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Gastrointestinal
Disorders
Linda H. Warren
EdD RN MSN CCRN
NUR 335
OBJECTIVES
 Review anatomy and physiology of the GI tract
 Review gastrointestinal intubation and nutrition
• TPN, enteral feedings
 Describe the clinical manifestations and management of acute GI
disorders
 Identify complications of acute GI disorders & the prevention
and management
ANATOMY AND PHYSIOLOGY
Alimentary canal:
 Oropharyngeal cavity (anterior to spine, posterior to trachea)
 Esophagus
 Stomach
 Small intestine (ABSORPTION)
 Large intestine (ELIMINATION)
Accessory organs:
 Pancreases
 Liver
 Gallbladder
 Gastroesophageal Junction
• Inlet into stomach
• LUQ
• Stores food & produces digestive
enzymes
 Stomach: HCl- acid secretion
• Cardia (main portion)
• Fundus
• Body
• Antrum
• Pylorus (inlet into small intestine)
GI Function
Functions of the GI system:
 Digestion /absorption of nutrients
 Elimination of waste products
 Detoxification and elimination of bacteria,
viruses, chemical toxins, & drugs
***Swallowing is a conscious / voluntary process
SMALL INTESTINE:
Largest segment of GI tract
-Duodenum (proximal portion)
• Ampulla of Vater
-Jejunum (medial portion)  where absorption begins
-Ileum (distal portion)
• Ileocecal valve
• Absorption of nutrients into blood stream thru intestinal wall
• Pancreas secretes enzymes for digestion
• Common bile duct
• ILEOCECAL VALVE: RLQ  where bowel sounds are heard best
• Controls passage of digestive material into large intestine
LARGE INTESTINE:
 Ascending
 Transverse
 Descending
 Sigmoid
 Rectum
 Anus
Colonoscopy: sigmoid colon  descending colon
-assessing for diverticulitis, bleeding, etc.
Reabsorption of water & electrolytes
Elimination of waste products
BILIARY SYSTEM
PANCREAS:
Exocrine functions:
 Production of digestive enzymes
Endocrine functions:
 Production of insulin & glucagon
Gallbladder: storage of bile
LIVER
 More than 400 functions
 Vascular functions
 Blood storage & filtration
 Secretory functions
 Bile production
 Bilirubin metabolism
 Metabolic functions
 Carbohydrate, fat & protein metabolism
 Clotting factors  liver disease = inc. bleeding
 Detoxification
 Vitamin & mineral storage
 LFT: AST/ALT
Abdominal Arterial System
BLOOD SUPPLY TO GI TRACT:
• Superior mesenteric artery
• Inferior mesenteric artery
Branch off of thoracic & abdominal aorta
Gastric artery: supplies oxygen & nutrients
Portal Venous System
 Superior Mesenteric
 Inferior Mesenteric
 Gastric
 Splenic
 Cystic
GENERAL ASSESSMENT
Health History:
 Pain (major reason why pts seek health care)
 Dyspepsia / indigestion (upper abdominal distress)
 Belching, regurgitation, abdominal fullness
 Intestinal Gas
 N / V
 Change in Bowel Habits / Stool Characteristics (clay-colored, greasy/fatty, etc)
 Weight changes / Diet
 Medications
 Melena (upper GI bleed) / hematochezia
Physical Assessment
INSEPCT ORAL CAVITY:
Gums, teeth, tongue
INSPECTION
-contour
-distention
-color / texture
-herniation
AUSCULTATION
PERCUSSION
-size/shape/density
-air sound smore hollow
PALPATION
-deep palpation for
identifying tumors or masses
INSPECTION & AUSCULTATION
Skin color / Texture
• Jaundice: liver dysFX
Symmetry / Contour
• Distention
Masses / Pulsations
• Hernias
• AAA
Peristalsis / Movement
 Bowel sounds: High pitched gurgling sounds
 Vascular sounds:
• Bruits (usually r.t dilated vessels)
• Venous Hums (cirrhosis  obstruction in portal circulation
PHYSICAL ASSESSMENT
Causes of Decreased Bowel Sounds
 Peritonitis
 Gangrene
 Reflux Ileus
 Surgical Manipulation of Bowel
 Late Bowel Obstruction
Causes of Increased Bowel Sounds
 Early Pyloric or Intestinal Obstruction
 Bleeding Ulcers/ Electrolyte Disturbances (blood is
irritating to the GI tract, wants to get rid of it = bloody
stools)
 Bleeding Esophageal Varices
 Diarrhea
 Subsiding Ileus
PHYSICAL ASSESSMENT
Percussion
 Detects fluid, gas or masses
 Tympany: presence of gas
 Dullness: presence of a mass, spleen, liver, kidneys
Palpation
 Evaluate major organs
 Tenderness / Rebound Tenderness (pain felt on release)
 Rigidity / Guarding
DIAGNOSTICS—
Serum Laboratory Studies:
 LFT
 BMP / electrolytes
 CBC
 Magnesium
 Phosphorus
 Amylase
 PT / pTT
 CEA protein: not normally detected in blood… can indicate malignancy.
 Stool Tests: Occult blood (turns blue  presence of blood)
 Imaging Studies: abdominal ultrasound (#1, noninvasive) / CT / MRI / PET
 Endoscopic Procedures: DIRECT visualization
 DNA Testing (BARRIER: insurance won’t pay for it)
ENDOSCOPIC PROCEDURES
 Upper GastrointestinaI Fibroscopy/ Esophagogastroduodenoscopy (EGD)
• Fasting 8-12 hrs before
 Endoscopic Retrograde Cholangiopancreatography (ERCP)
• Gallbladder studies
• FAT FREE DIET
 Fiberoptic Colonoscopy
• Virtual Colonoscopy (swallow a pill with a camera in it... Eliminated in stool)
• Sigmoidoscopy
 Endoscopy through an Ostomy
• Assess FX of stoma, presence of necrosis, tissue viability (how well it is doing)
INTERVENTIONS
 Provide pre & post-procedure instruction
 Reassurance
 Alleviate anxiety
 Report abnormal lab values
 Assess for adequate hydration
INTERVENTIONS
 Clear liquid diet or NPO after midnight
 Bowel preps / Cleansing enemas
 Allergies to Contrast (CT scans, allergies to shellfish or iodine)
 Renal Protective Measures:
• Mucomyst, IV bicarb = help isolate free radicals & prevent complications
 Conscious sedation – need anesthesia present
-Versed
-Propofol  hypoTN
 Post-procedure assessments / frequent vitals
GI INTUBATION
 Decompression  reduced N/V
 Lavage  put water in & pulling it back out…used for active bleeding
• Iced saline lavage for esophageal varices  vasoconstriction and dec. bleeding
 Diagnose GI Motility Disorders
 Administer Medications and Feedings
 Treat smaller obstructions:
• NGT/ OGT to decompress stomach
• Prevention of invasive surgery
 Compression of Bleeding Sites
 Aspiration of Gastric Contents
NASOGASTRIC / NASOENTERIC
TUBE FEEDINGS
 Meet Nutritional Requirements  enteral > parenteral
 Low cost
 Well Tolerated
 Ease of Use
 Preserve GI Integrity
 Preserve Intestinal & Hepatic Metabolism
 Maintain Fat Metabolism & Lipoprotein synthesis
 Maintain Normal Insulin / Glucagon Ratios
NASOGASTRIC / NASOENTERIC TUBES
 Nasogastric Tubes
• Levin (no air vent)
• Gastric or Salem Sump (air vent, low continuous wall suction)
• Sengstaken-Blakemore (SMALL diameter… crushed meds can clog up
tube)
***after administering crushed meds thru gastric tube… need to flush with a
decent amt of saline to PREVENT CLOGGING of the tube.
