GI Case Management Flashcards
Oropharyngeal Diseases
Patients with pharyngeal dysphagia more prone to regurgitation, aspiration esp in cases where large space-occupying lesion compressing CN IX, X – responsible for series of involuntary movements that transport food bolus into stomach, protect airway during swallowing
Why Mandiblectomies Prone to Hemorrhage
inferior alveolar artery (br mandibular artery) runs through ramus of mandible, almost always transected during surgery
Coags before sx
Why Maxillectomies Prone to Hemorrhage
transection of either or both major palatine artery, infraorbital artery
o Transection depends on location of tumor
o Both = branches of maxillary artery
Rostral maxillectomy: diffuse bleeding from highly vascularized nasal turbinates
Oral Pharyngeal Dz and Intubation
Potential challenges for intubation- retrograde
eg TMJ ankylosis, MMM
o Puncture cricothyroid membrane with needle or IVC
o Insert guide wire through needle and advanced retrograde through mouth opening then feed ET over guide wire into larynx
o Remove guidewire so further advanced ET into trachea
Reflex Assoc with Maxillofascial Sx
trigeminovagal reflex (rarely reported in vet med)
Bezold-Jarish Reflex
stimulation of [ventricular] cardiac chemoR or stretch R (mechanoR) – induction of sinus bradycardia, hypotension, peripheral VD
Bainbridge Reflex
increase HR caused by rise in BP in great veins as enter RA
Fluid Bolus
Vasovagal Reflex
decrease in venous return to heart (hypovolemia, compression of caudal VC, regional analgesia) – sinus bradycardia, vasodilation
Esophageal Composition
o Dogs: striated m
o Cats, pigs, horses, primates: proximal 2/3 striated m, distal 1/3 SmM
Muscles that Compose UES
cricopharyngeus, thyropharyngeus m
What is the most common cause of benign esophageal stricture in dogs, cats?
GA-related GER –> esophagitis
Esophagitis Related to GER
esophageal mucosa exposed to caustic substances for prolonged periods +/- esophageal defense mechanisms (EDMs) impaired/overwhelmed
What are esophageal defense mechanisms?
superficial mucus/bicarb layer, tight junctions btw epithelial cells, intracellular/interstitial buffering capacity dependent on BF
Incidence, Consequence of GER/esophagitis?
Signs: days to three weeks to appear
Mortality: 21-30%, low incidence (~0.1%)
Greater risk with intraabdominal sx, esp OVH
CS perforation: pneumothorax, pleuritis, pyothorax, resp distress
MOA GER Esophagitis
Reduced LES pressure allows contents to enter esophagus more easily
Swallow reflex absent; acidic gastric acid contents (pH <4) cannot be neutralized by patient swallowing basic saliva
Reduced esophageal peristalsis
Factors that Increase GER/Decrease LES Pressure
Older or younger animals
Dogs >40kg
Large, deep chested dogs esp in sternal recumbency
Dorsal recumbency
Change in Position During GA
Prolonged fasting times (>10hr), shorter fasting times (3h)
Intraabdominal sx, including laparoscopy
Ax duration >105’
GA during second half of pregnancy
What percentage of animals that experience GER will actually regurgitate?
Only 0-15% in patients experiencing GER will actually regurg
Incidence of GER in dogs, cats without hx of GI or esophageal dz: 12-67% based on esophageal pH meters
Treatment of Esophagitis/GER
H2RA tachyphylaxis may occur in 3-13d – PPIs more effective at treating reflux esophagitis, maintaining effects on pH
Should you include an anticholinergic indiscriminately in your canine, feline premeds?
NO!
