Ex1 OB 3 Flashcards
PIH
Encompasses a range of disorders collectively
Formerly known as “toxemia of pregnancy”, which includes:
- isolated systemic hypertension (nonproteinuric hypertension)
- preeclampsia (proteinuric hypertension)
- eclampsia
HTN during pregnancy
Common, ~ 10% of pregnancies
Associated with a higher incidence of maternal, fetal, and neonatal mortality and morbidity
PIH Etiologies
- Vasospasm caused by abnormal sensitivity of vascular smooth muscle to catecholamines
- -Antigen-antibody reactions between fetal and maternal tissues during first trimester that initiates placental vasculitis
- An imbalance of vasoactive prostaglandins (thromboxane A and prostacyclin) leading to vasoconstriction of small arteries and aggregation of platelets
Hypertensive States
- Gestational hypertension
- Preeclampsia, eclampsia
- Chronic essential hypertension
- Chronic hypertension (secondary to renal disease, endocrine disease, coarctation of the aorta)
- Chronic hypertension with superimposed preeclampsia
Gestational HTN
Characterized by onset of systemic HTN, without proteinuria or edema
Usually mild with minimal impact on pregnancy
Resolves before 12 weeks postpartum
-BP normalizes during first few weeks postpartum but systemic HTN often recurs with subsequent pregnancies
-Risk of developing essential HTN later in life increased in women with gestational HTN
Preeclampsia
Occurs in 5 – 8% of pregnancies in US
Incidence varies with geographical location (up to 18% in parts of Africa)
Disease is mild in 75% of patients
Preeclampsia is primarily a disease of
Primigravidas
Preeclampsia is associated with
High rates of neonatal mortality
-d/t decreased placental blood flow, decreased oxygen delivery to fetus, etc.
Preeclampsia maternal mortality
Cerebral hemorrhage (30 – 40%) Pulmonary edema (30 – 38%) Renal failure (10%) Cerebral edema (9%) DIC (9%) Airway obstruction (6%)
Preeclampsia risk factors
Predisposing factors: Nulliparity Black race Maternal age < 20 years or > 35 years Low socioeconomic status Multiple gestation Hydatidiform mole Polyhydramnios Obesity Chronic hypertension Diabetes Underlying renal disease
Preeclampsia diagnosis
development of HTN + proteinuria after 20 weeks of gestation
-2 categories
“classic” preeclampsia
Classic triad:
HTN, generalized edema, proteinuria
Mild Preeclampsia
HTN with SBP > 140 mmHg or DBP > 90 mmHg in patient who had normal BP prior to pregnancy
Proteinuria > 300 mg over 24 hours
Severe Preeclampsia
-SBP > 160 mmHg or DBP > 110 mmHg on two occasions < 6h apart
- Proteinuria > 2g in a 24h period or 2-4+ on urine dipstick testing
- Increased serum creatinine (>1.2 mg/dL)
- Oliguria = 500 mL/24h
Preeclampsia with severe features
Visual or other cerebral disturbances Epigastric pain Retinal hemorrhages, exudates, or papilledema Pulmonary edema *difficult IV access d/t pitting edema
Pathophysiology of preeclampsia
“A disease of theories”
The current concepts recognize that its a multisystem disorder characterized by vasoconstriction, metabolic changes, endothelial dysfunction, and activation of the coagulation cascade in conjunction with an inflammatory response
2-stage model has been proposed:
- failure of placental vascular remodeling results in reduced placental perfusion
- ischemic placenta may then produce circulating anti-angiogenic factors that promote generalized maternal vascular endothelium dysfunction, leading to systemic manifestations of preeclampsia
Normal Placentation
involves transformation of branches of maternal uterine arteries, spiral arteries, from thick-walled muscular arteries into sac-like flaccid vessels that permit delivery of greater volumes to uteroplacental unit
In an uncomplicated pregnancy: normal placenta connection to uterine wall.
