ASPIRATION and DIC Flashcards
What is the single most important factor leading to the decrease in aspiration ?
Neuraxial Anesthesia
A decrease incidence of aspiration due to multiple factors include (MARIN)
More neuraxial anesthesia Antacids prophylaxis RSI for GETA Improve training NPO policies
Regulation intubation vs RSI
RSI
- normal ventilation
- Muscle relaxants are given right away
If you give can ventilate
Use LMA (worst case scenario) Wake them up
Anesthesia maternal mortality related to
Airway issues
Prior to 1990, most common cause of anesthesia related death was
aspiration
Morbidity and mortality from aspiration depends on
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
Esophagus about _____long
40cm
Muscular shincters at both ends normally _______
Closed
What is the role of the CRICOPHARYNGEAL SPHINCTER?
prevents entry of air into esophagus during respiration
Decrease Esophageal sphincter is usually
8-20mmHg above gastric pressure
What is the hormone responsible to relaxes
Relaxin and progesterone
You get more air at the end of a case because of
Nitrous Oxide (thats why its contraindicated in pneumothorax)
Capacity of stomach is about ______why?
1-1.5L ; ability to stretch
Propulsion of food is via _____not _____
peristalsis ; gravity
Peristalsis is the
contractile ring of muscular activity progressing down the gut
Pyrolus closes midway through contraction wave allowing
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
What occurs with Large particles?
lag behind in retrograde fluid
Which kind of molecules move faster ?
Fluids and small particles exit the stomach faster than larger particles
Also affects exit of particles is the ___
Viscosity of suspension
What limits outflow
Tone and anatomical position of pylorus
_____always higher than most dependent portion of stomach
• Pylorus
Gastric Bypass patients usually at risk for
DUMPING SYNDROME
Up to _____highly acidic fluid is produced per day
by the stomach
1500 ml
Pyloric glands : Chief cells secrete
• Chief cells secrete
pepsinogen →pepsin
Oxyntic glands: Oxyntic cells secrete
• Oxyntic cells secrete with a ph of ______
HCl (pH 0.8)
This is where PPIs work
Oxyntic glands and Oxyntic cells
Vagus stimulates G cells to secrete
__________ →bind to________ and stimulates_______
gastrin; oxyntic cells ; HCl secretion
H-2 receptors______cAMP, _____calcium → dramatic________
acid production
↑; ↑; ↑
Ach binds to________ and________ Ca2+
muscarinic receptors; ↑
• Histamine potentiates both
gastrin and acetylcholine
When you antagonize H1
Tachycardia
Agonizing H1 leads to
Bradycardia
Acid is secreted at a ______________ ____of approximately __________ of ________even
when stomach is empty
Low basal rate of approximately 10% of maximal output,
Diurnal variation means acid
lowest in morning, highest in evening (take antacids @hs)
↑ dramatically with
ingestion
Cephalic phase:
Gastric acid output ↑ to_______
chewing, smelling, or tasting without significant ingestion ↑ vagal stimulation; 55% of peak levels
Gastric phase is the
entry into stomach of ingested contents, acid output peaks
• Intestinal phase:
begins with movement of food into small intestine
What are the 3 phases of digestion
Cephalic
Gastric
Intestinal
3 things Normally slowing GASTRIC EMPTYING :
↑ lipid content
↑ caloric load
Large particle size
*****Gastric emptying is
NOT slowed during pregnancy
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)
↑ progesterone
Relaxes ↓ esophageal sphincter
• GERD
Basal gastric acid secretion between
pregnant and nonpregnant women
No significant differences in basal gastric acid secretion
What are the mechanical effects of expanding uterus
- Increasing intragastric pressure
* Distorts normal anatomic relationship of esophagus/diaphragm/stomach
During labor always assume
Decrease GASTRIC EMPTYING
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
Mendelson demonstrated that sequelae from aspiration of liquids compared to solids were
more severe clinically and pathologically when the liquid was highly acidic
Aspirates with a pH _______ cause a granulocytic reaction
pH ↓ than 2.5
• General rule of Aspiration pneumonitis
pH < 2.5
gastric volume > 25 mL
pH somewhat evidence based, but gastric volume is not but
↓ is always better
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.”
