Complications of Pregnancy Flashcards
1
Q
3rd leading cause of maternal death
A
Pre-eclampsia
2
Q
1st and 2nd cause of maternal death
A
Hemorrhage/ Thromboembolism
3
Q
Pre-Eclampsia is a
A
Hypertensive disorders in pregnancy
4
Q
Hypertensive disorders of pregnancy
A
In pregnancy there is decreased sensitivity to vasopressors, Does not happen in pre-eclampsia
5
Q
Gestational HTN
A
Defined: HTN without proteinuria developing after 20
wks gestation with subsequent resolution postpartum
• 25% will develop preeclampsia
6
Q
Preeclampsia
A
HTN and proteinuria after 20 wks gestation
7
Q
Term Eclampsia only when
A
CNS involvements lead to seizures
8
Q
Creatinine should be
A
Lower
9
Q
Inflammatory mediators are
A
Hurtful
10
Q
HELLP stands for
A
Hemolytic Elevated LFT, Low Platelets
11
Q
Typically absent in less than 20 weeks gestation
A
Hemoconcentraton, Thrombocytopenia, Proteinuria
12
Q
Typically rare in less than 20 weeks gestation
A
Serum uric acid 5.5mg/dl
13
Q
Present in ALMOST ALL CASES in >20 weeks of gestation
A
Serum uric acid 5.5mg/dl
14
Q
Typically absent in third trimester
A
Proteinuria, Serum uric acid 5.5, hemoconcentration and thrombocytopenia
15
Q
Both present in SEVERE disease at >20 weeks of gestation
A
Hemoconcentration
Thrombocytopenia
16
Q
Typically present in >20 weeks gestation
A
Proteinuria
17
Q
Mild or severe HTN during those two times
A
<20 weeks gestation or >20 weeks gestation
18
Q
Define Gestational HTN
A
HTN without proteinuria developing after 20 weeks gestation with subsequent resolution postpartum
25% develop preeclampsia
19
Q
Define Pre-eclampsia
A
HTN and Proteinuria that develops AFTER 20 WEEKS of gestation
20
Q
When is the term eclampsia useed?
A
When there is HTN with CNS involvement resulting in seizures
21
Q
Diagnostic Criteria for Preeclampsia : Preeclampsia WITHOUT severe features (BPP 1)
A
BP ≥ 140/90mmHg after 20 weeks gestation Proteinuria ≥ 300mg/24h Protein-Creatinine ratio ≥0.3 1+ on urine dipstick specimen EDEMA
22
Q
Diagnostic Criteria for Preeclampsia : SEVERE Pre-eclampsia (BTSPNI)
A
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)
23
Q
Serum Cr in the pregnant woman should be much _______why?
A
lower because of GFR which is much higher
24
Q
Most cases of preeclampsia is with
A
Nulliparous (first pregnancy)
25
Risk Factors of Preeclampsia: Demographic factors (ABH)
Advanced maternal age > 35 years
Black race
Hispanic ethnicity
26
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)
27
Risk Factors of Preeclampsia: Medical Conditions (CODCAS)
```
Chronic HTN
Obesity
Diabetes Mellitus
Chronic Renal Disease
Antiphospholipid antibody syndrome
Systemic Lupus Erythematus
```
28
Risk Factors of Preeclampsia:Obstetric conditions
Multiple Gestation
| Hydatidiform mole
29
Risk Factors of Preeclampsia: Behavioral factor
Cigarette smoking (risk reduction)
30
Risk Factors of Preeclampsia: Partner related risk factors
Nulliparity
| LIMITED PRE-CONCEPTIONAL EXPOSURE TO PATERNAL SPERM
31
Preeclampsia Pathophysiology : Related to which factorts
NO exact pathogenic mechanism defined but probably related to maternal, paternal, fetal and placental factors
32
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
```
33
Blood flow in normally
Low resistance / High Flow
34
In preeclampsia , blood flow is , which leads to
High resistance / low flow leading to Placental ischemia and hypoxia
35
Familial tendency of PIH is
Recessive genetic inheritance
36
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)
```
37
My note : imbalance betwwen
Thromboxane --> Vasoconstriction
| Prostacyclin --> Vasodilation
38
Platelet factors in preeclampsia
Damaged endothelium --> platelet activation, aggregation and adhesion
39
What do platelets release that causes vasoconstriction?