 Nasoenteric Feeding Tubes
• Dobhoff
 Gastrostomy
 Jejunostomy
NGT NURSING INT:
 Patient Preparation
 Insertion of Gastric Tube: lean forward, give pt sips of water / swallowing.
 Make sure lubricant is water souble to prevent aspiration!!! (ex: Vaseline is NOT
water soluble)
 Confirm Placement: MUST HAVE AN XRAY
• Inject air, auscultate LUQ (stomach), should hear gurgling.
• Aspirate: are we getting gastric contents back?
 Secure the Tube
 Monitor Patient / Maintain Tube Function
 Oral / Nasal Hygiene
 Potential Complications: skin breakdown,
 Removal of Gastric Tube: intentional vs accidental
Nasogastric Tube
DO NOT place a NGT in a pt with a
history of esophageal varices…
HIGH RISK OF BLEEDING
Sengstaken-Blakemore Tube
Esophageal balloon: inflated to
compress bleeding esophageal varices
Gastric balloon: inflation + traction for
bleeding ulcers
COMPLICATIONS OF TUBE FEEDS:
GI:
 Diarrhea
 Nausea / vomiting  electrolyte disturbances
 Gas / bloating / cramping / Dumping Syndrome
 Constipation
Mechanical:
 Aspiration
 Tube displacement / obstruction / clog
 Residue
 Nasopharyngeal irritation
Metabolic:
 Hyperglycemia…may need sliding scale insulin coverage
 Dehydration and azotemia
PARENTERAL NUTRITION: indications
Intake insufficient to maintain anabolic state:
 Impaired ability to ingest food orally / tube
 Inability / unwillingness to ingest adequate nutrition (anorexia, elderly post-op pts)
 Medical condition prevents oral / tube feedings
 Prolonged pre / postoperative nutritional needs
• ACUTE PANCREATITS
• Fistulas
• Extensive bowel surgery
• Burn pts
• AIDs
• Sepsis
• Paralytic ileus
• Chrons disease
• Hyperemesis graviderum
ACUTE GI BLEEDING
Upper GI Bleeding:
 Peptic Ulcer Disease (PUD):
 Duodenal Ulcers
 Gastric Ulcers
 Stress Ulcers
• Cushing’s Ulcers:) overstimulation of the vagal nerve (assoaicted with
severe head trauma, brain surgery)
• Curling’s Ulcers: sympathetic response that causes a dec. in mucosal blood
flow  ischemia CAUSES: massive burns, shock, anoxia
 Esophageal / Gastric Varices (hemorrhoids)
 Mallory-Weiss Tear (usually resolves spontaneously)
• Longitudinal arterial hemorrhage
• Forceful episodes of retching / dry-heaving/ vomiting
• Seizures
• Alcoholism
Peptic Ulcer Disease (PUD)
Risk Factors:
 Smoking / chewing tobacco
 H. pylori bacteria
 Medications
• NSAID’s
• ASA
• Steroids (administer PPI / antacids)
 Alcohol
• Gnawing, burning pain in mid to upper
abdomen
• Between meals or at night
• Bloating
• N/V
• Heartburn
• Severe cases: melena, hematochezia,
coffee-ground emesis, weight loss
Types of Peptic Ulcers
 Gastric ulcers: Form in the lining of the stomach
 Duodenal ulcers: Form in the upper portion of small intestine
Symptoms of gastric and duodenal ulcers
similar, except for when pain occurs
Pain from a gastric ulcer:
• Occurs when food is still in the stomach,
SHORTLY AFTER EATING.
Pain from a duodenal ulcer:
• Occurs when the stomach is EMPTY…several
hours after eating
• Pain may improve after eating.
• Pain may wake you in the middle of the night.
Duodenal Ulcer
Stress Ulcer
Etiology: Ischemia
 Hemorrhage
 Trauma
 Sepsis
 Burns (Curling’s ulcer)
 Head trauma or brain surgery (Cushing’s ulcer)
Prevention
 Antacids (Mylanta, tums, help neutralize gastric acid / heartburn)
 Antacids: contain BICARBONATE  METABOLIC ALKALOSIS (fatigue, lethargy,
nausea)
 H2-receptor blockers (reduce gastric acid in stomach, cimetidine)
 Proton Pump Inhibitors (PPI’s) = Prilosec
Mallory-Weiss Tear
 Arterial Hemorrhage
 Longitudinal tear
 Forceful retching / vomiting
 Forceful coughing
 Epileptic seizures
 Long-term use of NSAID’s / ASA
 Excessive alcohol intake
Assess on XRAY
Longitudinal tear = air enters space (can be seen on XRAY)
INT: usually heal on their own, may give PPIs or H2-blockers
Esophageal Varices
 Portal hypertension  distended vessels
 Veins become distended & varices develop  fragile and prone to rupture
 Lower esophagus
 Upper portion of stomach
 Tend to bleed easily
 Enlarged vessels in esophagus
 Any chronic liver disease can cause esophageal varices
 S&S of acute alcoholism
Esophageal Varices
LFTs
Jaundice
Clay-colored stools
Symptoms
 People with chronic liver disease and esophageal varices may have no symptoms
 Small amount of bleeding: Dark or black streaks in the stools = Melena
 Larger amounts of bleeding  type & cross-match pts on admission
• Black, tarry stools
• Bloody stools
• Light-headedness
• Paleness
• Symptoms of chronic liver disease
• Vomiting
• Vomiting blood
• Dec Hgb/Hct
• May be hypotensive if bleeding is severe
TX: PRBCs
0.9% NS if hypotensive
MANAGEMENT of BLEEDING VARICES
 Somatostatin or Octreotide  reduce portal pressure / splanchnic blood flow
 Vasopressin  reduce portal pressure / dec blood flow thru. liver
 Endoscopic Procedures
• Banding if pouch  stops bleeding
• Cauterization
 Transjugular Intrahepatic Portosystemic Shunt (TIPS)
 Esophagogastric Tamponade
• Balloon inflation to cause vasoconstriction
 Surgical Intervention: Portacaval Shunt
ACUTE GI BLEEDING
Lower Gastrointestinal Bleeding
 Polyps
 Inflammatory Diseases
 Diverticulosis
 Cancer
 Vascular Ectasias (dilation of a vessel)
 Hemorrhoids
CLINICAL SIGNS AND SYMPTOMS
 Hematemesis
 Melena  black / tarry stool
 Hematochezia  bright red blood in stool
 Abdominal Discomfort
 Hypovolemic Shock r/t fluid loss:
• Hypotension
• Tachycardia
• Angina, cardiac ischemia on EKG
• Cool, clammy skin
• Change in level of consciousness
• Dec. CO
• Decreased urine output
• Decreased gastric motility
Laboratory Studies
 Complete Blood Count (CBC)
• #1: Hemoglobin & hematocrit!!!
• WBCs (H. pylori bacteria common cause)
• Platelet
 Electrolyte imbalances
 Increased BUN & creatinine
 Liver function
 Clotting profile (pT/PTT)
 Ammonia levels (byproduct of protein breakdown)
 Type & cross match (2-4 units typically ordered)
Diagnostic Tests
Endoscopy:
 Procedure of choice
 Upper vs lower GI bleed
 Diagnosis & treatment
Barium studies:
 Ulcers/bleeding tumors
MANAGEMENT of UPPER GI BLEEDING
 Hemodynamic Stabilization
• Oxygen administration (dec. Hgb & Hct)
• IVF resuscitation
• Colloids
• Blood / Blood products
 Gastric Lavage / decompression
• Only use orogastric tube if pt is intubated.
• Nasogastric tube used for A&O pts.
