Liver, GI, and Biliary Diseases Flashcards
• Liver receives
25 -30% of the cardiac output
The Hepatic plexus is innervated by:
Sympathetic nerve fibers from T6-T11
Parasympathetic fibers from the
right and left vagus and right phrenic nerves.
Blood-cleansing function
(Kupffer Cells).
Major Physiologic Functions of the Liver
- Blood reservoir (up to 300 mls).
- Blood-cleansing function (Kupffer Cells).
- Metabolic functions
• Metabolism of fat, carbohydrates, and
proteins - Drug metabolism
• Production of plasma proteins, albumin,
and plasma cholinesterases - Bile formation/excretion
- Bilirubin Excretion
Check for liver function
PT/INR
Bilirubin
ALT
Does not measure liver function
Total bilirubin normal
<1mg/dl
>3mg scleral icterus
>4 mg overt jaundice
Alanine aminotransferase (ALT) is a
cytoplasmic enzyme highly specific to the liver.
Aspartate aminotransferase (AST) is an
enzyme that exists in hepatic and extrahepatic tissues
Most important enzymes
ALT
- When both liver enzymes are elevated, ALT/AST ratio is considered:
- < 1 =
nonalcoholic steato-hepatitis (NASH) (non-alcohol fatty liver)
• When both liver enzymes are elevated, ALT/AST ratio is considered:• 2 to 4 =
alcoholic liver disease
Portal vein is
Bigger than portal artery
Albumin • Synthesized
exclusively by hepatocytes
Severe impairment of the synthetic
capacity of the liver
• INR•
Correlated to liver dysfunction • Reliable predictive value for survival of patients c/ liver disease
• Impairment of the hepatic synthetic function of coagulation factors.
Direct correlation with liver dysfunction
INR
Risk for surgery
Screen INR
Acute Cholecystitis
Obstruction of the cystic duct or common bile duct by a
gallstone causes acute inflammation of the gall bladder
90% of gallstones are composed of
cholesterol, due to “Western diet”
Signs and symptoms of Acute cholecystitis
- Nausea and vomiting
- Fever
- Abdominal pain
- RUQ tenderness
• Severe mid-epigastric pain that moves to the RUQ and radiates to the back = biliary colic • Murphy’s sign • Dark urine • Scleral icterus
Treatment of Acute Cholecystitis
- IV fluids, opioids for pain, antibiotics for leukocytosis
- Laparoscopic cholecystectomy
- 5% of “lap choles” convert to open because inflammation obscures the anatomy
Anesthesia considerations Immediate ↓ in venous return and cardiac output ➔ ↑ MAP and systemic vascular
resistance
• Opioid induced sphincter of Oddi spasm occurs in less than 3% of patients
• Treated c/ glucagon, naloxone, or nitroglycerin
• Insufflation ➔ ↑ intra-abdominal pressure ➔interferes c/ ventilation and venous return, can result in bradycardia (glycopyrrolate vs atropine)
Anesthesia considerations Insufflation
• Insufflation ➔ ↑ intra-abdominal pressure ➔interferes c/ ventilation and venous return, can result in bradycardia (glycopyrrolate vs atropine)
Anesthesia considerations:• Reverse Trendelenburg
can help c/ BP and SVR
Anesthesia considerations: Opioid induced
sphincter of Oddi spasm occurs in less than 3% of patient
Sphincter of Oddi spasms treated with
Treated c/ glucagon, naloxone, or nitroglycerin
Choledocholithiasis
Gallstones present in the common bile
duct• Signs and symptoms: cholangitis • Fever, shaking chills, jaundice, RUQ pain • Serum bilirubin and alkaline phosphatase
are sharply ↑ (distinguishing this
condition from ureterolithiasis and acute
intermittent porphyria)
Choledocholithiasis
Gallstones present in the common bile duct•
Choledocholithiasis Signs and symptoms:
cholangitis • Fever, shaking chills, jaundice, RUQ pain •
Biliary colic
Pain moves from mid-epigastric
Bilirubin and alk phosp
Serum bilirubin and alkaline phosphatase are sharply ↑ (distinguishing this condition from ureterolithiasis and acute intermittent porphyria)
WHat is Hepatitis?