Thomboxane
| Serotonin
40
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
41
Mild preeclampsia activate RAAS doing what to placental flow?
Improves uteroplacental perfusion
42
What happens in SEVERE PREECLAMPSIA?
Too much endothelial damage leads to serotonin-induced GREATER platelet aggregation via feedback loop
43
Coagulation factors leads to ________risk
Thromboembolic risk
44
Increase thromboembolic risk due to
Endothelial damage --> release of vWF factor VIII
45
PRE-ECLAMPSIA CAUSES AN
Exaggerated risk of thromboembolism
46
What is the role of von Willebrand with platelet
Tell platelet where to go
47
Both a direct and indirect cause of HTN
Endothelin and Calcium
48
Pre-Eclampsia and Hepatic factors
Increase uptake of free fatty acids-->hypertriglyceremia and increased risk for fatty liver.
49
What does the increase in triglycerides cause
Inhibit release of PROSTACYCLIN by damaged endothelium (vasodilator) and contributes to Liver dysfunction
50
CV hallmark of Pre-eclampsia
Increase BP
51
Cardiovascular changes in Pre-Eclampsia include
Increase BP
| Increase sensitivity to cathecholamines and overactive SNS
52
CV changes normalize
shortly after delivery
53
Hemodynamics changes in preeclampsia
| CO, SVR , PCWP/CVP
High CO
Normal to elevated SVR
Slighly low PCWP /CVP
54
Hemodynamics Preload , contractility and SVR
Decrease preload
Increase contractility
SVR normal or increase
55
Normal CVP /PCWP in severe preeclampsia
vasoconstriction
56
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
57
Greater than 1L bolus can lead to
Pulmonary edema
58
Normal pregnancy Colloid oncotic pressure usually-________but there is an ____________ in preeclampsia
Decrease due to decrease albumin: exaggerated decreased.
59
______-COP and _____ lead to Pulmonary Edema
Decreased; Increase Vascular permeability.
60
What helps lung issue from water
Surfactant
61
Hypercoagubility in pregnancy due to
Accelerated (shorter) prothrombin Time
Increase activation of factors II, V, X
Decrease Fibrinogen
62
Hypercoagubility in pregnancy due to
Decreased antithrombin III levels
| normally inhibit factors IX, X, XI, XII
63
Severe pre-eclamptic patients may need this concentrate
Antithrombin
64
Pre-eclampsia renal effects are
Glomerular enlargement --> ischemia --> Glomerulopathy --> proteinuria and 25% decrease in GFR
65
A decrease in UOP of _________requires assessment of Intravascular volume
<400ml/24 h
66
Endocrine and metabolic changes in preeclampsia include
Disruption of balance between vasodilators and vasoconstrictors
67
Vasodilators are
Nitrous
| PGI2
68
Vasoconstrictors are
Endothelin
Angiotensin II
Thromboxane A2
Serotonin
69
Serum Cr. should not be
1.1
70
Edema --> increase
Risk airway narrowing
71
What is an OMINOUS sign with Pre-eclampsia
EPIGASTRIC /SUBCOSTAL PAIN
Indicate hemorrhage /bleeding
SUBCAPSULAR HEMORRHAGE and INTRAPERITONEAL Bleeding
72
There can be epigastric subcostal pain because
Liver capsule can be distended by edema and hemorrhage
73
What is subcapsular hemorrhage and intraperitoneal bleeding confirmed by
US/CT scan
74
Classic findings in preeclampsia include
Severe Headaches
Visual Changes
Hyperreflexia
75
Unknown etiology of seizures may be HTN (HEVEHI)
```
Encephalopathy
Vasospasm
Edema
Hemorrhage