Definitive / Supportive Therapies:
 Pharmacological Therapies
• Antacids (risk for alkalosis)
• Histamine Blockers
• Proton Pump Inhibitors (PPIs)
• Mucosal Barrier Enhancers  especially in H. pylori (Prilosec)
• Antibiotics
MANAGEMENT of UPPER GI BLEEDING
 Endoscopic Therapies to stop bleeding:
• Sclerotherapy: inject a caustic agent that clots.
• Clips / Band Ligation
• Thermal methods: cauterization
 Surgical Therapies:
• Gastric Resections
• BILLROTH I: stomach joined to duodenum
• BILLROTH II: stomach joined to jejunum
• Done with a vagotomy to ↓ amt of stomach
acid production.
MANAGEMENT of UPPER GI BLEEDING
ACUTE GASTRIC PERFORATION
 Abrupt onset of severe abdominal pain
 Abdominal tenderness
 Board-like abdomen
 Absent bowel sounds
 Leukocytosis r/t infection (gastric contents enter peritoneum)
 Presence of free air in peritoneum on chest x-ray:
 Hole in the stomach  air enters peritoneum
 Will see presence of air just below the diaphragm—air rises
 Gastric decompression
 Start on ABX
 May require emergent surgery if free air doesn’t spontaneously resolve.
BOWEL OBSTRUCTION
 Blockage prevents normal flow through intestinal tract
 Can lead to ischemia & necrosis.
Mechanical Obstruction:
 Intra-luminal pressure on intestinal wall
 Intussusception: bowel telescopes on itself
 Tumors
 Hernias (incarcerated hernia—bowel closes off)
 Volvulus
 Strictures, adhesions, stenosis
 Scar tissues
Functional Obstruction:
 Musculature is unable to propel contents forward in the bowel.
 Paralytic ileus
 Crohns
 Diabetes
 Neurological disorders (Parkinsons)
 Surgical manipulation of bowel
 Amyloidosis: protein deposits on internal walls  fibrosis
SMALL BOWEL OBSTRUCTION
 Abdominal distention
 ↓ venous and arteriolar capillary pressure
 Edema, congestion, necrosis to rupture/perforation
 Peritonitis
 Reflux vomiting
 Metabolic Alkalosis
• Loss of Hydrogen, Chloride, and Potassium
 Dehydration & Acidosis (if persistent)
• Loss of Sodium and Water
 Hypovolemic Shock
LARGE BOWEL OBSTRUCTION
 Accumulation of intestinal contents, gas & fluid proximal to (above) obstruction
 Most common: Adenocarcinoma’s
 Severe distention
 Can cause a perforation
 Dehydration occurs slower (not vomiting)
 ↑ intrathoracic pressure:
 Intestinal strangulation & necrosis
 Interrupted blood supply
TX: bowel resection with anastomosis
MANAGEMENT
SMALL BOWEL:
 Decompression: Nasogastric tube
 IVF resuscitation
 Electrolyte repletion
 Surgical Intervention: depends on cause, duration of obstruction, &
condition of intestine
LARGE BOWEL:
 Decompression
 IVF resuscitation
 Electrolyte repletion
 Colonoscopy: untwist affected portion of bowel/ decompress
 Surgical Intervention: Cecostomy / Colostomy with stoma.
 Colostomy can be reversed.
PERITONITIS
 Inflammation of the peritoneum
 Bacterial Infection
 Leakage of abdominal contents into peritoneal cavity
 Peritoneal fluid:
 Turbid, cloudy
 ↑ protein, WBCS
 Cellular debris & blood
 Intestinal hypermotility (small intestine) paralytic ileus
 Air & fluid accumulation in the bowel
 Pain: Diffuse, Intense, Rebound tenderness
PERITONITIS
 Sepsis
 Major cause of death
 Bacteremia
 Septic Shock
 Septicemia progressing to hypovolemia
MANAGEMENT of PERITONITIS
 IVF resuscitation
 Electrolyte repletion
 Analgesics / Antiemetics (Zofran)
 Antibiotic Therapy
 Surgical Intervention: Remove infected material & correct the cause
 Post-op complications:
• Evisceration / Dehiscence
• first action: cover with saline-soaked sterile gauze, don’t want bowel to dry out)
• Staples with retention sutures, mesh placement to hold organs in place.
• Abscess formation
• Tx: surgical drains/JPs, start on broad-spectrum ABX, culture & sensitivity testing
WASHOUT with liters of fluid: done to prevent recurrent infection & remove as much
infected material out as possible.
PANCREATITIS
 Inflammation of the Pancreas
 Rapid progression
 Can reoccur in the same pt.
 Due to premature activation of pancreatic enzymes
 These enzymes are very corrosive to organs/tissues.
 Autodigestion of pancreas
 Converts Trypsinogen to active form, trypsin
Most damaging pancreatic enzymes:
 Phospholipase A
 Digests phospholipids on cell membranes  causes cell membrane destruction
 Elastase
 Digests elastic tissue of vessel walls
Results in hemorrhage & edema
ACUTE PANCREATITIS
Mild: Interstitial /Edematous
 Areas of fat necrosis in & around pancreas
 Resolves in 5-7 days
 TX: NPO, pain control
Severe: Necrotizing (destruction of cell membrane)/ Hemorrhagic
(elastase destroys lining of vessels)
 Extensive necrosis in & around pancreas
 Pancreatic cellular necrosis
 Hemorrhage within the pancreas
 Associated with local & systemic complications  infection/sepsis, MODS
MAJOR CAUSES OF ACUTE
PANCREATITIS
 Alcohol abuse
 Biliary disease (gallstones, biliary obstruction)
 Medications (estrogens, corticosteroids, LASIX, thiazides, sulfonamides)
 Infections
 Idiopathic
 Traumatic Injury (blunt or penetrating injury)
 Tumors
SIGNS & SYMPTOMS OF ACUTE
PANCREATITIS
 Pain*** NEEDS TO BE ADDRESSED!
 Nausea and vomiting
 Fever
 Dehydration
 Abdominal guarding / distention
 Tender abdomen
 Grey Turner’s Sign: flank pain
 Cullen’s Sign: umbilical pain
PANCREATITIS LABS:
Elevated:
 Serum amylase
 Serum lipase
 WBC’s
 Glucose  hyperglycemia
 LFT’s
 Bilirubin gallstones,
biliary obstruction
 Triglycerides
Decreased:
 Calcium
 Albumin
 Total Protein
 Potassium
 PaO2 r/t pleural effusion
• Fluid that moves out into space under
diaphragm
• If effusions become large enough  inc
pressure on lungs  atelectasis,
pneumonia, hypoxia
• TX of pleural effusion: thoracentesis or
chest tube to drain fluid.
DIAGNOSTIC TESTS
 X-Rays
 Abdomen
 Chest
 CT Scan
 Ultrasound
 Endoscopic Retrograde Cholangiopancreatography (ERCP)
 MRCP ( Magnetic Resonance)
 Aspiration Biopsy to determine severity of tissue damage
RANSON CRITERIA: SEVERITY SCALE
Present on Admission:
 Age >55
 WBC’s >16,000
 Serum glucose >200
 Serum LDH >350
 Serum SGOT >250
Mortality Rates:
• Less than 3 criteria 1-2%
• 3 or more: severe acute
pancreatitis
• 3-4 criteria: 15%
• 5-6 criteria: 40%
• 7 or more = 100%
Did any occur in the Initial 48 Hours...
