High Risk Disorders Part I (final) Cheat Sheet (DRAFT) by hellokitty2000

•^{5-10% of pregna­ncies} •^{↑mater­nal­-fetal morbidity & mortality worldwide} •Risk of matern­al/­fetal injury related to CNS irrita­bility^{•seizures•placental abruption•IUGR}

•after 20 weeks •BP > 140/90 x 2 •with or without protei­nuria (PCR > 0.3)

inadequate vascular remodeling →⬇ placental perfusion & hypoxia → endoth­elial cell dysfun­ction → vasospasm & ↓ tissue perfusion

•Primipara < 19 yrs or > 40 yrs •Previous hx of PEC •Family hx of PEC •Multiples •Obesity •African descent

34yo G4P3 @ 34 weeks with BP 142/88, 145/90

Prenatal follow-up? ➡•Weekly visits with AFI •BP 2x week •NST 2x week •platelets and LFTS weekly •FKC •Consider IOL @ 37 weeks

•BP >16­0/>110 •Severe features

Frequent assessment Vitals ➡•q 10 Assess edema, clonus, DTRs •HA, visual changes •Epiga­stric pain (liver is getting involved) •Foley – strict I&O •Fetal well-being •Plate­lets, liver enzymes

•Decreases neurom­uscular irrita­bility •Decreases CNS irrita­bility •Promotes maternal vasodi­lation

•MAG: 4g loading dose, then 2g/hr to depress (not eliminate) reflexes •Strict I&O (consider Foley) q hour •BP check q 15-30 mins
•Pulse Ox, Lung Sounds •DTRs, Clonus, and hand grasps •FLUID RESTRI­CTION •Control hypert­ension^{•BP meds via IV meds if severe •Continue observ­ations 24-48hrs PP •Symptoms usually resolve within 48 hours PP}

You are caring for a 34yo G2P1 who was admitted for IOL at 36 weeks for PEC with severe features. After you administer the Mag Sulfate bolus, the patient reports that she feels “sleepy and a little nausea­ted.” You also notice that the variab­ility of the FHR tracing is now minima­l.a­dmi­nister the Mag Sulfate bolus, the patient reports that she feels “sleepy and a little nausea­ted.” You also notice that the variab­ility of the FHR tracing is now minimal.
•What is your first action? •What would you assess? •What would you antici­pate? •What monitoring is necessary for this patient?

•Onset of seizure activity or coma in pregnancy without CNS lesion •Treat with Magnesium Sulfate + PEC measures
•Asses­sment ➡ ^{↑HTN precedes seizure followed by hypote­nsion and collapse •Coma may occur •Labor may begin, putting fetus in great jeopardy}

•Patent airway & patient safety •ABCs •Side rails up •Call for help!^{Do not leave!} •Suction •Prevent aspiration •Fetal Monitoring •Maternal VS •Meds^(O2)

Diagno­sis➡•Before pregnancy or diagnosed before 20 weeks. •Use of anti-h­ype­rte­nsives before pregnancy
•Monitor ➡Labs, u/s, NST AFI, IOL (37-38 weeks) •Persists > 12 weeks postpartum
•Risk: IUGR, PTL, placental abruption, renal failure, CHF, CVA, and superi­mposed PEC •Low dose ASA (12-36wks)
•Mild-­mod­erate: no evidence of improved outcomes with meds •CHTN with superi­mposed PEC

•HTN before 20 weeks with new onset protei­nuria •Worsening HTN plus one
1•New onset of sx2•Thro­mbo­cyt­openia3•↑liver enzymes4•Pulm­onary Edema5•New onset renal insuff­iciency ^{•↑morb­idity for mom & fetus}

•Elevated BP > 20 weeks •>1­40/­>90 •No protei­nuria •25% will develop PEC •If persists > 12 weeks PP ➡ CHTN

•Hemolysis •Elevated •Liver Enzymes •Low •Platelets (<100K)
•Labor­atory diagnosis with PEC •Non-s­pecific clinical presen­tation •Prompt delivery on dx vs. wait 48hrs for steroids if < 37wks
•Life threat­ening •Pulmonary edema •Acute renal failure •DIC •Abruption •Liver failure, hemorrhage •ARDS •Sepsis •Stroke

Preecl­ampsia •After 20 weeks •BP >14­0/>90 x2 •Prote­inuria and/or severe features
Chronic Hypert­ension •Before 20 weeks •>1­40/­>90
Gestat­ional Hypert­ension •After 20 weeks •>1­40/­>90

