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    Preeclampsia by Timothy Bilash MD MS
    www.DrTimDelivers.com

    Lovelace Medical Center, NM
    07July1996
    (first given Covenant Medical Center, IL 19October1995)
TABLE OF CONTENTS
  1. Case presentation
  2. Definitions
  3. Multisystem disease of microvasculature
  4. Assessment
  5. Physiology
  6. Labs in PIH
  7. Treatment
  8. Mortality
  9. Etiology Netter placenta
  10. Other diseases
  11. More info
  12. Bibliography
  13. Evaluations



  1. -(O)- Case presentation
    1. Clinical Triad
      1. hypertension
      2. proteinuria
      3. edema
      4. -(S)- Netter embryo


  2. Definitions
    1. Preeclampsia
      1. Mild
        1. BP >140/90, systolic 30/diastolic 15 mmHG increase, MAP>105
        2. proteinuria 100mg/L spot, 300mg/L/24hours
      2. Severe
        1. BP >160 systolic, >110 diastolic, >120 MAP x2, 6 hours apart
        2. proteinuria > 5g/24 hours (>3+ on spot)
        3. oliguria (<400ml/24 hours)
        4. thrombocytopenia
        5. epigastric pain, pulmonary edema, abnormal LFT
        6. -(O)- ACOG signs/symptoms
      3. Eclampsia = seizure/convulsion
        1. note onset, progress, body involvement, length
        2. 25% post partum
      4. HELLP (4-18%)
        1. hemolysis
          1. abnormal peripheral smear, bilibrubin >1.2 mg/dl
        2. elevated liver enzymes
          1. SGOT >70 U/L
        3. low platelet count (early finding)
          1. < 100,000
      5. Disseminated Intravascular Coagulation (DIC)
    2. Chronic Hypertension preceeding pregnancy
    3. Both


  3. Multisystem disease of microvasculature Netter vascular tree
    1. Visual
      1. "spots/flashes"
      2. AV nicking
      3. retinal edema
    2. CNS
      1. headache not relieved by tylenol
      2. altered consciousness
      3. hyperreflexia, clonus
      4. "aura"
    3. Cardiac
      1. cardiomyopathy
      2. high systemic vascular resistance
    4. Placenta
      1. decreased placental perfusion (improved by lateral position)
      2. spasm of spiral arteries
    5. Blood vessels
      1. Endothelial damage, decreased prostacylin I (vasodilator)
      2. Platelet damage, increased thromboxane A2 (vasoconstrictor)
      3. capillary leakage
    6. Renal
      1. 3 subsets of oliguria
        1. low volume (low PCWP, high SVR)
        2. renal artery spasm (normal or PCWP)
        3. high volume (high PCWP and SVR)
    7. Extremities
      1. non-dependent peripheral edema
    8. -(O)- Global pathophysiology list


  4. Assessment
    1. History
    2. Blood pressure
      1. sitting position most sensitive
      2. widened pulse pressure with dynamap is normal vs MAP increase
      3. diastolic
    3. Level of consciousness
    4. Respiratory rate
    5. Breath sounds
    6. Deep tendon reflexes
    7. Urine output (proteinuria)
    8. Pulse oximetry
    9. Pain/tenderness
      1. Epigastric/Back/RUQ
      2. Uterine
    10. Fetal well being
    11. Retinal vasospasm (sausage link)
    12. -(S)- Netter retina


