Complications of Pregnancy Flashcards
3rd leading cause of maternal death
Pre-eclampsia
1st and 2nd cause of maternal death
Hemorrhage/ Thromboembolism
Pre-Eclampsia is a
Hypertensive disorders in pregnancy
Hypertensive disorders of pregnancy
In pregnancy there is decreased sensitivity to vasopressors, Does not happen in pre-eclampsia
Gestational HTN
Defined: HTN without proteinuria developing after 20
wks gestation with subsequent resolution postpartum
• 25% will develop preeclampsia
Preeclampsia
HTN and proteinuria after 20 wks gestation
Term Eclampsia only when
CNS involvements lead to seizures
Creatinine should be
Lower
Inflammatory mediators are
Hurtful
HELLP stands for
Hemolytic Elevated LFT, Low Platelets
Typically absent in less than 20 weeks gestation
Hemoconcentraton, Thrombocytopenia, Proteinuria
Typically rare in less than 20 weeks gestation
Serum uric acid 5.5mg/dl
Present in ALMOST ALL CASES in >20 weeks of gestation
Serum uric acid 5.5mg/dl
Typically absent in third trimester
Proteinuria, Serum uric acid 5.5, hemoconcentration and thrombocytopenia
Both present in SEVERE disease at >20 weeks of gestation
Hemoconcentration
Thrombocytopenia
Typically present in >20 weeks gestation
Proteinuria
Mild or severe HTN during those two times
<20 weeks gestation or >20 weeks gestation
Define Gestational HTN
HTN without proteinuria developing after 20 weeks gestation with subsequent resolution postpartum
25% develop preeclampsia
Define Pre-eclampsia
HTN and Proteinuria that develops AFTER 20 WEEKS of gestation
When is the term eclampsia useed?
When there is HTN with CNS involvement resulting in seizures
Diagnostic Criteria for Preeclampsia : Preeclampsia WITHOUT severe features (BPP 1)
BP ≥ 140/90mmHg after 20 weeks gestation Proteinuria ≥ 300mg/24h Protein-Creatinine ratio ≥0.3 1+ on urine dipstick specimen EDEMA
Diagnostic Criteria for Preeclampsia : SEVERE Pre-eclampsia (BTSPNI)
BP ≥ 160/110 mmHg Thrombocytopenia (plt count < 100,000) Serum Cr > 1.1mg/dl OR 2 times the baseline Cr. Pulmonary Edema New onset CEREBRAL+ Visual disturbances Impaired liver function (HELLP)
Serum Cr in the pregnant woman should be much _______why?
lower because of GFR which is much higher
Most cases of preeclampsia is with
Nulliparous (first pregnancy)
Risk Factors of Preeclampsia: Demographic factors (ABH)
Advanced maternal age > 35 years
Black race
Hispanic ethnicity
Risk Factors of Preeclampsia: Genetic Factors (HFHP)
History of Preeclampsia in previous pregnancy
Family Hx of Preeclampsia
History of Placental Abruption, Fetal growth restriction, or fetal death (PFD)
Partner who fathered a preeclamptic pregnancy pregnancy in another woman (through fetal genes)
Risk Factors of Preeclampsia: Medical Conditions (CODCAS)
Chronic HTN Obesity Diabetes Mellitus Chronic Renal Disease Antiphospholipid antibody syndrome Systemic Lupus Erythematus
Risk Factors of Preeclampsia:Obstetric conditions
Multiple Gestation
Hydatidiform mole
Risk Factors of Preeclampsia: Behavioral factor
Cigarette smoking (risk reduction)
Risk Factors of Preeclampsia: Partner related risk factors
Nulliparity
LIMITED PRE-CONCEPTIONAL EXPOSURE TO PATERNAL SPERM
Preeclampsia Pathophysiology : Related to which factorts
NO exact pathogenic mechanism defined but probably related to maternal, paternal, fetal and placental factors
Preeclampsia Pathophysiology
DDEEHHPPS
Defective spiral artery/remodeling Placental Hypoperfusion Systemic Vasoconstriction ENDOTHELIAL DYSFUNCTION Disease PLACENTA releases PRO-INFLAMMATORY PROTEINS into MATERNAL CIRCULATION Hypertension END ORGAN DAMAGE Proteinuria HELLP
Blood flow in normally
Low resistance / High Flow
In preeclampsia , blood flow is , which leads to
High resistance / low flow leading to Placental ischemia and hypoxia
Familial tendency of PIH is
Recessive genetic inheritance
Endothelial Factors (VADA)
Vascular endothelial damage/dysfunction (in placenta and renal vessels) Arterial vasospasm ( liver, heart , brain) Decreased NO and prostaglandins (vasodilators), Increase ENDOTHELIN (vasoconstriction) Abnormal stimulation of RASS (increase snsitivy to angiotensin 2 and NE)
My note : imbalance betwwen
Thromboxane –> Vasoconstriction
Prostacyclin –> Vasodilation
Platelet factors in preeclampsia
Damaged endothelium –> platelet activation, aggregation and adhesion
What do platelets release that causes vasoconstriction?
