Post Partum Hemorrhage and Infections and other shit Flashcards
list risk factors for PPH
- abnormal placentation–> placenta previa, placenta accreta, hyaditiform mole
- 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
- 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)
- 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
when does PPH usually occur
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
define PPH
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
what are the common causes of PPH
UTERINE ATONY
retained POCs
placenta accreta
cervical lacerations
vaginal lacerations
how should you manage a PPH acutely
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
what is sheehan syndrome
pituitary infarction
manifests with absence of lactation secondary to the lack of prolactin or failure to restart menstruation secondary to the absence of gonadotropins
what is the etiology of PPH in vaginal births
vaginal lacerations
cervical lacerations
uterine atony
placenta accreta
vaginal hematoma
retained POCs
uterine inversion
uterine rupture
what is the etiology of PPH in C/S delivery
uterine atony
surgical blood loss
placenta accreta
uterine rupture
what usually causes cervical laceration
rapid dilation of the cervix in stage 1 of labour or maternal expulsive efforts prior to complete dilation of the cervix
what is the leading cause of PPH
uterine atony
what factors increase the risk for uterine atony
chorioamnionitis
exposure to magnesium sulfate
multiple gestation
macrosomic fetus
polyhydramnios
prolonged labour
history of atony
multiparous (especially grand multipara)
how is the diagnosis of uterine atony made
palpation of the uterus –> soft, enlarged, boggy
fundus may be well contracted but the lower uterine segment (less contractile tissue) may not be
how do you treat uterine atony initially
IV oxytocin (Pitocin)
while oxy is being administered, strong uterine massage should be performed to assist with contraction
what should you do it uterine atony persists after IV oxytocin and vigorous uterine massage
Methergine (not in HTN patients)
what should you do it uterine atony persists after IV oxytocin, vigorous uterine massage and methergine
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
what should you do it uterine atony persists after maximal medical management (with IV oxytocin, uterine massage, methergine, hemabate, and maybe misoprostol)
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
what should you do if suspicion is high for retained POCs
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
when should you suspect placenta accreta and what do you do
if PPH persists despite management with uterine massage, oxytocin, methergine etc
take them to OR for surgical management via exploratory laparotomy
treatment of uterine rupture
laparotomy and repair of uterus–if hemorrhage not controlled, may have to do hysterectomy
risk factors for uterine inversion
fundal implantation of placenta
uterine atony
placenta accreta
excessive traction on cord during third stage
how do you diagnose uterine inversion
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
how do you manage uterine inversion
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
describe the approach to PPH after a vaginal delivery
- stabilize the patient
- quickly investigate causes:
- rule out vaginal and cervical lacerations first
- attempt uterotonic agents and massage
- if unresponsive to above, move to the OR and attempt a D and C
- if this fails to stop bleeding, place an inflatable balloon in the uterine cavity to limit further hemorrhage
- if these measures fail–> laparotomy
describe the operative management of PPH once the decision has been made to do a laparotomy
- on entering abdo–> note whether there is blood in abdo–> suggests uterine rupture
- unless unstable and coagulopathic secondary to excessive blood loss, first surgical procedure is usually bilateral O’LEARY SUTURES to tie off the uterine arteries
- ligate the hypogastric or internal iliac arteries
- if uterine atony is cause–> B-LYNCH SUTUREScan be placed to attempt to compress the uterus and achieve hemostasis
- if all this fails, often require hysterectomy
why might seizure frequency increase during pregnancy in women with seizure disorders
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
list seizure meds that have known fetal congenital effects
phenytoin (REALLY bad…causes all the bad things)
phenobarbitol (also really bad)
primidone
valproate
carbamazepine
trimethadione
what fetal anomalies are associated with AEDS
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
what congenital anomaly is associated specifically with carbamazepine and valproate
NTDs
how should you manage an epileptic patient during pregnancy
- check total and free levels of AEDs on a monthly basis
- consider early genetic counseling
- check MSAFP
- level II U/S for fetal survey at 19-20 weeks
- consider amniocentesis for AFP and acetylcholinesterase
- supplement with oral vitamin K 20 mg QD starting at 37 weeks
if a woman with a seizure disorder develops preeclampsia, what drug do you use to prevent seizures
phenytoin (instead of magnesium in the non epileptic patient)
what common cardiac drugs are contraindicated in pregnancy
ACEi
diuretics
warfarin
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)
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)
what is the risk of pregnancy in a woman with marfan’s
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
what are the risks to the mother who gets pregnancy with pre-existing renal disease
increased risk of requiring dialysis
preeclampsia
preterm delivery
IIGR
worsening renal disease
how do you treat DVT in pregnancy
use adjusted dose LMWH (enoxaparin 1mg/kg BID) or unfractionated heparin (goal aPTT of 1.5 to 2.5 times normal)
LMWH better
what congenital abnormalities are caused by warfarin
nasal hypoplasia and skeletal abnormalities as well as diffuse CNS abnormalities including optic atrophy
what are two signs on CXR that can indicate PE
abrupt termination of a vessel as it is traced distally
area of radiolucency in the region of the lung beyond the PE
what diagnostic tool is best for PE
spiral CT (same as non pregnant)
how do you treat PE in the hemodynamically stable pregnant patient
LMWH (enoxaparin)
how do you treat PE in the hemodynamically UNSTABLE pregnant patient
IV heparin
how do you treat PE in a patient with massive PE leading to unstable hypoxic states
streptokinase for thrombolysis in addition to supportive measures
what is the most common cause of hyperthyroidism
graves disease
how do you manage patients with hyperthyroidism in pregnancy
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
what is the most common etiology for hypothyroid
hashimoto thyroiditis
second is ablation or removal of thyroid due to graves or cancer
how do you manage the hypothyroid woman in pregnancy
increase dose of levothyroxine 25-30% due to increased demand for thyroid hormone in pregnancy
keep TSH low normal and follow levels throughout pregnancy
what is the natural history of SLE in pregnancy
rule of 1/3–>
1/3 improve
1/3 worsen
1/3 remain unchanged
how do you manage SLE in pregnancy
continue meds like aspirin and corticisteroids
stop cyclophosphamide and methotrexate
remember methotrexate has a long half life
why do patients with SLE and antiphospholipid antibody syndrome have a higher rate of first and second trimester pregnancy loss
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
what cardiac complication is of concern in fetuses developing in SLE positive or Sjogrens positive mothers
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
