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P&P 3 > Ex1 OB 3 > Flashcards

Ex1 OB 3 Flashcards

1
Q

PIH

A

Encompasses a range of disorders collectively

Formerly known as “toxemia of pregnancy”, which includes:

  • isolated systemic hypertension (nonproteinuric hypertension)
  • preeclampsia (proteinuric hypertension)
  • eclampsia
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2
Q

HTN during pregnancy

A

Common, ~ 10% of pregnancies

Associated with a higher incidence of maternal, fetal, and neonatal mortality and morbidity

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3
Q

PIH Etiologies

A
  • 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
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4
Q

Hypertensive States

A
  • Gestational hypertension
  • Preeclampsia, eclampsia
  • Chronic essential hypertension
  • Chronic hypertension (secondary to renal disease, endocrine disease, coarctation of the aorta)
  • Chronic hypertension with superimposed preeclampsia
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5
Q

Gestational HTN

A

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

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6
Q

Preeclampsia

A

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

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7
Q

Preeclampsia is primarily a disease of

A

Primigravidas

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8
Q

Preeclampsia is associated with

A

High rates of neonatal mortality

-d/t decreased placental blood flow, decreased oxygen delivery to fetus, etc.

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9
Q

Preeclampsia maternal mortality

A 
Cerebral hemorrhage (30 – 40%)
Pulmonary edema (30 – 38%)
Renal failure (10%)
Cerebral edema (9%)
DIC (9%)
Airway obstruction (6%)
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10
Q

Preeclampsia risk factors

A 
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
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11
Q

Preeclampsia diagnosis

A

development of HTN + proteinuria after 20 weeks of gestation

-2 categories

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12
Q

“classic” preeclampsia

A

Classic triad:

HTN, generalized edema, proteinuria

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13
Q

Mild Preeclampsia

A

HTN with SBP > 140 mmHg or DBP > 90 mmHg in patient who had normal BP prior to pregnancy

Proteinuria > 300 mg over 24 hours

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14
Q

Severe Preeclampsia

A

-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
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15
Q

Preeclampsia with severe features

A 
Visual or other cerebral disturbances
Epigastric pain
Retinal hemorrhages, exudates, or papilledema
Pulmonary edema
*difficult IV access d/t pitting edema
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16
Q

Pathophysiology of preeclampsia

A

“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:

  1. failure of placental vascular remodeling results in reduced placental perfusion
  2. ischemic placenta may then produce circulating anti-angiogenic factors that promote generalized maternal vascular endothelium dysfunction, leading to systemic manifestations of preeclampsia
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17
Q

Normal Placentation

A

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.

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18
Q

Normal placentation involves the invasion of spiral arterial walls with

A

endovascular trophoblastic cells

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19
Q

In preeclampsia, what does not occur (pathogenesis)?

A

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

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20
Q

Preeclampsia is associated with what abnormalities

A

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

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21
Q

Preeclampsia: coagulation findings

A

thrombocytopenia, increased fibrin split products, + prolonged PT may occur
DIC rare but possible

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22
Q

Preeclampsia creates an imbalance in ________ ratio due to _______

A

imbalance in thromboxane to prostacyclin ratio

due to decreased prostacyclin production

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23
Q

Clinical effects of prostacyclin

A

decreased vasoconstriction, platelet aggregation, uterine activity
Increased uteroplacental blood flow

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24
Q

Clinical effects of thromboxane

A

Increased vasoconstriction, platelet aggregation, uterine activity
Decreased uteroplacental blood flow

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25
Q

One of the most serious forms of preeclampsia

A

HELLP Syndrom

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26
Q

HELLP Syndrome

A

Hemolysis, Elevated Liver Enzymes, and Low Platelets

*only in this if mom has all - otherwise pre-eclampsia with severe features

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27
Q

HELLP Syndrome: Labs

A

-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
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28
Q

HELLP syndrome: clinical indications

A

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

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29
Q

HELLP syndrome: most important factor relating to anesthesia

A

Platelet count dropping precipitiously –> catch mom in time (normal platelets:: 90 to 70) to place epidural, but cannot remove until plt count resolves

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30
Q

Medical Management:Mild Preeclampsia

A

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

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31
Q

Medical management: Severe Preeclampsia

A

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

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32
Q

Preeclampsia: Indications for Delivery

A
  • 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
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33
Q

Delivery – preeclampsia

A
  • 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
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34
Q

Why is vaginal delivery preferred over C/S in preeclampsia?