Acute inflammation or swelling of the liver
Causes of Hepatitis
Causes: virus, drugs, or toxins
If unable to retract gallbladder due to ______
enlarged liver
Viral hepatitis:
A, B, C, D, E, Epstein-Barr virus, Cytomegalovirus
What about Hep C?
is the most virulent ➔ chronic hepatitis (40%) and cirrhosis ➔ endstage liver disease requiring liver transplantation
Meds that can cause Hepatitis
• Analgesics, anticonvulsants, antibiotics, antihypertensives, etc.
Acetaminophen overdose occurs when glutathione stores are
insufficient to conjugate toxic metabolites of the drug
CO2 in diaphragm
Shoulder pain
Ischemia in closed system
Compartment syndrome
Normal intraabdominal pressure
<15 mmHg
Increase Abdominal pressure
Bradycardia due to Vagal response
S/Sx:
dark urine, fatigue, anorexia, nausea, fever, emesis,
headache, abdominal discomfort, light-colored stools, pruritus
Enzyme MOST indicative of liver damage
ALT
If patient gets bradycardic
Tell surgeon
Cardiac thump
Hit chest or glucagon
Give epi
Dose of glucagon for spasm of sphincter oddi
1mg IVP
Acute Hepatitis
Anesthesia Considerations
•
Volatile gases produce mild, self-limiting postoperative liver dysfunction related to alterations in hepatic oxygen supply
• α glutathione-S-transferase (sensitive marker for hepatocellular damage) ↑ transiently after administration of isoflurane, desflurane, and sevoflurane
Acute Hepatitis
Anesthesia Considerations
• Vasoactive drugs can cause splanchnic
vasoconstriction leading to inadequate hepatic BF
and impaired hepatocyte oxygenation
Hepatitis (acute) ;One unit of PRBC =
250 mg of bilirubin, which can overwhelm someone c/ hepatic disease
Stent for choledocholithiasis
Need to be removed
Choledocholithiasis –>
NEVER DO MAC
Immune-Mediated Hepatotoxicity
Administration of volatile anesthetics (especially halothane) leads to
immune-mediated hepatotoxicity (IgG)
Immune-Mediated Hepatotoxicity
Administration of volatile anesthetics (especially halothane) leads to
immune-mediated hepatotoxicity (IgG)
Fluorinated volatile anesthetics (enflurane, isoflurane, and desflurane) form
trifluoroacetylated metabolites, which have a cross sensitivity c/ halothane; sevoflurane does NOT have this property.
Fluorinated volatile anesthetics (enflurane, isoflurane, and desflurane) form
trifluoroacetylated metabolites, which have a cross sensitivity c/ halothane; **sevoflurane does NOT have this property
Cirrhosis
• Definitive diagnosis: Percutaneous liver biopsy
• Excessive chronic alcohol ingestion, chronic viral
hepatitis, or a variety of other progressive liver
diseases ➔ Scarring of the liver
Scarring of the liver leads to
➔Disruption of normal liver architecture and
parenchymal nodules are regenerated
Symptoms Cirrhosis :
fatigue, malaise, palmar erythema, spider angiomata, gynecomastia,
testicular atrophy, portal hypertension,
Symptoms Cirrhosis :
fatigue, malaise, palmar erythema, spider angiomata, gynecomastia, testicular atrophy, portal hypertension,
Light colored stools in Hepatitis Why?
