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4. Responses To Altered Metabolic-GI-Liver Alterations

Emergency and Critical Care Nursing (Velez College)

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RESPONSES TO METABOLIC-GASTROINTESTINAL AND LIVER ALTERATIONS

I. ASSESSMENT
- Assess px’s physical & psychological statuses & interpret lab data
A. Altered Gastrointestinal Function
1. General Nutritional Status Interview
 Should begin with questions regarding client’s dietary habits
 Questions should elicit information about average daily intake of food and
liquids, types and quantities consumed, where and when food is eaten, and any
conditions or diseases that affect intake or absorption
 What questions do you ask?
o Food intake history, Time, Food/drink, Amount, Method of preparation
2. Health History
 Elicit a description of present illness and chief complaint or symptoms through
COLDSPA
o Characteristics, onset, location, duration, severity, precipitating &
alleviating factors
 Family history, prenatal history, medications, use of tobacco and alcohol
 Complete nutritional history including 24-hour dietary intake

B. Focused Assessment of Clients with Hepato-Biliary & Pancreatic Disorders

1. Health History
 Elicit description of present illness and chief complaint
o Onset, course, duration, location, and precipitating and alleviating factors
o Cardinal signs and symptoms indicating altered hepatic, biliary, and
pancreatic function include:
 Jaundice, pruritus
 Jaundice can produce pruritus due to impaired bile-acid
excretion
 Changes in urine and stool color
 Vague to severe abdominal pain especially after eating fatty foods
 Abdominal tenderness and distention
 Easy bruising and bleeding
 Alcohol consumption
 Diet high in fat
 Infectious agents (transmitted thru nonsterile needle puncture, unprotected
sexual activity, ingestion of potentially contaminated food, etc)
 Recent blood transfusions
 Medications and herbal remedies
o Some sample drugs with high potential for hepatotoxicity:
 NSAIDS – such as ibuprofen, acetaminophen

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 Antiseizure meds – phenytoin, valproic acid

 TB drugs – isoniazid, pyrazinamide
II. PHYSICAL ASSESSMENT
- Px lies supine, knees flexed, slightly for inspection, auscultation, percussion & palpation of
the abdomen

1. Inspection
- Performed first noting any skin changes, nodules, skin lesions, scarring and/or discolorations
- Lesions are of particular importance bec GI dses often produce skin changes
- Inspect contour & symmetry of the abdomen noting for any localized bulging & distention
o Expected contours of the anterior abdominal wall: flat, rounded, or scaphoid
- Nsg priorities during inspection:
o Focuses on oral cavity, skin over the abdomen, & shape of the abdomen
 Skin, mucosa & sclerae: jaundice, petechiae or ecchymotic areas, spider angiomas,
palmar erythema
 Extremities: muscle atrophy, edema, skin excoriation s/t scratching
 Abdomen: contour, girth, pigmentation, color, scars, striae, visible masses, peristalsis
& pulsations
 Cognitive & Neurologic Status

2. Auscultation
- Always precedes percussion & palpation bec this may alter bowel sounds
- Determines character, location, frequency of bowel sounds
- Identifies vascular sounds
- Bowel sounds are using the diaphragm of the stethoscope for soft clicks & gurgling sounds
- Frequency & character of the sounds are usually heard as clicks & gurgles that occur
irregularly
 Auscultate bowel sounds before percussion and palpation (5-30 clicks/min – using
diaphragm of stethoscope for 5 minutes)
 Normal bowel sounds occur 5-30 times a min or every 5-15 seconds
 Auscultate in all abdominal quadrants
o Auscultate for vascular sounds (e.g. bruits, hepatic friction rub)

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3. Percussion
- Size, density of the abdominal organs
- Detect of air-filled, fluid-filled or sold masses
 Percuss all 4 quadrants noting tympany and dullness

4. Palpation
- Performed last so that the sounds from palpation aren’t auscultated
 Palpate deeply over all 4Qs for any masses and note location, size and shape,
pulsation
 Palpate liver, spleen, kidneys, and aorta for enlargement
 Always palpate tender areas last

III. DIAGNOSTIC ASSESSMENT

A. Non-Invasive
1. Guaiac Test (Stool for Occult Blood)
 Looks for hidden (occult) blood in a stool sample
o Involves putting a fecal sample on guaiac paper & applying hydrogen
peroxide w/c in the presence of blood, yields a blue rxn product w/in
seconds
 Detect GI bleeding (GI cancer)
 Instruct px to:
o Increase fiber diet 48-72 hours prior to the test
o No red meats, poultry, fish, turnips, horseradish, melons, salmon,
sardines
o Withhold 48 hours: Iron, steroids, indomethacin, colchicine, Vitamin C
 Done to avoid false + results
o Need to submit 3 stool specimens for 3 successive days

2. Hepatobiliary Scan
 Otherwise known as liver scan
 A non-invasive nuclear medicine study using radioactive materials to show size
and shape of liver tissue & to visualize replacement of liver tissue with scars,
cysts, & tumor
o Technetium, gallium, gold
 Radioactive agent is injected I.V which is taken up by the liver/hepatocyte &
excreted rapidly through the biliary tract
 Patient is placed on NPO & NO opioids given 4H before procedure
o S/E of opioids: constipation
o Withhold this to facilitate excretion of radioactive agent after the
procedure

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3. Radionuclide Imaging or Cholecystography

 Procedure is more or less the same with liver scan but this time, images of the
gallbladder & biliary tract are obtained after I.V administration of radioactive
agent

4. Upper GIT study/series (Barium Swallow

 An examination of the upper GIT under fluoroscopy after the client drinks barium
sulfate (BaSO4)
o Contrast agent
o Tasteless, odorless
o Non-absorbable suspension
 To visualize the esophagus, stomach, duodenum, and jejunum
 Pre-op
o NPO after midnight or 6-8 H before the day of test
o Withhold opioids 24H before test
 Post-op
o Laxative
o EOF
 Facilitate excretion of contrast agent
o Monitor for passage of barium (stools will appear chalky white for 24-72
hours)

