Hypertension and Diabetes in Pregnancy Flashcards
why does BP routinely decrease during pregnancy
decreased systemic vascular resistance
lowest in mid second trimester–> increases back to baseline by around term (should not be higher than pre pregnancy)
what two conditions are associated with HTN and liver injury in pregnancy
HELLP syndrome and acute fatty liver of pregnancy (AFLP)
what is the classic triad of symptoms in preeclampsia
nondependent edema, HTN, proteinuria in the pregnant woman
- nondependent edema is no longer part of the diagnosis, though it is often how women present
- classic presentation is of a nulliparous woman in her third trimester
is there a definitive known cause for preeclampsia
no
what is the presumed pathophysiology of preeclampsia
underlying pathology involved a generalized arteriolar constriction (vasospasm) and intravascular depletion secondary to a generalized transudative edema that can produce symptoms related to ischemia, necrosis, and hemorrhage of organs
- one of the fundamental aspects of the disease is VASCULAR DAMAGE and an imbalance in the relative concentrations of PROSTACYCLIN and THROMBOXANE –> primarily thought to be related to circulating antibodies or antibody-antigen complexes (i.e like SLE) that damage the endothelial lining of vessel walls leading to exposure of the underlying collagen structure
- vascular injury may also be related to the hyperdynamic state of pregnancy rather than immune
list the possible hypertensive states of pregnancy
gestational/pregnancy induced HTN
preeclampsia
severe preeclampsia
chronic hypertension
chronic hypertension with superimposed preeclampsia
HELLP syndrome
AFLP
list the maternal manifestations/complications of preeclampsia
seizure
cerebral hemorrhage
DIC and thrombocytopenia
renal failure
hepatic rupture or failure
pulmonary edema
*these complications are due to the generalized arteriolar vasoconstriction affecting the organs
list the obstetric manifestations/complications of preeclampsia
uteroplacental insufficiency–> can lead to fetal hypoxia, or if chronic, may lead to IUGR
placental abruption
increased premature deliveries
increased C/S deliveries
how do you diagnose severe preeclampsia
severely elevated BPs–> sBP above 160 and dBP above 110 or presence of any of the clinical findings
what % of patients with severe preeclampsia develop HELLP syndrome
10%
what is HELLP syndrome
subcategory of preeclampsia in which the patient presents with HEMOLYSIS, ELEVATED LIVER ENZYMES, LOW PLATELETS
HTN and proteinura may be minimal in these patients
uncommon but patients who get it decline rapidly and have poor maternal and fetal outcomes
even with careful management–> results in high rate of stillbirth (10-15%) and neonatal death (20-25%)
what % of live births experience preeclampsia
5-6%
when does preeclampsia typically develop
can develop any time after 20th week but most common in third trimester near term
what should you consider if HTN presents early in the second trimester (14-20 weeks)
hydatidiform mole or previously undiagnosed chronic HTN should be considered
what % of patients who develop HELLP were first diagnosed with preeclampsia
80%–> but the remainder of HELLP patients present with no previous history of HTN and will present with just symptoms of RUQ pain
*these women need to make sure to have HELLP ruled out despite benign initial presentation
what are the risk factors for preeclampsia
- those related to the manifestations of the disease
- -chronic HTN
- -renal disease
- -african american race (more likely to have T2DM, chronic HTN and obesity)
- -collagen vascular disease (SLE)
- -pregestational diabetes
- -maternal age below 20 or above 35 - those related to the immunogenic nature of preeclampsia
- -nulliparity
- -previous preeclampsia
- -multiple gestation
- -abnormal placentation
- -new paternity - family history
- -female relative of parturient
- -mother in law
- -cohabitation less than 1 year (“tolerance effect”)
- -parental ethnic discordance
how do you diagnose gestational HTN
BPs elevated above sBP 140/dBP 90 mmHg needed to diagnose PIH/GH