Normal placentation involves the invasion of spiral arterial walls with
endovascular trophoblastic cells
In preeclampsia, what does not occur (pathogenesis)?
transformation of spiral arteries does not occur bc the placental trophoblastic cells do not invade the spiral arteries, resulting in…
Narrow vessels –> placental hypoperfusion –> ischemia
Preeclampsia is associated with what abnormalities
Elevated levels of circulating renin, angiotensin, aldosterone, catecholamines
–> resulting in generalized vasoconstriction + endothelial damage; edema, hypoxemia, hemoconcentration
–> decreased renal blood flow, GFR, urine output
*puffy, swollen, but dehydrated
Preeclampsia: coagulation findings
thrombocytopenia, increased fibrin split products, + prolonged PT may occur
DIC rare but possible
Preeclampsia creates an imbalance in ________ ratio due to _______
imbalance in thromboxane to prostacyclin ratio
due to decreased prostacyclin production
Clinical effects of prostacyclin
decreased vasoconstriction, platelet aggregation, uterine activity
Increased uteroplacental blood flow
Clinical effects of thromboxane
Increased vasoconstriction, platelet aggregation, uterine activity
Decreased uteroplacental blood flow
One of the most serious forms of preeclampsia
HELLP Syndrom
HELLP Syndrome
Hemolysis, Elevated Liver Enzymes, and Low Platelets
*only in this if mom has all - otherwise pre-eclampsia with severe features
HELLP Syndrome: Labs
-hemolysis: indicated by abnormal peripheral blood smear + an increased bilirubin level
- Elevated liver enzymes:
- aspartate aminotransferase (AST) >70 U/L
- lactate dehydrogenase (LDH) >600 U/L
- Platelet count < 100,000/mm3
HELLP syndrome: clinical indications
Assuming no other coagulopathy, hemostasis not problematic unless platelet count < 40,000 /mm3
rate of fall is of clinical significance:
Regional anesthesia C/I if platelets drop dramatically over short period
-Platelet count usually returns to normal within 72h of delivery, but thrombocytopenia may persist for longer periods
HELLP syndrome: most important factor relating to anesthesia
Platelet count dropping precipitiously –> catch mom in time (normal platelets:: 90 to 70) to place epidural, but cannot remove until plt count resolves
Medical Management:Mild Preeclampsia
Tx for preeclampsia: Bedrest + delivery of infant
Hospitalization diminishes chances of convulsions + enhances fetal survival
Outpatient management includes bedrest, daily urine dip for protein, and BP measurement
Antihypertensives for DBP > 100 mmHg and gestation > 30 weeks
Medical management: Severe Preeclampsia
Goals include prevention of convulsions, control of maternal blood pressure, and initiation of delivery
Antihypertensives for control of blood pressure and corticosteroids used to accelerate fetal lung maturity
Preeclampsia: Indications for Delivery
- DBP consistently > 100 mmHg in a 24-hour period or confirmed > 110 mmHg
- Rising serum creatinine
- Persistent or severe headache
- Epigastric pain (liver distension)
- Abnormal LFTs
- Thrombocytopenia
- HELLP syndrome
- Eclampsia
- Pulmonary edema
- Abnormal FHR
- SGA fetus
Delivery – preeclampsia
- Vaginal delivery is preferable to C/S and labor induction is generally aggressive
- A clear endpoint for delivery should be determined, usually w/in 24h
- If delivery is not achieved within the set time frame, then a cesarean is warranted
Why is vaginal delivery preferred over C/S in preeclampsia?