Because of the bilirubin
Viral Hepatitis leading to chronic liver diseases
Hepatitis C
Hepatitis Co infection B
B and D
Hepatitis CO infection C and
E
Complications of Cirrhosis : Portal hypertension
Portal hypertension (combined c/ hypoalbuminemia and ↑
ADH → ascites) = hallmark of end-stage cirrhosis, leads to
extensive collateral circulation
• Fibrotic degeneration in liver ↑ resistance to BF
• Propranolol ↓ portal venous pressure
—> Gastroesophageal varices (accounts for 1/3 of deaths due to cirrhosis)
After administration of Iso, des and sevo
Alpha glutathione-S elevated
Vasoactive drugs leads to
Hepatic artery vasoconstriction ( do not vasoconstrict too much )
Hallmark of end-stage cirrhosis, leads to extensive collateral circulation
Portal hypertension (combined c/ hypoalbuminemia and ↑ ADH → ascites)
When anesthetic metabolized
TFA–? Go to surface cell of liver and covalently attached to liver cell, body sees as antigen
*****When anesthetic metabolized how they cause TFA?
***TFA– Go to surface cell of liver and covalently attached to liver cell, body sees as antigen
Hepatorenal syndrome
renal failure associated c/ severe liver disease due to hypovolemia and reduced renal blood flow
Liver can
Regenerate
***scar tissue
Complications of Cirrhosis
4. Hyperdynamic circulation:
↑ cardiac output (peripheral and splanchnic vasodilation via prostaglandins and interleukins), ↑ intravascular fluid
volume, ↓ blood viscosity, arteriovenous communications
Comlications of Hyperdynamic circulation:
↑ cardiac output (peripheral and splanchnic vasodilation via prostaglandins and interleukins), ↑ intravascular fluid
volume, ↓ blood viscosity, arteriovenous communications
Thrombocytopenia with cirrhosis is because of
Spleen –> Eats platelets and store
Definitive Dx of cirrhosis
Percutaneous liver biopsy
Complications of Cirrhosis : Hepatopulmonary syndrome:
significant intrapulmonary shunting and V/Q mismatch
Cirrhosis Complications Portopulmonary hypertension:
co- existing portal vein and pulmonary artery hypertension
Complications of Cirrhosis 8-10
8.Hypoglycemia (↓ glycogen storage)
9. Impaired immune defense
10. Hepatic encephalopathy
• Made worse by transjugular intrahepatic portosystemic shunt placement (TIPS) 35%
• Restrict protein
To decrease portal venous pressure beta blocker
Propranolol
Complications of Cirrhosis Coagulopathy:
hepatocytes produce fibrinogen, prothrombin, factor V, VII, IX, X, XI, XII and protein C and S, and antithrombin
Sinusoidal endothelial cells produce factor VIII and vWF
• The liver clears activated coagulation factors from circulation
Complications of Cirrhosis 11. Splenomegaly leading to
thrombocytopenia
Cirrhosis leads to
Hyperdynamic
Between arteries and venous
Capillaries
Cirrhosis ANESTHESIA CONSIDERATIONS: Optimize medically
Evaluate
ADminister
Treat
- Optimize medically
• Evaluate and correct coagulation status
• Administer Vit. K if PT/INR prolonged
• Treat thrombocytopenia
Cirrhosis anesthetic management: Chronic alcohol ingestion
↑ anesthetic requirement (MAC) for isoflurane due to
alcohol-induced microsomal enzyme induction
Anesthetic considerations for Cirrhosis Acutely intoxicated patients require
LESS anesthesia because of the additive depressant effects of alcohol (vulnerable to regurgitating gastric contents; bleeding may be altered due to alcohol-induced platelet aggregation interference)
Anesthetic Considerations for cirrhosis ↓ protein binding
due to hypoalbuminemia = ↑ pharmacologically active formsmof IV drugs
What is protein C
Naturally occurring anticoagulants
inactivate factors 5 and 8
What is protein S
Inactivate factors, naturally occurring anticoagulants
Anesthetic Considerations Cirrhosis Administer
- Volume distribution is ↑, so the initial dose of nondepolarizing muscle relaxant
needs to be larger than normal, however subsequent doses should be ↓ due to
↓ hepatic clearance
• The elimination half time of vecuronium is NOT ↑ until the dose exceeds 0.1mg/kg
blood slowly
• Clearance of citrate is ↓ in the cirrhotic live
In Cirrhosis Avoid instrumentation of
the esophagus c/ known esophageal varices (gastric
tubes, esophageal probes, etc.)