Aspiration pneumonitis: CXR
• CXR: “irregular soft mottled shadows without mediastinal shift
Clinical course Aspiration pneumonitits =
chemical injury from sterile acid gastric contents
Basic aspirate_____ surfactant levels
↓
Aspiration pneumonitis MOA:
↑ intra-alveolar water and protein content and a loss of lung volume = ↓ in pulmonary compliance and intrapulmonary shunting of blood
Bronchial obstruction due to
Cellular debris and bronchial denuding
Pathophysiological disturbances following Aspiration pneumonitis
EBDSHII
Exudative pulmonary edema bronchial obstruction ↓ lung compliance, and shunting → Hypoxemia ↑pulmonary vascular resistance increased work of breathing
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
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
The activation of neutrophils release
oxidants, proteases, leukotrienes, and other proinflammatory molecules
Aspiration pneumonitis content is
STERILE
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
Aspiration signs : if in Semi-recumbent or upright which part of lung is usually injured?
injury to lower lobes
What is the most common site of aspiration?
RLL most common site of aspiration d/t large size of right mainstem bronchus
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)
In aspiration pneumonitis PaO2 ↓
•
secondary to ↑ shunt
85-90% of patients eventually develop______when ?
abnormal CXR; CXR is often normal until 12-24 hours after aspiration
Recovery of Aspiration pneumonitis involves
proliferation and differentiation of surviving type II pneumocytes in alveolar epithelial cells
Aspiration pneumonitis Soluble proteins are removed by
paracellular diffusion and endocytosis
Aspiration pneumonitis Insoluble proteins are removed by
macrophages.
Aspiration pneumonitis Neutrophils are removed by
programmed cell death and phagocytosis by macrophages
________gradually restore normal composition of surfactant
• Type II pneumocytes
Aspiration pneumonitis, how is Na+ and H2o removed
Actively transport Na+ out of alveolus, water follows
Most common site of aspiration is
right
Pathophysiology of Acidic liquid aspiration : Acidic liquid aspiration injures______leading to ______
(FACER)
alveolar epithelium → alveolar exudate (edema,
albumin, fibrin, cellular debris, and RBCs)
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
ASPIRATION : NEUTRAL NONPARTICULATE LIQUID
MSN
- Neutral aspirate → alveolar exudate with minimal damage to the alveoli
- Slight ↑ in shunt and ↓ in PaO2
- Minimal pathologic changes
PATHOPHYSIOLOGY: PARTICLE ASPIRATION; large
Direct airway obstruction from larger particles = atelectasis
OBSTRUCTING LARGER AIRWAYS
PATHOPHYSIOLOGY: PARTICLE ASPIRATION: SMALL
Smaller particles: similar response as with acidic liquid
Causes exudative neutrophilic response at
levels of bronchioles and alveolar ducts
Small particles aspiration causes
Causes exudative neutrophilic response at levels of bronchioles and alveolar ducts leading to pulmonary edema
ARDS Clinical diagnosis criteria
within1 week of known clinical insult
ARDS Chest imaging clinical diagnosis of ARDS
Bilateral opacities NOT EXPLAINED by effusions
Biochemical ARDS PAO2/FIO2 ratio
<300 with CPAP or PEEP >5 cm H20
Origin of pulmonary edema: ARDS with diagnosis
Not explained by cardiac failure or overload.
Aspiration pneumonitis Treatment: when is it appropriate to do a rigid bronchoscopy?
Only if large particles obstruct airway
What does not help in the treatment of Aspiration pneumonitis
Lavage with saline/bicarbonate: does not remove acid, can worsen hypoxemia
Shunting + Hypoxemia treated with
positive pressure (CPAP or PEEP with supplemental oxygen), help decrease shunting . It improves FRC, reduces pulmonary shunting, reverse hypoxemia
Steroids in the treatment of Aspiration pneumonitis
Failed to demonstrate benefit on pulmonary function
What is not a component of acidic lung injury?
Infection is not a component of acidic
lung injury
• “Prophylactic” antibiotics are proven to cause
resistant organism infection
Antibiotics started ONLY if clinical evidence of
infection such as (3)
- Fever, ↑WBC
- Worsening CXR infiltrate
- Positive sputum gram stain
Minimizing risk factors of aspiration predisposing factors are
Emergency surgery
Difficult/failed tracheal intubation
Light anesthesia
GERD
____can happen just as often on emergence as induction
• Aspiration
• 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
MINIMIZING RISK: CHOICE OF
ANESTHESIA : General vs Regional
Risk of maternal death is approximately 17 times greater with general anesthesia compared with regional
Majority of general anesthesia
aspiration and/or hypoxemia injury
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
Should be administered within
20 minutes of induction of GETA
Particulate antacid
(e.g.. Maalox, Mylanta) when aspirated causes serious pneumonitis!
