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adv.princ II: exam 1 (5/13) > pre-eclampsia/eclampsia > Flashcards

pre-eclampsia/eclampsia Flashcards

0
Q

gestational hypertension

A
  • HTN not accompanied by proteinuria or gen. edema

- occurs during the last weeks of pregnancy or immediately after delivery

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1
Q

chronic hypertension

A

persistant hypertension before 20th week and beyond 6 weeks post delivery

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2
Q

pregnancy induced hypertension

A

includes pre-eclampsia, eclampsia, and any hypertensive disorders associated with pregnancy

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3
Q

pre-eclampsia:

  1. definition: (also termed as)
  2. when does it manifest?
  3. incidence:
  4. risk factors:
A
  1. occurence of hypertension, proteinuria and edema in second half of gestation (toxicemia of pregnancy)
  2. manifests after 20th week (except for with hydatiform mole)
  3. nulliparous, young females with poor prenatal care
    - diabetes
    - chronic HTN
    - multiple gestation
    - trophoblastic disease
    - advanced maternal age
    - grand multiparity
    - morbid obesity
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4
Q

eclampsis:

  1. defn
  2. mortality rank:
  3. etiology:
A
  1. ecalmpsia with accompanying seiaure (not from previous cerebral condition)
  2. 3rd leading cause of mortality in maternal and fetus
  3. faliure to lose muscular wall of spiral arteries (which happens in normal pregnancy). therefore instead of becoming distended, these arteries constrict causing a 30-40% decrease in uterine blood flow.
    - -the vasomotor receptors in the myometrium are responsive to stimulus and vasoconstrict causing ischemia to placenta
    - -in response to ischema, trophoblasts secrete substances that cause endothelial vessel damage.
    - -this damage causes the releas of mitogens called FIBRINOCTIN which causes a decrease in vasorelaxing substances and inpaired synehteis of endogenous anticoagulants.
    - -lack of anticoagluants causes activation of coagulation and platelet aggregation
    - -vasoconstriction causes loss of capillary endothelial integrity leading to leakage of fluid and protein
    - -protein leakage leads to decreased colloid oncotic pressures leading to protein uria and edema
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5
Q

side effects of eclampsia:

A
  • loss of plasma protein (decreased colloid oncotic pressure)
  • renal damage
  • vasoconstriction
  • coagulation abnormalities
  • myocardial and placental endothelial damage
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6
Q
  1. what is the problem with prostaglandins in preeclampsia?

2. what is the treatment?

A
  • -there are 2 placental prostaglandins: prostacyclin and thromboxane which are produced equally.
  • -thromboxane causes platelet aggregation and vasoconstriction
  • -prostacyclin inhibits platelet aggregation and is a vasodilator
  • -in pre-eclampsia there is 7x more thromboxane than prostacyclin leading to vasoconstriction and platelet aggregation decreasing blood flow to the placenta (by up to 70%) and endothelial injury
  • -this results in the placenta excreting a renin like substance (the parturient is more sensitive to renen/angiotensin anyway) causing systemic release of angiotensin II & aldosterone increasing vasoconstriction
    2. treatment may involve prostaglandin synthase inhibitors such as aspirin (low dose).
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7
Q
  1. what may be a cause of pre-eclampsia that is a reaction to the baby?
  2. how does this happen?
A
  1. immunological:
  2. AB/AG of the baby and mother interact and cause placental vasculitis which leads to tissue anoxia and release of thromboplastin like substance into maternal blood supply
    - - this causes platelet consumption, activation of coagulation mechanisms and pathogenesis (15-30% of pre-eclamptic patients have thrombocytopenia)
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8
Q
  1. what electrolyte imbalance may contribute to pre-eclampsia?
  2. how does this happen?
A
  1. hypocalcemia
  2. may be due to calcium metabolism or deficet which increases reactivity of vessels by 40%
    - -may be due to obligate loss to fetus or by inability to absorb calcium from GI tract (pre-eclamptic women show decreased urinary calcium).
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9
Q

what BP numbers and criteria are part of the diagnosis of pre eclampsia?

A

2 out of 3 of these:

  1. increase in systolic of >30 torr or >140 torr
  2. increase in diastolic of >15 torr or >90 torr
  3. hypertension at rest
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10
Q
  1. what proteinuria numbers are part of the diagnosis of pre eclampsia?
  2. what does this cause that is also part of the criteria?
A
  1. proteinuria: >0.3 grams of protein/ liter of urine in 24 hours (causing decreased plasma oncotic pressures) this leads to …
  2. Edema: generalized (legs and ankles especially)-not good criteria by itself since edema is common in pregnancy.
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11
Q

what is the criteria for SEVERE pre eclampsia?

