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SNRAObPedGer > ASPIRATION and DIC > Flashcards

ASPIRATION and DIC Flashcards

1
Q

What is the single most important factor leading to the decrease in aspiration ?

A

Neuraxial Anesthesia

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2
Q

A decrease incidence of aspiration due to multiple factors include (MARIN)

A 
More neuraxial anesthesia
Antacids prophylaxis
RSI for GETA
Improve training
NPO policies
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3
Q

Regulation intubation vs RSI

A

RSI

  1. normal ventilation
  2. Muscle relaxants are given right away
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4
Q

If you give can ventilate

A 
Use LMA (worst case scenario)
Wake them up
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5
Q

Anesthesia maternal mortality related to

A

Airway issues

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6
Q

Prior to 1990, most common cause of anesthesia related death was

A

aspiration

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7
Q

Morbidity and mortality from aspiration depends on

A

Physical status (if you have other issues such as asthma
and COPD you are at higher risk )
Type and volume of aspirate (less is better)
Therapy administered
Criteria use for diagnosis

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8
Q

Esophagus about _____long

A

40cm

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9
Q

Muscular shincters at both ends normally _______

A

Closed

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10
Q

What is the role of the CRICOPHARYNGEAL SPHINCTER?

A

prevents entry of air into esophagus during respiration

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11
Q

Decrease Esophageal sphincter is usually

A

8-20mmHg above gastric pressure

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12
Q

What is the hormone responsible to relaxes

A

Relaxin and progesterone

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13
Q

You get more air at the end of a case because of

A

Nitrous Oxide (thats why its contraindicated in pneumothorax)

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14
Q

Capacity of stomach is about ______why?

A

1-1.5L ; ability to stretch

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15
Q

Propulsion of food is via _____not _____

A

peristalsis ; gravity

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16
Q

Peristalsis is the

A

contractile ring of muscular activity progressing down the gut

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17
Q

Pyrolus closes midway through contraction wave allowing

A

Pylorus closes midway through contraction wave, allowing some fluid to exit into the duodenum but causing remaining fluid to move retrograde toward body of the stomach

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18
Q

What occurs with Large particles?

A

lag behind in retrograde fluid

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19
Q

Which kind of molecules move faster ?

A

Fluids and small particles exit the stomach faster than larger particles

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20
Q

Also affects exit of particles is the ___

A

Viscosity of suspension

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21
Q

What limits outflow

A

Tone and anatomical position of pylorus

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22
Q

_____always higher than most dependent portion of stomach

A

• Pylorus

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23
Q

Gastric Bypass patients usually at risk for

A

DUMPING SYNDROME

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24
Q

Up to _____highly acidic fluid is produced per day

by the stomach

A

1500 ml

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25
Q

Pyloric glands : Chief cells secrete

• Chief cells secrete

A

pepsinogen →pepsin

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26
Q

Oxyntic glands: Oxyntic cells secrete

• Oxyntic cells secrete with a ph of ______

A

HCl (pH 0.8)

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27
Q

This is where PPIs work

A

Oxyntic glands and Oxyntic cells

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28
Q

Vagus stimulates G cells to secrete

__________ →bind to________ and stimulates_______

A

gastrin; oxyntic cells ; HCl secretion

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29
Q

H-2 receptors______cAMP, _____calcium → dramatic________

acid production

A

↑; ↑; ↑

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30
Q

Ach binds to________ and________ Ca2+

A

muscarinic receptors; ↑

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31
Q

• Histamine potentiates both

A

gastrin and acetylcholine

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32
Q

When you antagonize H1

A

Tachycardia

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33
Q

Agonizing H1 leads to

A

Bradycardia

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34
Q

Acid is secreted at a ______________ ____of approximately __________ of ________even
when stomach is empty

A

Low basal rate of approximately 10% of maximal output,

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35
Q

Diurnal variation means acid

A

lowest in morning, highest in evening (take antacids @hs)

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36
Q

↑ dramatically with

A

ingestion

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37
Q

Cephalic phase:

Gastric acid output ↑ to_______

A

chewing, smelling, or tasting without significant ingestion ↑ vagal stimulation; 55% of peak levels

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38
Q

Gastric phase is the

A

entry into stomach of ingested contents, acid output peaks

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39
Q

• Intestinal phase:

A

begins with movement of food into small intestine

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40
Q

What are the 3 phases of digestion

A

Cephalic
Gastric
Intestinal

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41
Q

3 things Normally slowing GASTRIC EMPTYING :

A

↑ lipid content
↑ caloric load
Large particle size

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42
Q

*****Gastric emptying is

A

NOT slowed during pregnancy

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43
Q

When does gastric emptying becomes delayed ?

