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Obstetrics and Gynecology > Post Partum Hemorrhage and Infections and other shit > Flashcards

Post Partum Hemorrhage and Infections and other shit Flashcards

1
Q

list risk factors for PPH

A
  1. abnormal placentation–> placenta previa, placenta accreta, hyaditiform mole
  2. trauma during labour and delivery –> episiotomy, complicated vaginal delivery, low or mid-forceps delivery, sulcal or sidewall lacerations, uterine rupture, C/S or hysterectomy, cervical laceration
  3. uterine atony–> uterine inversion, overdistended uterus (i.e due to macrosomic fetus, multiple gestation, polyhydramnios), exhausted myometrium (rapid labour, prolonged labour, oxytocin or prostaglandin stimulation, chorioamnionitis)
  4. coagulation defects–> these intensify other causes–> placental abruption, prolonged retention of demised fetus, amniotic fluid embolism, severe intravascular hemolysis, severe preeclampsia and eclampsia, congenital coagulopathies, anticoagulant treatment
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2
Q

when does PPH usually occur

A

within the first 24 hours while patient still in hospital

however, can also occur in those with retained POCs for up to several weeks postpartum

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3
Q

define PPH

A

blood loss above 500 mL in vaginal delivery and above 1000 mL in C/S

if within first 24 hours–> early PPH

after, it is late/delayed PPH

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4
Q

what are the common causes of PPH

A

UTERINE ATONY

retained POCs

placenta accreta

cervical lacerations

vaginal lacerations

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5
Q

how should you manage a PPH acutely

A

while investigating the cause, start on fluid rescusitation and make preparations for blood transfusion

with blood loss above 2-3 L, patients may develop consumptive coagulopathy and require coagulation factors and platelets

if become hypovolemic and hypotensive–> consider SHEEHAN syndrome

may have to investigate and/or treat several causes of PPH simultaneously

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6
Q

what is sheehan syndrome

A

pituitary infarction

manifests with absence of lactation secondary to the lack of prolactin or failure to restart menstruation secondary to the absence of gonadotropins

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7
Q

what is the etiology of PPH in vaginal births

A

vaginal lacerations

cervical lacerations

uterine atony

placenta accreta

vaginal hematoma

retained POCs

uterine inversion

uterine rupture

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8
Q

what is the etiology of PPH in C/S delivery

A

uterine atony

surgical blood loss

placenta accreta

uterine rupture

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9
Q

what usually causes cervical laceration

A

rapid dilation of the cervix in stage 1 of labour or maternal expulsive efforts prior to complete dilation of the cervix

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10
Q

what is the leading cause of PPH

A

uterine atony

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11
Q

what factors increase the risk for uterine atony

A

chorioamnionitis

exposure to magnesium sulfate

multiple gestation

macrosomic fetus

polyhydramnios

prolonged labour

history of atony

multiparous (especially grand multipara)

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12
Q

how is the diagnosis of uterine atony made

A

palpation of the uterus –> soft, enlarged, boggy

fundus may be well contracted but the lower uterine segment (less contractile tissue) may not be

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13
Q

how do you treat uterine atony initially

A

IV oxytocin (Pitocin)

while oxy is being administered, strong uterine massage should be performed to assist with contraction

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14
Q

what should you do it uterine atony persists after IV oxytocin and vigorous uterine massage

A

Methergine (not in HTN patients)

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15
Q

what should you do it uterine atony persists after IV oxytocin, vigorous uterine massage and methergine

A

Hemabate (PGF2) (not in asthma patients)

thought to be more effective if injected directly into uterine musculature either transabdominally or transcervically

can also give misoprostol SL or rectally (off label)–> can help decrease the blood loss associated with atony when patients are without IV access

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16
Q

what should you do it uterine atony persists after maximal medical management (with IV oxytocin, uterine massage, methergine, hemabate, and maybe misoprostol)