Preecl­ampsia with severe features •BP >16­0/>110 x2 or severe features •Magnesium Sulfate* •Seizure precau­tions
HELLP •May not have s/s of PEC •High maternal and fetal mortality •Progr­esses rapidly

•Labetalol •Nifed­ipine •Methy­ldopa •Hydra­lazine •Magnesium Sulfate^{•Calcium Gluconate} •No ACE inhibitors •Avoid Methergine for PPH

Intrap­artum Care ➡•Mate­rna­l-Fetal VS •Conti­nuous EFM •Epidural? •Fluid restri­ction? •Quiet, dark, environment
•Emergency drugs, 02 @ 10L, suction ready •Magnesium Sulfate^{•Calcium gluconate}

•Pre-e­xisting DM type 1 & 2 •GDMa-1 •GDMA-2 •Hyper­emsis gravidarum •Hyper & hypo thyroidism •PKU

•Metabolic changes in pregnancy ➡ •Normal pregnancy alters maternal glucose metabo­lism, insulin produc­tion, and metabolic homeos­tasis
•Glucose is the primary fuel for the fetus•Glucose crosses the placenta, insulin does not
•Insulin needs↓­during the first trimester^{•Risk of hypogl­ycemia for IDM patients}
•Diabe­togenic effect in second and third trimesters^{•↑insulin resistance•Placental hormones act as insulin antago­nists}
•Expulsion of the placenta drops insulin requir­ements

•Gesta­tional DM ➡•Common-^{Hispanic, Native American, Asian, AA}•DX 2nd trimester with 1 & 3 hr. GTT •Screening algorithm •↑risk should screen early
•GDMA1- well controlled with diet •GDMA2- need meds

•Glucose crosses the placenta •↑ fetal insulin production in response to high glucose from maternal circulation
•Fetal macrosomia •Labor risks^{•Maternal Risks •Fetal Risks} •Newborn Risks

•Patient Counseling^{•Pathology of disease} •Low-g­lycemic diet •Exercise •Teach­/De­mon­strate^{•Glucose monitoring •Insulin Admini­str­ation}
•Signs of hypo- and hyperg­lycemia & immediate actions to be taken if signs noted •Fetal survei­llance

•Glucose Screen Gold standard is 3hr GTT.•GDMA1 – Diet controlled GDMA2 – on medication (metfo­rmin, glyburide, insulin)

Monitoring and TX➡•Blood Sugar Testing •Dietary Counseling •Exercise •Insulin •Oral hypogl­ycemic •Fetal monitoring •IOL →SVB or C/S
Risks and Conseq­uences➡•IUFD •Conge­nital malfor­mations •Macro­somia •RDS •Infec­tions •Polyh­ydr­amnios •PEC, CHTN •Hyper­gly­cemia •DKA

Intrap­artum➡ •Testing q hour •Fluids and insulin^{•(70-100 mg/dl) •Risks?} •Polyh­ydr­amnios •Macro­somia
Postpartum➡ •First 24hrs: ↓insulin demands^{•½ dosage of insulin} •PPH •Infec­tions •Breas­tfe­eding •Family planning

•Severe and persistent NVP •Weight loss, electr­olyte imbalance, nutrit­ional defici­encies and ketonuria.
•Idiop­ath­ic/­Mul­tif­act­orial •Can be a debili­tating complex metabolic disorder •Linked to Hydati­diform mole

•Persi­stent vomiting before 9 weeks •Ketonuria •Dehyd­ration •> 5% weight loss •Altered nutrit­ional status •Elect­rolyte imbalance (hypok­alemia)

•Small frequent meals •Don’t over eat •Eat what sounds good •Avoid triggers (odors) •Avoid spicy •Bland, low fat
•Cold may be more tolerable than warm •Drink from a cup with a lid and straw •Carbo­nated beverages- real ginger ale

•Inborn error of metabolism caused by an autosomal recessive trait that creates a deficiency in the enzyme phenyl­alanine hydrolase,
which impairs the body’s ability to metabolize foods with protein
•If unreco­gnized, can cause cognitive impairment
•Prompt diagnosis and therapy with a phenyl­ala­nin­e-r­est­ricted diet signif­icantly decreases the incidence of cognitive impair­ment.
•Women with PKU may be advised against breast­feeding because their milk contains a high concen­tration of phenyl­ala­nine.