5. Lower GI study/series (Barium enema)

 A fluoroscopic and radiographic examination of large intestine is performed after
rectal instillation of BaSO4
 Indicated for detecting bowel obstruction and cause of diarrhea and constipation
 C/I to pxs with colon perforation or fistula
o Barium contrast agents may cause peritonitis if they leak into the
peritoneal space
 Pre-op
o Low residue diet 1-2 days
o Clear liquid diet and a laxative the evening before test

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o NPO after midnight before day of test

o Suppository/Cleansing enema on morning of test
 Post-op
o EOF
o Administer mild laxative as prescribed
o Monitor passage of Ba and notify physician if bowel does not occur 2 days
after

6. Capillary Blood Glucose Monitoring

 Convenient way of monitoring blood glucose patterns and can be useful aid in
guiding treatment changes in patients with Type 1 and Type 2 diabetes,
especially during periods of illness or frequent hypoglycemia
 Let patient fast prior to extraction
o Fast 2-3 H before extraction
 Rotate sites
 Discard first drop of blood
o To prevent serous fluid from causing false + result

B. Invasive
1. Esophagogastroduodenoscopy (EGD)
 An upper GI fibroscopy
 Done with fiberscopes
o Flexible scope
 After sedation, an endoscope is passed down the esophagus to view the gastric
wall, sphincters, and duodenum; tissue specimens can be obtained for direct
visualization of Esophagus, stomach, and duodenum
o A local anesthetic is administered alongside midazolam versed IV
 Sedative
 Local anesthetic is administered to decrease anxiety & cause mild
sedation
 Pre-op

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o Obtain written consent

o NPO 6-8H or 12H before test
o Sedatives, narcotics, tranquilizers as prescribed (e.g. diazepam,
meperidine hydrochloride)
 To relax px
o AtSO4 and glucagon as ordered
 Atropine sulfate
 Cholinergic
 Given to reduce salivation/secretion
 Glucagon
 To relax smooth muscles of esophagus
o Remove denture to prevent airway obstruction
o Airway patency is monitored during the test
o Apply mouthguard
 Post-op
o Patient is positioned on left side
 To facilitate drainage of secretions
o NPO until gag reflex returns
 Usually would return 1-2 or 2-4 H
o Monitor for signs of perforation
 Pain, bleeding, unusual difficulty swallowing, elevated temp
o Maintain bedrest for the sedated px until alert and advise to avoid
driving 12H if sedative was used
o Lozenges, saline, gargles, or oral analgesics can relieve minor sore throat,
after the gag reflex returns
2. Endoscopic Retrograde Cholangiopancreatography (ERCP)
 Endoscopic visualization of common bile, pancreatic, and hepatic ducts with a
flexible fiber-optic endoscope inserted into the esophagus, passed through the
stomach and into the duodenum; the common bile duct and the pancreatic duct
are cannulated and contrast medium is injected into the ducts, permitting
visualization and radiographic evaluation

 Nursing considerations:
o Pre-procedure:
 Assess for allergies to iodine, seafood, or contrast media
 Place px on NPO 4H before procedure
 Remove dentures & instruct to gargle and swallow topical
anesthetic to decrease gag reflex, as ordered
 Verify informed consent BEFORE sedation
 Establish baseline v/s & IV access

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Administer antibiotic prophylaxis, glucagon & anticholinergics as

ordered
o Post-procedure
 Monitor and document v/s
 Monitor complications (i.e. esophageal bleeding, GI perforation,
pancreatitis, sepsis)
 Invasive diagnostic testing can cause GI perforated bowel
o Perforation: 1 of the most serious complications of
endoscopy of the lower GI tract
 Monitor for return of gag reflex

3. Percutaneous Transhepatic Cholangiography (PTC)

 A fluoroscopic examination of the intrahepatic and extrahepatic biliary ducts
after injection of contrast medium into the biliary tree through percutaneous
needle injection
 Useful for distinguishing jaundice caused by liver disease (hepatocellular
jaundice) from that caused by biliary obstruction, for investigating the
gastrointestinal symptoms of a patient whose gallbladder has been removed, for
locating stones within the bile ducts, and for diagnosing cancer involving biliary
system
 Pre-procedure:
o Assess allergies to iodine, seafood
o Place px on NPO 4H prior to procedure
o Verify informed consent BEFORE sedation
o Establish baseline v/s & ensure coagulation parameters and platelet
count is within normal limits
o Establish IV access & administer prophylactic antibiotics as ordered
 Post-procedure:
o Monitor & document v/s
o Assess puncture site for bleeding, hematoma, or bile leakage
o Monitor for signs of peritonitis & sepsis
o Report presence of pain immediately

4. Liver Biopsy
 Sampling liver tissue by needle aspiration for histologic analysis
 Can establish a diagnosis of specific liver disease
 Physician inserts biopsy needle by way of transthoracic (intercostal) or
transabdominal (subcostal) route
 Pre-procedure:
o Establish baseline hemoglobin level, hematocrit, & PLT count

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o Make sure prothrombin time (PT) is within normal limits

o Verify informed consent
o Establish baseline v/s
o Positioning for liver biopsy: supine/left lateral w/ right side of upper
abdomen and with patient’s right arm raised & extended over left
shoulder behind the head
o Tell patient that cooperation during procedure is important; he/she is
instructed to exhale & hold breath at end of expiration for at least 10
seconds as the biopsy needle is introduced
 Post-procedure:
o Positioning immediately after biopsy: right lateral/side-lying with small
pillow or folded towel placed under costal margin of puncture site
(patient is instructed to remain immobile & maintain position for at least
3H)
o Monitor v/s and biopsy site for hemorrhage and drainage
o Instruct patient to avoid coughing or straining
o Also instruct patient to avoid heavy lifting & strenuous activity for 1 week

5. Serum Blood Studies

- Usually begin w/ serum lab studies: CBC, Complete metabolic panel, PT, APTT, liver fxn test
i. Liver Function Tests
 Serum Enzymes
o Alkaline phosphatase (ALP) = in absence of bone disease, it is a sensitive
measure of biliary tract obstruction (NV: 13-19 units/L)
o Lactate Dehydrogenase (LDH) = may be increased in liver damage (NV:
100-120 units)
o Aminotransferase/Transaminases = enzyme which are increased in liver
cell damage as damaged liver cells primarily release these liver enzymes
 Alanine aminotransferase (ALT)
 Previously called Serum glutamic pyruvic transaminase
(SGPT)
 Levels are increased primarily in liver d/o
 Used to measure course of hepatitis or cirrhosis, effects of
ttt that may be toxic to the liver
 N.V.: 5-35 units
 Aspartate Amine Transferase (AST)
 Previously called serum glutamic-oxaloacetic transaminase
(SGOT)
 Not a sensitive index of liver function since levels are also
high in damage to heart, skeletal muscle, & kidney