  5. Physiology
    1. Normal pregnancy
      1. increased sodium
        1. decreased extretion of sodium
        2. increased renin, aldosterone
      2. increased protein retention (by growth hormone)
      3. increased prostacylin (vasodilator)
      4. increased thromboxane A2 (vasoconstrictor)
      5. decreased sensitivity to pressor Angiotensin II
    2. preeclampsia
      1. decrease in circulating blood volume (15% vs 45% increase)
        -(O)- Blood volumes in PIH
         Plumbing Analogy
        1. but excess ECF in the extravascular space- ie volume contraction with edema
        2. decreased GFR
          1. decreased albumin
        3. loss of body Na from all tissues
      2. vascular endothelial injury and vasospasm
        -(S)- Netter vascular tree
        1. vascular smooth muscle more sensitive to pressors (like angiotensin II)
          1. contraction of vascular smooth muscle
          2. peripheral resistance is increased
            1. less PGI2 from endothelium
            2. poor trophoblast infiltration leads to poor dilation
        2. endothelial damage by 6 weeks
          1. capillary leakage
          2. glomerular endotheliosis
      3. Biochemical changes
        1. plasma endothelin
          1. elevated only if clinical symptoms
          2. injection causes HELLP in rabbit model
          3. causes rhytmic uterine ctx in rats
          4. intracellular Ca increased in human myometrium
          5. inactivated in lungs
        2. elevated plasma fibronectin prior to symptoms
        3. elevated thrombomodulin in preeclampsia
        4. endothelium derived relaxing factor (nitric oxide) decreased
          1. impaired release
        5. free radical oxidation products precede clinical symptoms
          1. glutathione peroxidase
            1. associated with IUGR
              1. superoxide anion
                1. inactivates EDRF
          2. lipid peroxidation products
        6. low aldosterone if severe
      4. Platelets
        1. Arachidonic acid from platelets
        2. seratonin relaxation on intact endothelium
        3. activation is surface mediated
        4. used platelets don't aggregate
        5. increased volume
      5. Placenta
        1. abnormal spiral arteries confined to decidua portion
          1. platelet adherence to non-endothelial portions
        2. placenta is large
        3. superficial implantation
        4. innappropriate trophoblastic immaturity
          1. increased intermediate trophoblast
        5. atypical implantation site, acute atherosis,villous infarction, increased syncytial knotting
      6. increased BP
        1. episodes probably 2nd to periodic release of adrenal catecholamines
        2. may compensate for increased placental resistance in mild PIH
        3. in 2nd trimester correlated to pregnancy outcome
          1. high negative predictive value
        4. BP falls less in preeclamptics at night then normal (inverse to BP)
      7. liver
        1. periportal or focal parenchymal necrosis
      8. Kidney
        1. decreased GFR from hypovolemia
        2. low Na gives low Na to distal tubule, so no diuresis and develops edema


  6. -(O)- Labs in PIH
    1. Platelets
      1. platlet decrease seen prior to clinical disease
    2. creatinine
    3. Fibrinogen/ Fibrin Split Products
    4. Liver Enzymes
    5. uric acid
      1. up to 30% diurnal variaton
      2. increase 4 weeks prior to delivery, but significant only 1 week prior
    6. possible Ca/Cr urine ration possible dx
    7. Maternal base deficit > - 8 mEq/L predicts:
      1. fetal acidosis
      2. fetal death
      3. maternal end-organ ischemic injury


  7. Treatment
    1. delivery
    2. magnesium sulfate -(O)- Cunningham protocol
      1. not true anti-seizure on neuron, but prevents seizure
        1. improves cerebral blood pressure (vascular resistance)
        2. ?better local blood flow/autoregulation?
      2. anti-vasospasm
      3. superior to dilantin
      4. 1 gm Calcium gluconate 10% for magnesium toxicity
      5. level 4-8 mg/dl
      6. fall in SVR (2465 to 1377), increase in cardiac index (3.6 to 4.6)
        1. lasts > 4 hours on MgSO4
    3. reduce diastolic BP to 90-100mmHg
      1. hydralazine
        1. vasodilator
        2. onset 10-20 min x 4-6 hrs
        3. 50mg PO bid no effect on placental or renal vascular resistance
      2. labetalol
        1. alpha/beta blocker
        2. not for > 1 deg heart block
      3. Nitroglycerin
      4. Aldomet
      5. ? Nifedipine
    4. Avoid
      1. barbiturates (decreases cerebral blood flow)
      2. diuretics (unless pulmonary edema)
    5. low-dose aspirin
    6. ? Phenytoin/Dilantin (15-25 mg/kg at < 25mg/min)


  8. Mortality
    1. perinatal death
      1. abruptio placenta
      2. intrauterine asphyxia
      3. extreme prematurity
    2. maternal death
      1. pulmonary edema
        1. highest 24-72 hours pp (decreased colloid osmotic pressure)
      2. liver rupture
      3. DIC