  1. blood pressure:
  2. proteinuria:
  3. oliguria:
  4. neurological:
  5. respiratory:
  6. liver:
  7. coagulation:
A
  1. SBP of > 160 mmHg or DBP of >100
    - at rest
    - on 2 separate occasions
    - 6 hours apart
  2. proteinuria >5 grams in 24 hours (or 3+ to 4+ by dipstick )
  3. oliguria (<500 cc urine in 24 hrs.)
  4. cerebral or visual disturbances (headache, blurred vision, altered LOC)
  5. pulmonary edema
  6. marked hepatic dysfunction
  7. thrombocytopenia or s/s of DIC (DIC occurs in 20%)
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12
Q

developing pre eclampsia which trimester gives one a worse prognosis?

A

early in second trimester= rapidly progressing, more severe & more chance of perinatal mortality

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13
Q

what does hyper reflexia have to do with pre eclampsia

A

hyper reflexia diagnosis worsens the prognosis for mother and fetus

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14
Q

pathophysiaological changes with pre eclampsia:

1. what is involved?

A
  1. involves almost every organ system
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15
Q

pre eclampsia:

-cardiovascular changes (12 things)

A
  1. increased levels of renin
  2. increased levels of angiotensin
  3. increased levels of aldosterone
  4. increased levels of catecholamines
  5. increased sensitivity to vasoconstricting drugs
  6. elevated BP d/t increased C.O. (more than d/t increased SVR)
  7. increased C.O. may precede hypertension
  8. severely increased C.O. may increase PAWP
  9. reduced blood plasma
  10. decreased colloid oncotic pressure
  11. tissue edema (also cerebral in eclamptic)
  12. increased blood viscositn decreases perfusion
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16
Q

pre-eclampsia:

hematological:

A
  1. increased blood viscosity
  2. coagulation abnormalities (elevated PTT, increased thromboplastin)
  3. thrombocytopenia (<150,000)d/t autoimmune
  4. increased tendancy toward thromboembolism
  5. increased fibrin split products
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17
Q

pre eclampsia

  • GI:
  • renal:
A

hepatic:
1. periportal hemorrhage, ischemic lesions, swelling and subscapular hemorrhage (HELLP)
2. increased liver enzymes
3. serum proteins lost in urine
renal:
1. increased GFR and creatnine clearance
2. acute renal failure with oliguria (may become permanent)

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18
Q

pre eclampsia systemic changes:

CNS:

A
  1. hyper reflexia and cns irritability (seizures)
  2. abnormal EEG in 75% of pre eclamptic patients
  3. leading cause of death -intracranial hemorrhage
  4. may even have seizures up to 48 hours post op
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19
Q

pre eclampsia symptoms

are they always obvious?

A

no, >20% have had no preceeding proteinuria, headache or hyper reflexia

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20
Q 
pre eclampsia systemic effects:
respiratory:
1. pulmonary issues d/t:
2. airway and larynx changes:
3. risk of apnea from...?
4. oxy hgb changes...?
5. when is highest risk of pulmonary edema?
A
  1. pulmonary edema d/t decreased oncotic pressure, capillary endothelial damage and marked vasoconstriction
  2. airway and laryngeal edema
  3. decreased resp effort from magnesium and narcotics
  4. oxy-hgb curve shifts to left (instead of right) causing less O2 availability to fetus
  5. greatest risk of pulm edema post partum d/t redistribution of fluids into intravascular space (from uterus)).
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21
Q

uterus and placental changes with pre-eclampsia:

  1. what happens to placenta?
  2. what happens to uterus?
  3. what happens to uterine circulation?
A
  1. placenta is small and shows evidence of premature aging, has infarcts, fibrin deposits, calcification, may abrupt or go into pre-term labor
  2. uterus becomes hyperactive and markedly sensitive to oxytocin; rapid labor with painful contractions is common
  3. uterine circulation decreases d/t hypovolemia, vasoconstriction and increased blood viscosity
22
Q

preeclampsia:

what are leading causes of intrauterine mortality?

A
  • placental infarction
  • retardation of placental growth
  • abruption
  • infection of amniotic fluid
23
Q

preeclampsia:

causes of maternal morbidity:

A
  • pulm edema (with CHF)
  • aspiration
  • hemorrhage
  • DIC
  • ARF
  • ruptured liver
  • septic shock
24
Q

what is the therapy for pre eclampsia and eclampsia?