A

thrombocytopenia + coagulopathy from preeclampsia increases risk of bleeding

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35
Q

Eclampsia

A

Preeclampsia + generalized seizures
Most seizures occur before delivery
-PP seizures occur most often w/in 48h after delivery

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36
Q

Pathophysiology of eclampsia

A

seizures attributed to platelet thrombi, hypoxia due to local vasoconstriction, and foci of hemorrhage in the cortex

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37
Q

Relationship between eclampsia + HTN

A

poor correlation with severity of HTN

25 – 40% of patients will have normal BP at time of their first eclamptic seizure

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38
Q

hallmarks of hypertensive encephalopathy

A

retinal hemorrhages, exudates, and papilledema

*very infrequent in eclampsia

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39
Q

Severe Preeclampsia: HTN Tx

A

*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

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40
Q

Severe Preeclampsia: Fluid management

A
  • Significant hypovolemia d/t shift of fluid/proteins to extravascular compartment
  • inverse relationship between intravascular volume + severity of HTN has been demonstrated
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41
Q

Severe preeclampsia: pts with very elevated DBP expected to have

A

negative CVP readings

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42
Q

Severe Preeclampsia: Coagulation Abnormalities

A
  • assess coag status

- administration of platelets, FFP, pRBCs may be necessary

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43
Q

Agent of choice for seizure prevention + control in preeclampsia/eclampsia

A

Magnesium Sulfate

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44
Q

Magnesium sulfate - outcomes

A
  • can reduce seizures by 50% w/o any serious maternal morbidity
  • beneficial effect may be vasodilation + increase in CO (by a reduction of SVR)
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45
Q

Magnesium Sulfate: MOA

A
  • 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
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46
Q

Magnesium Sulfate Dosing

A
  • 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
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47
Q

Magnesium Therapeutic Index

A
  • Narrow therapeutic index
  • therapeutic range: serum levels 4 to 8 mEq/L
  • normal serum magnesium level is 1.5 – 2.0 mEq/L
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48
Q

Magnesium Toxicity: Plasma Mag Level 5-10

A

Effects: EKG changes

  • PR prolonged
  • widened QRS
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49
Q

Magnesium Toxicity: Plasma Mag Level 10

A

Loss of DTRs

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50
Q

Magnesium Toxicity: Plasma Mag Level < 15

A

SA + AV Block

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51
Q

Magnesium Toxicity: Plasma Mag Level > 15

A

Respiratory paralysis

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52
Q

Magnesium Toxicity: Plasma Mag Level 25

A

Cardiac arrest

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53
Q

Tx: Magnesium Toxicity

A

10 mL of 10% calcium gluconate slow IV push to counteract effects

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54
Q

Why calcium gluconate and not chloride for mag toxicity tx?

A

Chloride is 3x as potent, but extremely irritating to vessels when given IV push

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55
Q

Magnesium: pros

A 
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)
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56
Q

Magnesium: cons

A

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

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57
Q

Anesthetic options for Severe preeclampsia: Technique of choice

A
  • 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
58
Q

Anesthetic options for Severe preeclampsia: Spinal

A

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
59
Q

Anesthetic options: Neuraxial C/I

A

Coagulopathy or C/I’s

= GETA

60
Q

Risks – GETA for C/S d/t preeclampsia

A
  • Periglottic edema (difficult airway)

- HD response to intubation: HTN

61
Q

In patients receiving mag sulfate who undergo GETA, what may occur?

A

activity of Sux + NDMR enhanced

62
Q

GETA for C/S in pt with preeclampsia: induction risk + Tx

A

Risk of HTN –> stroke + pulmEdema
Prophylaxis: Labetolol 10mg IV
Tx: SNP or NTG

63
Q

Most common medical complication of pregnancy

A

Diabetes Mellitus

64
Q

any degree of glucose intolerance with first recognition during pregnancy

A

Gestation Diabetes (GDM)

65
Q

Midline defect

A

occurs on the anterior (front) portion of body, usually in middle or center of body.
Like cleft palate or imperforate anus

66
Q

Hyperglycemia around _____ results in 6x increase in ______

A

Hyperglycemia around conception or early organogenesis results in a 6-fold increase in midline birth defects

