action unknown.
•
*4-6g bolus over 20 min followed by 1-3g/h infusion
– Target level: 2 – 3 mmol/L
Other Options
• Phenytoin (less effective than Mg sulfate)
– N Engl J Med 1995 Jul 27;333(4):201-5
– Cochrane Database Syst Rev 2003; (4) :CD000128
• Nimodipine (less effective than Mg Sulfate)
– N Engl J Med 2003 Jan 23;348(4):304-11.
• Benzodiazepines (diazepam and lorazepam) may be
used in acute management (not prevention), but
beware depressant effect on fetus.
– Employed after attempting repeat bolus of Mg sulfate.
Fetal Monitoring
• Frequent ultrasound/ non-stress test.
• Biophysical profile, time permitting.
• Scalp electrodes if possible.
Delivery
• Essentially any patient past 37 weeks GA, or
meeting criteria for “severe” preeclampsia
should be considered for delivery.
Indications for Delivery in Preeclamsia
• Specifically:
–
–
–
–
–
–
–
Thrombocytopenia
Deteriorating liver function
Deteriorating renal function
Abruptio placentae
Persistent severe headaches or visual changes
Persistent epigastric pain, nausea/vomiting
Fetal indications: IUGR, oligohydramnios, nonreassuring
results from fetal testing
Delivery
• Delivery is the rule in severe preeclampsia at >
32 wks gestational age.
• Cesarean section or vaginal delivery are
possible, depending upon clinical
circumstances.
Case # 2 (cont’d)
• You call the obstetrics senior to tell her this
woman needs to be induced, when the nurse
calls you over to inform you that the patient’s
breathing has become shallow, and that she
can no longer move her arms or legs.
Question # 9
• What is magnesium toxicity? How should you
monitor for it? How do you treat it? (Neil)
What is magnesium toxicity?
• Pharmacologic myasthenic syndrome
• Decreased motor end plate sensitivity to Ach
• Reduced excitability of muscle fibre
membrane
What is magnesium toxicity?
• Initially can get flushing, mild hypotension,
nausea and headaches
How should you monitor for it?
•
•
•
•
•
•
•
•
•
•
Significant changes in BP from baseline values.
Double (or blurring of) vision.
Tachycardia or bradycardia.
Respiratory rate <14 or >24.
Oxygen saturation <95%.
Changes in breath sounds suggestive of pulmonary
edema.
Changes in level of consciousness or neurologic status.
Absent DTRs.
Urinary output <30 mL/hr.
Nonreassuring fetal heart rate pattern.
How do you treat it?
• Calcium 1g IV over 3 mins
• Stop MgSO4
• Supportive care
Case # 2 (cont’d)
• The anesthetist brings the patient back from
the OR and tells you that the patient was a
little “oozy” after delivery, having received 2
units of blood, and 2 units of FFP.
• He adds that the OB ruled out a tear or
retained products, and that the bleeding had
now slowed to a “trickle” on oxytocin.
Question 10
What are the major causes of post-partum
hemorrhage, and how should it be worked
up? (Yoan)
Post Partum Hemorrhage
• Postpartum hemorrhage (PPH) is the most
important single cause of maternal death,
accounting for about 25% of the total and
claiming an estimated 150 000 lives annually.
• The majority of these deaths (88%) occur
within four hours of delivery
PPH
• Defined as the loss of 500mL or more of blood from the genital tract.
– Primary PPH occurs within the first 24 hours after delivery
– secondary PPH occurs after this time.
• The ability of a woman to cope with blood loss depends on a number of
factors
– Previous health
– Anemia
– Volume contraction due to dehydration or preeclampsia
• Emergency measures if loss > 1/3 of estimated blood volume (EBV)
(blood volume [mL] = weight [kg] x 80) or loss of 1000 mL or a change in
vital signs.)
PPH Risk Factors
• Increased Maternal age
• Great multipara
• Multiple pregnancies
• Post C/S
• Assisted conception
PPH Prevention
• Early oxytocic therapy
• Early Cord clamping
• Early Placental delivery by gentle controlled cord
traction following signs of placental separation
Reduce the incidence and severity of PPH, postpartum
anemia, and the need for blood transfusion
JOGC 2006 Review:
The 4 Ts
• If exploration shows no trauma and no
retained tissue + well contracted uterus
• Then coagulopathy
– R/O AFLP
– R/O HELLP
– Sepsis
– Amniotic fluid embolus
Case # 2 (cont’d)
• As the anesthetist walks out of the unit, the
nurse looks at you and notes that the patient
is sitting in a pool of blood and is looking pale.
• You quickly order 4 units of blood, and call for
stat bloodwork . As you examine the patient
to figure out what kind of access you have,
you do a double take when the nurse asks if
you want her to go find a Blakemore tube.