Decreases LES tone
Minimal effect on gastric pH at clinical doses – higher doses, will inhibit H plus secretion by gastric parietal cells via M1
Congenital or Idiopathic ME
defect of vagal sensory innervation where esophageal peristalsis does not occur, no detection of dilation caused by food bolus
Acquired Megaesophagus
mechanical obstruction –> Vascular ring anomaly, esophageal stricture, hiatal hernia, tumor, granuloma, FBs
* Over time, dilation of esophagus proximal to lesion becomes irreversible
Idiopathic acquired: most common form in adults – loss of normal esophageal motility eventually results in dilation
Secondary to/assoc with other diseases:
* Peripheral neuropathy, laryngeal paralysis, MG, severe esophagitis, lead poisoning, lupus myositis, chronic/recurrent GD or GDV
Main Anesthetic Concerns Assoc with ME
GER, regurg, aspiration
Prolonged fasting not necessary: dysmotility, dilation prevent complete emptying of esophageal contents
Potential for repeated episodes of asp pneumonia, greater risk for postop hypoxemia
Stricture Ballooning/Upper GI Endoscopy
o Pyloric sphincter tone may increase with pure MOR agonists, ketamine
o Gastric distention: hypoventilation, decreased venous return; vagal nerve stimulation from distended viscous
o Overdistention of GIT = activation of stretch R within walls, sudden/profound vagally-mediated bradycardia, tx: immediate deflation, atropine
o Inflation of hollow viscus with air = dull cramping pain of poorly localized discomfort ; Intraop analgesia +/- TAP block: more stable plane of ax
Laparoscopy - Effects of CO2 Insufflation
Decrease venous return, impair ventilation
Increase in SVR, decreased preload, potential for hypotension
Decreases FRC, reduced compliance – predisposed to VQ mismatch
Cranial displacement of diaphragm – more difficult for SpV to maintain adequate minute ventilation, IPPV may be required
PPV: decreases HBF
CO2 freely diffuses into splanchnic circulation
Levels of Abdominal Pressure Assoc with Laparoscopy
Intraabdominal pressure 10-16 mmHg, HBF increased >12mm Hg (humans)
o Ideally want intraabdominal pressure as low as possible
o Decrease in blood flow to GIT
o Decreased GFR = AKI
Transient increases in hepatic transaminases up to 48hr after desufflation
o Increases in ALT, AST directly proportional to intra-abdominal pressure, duration of insufflation
Other Effects of Laparoscopy
VQ mismatch: potential for large differences btw ETCO2, PaO2, worse with Trendelenburg
Increased ICP
Hypercapnia
Air Embolism
Air Embolism with Laparoscopy
Absorption of CO2 via ruptured blood vessel, etc: rapid absorption of CO2 into tissues (as opposed to nitrogen) means that it seldom causes clinical problems
Microemboli don’t cause as severe issues as pass through right side of heart»_space; Wedge in pulmonary vessels where they create V/Q mismatching/ pulmonary hypertension/ atelectasis, can be eliminated through lungs
Large gas emboli can become lodged in RA or RV or PA where they stop passage of blood through the heart»_space; Rapidly fatal
If reach systemic circulation, obstruct BF - cause hypoxia in critical organs (eg cerebral, coronary arteries most vulnerable)
Tolerable Levels of Air in Circulation
0.35mL/kg/min in dogs, pigs 2mL/kg
How Reduce Risk of Embolism with Laparoscopy
by slowing rate of abdominal insufflation to <1 L/min more time for pulmonary clearance of air bubbles
Diagnosis of Air Embolism
Behavior changes (agitation, change in demeanor)
changes in ETCO2 readings (V/Q mismatch with rapid drop in CO2 when ventilation held constant)
development of mill-wheel heart murmur (harsh, churning, splashing, metallic)
Hypotension, tachypnea
TEE = definitive diagnosis
Treatment of Air Embolism
Remove insufflated gas from abdomen
Address any non-ligated vasculature
increase CVP (to encourage bleeding rather than air entrainment)
discontinue N2O admin, administer 100% O2
Nitrous and Air Emboli
Admin of N2O: exacerbates gas emboli as diffuses into air pockets, expands them
Induction and Maintenance of Patients with GDV, Splenic Masses
TP, propofol sensitize myocardium to catecholamine-assoc arrhythmias
o Also why des, iso, sevo preferred for maintenance vs halothane
* DO NOT INDUCE VIA INHALANT TECHNIQUE
Pathogenesis of SI Intraluminal Obstruction
Intestine rostral to FB extends with gas, fluid (fluid DT increased secretion from intestinal glands, retention of fluid)
Fluid shifts from serosa into peritoneal cavity