67
Q

Ketoacidosis

A
  • immediate threat to life
  • leading cause of perinatal morbidity
  • 40% of perinatal mortality
68
Q

GDM Complications

A 
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

69
Q

GDM effect on placenta

A

Associated with placental abnormalities

-uteroplacental blood flow index lower by 35-40% in diabetic parturients

70
Q

GDM: poorly regulated + higher HbA1c effect at tissue level

A

2,3-DPG levels lower = blood oxygen release at tissue level impaired

71
Q

Most common cause of 3rd trimester bleeding

A

placenta previa
abruptio placentae
uterine rupture

72
Q

Postpartum hemorrhage is most often due to

A

uterine atony (soft)
retained placenta
placenta accreta (grew thru uterus)
uterine inversion

73
Q

Obstetrical Hemorrhage

A 
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
74
Q

Abruptio placenta

A

placental abruption

a partial or complete separation of the placenta before delivery of the fetus

75
Q

Most common cause of OB hemorrhage + maternal death

A

Abruptio placenta

76
Q

Placenta Previa

A

Occurs when placenta is implanted low in uterus, either overlying or encroaching cervical opening (cervical os)

77
Q

Types of placenta previa

A

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

78
Q

Placenta Previa is more common

A
  • in multiparous women

- previous C/S or uterine myomectomy

79
Q

Placenta Previa is characterized by

A

painless vaginal bleeding in 3rd trimester

80
Q

Bleeding d/t placenta previa

A

may stop spontaneously, risk of severe bleeding can occur at any time

81
Q

Placenta Previa: Tx

A

< 37 weeks, mild to moderate bleeding: bedrest + observation

> 37 weeks: C/S

82
Q

Abruptio Placenta Risk Factors

A

chronic HTN, PIH, preeclampsia, maternal cocaine use, excessive alcohol intake, smoking, + previous history of abruption

83
Q

Abruptio Placenta manifestations

A

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

84
Q

Abruptio Placenta Risks

A

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%

85
Q

Placenta Accreta

A

Abnormally firm attachment of placenta to uterine wall

placenta becomes difficult or impossible to separate from uterus + produce life-threatening maternal hemorrhage

86
Q

Placenta Accreta - increased risk if

A

history of placenta previa or C/S

87
Q

Placenta increta

A

placenta invades the myometrium

88
Q

Placenta percreta

A

placenta has invaded the myometrium and serosa, sometimes into adjacent organs, such as the bladder

89
Q

Uterine rupture

A
  • 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)
90
Q

What must be available for TOLAC?

A

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)

91
Q

Uterine rupture S/S

A
  • non-specific
  • fetal bradycardia almost always occurs
  • Maternal hypotension along with loss of function of uterine pressure monitors often evident
92
Q

Tx Uterine Rupture

A

emergency laparotomy

GA indicated

93
Q

Vasa Previa

A

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

94
Q

Vasa Previa risks

A

bleeding from fetal circulation = fetus at risk

95
Q

Vasa Previa Tx

A

immediate delivery

96
Q

PPH

A

postpartum hemorrhage

causes: uterine + non-uterine

97
Q

Uterine causes - PPH

A

most frequent: uterine atony + retained placental products

others: uterine rupture + uterine inversion

98
Q

Non-uterine causes - PPH

A

vaginal tears, perineal hematoma, maternal coagulopathy

99
Q

Uterine Atony: risk factors

A 
Prolonged labor
Overdistended uterus (macrosomia or multiple births)
Infection
Grand multiparity
Administrations of drugs that relax uterus:
-Halogenated anesthetics
-β-sympathomimetic agonists
-Magnesium sulfate
100
Q

Uterine Atony Tx

A

-oxytocin
Doses can precipitate HOTN (continuous infusions preferable)

-Hemabate + ergot alkaloids (Methergin) are potent uterotonic agents used to treat atony

101
Q

Retained Placenta Tx

A

~ 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

102
Q

Amniotic fluid embolism

A

Mortality ~ 80%
Survival uncommon, survivors often have neurological dysfxn
Most occur during or immediately after labor

103
Q

AFE Pathogenesis

A

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

104
Q

AFE presentation

A

Acute SOB, +/- cough, followed by severe HOTN
Fetal distress evidenced by fetal bradycardia from hypoxic insult
Cyanosis
Asystole

105
Q

Phases of AFE

A

Early phase:
Pulm vasospasm
Acute RHF
Often fatal early (50% die w/in 1h)

Second phase: LVF + pulmEdema

106
Q

AFE Tx

A

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 ?