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 NV: 10-40 units

 Gamma glutamyl transferase (GGT)
 Also called G-glutamyl transpeptidase
 Levels are high in alcohol-induced liver damage
 Also a sensitive indicator of biliary cholestasis
 NV: 10-48 IU/L
 Serum proteins = measures ability of liver to synthesize proteins
o Albumin = NV: 4.0 - 5.5 g/dL
 Decreases w/ hepatocellular injury
o Globulin = NV: 1.7 - 3.3 g/dL
 Increases w/ hepatitis
o Albumin/Globulin (A/G) ratio = normally 2:1; low in chronic liver disease

 Pigment Studies = measures ability of the liver to conjugate and excrete

bilirubin; abnormal in liver & biliary tract disease associated with jaundice
clinically
o In the liver, bilirubin is changed into a form that the body can get rid of
called the conjugated/direct bilirubin
o Px is instructed to eat a diet low in yellow food for 3-4 days and to fast
for 4H before blood is drawn
 Carrots, yams, yellow beans
o Total bilirubin = used as screening test for liver or biliary dysfunction; NV:
 1.5 mg/dL
o Direct (Conjugated) Bilirubin = increased in bile obstruction; NV: 0.03
mg/dL
o Indirect (Unconjugated) Bilirubin = increased in hepatocellular failure &
hemolytic jaundice; NV: 0.1 -1.1 mg/dL
o Urine bilirubin = high if direct bilirubin is also high

 Serum Ammonia = increased in liver failure, indicated decreased ability of liver

to convert ammonia to urea; NV: 35 - 65 mcg/dL

 Blood coagulation studies = prolonged in liver failure (e.g. PT, APTT)

o Prothrombin Time = 10-40 sec or 90% of control
 Increases w/ chronic liver dse or vit K deficiency
o International Normalized Ratio (INR) = 0.9-1.3
 Increases w/ presence of high chance of bleeding
 Useful for monitoring effects of drugs such as warfarin
o Partial Thromboplastin time (PTT) = 25-40 sec
 Increases w/ severe liver dse or heparin therapy

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IV. NURSING DIAGNOSES:

- Acute/Chronic Pain related to Lesions Secondary to Increased Gastric secretions
- Imbalanced Nutrition: Less than Body Requirements related to Anorexia
- Impaired Comfort related to Pruritus
- Excess Fluid Volume related to Portal Hypertension
- Pain related to Liver Enlargement
- High Risk for Ineffective Therapeutic Regimen related to Lack of Knowledge
- Decreased Cardiac Output related to Alterations in Preload
- Deficient Fluid Volume related to Absolute Blood Loss
- Anxiety related to Threat to Biologic, Psychologic and or Social Integrity
- Hyperthermia related to Increased Metabolic Rate

V. PLANNING
 Administering Volume Replacement
 Controlling bleeding
 Maintaining surveillance for complications
 Administering fluids, insulin, and electrolytes
 Monitor Response to therapy
 Normalize body temperature
 Patient education

VI. METABOLIC-GASTROINTESTINAL AND LIVER ALTERATIONS

1. Acute GI Bleeding
 Gastrointestinal Bleeding = any bleeding that starts in the gastrointestinal tract
o Symptoms can occur w/o warning, be sudden & severe or have a slow onset
o Acute GI bleeding can be life threatening if the cause of bleeding can’t be
treated/controlled
 Common reason for a px to be admitted to the ICU
 74-100% of critically ill pxs develop stress-related GI mucosal erosions w/in
24H of admission that can lead to serious GI bleeding
 Bleeding may come from any site along the GI tract, but is often divided into:
o Upper GI bleeding: The upper GI tract includes the esophagus (the tube from mouth
to stomach), stomach, and first part of small intestine
 Medical emergency associated w/ morbidity, mortality, & costly care
 4x more common than lower GI bleeding

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 Commonly has s/s of hypovolemic shock

o Lower GI bleeding: The lower GI tract includes much of the small intestine, large
intestine or bowels, rectum, and anus
 Has a lower morbidity & mortality
 Bleeding resolves spontaneously in the vast majority of pxs
Distinguishing upper & lower GI bleeding by origin is an impt consideration
- A rapid upper GI bleed may present as a presence of blood in the lower GI tract
 Etiology: may be due to conditions including:
Upper GI tract disorders:
o Peptic Ulcer Disease
 Duodenal ulcer (20-30%)
 Gastric ulcer (10-20%)
 PUD: Most common cause of upper GI bleeding
o Gastric or duodenal erosions (20-30%)
o Gastroesophageal Varices (15-20%)
o Occurs when there is an increased pressure in the portal venous system
of the liver
o If blood X flow easily through the liver bec of obstructive dse, it is
diverted into collateral channels
 Normally the low pressure vessels found in distal esophagus
 Such as esophagus varices
o Acute upper GI hemorrhage occurs when esophageal and/or varices
rupture from increased portal vein pressure such as that of portal
hypotension
Lower GI tract disorders:
o Anal fissures
o Colitis: Radiation, ischemic, infectious
o Colonic sarcoma
o Colonic polyps
o Diverticular disease
o IBD – Inflammatory Bowel Dse (Ulcerative Colitis, Crohn disease)
o Internal hemorrhoids
 Clinical Presentation:
o Hematemesis
 Bright red bloody vomitus
 Associated w/ fresh bleeding indicating upper GI bleeding
 Coffee-ground emesis
 Caused when blood is mixed w/ digestive juices
 Usually indicates that the bleeding has slowed/stopped

