GI/Liver Flashcards
Post op jaundice causes
Prehepatic: hematoma abs, hemolytic transfusion rxn (increased indirect unconjugated bili-delayed or acute
Hepatic:
- Chonic dz (viral hepatitis)
- Ischemic or hypoxic injury/sepsis (would see abnl LFT’s/coags/plts indicating liver dysfunction)
- Drug induced (can detect this from reviewing records for drugs such as a-methyldopa, Tylenol, chloramphenicol, isoniazid, sulfonamides, and of course r/o halothane for anes record.)
- Inborn errors of metabolism (gilberts-unconjugated hyperbillirubemia), crigler Najjar (decreased or absent gluonyl transferase, unconjugated hyerbili), n dubin johnson-conjugated hyperbil
- Intrahepatic cholestasis
post hepatic
Cholecystitis, Common Bile duct stone, Pancreatitis (would see conjugated hyperbiirubinemia)
Etio of hemodyamic changes during esophagectomy
cardiac/great vessel compression
vagal stimulation
hemorrhage
dysarrthymias
PTX
epidural
synthetic liver fxn tests
- Albumin 2-3 week half life 3.5-5.5
- PT: measures 2 7,,10 (7 half life 4-6 hrs)
halothane hepatitis etiologt
hepatitis 2/2 oxidatitve metabolites such as trifluroacetic acid, and they induce autoimmine response or hve direct hepatotoxic effect
RF: F middle age, obese, repeated exposure
iso des 1:300,000 vs halothane 1:35,000
Functions of the liver
- metabolism carbs, fats proteins
- synthesis of serum proteins-albumin/clotting factors
- metabolism of drugs hormones, toxins (Phase 1-oxidation/reduction (benzo barbs), Phase 2 (conjugation-morphine)
- production urea and bile (absorption ADEK)
factors that effect HBF
how to preserve hepaptic blood flow intraop
- hypotension (RA GETA
- vasoconstriction of HA or GI/splanchnic circ 2/2 sympathetic stim
- BB that block B2 mediate HA vasodilation
- alpha agonists that cause HA and PV vasoconstriction
- excessive PEEP or postive pressure (increased hepatic venous pressure, decreased venous return
- H2 blocks decrease HBF
- direct surgical compression
maintain euvolemia, avoid hypotension, use iso (reduces portal flow least), min sympathetic stim, avoid BB and alpha agonist if possible
What is cirrhosis?
Head to toe effects
heapatic necrosis, fibrosis, and nodal regeneration/ leading to portal HTN >10mmHg. causes ETOH, hepatitis, toxins
Anesthesia:
1) paralysis: may need more larger initial dose due to larger VD, decreaed proetin binding larger free fraction may off set this, and impaired metabolism few doses may be needed
2) citrate intoxication more likely w blood
3) psueocholinesterase def
Neuro: encephalopathy AMS, asterxisis, hyperreflexa, wernicke korsakoff (more permeable BBB, ammonia broken down from blood in GI tract or transfusion)
Cards: hyperdynmaic state =high mixed venous(increased CO, low SVR, anemia, systemic shunts), systemic AV shunts
resp: decreased FRC and restrictive dz from ascites, increased AV shunts, plerual effusions, inhibition of HPV (from vasodilating substances - VIP, glucagon)–>hypoxemia, resp alkalosis
GI: Portal HTN causing 1) ascities (2/2 portal HTN, hypoalbumin, renal rentention of fluids),2) varices/hemorrhids, aspiration risk
renal: decrease renal perfusion, sodium retentiom. (increase in total body andvolume but decrease in effective volume, HRS (prerenal oliguria w NA retention, azotemia, and ascites
Heme: thrombocytopenia (splenic sequestration), anemia (bleeding, RBC destruction, malnutrition, SBP
Electrolytes: hyponatremia (dilutional), hypokalemia (diuresis or hyperaldosteronism), hypoalbumin, hypoglycemia
esophagel cancer considerations
cardio: often after ETOH and smoker, high risk post op a fib
pulm: smokers often, chronic aspiration–>pulm fibrosis,
GI: nutrional status poor (increased MM), liver fxn, aspiration risk (obstruction, altered motility and spincter dysfunction
chemo: doxorubicin (cardiomyopathy, belomycin lung, radiation (pnumonitis, pericarditis
medical management of PHTN and varicela hemorrhage
BB (propranolol), or isosorbide if BB not tolerated, TIPS
variceal bleed: vasoconstriction-somatostatin, octreotide (lower portal pressures) via vasocosnstrction; vasopressin, sclerotherapy, ligataion, balloon tamponade,
causes of hepatitis
ETOH,
halothane, amiodarone,
rifampin, INH
steriods, OCP
concerns with chronic alcoholics
Anesthesia: intoxiciation effect on MAC
neuro: AMS, encephalopathy, wernicke korsaoff (ataxia, confusion, occular issues; tx thiamine), withdrawl (sezizures DT)
cards: acute HTN tachy; cardiomyopathy, arrythmia
resp: smoker?