Infaction
```
76
Severe eclampsia asssociated wtih (2) in uterine
Intrauterine Growth retardation
| Oligohydramnios
77
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
78
Central anticonvulsant effect of magnesium by
Decreased cerebra vasoconstriction/ischemia
79
Other effects of Magnesium
decrease vascular response to catecholamines
decrease ACE levels
Increase PGI2 production by endothelium
80
Magnesium effect on NMB
Potentiate the NMB
81
Placental relief of vasoconstriction by
Inhibiting TXA2 synthesis
Calcium channel blockade
Increase UBF
82
Magnesium Sulfate: therapeutic levels: 1.7-2.4
Normal , untreated patient
83
Magnesium Sulfate: therapeutic levels: 5-9
Therapeutic
84
Magnesium Sulfate: therapeutic levels: 12
Loss of DTRs
85
Magnesium Sulfate: therapeutic levels: 15-20
RESPIRATORY ARREST
86
Magnesium Sulfate: therapeutic levels: >25
ASYSTOLE
87
How do you treat Mg toxicity
Stop infusion
IV Calcium
Bircarbonate for acidemia
Intubation/Ventialtion for resp impairment
88
Magnesium antagonizes
Calcium, giving more calcium help
89
No clear benefit of those
AntiHTN
90
What can be used to minimize maternal morbidity associated with
Encephalopathy
CVA
Placental abruption
End organ damage
91
Treatment goals BP
DBP 90-105mmHg
| MAP 105-125 mmHg
92
Most common used antihypertensive
Hydralazine
93
Hydralazine effects
Relaxes arterioles
Decrease SVR, BP and may Increase HR
NO effect on UP/FP BF
94
2nd most common use antihypertensive (LADA)
Labetalol
Alpha:beta 1:7
Decrease SVR with Increase HR
AVoid in asthmatic /liver dysfunction , crosses the placenta
95
Characteristics of Nitroglycerin VDVU
Venous>arterial relaxation
Decrease preload> afterload
Very rapid onset (hypotension)
UBBF preserved but crosses UP/FP
96
Nitroprusside characteristics
```
Powerful Vadodilator arterial>venous
Decrease Afterload
Crosses Placenta (worry about cyanide toxicity)
```
97
Nifedipine characteristics
Arterial dilator with little cardiodepresion
| Can exaggerate HoTN if receiving MgSO4
98
ESMOLOL characteristics
IV bolus for sympathetic block during intubation.
99
4 complications of Pre-eclampsia PPOH
Oliguria
HELLP
Pulmonary Edema
Placenta abruption with preeclampsia
100
Oliguria best diagnosted with
Decrease in UOP w/ serial measurements over time
101
Refractory oliguria is
<30ml for 3 hours responding to IVF bolus
| Can be pre-renal, intra-renal, or post-renal
102
What is the hallmark of HELLP?
Hemolysis
103
HELLP is secondary to
Severe form of Pre-eclampsia
104
HELLP is due to unknown insult but most likely
Intravascular platelet activation
| Microvascular endothelial damage
105
Hallmark for Pre-eclampsia is
Increase BP
106
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
107
Many HELLP patients have
Pre-eclampsia first
108
What does RUQ/neck? shoulder pain indicate?
50% chance of hepatic subscapular hematoma/bleeding
109
AST vs ALT which is more specific to the liver
ALT
110
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)
```
111
All HELLP patients show some evidence of
compensated DIC
112
Treatment of HELLP and preEclampsia
Delivery of fetus
113
HELLP patients have better outcomes with this medication
Dexamethason
114
HELLP postpartum check for
Retained produces of placental or fetus with Ultrasound.