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o Melena
 Black, tarry stool w/ a characteristic foul order
 Usually indicates upper GI bleeding sources
 Bec blood has gone through the GI tract

o Hematochezia
 Fresh, red maroon stools
 Regardless of source, lower GI bleeding typically presents as this
 But it can also occur w/ massive upper GI bleeding w/c is usually
associated w/ orthostatic hypotension but most of the time, it’s usually a
lower GI bleeding source
o Syncope
o Dyspepsia (indigestion)
o Epigastric pain
o Heartburn
o Diffuse abdominal pain
o Dysphagia
o Weight loss
o Signs of shock: hypotension, decreased pulses, decreased urine output
o Jaundice
 Diagnostics:
o Endoscopy = considered “gold standard” for diagnosis of GI bleeding
o Provides direct visualization of GI tract & bleeding site
o EGD
o Colonoscopy
o Radiographic procedures
o Upper & lower GI studies
o Serum blood studies
o CBC, metabolic profiles, coagulation profiles
 Treatment:
Fundamental goal of initial ttt: securing airway & initiating volume resuscitation
Focus: hemodynamic stabilization, identification of bleeding
Endoscopy w/in 12-24 H of admission is essential for those unstable upon admission or those who
continue to actively bleed after resuscitation
o Fluid resuscitation
 Adequate resuscitation and stabilization is essential

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 Patients with active bleeding should receive IVF (e.g 500 mL of NS or RL over 30
minutes) while being crossmatched for blood transfusion
 Blood transfusion
 Must be individualized
 Approach is to initiate blood transfusion if hemoglobin is < 7 g/dL (70g/L)
o Hemostasis
 GI bleeding stops spontaneously in abt 80% of pxs
 Remaining pxs require some type of interventions
 Early intervention to control bleeding is important to minimize mortality,
particularly in elderly patients
o Airway
 Major cause of morbidity & mortality in pxs w/ active upper GI bleeding is
aspiration of blood w/ subsequent compromise
 To prevent these probs, endotracheal intubation should be considered in patients
who have inadequate gag reflexes or are obtunded or unconscious—particularly
if they will be undergoing upper endoscopy
o Active variceal bleeding
 Can be treated with endoscopic banding, injection sclerotherapy, or transjugular
intrahepatic portosystemic shunting (TIPS) procedure
o General Support
 Supplemental oxygen via nasal cannula
 NPO
 Shock & bleeding must be controlled before oral intake
 Client should receive nothing by mouth during acute phase of GI bleeding
 When bleeding is controlled, diet can gradually be increased starting w/
ice chips & then clear liquids
 PIVC (16G/18G) or a central venous line should be inserted
 Placement of a pulmonary artery catheter
 Elective endotracheal intubation
 Nursing Management:
o All critically ill patients should be considered at risk for stress ulcers and therefore GI
hemorrhage. Maintaining gastric fluid pH 3.5-4.5 is a goal of prophylactic therapy
o Major nursing interventions are:
 Administering volume replacement
 Controlling bleeding
 Maintaining surveillance for complications (i.e. hemorrhagic shock)
 Educating family and patient

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2. Intra-abdominal Hypertension and Abdominal Compartment Syndrome

What is IAH and ACS?
 Intra-abdominal Pressure = pressure concealed within the abdominal cavity
 Intra-abdominal Hypertension (IAH)
o Sustained pathological elevation of IAP greater than or equal to 12 mmHg
 Grade I: IAP between 12 - 15 mmHg
 Grade II: IAP between 16 - 20 mmHg
 Grade III: IAP between 21 - 25 mmHg
 Grade IV: IAP > 25 mmHg
o If untreated, IAH can lead to abdominal compartment syndrome
 Medical emergency that accts for significant morbidity & mortality in critically ill
pxs
 Abdominal Compartment Syndrome (ACS)
o Organ dysfunction caused by intra-abdominal pressure > 20 mmHg– This is a medical
emergency!
o End-stage complication of untreated IAH
o Affects mesenteric, hepatic, & intestinal systems & can diminish blood flow to intra-
abdominal organs
 Prevalence:
o IAH and ACS are not only related to trauma
 IAH and ACS are equally prevalent in medical patients
 Can be found in every critical care population
 Pathophysiology
o Initial injury (caused by trauma, hemorrhage, sepsis, hypotension, etc)  produces
hypoxia of intestinal tissues  results in mild systemic inflammatory response (3
sequelae which develops positive feedback loop: (1) release of cytokines, (2) oxygen
free radicals produced, and (3) decreased production of adenosine triphosphate (ATP);
translocation of bacteria from gut to mesenteric lymph nodes)
o Any secondary injury causes an exaggerated systemic inflammatory response

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 Possibly caused by bacterial translocation  additional release of cytokines 

perpetuates the positive feedback loop
o Combination results in increasing IAP and hypoxia
 Effects of Increase Intra-abdominal Pressure
o Renal
 Compression of renal veins and collecting systems
 Oliguria, activation of RAA system, acute tubular necrosis and renal
failure (if prolonged)
o Neurological
 Increased ICP
 Decreased Cerebral perfusion pressure (CPP)

o Gastrointestinal
 Edema
 Necrosis

 Intra-abdominal Pressure Monitoring = the gold standard for diagnosing intra-abdominal

hypertension.
o Measure IAP at least every 4-6 hours
o IAP is measured by measuring bladder pressure
 Requires placement of indwelling urinary catheter
 Drainage bag clamped
 Patient in flat supine position (recommended) to avoid muscle contraction
 If not tolerated, may place in supine 30-degree reverse Trendelenburg
 Note patient’s position at time of pressure measurement in medical
record
 Instill 25 mL of sterile 0.9% normal saline through catheter
 Transducer attached to catheter sample port (transducer zeroed to mid-
axillary line at the level of the iliac crest)
 Obtain pressure reading during end-expiration
 Subtract instilled volume from urinary output

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 Monitor for trends and signs of organ dysfunction

 Treatments:
o Titrate therapies for IAP lesser than or equal to 15mmHg
o Optimize fluid status
o Optimize systemic perfusion
 Goal abdominal perfusion pressure (APP) of greater than or equal to
60mmHg
 APP = MAP – IAP
o Mean arterial pressure
o Intra-abdominal pressure
o Evacuate intraintestinal contents
o Evacuate intra-abdominal lesions
o Improve abdominal wall compliance
o Consider emergent abdominal decompression
 Percutaneous drain to remove fluid
 Decompressive Celiotomy
 Bedside laparotomy