Cirrhosis and BP
Maintain normal BP because perfusion to the liver is already compromised
Cirrhosis and Muscle relaxants Severe liver disease may
Alter plasma cholinesterase activity and prolong
succinylcholine
**Cirrhosis and volume of distribution
*****Volume distribution is ↑, so the initial dose of nondepolarizing muscle relaxant needs to be larger than normal, however subsequent doses should be ↓ due to
↓ hepatic clearance
DO NOT Do this in cirrhosis
PUT ANYTHING DOWN THROAT
For cirrhosis The elimination half time of vecuronium is NOT
↑ until the dose exceeds 0.1mg/kg
Cirrhosis and Vecuronim
Greater than Intubation dose
Acute liver failure =
rapid development of severe liver damage c/ impaired function and encephalopathy in someone who
previously had normal liver function.
• Fulminant hepatic failure develops
8 days of the new onset of symptoms
Hepatic Failure Signs and SYmptoms
• Signs and symptoms (rapid progression of symptoms): malaise, nausea, jaundice, altered mental status, coma, respiratory alkalosis, cerebral edema, hypotension, hypoglycemia, coagulopathy, neutropenia, oliguric renal failure •
Hepatic Failure Hallmark signs:
altered mentation, prolonged prothrombin time
Treatment of Hepatic Failure
Supportive, cause of failure needs to
be established and treated.
Management of Anesthesia of hepatic Failure
• End stage liver disease is associated c/ very low SVR
• No elective procedures
• Correct coagulation c/ fresh frozen plasma (has all
clotting factors)
• Critically ill patients should receive low doses of volatiles
or N2O c/ TIVA
Hepatic Lactulose therapy preoperative can
help decrease ammonia load and prevent hepatic
encephalopathy
Hepatic failure metabolic disturbance
Respiratory Alkalosis
Hepatic Failure correct_____
• Maintain____
Correct imbalances and abnormalities
urine output c/ IV fluids
Hepatic Failure Invasive monitors may be necessary because
patients are at risk for arterial hypoxemia,
metabolic acidosis, hypokalemia, hypocalcemia,
and hypomagnesemia, RESP ALKALOSIS
Preservative for liver transplant rich in
potassium
Anesthesia for Liver Transplant • Fluid warmers and rapid infusion should be considered • Transplanted liver has impaired vasoconstrictive response = impaired protection of hepatic blood flow, no longer a source for autotransfusion
• Anesthesia maintained c/ opioids and inhaled anesthetics combined c/ muscle relaxants that are NOT dependent on hepatic clearance (atracurium, cisatracurium)
Anesthesia for Liver Transplant
should be considered
Fluid warmers and rapid infusion
• Transplanted liver has impaired
vasoconstrictive response = impaired protection of hepatic blood flow, no longer a source for autotransfusion
Phases of Liver Transplantation I. Dissection
– mobilizing vasculature around liver (hepatic artery, portal vein, supra/infrahepatic vena cava), isolating common bile duct, and removing native liver
• CV instability due to hemorrhage, venous pooling, ↓ venous return
III. Reperfusion (neohepatic) phase –
Phases of Liver Transplantation II. Anhepatic
– blood supply to native liver is clamped (venovenous shunt usually
placed)
• Vigorous retraction may impair ventilation, lack of liver metabolism leads to metabolic
acidosis, ↓ drug metabolism, and citrate toxicity
Phases of Liver Transplantation III. Reperfusion (neohepatic) phase
reanastomosis of major blood vessels to donor liver
• Most hemodynamically unstable phase:
• Dysrhythmias, severe bradycardia, hypotension, hyperkalemic arrest
• Will normalize soon after graft is rep
Most hemodynamically unstable phase
Reperfusion
• Bound to proteins to form hemoproteins including
hemoglobin and cytochromes P-450
• Genetic errors of metabolism characterized by
overproduction of porphyrins and their precursors
= most important porphyrin
• Heme
relevant to anesthesia because they produce life-threatening reactions to certain drug
• Only acute porphyrias
• Porphyrias are classified by the
site of enzyme blockage along the heme production pathway
Acute intermittent porphyria is the
most common acute form of porphyria, producing
the most serious symptoms such as hypertension, renal dysfunction, and CNS symptoms and can be precipitated by the administration of certain drugs.