A
  1. delivery of fetus and placenta is DEFINITIVE.

2. control the disease as long as uterine evnironment is condusive with fetal development

25
Q

what are the goals of controling pre eclampsia/eclampsia (8 things)

A
  1. minimize vasospasm
  2. improve circulation to uterus and placenta (also kidneys)
  3. improve vascular volume
  4. correct acid-base imbalances
  5. decrease CNS and reflex hyperactivity
  6. treatment is usually symptomatic
  7. no sodium or fluid restrictions
  8. no furosemide until post partum if urine is less than 30 cc/hr in spite of fluid challenges OR if there is CHF with pulmonary edema
26
Q

what is the role of magnesium in pre eclampsia and eclampsia?
(8 things)

A
  1. first line drug in treatment of the “eclampsias”
  2. reduces hyper-reflexia and controls convulsions
  3. mild vasodilator
  4. depresses catecholamine release
  5. cerebral vasodilator, reduces cerebral vasospasm
  6. increases uterine blood flow
  7. increases production of prostacyclin (which vasodilates vessels to placenta)
  8. some sedation properties
27
Q

how does magnesium decrease hyperreflexia and control convulsions?

A
  • it decreases the amount of acetylcholine liberated at the NMJ
  • decreases sensitivity of the end plate to Ach
  • depresses the excitability of the muscle membrane
28
Q

how does magnesium work as a vasodilator?

A

-depresses smooth muscle contraction
-depresses catecholamine release
also:
-decreases renin and angiotensin converting enzyme action
-increases prostacycline release

29
Q
  1. what does overdose of magnesium lead to?
  2. at what dose is magnesium overdose seen?
  3. what is the treatment of mag overdose for mother?
  4. what is treatment of mag overdose for neonate?
A
  1. -muscle weakness
    - respiratory insuffeciency
    - cardiac failure
  2. at greater than 10-15 mEq/L (when deep tendon reflexes are depressed).
  3. -decrease or discontinue gtt;
    - give 10% (10gm/dL) solution in 10cc over 10 min for mother (however it is best to support respirations and avoid unless cardiac suppression)
  4. give 0.5-1 cc slowly (of a 10% solution) for neonate (monitor HR)
30
Q

what must you monitor when giving mag?

A

mag is excreted by kidneys, so be careful with administration if urine output is decreased or renal impairment.

31
Q

magnesium administration:

  1. loading dose:
  2. gtt dose
  3. duration
  4. goal for magnesium levels:
A
  1. 2-4 grams over 15 minutes
  2. infusion of 2-4 grams/hr
  3. maintain for 24-48 hours
  4. keep glood levels at 4-6 (some say 4-8) meq/L (normal level is 1.5-2.0 meq/L)
32
Q

how does magnesium work on pre term labor

A

-antagonizes uterine activity

33
Q

magnesium effects on lungs

A

bronchodilator

34
Q

what are detremental effects of magnesium?

A
  • slows down contractions (prolongs labor and higher risk of bleeding post partum)
  • decreases fetal heart variability (and apgar scores with maternal overdose)
  • increases sensitivity to muscle relaxants (especially NDMRs)
35
Q

treatment of pre eclampsia and eclampsia:
antihypertensives:
1. what is the #1 antihypertensive used?
2. what does it do?
3. what are negative attributes of this drug?

A
  1. hydralizine (apresoline); widely used for diastolic pressure >100 mmHg
  2. -decreases maternal MAP;
    - decreases uterine vascular resistance;
    - increases uterine artery blood flow
  3. long onset time (10-20 minutes)
36
Q

treatment of pre eclampsia or eclampsia:

5 other drugs used (and action):

A
  1. clonidine- presynaptic alpha 2 blocker
  2. prazosin-alpha blocker
  3. nipride- arterial vasodilator
  4. nitroglycerine-venous vasodilator
  5. labetolol-beta blocker
37
Q

what are pros and cons of beta blockers (labetolol, esmolol) (2 pros and 3 cons)?

A

pros:
1. has not been associated with decreased uterine activity or placental perfusion
2. can be used during induction to blunt sympathetic effects of laryngoscopy in pre eclamptic or eclamptic patient
cons:
1. can depress heart action particularly in CHF patient
2. decreased BP can decrease utero-placental circulation
3. esmolol crosses placental-fetal membrane causing fetal bradycardia

38
Q

calcium channel blockers:

  1. how often used?
  2. what does it do?
  3. action:
A
  1. gaining importance and regarded as safe
  2. improves placental and renal blood flow (increased urine output)
  3. works with magnesium (which is also a calcium channel blocker) to decrease arterial muscle constriction
39
Q

eclampsia:
control of convulsions
–what drugs are used (and doses)

A
  1. thiopental 50-100 mg
  2. valium 2.5-5 mg
  3. magnesium 2-4 grams
40
Q

eclampsia:
control of convulsions-if cerebral edema suspected:
–what meds are used?

