CCRN Exam Blueprint – ~6%

 Acute abdominal trauma

 Acute GI hemorrhage

 Bowel infarction/obstruction/perforation (i.e. mesenteric

ischemia, adhesions)

 Gastroesophageal reflux

 GI surgeries

 Hepatic failure/coma (i.e. portal hypertension, cirrhosis,

esophageal varicies, fulminant hepatitis, biliary atresia)

 Malnutrition & malabsorption

 Pancreatitis

Abdominal assessment

 Inspection

 Auscultation

 Percussion

 Palpation – always

last!

RUQ : Liver, Gallbladder, Duodenum, Head of Pancreas

LUQ : Pancreas, Liver, Spleen, Stomach

RLQ : Appendix, Cecum

LLQ : Sigmoid Colon

 Pyloric sphincter to the cecum

 18 to 20 feet in length

 Major role is digestion & absorption

•  Carbohydrates
•  Fats
•  Protein/Amino acids
•  Water
•  Electrolytes

 3 segments

•  Duodenum
•  10 in long
•  Jejunum
•  8 feet
•  Ileum
• 12 feet

Large Intestine

 5 to 6 feet long, 2.5 in diameter

 Extends from the ileum to the anus

 Responsible for absorption of H2O,

electrolytes & elimination of wastes

3 sections:

 Cecum

 Large intestine

 Rectum

Subdivided:

 Ascending

 Transverse

 Descending

Sigmoid

 Absorbs 800 – 900 ml

fluid

 Bacteria cause

formation of gas

 Synthesize vitamin K,

thiamine, riboflavin,

B12, folic acid, biotin

& nicotinic acid

 Main aerobic bacteria

is E. coli

Intestinal Infarction

 20% of the cardiac output goes to the

intestines after eating

 Infarction is rare d/t collateral flow

2 main types of infarction:

 Occlusive:

 Embolus or thrombosis to the superior

mesenteric artery or major vessel

 Adequate C.O.

 Non-occlusive:

 Associated with decreased C.O. or BP

 At risk: patients with atherosclerosis

 Ischemia is secondary to overall low

perfusion stat

Intestinal Infarction Diagnosis/Treatment

Diagnosis

 Clinical presentation

 Rule out other causes

 Perforated ulcers

 CT scan – assess for free air

 Radiographic Angiography

 Assess for embolus or thrombus

 Surgery

 Assess for ischemic or infarcted

bowel (more difficult)

 Labs

 Nonspecific

 Leukocytosis, elevated lactate,

elevated LDH, amylase, ABG

(acidosis)

Treatment

 Supportive

 Adequate resuscitation

 Occlusive:

 Surgery

 Angio

 Thrombolytic therapy if

present within 8 hours of

onset of symptoms

 Non-occlusive:

 Vasodilator therapy to

dilate the mesenteric

artery

 Resect infarcted bowel

Bowel obstruction - Causes

 Adhesions from previous surgery

 Hernias

 Incarceration

 Tumors

 Can cause partial or complete obstruction

 Ulcers

 Infections

 Abscesses

 Diverticulitis

Bowel obstruction – signs & symptoms

Duodenal or Proximal Small

Bowel:

 Depends on location &

etiology

 **Vomiting

 Crampy, epigastric pain

 Dehydrated

Distal small bowel or large bowel

 Vague abdominal pain

 Decreased passing of stool

or gas

 Constipation

 Vomiting (late – hours to

days after)

 Both:

 Decreased intake

 Fluid trapped in intestinal

loops

 Early – bowel sounds are

increased, late - decreased

Bowel Obstruction con’t

Diagonsis

 Clinical presentation &

history

 Abdominal radiograph

 Dilated loops of bowel

 Endoscopy

 CT Scan

 Upper GI

 Abdominal Ultrasound

Treatment

 Adequate fluids

 Electrolyte replacement

 Monitor for ileus

 NG tube! (removes air)

 Surgery

 Adhesions

 Incarcerated hernia

 Antibiotics (if indicated)

 Rare, can be fatal

 Stomach, duodenum,

appendix, colon

 “Rigid” abdomen

 Leakage of intestinal content

into the peritoneum

•  Systemic inflammatory response (SIRS)