3. Liver Failure
 Liver: largest organ of the body
o Essential role in regulating body’s metabolism
 An uncommon condition in which rapid deterioration of liver function results in
coagulopathy and alteration in mental status
o Common adverse complication: hepatic encephalopathy
 Liver failure indicates that liver has sustained injury
 Types of Liver Failure:
o Fulminant Hepatic failure = encephalopathy starts within 8 weeks
 Otherwise known as acute failure
 Results in a rapid deterioration of liver fxn in a person w/o prior liver dse
 Cellular insult results in a massive cell necrosis leading to multiple organ
dysfxn
o Non fulminant hepatic failure = encephalopathy starts between 8-26 weeks
 Acute Liver Failure
o Is a rare condition characterized by the abrupt onset of severe liver injury
o Loss of liver function that occurs rapidly – in days or weeks – usually in a person who
has no pre-existing liver disease
o It’s a medical emergency that requires hospitalization
o Leading cause
 Acetaminophen overdose
o Other causes:

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 Viral hepatitis (A, B, E)

 Thrombosis
 Shock
o Px hx:
 Focus: exposure to viral infxns, drugs or other toxins or other recent
injuries/illnesses
 Px & family should be questioned abt acetaminophen intake
 Acetaminophen toxicity
o Antidote:
 N-acetylcysteine (NAC or Mucomyst)
 Activated charcoal
 Decontamination agent
 Prevents absorption of acetaminophen by
absorbing drug in the intestine
o Clinical Manifestation:
 Jaundice
 2ndary to excessive deposition of bilirubin in skin tissues, mucous
membrane, sclera
o Represents failure of liver to adequately uptake, conjugate &
excrete bilirubin
o Bec of this, jaundice is typically evident when bilirubin exceeds
2-3 mg/dL
 Hepatic encephalopathy (mental confusion, difficulty concentrating and
disorientation)
o Altered mental status & level of consciousness
o Neurological status requires vigilant assessment bec hepatic
encephalopathy, cerebral edema, & increased ICP can rapidly
progress into brain __ & death)
 Pain and tenderness in the upper right side of the stomach
 Electrolyte imbalances (hypoglycemia, hypokalemia, hypomagnesemia,
hypocalcemia, and hypophosphatemia)
o Hypoglycemia develops due to massive hepatic cell necrosis
thus there will be a diminished glucose release
o Hypokalemia may occur from inadequate oral intake
potassium loss from vomiting
 Melena
 Ascites
o Accumulation of fluid in the stomach due to a lot of factors

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 Portal hypotension, hypoalbuminemia, inactivation of

RAA mechanism (aldosterone-antidiuretic hormone)
thereby promoting fluid retention in the body
 Ankle edema
o Albumin is responsible for maintaining colloid osmotic
pressure in the vascular system
o In the absence of albumin, fluids from the vascular system
could cross over into the interstitial space thus the
accumulation of fluid in the legs, ankle, & feet
 Malaise, drowsiness, and muscle tremors
 Bleeding, cerebral edema, hematemesis, coma
o Bleeding: Increased PT or INR > 1.5

o Management:
 Treatment of acute liver failure consists of drugs and liver transplantation
 Pharmacological management includes certain antidotes to reverse the
effects of ALF and various medication to reduce ICP
 Penicillin G, activated charcoal, N-acetylcysteine, osmotic diuretics
(mannitol to decrease cerebral edema), barbiturate (phenobarbital
when severe intracranial hypertension doesn’t respond to any
measures), benzodiazepine, and anesthetic agents (propofol –
sedative hypnotic to reduce cerebral blood flow)
 Nursing Interventions:
 Assess, report, and record signs and symptoms and reactions to
treatment
 Monitor fluids input and output closely
 Observe for signs of dehydration, 2ndary infxn,
neurologic disturbances, edema, jaundice
 Provide adequate diet with high proteins, CHO, and vitamins
(carefully monitor this in encephalopathy)
 Monitor for signs of possible bleeding
 Other interventions:
 For coagulopathy/GIT bleeding – vitamin K can be given to treat
abnormal PT
 Correction is needed prior to undergoing invasive
procedures
 Hypotension should be treated with fluids
 Pulmonary complications – mechanical ventilation may be
required esp for mgmt. of cerebral edema & acute respiratory
distress syndrome

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 Head of bed should be elevated to 30 degree

 Monitor neurologic status
o Hepatic encephalopathy is a major complication of ALF & a
prognostic marker bec it is progressive unless LF is resolved
o Goal is to maintain intracranial pressure below 20 mmHg, and
cerebral perfusion pressure above 50-60 mmHg
o Judicious administration of sedation and analgesia for patients
experiencing agitation during certain stages of Hepatic
encephalopathy.
 Ttt would focus on resolution of LF, decreasing ammonia lvl, & monitoring
ICP w/ interventions to decrease cerebral edema

4. Acute Pancreatitis
 Occurs suddenly as 1 attack or can be recurrent with resolutions; can be a medical emergency
 Due to self-digestion of pancreas by its own proteolytic enzymes
o Trypsin
 Other common causes aside from auto-digestion:
o Alcoholism: one of the most common cause
o Drug toxicity
o Abdominal trauma
o Biliary duct obstruction
 Assessment:
o Acute steady & severe epigastric pain that occur in the umbilical area and may radiate
into the back. It is associated with ingestion of alcohol or a fatty meal (cardinal sign)
 Pain is usually the main symptoms in pancreatitis and is aggravated when lying
down
o Nausea and vomiting worsen with oral intake and does not relieve the pain
 Caused by the hypermotility or paralytic ileus 2ndary to pancreatitis or
peritonitis
o Vital signs: fever, hypotension, tachycardia
o Abdominal rigidity, tenderness, distention, and decreased bowel sounds
o Grey Turner’s sign = reddish-brown to bluish discoloration along the flanks and
represents accumulation of blood in the area; a sign of severe necrotizing pancreatitis
 Death of pancreatic tissue causes bleeding into the abdomen
o Cullen’s sign = bluish discoloration around the umbilicus; also a sign of severe
necrotizing pancreatitis
o Steatorrhea = fat content increases in volume as pancreatic insufficiency worsens
 Bulky, fatty, foul-smelling stool
 Diagnostic Evaluation