MINIMIZING RISK: H-2 RECEPTOR ANTAGONISTS
Cimetidine
Ranitidine
Famotidine
H2 antagonists effect
reduces gastric acidity significantly approx. 30 minutes after IV administration maximal effect at 60-90 min
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
Duration of action of H2
is sufficiently long to cover emergence from GA for a Csection
PPIs
Omeprazole and lansoprazole
PPI and onset of action
Take forever to work PO
But IV start of action similar to H2 antagonsist.
PPI MOA
inhibit the H+ pump on gastric surface of OXYNTIC CELL
PREVENT stomach from making further acid
H2 antagonists
You cannot give metoclompramide to this patients
Parkinson’s
Cannot give metoclopramide in this type of GI disorder
Bowel obstruction
Class of metoclopramide
Central dopamine receptor antagonists
Metoclopamide effect
Increase LES tone
Decrease gastric volume by increasing gastric peristalsis
Metoclopramide starts in
15 min
Major side effect of Metoclopramide is
EPS
What antagonize the effect of metoclopramide is
Prior admin with opiod and atropine
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”
Normal laboring patients should not
receive aspiration prophylaxis unless they are high risk for C-section
DISSEMINATED INTRAVASCULAR COAGULATION (DIC): ACQUIRED COAGULOPATHY
Results from an abnormal activation of the coagulation system
4 main issues with DIC
- Formation of large amount of thrombin
- Depletion of coagulation factors
- Activation of fibrinolytic system
- Hemorrhage
Progression of DIC
• If severe enough, diffuse microvascular thrombosis → end-organ injury
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
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
DIC:pathophysiology
• Complicated & poorly understood
• 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
• Dead tissue and amniotic fluid contains
thromboplastic substances that trigger
coagulation.
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.
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.
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
Coagulation consumption
- Accelerated turnover of various factors
* Levels at any given time depend upon rate of destruction and repletion
The Proteins other than coagulation factors may be depleted due to DIC
- Antithrombin 3
- Fibronectin
- Plasminogen
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
Does not reflect severity of DIC_________
Platelet count depression
Thrombocytopenia may result from processes other than clot function
- Adhesion to damaged endothelium
* Intravascular platelet “clumping”
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)
Present with every patient wit DIC
Fibrinolysis
• 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!)
DIC: CLINICAL FEATURES OF ACUTE
DIC
• Clinical emergency
• Bleeding of all kinds from anywhere in/on the body
•
Most common bleeding sites for DIC
Gums, epistaxis, GI, pulmonary, hematuria, cutaneous are most common sites
Chronic DIC
Intermediate between hypercoagulable state and acute DIC
more likely to produced clot
physiologic DIC
Differential dx of abrupt onset of severe bleeding
Rule out severe liver disease (elevated platelets, elevated PT)
Always the result of serious obstetric
DIC
Definitive treatment preeclampsia
Tx deliver baby
Definitive tx of Abruptio
Tx deliver baby and placenta
Tx of sepsis
ABT
Tx of retained products of conception
D and C
Ultimat cure of DIC
Treatment of primary disorder or Underlying condition
Provide ventilation and multiorgan support
DIC supportive Treatment while you look for etiology if
Active bleeding or invasive procedure required
How do you treat bleeding in DIC with FFP
15-30ml/kg to maintain PT and aPTT 1.5 times normal values
How do you treat bleeding in DIC with CRyoprecipitate or Fibrinogen concentrate
Maintain fibrinogen above 150-200mg/dl
Platelets to maintain
platelet count above 50,000
Cryoprecipitate factors are
Fibrinogen
Von Willebrand (Factor VIII)
Fibronectin
Heparin only work if
Antithrombin III level is adequate
New agent in treatment of massive bleeding
rFVIIa (replacing cryo and FFPs)
EACA
prevents breakdonw of clotting (aminocaproic and tranxemic acid)
Better throughout pregnancy Warfarin vs heparin
Heparin or LMWH
If on warfarin
D/C before onset of labor
If onset of labor occurs and patient is on warfarin
Revers with Vit K and IV prothrombin complex concentrate (PCC)
What is better warfarin vs Four-factor concentrte
Four factor Prothrombin concentrate (KCENTRA) better option for warfarin reversal than FFP
If condition require immediate reversal of anticoagulatio
IV protamine 12.5-50mg administered
Protamine reversal of heparin CONTRAINDICATED to
allow administration of neuraxial anesthesia is NOT RECOMMENDED.
Reversal of lovenox with protamine sulfate is
not predictable
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.
IF the patient has DIC no
spinal anesthesia
Alternative GA