Thomboxane
Serotonin
What is the role of serotonin in MILD preeclampsia?
It will increase Prostaglandin and NO , but ACTIVATES RAAS via positive feedback loop –> Increase uteroplacental perfusion
Mild preeclampsia activate RAAS doing what to placental flow?
Improves uteroplacental perfusion
What happens in SEVERE PREECLAMPSIA?
Too much endothelial damage leads to serotonin-induced GREATER platelet aggregation via feedback loop
Coagulation factors leads to ________risk
Thromboembolic risk
Increase thromboembolic risk due to
Endothelial damage –> release of vWF factor VIII
PRE-ECLAMPSIA CAUSES AN
Exaggerated risk of thromboembolism
What is the role of von Willebrand with platelet
Tell platelet where to go
Both a direct and indirect cause of HTN
Endothelin and Calcium
Pre-Eclampsia and Hepatic factors
Increase uptake of free fatty acids–>hypertriglyceremia and increased risk for fatty liver.
What does the increase in triglycerides cause
Inhibit release of PROSTACYCLIN by damaged endothelium (vasodilator) and contributes to Liver dysfunction
CV hallmark of Pre-eclampsia
Increase BP
Cardiovascular changes in Pre-Eclampsia include
Increase BP
Increase sensitivity to cathecholamines and overactive SNS
CV changes normalize
shortly after delivery
Hemodynamics changes in preeclampsia
CO, SVR , PCWP/CVP
High CO
Normal to elevated SVR
Slighly low PCWP /CVP
Hemodynamics Preload , contractility and SVR
Decrease preload
Increase contractility
SVR normal or increase
Normal CVP /PCWP in severe preeclampsia
vasoconstriction
For example, In normal patient, if you give fluid with CVP of 8 itll go up to 14, with pre-eclampsia it will go up to
20
Greater than 1L bolus can lead to
Pulmonary edema
Normal pregnancy Colloid oncotic pressure usually-________but there is an ____________ in preeclampsia
Decrease due to decrease albumin: exaggerated decreased.
______-COP and _____ lead to Pulmonary Edema
Decreased; Increase Vascular permeability.
What helps lung issue from water
Surfactant
Hypercoagubility in pregnancy due to
Accelerated (shorter) prothrombin Time
Increase activation of factors II, V, X
Decrease Fibrinogen
Hypercoagubility in pregnancy due to
Decreased antithrombin III levels
normally inhibit factors IX, X, XI, XII
Severe pre-eclamptic patients may need this concentrate
Antithrombin
Pre-eclampsia renal effects are
Glomerular enlargement –> ischemia –> Glomerulopathy –> proteinuria and 25% decrease in GFR
A decrease in UOP of _________requires assessment of Intravascular volume
<400ml/24 h
Endocrine and metabolic changes in preeclampsia include
Disruption of balance between vasodilators and vasoconstrictors
Vasodilators are
Nitrous
PGI2
Vasoconstrictors are
Endothelin
Angiotensin II
Thromboxane A2
Serotonin
Serum Cr. should not be
1.1
Edema –> increase
Risk airway narrowing
What is an OMINOUS sign with Pre-eclampsia
EPIGASTRIC /SUBCOSTAL PAIN
Indicate hemorrhage /bleeding
SUBCAPSULAR HEMORRHAGE and INTRAPERITONEAL Bleeding
There can be epigastric subcostal pain because
Liver capsule can be distended by edema and hemorrhage
What is subcapsular hemorrhage and intraperitoneal bleeding confirmed by
US/CT scan
Classic findings in preeclampsia include
Severe Headaches
Visual Changes
Hyperreflexia
Unknown etiology of seizures may be HTN (HEVEHI)
Encephalopathy Vasospasm Edema Hemorrhage Infaction
Severe eclampsia asssociated wtih (2) in uterine
Intrauterine Growth retardation