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o Increase serum lipase, amylase levels

 Used in making dx for acute pancreatitis
 Although in most cases, both are elevated w/in 24H of the onset of symptoms
 A: usually returns to n° in 48-72 hrs
 SL: Remain elevated for a longer period, often days longer than amylase
o Increase urine amylase
o Leukocytosis or elevated WBC
o Hyperglycemia
 Impt to closely monitor blood glucose lvls in pxs w/ pancreatitis bec of the
malfxn in the insulin production
o Hypocalcemia
 If calcium is sequestered by fat necrosis
o Increase C-reactive protein
o Increase bilirubin and liver function test (indicates hepatic involvement)
o Imaging studies (e.g. Abdominal X-ray, UTZ, Ct-scan)
 Medical Therapy: directed towards relieving symptoms & preventing/treating complications
o Narcotic analgesics:
 Drug of choice: meperidine (Demerol)
 Med of choice to treat pain
 Morphine sulfate can cause spasms in the sphincter of Oddi thereby
increasing bowel obstruction & exacerbating the condition
o Antiemetics, antispasmodics and anticholinergics
 Decrease vagal stimulation, pancreatic secretion, & ampullary spasm
o Somatostatin = a treatment for acute pancreatitis, inhibits the release of pancreatic
enzymes; known to inhibit GI, endocrine, exocrine, pancreatic, and pituitary secretions,
as well as modify neurotransmission and memory formation in the CNS
o Fluid resuscitation and electrolyte replacement
 Maintain circulatory volume & provide emergency ttt for shock
o Insulin administration as prescribed due to malfxn of insulin production
o Antibiotics
 Therapeutic and Surgical Management:
o NPO with NGT
 All oral intake is withheld to prevent stimulation of pancreas & secretion of
enzymes
o IV and total parenteral nutrition
 Hypovolemic shock from fluid shift: major factor in acute pancreatitis
 Early fluid therapy is a cornerstone of ttt & is universally recommended
for pxs w/ acute pancreatitis
o Peritoneal lavage
o Cholecystectomy after acute pancreatitis is resolved

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 Nursing Management:
o Administer pain management as ordered
o Keep NPO with gastric suction
 Nasogastric suction is an option for pxs w/ consistent vomiting, gastric
distention, ileus
 Reduces stimulation of pancreatic secretions by decreasing the contents that
enters the small intestine
 Usually NG intubation w/ low intermittent suction
o Monitor lab results, v/s, intake/output bowel sounds
 Acute pancreatitis can cause decrease urine output w/c results from the renal
failure that sometimes accompanies this condition
o Maintain bed rest and may increase activity as tolerated
 Bed rest: to decrease metabolic rate & reduce secretion of pancreatic & gastric
enzymes
o Place patient in a knee-chest position to facilitate relief of pain to reduce abdominal
pressure & tension providing some measure of comfort & pain relief
o Oral feeding is resumed when amylase levels return to normal and when pain is relieved
o Small frequent, low fat, feedings with no alcohol after acute phase
 Px w/ pancreatitis should avoid high fat food & alcohol
5. Hyperglycemia
o During acute illness, liver produces & releases glucose in response to glucocorticoids,
catecholamines, growth hormones, etc.
o As a result of this, fat & proteins are catabolized & blood sugar surges
o Conditions such as MI, stroke, surgery, trauma, pain may cause release of these
biological mediators & counter regulatory hormones
o The greater the stress response, the higher the blood pressure
 Rigorous glucose monitoring & effective mgmt. of blood glucose are essential
o Usually accomplished in critically ill pxs by frequent blood glucose monitoring paired
w/ continuous insulin infusion
 Medical term describing an abnormally high blood glucose level
 Hallmark sign of diabetes (both type 1 and type 2 DM)
 Signs and symptoms:
o 3 Ps: Polyuria, Polydipsia, Polyphagia
o Viscous blood w/c could lead to poor circulation
o Altered sensation
o Glycosuria due to damaged glomeruli
o Diabetic foot w/c could be a complication of hyperglycemia/diabetes
o Risk for infection and dehydration
o Hot and dry skin
o Hypertension (with headache)

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o Fatigue, blurred vision, slurring of speech

 Precautionary measures:
o Follow diabetes meal plan, exercise program, and medication routine
o If blood sugar levels are above target range, drink extra liquids
 Helps replace fluids lost through urine
 Water & sugar-free drinks are best
 Drink non-caffeinated & non-alcoholic beverages that do not contain sugar
 Instruct px to avoid drinks w/ a lot of sugar (fruit juice)
o Monitor blood sugar often
o Normal blood glucose ranges from 70 to 110 mg/dL
 Treatment:
o Control of high glucose level:
 Raise insulin dose as prescribed & titrate thereafter
 Recommend dietary changes
 Recommend more exercise (at least three times a week to meet goals of
planned exercise, thereby lowering blood glucose levels, reducing/maintaining
proper weight)
 Recommend closer glucose monitoring

6. Diabetic Ketoacidosis
 A life-threatening complication of DM that develops when severe insulin deficiency occurs
 Main clinical manifestations:
o Hyperglycemia, dehydration and electrolyte loss due to polyuria, and acidosis
o During acute illness, things such as breakdown of fat increases due to increased
metabolic demands, thereby increasing ketones. That is why there is a presence of
acidosis in DKA
 More common to occurs in patients with Type 1 DM
 Causes:
o Decreased or missed dose of insulin
o Illness or infxn
 Release of cortisol due to stress decreases production of insulin. Thus, increasing
risk of DKA
 Assessment:
o Elevated blood glucose level 300-800 mg/dL
o Decreased serum bicarbonate and pH
o Sodium and potassium may be low
o Glycosuria; polyuria; dehydration
o Metabolic acidosis
 As a compensation, px will exhibit Kussmaul’s respiration/breathing
 Deep, labored, fast breathing