107
Q

Leading cause of maternal death globally

A

hemorrhage

108
Q

Maternal hemorrhage usually occurs

A

immediately after delivery (35%)

109
Q

Abnormal OB blood loss

A

> 500 mL vaginal delivery

> 1L C/S

110
Q

Major hemorrhage

A

Blood loss 2,500 mL or +
Transfusion of 5 or + units blood
Treatment for coagulopathy

111
Q

Causes of maternal hemorrhage: antepartum

A

Placenta previa
Placental abruption
Uterine rupture
Vasa previa

112
Q

Causes of maternal hemorrhage: postpartum

A 
Uterine atony
Genital trauma
Retained placenta
Placenta accreta
Uterine inversion
113
Q

PPH risk factors

A 
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
114
Q

strong predictor for subsequent development of severe postpartum hemorrhage

A

Fibrinogen levels of < 2 g/dL in early stage of postpartum bleeding

115
Q

Accounts for 80% of PPH

A

uterine atony

116
Q

uterine atony is the loss of tone in uterine musculature following delivery as a result of failure to respond to ________

A

normal endogenous oxytocic substances, oxytocin, and prostaglandin

117
Q

No vaginal bleeding, can mom have uterine atony?

A

Yes - can be atonic, engorged uterus with > 1L blood

118
Q

Prevention of uterine atony is facilitated how?

A

Administration of oxytocin immediately after delivery

119
Q

s/s hypovolemia

A

may not be present until > 1200-1500mL blood loss

120
Q

Circulating blood volume expands from ____

A

20-100%

121
Q

RBC volume increases by

A

30%

122
Q

CO increases by

A

50%

123
Q

Risks of hypovolemia or hypovolemic shock in pregnancy

A

Masked s/s d/t normal increases in pregnancy:
HR increases 15-20 bpm
Peripheral vasodilation
Widened pulse pressure

124
Q

Hypovolemic shock: moms SBP may not drop until ____

A

2-3L blood have been lost

125
Q

Surgical management of maternal hemorrhage

A 
Bimanual compression of uterus
Uterine balloon tamponade
Uterine compression sutures
Arterial ligation
Peripartum hysterectomy
Angiographic arterial embolism
126
Q

Crystalloids are distributed between intravascular and extravascular space by a ratio of

A

1:3

127
Q

Exsanguinating hemorrhage tx

A

immediate resuscitation with any fluid; blood products = saving
**O negative should be considered

128
Q

Transfusion of red blood cells is usually unnecessary in patients with

A

Hgb = 10 g/dL or +

129
Q

Transfusion of pRBCs should be administered if

A

Hgb < 6 g/dL

130
Q

Transfusion Guidelines

A

Once > 10 units pRBCs given:
1:3 FFP:pRBC
+ 6u platelets

(avoid dilutional coagulopathies)
*ongoing measurement of Hgb, coags, + platelets guide therapy

131
Q

Key strategy to avoid coagulopathy during MTP

A

Administer FFP before abnormal PTT values occur

132
Q

Resuscitative goals

A

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

133
Q

External Bimanual uterine compression

A
  • 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’
134
Q

Complications of resuscitation and transfusion include:

A 
Accidental admin of ABO incompatible blood
Dilutional coagulopathies
Transfusion reactions
Hypothermia
Hyperkalemia + hypocalcemia
135
Q

Principle duties of anesthesia providers (during maternal hemorrhage)

A

Maintain vital functions
Replace blood loss
Provide the conditions under which hemorrhage can be controlled

136
Q

Advent of ultrasonography has also allowed providers to

A

anticipate patients at high risk for hemorrhage, such as those with placental abnormalities, thus guiding planning for care + predicting blood loss

137
Q

Initial responsibilities of anesthesia provider in unexpected hemorrhage:

A

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

138
Q

Non-initial responsibilities of anesthesia provider in unexpected hemorrhage:

A

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

139
Q

In the event of massive uncontrollable hemorrhage, anesthesia provider should be prepared for

A

emergency hysterectomy

Patient under regional may have to be converted to GA

140
Q

Anticipated Hemorrhage

A
  • 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
141
Q

After team assembled, Anesthetic management: Anticipated Hemorrhage

A

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)

P&P 3 (9 decks)

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