should be elevated on at least two occasions 4-6 hours apart and taken while patient seated
*if patients 24 hour urinary protein total is less than 300 mg, preeclampsia is ruled out and patient can be managed expectantly, but these patients are at risk of developing preeclampsia so follow closely with labs etc
fetal complications of preeclampsia
complications related to prematurity, if early delivery necessary
acute uteroplacental insufficiency–> placental infarct and/or abruption, intrapartum fetal distreass, stilbirth
chronic uteroplacental insufficiency–> asymmetric and symmetric SGA fetuses, IUGR
oligohydramnios
diagnosis definition of mild preeclampsia
sBP above 140 mmHg
dBP above 90 mmHg
proteinuria above 300 mg/24 hours or above 1 but less than 2 on dipstick
diagnosis of severe preeclampsia
by symptoms
neuro–> severe headache not relieved by acetaminophen
visual changes, scotoma
CV–> sBP above 160, dBP above 110
pulmonary edema
acute renal failure with rising creatinine
oliguria less than 500 mL/24hours
proteinuria or more than 5 g/24 hours or more than 3+ on dipstick
RUQ pain
elevation of transaminases, AST, ALT
hemolytic anemia
thrombocytopenia less than 100 000 platelets/mL
DIC
IUGR, abnormal fetal dopplers
diagnosis of eclampsia
preeclampsia with seizures
how do you diagnose HELLP
- hemolytic anemia–> schistocytes on peripheral blood smear, elevated LDH, elevated total bili
- elevated liver enzymes–> increase in AST, ALT
- low platelets–> thrombocytopenia
is urine dipstick a good way to rule out preeclampsia
no, especially not in the setting of HTN–> a clean urine dip does not mean they wont have elevated 24 hour protein in their urine
a better predictor in acute setting is spot urine-to-creatinine ratio because creatinine secretion is relatively constant –> ratio of 0.2 to 0.3 is concerning for preeclampsia and should warrant prompt further evaluation
what should you screen for in a woman with HELLP who presents with frank hepatic failure
AFLP
what is AFLP
unclear whether own disease, or on the spectrum of preeclampsia
more than 50% of people with AFLP will also have HTN and proteinura
high mortality rate
how do you differentiate AFLP from HELLP
lab tests associated with liver failure–> elevated ammonia level, blood glucose less than 50 mg/dL, markedly reduced fibronogen and antithrombin III levels
how do you manage AFLP
supportive
liver transplant has been used but some studies report AFLP can be treated in many patients without this aggressive intervention
what is the ultimate treatment of preeclampsia
delivery –> induction of labour is the treatment of choice for pregnancies at term, unstable preterm pregnancies or pregnancies where there is evidence of fetal lung maturity
vaginal delivery may be attempted with assistance of prostaglandins, foley bulb, oxytocin or amniotomy as needed
C/S only for obstetric indications
how would you manage a patient with preeclampsia who is stable and preterm
bed rest and expectant management until delivery at 37 weeks or until delivery otherwise indicated
most commonly manage in hospital
betamethasone given to enhance fetal lung maturity
what medication is often started in women with preeclampsia and what is the dosing
magnesium sulfate
should continue for 12 -24 hours after delivery
this is for seizure prophylaxis during labour and delivery –> 4 g load and 1g/hour maintenance // some places still use 4-6 g load and 2g/hour maintenance
what are the goals of treatment in severe preeclampsia
prevent eclampsia, control maternal BP and deliver the fetus
management varies depending on gestational age
describe an approach to managing a patient with severe preeclampsia
- stabilize with magnesium sulfate for seizure prophylaxis, hydralazine for ateriolar dilation and labetolol for BP control
- once stable–> if gestational age between 24-32 weeks, expectant management to allow time for treatment with betamethasone and further fetal maturity
- beyond 32 weeks or in severe preeclamptic patients with signs of renal failure, pulm edema, hepatic injury, HELLP or DIC–> delivery should ensue immediately
what is the point of using magnesium sulfate in the setting of preeclampsia