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 Happens when body tries to remove Co2 & acid from the body by quickly
breathing it out
 Compensatory mechanism of the body to correct acidosis
o Sweet breath odor
 Due to high lvs of ketones
 Indications WHEN to contact a medical practitioner
o Decreased consciousness
o Difficulty breathing
o Fruity breath
 Implementation:
o Restore circulating blood volume
o Treat dehydration with rapid IV infusions
 e.g bolus PNSS/.9 NACL to promote circulation and dilute sugar
o Treat hyperglycemia with IV regular insulin
 Usually, IV bolus is done for correction first then continuous infusion thereafter
to titrate it depending on the px’s blood glucose lvls
o Cardiac monitoring & electrolyte replacement
o Treat acidosis according to cause (check ABG)
 Give antacids: Sodium bicarbonate to correct acidosis
 Prevention:
o Restore circulating blood volume
o Educate patients in recognizing early S/S of DKA
o Emphasize not to eliminate insulin doses when nausea and vomiting occur
o Should have available foods for use on a “sick day”
o Drink fluids every hour to prevent dehydration
o In people with infections or who are on insulin pump therapy, measuring urine
ketones can give more information than glucose measurements alone
 Ex. Spot test
o Measures ketones in urine
o Kit contains dipsticks coated w/ chemicals that react w/ ketone
bodies
o Dipstick is dipped in urine sample & a color change would
indicate presence of ketones

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7. Hyperglycemic-Hyperosmolar Nonketotic Syndrome (HHNS/HONKS)

 Also known as “Hyperosmolar hyperglycemic state”
 Extreme hyperglycemia without ketosis and acidosis
 Characterized by hyperglycemia, hyperosmolarity, & dehydration w/o ketosis
 Occurs in patients with Type 2 DM
o DKA: Type 1
 Onset is usually slow and takes hours or days to develop
 Causes:
o Leading cause: Inadequate fluid replacement
o Insufficient insulin
o Major stresses
 Assessment:
o Blood glucose is from 600 - 1200 mg/dL
o Hypotension
o Dehydration
o Tachycardia
o Mental status changes and neurological deficits
o Seizures
o Polydipsia (special craving for cold water), polyuria, increased plasma osmolality
(>320mosm/kg) [NV: 275-295 mOsm/kg], high urine specific gravity (>1.010)
 Higher urine specific gravity = higher risk for dehydration
 Implementation:
o Similar treatment with DKA
o Includes fluid replacement, correction of electrolyte imbalances
o Hypokalemia
 Administer KCL & insulin administration

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VII. IMPLEMENTATION

A. Medical/Surgical Management

 Volume Restoration
 Nasogastric Suction Tubes
o Nasogastric tubes = primarily inserted for decompression of stomach
o Types:
 Levin = single lumen (channel within a tube or catheter) and is made
of plastic/rubber. This tube is connected to low intermittent suction
(30-40 mmHg) to avoid erosion or tearing of the stomach lining w/c
can result from the tube’s adherence to the mucosa of the stomach
 Salem (Double Lumen) Pump = radiopaque (easily seen on x-ray),
clear plastic, double-lumen gastric tube. The blue port vent is always

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open to air for continuous atmospheric irrigation; prevent reflux by

having the blue vent port above patient’s waist

o Things to remember when feeding:

 Residual volume shouldn’t exceed 150 mL
 If volume is > 150, hold the feeding & notify physican
 Maintain patency of the tube at all times & assess patency prior to
feeding
 Air insufflation method
o Introducing air into the tube

 Esophagogastric Balloon Tamponade Tubes

o Done via placement of Sengstaken-blakemore or Minnesota tube which are
multi-lumen gastric tubes, placed nasally & extended into the stomach; there
are two balloons, one in the esophageal area that, when inflated, tamponades
the bleeding varices in the esophagus & the gastric balloon, which serves as
anchor

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o Sengstaken-Blakemore tube = triple lumen gastric tube (one lumen allows

inflation of esophageal balloon, the other allows inflation of gastric balloon
while third lumen allows for gastric aspiration)

o Minnesota tube = 4-lumen gastric tube; a modified Sengstaken-blakemore

tube with an additional lumen for aspirating esophagopharyngeal secretions
o Nursing Considerations:
 Closely monitor patient’s condition and lumen pressure
 If pressure changes or decreases, check for bleeding & notify
physician immediately
 Check for esophageal rupture
o Shock, increase respiratory difficulty, increased bleeding
 Careful surveillance of patient’s vital signs, oxygen saturation, and
cardiac rhythm (a change may indicate new bleeding)
 Monitor respiratory status and observe for respiratory distress. Cut
balloon ports and remove tube.
 If px manifests respiratory distress while the balloon is inflated,
cut the Cut balloon ports and remove tube.
o Keep scissors at bedside in case of emergencies
 Provide support for px
 Give rationales as to why we are doing certain things especially
when explaining the placement of the tamponade tube so as to
obtain cooperation & reduce anxiety from the procedure
 Deflate esophageal balloon for about 30 minutes every 12 hours or
according to hospital policy/procedure
 Impt to release this pressure periodically to prevent tissue
necrosis
 Shouldn’t be left inflated for more than 24 H

 Billroth I and II
o Subtotal Gastrectomy = a generic term referring to any surgery that involves
partial removal of the stomach, may be accomplished by either a Billroth I or a
Billroth II procedure.