115
Etiology of Pulmonary placenta with severe eclampsia (DIIL)
Decrease colloid oncotic pressure
Increase pulmonary capillary permeability
Increase intravascular hydrostatic pressure
LVF (SVR increase)
116
A respiratory complication of severe pre-eclampsia is
ARDS
117
In Placental Abruption, if fetal death occurs with abruption will have
50% maternal blood loss
118
Severe abruption can be complicated by
DIC
119
Treat severe abruption by (DFPP)
Delivery baby
PRBCs
FFPs
Platelets
120
When to avoid regional
Clinical bleeding + Thrombocytopenia
121
If there is a short interval
Clinical judgement call of risk vs benefit
122
DIC development mostly with (ASA)
Abruption
Amniotic fluid embolism
Sepsis
123
For PT/PTT
Trach platelet count and Fibrin degradation products
124
MAG sulfate and anesthesia: Combined with epidural
AT risk for hypotension due to sympathectomy
| Titrate epidural slowly and treat with EPHEDRINE PRN
125
Action of magnesium on vasoconstrictors
Mg blunts contractile response to vasoconstrictions
| Also inhibits catecholamines release after SNS stimulation (like intubation)
126
Magnesium action on calcium release
Magnesium inhibits Ca2+ facilitate presynaptic transmitter release (no depolarization for you )
127
MG act like a NMB at
>12mg/dl
128
Hypermagnesemia enhances sensitivity to __________ what is not affected_____
All NDNMBs ; Succinylcholine
129
What happens at mag level > 12mg/dl
Loss of DTRs
130
Consider use of CVP and PCWP
Severe preeclampsia with persistent oliguria and renal failure
A-LINE
131
Absolute contraindications to anesthesia is
Patient's refusal (can be charged with battery)
132
AT this level in thoracic spine, may vomit and have hypotension
T6
133
Epidural vs General Endotracheal anesthesia advantage
Epidural @ T4 blunts hemodynmaic and neuroendocrine responses better than GETA
134
With coagulopathy and decreased platelet which anesthesia is better?
Spinal preferred over epidural
135
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 )
136
How do you know HOw high Epidural has reached
T4 hypotension
C3 stop breathing
ASK if they feel anything
137
Long epidural needle for women with
BMI> 50
138
C-section with GETA INDICATIONS
Coagulopathy
Placental abruption
Severe fetal distress
139
Causes the highest mortality in preeclamptic women
Intracranial hemorrhage (intubation leads to increase ICP and risk of hemorrhagic veins)
140
Postpartum management": Severe preeclampsia;
| Magnesium infusion
Continue Mag 24 hours after delivery or until diuresis begins
141
Why monitoring bed for 24 hours unless complications arise?
Possible pulmonary edema and HELLP
142
Persistent eclampsia
HTN oliguria, higher risk of M&M
143
What is eclampsia
Convulsion and or coma occuring during pregnancy in a woman who ALSO MEETS diagnostic criteria for preeclampsia (Proteinuria, HTN, edema)
144
Until proven otherwise
Seizures during pregnancy = Eclampsia
145
What terminates the seizure during eclamptic seizures?
Pt stop breathing
| Increased CO2 levels in the brain terminate seizures
146
Pt can go from Normal to Full eclamsia skipping
Pre-eclampsia
147
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
```
148
Maternal complications of Eclampsia
| DAHN-PPCA
```
Abruption
HELLP
DIC
Neurological deficit
Pulmonary aspiration
Pulmonary Edema
CP arrest
Acute renal failure
```
149
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.
150
Things complicating seizures include
Aspiration of stomach contents
| CR arrest
151
Goals of anesthetic management during seizures: Primary
| SPE
Stop the convulsions
Establish clear airway
Prevent major complications
152
Other Goals of anesthetic management during seizures: Primary ADIG
Antihypertensive
Induce/augment labor
Delivery should be expedited (UBF goes down, fetal bradycardia)
Give magsulfate
153
Increase ICP not a concern if a patient is
Conscious
| Alert and seizure free
154
Indicate possible major intracranial pathology
Persistent coma
| neurologic deficits
155
BP control for anesthesia
Do not let get DBP get to >110
156
Epidural ok if
Alert, awake and seizure controlled
157
Neurosurgical anesthetic with opioids , relaxants, ___________ and mild _____
VA, hyperventilation (CO2 decrease-> ICP decrease)
158
Major contraindications to Spinal
Increased ICP --> Herniation
159
Meds use in spinal that can lead to seizures
Lidocaine
| Bupivacaine
160
Decreases DVT incidence
Early ambulation
161
3 possible origins of DVT
Superficial vein
Pelvic vein
Ovarian vein
162
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
163
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.