thrombocytopenia + coagulopathy from preeclampsia increases risk of bleeding
Eclampsia
Preeclampsia + generalized seizures
Most seizures occur before delivery
-PP seizures occur most often w/in 48h after delivery
Pathophysiology of eclampsia
seizures attributed to platelet thrombi, hypoxia due to local vasoconstriction, and foci of hemorrhage in the cortex
Relationship between eclampsia + HTN
poor correlation with severity of HTN
25 – 40% of patients will have normal BP at time of their first eclamptic seizure
hallmarks of hypertensive encephalopathy
retinal hemorrhages, exudates, and papilledema
*very infrequent in eclampsia
Severe Preeclampsia: HTN Tx
*Hydralazine
-longer onset time, not good for urgent situations
*Labetalol
-quick onset
-doses up to 1mg/kg do not effect baby blood flow
Nifedipine
-CCB + increases UBF
**assoc. with: lowering moms bp, prolonging pregnancy, improving fetal O2
*Sodium Nitroprusside
-risk of fetal cyanide toxicity
Nitroglycerin
Severe Preeclampsia: Fluid management
- Significant hypovolemia d/t shift of fluid/proteins to extravascular compartment
- inverse relationship between intravascular volume + severity of HTN has been demonstrated
Severe preeclampsia: pts with very elevated DBP expected to have
negative CVP readings
Severe Preeclampsia: Coagulation Abnormalities
- assess coag status
- administration of platelets, FFP, pRBCs may be necessary
Agent of choice for seizure prevention + control in preeclampsia/eclampsia
Magnesium Sulfate
Magnesium sulfate - outcomes
- can reduce seizures by 50% w/o any serious maternal morbidity
- beneficial effect may be vasodilation + increase in CO (by a reduction of SVR)
Magnesium Sulfate: MOA
- Anticonvulsant effect likely from acting as an N-methyl-D-aspartate (NMDA) receptor antagonist
- Increased production of endothelial vasodilator, prostacyclin
- Protects against ischemic damage of cells by substitution of calcium
Magnesium Sulfate Dosing
- Initial dose: 4–6g IV over 10–20 min, followed by maintenance infusion 1–2g/h
- In presence of renal failure, rate of infusion should be modified by evaluating serum magnesium levels
Magnesium Therapeutic Index
- Narrow therapeutic index
- therapeutic range: serum levels 4 to 8 mEq/L
- normal serum magnesium level is 1.5 – 2.0 mEq/L
Magnesium Toxicity: Plasma Mag Level 5-10
Effects: EKG changes
- PR prolonged
- widened QRS
Magnesium Toxicity: Plasma Mag Level 10
Loss of DTRs
Magnesium Toxicity: Plasma Mag Level < 15
SA + AV Block
Magnesium Toxicity: Plasma Mag Level > 15
Respiratory paralysis
Magnesium Toxicity: Plasma Mag Level 25
Cardiac arrest
Tx: Magnesium Toxicity
10 mL of 10% calcium gluconate slow IV push to counteract effects
Why calcium gluconate and not chloride for mag toxicity tx?
Chloride is 3x as potent, but extremely irritating to vessels when given IV push
Magnesium: pros
Anticonvulsant Vasodilation Increased uterine blood flow Increased renal blood flow AntiHTN Increased prostacyclin release by endothelial cells Decreased plasma renin activity Decreased ACE Attenuation of vascular responses to pressor substances Reduced platelet aggregation Bronchodilation Tocolysis (improves uterine blood flow and antagonizes uterine hyperactivity)
Magnesium: cons
Tocolysis with prolonged labor + increased postpartum hemorrhage
Decreased FHR variability
Generalize muscle weakness
Increased sensitivity to muscle relaxants
Neonatal effects: lower APGAR scores + decreased muscle tone
*mag can relax mom = can relax uterus + baby too
Anesthetic options for Severe preeclampsia: Technique of choice
- Epidural anesthesia recommended for C/S delivery in severe preeclamptic pt as technique of choice
- Epidural analgesia early in labor may help to reduce circulating levels of maternal catecholamines, thus improving uteroplacental perfusion
Anesthetic options for Severe preeclampsia: Spinal
Spinal anesthesia in context of severe preeclampsia has not been recommended in the past, bc concern rapid onset of sympathectomy would precipitate HOTN
- But single-shot spinal for C/S can be safely used in pt with severe preeclampsia
- HOTN avoided w/ meticulous attention to technique + volume expansion
Anesthetic options: Neuraxial C/I
Coagulopathy or C/I’s
= GETA
Risks – GETA for C/S d/t preeclampsia
- Periglottic edema (difficult airway)
- HD response to intubation: HTN
In patients receiving mag sulfate who undergo GETA, what may occur?
activity of Sux + NDMR enhanced
GETA for C/S in pt with preeclampsia: induction risk + Tx
Risk of HTN –> stroke + pulmEdema
Prophylaxis: Labetolol 10mg IV
Tx: SNP or NTG
Most common medical complication of pregnancy
Diabetes Mellitus
any degree of glucose intolerance with first recognition during pregnancy
Gestation Diabetes (GDM)
Midline defect
occurs on the anterior (front) portion of body, usually in middle or center of body.