 ↓ Hct >10%
 BUN Rise >5.0
 Serum Ca+ <8.0
 PaO2 <60  intubation
 Base Deficit >4 mEq/L
 Estimated fluid sequestration >6L with no
improvement
Obesity increases poor
prognosis:
• increase fat deposits=
increase risk of fat necrosis
SYSTEMIC COMPLICATIONS:
Pulmonary:
 Hypoxemia (PaO2<60)
 Fluid accumulation  diaphragmatic restriction  atelectasis
 Pneumonia / pleural effusions
 ARDS
Cardiovascular:
 Hypovolemic shock
 Myocardial depression
 Cardiac dysrhythmias
 Hypoperfusion / ↓CO = elevated LACTATE
Hematologic:
 Coagulation abnormalities
 DIC
SYSTEMIC COMPLICATIONS
Gastrointestinal
 Gastrointestinal bleeding
 Pancreatic pseudocyst
 Pancreatic abscess
Renal
 Azotemia
 Oliguria
 AKI due to hypoperfusion / ↓ CO
Metabolic
 Hypocalcemia
 Hyperglycemia
 Hyperlipidemia
 Metabolic acidosis
SUPPORTIVE THERAPY
Hemodynamic Stability:
 IV Fluids (massive amts, assess for hemodilution, may need to give blood)
 Inotropes
 Electrolyte repletion
 Blood transfusion
 Antibiotic Therapy
 Respiratory
 Renal
 Nutrition: enteral or parenteral, monitor total protein & albumin levels
Control Pain!
 Opiates
Correct Underlying Cause
(lithotripsy for gallstones, cholecystectomy, gallbladder decompression)
ACUTE LIVER FAILURE
Liver Failure:
 Unable to perform its many functions
 Results from necrosis or decreased blood supply to liver cells
 Hepatitis
 Inflammation of the liver
 Cirrhosis
 Chronic disease: liver tissue replaced by fibrotic tissue
 Fatty liver disease
 Liver cells replaced by fatty cells or tissue
LIVER FUNCTIONS
 Very vascular organ
 Secretory:
• Production / secretion of bile
• Conjugation of bilirubin:
• byproduct of Hgb degradation, enters blood stream bc bound to proteins
 Metabolic:
• Metabolism: carbs, proteins, fats (NEED TO BE LIMITED IN LIVER FAILURE, esp. proteins)
• Synthesis: prothrombin, fibrinogen & factors VII, IX, and X (clotting factors)
• Detoxification: hormones, drugs (Tylenol, Dilantin, oral contraceptives, sulfonamides, psych meds.)
 Storage:
• Blood
• Glucose
• Vitamins
• Fat
EVALUATION OF LIVER FUNCTION
 Liver Enzymes
• ALT / SGPT
• AST / SGOT
• Alk Phos
 Bilirubin (conjugated/unconjugated)
 Coagulation (PT/PTT)
 Serum Ammonia
 Serum Albumin
ACUTE HEPATITIS
 Inflammatory liver disease:
• Inflammation of hepatocytes
• Edema
• Interrupts normal blood supply
• Necrosis of healthy cells  portal HTN / congestion of portal system
 Viral
 Liver injury / necrosis
 Acute: lasts about 6 months
• Complete resolution of injured hepatic tissue.
• Rapid deterioration to liver failure and death.
ACUTE VIRAL HEPATITIS
Hepatitis A: Fecal-oral route
 Contaminated food & water
 Contaminated raw shellfish
Hepatitis B: Blood / body fluid  contact precautions
 Chronic infection: Hepatitis & cirrhosis
 Contaminated needles / sexually transmitted (STDs)
 Vaccine (2 doses)
Hepatitis C: Blood / blood products
 Transfusions prior to 1992
 IV drug abusers (contaminated needles)
 Occupational exposure
 Major cause: chronic hepatitis, cirrhosis & hepatocellular cancer
 Major indication for liver transplant
Acute Hepatitis
Symptoms:
 GI pain (RUQ)
 Fever, chills
 Jaundice (starts in sclera  skin)
 Severity of jaundice depends on
disease progression.
 Caused by accumulation of bilirubin.
 N/V
 Fatigue
Management:
 Rest
 Nutritional support
 Prevent spread of the virus
HEPATIC CIRRHOSIS
 Liver enlargement
 Portal hypertension
 Ascites
 Jaundice
 Infection / Peritonitis which can lead to…
• Bacteremia
• Bacterial peritonitis
 GI Varices r/t portal HTN  vasodilates vessels
 Edema
• Decreased plasma albumin / total protein
 Vitamin Deficiencies & Anemia
 Mental Deterioration (hepatic encephalopathy due to build up of
ammonia) TX: lactulose to get rid of ammonia
ACUTE HEPATIC FAILURE
 Shock
• Hypotensive episode:
• insufficient oxygenation, capillary permeability,
microthrombi develop cause tissue ischemia & necrosis
 Fulminant Hepatic Failure (FHF)
• Viral Infections
• Hepatotoxins (ex: Tylenol, psych meds)
 Systemic Inflammatory Response (SIRS)
• Sepsis: major body insult /systemic malignant process
• Vascular permeability increases
• Microemboli
• MODS
CLINICAL SIGNS & SYMPTOMS
 Hepatic Failure
 Vague
 Weakness
 Fatigue
 Loss of appetite
 Weight loss
 Abdominal discomfort
 Nausea / vomiting
 Change in bowel habits
 Clay colored stools, dark urine
 Fulminant Hepatic Failure (severe)
 Hyperexcitability & asterixis r/t
ammonia build up & hypocalcemia
 Insomnia
 Irritability
 Decreased LOC / coma
 Convulsions
 Sudden onset high fever
 Nausea / vomiting
 Chills
 Jaundice
COMPLICATIONS OF
HEPATIC FAILURE
 Hepatic Encephalopathy
• Ammonia
• Nitrogenous wastes
• Asterixis
• Cerebral edema
 Portal Hypertension
• Disruption of blood flow
• Dilation of vessels
 Esophageal Varices
• Engorgement of esophageal veins
• Rupture: medical emergency
 Ascites
• Fluid in abdominal cavity
• Decreased colloid osmotic pressure r/t dec. albumin
• Abdominal compartment syndrome  ascites causes compression of abdominal organs.
Ascites Management
Medical management:
 Bed rest
 Sodium & fluid restriction
 Diuretics
 Paracentesis: complications—organ perforation, hypotension if too much fluid removed, F&E imbalance
• May not remove all the fluid to prevent complications.
• If pt becomes hypotensive…need to administer fluids!
 Albumin
 Nutritional support
 Peritoneovenous shunt – long term management
• LeVeen shunt
• Denver shunt
Denver Shunt
• Used for chronic ascites management
• Has pump attached
• Recirculates volume / replete intravascular space
• Retains nutrients
• Inc renal blood flow
• Inc. CO
• Inc. u/o
• Eases WOB and enhances gas exchange
Ascites Management
 Nursing Management:
 Monitor volume status
 I&O
 Daily weights
 Assess respiratory status
 Supplemental O2
 Assist with procedures to relieve pressure
 Paracentesis, thoracentesis, chest tube placement
COMPLICATIONS OF
HEPATIC FAILURE
 Hepatorenal Syndrome
• Renal failure in the absence of pathology
• Decreasing glomerular filtration rate (GFR)
• Reduced urine sodium
• Presence of azotemia
• Oliguria  anuria
• High BUN/creatinine ratio
 Sepsis / SIRS
 Spontaneous Bacterial Peritonitis
 Transposition of bacteria across cell membrane to ascitic fluid.
 Mvmt of bacteria across cell membrane into peritoneum.
SUPPORTIVE THERAPY
 Encephalopathy
• Correct underlying cause
• Control protein intake
• Lactulose / Neomycin / Metronidazole
• Intubation /mechanical ventilation
 Hypoglycemia
• Monitor serum glucose
• IV replacement with dextrose.
 Metabolic abnormalities
• Monitor serum electrolytes & repletion
• Acidosis: Bicarbonate administration if pH<7.
SUPPORTIVE THERAPY
 Gastrointestinal Hemorrhage
 FFP /platelets to replace clotting factors with Vitamin K
 Vitamin K takes longer to work so need FFP as emergent measure.