seizure prophyalxis
what 3 meds are commonly used to treat severe preeclampsia
magnesium sulfate
hydralazine
labetolol
does preeclampsia resolve immediately after delivery
no–can have effects lingering for several weeks
can even worsen acutely in the immediate post partum phase, possibly due to increased placental antigen exposure during labour and delivery
seizure prophylaxis is thus continued 24 hours post partum or until patient is markedly improved
what meds are usually used in the setting of chronic HTN in pregnancy
labetolol and nifedipine (adalat)
what is the recurrence rate of preeclampsia in subsequent pregnancies
25-33%
in patients with both chronic HTN and preeclampsia, recurrence up to 70%
how do you manage patient to try and reduce risk of recurrence of preeclampsia
low doses of aspirin prior to and during subsequent pregnancies
calcium supplementation
define eclampsia
grand mal seizures in the preeclamptic patient that cannot be attributed to other causes
*eclampsia may also occur without proteinuria
complications of eclampsia
cerebral hemorrhage
aspiration pneumonia
hypoxic encephalopathy
thromboembolic events
what is the clinical manifestation of eclampsia
tonic clonic seizures
may or may not be proceeded by aura
25% before labour, 50% during labour, 25% after delivery
most post partum seizures will occur within 48 hours of delivery but can occur as late as weeks later
how does magnesium sulfate achieve seizure prophylaxis in the eclamptic patient
decreases hyperreflexia
raises seizure threshold
*as good or better than phenytoin, carbamazepine, and phenobarbital in prevention of recurrence of seizures in eclamptic patients
how long do you treat eclamptic patients with magnesium sulfate for
initiate at time of diagnosis and continued until 12-24 hours after delivery
how do you treat magnesium sulfate overdose
10 mL of 10% calcium chloride or calcium gluconate should be rapidly administered through IV
cardiac protection
what % of women with chronic HTN will develop preeclampsia
1/3
what are the risks to mom and baby with chronic HTN
IUGR in fetus due to poor vascular development
superimposed preeclampsia, premature delivery and placental abruption in mom
how do you treat women with chronic HTN who are pregnant
if BP 140/90 or below consistently, can manage expectantly
use antihypertensives in those with persistently elevated BPs or in those who were already on meds prior to pregnancy
two most common meds: labetolol
nifedipine
what type of med is labetolol
beta blocker with concomitant alpha blockade
what type of med is nifedipine
(adalat)
peripheral calcium channel blocker
what is the risk of labetolol in pregnancy
associated with low birth weight but unclear if it is the med or the severity of the HTN that causes this
define true gestational diabetes
impairment of carbohydrate metabolism that first manifests during pregnancy
may have borderline impairments at baseline or be entirely normal in non pregnant state
why does gestational diabetes happen
in pregnancy, human placental lactogen and other hormones produced by the placenta act as anti-insulin agents leading to increased insulin resistance and generalized carb intolerance
this increased insulin resistance occurs in all pregnant women but those in whom the balance tips in favour of insulin resistance will have elevated post prandial BG and occasionally elevated fasting glucose
*in animal models, there has been shown to be pancreatic beta cell hyperplasia in the first part of pregnancy, possibly to overcome this insulin resistance from the placental hormones, but not sure if this is the case in humans
when is GDM usually diagnosed and why is this important
late second, early third trimester (placental hormones increase in volume with size of placenta)
therefore, women with GDM are usually not at risk for congenital anomalies like those with pregestational diabetes
*there is still an increased risk of fetal macrosomia and birth injuries as well as neonatal hypoglycemia, hypocalcemia, hyperbilirubinemia and polycythemia like those with pregestational diabetes
do women who develop GDM go on to get T2DM?