Oligohydramnios
What is the effect of Magnesium at the NMJ
Decrease uptake , binding and distribution of Ca2+ in vascular smooth muscle which prevents the interraction of myosin with actin
Central anticonvulsant effect of magnesium by
Decreased cerebra vasoconstriction/ischemia
Other effects of Magnesium
decrease vascular response to catecholamines
decrease ACE levels
Increase PGI2 production by endothelium
Magnesium effect on NMB
Potentiate the NMB
Placental relief of vasoconstriction by
Inhibiting TXA2 synthesis
Calcium channel blockade
Increase UBF
Magnesium Sulfate: therapeutic levels: 1.7-2.4
Normal , untreated patient
Magnesium Sulfate: therapeutic levels: 5-9
Therapeutic
Magnesium Sulfate: therapeutic levels: 12
Loss of DTRs
Magnesium Sulfate: therapeutic levels: 15-20
RESPIRATORY ARREST
Magnesium Sulfate: therapeutic levels: >25
ASYSTOLE
How do you treat Mg toxicity
Stop infusion
IV Calcium
Bircarbonate for acidemia
Intubation/Ventialtion for resp impairment
Magnesium antagonizes
Calcium, giving more calcium help
No clear benefit of those
AntiHTN
What can be used to minimize maternal morbidity associated with
Encephalopathy
CVA
Placental abruption
End organ damage
Treatment goals BP
DBP 90-105mmHg
MAP 105-125 mmHg
Most common used antihypertensive
Hydralazine
Hydralazine effects
Relaxes arterioles
Decrease SVR, BP and may Increase HR
NO effect on UP/FP BF
2nd most common use antihypertensive (LADA)
Labetalol
Alpha:beta 1:7
Decrease SVR with Increase HR
AVoid in asthmatic /liver dysfunction , crosses the placenta
Characteristics of Nitroglycerin VDVU
Venous>arterial relaxation
Decrease preload> afterload
Very rapid onset (hypotension)
UBBF preserved but crosses UP/FP
Nitroprusside characteristics
Powerful Vadodilator arterial>venous Decrease Afterload Crosses Placenta (worry about cyanide toxicity)
Nifedipine characteristics
Arterial dilator with little cardiodepresion
Can exaggerate HoTN if receiving MgSO4
ESMOLOL characteristics
IV bolus for sympathetic block during intubation.
4 complications of Pre-eclampsia PPOH
Oliguria
HELLP
Pulmonary Edema
Placenta abruption with preeclampsia
Oliguria best diagnosted with
Decrease in UOP w/ serial measurements over time
Refractory oliguria is
<30ml for 3 hours responding to IVF bolus
Can be pre-renal, intra-renal, or post-renal
What is the hallmark of HELLP?
Hemolysis
HELLP is secondary to
Severe form of Pre-eclampsia
HELLP is due to unknown insult but most likely
Intravascular platelet activation
Microvascular endothelial damage
Hallmark for Pre-eclampsia is
Increase BP
Hemolysis indicators are (ALIT)
Abnormal peripheral blood smear + Increase bilirubin level >1.2mg/dl
Increase liver enzymes AST (SGOT) >70
LDH >600
Thrombocytopenia < 100,000
Many HELLP patients have
Pre-eclampsia first
What does RUQ/neck? shoulder pain indicate?
50% chance of hepatic subscapular hematoma/bleeding
AST vs ALT which is more specific to the liver
ALT
Maternal complications with HELLP include: (CCDPA)
Which one occurs more with HELLP than preeclampsia
CVA CV DIC Placental abruption ARF (occurs more frequently with HELLP than preeclampsia)
All HELLP patients show some evidence of
compensated DIC
Treatment of HELLP and preEclampsia
Delivery of fetus
HELLP patients have better outcomes with this medication
Dexamethason
HELLP postpartum check for
Retained produces of placental or fetus with Ultrasound.
