ASPIRATION and DIC Flashcards
1
Q
What is the single most important factor leading to the decrease in aspiration ?
A
Neuraxial Anesthesia
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
3
Q
Regulation intubation vs RSI
A
RSI
- normal ventilation
- Muscle relaxants are given right away
4
Q
If you give can ventilate
A
Use LMA (worst case scenario) Wake them up
5
Q
Anesthesia maternal mortality related to
A
Airway issues
6
Q
Prior to 1990, most common cause of anesthesia related death was
A
aspiration
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
8
Q
Esophagus about _____long
A
40cm
9
Q
Muscular shincters at both ends normally _______
A
Closed
10
Q
What is the role of the CRICOPHARYNGEAL SPHINCTER?
A
prevents entry of air into esophagus during respiration
11
Q
Decrease Esophageal sphincter is usually
A
8-20mmHg above gastric pressure
12
Q
What is the hormone responsible to relaxes
A
Relaxin and progesterone
13
Q
You get more air at the end of a case because of
A
Nitrous Oxide (thats why its contraindicated in pneumothorax)
14
Q
Capacity of stomach is about ______why?
A
1-1.5L ; ability to stretch
15
Q
Propulsion of food is via _____not _____
A
peristalsis ; gravity
16
Q
Peristalsis is the
A
contractile ring of muscular activity progressing down the gut
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
18
Q
What occurs with Large particles?
A
lag behind in retrograde fluid
19
Q
Which kind of molecules move faster ?
A
Fluids and small particles exit the stomach faster than larger particles
20
Q
Also affects exit of particles is the ___
A
Viscosity of suspension
21
Q
What limits outflow
A
Tone and anatomical position of pylorus
22
Q
_____always higher than most dependent portion of stomach
A
• Pylorus
23
Q
Gastric Bypass patients usually at risk for
A
DUMPING SYNDROME
24
Q
Up to _____highly acidic fluid is produced per day
by the stomach
A
1500 ml
25
Pyloric glands : Chief cells secrete
| • Chief cells secrete
pepsinogen →pepsin
26
Oxyntic glands: Oxyntic cells secrete
| • Oxyntic cells secrete with a ph of ______
HCl (pH 0.8)
27
This is where PPIs work
Oxyntic glands and Oxyntic cells
28
Vagus stimulates G cells to secrete
| __________ →bind to________ and stimulates_______
gastrin; oxyntic cells ; HCl secretion
29
H-2 receptors______cAMP, _____calcium → dramatic________
| acid production
↑; ↑; ↑
30
Ach binds to________ and________ Ca2+
muscarinic receptors; ↑
31
• Histamine potentiates both
gastrin and acetylcholine
32
When you antagonize H1
Tachycardia
33
Agonizing H1 leads to
Bradycardia
34
Acid is secreted at a ______________ ____of approximately __________ of ________even
when stomach is empty
Low basal rate of approximately 10% of maximal output,
35
Diurnal variation means acid
lowest in morning, highest in evening (take antacids @hs)
36
↑ dramatically with
ingestion
37
Cephalic phase:
| Gastric acid output ↑ to_______
chewing, smelling, or tasting without significant ingestion ↑ vagal stimulation; 55% of peak levels
38
Gastric phase is the
entry into stomach of ingested contents, acid output peaks
39
• Intestinal phase:
begins with movement of food into small intestine
40
What are the 3 phases of digestion
Cephalic
Gastric
Intestinal
41
3 things Normally slowing GASTRIC EMPTYING :
↑ lipid content
↑ caloric load
Large particle size
42
*****Gastric emptying is
NOT slowed during pregnancy
43
When does gastric emptying becomes delayed ?
| Factors that may delay are
Normal in early labor but becomes delayed as labor advances (pain, opioids, epidural dose >100mcg Fent)
44
↑ progesterone
Relaxes ↓ esophageal sphincter
| • GERD
45
Basal gastric acid secretion between
| pregnant and nonpregnant women
No significant differences in basal gastric acid secretion
46
What are the mechanical effects of expanding uterus
* Increasing intragastric pressure
| * Distorts normal anatomic relationship of esophagus/diaphragm/stomach
47
During labor always assume
Decrease GASTRIC EMPTYING
48
RISK FACTORS FOR ASPIRATION PNEUMONITIS
| CDPV
Chemical nature (↑ acidity = worse)
• Physical nature (liquid worse than solid)
• Volume (more is worse)
• Disruption of surfactant by the large volume of liquid
49
Mendelson demonstrated that sequelae from aspiration of liquids compared to solids were
more severe clinically and pathologically when the liquid was highly acidic
50
Aspirates with a pH _______ cause a granulocytic reaction
pH ↓ than 2.5
51
• General rule of Aspiration pneumonitis
pH < 2.5
| gastric volume > 25 mL
52
pH somewhat evidence based, but gastric volume is not but
↓ is always better
53
ASPIRATION PNEUMONITIS: “MENDELSONS SYNDROME”
| What develop immediately ?
