CBP Obstetrics April 30 2009 CASE

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 R 2 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 R 2 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 -6 mg/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/m. L to 500012000/m. L 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 factor 8. 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 O 2 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 R 2 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. ]: S 248 –S 255

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 R 2 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 p. CO 2 28 – 35 mm. Hg • PO 2 > 90 mm. Hg • 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 Fi. O 2 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 P 2, and what you think is a right-sided S 3. Her lungs are clear, and her legs look remarkably svelte for a pregnant woman.

Case # 1 (cont’d) • Your R 2 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 R 1 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, 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 m. Gy] 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 Fi. O 2 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.

$Initial Treatment • Treatment with LMW heparin or unfractionated heparin is recommended until the$

Initial Treatment • Treatment with LMW heparin or unfractionated heparin is recommended until the diagnosis is ruled out by objective testing

$Heparin • Neither unfractionated heparin nor LMWH crosses the placenta, • advantages of LMWH$

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,

$• The pharmacokinetics and pharmacodynamics of subcutaneous unfractionated heparin are unpredictable during the$

• The pharmacokinetics and pharmacodynamics of subcutaneous unfractionated heparin are unpredictable during the 3 rd trimester, • Meticulous monitoring of the a. PTT 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 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’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 Bi. PAP and gives you the story “ 32 year old G 1 P 0 A 0, 38 weeks in, has a 48 h 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)

Preeclampsia Dx Severe PEclampsia HELLP Acute fatty liver -HTN -Proteinuria (>2+ or 300/d) • Sustained s. BP >160 • Sustained d. BP>110 • Pulmonary oedema • Proteinuria >5 g/24 h • Oliguria <500 m. L/24 h • Persistent headaches or scotomata • Persistent RUQ or epigastric pain • Plt <100 000/mm 3 • I/U growth restriction <10 th percentile -Smear: Schistocytes -Bili > 20 -ALT > 3 x LDH > 600 Plt < 100 000 3 rd trimester Hyperbili Hypoglyc Hyperammoniemia DDx Pre. Eclampsia-AFL-HELLP Patients -Nullipara -non White -Low social status -early 20 s 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 24 h, fetal U/S, CBC Creat + LFTs q 6, then daily post delivery Evolution Polyuria = resolution Resolve 96 h post delivery (majority) -White -Multipara -> 35 yo Indicated (urgent) Vag or C/S ±steroids 6 -12 dex q 6 h Death 10 -15% Fetal death 15 -66% Hypoglyc 50% Coagulopathy 50% Renal failure Encephalopathy Pancreatitis

Severe Pre. Eclampsia

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 + 24 h urine protein • Coags, fibrinogen • Liver enzymes + direct bilirubin • TSH • 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 R 2; 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 2 g IV, repeated q 15 min to maximum 6 g* – Obtain serum Mg level after 1 st dose in patients receiving prophylaxis with magnesium sulfate (please refer to Dr. Mclean’s slides). – Mechanism of anticonvulsant action unknown. • *4 -6 g bolus over 20 min followed by 1 -3 g/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) : CD 000128 • 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 m. L/hr. Nonreassuring fetal heart rate pattern.

How do you treat it? • Calcium 1 g IV over 3 mins • Stop Mg. SO 4 • 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 500 m. L 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 [m. L] = weight [kg] x 80) or loss of 1000 m. L 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 Ø 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 m. L of saline, and strength to withstand a maximum internal and external pressure of 300 mm. Hg. 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 m. L balloon can be guided into the uterine cavity and inflated with 60 to 80 m. L 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 m. L 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 40 U in 500 NS at 125 cc/hr 2. PGF 2α a. 0, 25 mg IM q 15 min ad 2 mg (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. rf. VIIa

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 -500 cc 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