Circulation in mucosa becomes ischemic, wall necrosis possible
Bacterial overgrowth, may translocate if normal mucosal barrier impaired by distention, ischemia
Consequences of Manipulation, Derotation of Ischemic Bowel
release of numerous inflammatory mediators that cause VD, cardiac dysfunction
Ischemic reperfusion injury, endotoxemic shower/shock
Lidocaine CRI, dexmedetomidine CRI
Analgesia in Abdominal Sx
Innervation: sympathetic chain T1-L3/4, abdominal wall innervation T11-13/L1-3
Innervated primarily by C fibers: poorly localized, may be assoc with autonomic responses DT adjacent travel with ANS fibers
Stimulus from distention, contraction, inflammatory mediators, ischemia
Referred pain: distant from source, DT convergence of afferent nerve pathwas onto same DH neurons
Pathophysiology of GDV
Gastric distention, torsion – compromised BF to stomach, surrounding organs
CV compromise DT obstruction of (low pressure) caudal VC, portal vein, splenic veins
Obstruction of vessels = decreases venous return, increased venous pressure –> severe hypovolemic shock, decreased oxygen delivery
DO CO, hypotension + splanchnic pooling/portal hypertension = interstitial edema, loss of IV volume
o Distention of stomach, increased abdominal pressure restricted ventilation via interference with diaphragmatic excursion
Respiratory compromise, possible partial lung collapse
Decreased VT, VQ mismatch – hypercapnia, hypoxemia despite increased RR, effort
Consequences of GDVs
- Arrhythmias
- Hemoabdomen - rupture of short, large bore gastric arteries
- Mixed Acid, base Disturbances
- Splenic Compromise/Vascular avulsion
Arrhythmias Assoc with GDV
Common – mainly ventricular, ~40% of GDV dogs
Coronary BF decreased by 50% in GDVs: myocardial ischemia establishes ectopic foci of electrical activity
* Supported by elevated cardiac troponins in GDV
Also circulating catecholamines, pro inflammatory cytokines
Tx: >160, multifocal, R on T, impact on hemodynamic status – lidocaine bolus, CRI
Acid Base Disturbances with GDV
- Initial hypochloremic metabolic alkalosis – sequestration of gastric HCl DT outflow tract obstruction, vomiting, salivation
- High anion gap (lactate) acidosis secondary to low DO2
–Ischemia, contributions from release of inflammatory mediators - Respiratory acidosis from hypoventilation, hypercapnia
Also hypokalemia
MOA hypokalemia with GDV
administration of large volumes of low K containing fluids, loss of K via vomiting, hypochloremic metabolic alkalosis with transcellular shifting, RAAS activation, catecholamine-induced intracellular shifting of K+
Gastric Necrosis with GDV
when >1 hemostatic test abnormal, lactate greatly elevated at presentation +/- fails to decrease significantly with fluid resuscitation predicting a poor outcome
MOA: gastric wall tension exceeds driving pressure in gastric wall arterioles, capillaries
Reduced CO –> gastric necrosis –> increased mortality
Risk Factors Assoc with Badness in GDVs
hypotension during hospitalization, combined splenectomy + partial gastrectomy, peritonitis, sepsis, DIC
Consider avoidance of hyperoxia – greater damage following reperfusion in patients maintained at higher than normal O2 levels
GI Neoplasia Considerations
Main considerations with GI Neoplasia:
*Hypercalcemia of malignancy
–Muscle tremors, weakness, arrhythmias
*Hypoproteinemia
*Anemia
*Monitor BG with GI stromal tumors - secrete insulin, also lymphoma, leiomyomas
*MCTs: histamine release
Hemoabdomen: volume replacement with crystalloids
3x volume for acute hemorrhage
8x gradual loss affecting intracellular volume
Losses 20-30% total blood volume replaced with FWB, plasma, colloids + pRBCs
Mesenteric Traction Syndrome
tachycardia, hypotension, cutaneous hyperemia in humans undergoing abdominal surgery
Release of prostacyclin, histamine, other vasoactive substances cause fluctuations in hemodynamic status when tension placed on mesenteric vasculature
Mortality with Septic Abdomen
31-64%
Higher survival rates with secondary peritonitis treated surgically vs medical management, primary peritonitis
Other risk factors: pre‐existing peritonitis, low albumin/protein levels, intraoperative hypotension, hyperlactatemia
Diagnosis of Septic Abdomen
AXR/AUS – specific lesion with or without effusion in secondary peritonitis
Confirmation: septic infiltrate cytology of peritoneal effusion or lavage fluid
Lactate often increased in serum +/- abdominal fluid.