“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.”
54
Aspiration pneumonitis: CXR
• CXR: “irregular soft mottled shadows without mediastinal shift
55
Clinical course Aspiration pneumonitits =
chemical injury from sterile acid gastric contents
56
Basic aspirate_____ surfactant levels
↓
57
Aspiration pneumonitis MOA:
↑ intra-alveolar water and protein content and a loss of lung volume = ↓ in pulmonary compliance and intrapulmonary shunting of blood
58
Bronchial obstruction due to
Cellular debris and bronchial denuding
59
Pathophysiological disturbances following Aspiration pneumonitis
EBDSHII
```
Exudative pulmonary edema
bronchial obstruction
↓ lung compliance, and shunting →
Hypoxemia
↑pulmonary vascular resistance
increased work of breathing
```
60
After direct acid-mediated injury of respiratory tract by aspiration pneumonitis an intense ___
Inflammatory response ensues from (MSIT)macrophage
| activation and secretion of cytokines, interleukins and tumor necrosis factor-alpha
61
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)
chemotaxis, accumulation, and activation of neutrophils in
alveolar exudate, up-regulation of adhesion molecules within pulmonary vasculature, and activation of the complement pathways
62
The activation of neutrophils release
oxidants, proteases, leukotrienes, and other proinflammatory molecules
63
Aspiration pneumonitis content is
STERILE
64
Often witnessed by anesthesia provider
• In supine position which part is usually injured?
•
injury to posterior segments of upper lobes and apical segments of lower lobes
65
Aspiration signs : if in Semi-recumbent or upright which part of lung is usually injured?
injury to lower lobes
66
What is the most common site of aspiration?
RLL most common site of aspiration d/t large size of right mainstem bronchus
67
Aspiration sign in a Spontaneously breathing patient →
HTTRA
HH
breath holding followed by tachypnea & tachycardia (slight resp. acidosis)
Hypoxemia (↑ shunting), bronchospasm
Hypotension (↑PVR results in ↓ cardiac index)
68
In aspiration pneumonitis PaO2 ↓
| •
secondary to ↑ shunt
69
85-90% of patients eventually develop______when ?
abnormal CXR; CXR is often normal until 12-24 hours after aspiration
70
Recovery of Aspiration pneumonitis involves
proliferation and differentiation of surviving type II pneumocytes in alveolar epithelial cells
71
Aspiration pneumonitis Soluble proteins are removed by
paracellular diffusion and endocytosis
72
Aspiration pneumonitis Insoluble proteins are removed by
macrophages.
73
Aspiration pneumonitis Neutrophils are removed by
programmed cell death and phagocytosis by macrophages
74
________gradually restore normal composition of surfactant
• Type II pneumocytes
75
Aspiration pneumonitis, how is Na+ and H2o removed
Actively transport Na+ out of alveolus, water follows
76
Most common site of aspiration is
right
77
Pathophysiology of Acidic liquid aspiration : Acidic liquid aspiration injures______leading to ______
(FACER)
alveolar epithelium → alveolar exudate (edema,
| albumin, fibrin, cellular debris, and RBCs)
78
In pathophysiology of acidic liquid Alveolar exudate/pulmonary edema leads to: (DLIB)
* ↓ in lung compliance
* Loss of lung volume
* Intrapulmonary shunting of blood
* Bronchial obstruction/ bronchospasm
79
ASPIRATION : NEUTRAL NONPARTICULATE LIQUID
| MSN
* Neutral aspirate → alveolar exudate with minimal damage to the alveoli
* Slight ↑ in shunt and ↓ in PaO2
* Minimal pathologic changes
80
PATHOPHYSIOLOGY: PARTICLE ASPIRATION; large
Direct airway obstruction from larger particles = atelectasis
OBSTRUCTING LARGER AIRWAYS
81
PATHOPHYSIOLOGY: PARTICLE ASPIRATION: SMALL
Smaller particles: similar response as with acidic liquid
Causes exudative neutrophilic response at
levels of bronchioles and alveolar ducts
82
Small particles aspiration causes
Causes exudative neutrophilic response at levels of bronchioles and alveolar ducts leading to pulmonary edema
83
ARDS Clinical diagnosis criteria
within1 week of known clinical insult
84
ARDS Chest imaging clinical diagnosis of ARDS
Bilateral opacities NOT EXPLAINED by effusions
85
Biochemical ARDS PAO2/FIO2 ratio
<300 with CPAP or PEEP >5 cm H20
86
Origin of pulmonary edema: ARDS with diagnosis
Not explained by cardiac failure or overload.