Etiology of Pulmonary placenta with severe eclampsia (DIIL)
Decrease colloid oncotic pressure
Increase pulmonary capillary permeability
Increase intravascular hydrostatic pressure
LVF (SVR increase)
A respiratory complication of severe pre-eclampsia is
ARDS
In Placental Abruption, if fetal death occurs with abruption will have
50% maternal blood loss
Severe abruption can be complicated by
DIC
Treat severe abruption by (DFPP)
Delivery baby
PRBCs
FFPs
Platelets
When to avoid regional
Clinical bleeding + Thrombocytopenia
If there is a short interval
Clinical judgement call of risk vs benefit
DIC development mostly with (ASA)
Abruption
Amniotic fluid embolism
Sepsis
For PT/PTT
Trach platelet count and Fibrin degradation products
MAG sulfate and anesthesia: Combined with epidural
AT risk for hypotension due to sympathectomy
Titrate epidural slowly and treat with EPHEDRINE PRN
Action of magnesium on vasoconstrictors
Mg blunts contractile response to vasoconstrictions
Also inhibits catecholamines release after SNS stimulation (like intubation)
Magnesium action on calcium release
Magnesium inhibits Ca2+ facilitate presynaptic transmitter release (no depolarization for you )
MG act like a NMB at
> 12mg/dl
Hypermagnesemia enhances sensitivity to __________ what is not affected_____
All NDNMBs ; Succinylcholine
What happens at mag level > 12mg/dl
Loss of DTRs
Consider use of CVP and PCWP
Severe preeclampsia with persistent oliguria and renal failure
A-LINE
Absolute contraindications to anesthesia is
Patient’s refusal (can be charged with battery)
AT this level in thoracic spine, may vomit and have hypotension
T6
Epidural vs General Endotracheal anesthesia advantage
Epidural @ T4 blunts hemodynmaic and neuroendocrine responses better than GETA
With coagulopathy and decreased platelet which anesthesia is better?
Spinal preferred over epidural
Spinal considerations advantage and risk
reliable dense block with rapid onset but can lead to profound HoTN and fetal compromise (treat with Ephedrine 50mg IM )
How do you know HOw high Epidural has reached
T4 hypotension
C3 stop breathing
ASK if they feel anything
Long epidural needle for women with
BMI> 50
C-section with GETA INDICATIONS
Coagulopathy
Placental abruption
Severe fetal distress
Causes the highest mortality in preeclamptic women
Intracranial hemorrhage (intubation leads to increase ICP and risk of hemorrhagic veins)
Postpartum management”: Severe preeclampsia;
Magnesium infusion
Continue Mag 24 hours after delivery or until diuresis begins
Why monitoring bed for 24 hours unless complications arise?
Possible pulmonary edema and HELLP
Persistent eclampsia
HTN oliguria, higher risk of M&M
What is eclampsia
Convulsion and or coma occuring during pregnancy in a woman who ALSO MEETS diagnostic criteria for preeclampsia (Proteinuria, HTN, edema)
Until proven otherwise
Seizures during pregnancy = Eclampsia
What terminates the seizure during eclamptic seizures?
Pt stop breathing
Increased CO2 levels in the brain terminate seizures
Pt can go from Normal to Full eclamsia skipping
Pre-eclampsia
Risk factors of Eclampsia (FMMN-PPRST)
First pregnancy Multiple Gestation Molar Pregnancy Triploidy Preexisting HTN Renal diseas Non-immune hydrops fetalis SLE Previous hx of preeclampsia/eclampsia
Maternal complications of Eclampsia
DAHN-PPCA
Abruption HELLP DIC Neurological deficit Pulmonary aspiration Pulmonary Edema CP arrest Acute renal failure
Describe seizures with Eclampsia
Begins with facial twitching f/b 20 second tonic phase with a generalized clonic seizure and apnea lasting an additional 60 sec–> Postictal stage with variable coma follows.
Things complicating seizures include
Aspiration of stomach contents
CR arrest
Goals of anesthetic management during seizures: Primary
SPE
Stop the convulsions
Establish clear airway
Prevent major complications
Other Goals of anesthetic management during seizures: Primary ADIG
Antihypertensive
Induce/augment labor
Delivery should be expedited (UBF goes down, fetal bradycardia)
Give magsulfate
Increase ICP not a concern if a patient is
Conscious
Alert and seizure free
Indicate possible major intracranial pathology
Persistent coma
neurologic deficits
BP control for anesthesia
Do not let get DBP get to >110
Epidural ok if
Alert, awake and seizure controlled
Neurosurgical anesthetic with opioids , relaxants, ___________ and mild _____
VA, hyperventilation (CO2 decrease-> ICP decrease)
Major contraindications to Spinal
Increased ICP –> Herniation
Meds use in spinal that can lead to seizures
Lidocaine
Bupivacaine
Decreases DVT incidence
Early ambulation
3 possible origins of DVT
Superficial vein
Pelvic vein
Ovarian vein
DVT pathophysiology
A blood clot or thrombus that forms in a deep vein of the leg or pelvis either partially or totally blocking the flow of blood
PE pathophysiology
1 . A DVT or parts of it breaks off from the vein
2. the break away clot travels through the bloodstream
to the heart and migrates toward the lung
3. The clot blocks a vessel to the lung interrupting blood supply.
If DVT untreated
24% risk of PE –> 15% whe PE occurs
if DVT treated
4.5%risk of pE
2/3 of pregnancy related PEs occur
Postpartum monitor >4 hours PP
4 risk of thromboembolism MECS
Smoking
Malignancy
Contraceptive
Endothelial injury
Why is there venous stasis?