Like cleft palate or imperforate anus
Hyperglycemia around _____ results in 6x increase in ______
Hyperglycemia around conception or early organogenesis results in a 6-fold increase in midline birth defects
Ketoacidosis
- immediate threat to life
- leading cause of perinatal morbidity
- 40% of perinatal mortality
GDM Complications
Pregnancy: Placental insufficiency Superimposed preeclampsia Diabetic nephropathy Diabetic ketoacidosis
Fetal macrosomia:
assoc. with operative delivery, shoulder dystocia, birth trauma
Neonatal complications: respiratory distress syndrome, hypocalcemia, hyperbilirubinemia, hypoglycemia
GDM effect on placenta
Associated with placental abnormalities
-uteroplacental blood flow index lower by 35-40% in diabetic parturients
GDM: poorly regulated + higher HbA1c effect at tissue level
2,3-DPG levels lower = blood oxygen release at tissue level impaired
Most common cause of 3rd trimester bleeding
placenta previa
abruptio placentae
uterine rupture
Postpartum hemorrhage is most often due to
uterine atony (soft)
retained placenta
placenta accreta (grew thru uterus)
uterine inversion
Obstetrical Hemorrhage
Blood loss assoc. w/ pregnancy or parturition and 1 or + : -Causes maternal or perinatal death -Requires blood transfusion -Decreases hematocrit by 10 points -Triggers emergency therapeutic response
Abruptio placenta
placental abruption
a partial or complete separation of the placenta before delivery of the fetus
Most common cause of OB hemorrhage + maternal death
Abruptio placenta
Placenta Previa
Occurs when placenta is implanted low in uterus, either overlying or encroaching cervical opening (cervical os)
Types of placenta previa
Low implantation: small portion of placenta covers cervical os. Possibility to deliver vaginally
Partial: can cause just as much bleeding as total.
Total: overlying cervical os
Placenta Previa is more common
- in multiparous women
- previous C/S or uterine myomectomy
Placenta Previa is characterized by
painless vaginal bleeding in 3rd trimester
Bleeding d/t placenta previa
may stop spontaneously, risk of severe bleeding can occur at any time
Placenta Previa: Tx
< 37 weeks, mild to moderate bleeding: bedrest + observation
> 37 weeks: C/S
Abruptio Placenta Risk Factors
chronic HTN, PIH, preeclampsia, maternal cocaine use, excessive alcohol intake, smoking, + previous history of abruption
Abruptio Placenta manifestations
vaginal bleeding + uterine tenderness
Categorized based on severity (degree of placental separation)
Blood loss can be underestimated d/t potential for substantial hemorrhage concealed behind placenta
Abruptio Placenta Risks
DIC (30%, high risk)
d/t open venous sinuses in uterine wall = amniotic fluid enters maternal circulation
Severe abruption: fetal mortality 50%, maternal mortality 1-3%
Placenta Accreta
Abnormally firm attachment of placenta to uterine wall
placenta becomes difficult or impossible to separate from uterus + produce life-threatening maternal hemorrhage
Placenta Accreta - increased risk if
history of placenta previa or C/S
Placenta increta
placenta invades the myometrium
Placenta percreta
placenta has invaded the myometrium and serosa, sometimes into adjacent organs, such as the bladder
Uterine rupture
- potentially life threatening complication
- May occur in a previously scarred uterus or result from uterine manipulation, trauma, or overly aggressive use of oxytocin (or VBAC)
What must be available for TOLAC?