Factors that may delay are

A

Normal in early labor but becomes delayed as labor advances (pain, opioids, epidural dose >100mcg Fent)

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44
Q

↑ progesterone

A

Relaxes ↓ esophageal sphincter

• GERD

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45
Q

Basal gastric acid secretion between

pregnant and nonpregnant women

A

No significant differences in basal gastric acid secretion

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46
Q

What are the mechanical effects of expanding uterus

A
  • Increasing intragastric pressure

* Distorts normal anatomic relationship of esophagus/diaphragm/stomach

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47
Q

During labor always assume

A

Decrease GASTRIC EMPTYING

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48
Q

RISK FACTORS FOR ASPIRATION PNEUMONITIS

CDPV

A

Chemical nature (↑ acidity = worse)
• Physical nature (liquid worse than solid)
• Volume (more is worse)
• Disruption of surfactant by the large volume of liquid

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49
Q

Mendelson demonstrated that sequelae from aspiration of liquids compared to solids were

A

more severe clinically and pathologically when the liquid was highly acidic

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50
Q

Aspirates with a pH _______ cause a granulocytic reaction

A

pH ↓ than 2.5

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51
Q

• General rule of Aspiration pneumonitis

A

pH < 2.5

gastric volume > 25 mL

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52
Q

pH somewhat evidence based, but gastric volume is not but

A

↓ is always better

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53
Q

ASPIRATION PNEUMONITIS: “MENDELSONS SYNDROME”

What develop immediately ?

A

“Cyanosis and labored respirations develop immediately, but death often ensues within minutes to hours, with a pink froth exuding from the respiratory passages in the terminal stages.”

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54
Q

Aspiration pneumonitis: CXR

A

• CXR: “irregular soft mottled shadows without mediastinal shift

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55
Q

Clinical course Aspiration pneumonitits =

A

chemical injury from sterile acid gastric contents

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56
Q

Basic aspirate_____ surfactant levels

A

↓

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57
Q

Aspiration pneumonitis MOA:

A

↑ intra-alveolar water and protein content and a loss of lung volume = ↓ in pulmonary compliance and intrapulmonary shunting of blood

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58
Q

Bronchial obstruction due to

A

Cellular debris and bronchial denuding

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59
Q

Pathophysiological disturbances following Aspiration pneumonitis
EBDSHII

A 
Exudative pulmonary edema
bronchial obstruction
↓ lung compliance, and shunting →
Hypoxemia
↑pulmonary vascular resistance
 increased work of breathing
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60
Q

After direct acid-mediated injury of respiratory tract by aspiration pneumonitis an intense ___

A

Inflammatory response ensues from (MSIT)macrophage

activation and secretion of cytokines, interleukins and tumor necrosis factor-alpha

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61
Q

The activation of macrophages Leads to
• Amplification of these inflammatory processes may result in development
of acute lung injury or acute respiratory distress syndrome (ARDS)

A

chemotaxis, accumulation, and activation of neutrophils in
alveolar exudate, up-regulation of adhesion molecules within pulmonary vasculature, and activation of the complement pathways

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62
Q

The activation of neutrophils release

A

oxidants, proteases, leukotrienes, and other proinflammatory molecules

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63
Q

Aspiration pneumonitis content is

A

STERILE

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64
Q

Often witnessed by anesthesia provider
• In supine position which part is usually injured?
•

A

injury to posterior segments of upper lobes and apical segments of lower lobes

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65
Q

Aspiration signs : if in Semi-recumbent or upright which part of lung is usually injured?

A

injury to lower lobes

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66
Q

What is the most common site of aspiration?

A

RLL most common site of aspiration d/t large size of right mainstem bronchus

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67
Q

Aspiration sign in a Spontaneously breathing patient →
HTTRA
HH

A

breath holding followed by tachypnea & tachycardia (slight resp. acidosis)
Hypoxemia (↑ shunting), bronchospasm
Hypotension (↑PVR results in ↓ cardiac index)

68
Q

In aspiration pneumonitis PaO2 ↓

•

A

secondary to ↑ shunt

69
Q

85-90% of patients eventually develop______when ?