 Antacids / H2 Blockers (lowers hydrochloric acid)
 Cerebral Edema
 ICP monitoring
 IV Mannitol
 Barbiturate induced coma to lower metabolism(phenobarbital, esp. if ICP is elevated)
 Elevate HOB 30 degrees
SUPPORTIVE THERAPY
 Hepatorenal Syndrome
• Fluid resuscitation
• TIPS Procedure
• Inotropes
• Low-dose dopamine to increase renal blood flow
• 80% mortality unless they get a Liver Transplant
 Spontaneous Bacterial Peritonitis
• Antibiotic therapy
• Third generation cephalosporin for 5-7 days, until
ascitic fluid cell count normal

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Gi disorders

  • 2. OBJECTIVES  Review anatomy and physiology of the GI tract  Review gastrointestinal intubation and nutrition • TPN, enteral feedings  Describe the clinical manifestations and management of acute GI disorders  Identify complications of acute GI disorders & the prevention and management
  • 3. ANATOMY AND PHYSIOLOGY Alimentary canal:  Oropharyngeal cavity (anterior to spine, posterior to trachea)  Esophagus  Stomach  Small intestine (ABSORPTION)  Large intestine (ELIMINATION) Accessory organs:  Pancreases  Liver  Gallbladder
  • 4.  Gastroesophageal Junction • Inlet into stomach • LUQ • Stores food & produces digestive enzymes  Stomach: HCl- acid secretion • Cardia (main portion) • Fundus • Body • Antrum • Pylorus (inlet into small intestine)
  • 5. GI Function Functions of the GI system:  Digestion /absorption of nutrients  Elimination of waste products  Detoxification and elimination of bacteria, viruses, chemical toxins, & drugs ***Swallowing is a conscious / voluntary process
  • 6. SMALL INTESTINE: Largest segment of GI tract -Duodenum (proximal portion) • Ampulla of Vater -Jejunum (medial portion)  where absorption begins -Ileum (distal portion) • Ileocecal valve • Absorption of nutrients into blood stream thru intestinal wall • Pancreas secretes enzymes for digestion • Common bile duct • ILEOCECAL VALVE: RLQ  where bowel sounds are heard best • Controls passage of digestive material into large intestine
  • 7. LARGE INTESTINE:  Ascending  Transverse  Descending  Sigmoid  Rectum  Anus Colonoscopy: sigmoid colon  descending colon -assessing for diverticulitis, bleeding, etc. Reabsorption of water & electrolytes Elimination of waste products
  • 9. PANCREAS: Exocrine functions:  Production of digestive enzymes Endocrine functions:  Production of insulin & glucagon Gallbladder: storage of bile
  • 10. LIVER  More than 400 functions  Vascular functions  Blood storage & filtration  Secretory functions  Bile production  Bilirubin metabolism  Metabolic functions  Carbohydrate, fat & protein metabolism  Clotting factors  liver disease = inc. bleeding  Detoxification  Vitamin & mineral storage  LFT: AST/ALT
  • 11. Abdominal Arterial System BLOOD SUPPLY TO GI TRACT: • Superior mesenteric artery • Inferior mesenteric artery Branch off of thoracic & abdominal aorta Gastric artery: supplies oxygen & nutrients
  • 12. Portal Venous System  Superior Mesenteric  Inferior Mesenteric  Gastric  Splenic  Cystic
  • 13. GENERAL ASSESSMENT Health History:  Pain (major reason why pts seek health care)  Dyspepsia / indigestion (upper abdominal distress)  Belching, regurgitation, abdominal fullness  Intestinal Gas  N / V  Change in Bowel Habits / Stool Characteristics (clay-colored, greasy/fatty, etc)  Weight changes / Diet  Medications  Melena (upper GI bleed) / hematochezia
  • 14. Physical Assessment INSEPCT ORAL CAVITY: Gums, teeth, tongue INSPECTION -contour -distention -color / texture -herniation AUSCULTATION PERCUSSION -size/shape/density -air sound smore hollow PALPATION -deep palpation for identifying tumors or masses
  • 15. INSPECTION & AUSCULTATION Skin color / Texture • Jaundice: liver dysFX Symmetry / Contour • Distention Masses / Pulsations • Hernias • AAA Peristalsis / Movement  Bowel sounds: High pitched gurgling sounds  Vascular sounds: • Bruits (usually r.t dilated vessels) • Venous Hums (cirrhosis  obstruction in portal circulation
  • 16. PHYSICAL ASSESSMENT Causes of Decreased Bowel Sounds  Peritonitis  Gangrene  Reflux Ileus  Surgical Manipulation of Bowel  Late Bowel Obstruction Causes of Increased Bowel Sounds  Early Pyloric or Intestinal Obstruction  Bleeding Ulcers/ Electrolyte Disturbances (blood is irritating to the GI tract, wants to get rid of it = bloody stools)  Bleeding Esophageal Varices  Diarrhea  Subsiding Ileus
  • 17. PHYSICAL ASSESSMENT Percussion  Detects fluid, gas or masses  Tympany: presence of gas  Dullness: presence of a mass, spleen, liver, kidneys Palpation  Evaluate major organs  Tenderness / Rebound Tenderness (pain felt on release)  Rigidity / Guarding
  • 18. DIAGNOSTICS— Serum Laboratory Studies:  LFT  BMP / electrolytes  CBC  Magnesium  Phosphorus  Amylase  PT / pTT  CEA protein: not normally detected in blood… can indicate malignancy.  Stool Tests: Occult blood (turns blue  presence of blood)  Imaging Studies: abdominal ultrasound (#1, noninvasive) / CT / MRI / PET  Endoscopic Procedures: DIRECT visualization  DNA Testing (BARRIER: insurance won’t pay for it)
  • 19. ENDOSCOPIC PROCEDURES  Upper GastrointestinaI Fibroscopy/ Esophagogastroduodenoscopy (EGD) • Fasting 8-12 hrs before  Endoscopic Retrograde Cholangiopancreatography (ERCP) • Gallbladder studies • FAT FREE DIET  Fiberoptic Colonoscopy • Virtual Colonoscopy (swallow a pill with a camera in it... Eliminated in stool) • Sigmoidoscopy  Endoscopy through an Ostomy • Assess FX of stoma, presence of necrosis, tissue viability (how well it is doing)
  • 20. INTERVENTIONS  Provide pre & post-procedure instruction  Reassurance  Alleviate anxiety  Report abnormal lab values  Assess for adequate hydration
  • 21. INTERVENTIONS  Clear liquid diet or NPO after midnight  Bowel preps / Cleansing enemas  Allergies to Contrast (CT scans, allergies to shellfish or iodine)  Renal Protective Measures: • Mucomyst, IV bicarb = help isolate free radicals & prevent complications  Conscious sedation – need anesthesia present -Versed -Propofol  hypoTN  Post-procedure assessments / frequent vitals
  • 22. GI INTUBATION  Decompression  reduced N/V  Lavage  put water in & pulling it back out…used for active bleeding • Iced saline lavage for esophageal varices  vasoconstriction and dec. bleeding  Diagnose GI Motility Disorders  Administer Medications and Feedings  Treat smaller obstructions: • NGT/ OGT to decompress stomach • Prevention of invasive surgery  Compression of Bleeding Sites  Aspiration of Gastric Contents
  • 23. NASOGASTRIC / NASOENTERIC TUBE FEEDINGS  Meet Nutritional Requirements  enteral > parenteral  Low cost  Well Tolerated  Ease of Use  Preserve GI Integrity  Preserve Intestinal & Hepatic Metabolism  Maintain Fat Metabolism & Lipoprotein synthesis  Maintain Normal Insulin / Glucagon Ratios