A
  1. mannitol

2. decadron 10-16 mg

41
Q

eclampsia: what monitors (cardiovascular)

A
  1. bp with NIBP, (art line if pulmonary edema, pressor therapy and/or frequent labs =(abgs etc.).
  2. cvp if severe eclampsia with marked HTN and oliguria
  3. pulm art catheter ONLY if refractory oliguria, cardiac lesions or s/s of CHF.
42
Q

eclampsia–anesthetic considerations:

analgesia

A
  1. contractions may be intense but minimal narcotics to avoid fetal depression (give small doses of fentanyl if they cannot have regional)
  2. pudendal block
  3. if too intense; GETA with RSI
  4. continuous lumbar epidural
43
Q

eclampsia:

  1. what are the pros of continuous lumbar epidural?
  2. what are the “DOs” of epidural with eclampsia?
A

1a. good for relaxation without neonatal depression
1b. decreases circulating catecholamines (namely epi which decreases uterine placental blood flow) therefore improving blood flow
2. hydrate well (sodium chloride, LR or albumin 5% if diastolic >100)
2b. avoid hypostension (small doses of ePHEDrine, fluids)
2c. supplemenatl oxygen

44
Q
  1. what should your CVP be with eclamptic patient?

2. what happens to fluid requirements to raise CVP if diastolic higher?

A
  1. cvp=4-6cm/H2O

2. the higher the diastolic pressure, the more fluids are needed to raise the CVP.

45
Q
  1. what is the best way to give an epidural to an eclamptic/pre eclamptic? to what level do you want your epidural?
  2. how long does it take; what is the benefit?
A

1a. give 8-10 cc(1/2 dose) of 1.5-2% lidocaine or 0.5% bupivicaine to get to level T10
1b. when CV is stable, giventhe other 1/2 to get to level T5
2. takes 30 minutes but less hypotension

46
Q
  1. what is the best anesthetic for eclamptic/ preeclamptic?

2. what would prevent you from doing regional on this patient?

A
  1. regional

2. coagulopathy, low platelet count, absolute emergency (no time)

47
Q

SAB

  1. risk:
  2. what to check before spinal?
  3. what does the literature say about SAB with eclampsia?
  4. SAB doses:
A
  1. high chance of sympathetomy (treat with small doses of ephedrine or phenylephrine)
  2. note coags
  3. some recommend no spinal d/t hypotension
  4. 5% lidocaine (70-80 mg)
    - -.75% bupivicaine (10-15 mg)
    - -.5% tetracaine (9-11 mg)
48
Q

what is the risk with muscle relaxants with pre/eclamptics

A

magnesium potentiates muscle relaxants

49
Q

pre/eclampsia:

  1. what induction med do you not want to use?
  2. why?
  3. what med should you use to preserve BP if dehydrated?
A
  1. ketamine
  2. increases blood pressure too much by inducing catecholamine release
  3. etomidate or thiopental if dehydrated
50
Q
  1. should you pre treat with NDMR when using sux?

2. can you use NDMRs?

A
  1. absolutely NOT if on magnesium (mag potentiates NDMRs).

2. is sux is contraindicated, use small doses of short acting NDMR

51
Q

HELLP:

  1. what is it?
  2. what is it?
A
  1. -hemolytic anemia
    - —elevated liver enzymes
    - —low platelets
  2. variant of severe preeclampsia;(12-14% of pre/eclamptics)
    - fibrin deposits in liver sinusoids leads to preiportal necrosis, subscapular rupture, intrahepatic hemorrhage and hepatic rupture
    - occurs in third trimester (11% before 27 weeks)
    - usually develops suddenly
52
Q

clinical presentation of HELLP

A
  1. epigastric pain, nausea and vomiting
  2. malise
  3. intravascular coagluopathy (platelets less than 50,000-can drop 35-50% in 24 hours)
  4. renal failure
  5. mortality: perinatal-60%
    - -maternal: 24%
53
Q

treatment of help:

A

delivery (especially if DIC)
control blood pressure
support (blood, hemodynamic monitoring, platelet transfusion)
platelet infusion for less than 40,000

adv.princ II: exam 1 (5/13) (8 decks)

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