 Tachycardia, tachypnea

 Fever, leukocytosis & severe

abdominal pain

 Elevated Hgb/Hct

•  Hemo-concentrated d/t dehydration

 Diagnosis

 Clinical presentation

 Abdominal films

 free air in abdomen

 Exploratory lap

 Treatment:

 Surgery

 Adequate volume

resuscitation

 Antibiotics

Acute GI Hemorrhage

Upper:

 Stomach or small intestine

 Ulcers/erosion

•  NSAIDS
• 
  
•  Excess acid production
• 
  
•  Stress

 Esophagogastric varicies

•  Portal Hypertension

 AV Malformations

 Mallory-Weiss tear

 Tumor

Lower

Distal small intestine &

colon

4 Types:

 Anatomic

•  Diverticuli

 Vascular

 Inflammatory

 Neoplastic

• 
  
•  Colon tumors

Acute GI Hemorrhage - Upper

Symptoms:

 Abdominal pain – right upper

quad

 Pain worse after eating

 Offenders: ETOH, aspirin,

spicy food

 Vomit blood – bright red or

coffee ground

 Blood in stool (dark)

 > 2 units loss, go into shock

Diagnosis & Treatment:

 Endoscopy***

 Active hemorrhage may require

angiography (embolization)

 Maintain optimal hemodynamics

 Crystalloids & transfusions

 H2 blockers or PPIs (IV, then PO)

•  Reduces the risk of mucosal lining
• damage

 Vasopressin infusion

•  0.1 – 0.8 units/min

 Octreotide acetate (Sandostatin)

•  50-150 mcg SQ BID/TID
•  Infusion: 25-50 mcg/hr x 24-48 hrs

Acute GI Hemorrhage - Lower

3 Main Causes

^{_{ Polyps/Tumors}}

• ^{_{ Diagnosed by colonoscopy}}
•  
• ^{_{ Barium enema}}
•  
• ^{_{ Endoscopic or Surgical removal}}

^{_{ Diverticulitis}}

• ^{_{ Outpouchings}}
•  
• ^{_{ Lack of fiber}}
•  
• ^{_{ Can become infected & bleed}}
•  
• ^{_{ Diagnosed by colonoscopy}}
•  
• ^{_{ Severe cases may require embolization or}}
•  
• ^{_{surgery (resection)}}

^{_{ Arteriovenous Malformations (AVMs)}}

• ^{_{ Diagnosed by colonoscopy}}
•  
• ^{_{ Endoscopic laser, thermal or electrical}}
•  
• ^_coagulation

Gastrointestinal Trauma

Blunt “closed” Trauma:

 Auto accident (“seat belt

sign”), sports injury

 Risk of bleeding or

contusion

 Risk of peritonitis

Also at risk:

•  Spleen
•  Kidney
•  Duodenum
•  Liver

Penetrating Trauma:

 Stab wounds, GSW

 High risk of bleeding

 Risk of peritonitis

Also at risk:

•  Liver
•  Stomach
•  Colon

FAST EXAM

 Focused

 Assessment with

 Sonography for

 Trauma

 Screen for blood

around heart &

abdominal cavity

Abdominal Trauma con’t

Diagnosis:

 CT Scan**

 Identify other organs injured

 Can detect hemorrhage, hematomas, ruptures, lacerations

 Diagnostic peritoneal

lavage

 Not used

 E-FAST exam

(ultrasound)

Treatment:

 Hemodynamic stability

 IV fluids

 Antibiotics

 Monitor Hgb & Hct

 Surgery if penetrating

trauma or active bleeding

 Liver or splenic injury may

require arterial

embolization

Abdominal Compartment Syndrome

 Increased intra-abdominal pressure

 Massive fluid resuscitation

•  Inflammation
•  Capillary leak

 Who’s at risk?