A

go to OR for dilation and curretage to rule out possible retained POCs

patients unresponsive to these conservative measures but are not bleeding TOO much may benefit from uterine packing with an inflatable tamponade (Bakri balloon) or occlusion of pelvic vessels (uterine artery embolization) by IR to prevent hysterectomy

if this is unsuccessful, can do exploratory laparotomy with ligation of pelvic vessels and possible hysterectomy if required

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17
Q

what should you do if suspicion is high for retained POCs

A

uterus should be explored either manually if cervix not contracted down or by U/S

if there is evidence of a normal uterine stripe, probability of retained products is lower

however, if still suspected, do D and C

if hemorrhage continues after confirmation of no retained POCs, suspect placenta accreta

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18
Q

when should you suspect placenta accreta and what do you do

A

if PPH persists despite management with uterine massage, oxytocin, methergine etc

take them to OR for surgical management via exploratory laparotomy

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19
Q

treatment of uterine rupture

A

laparotomy and repair of uterus–if hemorrhage not controlled, may have to do hysterectomy

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20
Q

risk factors for uterine inversion

A

fundal implantation of placenta

uterine atony

placenta accreta

excessive traction on cord during third stage

21
Q

how do you diagnose uterine inversion

A

witnessing the fundus of the uterus attached to the placenta on placental delivery

patients often experience an intense vasovagal episode from the inversion and may require stabilization with aid of anesthesiologist before manual replacement can be attempted

22
Q

how do you manage uterine inversion

A

stabilize patient, maybe with help of anesthesiologist of have vagal episode

first, attempt manual replacement of uterus

uterine relaxants like nitroglycerin of general anesthesia with halogenated agents may be given to aid uterine relaxation and replacement

if this is unsuccessful, laparotomy is required to surgically replace the uterus

23
Q

describe the approach to PPH after a vaginal delivery

A
  1. stabilize the patient
  2. quickly investigate causes:
  3. rule out vaginal and cervical lacerations first
  4. attempt uterotonic agents and massage
  5. if unresponsive to above, move to the OR and attempt a D and C
  6. if this fails to stop bleeding, place an inflatable balloon in the uterine cavity to limit further hemorrhage
  7. if these measures fail–> laparotomy
24
Q

describe the operative management of PPH once the decision has been made to do a laparotomy

A
  1. on entering abdo–> note whether there is blood in abdo–> suggests uterine rupture
  2. unless unstable and coagulopathic secondary to excessive blood loss, first surgical procedure is usually bilateral O’LEARY SUTURES to tie off the uterine arteries
  3. ligate the hypogastric or internal iliac arteries
  4. if uterine atony is cause–> B-LYNCH SUTUREScan be placed to attempt to compress the uterus and achieve hemostasis
  5. if all this fails, often require hysterectomy
25
Q

why might seizure frequency increase during pregnancy in women with seizure disorders

A

increased levels of circulating estrogens during pregnancy may increase function of the CYP450 enzymes which leads to more rapid hepatic metabolism of AEDs.

renal function also increases in pregnancy–> 50% rise in Cr clearance which affects metabolism of carbamazepine, primidone and the benzodiazepines

increase in total blood volume leads to decreased levels of circulating AEDs

hormonal changes, added stress and decreased sleep occur during pregnancy–> may lower seizure threshold and increase seizure frequency

decreased compliance with AEDs in pregnancy due to concerns over fetal effects

estrogen is epileptogenic and decreases seizure threshold

26
Q

list seizure meds that have known fetal congenital effects

A

phenytoin (REALLY bad…causes all the bad things)

phenobarbitol (also really bad)

primidone

valproate

carbamazepine

trimethadione

27
Q

what fetal anomalies are associated with AEDS

A 
NTDs
IUGR
microcephaly
low IQ
ptosis
cardiac anomalies 
distal digital hypoplasia
low set ears
epicanthal folds
short nose
long philtrum
lip abnormalities
hypertelorism
developmental delay
  • 4x increased risk of cleft palate
  • 3-4x increased risk of cardiac anomalies
28
Q

what congenital anomaly is associated specifically with carbamazepine and valproate