Trial of Labor after C/S
-ACOG recommends physician capable of performing C/S + anesthesia provider be immediately available (< 30 minutes away if in rural area)
Uterine rupture S/S
- non-specific
- fetal bradycardia almost always occurs
- Maternal hypotension along with loss of function of uterine pressure monitors often evident
Tx Uterine Rupture
emergency laparotomy
GA indicated
Vasa Previa
fetal umbilical cord passes in front of the presenting part of fetus
-vessels of umbilical cord are vulnerable to trauma during vaginal exam or aROM
Vasa Previa risks
bleeding from fetal circulation = fetus at risk
Vasa Previa Tx
immediate delivery
PPH
postpartum hemorrhage
causes: uterine + non-uterine
Uterine causes - PPH
most frequent: uterine atony + retained placental products
others: uterine rupture + uterine inversion
Non-uterine causes - PPH
vaginal tears, perineal hematoma, maternal coagulopathy
Uterine Atony: risk factors
Prolonged labor Overdistended uterus (macrosomia or multiple births) Infection Grand multiparity Administrations of drugs that relax uterus: -Halogenated anesthetics -β-sympathomimetic agonists -Magnesium sulfate
Uterine Atony Tx
-oxytocin
Doses can precipitate HOTN (continuous infusions preferable)
-Hemabate + ergot alkaloids (Methergin) are potent uterotonic agents used to treat atony
Retained Placenta Tx
~ 1% of vaginal deliveries
Usually reqs manual exploration of uterus + facilitated by epidural/spinal
Additional uterine relaxation achieved w/ nitroglycerine 50–100mcg IV
Ketamine can be used if regional not in place
If bleeding excessive + hypovolemia present, regional may be C/I d/t HOTN
GA + RSI may be necessary
As soon as uterus is relaxed sufficiently to allow extraction, volatile should be d/c’ed to prevent uterine atony + further bleeding
Amniotic fluid embolism
Mortality ~ 80%
Survival uncommon, survivors often have neurological dysfxn
Most occur during or immediately after labor
AFE Pathogenesis
initiating event poorly understood
Usually during labor or other procedure, amniotic fluid + debris enters maternal circulation
-may trigger a massive anaphylactic rxn, activation of complement system, or both
AFE presentation
Acute SOB, +/- cough, followed by severe HOTN
Fetal distress evidenced by fetal bradycardia from hypoxic insult
Cyanosis
Asystole
Phases of AFE
Early phase:
Pulm vasospasm
Acute RHF
Often fatal early (50% die w/in 1h)
Second phase: LVF + pulmEdema
AFE Tx
supportive
Administer O2 + intubate
Aggressive CPR if arrests
Treat HOTN w/ crystalloid + blood products
Use vasopressors
*early delivery of fetus = may improve survival of mom + may result in survival of fetus
*HD, plasmapheresis, ECMO w/ IABP ?
Leading cause of maternal death globally
hemorrhage
Maternal hemorrhage usually occurs
immediately after delivery (35%)
Abnormal OB blood loss
> 500 mL vaginal delivery
> 1L C/S
Major hemorrhage
Blood loss 2,500 mL or +
Transfusion of 5 or + units blood
Treatment for coagulopathy
Causes of maternal hemorrhage: antepartum
Placenta previa
Placental abruption
Uterine rupture
Vasa previa
Causes of maternal hemorrhage: postpartum
Uterine atony Genital trauma Retained placenta Placenta accreta Uterine inversion
PPH risk factors
Multiple gestation Macrosomia Polyhydramnios High parity Prolonged labor Chorioamnionitis Augmented labor Tocolytics Maternal blood disorders > 35 years HTN disorders High concentrations of volatile anesthetic agents
strong predictor for subsequent development of severe postpartum hemorrhage
Fibrinogen levels of < 2 g/dL in early stage of postpartum bleeding
Accounts for 80% of PPH
uterine atony
uterine atony is the loss of tone in uterine musculature following delivery as a result of failure to respond to ________
normal endogenous oxytocic substances, oxytocin, and prostaglandin
No vaginal bleeding, can mom have uterine atony?
Yes - can be atonic, engorged uterus with > 1L blood
Prevention of uterine atony is facilitated how?