•  Up to 30% of trauma patients
•  Over 35% of major abdominal surgery
•  Up to 8% of critically ill patients

Signs/Symptoms of abdominal hypertension

 Abdominal distention

 Intra-abdominal pressure

> 25 mmHg

•  Normal bladder pressure is

5 – 10 mmHg

 Decreased urine output

 Abdominal perfusion

pressure:

MAP

(-) Bladder pressure (IAP)

> 60 mmHg (ideal)

 Respiratory Compromise:

•  Shortness of breath, increased respiratory rate
  
•  Increased airway pressure
  
•  Difficult ventilation

Hemodynamic effects:

•  Decreased venous return
•  Decreased C.O.
•  Increased afterload (SVR)
•  Increased preload (CVP/PAOP)

Abdominal Compartment Syndrome

Monitoring/ Treatment:

 Monitor bladder pressure via

urinary catheter

 If IAP > 25 – indication of

IACS

 Decompressive laparotomy

 Abdomen is left open

 Monitor for organ ischemia

 Follow lactate levels

Hepatic failure

Functions of the liver:

 75-90% of hepatocytes

lost before failure occurs

 Filters toxins

•  NH3 – ammonia

 Synthesize plasma

proteins

•  Albumin/coagulation factors

Causes of failure:

 Hepatitis

 Fatty Liver

•  ETOH
•  Starvation
•  Obesity
•  Diabetes

 Advanced Cirrhosis

•  Cirrhosis, tumors

 Fulminant

•  Viral
•  Toxin induced (acetaminophen, ecstasy)

Advanced Cirrhosis

Physical S/S

Atrophied muscles

 Splenomegaly

 Distended abdomen

(ascites)

 Tissue paper thin skin

 Hemorrhoids

 Jaundice

 Lower extremity edema

 Spider angiomas

Labs

 ↓ Albumin, protein

 ↓ Platelet count, fibrinogen

 ↓ Na, K+, Mg, Ca, glucose

 ↑ RBCs, ↑/ ↓ WBCs

 ↑ Hepatic Transaminases

 AST, ALT, LDH, alkaline

phosphatase

 AST/ALT ratio > 1 = chronic failure

 ↑ PTT/PT/INR

 ↑ Lactate

 ↑ Bilirubin

 ↑ Ammonia

Clinical Presentation

 Hypotension

 GI Bleed

 Weight loss

 Poor appetite

 Ascites (shortness of breath)

 Chronic low albumin level

•  Liver unable to make albumin

 Portal HTN

•  Hydrostatic pressure pushes fluid into abdominal space

 Poor renal perfusion

 ↑ Aldosterone & ADH contribute to

fluid retention

 Jaundice (↑ bilirubin)

 Usually scleral first

Neuro:

 Lethargic

 Slow to respond

 Slurred speech

 Decreased LOC

 Asterixis

•  Flapping hands

 Hepatic encephalopathy

 Cerebral edema

 Increased ICPs

 Seizures

 Coma

Cirrhosis Diagnosis

 Hepatic parenchymal

cells destroyed,

replaced with fibrotic

tissue

 Constriction of blood

flow leads to portal

hypertension

 Liver biopsy

 Ultrasound

•  Assess portal hypertension & nodules

Treatment

 Assess causative reason

 Eliminate cause (ETOH)

 Symptom management

 Evaluate for liver

transplant

Ascites Management

 Low Na+ diet

 Fluid restriction

•  1.5 L/day

 Diuretics

•  Aldosterone antagonists
• (Spironolactone)
•  Loop diuretics

 Paracentesis

 Little evidence to

protein restrict

 Nursing care:

 Measure abdominal

girth

 Daily weights

 Monitor labs

 Monitor for hepatorenal

syndrome

•  Oliguria
•  Decreased urine Na+
•  Increased
• BUN/Creatinine

 Monitor for bleeding

•  Vitamin K abnormalities

 High risk of developing

liver carcinoma

 Monitor for sepsis

•  Translocation of bacteria
•  GI tract  blood stream

 Severity of disease

•  Childs-Pugh
• Classification

Grading severity of cirrhosis

Grading severity of cirrhosis

Nursing con’t

 Monitor neuro changes &

LOC

 Drug clearance

 Caution with sedatives

 If ammonia elevated –

Lactulose

•  Poorly absorbed sugar
•  Decreases bowel pH
•  Ammonia excreted in stool

Neomycin

•  Poorly absorbed antibiotic
•  Destroys normal flora of large intestine

 Nutrition

•  TPN or tube feeding if unable to take PO

 Assess for bleeding

 Daily weights

 Fluid & Na restrict

 Paracentesis – Not first

line treatment; reaccumulation

 Monitor respiratory status

•  Pressure on diaphragm

Esophageal Varices

Clinical Presentation

Dilated, engorged submucosal

veins in the mid to

distal esophagus

 Caused by portal

hypertension

 30% mortality associated

with a bleed

 Elevated liver enzymes,

bilirubin, coag times (PT/INR)