Peritoneal lactate, comparison of serum with peritoneal lactate diagnostic in ≥90% of dogs, not accurate in cats
Sepsis
presence of SIRS in response to most often bacterial but fungal or protozoal infections
o May progress to severe sepsis with multiple organ dysfunction (MODS), poor perfusion, hypotension
Septic Shock
Acute circulatory failure, persistent arterial hypotension despite volume resuscitation assoc with sepsis
SAP <90, MAP <60
Bacteremia
Presence of live bacterial organisms in bloodstream
Sepsis Definition
Clinical syndrome caused by infection, host’s systemic inflammarioty response to it
May be bacterial, viral, protozoal, fungal in origin
SIRS - definition
Clinical signs of SIRS to infectious or noninfectious insults
MODS - def
Physiologic deranges of endothelial, cardiopulmonary, renal, nervous, endocrine, GI systems assoc with progression of uncontrolled systemic inflammation or DIC
Hypovolemic Shock
Decrease in circulating blood volume
hemorrhage, severe dehydration, trauma
Cardiogenic Shock
Decrease in forward flow from heart
CHF, arrhythmias, tamponade, drug overdose
Distributive Shock
Marked decrease or increase in SVR or maldistribution of blood
Sepsis, anaphylaxis, obstruction (HW dz, saddle thrombosis), catecholamine excess, GDV
Metabolic Shock
Deranged Cellular Metabolic Machinery
Hypoglycemia, cyanide toxicity, mitochondrial dysfunction, cytopathic hypoxia of sepsis (maybe MH)
Hypoxemia Shock
Decrease in PaO2
Anemia, severe pulmonary dz, CO toxicity, methemoglobinemia
Type I Hyprsensitivity Run
Immediate, IgE dependent - histamine release
Anaphylaxis
Type II Hypersensitivity Run
Cytotoxic, IgG, IgM dependent
Type III Hypersensitivity Run
Immune complex mediated, IgG/ IgM complex dependent
Type IV Hypersensitivity Run
Delayed, T lymphocyte dependent
Type IV Hypersensitivity Run
Delayed, T lymphocyte dependent
Histamine Receptors
H1, H2, H3
Role of H1
● Mediate coronary artery VC, cardiac depression
● Rhinitis
● Pruritus
● Bronchoconstriction
● Stimulation causes endothelial cells to convert L-arginine into NO (potent vasodilator)
Role of H2
gastric acid production
produce systemic coronary and systemic vasodilation, increases in HR/ventricular contractility
Role of H3
On presynaptic terminals of sympathetic effector nerves that innervate heart, systemic vasculature
These receptors inhibit endogenous norepi release from sympathetic nerves, so activation accentuates degree of shock observed during antigen challenge because compensatory neural adrenergic stimulation is blocked
Role of Epi in Anaphylaxis
Stimulation of beta-adrenergic receptors enhances production of adenyl cyclase, subsequent conversion of adenosine triphosphate to cAMP
Inhibits antigen-induced release of histamine and other anaphylactic mediators
Improvement in MAP attributed to increase in CO from epi’s beta adrenergic effects on the heart, not its alpha 1 vasoconstrictive effects on systemic vasculature
Pathophysiology of Sepsis
organisms +/- toxins gain access to circulation
Classic explanation: release of endotoxin from Gram-negative organisms (LPS) and exotoxins/peptidoglycans from Gram-positive organisms
Activation of WBCs > release of potent inflammatory mediators
Damage to microvascular endothelium = loss of control of permeability, develop coagulopathy
Body generates anti-inflammatory response to maintain homeostatic balance: initially SIRS phase, then CARS phase
SIRS Phase
Initially: ‘hyperdynamic’ stage (in dogs) with increased CO, tachycardia, vasodilation (bright red MM), shortened CRT
CARS Phase
counter anti-inflammatory response syndrome, immunosuppressive phase
What happens following hyper dynamic phase of shock?
Proinflammatory effects overwhelm anti‐inflammatory response = CV collapse ensues with continued VD, myocardial dysfunction, poor perfusion, decreased CRT, bluish or pale MM, obtundation, hypothermia.