A

NTDs

29
Q

how should you manage an epileptic patient during pregnancy

A
  1. check total and free levels of AEDs on a monthly basis
  2. consider early genetic counseling
  3. check MSAFP
  4. level II U/S for fetal survey at 19-20 weeks
  5. consider amniocentesis for AFP and acetylcholinesterase
  6. supplement with oral vitamin K 20 mg QD starting at 37 weeks
30
Q

if a woman with a seizure disorder develops preeclampsia, what drug do you use to prevent seizures

A

phenytoin (instead of magnesium in the non epileptic patient)

31
Q

what common cardiac drugs are contraindicated in pregnancy

A

ACEi

diuretics

warfarin

32
Q

what are the two main sources of massive fluid shift that occur in the immediately post partum woman (and are of particular concern to those who have underlying cardiac disease)

A

increased venous return as no longer have an enlarged uterus compressing the vena cava

uterus clamps down after placental expulsion, and demands less circulation, leading to effective autotransfusion of its blood supply (approx 500 mL)

33
Q

what is the risk of pregnancy in a woman with marfan’s

A

hyperdynamic state of pregnancy can cause increased risk of aortic dissection and/or rupture particularly in those with an aortic root diameter greater than 4 cm

should be encouraged to pursue sedentary lifestyle and be started on beta blockers

34
Q

what are the risks to the mother who gets pregnancy with pre-existing renal disease

A

increased risk of requiring dialysis

preeclampsia

preterm delivery

IIGR

worsening renal disease

35
Q

how do you treat DVT in pregnancy

A

use adjusted dose LMWH (enoxaparin 1mg/kg BID) or unfractionated heparin (goal aPTT of 1.5 to 2.5 times normal)

LMWH better

36
Q

what congenital abnormalities are caused by warfarin

A

nasal hypoplasia and skeletal abnormalities as well as diffuse CNS abnormalities including optic atrophy

37
Q

what are two signs on CXR that can indicate PE

A

abrupt termination of a vessel as it is traced distally

area of radiolucency in the region of the lung beyond the PE

38
Q

what diagnostic tool is best for PE

A

spiral CT (same as non pregnant)

39
Q

how do you treat PE in the hemodynamically stable pregnant patient

A

LMWH (enoxaparin)

40
Q

how do you treat PE in the hemodynamically UNSTABLE pregnant patient

A

IV heparin

41
Q

how do you treat PE in a patient with massive PE leading to unstable hypoxic states

A

streptokinase for thrombolysis in addition to supportive measures

42
Q

what is the most common cause of hyperthyroidism

A

graves disease

43
Q

how do you manage patients with hyperthyroidism in pregnancy

A

can continue with PTU or methimazole (which decrease production of T4)

use minimum dosage due to risk of fetal goiter

TSH should be kept netween 0.5 and 2.5, and closer to 0.5 if possible

44
Q

what is the most common etiology for hypothyroid

A

hashimoto thyroiditis

second is ablation or removal of thyroid due to graves or cancer

45
Q

how do you manage the hypothyroid woman in pregnancy

A

increase dose of levothyroxine 25-30% due to increased demand for thyroid hormone in pregnancy

keep TSH low normal and follow levels throughout pregnancy

46
Q

what is the natural history of SLE in pregnancy

A

rule of 1/3–>

1/3 improve

1/3 worsen

1/3 remain unchanged

47
Q

how do you manage SLE in pregnancy

A

continue meds like aspirin and corticisteroids

stop cyclophosphamide and methotrexate
remember methotrexate has a long half life

48
Q

why do patients with SLE and antiphospholipid antibody syndrome have a higher rate of first and second trimester pregnancy loss

A

placental thrombosis

  • high rate of second trimester loss is hallmark of these diseases and they will often show symmetric IUGR by 18-20 weeks gestation
  • treatment with low dose aspirin, heparin and corticosteroids have been tried with some improvement in prognosis
49
Q

what cardiac complication is of concern in fetuses developing in SLE positive or Sjogrens positive mothers

A

AV block, irreversible

due to anti-Ro and anti-La antibodies that can cross the placenta and are tissue specific to the fetal cardiac conduction system

Obstetrics and Gynecology (21 decks)

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