  9. Etiology Netter placenta
    1. Chorionic villi must be present
      1. trophosblast without villous stroma does not promote
      2. fetus not necessary
      3. Increased chorionic villi (multiple gestation, hydatidiform mole) increases risk
    2. imbalance of prostaglandins
      1. decrease in prostacyclin (decreased prostacyclin/prostaglandin ratio)
    3. Increased risks
      1. History of PIH
      2. Vascular disease
    4. Immune system
      1. New partner, first pregnancy increases risk (sperm)
      2. decreased IgG in maternal serum
      3. Plasma from preeclamptic suppresses endothelial cell growth
    5. Genetic predisposition
      1. recessive
    6. Calcium deficiency (?) (role of potassium in hypertension)
    7. High BP had low vitamin E and high lipid peroxidation products
      1. 8-fold increase in preeclampsia risk if low erythrocyte omega-3 fatty acids
      2. 15% increase in omega-3 gives 46% decrease risk preeclampsia


  10. Other diseases
    1. Thrombotic Thrombocytic Purpura (TTP)
      1. microangiopathic hemolytic anemia
      2. thrombocytopenia
      3. neurological abnormalitiess
      4. fever
      5. renal dysfunction
    2. Hemolytic Uremic Syndrome (HUS)
      1. acute nephropathy
      2. microangiopathic hemoltyic anemia
    3. Acute Fatty Liver of Pregnancy (AFLP)
      1. fatty infiltration of the liver (most prominent in central zone rather then periportal)
      2. often nonspecific GI/flu symptoms, epigastric pain
    4. Acute Renal Failure (ARF)


  11. More info
    1. Comparison to nonpregnant hypertension
      1. Na restriction effectivly lowers all forms of hypertension
        1. increased angiotensin with pressor response noted in nonpregnant,
      2. if maintain K balence, no increased BP with increased Na
        1. rice-fruit-sugar diet high in K
      3. Ca- increase in water decreases BP and mortality
        1. HTN patients ingest less calcium then normotensive
      4. Salt sensitive individuals/rats require higher BP and renal perfusion before excrete Na
    2. Na- sodium
      1. increased Na need in pregnancy
      2. convulsions and coma in eclampsia may be related to hyponatremia
        1. symptoms of toxemia similar to symtoms of Na depletion
        2. Na restriction
          1. in pregnant animals decreases Na stores in muscle, bone, brain
          2. increased angiotensin with Na retention response noted in pregnant
            1. thus dietary Na restriction stimulates Na retention
          3. depletes renin from juxtaglomerular apparatus, reversed by NaCl
          4. depletes aldosterone (adrenal) if severe)
      3. often edema decreased after salt treatment
    3. Mg- magnesium
      1. may not be anticonvulsant (acton neurons), but may improve vascular autoregulation in CNS which prevents seizures
      2. infusion cause vasodilation
    4. K- potassium
      1. may effect naturesis following added K
    5. Ca- calcium
      1. BP falls after 1g/day in normal pregnancy and young adults
      2. may be mediated by phosphate deficiency
    6. Cl- chloride
      1. angiotensin I converting enzyme is chloride activated
    7. cell adhesion molecule VCAM-1 elevated


  12. Bibliography
    1. *Sibai BM et al, Current understanding of severe preeclampsia, Current Opinion in Nephrology and Hypertension , 1994 (4), 436-445
    2. *How Should Hypertension During Pregnancy Be Managed, Medical Clinics of North America , Cunningham F and Pritchard J, 1984(68), 2:505-526
    3. Precis V, An Update in Obstetrics and Gynecology, 1994, American College of Obstetricians and Gynecologists
    4. *Crisis Obstetrics, Part III (1995), 3 videocassettes with study guide, Poole JH, (Mosby/Saint Louis)
    5. Harvey C and Burke M, in High-Risk Intrapartum Nursing (1992), Mandeville L and Trojano N, Eds., NAACOG, (Lippincott)
    6. *Zeeman, GG and Decker GA, Pathogenisis of Preeclampsia: a Hypothesis, Clinical Obstetrics and Gynecology , 1992, 35;317-337 (complete clinic on hypertension follows)
    7. Women Diagnosed with Pregnancy-Induced Hypertension (Pre-Eclampsia) Should Be Placed on Sodium Resticted Diets, Critical Care Nurse , Mathewson M, May/June 1983
    8. A Reappraisal of Sodium Restriction during Pregnancy, International Journal of Gynaecology and Obstetrics, Pike R and Smiciklas A, 1972(10), 1:1-7


  13. Evaluations
    1. 19October1995 Covenant Medical Center
    2. 07July1996 Lovelace Medical Center


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