  • 24. NASOGASTRIC / NASOENTERIC TUBES  Nasogastric Tubes • Levin (no air vent) • Gastric or Salem Sump (air vent, low continuous wall suction) • Sengstaken-Blakemore (SMALL diameter… crushed meds can clog up tube) ***after administering crushed meds thru gastric tube… need to flush with a decent amt of saline to PREVENT CLOGGING of the tube.  Nasoenteric Feeding Tubes • Dobhoff  Gastrostomy  Jejunostomy
  • 25. NGT NURSING INT:  Patient Preparation  Insertion of Gastric Tube: lean forward, give pt sips of water / swallowing.  Make sure lubricant is water souble to prevent aspiration!!! (ex: Vaseline is NOT water soluble)  Confirm Placement: MUST HAVE AN XRAY • Inject air, auscultate LUQ (stomach), should hear gurgling. • Aspirate: are we getting gastric contents back?  Secure the Tube  Monitor Patient / Maintain Tube Function  Oral / Nasal Hygiene  Potential Complications: skin breakdown,  Removal of Gastric Tube: intentional vs accidental
  • 26. Nasogastric Tube DO NOT place a NGT in a pt with a history of esophageal varices… HIGH RISK OF BLEEDING
  • 27. Sengstaken-Blakemore Tube Esophageal balloon: inflated to compress bleeding esophageal varices Gastric balloon: inflation + traction for bleeding ulcers
  • 28. COMPLICATIONS OF TUBE FEEDS: GI:  Diarrhea  Nausea / vomiting  electrolyte disturbances  Gas / bloating / cramping / Dumping Syndrome  Constipation Mechanical:  Aspiration  Tube displacement / obstruction / clog  Residue  Nasopharyngeal irritation Metabolic:  Hyperglycemia…may need sliding scale insulin coverage  Dehydration and azotemia
  • 29. PARENTERAL NUTRITION: indications Intake insufficient to maintain anabolic state:  Impaired ability to ingest food orally / tube  Inability / unwillingness to ingest adequate nutrition (anorexia, elderly post-op pts)  Medical condition prevents oral / tube feedings  Prolonged pre / postoperative nutritional needs • ACUTE PANCREATITS • Fistulas • Extensive bowel surgery • Burn pts • AIDs • Sepsis • Paralytic ileus • Chrons disease • Hyperemesis graviderum
  • 30. ACUTE GI BLEEDING Upper GI Bleeding:  Peptic Ulcer Disease (PUD):  Duodenal Ulcers  Gastric Ulcers  Stress Ulcers • Cushing’s Ulcers:) overstimulation of the vagal nerve (assoaicted with severe head trauma, brain surgery) • Curling’s Ulcers: sympathetic response that causes a dec. in mucosal blood flow  ischemia CAUSES: massive burns, shock, anoxia  Esophageal / Gastric Varices (hemorrhoids)  Mallory-Weiss Tear (usually resolves spontaneously) • Longitudinal arterial hemorrhage • Forceful episodes of retching / dry-heaving/ vomiting • Seizures • Alcoholism
  • 31. Peptic Ulcer Disease (PUD) Risk Factors:  Smoking / chewing tobacco  H. pylori bacteria  Medications • NSAID’s • ASA • Steroids (administer PPI / antacids)  Alcohol • Gnawing, burning pain in mid to upper abdomen • Between meals or at night • Bloating • N/V • Heartburn • Severe cases: melena, hematochezia, coffee-ground emesis, weight loss
  • 32. Types of Peptic Ulcers  Gastric ulcers: Form in the lining of the stomach  Duodenal ulcers: Form in the upper portion of small intestine Symptoms of gastric and duodenal ulcers similar, except for when pain occurs Pain from a gastric ulcer: • Occurs when food is still in the stomach, SHORTLY AFTER EATING. Pain from a duodenal ulcer: • Occurs when the stomach is EMPTY…several hours after eating • Pain may improve after eating. • Pain may wake you in the middle of the night.
  • 34. Stress Ulcer Etiology: Ischemia  Hemorrhage  Trauma  Sepsis  Burns (Curling’s ulcer)  Head trauma or brain surgery (Cushing’s ulcer) Prevention  Antacids (Mylanta, tums, help neutralize gastric acid / heartburn)  Antacids: contain BICARBONATE  METABOLIC ALKALOSIS (fatigue, lethargy, nausea)  H2-receptor blockers (reduce gastric acid in stomach, cimetidine)  Proton Pump Inhibitors (PPI’s) = Prilosec
  • 35. Mallory-Weiss Tear  Arterial Hemorrhage  Longitudinal tear  Forceful retching / vomiting  Forceful coughing  Epileptic seizures  Long-term use of NSAID’s / ASA  Excessive alcohol intake Assess on XRAY Longitudinal tear = air enters space (can be seen on XRAY) INT: usually heal on their own, may give PPIs or H2-blockers
  • 36. Esophageal Varices  Portal hypertension  distended vessels  Veins become distended & varices develop  fragile and prone to rupture  Lower esophagus  Upper portion of stomach  Tend to bleed easily  Enlarged vessels in esophagus  Any chronic liver disease can cause esophageal varices  S&S of acute alcoholism
  • 39. Symptoms  People with chronic liver disease and esophageal varices may have no symptoms  Small amount of bleeding: Dark or black streaks in the stools = Melena  Larger amounts of bleeding  type & cross-match pts on admission • Black, tarry stools • Bloody stools • Light-headedness • Paleness • Symptoms of chronic liver disease • Vomiting • Vomiting blood • Dec Hgb/Hct • May be hypotensive if bleeding is severe TX: PRBCs 0.9% NS if hypotensive
  • 40. MANAGEMENT of BLEEDING VARICES  Somatostatin or Octreotide  reduce portal pressure / splanchnic blood flow  Vasopressin  reduce portal pressure / dec blood flow thru. liver  Endoscopic Procedures • Banding if pouch  stops bleeding • Cauterization  Transjugular Intrahepatic Portosystemic Shunt (TIPS)  Esophagogastric Tamponade • Balloon inflation to cause vasoconstriction  Surgical Intervention: Portacaval Shunt
  • 41. ACUTE GI BLEEDING Lower Gastrointestinal Bleeding  Polyps  Inflammatory Diseases  Diverticulosis  Cancer  Vascular Ectasias (dilation of a vessel)  Hemorrhoids
  • 42. CLINICAL SIGNS AND SYMPTOMS  Hematemesis  Melena  black / tarry stool  Hematochezia  bright red blood in stool  Abdominal Discomfort  Hypovolemic Shock r/t fluid loss: • Hypotension • Tachycardia • Angina, cardiac ischemia on EKG • Cool, clammy skin • Change in level of consciousness • Dec. CO • Decreased urine output • Decreased gastric motility
  • 43. Laboratory Studies  Complete Blood Count (CBC) • #1: Hemoglobin & hematocrit!!! • WBCs (H. pylori bacteria common cause) • Platelet  Electrolyte imbalances  Increased BUN & creatinine  Liver function  Clotting profile (pT/PTT)  Ammonia levels (byproduct of protein breakdown)  Type & cross match (2-4 units typically ordered)
  • 44. Diagnostic Tests Endoscopy:  Procedure of choice  Upper vs lower GI bleed  Diagnosis & treatment Barium studies:  Ulcers/bleeding tumors
  • 45. MANAGEMENT of UPPER GI BLEEDING  Hemodynamic Stabilization • Oxygen administration (dec. Hgb & Hct) • IVF resuscitation • Colloids • Blood / Blood products  Gastric Lavage / decompression • Only use orogastric tube if pt is intubated. • Nasogastric tube used for A&O pts.