Administration of oxytocin immediately after delivery
s/s hypovolemia
may not be present until > 1200-1500mL blood loss
Circulating blood volume expands from ____
20-100%
RBC volume increases by
30%
CO increases by
50%
Risks of hypovolemia or hypovolemic shock in pregnancy
Masked s/s d/t normal increases in pregnancy:
HR increases 15-20 bpm
Peripheral vasodilation
Widened pulse pressure
Hypovolemic shock: moms SBP may not drop until ____
2-3L blood have been lost
Surgical management of maternal hemorrhage
Bimanual compression of uterus Uterine balloon tamponade Uterine compression sutures Arterial ligation Peripartum hysterectomy Angiographic arterial embolism
Crystalloids are distributed between intravascular and extravascular space by a ratio of
1:3
Exsanguinating hemorrhage tx
immediate resuscitation with any fluid; blood products = saving
**O negative should be considered
Transfusion of red blood cells is usually unnecessary in patients with
Hgb = 10 g/dL or +
Transfusion of pRBCs should be administered if
Hgb < 6 g/dL
Transfusion Guidelines
Once > 10 units pRBCs given:
1:3 FFP:pRBC
+ 6u platelets
(avoid dilutional coagulopathies)
*ongoing measurement of Hgb, coags, + platelets guide therapy
Key strategy to avoid coagulopathy during MTP
Administer FFP before abnormal PTT values occur
Resuscitative goals
Avoidance of hypothermia
Early support of coagulation system (1: 1: 1)
Cell salvage: autologous transfusion using suction + washing systems
Administration of antifibrinolytic therapy (tranexamic acid)
Recombinant factor VIIa
External Bimanual uterine compression
- Emergency maneuver to reduce PPH + permit time for resuscitation + control of bleeding
- Aorta compressed with closed fist just above umbilicus to temporarily halt uterine blood flow
- ‘External aortic abdominal pressure’
Complications of resuscitation and transfusion include:
Accidental admin of ABO incompatible blood Dilutional coagulopathies Transfusion reactions Hypothermia Hyperkalemia + hypocalcemia
Principle duties of anesthesia providers (during maternal hemorrhage)
Maintain vital functions
Replace blood loss
Provide the conditions under which hemorrhage can be controlled
Advent of ultrasonography has also allowed providers to
anticipate patients at high risk for hemorrhage, such as those with placental abnormalities, thus guiding planning for care + predicting blood loss
Initial responsibilities of anesthesia provider in unexpected hemorrhage:
Assess VS, BP, O2 sat, HR, capillary refill, peripheral + core temp, + LOC
Obtain abbreviated history
Assess airway, anticipated difficulty with intubation
Achieve proper venous access (2x18g min)
Call for help early, especially in cases of brisk bleeding
Non-initial responsibilities of anesthesia provider in unexpected hemorrhage:
Ensure adequate pain control
Indwelling epidural catheter for analgesia can be used for procedures with minor -moderate hemorrhage
Early transfer to OR should be considered at beginning of hemorrhage management in order to provide appropriate neuraxial or GA
Compare VS to stated EBL
Communicate discrepancies to OB team
Review ongoing fluid resuscitation + pharmacotherapy + assume responsibility for management
Send initial laboratory assays (Hgb/Hct, coags)
Order blood + blood products as needed
In the event of massive uncontrollable hemorrhage, anesthesia provider should be prepared for
emergency hysterectomy
Patient under regional may have to be converted to GA
Anticipated Hemorrhage
- Early consultation w/ anesthesia staff = essential in pts w/ known elevated risk of severe hemorrhage
- Transfer to another facility (if inadequate resources for MTP not available)
- Assemble anesthesia team: do not attempt to do cases of anticipated hemorrhage alone
After team assembled, Anesthetic management: Anticipated Hemorrhage
Ensure/have the following:
- all uterotonic Rx in OR
- immediate availability of vasopressors
- Procure a supply of calcium chloride (Tx: low ionized calcium d/t rapid transfusion)
- Order blood products for immediate availability: 10 units PRBC, 10 units FFP, 10 units of platelets
- Prepare transfusion lines, assemble rapid infusion devices, or pressure bags
- Set up fluid warmer/blanket
- Establish communication lines w/ central lab + blood bank
- Have POC devices for hemoglobin, electrolytes available
- Plan for GA
- Establish min 2 large IVs
- Place CVC w/ 7+ Fr cordis
- Utilize invasive ABP monitoring (beat-to-beat pressure measurement + frequent blood sampling)