gi: ulcer, cirrhosis, aspiration risk
heme: pancytopenia
goals fir a cirrhoric pt
preop
- determine extent of multisystem dz
- optimize the pt: encepalopathy volume status, hyperdynamic state, hypoxemia, coaguopthy, anemia, electrolytes,
- delay if active hepatitis
intraop
- increased aspiration risk
- anesthetic that accounts for impaired hepatic drug clearance, increased VD, decreased protein binding, and altered MAC
- careful fluid management: low oncotic pressure predisposes to pulm edema need adeuquate hydration to preserve hepatic and renal perfusion
- have blood available to treat bleeding and coagulopathy from thrombocytopenia
post op
- AMS withdrawl or enceph
- same as above
Labs for cirrhotic
- CBC plt, PT PTT -pancytopenia from plt sequestration, anemia from bleeding, malnutriion and RBC destruction, coagulopathy from factor def
- electrolytes: BUN cr, glucose, na, K-hyponatremia from dlution, hypokalemia from diuresis and hyperaldosteronism, hypoglycemia from severe liver failure, azotemia from dehydration or HRS
- LFT for baseline values and albumin
why are cirrotics hypoxic
- atelectasis, restrictive lung dz, low FR from ascites
- attenuation of HPV via vasodilators, intrapulmonary A shunts
- plerual effusions,
Stages of liver transplant/complications
how to reduce reperfusion
- preanhepatic- dissection
bleeding
- anheppatic-liver is seperated from circulation and replaced w donor
- clamp IVC above and below, hepatic artery, PV
- CO drops, distal venous pressure increases
- consider V-v bypass
- complications-embolism of air/clots, bleeding/coagulopathy, hypothermia, citrate intoxication, acidosis, RF, brachial plexus injury - transplanted liver connected to circulation
- clamps removed, HA reanastamosed, CBD reconnected
- complications: hyperkalemia, acid metabolites/vasoactive suvstances kfrom lower body,cold blood, cytokines
- flush graft prior to reperfusion, current any current met acidosis to counter acid load from graft, admin calcium ro counter effects of K on heart, admin vasopressors/inotropes to correct any prexisting hypotension
how can veno-venous bypass be used during transplant, complications
what is a piggyback technique
when to use techniques
maintains venous return to heart during IVC clamping by diverting blood from IVC via pump (no oxygenator) to axillary vein/ SC/IJ.