 Quickly go into hypovolemic,

hemorrhagic shock

Esophageal Varices con’t

Treatment

 Difficult to control

bleeding

 Correct coags

 Airway protection

 Hemodynamic support

 Vasopressin infusion

•  0.4 – 1 unit/min
•  Reduces portal pressure

To achieve hemostasis:

 Somatostatin

•  Short acting
•  Causes decrease in portal inflow

 Octreotide

•  Long acting – continue for up to 5 days post bleed

Esophageal Varices Treatment

Endoscopic

 Banded ligation

 Sclerotherapy

 High incidence of re-bleed

 Beta blockers

(propranolol)

 Nitrates

 Band ligation

Transjugular Intrahepatic

Portosystemic Shunting (TIPS)

 Done in IR

 Blood directed from

the portal vein to the

hepatic vein

^Relieves

^pressure

^{in the}

^portal

^system

Esophageal Varices – Uncontrolled bleeding

 Esophageal Balloon

•  Minnesota Tube, Blakemore

 Tamponade bleeding area

 High incidence of re-bleeding

after removal

 Placement verified via x-ray

 Airway

•  Endotracheal intubation
•  Aspiration

 Safety:

•  Scissors always at the bedside

Gastric balloon inflation:

250 – 500 cc SB

450 – 500 cc Minnesota

Pancreatitis

 Pancreas

 Composed of head, body

& tail

 Endocrine gland

•  Secretion of insulin
•  Secretion of glucagon

 Exocrine gland

 Release digestive enzymes

•  10% of pancreatic
• enzymes must be present to
• prevent malabsorption

Pancreatic enzymes

 Amylase

 Alpha amylase released in saliva

 Breaks down carbohydrates

 Pancreatic amylase

 Breaks down raw & cooked starches

 Lipase

 Digest fats

 Bile salts are essential for this!!!

Acute Pancreatitis

 Enzymatic auto-digestion

 Acute, local inflammation

 Triggers systemic inflammation

 Enzymes are activated prior to

release from the pancreas

 Obstruction can lead to

activation of the enzymes

 2 most common causes:

 ETOH

 Gall stones

 Both – duct obstruction

Acute Pancreatitis – Clinical Presentation

 Pain

•  Upper abdomen, radiates to the back

 Distended abdomen

 Bowel sounds decreased or absent

Other symptoms:

 Nausea, vomiting

 Fever

 Tachycardia

 Hypotension

 Pleural effusions

•  Left sided or bilateral

 Atelectasis

 Elevated hemi-diaphragm

 Pulmonary infiltrates

 Monitor for ARDS!!!

 Necrotizing pancreatitis –

Severe form

•  Necrosis of pancreas, peripancreatic
• tissue & fatHemorrhage

 S/S Hypovolemic shock

 Sequestration of fluids in the

peritoneum

Other S/S of Pancreatitis:

 Cullen’s sign

 Grey-Turner’s

•  May appear within 1-2 weeks
• with hemorrhagic pancreatitis

Diagnosis of Acute Pancreatitis

 Clinical signs & symptoms

 Elevation of amylase***

(elevates within 24 hours)

•  Many times over 500
•  Can return to normal within
• 3 to 5 days after onset
•  Note: Not a marker of severity

 Elevated lipase

•  Stays elevated longer than amylase

 Elevated urinary amylase

 Hypocalcemia

•  Follow ionized calcium

 H/H – may be increased

or decreased (esp later)

 Leukocytosis

 Hypoxemia

 Hypoalbuminemia

 Hyperglycemia

 Hypokalemia

 Hypomagnesemia

 Steatorrhea

Ranson’s Criteria for Acute Pancreatitis

Present on Admission:

 Age > 55

 WBC > 16,000

 Glucose > 200 mg/dL

 Serum LDH >350 IU/L

 SGOT (AST) > 250

IU/L

Developing during the first 48

hours:

 Hct drop > 10%

 BUN increase > 8 mg/dL

 Serum Calcium < 8 mg/dL

 Arterial oxygen sat < 60

mmHg

 Base deficit > 4 mEq/L

 Estimated fluid

sequestration > 600 ml

Score 0 – 2: Minimal mortality

Score 3 – 5: 10 – 20% mortality

Score > 5: More than 50% mortality, associated with increased systemic complications

Highest risk – Modified Glasgow

P = PaO2 (< 60, ARDS)

A = Age (> 55 yo)

N = Neutrophils (Increased WBCs)

C = Calcium (Hypocalcemia)

R = Renal function (Increased BUN)

E = Enzymes (Elevated ALT/LDH)

A = Albumin (hypoalbuminemia)

S = Sugar (Hyperglycemia)

Diagnostics & Treatment Pancreatitis

 Serum amylase & lipase

 CT Scan

•  Caution with contrast

 Ultrasound

•  Assess for gall stones & pancreatic fluid collections
•  If gallstone obstruction – ERCP (Endoscopic Retrograde
•      Cholangiopancreatography)

 MRI

 Visual fluid collections or

masses

 Supportive – Multi-system organ

failure

 Rest the pancreas

•  NG tube if ileus is present

 Prevent complications

•  Pulmonary
•  Needle aspiration of fluid –
• guide antibiotic therapy

 Cardiovascular & hemodynamic

monitoring

•  Adequate volume resuscitation

 Pain management

 Nutritional support

•  Feeding tube past the duodenum
•  Parenteral

Nursing Interventions Pancreatitis

 Pain management

 Close monitoring of

•  Hgb/Hct
•  BUN/Creat/Creatinine
• clearance Electrolytes

 Monitor for:

•  Respiratory compromise
•  Hypovolemia

 Why such severe

hypocalcemia?

Answer:

 Calcium binds with

fatty acids from

necrotic fat

 Hypoalbuminemia

Malnutrition

 Minimal caloric needs: 25 kcal/kg/day

 Protein needs: 1 gram/kg/day

 Assessing nutritional status

 Pre-Albumin

 Albumin

 Malabsorption

 Steatorrhea – fat in stool

Bariatric Surgery: Who qualifies?

 > 18 years

 Low BMI (30-34.9) with co-morbid condition

 BMI > 35 with co-morbid condition

 BMI > 40

 Loss of > 50% of excess body weight = SUCCESS

 Surgery is the only proven method to have long

term effects

Pre-Op requirements:

Bariatric Surgery

 MD Consult

 Mental Health consult

 Nutrition consult & education

•  Labs (baseline vitamin levels, lipid panel, CBC,
• chemistry panel)
•  ABG
•  Sleep Testing
•  12 Lead EKG (over age 50)
•  Endoscopy
•  Consults (Cardiology, Pulmonary, Pain)

 Adjustable Gastric Banding

 Gastric Sleeve

 Gastric Bypass (Roux en Y)

 Bilio-Pancreatic Duodenal Switch - rare

Weight Loss Expectations:

Weight Loss Expectations:

 Laparoscopic only

 Surgery takes about 30 min

 Home same day or next day

 FDA approved for BMI 30-35

 Return 4-6 weeks post-op for “fill”

 Weight loss slower

 Lower risk

Gastric Sleeve

Gastric Sleeve

 Laparoscopic or open

 2/3 of stomach is removed

 Stomach is now a tube with restriction at the

proximal end

 Inner diameter ~ 16 mm

 Surgery takes about 45 min

 Overnight hospital stay

 Monitor for bleeding or leak

Gastric Bypass (Roux-en-Y)

 Laparoscopic or open

 Small intestine anastomosed to upper portion of stomach

 Creates a “pouch”

 Pouch only holds ~30 cc

 UGI post-op am

 1-3 day hospital stay –

•  1st night close observation

 Initial rapid weight loss

 Monitor for bleeding & leak

Post-Op concerns Bariatric

 Monitor for signs of bleeding

•  Increased HR, decreased BP

 Monitor for signs of leaking

•  SIRS, signs of sepsis

 High risk for DVT, Pulmonary embolism,

 Monitor for hypoglycemia

 Small, frequent, usually liquid meals for 1st week

 Protein based

 Long term:

 Dumping syndrome

 Vitamin deficiencies

 Lactose intolerance