87
Aspiration pneumonitis Treatment: when is it appropriate to do a rigid bronchoscopy?
Only if large particles obstruct airway
88
What does not help in the treatment of Aspiration pneumonitis
Lavage with saline/bicarbonate: does not remove acid, can worsen hypoxemia
89
Shunting + Hypoxemia treated with
positive pressure (CPAP or PEEP with supplemental oxygen), help decrease shunting . It improves FRC, reduces pulmonary shunting, reverse hypoxemia
90
Steroids in the treatment of Aspiration pneumonitis
Failed to demonstrate benefit on pulmonary function
91
What is not a component of acidic lung injury?
Infection is not a component of acidic
| lung injury
92
• “Prophylactic” antibiotics are proven to cause
resistant organism infection
93
Antibiotics started ONLY if clinical evidence of
| infection such as (3)
* Fever, ↑WBC
* Worsening CXR infiltrate
* Positive sputum gram stain
94
Minimizing risk factors of aspiration predisposing factors are
Emergency surgery
Difficult/failed tracheal intubation
Light anesthesia
GERD
95
____can happen just as often on emergence as induction
• Aspiration
96
• Small volumes __________ of_____ other than_____ and pulp containing juices consumed up to 2 hours
150 mL; 5.7 fluid ounces; fluid; milk
| before elective surgery do not ↑ the risk of aspiration in the otherwise healthy parturient
97
MINIMIZING RISK: CHOICE OF
| ANESTHESIA : General vs Regional
Risk of maternal death is approximately 17 times greater with general anesthesia compared with regional
98
Majority of general anesthesia
aspiration and/or hypoxemia injury
99
Non particulate antacid: ______citrate (Bicitra) can neutralize ______ml of HCL with a pH of _____
30 mL Na citrate [Bicitra] can neutralize 255 mL of hydrochloric acid with a PH of 1.0
100
Should be administered within
20 minutes of induction of GETA
101
Particulate antacid
(e.g.. Maalox, Mylanta) when aspirated causes serious pneumonitis!
102
MINIMIZING RISK: H-2 RECEPTOR ANTAGONISTS
Cimetidine
Ranitidine
Famotidine
103
H2 antagonists effect
reduces gastric acidity significantly approx. 30 minutes after IV administration maximal effect at 60-90 min
104
How does H2 antagonists work
Block histamine receptors on oxyntic cell → ↓diminish gastric acid production → leading to a slight ↓ in gastric volume in fasting patient
105
Duration of action of H2
is sufficiently long to cover emergence from GA for a Csection
106
PPIs
Omeprazole and lansoprazole
107
PPI and onset of action
Take forever to work PO
| But IV start of action similar to H2 antagonsist.
108
PPI MOA
inhibit the H+ pump on gastric surface of OXYNTIC CELL
109
PREVENT stomach from making further acid
H2 antagonists
110
You cannot give metoclompramide to this patients
Parkinson's
111
Cannot give metoclopramide in this type of GI disorder
Bowel obstruction
112
Class of metoclopramide
Central dopamine receptor antagonists
113
Metoclopamide effect
Increase LES tone
| Decrease gastric volume by increasing gastric peristalsis
114
Metoclopramide starts in
15 min
115
Major side effect of Metoclopramide is
EPS
116
What antagonize the effect of metoclopramide is
Prior admin with opiod and atropine
117
Guidelines for perinatal care (American College of Obstetrics & Gynecology, American Academy of Pediatrics)
“Patients in active labor should avoid oral ingestion of anything excepts sips of clear liquids, occasional ice chips, or moistening of mouth/lips”
118
Normal laboring patients should not
receive aspiration prophylaxis unless they are high risk for C-section
119
DISSEMINATED INTRAVASCULAR COAGULATION (DIC): ACQUIRED COAGULOPATHY
Results from an abnormal activation of the coagulation system
120
4 main issues with DIC
* Formation of large amount of thrombin
* Depletion of coagulation factors
* Activation of fibrinolytic system
* Hemorrhage
121
Progression of DIC
• If severe enough, diffuse microvascular thrombosis → end-organ injury
122
Effect of systemic activation of coagulation (ID)
Intravascular deposition of fibrin -->Thrombosis of small and midsize vessels and organ failure
Depletion of platelets and anticoagualtion factors-> Bleeding
123
DIC: OBSTETRIC ETIOLOGY
```
• 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
DIC:pathophysiology
• Complicated & poorly understood
125
• Obstetric “triggers” of DIC
include entry of procoagulant tissue extracts and into the blood which interact with Factor VII and activate the extrinsic coagulation pathway
126
• Dead tissue and amniotic fluid contains
thromboplastic substances that trigger
| coagulation.