they can–4 to 10x increased risk of developing it in their lifetime
what is the incidence of GDM
1-12% of pregnant women depending on population
5-8% in USA
more common in women of hispanic/latina origin, asian/pacific islander and native american descent
paternal ethnicity in these groups can also contribute
what are the risk factors for developing GDM
race/ethnicity
maternal BMI/obesity
increasing maternal age
family history of diabetes
previous infant weighing more than 4000 g
previous stillborn infant
when is the best time to screen for GDM
end of second trimester between 26-28 weeks in women low risk for GDM
those with one or more risk factors however should be screened at first prenatal visit as part of initial lab tests
how is GDM screened for
most common: 50 g glucose load given and plasma glucose measured 1 hour later–> if positive (BG above 130-140 mg/dL), do glucose tolerance test
how do you do the GTT
3 days of special carb diet–> 8 hour fast–> measure BG before admin of load–> give 100g glucose load–> measure BG at 1, 2, and 3 hours after load
if 2 or more of the 4 values are elevated, diagnosis of GDM made
describe a classification system for diabetes during pregnancy
white classification
Class A1, A2, B etc –> T
Class A1–> GDM, diet controlled
Class A2–> GDM, insulin dependent
other classes are various types of diabetes with ages of onset, symptoms etc
how do you manage GDM once diagnosed
patient usually started on diet recommended for patients with diabetes –> total carb intake is most important
recommended carb intake is approx 200-220 g per day
monitor BG 4 times per day (1 fasting, 3 post prandial)
when should you start diabetic meds in a GDM patient
if more than 25-30% of her BG readings are elevated
start insulin or another oral hypoglycemic agent
what insulin should be used in the true GDM patient
usually fasting BG is fine–> there isnt a problem with baseline metabolism, but with dealing with large carb boluses–> thus post prandial values are high
can thus use a short acting insulin in combo with an intermediate acting insulin in morning to cover breakfast and lunch (short acting at dinner)
- short acting–> Lispro (Humalog)
- intermediate acting–> NPH
what else needs to be done in the management of Class A2 GDM patients once started on insulin
fetal monitoring with NSTs or modified BPPs begun between 32-36 weeks and continued until delivery weekly or biweekly
often get obstetric U/S between 34-37 weeks due to risk of macrosomia
*those with Class A1 GDM are not commonly offered fetal monitoring
when do GDM patients on insulin usually get induced
39 weeks
patients with poor glycemic control are offered delivery between 37-39 weeks after verification of fetal lung maturity
what is the recurrence rate of GDM in subsequent pregnancies
50%
25-35% will go on to develop overt diabetes within 5 years
what is the effect of GDM on the kids in childhood
increased incidence of childhood obesity and T2DM later in life
what is the relationship between pregestational diabetes and preeclampsia?
4x more likely to get preeclampsia or eclampsia
list the possible obstetric complications from pregestational diabetes in pregnancy
polyhydramnios
preeclampsia
miscarriage
infection
PPH
increased C/S
list the possible diabetic emergencies than can occur with pregestational diabetes in pregnancy
hypoglycemia
ketoacidosis
diabetic coma
list the possible vascular and organ involvement complications that can happen to mom in the setting of pregestational diabetes in pregnancy
cardiac
renal
ophthalmic
peripheral vascular
list the possible neuro complications that can happen to mom due to pregestational diabetes in pregnancy
peripheral neuropathy
GI disturbance
what are the possible fetal complications of pregestational diabetes in pregnancy
- macrosomia–> traumatic delivery, shoulder dystocia, Erb palsy
- delayed organ maturity–> pulm, hepatic, neuro, pituitary-thyroid axis
- congenital malformations–> CV defects, NTDs, caudal regression syndrome, situs inversus, duplex renal ureter, IUGR
- IUFD
- 5x increase in perinatal death
- 2-3x increase in risk of congenital malformations, depending on glycemic control
what is the risk of perinatal mortality in a woman with poor glycemic control in pregestational diabetes in pregnancy
as high as 30%
decreases to 1% with careful management
how can you use HbA1c to predict perinatal outcomes
less than 6/5%–> generally good outcomes
above 12%–> poorer outcomes, and 25% rate of congenital anomalies
why dont we generally use oral hypoglycemics in pregnancy
concerns regarding fetal hypoglycemia or potential teratogenicity
not shown to actually be much of a problem in some studies
*but also, likely wont be enough to control hyperglycemia in pregnant patients