  • 46. Definitive / Supportive Therapies:  Pharmacological Therapies • Antacids (risk for alkalosis) • Histamine Blockers • Proton Pump Inhibitors (PPIs) • Mucosal Barrier Enhancers  especially in H. pylori (Prilosec) • Antibiotics MANAGEMENT of UPPER GI BLEEDING
  • 47.  Endoscopic Therapies to stop bleeding: • Sclerotherapy: inject a caustic agent that clots. • Clips / Band Ligation • Thermal methods: cauterization  Surgical Therapies: • Gastric Resections • BILLROTH I: stomach joined to duodenum • BILLROTH II: stomach joined to jejunum • Done with a vagotomy to ↓ amt of stomach acid production. MANAGEMENT of UPPER GI BLEEDING
  • 48. ACUTE GASTRIC PERFORATION  Abrupt onset of severe abdominal pain  Abdominal tenderness  Board-like abdomen  Absent bowel sounds  Leukocytosis r/t infection (gastric contents enter peritoneum)  Presence of free air in peritoneum on chest x-ray:  Hole in the stomach  air enters peritoneum  Will see presence of air just below the diaphragm—air rises  Gastric decompression  Start on ABX  May require emergent surgery if free air doesn’t spontaneously resolve.
  • 49. BOWEL OBSTRUCTION  Blockage prevents normal flow through intestinal tract  Can lead to ischemia & necrosis. Mechanical Obstruction:  Intra-luminal pressure on intestinal wall  Intussusception: bowel telescopes on itself  Tumors  Hernias (incarcerated hernia—bowel closes off)  Volvulus  Strictures, adhesions, stenosis  Scar tissues Functional Obstruction:  Musculature is unable to propel contents forward in the bowel.  Paralytic ileus  Crohns  Diabetes  Neurological disorders (Parkinsons)  Surgical manipulation of bowel  Amyloidosis: protein deposits on internal walls  fibrosis
  • 50. SMALL BOWEL OBSTRUCTION  Abdominal distention  ↓ venous and arteriolar capillary pressure  Edema, congestion, necrosis to rupture/perforation  Peritonitis  Reflux vomiting  Metabolic Alkalosis • Loss of Hydrogen, Chloride, and Potassium  Dehydration & Acidosis (if persistent) • Loss of Sodium and Water  Hypovolemic Shock
  • 51. LARGE BOWEL OBSTRUCTION  Accumulation of intestinal contents, gas & fluid proximal to (above) obstruction  Most common: Adenocarcinoma’s  Severe distention  Can cause a perforation  Dehydration occurs slower (not vomiting)  ↑ intrathoracic pressure:  Intestinal strangulation & necrosis  Interrupted blood supply TX: bowel resection with anastomosis
  • 52. MANAGEMENT SMALL BOWEL:  Decompression: Nasogastric tube  IVF resuscitation  Electrolyte repletion  Surgical Intervention: depends on cause, duration of obstruction, & condition of intestine LARGE BOWEL:  Decompression  IVF resuscitation  Electrolyte repletion  Colonoscopy: untwist affected portion of bowel/ decompress  Surgical Intervention: Cecostomy / Colostomy with stoma.  Colostomy can be reversed.
  • 53. PERITONITIS  Inflammation of the peritoneum  Bacterial Infection  Leakage of abdominal contents into peritoneal cavity  Peritoneal fluid:  Turbid, cloudy  ↑ protein, WBCS  Cellular debris & blood  Intestinal hypermotility (small intestine) paralytic ileus  Air & fluid accumulation in the bowel  Pain: Diffuse, Intense, Rebound tenderness
  • 54. PERITONITIS  Sepsis  Major cause of death  Bacteremia  Septic Shock  Septicemia progressing to hypovolemia
  • 55.
  • 56. MANAGEMENT of PERITONITIS  IVF resuscitation  Electrolyte repletion  Analgesics / Antiemetics (Zofran)  Antibiotic Therapy  Surgical Intervention: Remove infected material & correct the cause  Post-op complications: • Evisceration / Dehiscence • first action: cover with saline-soaked sterile gauze, don’t want bowel to dry out) • Staples with retention sutures, mesh placement to hold organs in place. • Abscess formation • Tx: surgical drains/JPs, start on broad-spectrum ABX, culture & sensitivity testing WASHOUT with liters of fluid: done to prevent recurrent infection & remove as much infected material out as possible.
  • 57. PANCREATITIS  Inflammation of the Pancreas  Rapid progression  Can reoccur in the same pt.  Due to premature activation of pancreatic enzymes  These enzymes are very corrosive to organs/tissues.  Autodigestion of pancreas  Converts Trypsinogen to active form, trypsin Most damaging pancreatic enzymes:  Phospholipase A  Digests phospholipids on cell membranes  causes cell membrane destruction  Elastase  Digests elastic tissue of vessel walls Results in hemorrhage & edema
  • 58. ACUTE PANCREATITIS Mild: Interstitial /Edematous  Areas of fat necrosis in & around pancreas  Resolves in 5-7 days  TX: NPO, pain control Severe: Necrotizing (destruction of cell membrane)/ Hemorrhagic (elastase destroys lining of vessels)  Extensive necrosis in & around pancreas  Pancreatic cellular necrosis  Hemorrhage within the pancreas  Associated with local & systemic complications  infection/sepsis, MODS
  • 59. MAJOR CAUSES OF ACUTE PANCREATITIS  Alcohol abuse  Biliary disease (gallstones, biliary obstruction)  Medications (estrogens, corticosteroids, LASIX, thiazides, sulfonamides)  Infections  Idiopathic  Traumatic Injury (blunt or penetrating injury)  Tumors
  • 60. SIGNS & SYMPTOMS OF ACUTE PANCREATITIS  Pain*** NEEDS TO BE ADDRESSED!  Nausea and vomiting  Fever  Dehydration  Abdominal guarding / distention  Tender abdomen  Grey Turner’s Sign: flank pain  Cullen’s Sign: umbilical pain
  • 61. PANCREATITIS LABS: Elevated:  Serum amylase  Serum lipase  WBC’s  Glucose  hyperglycemia  LFT’s  Bilirubin gallstones, biliary obstruction  Triglycerides Decreased:  Calcium  Albumin  Total Protein  Potassium  PaO2 r/t pleural effusion • Fluid that moves out into space under diaphragm • If effusions become large enough  inc pressure on lungs  atelectasis, pneumonia, hypoxia • TX of pleural effusion: thoracentesis or chest tube to drain fluid.
  • 62. DIAGNOSTIC TESTS  X-Rays  Abdomen  Chest  CT Scan  Ultrasound  Endoscopic Retrograde Cholangiopancreatography (ERCP)  MRCP ( Magnetic Resonance)  Aspiration Biopsy to determine severity of tissue damage
  • 63. RANSON CRITERIA: SEVERITY SCALE Present on Admission:  Age >55  WBC’s >16,000  Serum glucose >200  Serum LDH >350  Serum SGOT >250 Mortality Rates: • Less than 3 criteria 1-2% • 3 or more: severe acute pancreatitis • 3-4 criteria: 15% • 5-6 criteria: 40% • 7 or more = 100% Did any occur in the Initial 48 Hours...  ↓ Hct >10%  BUN Rise >5.0  Serum Ca+ <8.0  PaO2 <60  intubation  Base Deficit >4 mEq/L  Estimated fluid sequestration >6L with no improvement Obesity increases poor prognosis: • increase fat deposits= increase risk of fat necrosis
  • 64. SYSTEMIC COMPLICATIONS: Pulmonary:  Hypoxemia (PaO2<60)  Fluid accumulation  diaphragmatic restriction  atelectasis  Pneumonia / pleural effusions  ARDS Cardiovascular:  Hypovolemic shock  Myocardial depression  Cardiac dysrhythmias  Hypoperfusion / ↓CO = elevated LACTATE Hematologic:  Coagulation abnormalities  DIC
  • 65. SYSTEMIC COMPLICATIONS Gastrointestinal  Gastrointestinal bleeding  Pancreatic pseudocyst  Pancreatic abscess Renal  Azotemia  Oliguria  AKI due to hypoperfusion / ↓ CO Metabolic  Hypocalcemia  Hyperglycemia  Hyperlipidemia  Metabolic acidosis
  • 66. SUPPORTIVE THERAPY Hemodynamic Stability:  IV Fluids (massive amts, assess for hemodilution, may need to give blood)  Inotropes  Electrolyte repletion  Blood transfusion  Antibiotic Therapy  Respiratory  Renal  Nutrition: enteral or parenteral, monitor total protein & albumin levels Control Pain!  Opiates Correct Underlying Cause (lithotripsy for gallstones, cholecystectomy, gallbladder decompression)
  • 67.