MODS
Progressive, potentially reversible dysfunction of two or more organ systems after acute life threatening disruption of homeostasis
Dysfunction of either respiratory, CV, renal, coag system independently associated with significantly increased odds of death
MOA MODS
Systemic activation, dysregulation of inflammatory cascade causes organ dysfunction and failure
Combined effect of inappropriate host defense response, dysregulation of immune/inflammatory responses leads to cell injury, tissue and organ failure
One Hit Model
Massive initial insult - major trauma, septic peritonitis
Two Hit Model
Multiple insults over short period of hours to days, eg major trauma followed by aspiration pneumonia
Second hit induces exaggerated inflammatory response, immune dysfunction
Three Hit Model
Sustained eg drug resistant bacterial infection
Cryptic Shock
Loss of hemodynamic coherence leading to hyperlactatemia, acidemia despite normal perfusion parameters
Normalization of CV parameters may not equate to improvements in microcirculatory perfusion – macrocirculation vs microcirculation
GIT and Role in SIRS
important role in generation of SIRS, sepsis even when intestinal serosa intact, primary source located elsewhere
Inflammation damages barrier function of GI mucosal lining – allows absorption of non-microbial factors into lymphatic system
Eventually drain into venous system via thoracic duct
Pathway contributes to magnification of ongoing SIRS, resp distress/dysfunction, MODS
Translocation of bacteria, bacterial product thought to occur via lymphatics vs portal system - not necessary for development of SIRS/MODS
SIRS Parameters in Dogs
Need at least 2
HR >120bpm
RR >40, PaCO2 <30
T <100.4, >104
Leukogram >18,000 or <5000
SIRS Parameters in Cats
Need at least 2
HR <140, >225
RR >40
T <100, >104
WBC >19,000 or <5000
Goals of Resuscitation Therapy
MAP >65mm Hg, central venous O2 saturation >70%, CVP 8-12mm Hg, urine output >0.5mL/kg/hr
First line therapy choice = Balanced crystalloid electrolyte solution
+/- albumin if protein/albumin low
4 Main MOA of Refractory Hypotension with Sepsis
- Unregulated synthesis of NO (increased with acidosis)
- Local acidosis from anaerobic metabolism - electrolyte changes prevent SmM contraction
- Activation of AC - prevents increased intracellular Ca
- Depletion of VP from neurohypophysis
MOA for refractory hypotension: acidosis
Local acidosis with hydrogen, lactic acid production from anaerobic metabolism
Opens ATP sensitive K channels in vascular SmM
Allows influx of K, prevents Ca from entering cells – SmM does not contract, vasoplegia
Hyperpolarization of vascular SmM cells
MOA for refractory hypotension: activation of AC, prevention of increased intracellular Ca
Prostaglandin, prostacyclin concentrations increase which activates adenylyl cyclase
AC –> stimulates formation of cAMP, activates PKA and prevents increase in cytoplasmic Ca leading to vasodilation
MOA for refractory hypotension: depletion of VP
Concentration increases 20 to 200 fold in hypotensive states, acute septic shock to help maintain vasoconstriction
Levels rapidly depleted, deficiency may contribute to pathogenesis of irreversible shock
Synthetic VP
V1A R in SmM – intense nonadrenergic VC at endothelial level, preferentially constricts arterioles in extracerebral tissues
Decrease in inducible NO synthase activity, inhibits VD in septic shock
Also modulates Na/KATP channels, potentiates adrenergic or other vasoactive agents, allows for decreased dose of other catecholamines, effective in presence of acidemia
CIRCI
Critical Illness-Related Corticosteroid Deficiency
Inadequate endogenous corticosteroid activity in relation to severity of patient’s illness
Corticosteroids = necessary for responsiveness to vasopressor therapy
Underlying pathophysiology unknown
Potential MOAs CIRCI
HPA dysfunction
Alterations in cortisol-plasma protein binding
Changes in glucocorticoid receptor function
Target cell enzymatic changes
Decreased production of ACTH, corticotropin releasing hormone, cortisol
Adrenal damage from infarction, hemorrhage
Adrenal suppression from chronic exogenous glucocorticoid administration
Inflammatory cytokines causing systemic inflammation associated with glucocorticoid release
Vasopressor Therapy in Sepsis
VPs: NE > epi > VP
Dopamine, phenylephrine not recommended in humans
No difference found with use of various VPs in animals
Lowest effective dose to avoid ischemia, mask persistent hypovolemia
Inotropes: myocardial depression
Alterations in BG: hyper or hypoglycemia – maintain normal levels
Relative adrenal insufficiency occurs in sepsis: consider physiologic doses of steroids
POI
horses, rabbits, ruminants, humans
Drugs: anticholinergics, opioids, a2, inhalants, N2O, induction agents
Which drug does not induce POI?
KETAMINE
Opioids and POI
delay gastric emptying, increase sphincter tone, variably affect SmM ctx
Inhibit propulsive motility, enhance segmental contractions esp in colon
Absorption increased, secretions decreased
Constipation: frequent SE
Epidural morphine: much faster return of GI motility in dogs, humans
Return of GI Motility
Dogs: distal intestine/colon first > proximal intestine stomach
MOA of POI
Paralysis of muscularis externa layer
Local inflammatory response within muscularis layer after intestinal handing
Resident macrophage activation proportional to intensity of damage
Increases NO –> Decreases motility
Exacerbated by effects of anesthetic agents on motility, presence or development of peritonitis/sepsis