164
If DVT untreated
24% risk of PE --> 15% whe PE occurs
165
if DVT treated
4.5%risk of pE
166
2/3 of pregnancy related PEs occur
Postpartum monitor >4 hours PP
167
4 risk of thromboembolism MECS
Smoking
Malignancy
Contraceptive
Endothelial injury
168
Why is there venous stasis?
Gravid uterus makes blood harder to go black
169
Pulmonary Embolism HTN
from embolus --> RV overload --> RV failure-> Rsided CHF
170
S/S of PE PAD-C
Dyspnea (JVD)
Palpitations
Angina
Cough with hemoptysis
171
ECG S/S of PE
RV strain
ST-T wave changes
SVT
172
CXR evidence of PE
25-40% of PE have normal CXR
173
Better works
V/Q scan, pulmonary angiography, spiral CT
174
For PE spiral CT scan shows
Pulmonary dead space
175
Anesthesia Focus with PE (VASA)
```
Adequate maternal/fetal oxygenation
Support maternal circulation
Anticoagulation
Venous interruption
Surgical embolectomy for rapidly deteriorating patients.
```
176
Clinical presentation depends on
```
Size and number
Rate of clot
Preexisting
Recurrence
Resp failure from extensive or pulmonary edema
```
177
Treatment of DVT goal
Prevent PE
178
IV heparin should be d'c'd
when active labor begins
179
Warfarin post pastrum
Continue for 3 months ( if no AC can be used, greenfield filter)
180
Does warfarin cross breastmilk
NO
181
Avoid
Esophageal temp probe
| Gastric tube
182
Diagnosis of exclusion after autopsy usually
Amniotic Fluid Embolism
183
Amniotic fluid embolism
Amniotic entering fluid vein
184
Etiology unclear but studies suggesting metabolites of
Arachidonic acid (leukotrienes) and meconium responsible
185
Early phase of AFE about____Mins
30 min
186
AFE Early phase symptoms
| PPRDVHH
```
Pulmonary Vasopasm
Pulmonary HTN
RVF
Decrease CO
V/Q mismatch
Hypoxemia
Hypotension
```
187
V/Q mismatch is a
Deadspace problems
188
Ventilation is a
Shunt problem
189
AFE 2nd phase symptoms (LPD)
LVF
Pulmonary Edema
DIC
190
Presentation of AFE
3rd trimester after abdominal trauma and postpartu
191
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)
192
When does amniotic Fluid embolism occur?
After maternal exposure to fetal issue
193
Amniotic fluid embolism is
anaphylactoid syndrome of pregnancy --> HELPFUL MEDICATION Is EPI
194
AFE presentation similar to
Shock and anaphylaxis
195
FHR during AFE
severe decelerations but FHR variability is present
196
Management of AFE: airway
100% oxygen
| Intubate the trachea and support ventilation as needed
197
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
198
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
199
Management of AFE: Hemostatic support (MES)
Massive transfusion protocol
Ensure normothemia
Send blood owrk
200
Venous Air Embolism most common with
General Anesthesia
| Less with regional because they are spontaneously breathing
201
Venous Air embolism pathophysiology
pressure gradient as small as -5cm2 between surgical field and heart allows venous air entrapment
202
2 things associated with the development of Venous Air Embolis
Steep Trendeleburg position
| Uterine Exterioriation during C-section
203
Fatal volume
>3mg/kg are fatal RV air lock
204
Small air volumes leads to (VAHH)
V/Q mismatch
Hypoxemia
Arrythmia
Hypotension
205
Venous Air embolism with patent FO
paradoxical air embolism
| CV/neuro complications
206
Venous Air embolism presentation
50% angina
25% Decrease SaO2
>20% drop in BP (2%)
207
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
```