A

abnormal CXR; CXR is often normal until 12-24 hours after aspiration

70
Q

Recovery of Aspiration pneumonitis involves

A

proliferation and differentiation of surviving type II pneumocytes in alveolar epithelial cells

71
Q

Aspiration pneumonitis Soluble proteins are removed by

A

paracellular diffusion and endocytosis

72
Q

Aspiration pneumonitis Insoluble proteins are removed by

A

macrophages.

73
Q

Aspiration pneumonitis Neutrophils are removed by

A

programmed cell death and phagocytosis by macrophages

74
Q

________gradually restore normal composition of surfactant

A

• Type II pneumocytes

75
Q

Aspiration pneumonitis, how is Na+ and H2o removed

A

Actively transport Na+ out of alveolus, water follows

76
Q

Most common site of aspiration is

A

right

77
Q

Pathophysiology of Acidic liquid aspiration : Acidic liquid aspiration injures______leading to ______
(FACER)

A

alveolar epithelium → alveolar exudate (edema,

albumin, fibrin, cellular debris, and RBCs)

78
Q

In pathophysiology of acidic liquid Alveolar exudate/pulmonary edema leads to: (DLIB)

A
  • ↓ in lung compliance
  • Loss of lung volume
  • Intrapulmonary shunting of blood
  • Bronchial obstruction/ bronchospasm
79
Q

ASPIRATION : NEUTRAL NONPARTICULATE LIQUID

MSN

A
  • Neutral aspirate → alveolar exudate with minimal damage to the alveoli
  • Slight ↑ in shunt and ↓ in PaO2
  • Minimal pathologic changes
80
Q

PATHOPHYSIOLOGY: PARTICLE ASPIRATION; large

A

Direct airway obstruction from larger particles = atelectasis
OBSTRUCTING LARGER AIRWAYS

81
Q

PATHOPHYSIOLOGY: PARTICLE ASPIRATION: SMALL

A

Smaller particles: similar response as with acidic liquid
Causes exudative neutrophilic response at
levels of bronchioles and alveolar ducts

82
Q

Small particles aspiration causes

A

Causes exudative neutrophilic response at levels of bronchioles and alveolar ducts leading to pulmonary edema

83
Q

ARDS Clinical diagnosis criteria

A

within1 week of known clinical insult

84
Q

ARDS Chest imaging clinical diagnosis of ARDS

A

Bilateral opacities NOT EXPLAINED by effusions

85
Q

Biochemical ARDS PAO2/FIO2 ratio

A

<300 with CPAP or PEEP >5 cm H20

86
Q

Origin of pulmonary edema: ARDS with diagnosis

A

Not explained by cardiac failure or overload.

87
Q

Aspiration pneumonitis Treatment: when is it appropriate to do a rigid bronchoscopy?

A

Only if large particles obstruct airway

88
Q

What does not help in the treatment of Aspiration pneumonitis

A

Lavage with saline/bicarbonate: does not remove acid, can worsen hypoxemia

89
Q

Shunting + Hypoxemia treated with

A

positive pressure (CPAP or PEEP with supplemental oxygen), help decrease shunting . It improves FRC, reduces pulmonary shunting, reverse hypoxemia

90
Q

Steroids in the treatment of Aspiration pneumonitis

A

Failed to demonstrate benefit on pulmonary function

91
Q

What is not a component of acidic lung injury?

A

Infection is not a component of acidic

lung injury

92
Q

• “Prophylactic” antibiotics are proven to cause

A

resistant organism infection

93
Q

Antibiotics started ONLY if clinical evidence of

infection such as (3)

A
  • Fever, ↑WBC
  • Worsening CXR infiltrate
  • Positive sputum gram stain
94
Q

Minimizing risk factors of aspiration predisposing factors are

A

Emergency surgery
Difficult/failed tracheal intubation
Light anesthesia
GERD

95
Q

____can happen just as often on emergence as induction

A

• Aspiration

96
Q

• Small volumes __________ of_____ other than_____ and pulp containing juices consumed up to 2 hours

A

150 mL; 5.7 fluid ounces; fluid; milk

before elective surgery do not ↑ the risk of aspiration in the otherwise healthy parturient

97
Q

MINIMIZING RISK: CHOICE OF

ANESTHESIA : General vs Regional

A

Risk of maternal death is approximately 17 times greater with general anesthesia compared with regional

98
Q

Majority of general anesthesia

A

aspiration and/or hypoxemia injury

99
Q

Non particulate antacid: ______citrate (Bicitra) can neutralize ______ml of HCL with a pH of _____

A

30 mL Na citrate [Bicitra] can neutralize 255 mL of hydrochloric acid with a PH of 1.0

100
Q

Should be administered within

A

20 minutes of induction of GETA

101
Q

Particulate antacid

A

(e.g.. Maalox, Mylanta) when aspirated causes serious pneumonitis!