Porphyrias causing drugs
KEPT MAN • Ketorolac • Etomidate • Pentazocine • Thiopental & Thiamylal • Methohexital •Nifedipine
Porphyrias Anesthesia Considerations:
• Carbohydrate administration can suppress porphyrin synthesis
(10% glucose in saline recommended)
• NPO time should be minimized
• Thorough neurological exam needed before administering regional anesthesia (document existing muscle weakness)
• Avoid all barbiturates
• Keep the patient warm
Treatment of Porphyria
Treatment:
• Remove triggering agents
• Adequate hydration and carbohydrate administration
• Treat symptoms as needed
• Hematin (3-4mg/kg IV over 20min) is the only specific therapy for acute porphyric crisis
• Benzodiazepines and propofol can help alleviate symptoms
Care for Patients c/ Decreased
Liver Function
• Patients c/ liver disease have a diminished physiologic reserve in
response to surgical stress
• ↑ risk for bleeding, infection, hepatic decompensation, and death
Significant liver disease NS vs LR
NS
Care for Patients c/ Decreased
Liver Function• Preoperative care:
- Malnutrition and malabsorption are common = vitamin deficiencies and hypoalbuminemia
- Monitor blood sugar
- Hyponatremia results from free water retention
- Degree of encephalopathy is directly correlated to perioperative mortality
Anesthesia for Patients c/ Decreased Liver
Function in a healthy liver
• In a healthy liver, lactated ringers is converted to
bicarbonate.
• A diseased liver is unable to do this conversion, so the
kidneys convert that lactate into lactic acid, leading to
hepatic encephalopathy
Anesthesia for Patients c/ Decreased Liver
Function
• Preoperative care:
• Patients c/ chronic liver disease (especially c/ ascites)
commonly have
↑ gastric volumes and delayed gastric
emptying ➔ Full Stomach
• Factors affecting pharmacokinetics: Decreased liver
• Impaired hepatic synthetic function, ↑ volume of distribution, ↓ plasma protein binding of medications, and ↓ clearance of drugs
Anesthesia for Patients c/ Decreased Liver
Function • Postoperative care •
Admit to ICU to maintain hemodynamics, ensure satisfactory oxygenation and ventilation, frequent
assessing of neurologic function, control electrolyte disturbances and coagulopathies
improves outcome in decreased liver function
• Early enteral feeding
Mallor Weiss Syndrome
• Mucosal tear - usually caused by vomiting, retching, or vigorous coughing
• May have large blood loss
• Bleeding usually stops c/out treatment in a
few hours- surgery rarely needed
• Esophagectomy
• Curative or palliative option for malignant esophageal
lesions
• High morbidity & mortality
• Most post op complications-respiratory
• Acute lung injury /(ARDS) may occur (10-20%)
• c/ ARDS- mortality = 50%
• Anesthesia considerations: Esophageal Disease
•
Malnourished
• Dehydration
• Pancytopenia
• May have had chemo or radiation-> difficult intubation
GERD
Reflux of gastric contents into esophagus
• Lower Esophageal Sphincter (LES) opens c/ swallowing closes after to prevent gastric acid in the stomach
from refluxing into the esophagus
• At rest, LES exerts pressure high enough to prevent
reflux
Inappropriate relaxation/weakness of LES ➔
gastric acid reenters the esophagus, causing irritation
Reflux into the pharynx, larynx, and tracheobronchial tree results
in chronic cough, bronchoconstriction, pharyngitis, laryngitis, morning hoarseness, bronchitis, or pneumonia
Recurrent pulmonary aspiration may result in
aspiration pneumonia, pulmonary fibrosis, or asthma.