Question # 11
• Outline the medical treatment of postpartum hemorrhage. Other than
hysterectomy, what options are available
when medical treatment fails? (Scot)
Sequential steps in managing postpartum hemorrhage
Uterine massage
Uterotonic drugs:
Oxytocin (10 to 40 U in 1 liter of normal saline via intravenous infusion; 80 U in 1 liter of normal saline may be given for a short time)
Methergine (0.2 mg intramuscularly every two to four hours) if not hypertensive
Carboprost tromethamine (Hemabate) (250 mcg intramuscularly every 15 to 90 minutes, as needed, to a total dose of 2 mg) if no asthma
Misoprostol (800 to 1000 mcg rectally) can be given to women with hypertension or asthma
Inspect the vagina and cervix for lacerations; repair as necessary
Transarterial embolization - If the woman is stable and there is time for personnel and facilities to mobilize
Uterine tamponade (Bakri or Sengstaken-Blakemore tube, Foley, packing) is performed if medical therapy fails and prior to or in conjunction with
preparations for surgery
Laparotomy - If the above measures fail, surgical approaches that are quick, relatively easy, and effective should be tried first. In utilizing these
measures, the surgeon should be cognizant of the amount of blood loss and the stability of the patient, and should perform hysterectomy rather than
resort to temporizing measures if her cardiovascular status is unstable or if it appears that the anesthesiologist will not be able to keep up with her fluid
needs.
Ligation of bleeding sites
Uterine artery ligation, including utero-ovarian arcade
B-Lynch stitch
Hysterectomy - Hysterectomy is the last resort, but should not be delayed in women who have disseminated intravascular coagulation and require
prompt control of uterine hemorrhage to prevent death
Suturing and tacking of deep pelvic bleeders
Pelvic packing
Recombinant activated factor VIIa
•
•
•
•
•
•
•
Tamponade — Tamponade is effective in many patients; however, in the
setting of cardiovascular instability, it is important to avoid prolonged, futile
attempts at temporizing measures rather than proceeding to laparotomy and, if
necessary, hysterectomy.
The Bakri tamponade balloon was specifically designed for uterine tamponade to
control postpartum bleeding. It is a silicone balloon with a capacity of 500 mL of
saline, and strength to withstand a maximum internal and external pressure of
300 mmHg.
If the Bakri device is not available, a Sengstaken-Blakemore tube can be used
to tamponade the uterus. This not only tamponades the uterus, but allows for
drainage of blood from sites proximal to the tube. Excessive bleeding suggests
that tamponade is not effective. In two series of patients with massive PPH, use
of a Sengstaken-Blakemore tube reduced the need for surgery or embolization
in most patients and was also useful for controlling bleeding while patients
waited for such procedures.
If these devices are not available, a #24 Foley catheter with a 30 mL balloon
can be guided into the uterine cavity and inflated with 60 to 80 mL of saline as
an alternative means of tamponading the uterus.
Uterine packs also have been used to control PPH with variable success; proper
technique requires firmly packing the entire uterine cavity with gauze, such as
Kerlix, to achieve tamponade. The gauze can be impregnated with 5000 units
thrombin in 5 mL sterile saline to enhance clotting. If packing does not control
hemorrhage, repacking is not advised.
Regardless of the form of tamponade employed, the hemoglobin and urine
output should be closely monitored. This is especially important when a gauze
pack is used because a large amount of blood can collect behind the pack.
Devices used to tamponade the uterus are removed after 24 hours.
PPH-Medical Tx
1. Oxytocin
a. 10 U IV slow bolus
b. Then 40U in 500NS at 125cc/hr
2. PGF2α
a. 0,25mg IM q 15 min ad 2mg (80-90% efficient)
3. Ergometrine 0.5 mg by slow IV injection
4. Methergine 0.2 mg intramuscularly,
5. 20 mg dinoprostone vaginally or rectally
6. misoprostol 1000 ug rectally
7. Tranexamic Acid: antifibrinolytic
8. rfVIIa
PPH Surgical Tx
1. R/O uterine inversion, atony, retention of
products
2. Bimanual massage
3. Packing
4. Blakemore, Bakri SOS or Rusch Urological
balloon: 300-500cc inflation, if bleeding stop
→ 87% chance no need for further Tx
– Condom in low ressource setting
PPH- Surgical Tx
• If tamponade test –
– Laparotomy + bimanual compression
• If + ( success at controlling) then compression suture)
• 68% success
– Devascularization
• Uterine, ovarian and internal Iliac (Int Iliac 50% success
and dangerous)
– Subtotal or total Hysterectomy
– Interventional radiology: unsure of role in
unstable pt
JOGC Review PPH 2006