102
Q

MINIMIZING RISK: H-2 RECEPTOR ANTAGONISTS

A

Cimetidine
Ranitidine
Famotidine

103
Q

H2 antagonists effect

A

reduces gastric acidity significantly approx. 30 minutes after IV administration maximal effect at 60-90 min

104
Q

How does H2 antagonists work

A

Block histamine receptors on oxyntic cell → ↓diminish gastric acid production → leading to a slight ↓ in gastric volume in fasting patient

105
Q

Duration of action of H2

A

is sufficiently long to cover emergence from GA for a Csection

106
Q

PPIs

A

Omeprazole and lansoprazole

107
Q

PPI and onset of action

A

Take forever to work PO

But IV start of action similar to H2 antagonsist.

108
Q

PPI MOA

A

inhibit the H+ pump on gastric surface of OXYNTIC CELL

109
Q

PREVENT stomach from making further acid

A

H2 antagonists

110
Q

You cannot give metoclompramide to this patients

A

Parkinson’s

111
Q

Cannot give metoclopramide in this type of GI disorder

A

Bowel obstruction

112
Q

Class of metoclopramide

A

Central dopamine receptor antagonists

113
Q

Metoclopamide effect

A

Increase LES tone

Decrease gastric volume by increasing gastric peristalsis

114
Q

Metoclopramide starts in

A

15 min

115
Q

Major side effect of Metoclopramide is

A

EPS

116
Q

What antagonize the effect of metoclopramide is

A

Prior admin with opiod and atropine

117
Q

Guidelines for perinatal care (American College of Obstetrics & Gynecology, American Academy of Pediatrics)

A

“Patients in active labor should avoid oral ingestion of anything excepts sips of clear liquids, occasional ice chips, or moistening of mouth/lips”

118
Q

Normal laboring patients should not

A

receive aspiration prophylaxis unless they are high risk for C-section

119
Q

DISSEMINATED INTRAVASCULAR COAGULATION (DIC): ACQUIRED COAGULOPATHY

A

Results from an abnormal activation of the coagulation system

120
Q

4 main issues with DIC

A
  • Formation of large amount of thrombin
  • Depletion of coagulation factors
  • Activation of fibrinolytic system
  • Hemorrhage
121
Q

Progression of DIC

A

• If severe enough, diffuse microvascular thrombosis → end-organ injury

122
Q

Effect of systemic activation of coagulation (ID)

A

Intravascular deposition of fibrin –>Thrombosis of small and midsize vessels and organ failure
Depletion of platelets and anticoagualtion factors-> Bleeding

123
Q

DIC: OBSTETRIC ETIOLOGY

A 
• Preeclampsia
• Placental abruption (40% of patients)
• Sepsis (abortion, chorioamnionitis)
• Retained dead fetus (no evidence of DIC until 3-5
weeks)
• Amniotic fluid embolism (the few who survive
usually → DIC)
• Postpartum hemorrhage
124
Q

DIC:pathophysiology

A

• Complicated & poorly understood

125
Q

• Obstetric “triggers” of DIC

A

include entry of procoagulant tissue extracts and into the blood which interact with Factor VII and activate the extrinsic coagulation pathway

126
Q

• Dead tissue and amniotic fluid contains

A

thromboplastic substances that trigger

coagulation.

127
Q

DIC generates

A

pro-inflammatory cytokines and the activation of monocytes, bacteria cause the up-regulation of tissue factor as well as the release of microparticles expressing tissue factor thus leading to activation of coagulation.

128
Q

What does proinflammatory cytokines cause?

A

cause the activation of endothelial cells, a process that impairs anticoagulants mechanisms and down regulates fibrinolysis by generating increase amounts of plasminogen activator inhibitor.

129
Q

Lab findings: Change how fast?