127
DIC generates
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
What does proinflammatory cytokines cause?
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
Lab findings: Change how fast?
* ↓Plt count
* ↓ fibrinogen and antithrombin III concentrations
* Variable ↑ in PT, aPTT, and thrombin and reptilase times
* ↑ levels of D-dimer, fibrin and FDP
130
Coagulation consumption
* Accelerated turnover of various factors
| * Levels at any given time depend upon rate of destruction and repletion
131
The Proteins other than coagulation factors may be depleted due to DIC
* Antithrombin 3
* Fibronectin
* Plasminogen
132
DIC pathophysiology (arrow)
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
Does not reflect severity of DIC_________
Platelet count depression
134
Thrombocytopenia may result from processes other than clot function
* Adhesion to damaged endothelium
| * Intravascular platelet “clumping"
135
DIC PATHOPHYSIOLOGY: INTRAVASCULAR FIBRIN FORMATION
Formation of small strands/microclots of fibrin is the immediate result of DIC (may lead to obstruction of pulmonary vessels) Obstruction (DEAD SPACE)
136
Present with every patient wit DIC
Fibrinolysis
137
• Fibrin degradation products (FDP): (APID)
Protein fragments that;
• Act as antithrombins (↑ bleeding)
• Produce defective fibrin polymer (↑bleeding)
• Impair platelet clearance
• Directly damage pulmonary vasculature (ARDS!)
138
DIC: CLINICAL FEATURES OF ACUTE
| DIC
• Clinical emergency
• Bleeding of all kinds from anywhere in/on the body
•
139
Most common bleeding sites for DIC
Gums, epistaxis, GI, pulmonary, hematuria, cutaneous are most common sites
140
Chronic DIC
Intermediate between hypercoagulable state and acute DIC
141
more likely to produced clot
physiologic DIC
142
Differential dx of abrupt onset of severe bleeding
Rule out severe liver disease (elevated platelets, elevated PT)
143
Always the result of serious obstetric
DIC
144
Definitive treatment preeclampsia
Tx deliver baby
145
Definitive tx of Abruptio
Tx deliver baby and placenta
146
Tx of sepsis
ABT
147
Tx of retained products of conception
D and C
148
Ultimat cure of DIC
Treatment of primary disorder or Underlying condition
| Provide ventilation and multiorgan support
149
DIC supportive Treatment while you look for etiology if
Active bleeding or invasive procedure required
150
How do you treat bleeding in DIC with FFP
15-30ml/kg to maintain PT and aPTT 1.5 times normal values
151
How do you treat bleeding in DIC with CRyoprecipitate or Fibrinogen concentrate
Maintain fibrinogen above 150-200mg/dl
152
Platelets to maintain
platelet count above 50,000
153
Cryoprecipitate factors are
Fibrinogen
Von Willebrand (Factor VIII)
Fibronectin
154
Heparin only work if
Antithrombin III level is adequate
155
New agent in treatment of massive bleeding
rFVIIa (replacing cryo and FFPs)
156
EACA
prevents breakdonw of clotting (aminocaproic and tranxemic acid)
157
Better throughout pregnancy Warfarin vs heparin
Heparin or LMWH
158
If on warfarin
D/C before onset of labor
159
If onset of labor occurs and patient is on warfarin
Revers with Vit K and IV prothrombin complex concentrate (PCC)
160
What is better warfarin vs Four-factor concentrte
Four factor Prothrombin concentrate (KCENTRA) better option for warfarin reversal than FFP
161
If condition require immediate reversal of anticoagulatio
IV protamine 12.5-50mg administered
162
Protamine reversal of heparin CONTRAINDICATED to
allow administration of neuraxial anesthesia is NOT RECOMMENDED.
163
Reversal of lovenox with protamine sulfate is
not predictable
164
If patient with an ISOLATED laboratory abnormality and no clinical evidence of coagulopathy what is the next step? What should you monitor closely
Can do NEURAXIAL anesthesia
| Do frequent neuro assessment to facilitate early detection of EPIDURAL hematoma during the postpartum period.
165
IF the patient has DIC no
spinal anesthesia
| Alternative GA