Succ
Increase LES tone,
Anesthesia Considerations for GERD
•
High aspiration risk-ETT, RSI
• Highest risk of aspiration pneumonitis c/ > 25ml and pH < 2.5 gastric
contents
• Famotidine decrease gastric acid secretion
• Sodium citrate-oral nonparticulate antacid ↑ gastric pH
• Gastrokinetic agent such as metoclopramide should be considered
2 drugs that increase LES tone
Neostigmine
Succinylcholine
Hiatal Hernia
• Adequate LES tone to keep acid out
• Herniation of part of the stomach into the thoracic cavity
through the esophageal hiatus in diaphragm
• Sliding hiatal hernia =
GEJ and fundus slide upward
• Paraesophageal hernia =
esophagogastric junction remains in normal location and pouch of stomach is herniated next to gastroesophageal junction through the esophageal hiatus
• Most patients c/ hiatal hernias
do not have symptoms of
reflux esophagitis
Carcinoid tumors origination
- 70% originate from one of three sites:
- Bronchus
- Jejunoileum
- Colon-rectum
Carcinoid tumors secrete
- Secrete GI peptides and/or vasoactive substances
* Serotonin, ACTH, GHRF
Found incidentally during surgery for suspected appendicitis
Carcinoid tumors
Carcinoid Syndrome
• Occurs in 20% of pts c/ carcinoid tumorsn•
Large amounts of serotonin & vasoactive substances enter systemic circulation
• Cardiac tumors may have cardiac manifestations resulting from
fibrosis involving the endocardium
Nicotinamide
Vitamin D3
Carcinoid tumor typical valvular lesions
Pulmonic stenosis and tricuspid regurgitation
Carcinoid triad is
cardiac involvement, flushing(histamine) & diarrhea
• Serotonin is over produced, histamine is released, & both may cause bronchoconstriction
Carcinoid triad Other clinical manifestations:
wheezing or asthma-like symptoms and skin
lesions (because of HISTAMINE RELEASE)
Carcinoid Tumors
• Potentially life -threatening complication of carcinoid syndrome
= carcinoid crisis
• Manifests as intense flushing, diarrhea, abdominal pain, and cardiovascular signs (tachycardia, hypertension or hypotension)
• Can occur spontaneously or provoked by stress, chemotherapy, or biopsy
Drugs that may provoke mediator release
- Epinephrine
- Norepinephrine
- Succinylcholine
- Mivacurium
- Atracurium
- D-tubocurarine
Carcinoid Syndrome Treatment
- Avoiding conditions that precipitate flushing
- Treating heart failure and/or wheezing
- Providing dietary supplementation c/ nicotinamide
- Controlling diarrhea
- If the patient continues to have symptoms, serotonin receptor antagonists
or somatostatin analogues are useful - Synthetic analogues of somatostatin, (octreotide) control symptoms in>80% of patients
Carcinoid syndrome Surgery is the
only potentially curative therapy for nonmetastatic carcinoid tumors
Carcinoid Syndrome Anesthesia Management
- A-Line d/t potential for rapid changes in hemodynamic variables
- Octreotide preoperatively and before manipulation of the tumor will attenuate most adverse hemodynamic responses
- General anesthesia typically used
- ↑ levels of serotonin have been associated c/ delayed awakening
- Ondansetron, a serotonin antagonist, is a useful and logicalantiemetic choice
- Use of epidural analgesia in pts who have been adequately treated c/ octreotide is safe
Carcinoid syndrome anesthesia preoperatively and before manipulation of the tumor will
attenuate most adverse hemodynamic responses
Octreotide
Continous disease
Ulcerative Colitis
Crohns Disease: WHat is it?