A
  • ↓Plt count
  • ↓ fibrinogen and antithrombin III concentrations
  • Variable ↑ in PT, aPTT, and thrombin and reptilase times
  • ↑ levels of D-dimer, fibrin and FDP
130
Q

Coagulation consumption

A
  • Accelerated turnover of various factors

* Levels at any given time depend upon rate of destruction and repletion

131
Q

The Proteins other than coagulation factors may be depleted due to DIC

A
  • Antithrombin 3
  • Fibronectin
  • Plasminogen
132
Q

DIC pathophysiology (arrow)

A

Precipitating event –> TF/Extrinsic pathway activation->Coagulation cascade–>Excess thrombin–> Conversion of plasminogen to plasmin–>Fibrinolysis with excess FDPs –> Excess bleeding –> Shock, hypotension, Increased vascular permeability

Precipitating event –> TF/Extrinsic pathway activation->Coagulation cascade–>Excess thrombin–> Excess clotting –>Ischemia, impaired organ perfusion, end organ damage

Microvascular and Macrovascular clotting –> Thrombocytopenia –>Consumption of clotting factors –> Fibrinolysis with excess FDPs

133
Q

Does not reflect severity of DIC_________

A

Platelet count depression

134
Q

Thrombocytopenia may result from processes other than clot function

A
  • Adhesion to damaged endothelium

* Intravascular platelet “clumping”

135
Q

DIC PATHOPHYSIOLOGY: INTRAVASCULAR FIBRIN FORMATION

A

Formation of small strands/microclots of fibrin is the immediate result of DIC (may lead to obstruction of pulmonary vessels) Obstruction (DEAD SPACE)

136
Q

Present with every patient wit DIC

A

Fibrinolysis

137
Q

• Fibrin degradation products (FDP): (APID)

A

Protein fragments that;
• Act as antithrombins (↑ bleeding)
• Produce defective fibrin polymer (↑bleeding)
• Impair platelet clearance
• Directly damage pulmonary vasculature (ARDS!)

138
Q

DIC: CLINICAL FEATURES OF ACUTE

DIC

A

• Clinical emergency
• Bleeding of all kinds from anywhere in/on the body
•

139
Q

Most common bleeding sites for DIC

A

Gums, epistaxis, GI, pulmonary, hematuria, cutaneous are most common sites

140
Q

Chronic DIC

A

Intermediate between hypercoagulable state and acute DIC

141
Q

more likely to produced clot

A

physiologic DIC

142
Q

Differential dx of abrupt onset of severe bleeding

A

Rule out severe liver disease (elevated platelets, elevated PT)

143
Q

Always the result of serious obstetric

A

DIC

144
Q

Definitive treatment preeclampsia

A

Tx deliver baby

145
Q

Definitive tx of Abruptio

A

Tx deliver baby and placenta

146
Q

Tx of sepsis

A

ABT

147
Q

Tx of retained products of conception

A

D and C

148
Q

Ultimat cure of DIC

A

Treatment of primary disorder or Underlying condition

Provide ventilation and multiorgan support

149
Q

DIC supportive Treatment while you look for etiology if

A

Active bleeding or invasive procedure required

150
Q

How do you treat bleeding in DIC with FFP

A

15-30ml/kg to maintain PT and aPTT 1.5 times normal values

151
Q

How do you treat bleeding in DIC with CRyoprecipitate or Fibrinogen concentrate

A

Maintain fibrinogen above 150-200mg/dl

152
Q

Platelets to maintain

A

platelet count above 50,000

153
Q

Cryoprecipitate factors are

A

Fibrinogen
Von Willebrand (Factor VIII)
Fibronectin

154
Q

Heparin only work if

A

Antithrombin III level is adequate

155
Q

New agent in treatment of massive bleeding

A

rFVIIa (replacing cryo and FFPs)

156
Q

EACA

A

prevents breakdonw of clotting (aminocaproic and tranxemic acid)

157
Q

Better throughout pregnancy Warfarin vs heparin

A

Heparin or LMWH

158
Q

If on warfarin

A

D/C before onset of labor

159
Q

If onset of labor occurs and patient is on warfarin

A

Revers with Vit K and IV prothrombin complex concentrate (PCC)

160
Q

What is better warfarin vs Four-factor concentrte

A

Four factor Prothrombin concentrate (KCENTRA) better option for warfarin reversal than FFP

161
Q

If condition require immediate reversal of anticoagulatio

A

IV protamine 12.5-50mg administered

162
Q

Protamine reversal of heparin CONTRAINDICATED to

A

allow administration of neuraxial anesthesia is NOT RECOMMENDED.

163
Q

Reversal of lovenox with protamine sulfate is

A

not predictable

164
Q

If patient with an ISOLATED laboratory abnormality and no clinical evidence of coagulopathy what is the next step? What should you monitor closely

A

Can do NEURAXIAL anesthesia

Do frequent neuro assessment to facilitate early detection of EPIDURAL hematoma during the postpartum period.

165
Q

IF the patient has DIC no

A

spinal anesthesia

Alternative GA

SNRAObPedGer (25 decks)

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