Gravid uterus makes blood harder to go black
Pulmonary Embolism HTN
from embolus –> RV overload –> RV failure-> Rsided CHF
S/S of PE PAD-C
Dyspnea (JVD)
Palpitations
Angina
Cough with hemoptysis
ECG S/S of PE
RV strain
ST-T wave changes
SVT
CXR evidence of PE
25-40% of PE have normal CXR
Better works
V/Q scan, pulmonary angiography, spiral CT
For PE spiral CT scan shows
Pulmonary dead space
Anesthesia Focus with PE (VASA)
Adequate maternal/fetal oxygenation Support maternal circulation Anticoagulation Venous interruption Surgical embolectomy for rapidly deteriorating patients.
Clinical presentation depends on
Size and number Rate of clot Preexisting Recurrence Resp failure from extensive or pulmonary edema
Treatment of DVT goal
Prevent PE
IV heparin should be d’c’d
when active labor begins
Warfarin post pastrum
Continue for 3 months ( if no AC can be used, greenfield filter)
Does warfarin cross breastmilk
NO
Avoid
Esophageal temp probe
Gastric tube
Diagnosis of exclusion after autopsy usually
Amniotic Fluid Embolism
Amniotic fluid embolism
Amniotic entering fluid vein
Etiology unclear but studies suggesting metabolites of
Arachidonic acid (leukotrienes) and meconium responsible
Early phase of AFE about____Mins
30 min
AFE Early phase symptoms
PPRDVHH
Pulmonary Vasopasm Pulmonary HTN RVF Decrease CO V/Q mismatch Hypoxemia Hypotension
V/Q mismatch is a
Deadspace problems
Ventilation is a
Shunt problem
AFE 2nd phase symptoms (LPD)
LVF
Pulmonary Edema
DIC
Presentation of AFE
3rd trimester after abdominal trauma and postpartu
Differential diagnosis of AFE (ONA)
OB complications (abruption, eclampsia)
NonOB complication (PE, VAE, sepsis, MI, anaphylaxis)
Anesthesia (High neuraxial block, LA systemic Tox, med
error)
When does amniotic Fluid embolism occur?
After maternal exposure to fetal issue
Amniotic fluid embolism is
anaphylactoid syndrome of pregnancy –> HELPFUL MEDICATION Is EPI
AFE presentation similar to
Shock and anaphylaxis
FHR during AFE
severe decelerations but FHR variability is present
Management of AFE: airway
100% oxygen
Intubate the trachea and support ventilation as needed
Management of AFE: CV support (SEAL)
Start CPR if needed
Ensure LEFT UTERINE DISPLACEMENT to RELIEVE AORTOCAVAL COMPRESSION if appropriate
AMINISTER FLUIDS and VASOPRESSORS
Large bore IV access, invasive pressure monitoring
Management of AFE: FETUS (ME)
Monitor fetal well being
Expedite delivery for nonreassuring status in VIABLE EVENT or in the event of maternal CPR in the 2nd half of pregnancy
Management of AFE: Hemostatic support (MES)
Massive transfusion protocol
Ensure normothemia
Send blood owrk
Venous Air Embolism most common with
General Anesthesia
Less with regional because they are spontaneously breathing
Venous Air embolism pathophysiology
pressure gradient as small as -5cm2 between surgical field and heart allows venous air entrapment
2 things associated with the development of Venous Air Embolis
Steep Trendeleburg position
Uterine Exterioriation during C-section
Fatal volume
> 3mg/kg are fatal RV air lock
Small air volumes leads to (VAHH)
V/Q mismatch
Hypoxemia
Arrythmia
Hypotension
Venous Air embolism with patent FO
paradoxical air embolism
CV/neuro complications
Venous Air embolism presentation
50% angina
25% Decrease SaO2
>20% drop in BP (2%)
Resuscitation of patient with massive venous air embolism
PDS -CEIP
Prevent air entrapment (change position, flood surgical field) Discontinue Nitrous give 100% oxygen Support ventilation and circulation Central venous catheter to aspirate air Expedite delivery Imaging to rule out intercerebral air. Paradoxical cerebral artery gas may benefit from Hyperbaric oxygen therapy