- Acute or chronic bowel inflammation
* Can occur anywhere from mouth to anus
Crohns: Most common site of inflammation =
terminal ileum
• Occurs in patches a.k.a. “Skip Lesions”
Crohn’s Disease
Crohns Disease
• Symptoms:
Diarrhea, anorexia, and fear of eating
• Causes weight loss of 10-20% of ideal body weight
• Over several years, persistent inflammation gradually progresses to fibrostenotic narrowing and stricture
• Diarrhea ↓ and is replaced by chronic bowel obstruction
• Loss of digestive & absorptive surfaces, which results in malabsorption & steatorrhea
Granulomas common
Crohn’s Disease
Granulomas uncommon
UC
Inflammatory Bowel Disease
Treatment
- Sulfasalazine is the mainstay of therapy
• Anti-inflammatory therapy
• 30% of pts experience allergic reactions or significant side effects such as headache, anorexia, nausea, and vomiting - Oral or parenteral glucocorticoids
- Methotrexate
• Impairs DNA synthesis - Cyclosporine: Alters the immune response by acting as a potent inhibitor of T cell–mediated
responses
Acute Pancreatitis
- Acute inflammatory disorder of pancreas
- Incidence: ↑ 10-fold since 1960s (alcohol abuse and/or improved diagnostic techniques and gallstones)
- Common in patients c/ AIDS,hyperparathyroidism (associated hypercalcemia)
- Trauma-induced acute pancreatitis associated c/ blunt trauma rather than penetrating injury
• Postoperative pancreatitis o
ccurs after
abdominal and non-cardiac or cardiac
thoracic surgery, especially procedures that
require CPB
• Clinical pancreatitis
develops in 1% to 2% of patients following (ERCP) • Indomethacin suppository
Signs & Symptoms of Pancreatitis
- Excruciating, unrelenting mid-epigastric abdominal pain that radiates to back ➔ Nausea and vomiting can occur at peak of pain
- Ileus ➔ abdominal distention
- Pleural effusions or ascites ➔ dyspnea (ARDS c/ 20% of pts.)
- Low-grade fever, tachycardia, and hypotension
- Obtundation and psychosis = alcohol withdrawal
- Hypocalcemia ➔ Tetany
- Hallmark- ↑ in serum amylase concentration
- Renal failure (25%)
Acute Pancreatitis Treatment
1. Hypovolemia, Bleeding, or Albumin Loss • Aggressive intravenous fluid • Colloid replacement 2. NPO to rest pancreas 3. Opioids for severe pain 4. NGT for persistent vomiting or ileus
Chronic Pancreatitis
May be asymptomatic or abdominal pain may be
attributed to other causes
• There is loss of both exocrine and endocrine
function
Signs & symptoms of chronic Pancreatitis
• Epigastric pain that radiates to the back
frequently postprandial
• Steatorrhea (fat in stool; foul smelling)
• At least 90% of pancreatic exocrine function is lost
• Diabetes mellitus is the end result of loss of
endocrine function
Pathogenesis Chronic pancreatitis
Chronic alcohol abuse
Treatment of chronic pancreatitis
Management of pain, malabsorption, and
diabetes mellitus
Appendicitis peak incidence
Peak incidence of acute appendicitis in 2 nd & 3rd decades of life
Appendicitis
Perforation & ↑ mortality are more common in infants and the elderly
Appencitis, In elderly,
pain & tenderness are often blunted, & diagnosis is frequently delayed, so there is a 30% incidence of
perforation in patients older than 70 years
Signs/Symptoms Initial:
mild crampy abdominal pain resulting from appendiceal contractions or distention of the appendiceal lumen
• Poorly localized pain c/ urge to defecate or pass flatus
• Appendectomy should be
performed as soon as the patient can be prepared
Anesthesia Considerations Anesthesia Considerations • Usually appear \_\_\_\_\_\_ • These patients are \_\_\_\_\_\_\_\_\_ • \_\_\_\_\_\_\_\_ induction • \_\_\_\_\_\_\_ tube • Either \_\_\_\_\_or \_\_\_\_\_\_\_\_procedure. • If Laparoscopic: \_\_\_\_\_\_\_\_\_\_ • Keep patient relaxed, but can be short procedure. • Low dose \_\_\_\_\_\_\_
• Usually appear after-hours (Add-On/Emergent
Cases)
• These patients are considered a full stomach
• Rapid sequence induction
• Oral gastric tube
• Either open or laparoscopic procedure.
• If Laparoscopic: Trendelenburg intraop c/ slight
left tilt position.
• Keep patient relaxed, but can be short procedure.
• Low dose NMBDs