minimizes hypotension/improved hemodynamics, improved preload/cardiac filling
reduction pulm edema (less blood and fluid admin)
splanchnic decompression–>faster return of guyt moility
potential decrease post op renal dysfunction
limited metabolic impairment interstitial edema, ischemia, and acid metabolites in lower extxremities,
air/clot embolism, vascular/brachial plexus injury, hematoma
improved surgical field
donor IVC is attached to recipients
cardiac dz, severe pHTN, or when clamping IVC results in severe hemodynamic instability, others believe in volume loading and pressors
Post op liver transplant complications
neuro: seziure (cyclospirone), encephalopathy
cards: hypo/hypervolemia, CHF (PPH, fluid overload)
resp: pleural effusion, R phrenic nerve injury, TRALI, pulm edema
GI: vascular or anastomitic leak, hepatic or PV thrombosis
renal: ARF (ATN prerenal, drug toxicity, HRS)
metabolic: metabolic alkalosis, hypokalemia (critrate metabolism)
heme: hemorrhage, coagulopathy, infections, rejection (1-6weeks)
causes of coagulopathy during liver transplant
massive blood transfusion: fdilutional coagulopathy
fibrinolysis-increase in tissue plasminogen activator (tissue plasmiogen activator inhibitor decreased)
hypothermia
DIC
residual heparin
inadequate clotting factor synthesis
uremia
What does meld consist of, what does it mean, and what does it exclude
INR bili, creatinine
6-40 higher the score the higher the short term mortality
excluded fulminant liver failure and life expectany <7 days -status 1 (higher priority)
Triad of hepatopulmonary syndrome
Pa02<70 on RA or A-a >20
liver dz
intrapulmonary vascular dilations
BENEFITS of paracentesis
How to replace fluid
cards: increased CO (relieves compression on IVC
pulm: improved pulm compliance and pulm case exchange (reduced VQ mismatch)-reduction of ascitc pressure on diaphrgam
GI; decreased risk of gastric aspirations (decreased ascetic fluid compression of stomach)
-50% immediate rest of 6 hrs: 6-8g/L
def of portopulm HTN
PPH: PAP>25 or PVR >240 dynes/sec/cm^5, (3 woods) in presence of normal PCWP
mild 25-35
moderate 35-45
severe >45
>35 and >250 increased risk of periop death from R heart failure or hepatic failure
severe >50 can be considered contraindication to liver transplant
confusion in cirrhotics
- intoxication
- wernicke encep (b1)
- chronic subdural ICP increase
- worsening encephalopathy (bleeding)
etiology reperfusion syndrome
reduce effect
- excessive K load from graft
- release vasoactive substances and metabolic metabolites,
- cold blood on heart
- release of cytokines
- flush graft before reperfusion
- correct any current met acidosis:: bicarb
- calcium to counter effect K on heart
- inotropes and vasopressors to correct any preexisting hypotension
Carcinoid triad
dx
caricinoid syndrome
preop optimization
Flushing diarrhea, cardiac involvement (TR PS-serotonin induced fiborsis), broncoconstrition
urine 5-HIAA: hydroxyindoleacetic acid (breakdown product of serotonin), chromogranin A elevated
- complex sx that occur when carcinoid tumor releases excessive amounts of hormones (serotonin, histamine, bradykinin) into systemic circulation (met to liver substances bypass portal circ or occur outside the GI tract
- somtaostatin analog-octreotide to decrease serotonin secretion, optimize fluid status
anxiolytic (reduce stress induced release vasoactive substances), H1 and H2 blockers to attenuate the effect of histamine,, alpha and BB blockeer to prevent catecholamine mediated release of vasoactive sustances, steriods
serotonin antagonist for nausea-zofran
ASPIRATION PNEUMONITIS
pathophy of aspiration pneumonitis
when do admin abx
- Aspirated material causes damage to surfactant producing cells (atelectasis), pulmonary capillary endothelium –>pulm edema
1. bacterial infection based on cx and sensitivity
2. high liklihood of negative or anerobic organism such as w feculent aspiration
3. clinical course fails to improve after several days
triad of compartment syndrome
increased abdominal pressure, abdominal distenion, evidence of end organ dysfunction
What to do during aspiration
Head down, suction mouth, intubate, then suction bf PPV to avoid distal disemmination
- baseline ABG and CXR
- bronch for particulate
- tx any broncospasm
monitor for 24-48 hrs
-no abx or steriods
Considerations for ETOh abuse
withdrawl: tremors 6 hrs, seizures 1-1.5 days,
delerium tremens-AMS, autononmic instability (fever tachycardia HTN) 3 days, agitation
Issues with cricoid
how it should be approached
- esophageus is displaced laterally in some pts (not compressed against vertebral bodies
- may reduce LES tone increasing risk of aspiration
- may increase dificulty of intubation
- may practioners apply excessive or insufficinet force–>ineffective or increased difficulty on intubation
proper application of cricoid may reduce risk of aspiration in high risk pt, but I would reduce or eliminatw if I felt it was interferring w rapid intubation.
why hydrophilic opioids used for thoracic epidural during esophectomy
covers larger number off dermatomes