  • 68. ACUTE LIVER FAILURE Liver Failure:  Unable to perform its many functions  Results from necrosis or decreased blood supply to liver cells  Hepatitis  Inflammation of the liver  Cirrhosis  Chronic disease: liver tissue replaced by fibrotic tissue  Fatty liver disease  Liver cells replaced by fatty cells or tissue
  • 69. LIVER FUNCTIONS  Very vascular organ  Secretory: • Production / secretion of bile • Conjugation of bilirubin: • byproduct of Hgb degradation, enters blood stream bc bound to proteins  Metabolic: • Metabolism: carbs, proteins, fats (NEED TO BE LIMITED IN LIVER FAILURE, esp. proteins) • Synthesis: prothrombin, fibrinogen & factors VII, IX, and X (clotting factors) • Detoxification: hormones, drugs (Tylenol, Dilantin, oral contraceptives, sulfonamides, psych meds.)  Storage: • Blood • Glucose • Vitamins • Fat
  • 70. EVALUATION OF LIVER FUNCTION  Liver Enzymes • ALT / SGPT • AST / SGOT • Alk Phos  Bilirubin (conjugated/unconjugated)  Coagulation (PT/PTT)  Serum Ammonia  Serum Albumin
  • 71. ACUTE HEPATITIS  Inflammatory liver disease: • Inflammation of hepatocytes • Edema • Interrupts normal blood supply • Necrosis of healthy cells  portal HTN / congestion of portal system  Viral  Liver injury / necrosis  Acute: lasts about 6 months • Complete resolution of injured hepatic tissue. • Rapid deterioration to liver failure and death.
  • 72. ACUTE VIRAL HEPATITIS Hepatitis A: Fecal-oral route  Contaminated food & water  Contaminated raw shellfish Hepatitis B: Blood / body fluid  contact precautions  Chronic infection: Hepatitis & cirrhosis  Contaminated needles / sexually transmitted (STDs)  Vaccine (2 doses) Hepatitis C: Blood / blood products  Transfusions prior to 1992  IV drug abusers (contaminated needles)  Occupational exposure  Major cause: chronic hepatitis, cirrhosis & hepatocellular cancer  Major indication for liver transplant
  • 73. Acute Hepatitis Symptoms:  GI pain (RUQ)  Fever, chills  Jaundice (starts in sclera  skin)  Severity of jaundice depends on disease progression.  Caused by accumulation of bilirubin.  N/V  Fatigue Management:  Rest  Nutritional support  Prevent spread of the virus
  • 74. HEPATIC CIRRHOSIS  Liver enlargement  Portal hypertension  Ascites  Jaundice  Infection / Peritonitis which can lead to… • Bacteremia • Bacterial peritonitis  GI Varices r/t portal HTN  vasodilates vessels  Edema • Decreased plasma albumin / total protein  Vitamin Deficiencies & Anemia  Mental Deterioration (hepatic encephalopathy due to build up of ammonia) TX: lactulose to get rid of ammonia
  • 75. ACUTE HEPATIC FAILURE  Shock • Hypotensive episode: • insufficient oxygenation, capillary permeability, microthrombi develop cause tissue ischemia & necrosis  Fulminant Hepatic Failure (FHF) • Viral Infections • Hepatotoxins (ex: Tylenol, psych meds)  Systemic Inflammatory Response (SIRS) • Sepsis: major body insult /systemic malignant process • Vascular permeability increases • Microemboli • MODS
  • 76. CLINICAL SIGNS & SYMPTOMS  Hepatic Failure  Vague  Weakness  Fatigue  Loss of appetite  Weight loss  Abdominal discomfort  Nausea / vomiting  Change in bowel habits  Clay colored stools, dark urine  Fulminant Hepatic Failure (severe)  Hyperexcitability & asterixis r/t ammonia build up & hypocalcemia  Insomnia  Irritability  Decreased LOC / coma  Convulsions  Sudden onset high fever  Nausea / vomiting  Chills  Jaundice
  • 77. COMPLICATIONS OF HEPATIC FAILURE  Hepatic Encephalopathy • Ammonia • Nitrogenous wastes • Asterixis • Cerebral edema  Portal Hypertension • Disruption of blood flow • Dilation of vessels  Esophageal Varices • Engorgement of esophageal veins • Rupture: medical emergency  Ascites • Fluid in abdominal cavity • Decreased colloid osmotic pressure r/t dec. albumin • Abdominal compartment syndrome  ascites causes compression of abdominal organs.
  • 78. Ascites Management Medical management:  Bed rest  Sodium & fluid restriction  Diuretics  Paracentesis: complications—organ perforation, hypotension if too much fluid removed, F&E imbalance • May not remove all the fluid to prevent complications. • If pt becomes hypotensive…need to administer fluids!  Albumin  Nutritional support  Peritoneovenous shunt – long term management • LeVeen shunt • Denver shunt
  • 79. Denver Shunt • Used for chronic ascites management • Has pump attached • Recirculates volume / replete intravascular space • Retains nutrients • Inc renal blood flow • Inc. CO • Inc. u/o • Eases WOB and enhances gas exchange
  • 80. Ascites Management  Nursing Management:  Monitor volume status  I&O  Daily weights  Assess respiratory status  Supplemental O2  Assist with procedures to relieve pressure  Paracentesis, thoracentesis, chest tube placement
  • 81. COMPLICATIONS OF HEPATIC FAILURE  Hepatorenal Syndrome • Renal failure in the absence of pathology • Decreasing glomerular filtration rate (GFR) • Reduced urine sodium • Presence of azotemia • Oliguria  anuria • High BUN/creatinine ratio  Sepsis / SIRS  Spontaneous Bacterial Peritonitis  Transposition of bacteria across cell membrane to ascitic fluid.  Mvmt of bacteria across cell membrane into peritoneum.
  • 82. SUPPORTIVE THERAPY  Encephalopathy • Correct underlying cause • Control protein intake • Lactulose / Neomycin / Metronidazole • Intubation /mechanical ventilation  Hypoglycemia • Monitor serum glucose • IV replacement with dextrose.  Metabolic abnormalities • Monitor serum electrolytes & repletion • Acidosis: Bicarbonate administration if pH<7.
  • 83. SUPPORTIVE THERAPY  Gastrointestinal Hemorrhage  FFP /platelets to replace clotting factors with Vitamin K  Vitamin K takes longer to work so need FFP as emergent measure.  Antacids / H2 Blockers (lowers hydrochloric acid)  Cerebral Edema  ICP monitoring  IV Mannitol  Barbiturate induced coma to lower metabolism(phenobarbital, esp. if ICP is elevated)  Elevate HOB 30 degrees
  • 84. SUPPORTIVE THERAPY  Hepatorenal Syndrome • Fluid resuscitation • TIPS Procedure • Inotropes • Low-dose dopamine to increase renal blood flow • 80% mortality unless they get a Liver Transplant  Spontaneous Bacterial Peritonitis • Antibiotic therapy • Third generation cephalosporin for 5-7 days, until ascitic fluid cell count normal