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 Billroth I
 Surgeon removes part of the distal portion of the stomach,
including the antrum. The remainder of the stomach is
anastomosed to the duodenum
 This combined procedure is more properly called
gastroduodenostomy
 It decreases the incidence of dumping syndrome that often
occurs after a Billroth II procedure.
o Rapid gastric emptying
o Medical condition in w/c the stomach empties its
contents into the 1st part of the small intestine
(duodenum) faster than normal
 What to do if dumping syndrome occurs:
o Instruct px to lie down 30 mins after eating to delay
gastric emptying
o Avoid high carb food
o Assume low fowler’s position during meals
o Limit fluid taken during meals as this exacerbates gastric
emptying
o Instruct px not to walk immediately after eating
 Billroth II
 Billroth II resection involves reanastomosis of the proximal
remnant of the stomach to the proximal jejunum
 Pancreatic secretions and bile continue to be secreted into the
duodenum, even after gastrectomy
o As these secretions are necessary for digestion, a route
to the intestine must be preserved
 Surgeons prefer the Billroth II technique for treatment of
duodenal ulcer because recurrent ulceration develops less
frequently after this surgery.
 Nurse should never irrigate or reposition the gastric tube
inserted after gastric surgery unless specifically ordered by the
physician
 Encourage px to do leg exercises, ambulate, & DBE and coughing
techniques to promote healing & circulation
 WOF: Dumping Syndrome

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 Transjugular Intrahepatic Portosystemic Shunt (TIPS)

o Involves the threading of a cannula into the portal vein via the transjugular
route; an expandable stent is inserted & serves as an intrahepatic shunt
between the portal circulation & hepatic vein, thereby reducing portal
hypertension.
 Liver Transplantation
o Surgery to remove a diseased liver and replace it with a healthy one.
o Px’s entire liver is removed & then replaced with a complete new liver or a
portion of a healthy liver
o Indications:
 Liver transplantations is needed for patients who are likely to die
because of liver failure
 Many dse can cause liver failure
 Most common: cirrhosis
o Scarring & death of liver cells
o Cirrhosis caused by hep C is the most common reason
for liver transplant
 Common conditions requiring liver transplant include:
 Noncholestatic cirrhosis
 Biliary atresia
 Acute hepatic necrosis

o Where does a liver for a transplant come from?

 Two types:
 Living donor transplantation
 Cadaveric transplantation
o Liver transplant surgery takes between 6 and 12 hours

o Post-op:
 Patient is advised to stay in the hospital for an average of 1-3 weeks to
ensure that new liver is working
 Patient is required to take lifetime medicines (e.g. immunosuppressive
medications) to prevent rejection and infections

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o Complications:
 Rejection
 Immune system works to destroy foreign substances that
invades the body. The immune system, however, can’t
distinguish between transplanted liver and unwanted invaders,
such as viruses and bacteria.
 Therefore, immune system may attempt to attack and destroy
the new liver. This is called rejection episode
o About 70% of all liver transplant pxs have some degree
of organ rejection prior to discharge
 Antirejection medications (immunosuppressive drugs) are given
to ward off the immune attack
 Infection
 Because antirejection drugs that suppress immune system are
needed to prevent the liver from being rejected, it places
patient at increased risk for infections
o This problem diminishes as time passes
o Not all pxs have probs w/ infection & most infections can
be treated successfully as they occur

 Bariatric Surgery
o Gastric bypass and other weight-loss surgeries—known collectively as bariatric
surgery—involves making changes to the digestive system to help lose weight.
 Done when diet and exercise haven’t worked or when you have serious
health problems because of your weight
o Some procedures limit hm you can eat, other procedures work by reducing
body’s ability to absorb nutrients, and some procedures do both

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o Types:
 Biliopancreatic diversion with duodenal switch
 Roux-en-Y Gastric bypass
 Laparoscopic roux-en-y gastric bypass results in both restriction
& malabsorption and is the gold standard for treating obesity
 Sleeve gastrectomy

o Indications:
 Done to help lose excess weight and reduce risk of potentially life-
threatening weight-related health problems, including:
 Heart disease and stroke
 High blood pressure
 Nonalcoholic fatty liver disease (NAFLD) or nonalcoholic
steatohepatitis (NASH)
 Sleep apnea
 Type 2 diabetes
 Typically done when you’ve tried to lose weight by improving diet &
exercise habits
 In general, bariatric surgery could be an option if:
 Body mass index (BMI) is 40 or higher (extreme obesity)
 BMI is 35 – 35.9 (obesity), and patient have a serious weight-
related health problems
o Post-op:
 Careful respiratory monitoring for 24-48 hours post-op
 Airway obstruction & oxygenation problems are important post-
op concerns following bariatric surgery
 Assess and educate patients of anastomotic leaks (leakage of gastric
contents at the site of anastomosis is a potentially life-threatening
complication which would lead to sepsis if left untreated)
 S/S of anastomotic leaks
o Fever, left shoulder pain, tachypnea, tachycardia
 Impt to educate pxs on s/s as leaks can occur weeks following
surgery

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 NPO for at least 1-2 days to allow healing of stomach & digestive system
 Diet progression: Liquids  pureed, very soft foods  regular foods
 Frequent medical checkups to monitor health in first several months
after surgery
 Lab testing, blood works
Other med/surgical mgmt. we can do to pxs w/ alterations in the GI, metabolic, liver fxn
 Reverse Hydration
 Reverse Ketoacidosis
 Electrolyte Replacement
 Rapid Hydration

B. Pharmacologic Management Complimentary/Alternative Therapy

1. Ginger
 Medicinal uses of Ginger:
o Ginger has been used to treat problems such as vomiting, diarrhea, coughing,
inflammatory joint diseases including rheumatism and arthritis.
o Ginger root is used to relieve motion sickness
o Ginger may lower cholesterol and help prevent blood from clotting.
 Help treat heart dse where BVs can become blocked & lead to heart
attack/stroke
o Other studies suggest that ginger may help improve blood sugar control among
people with type 2 diabetes
 How to take it:
o Pediatric:
 DO NOT give ginger to children under 2 yrs old
 Ginger could be too harsh on their developing systems
 Children over 2 may take ginger to treat nausea, stomach cramping, and
headaches. However, a consult with a physician is recommended to find
the right dose
o Adult:
 In general, do not take more than 4 g of ginger per day, including food
sources. Pregnant women should not take more than 1g/day.
 Possible Interactions:
o Blood-thinning medications
 Warfarin (Coumadin), clopidogrel (Plavix), aspirin
 Ginger may increase risk of bleeding
o Diabetes medications
 Ginger may lower blood sugar that can raise the risk of
developing hypoglycemia or low blood sugar

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o High blood pressure medications

 Ginger may lower blood pressure, thereby raising the risk of
hypotension or irregular heartbeat

2. Bitter Gourd or Bitter Melon (Ampalaya)

 Scientific name: Momordica charantia
 A climbing vine with tendrils that grow up to 20 cms long
 Fruits have ribbed and wrinkled surface that are fleshy green with pointed end at length
and has a bitter taste
 Uses:
o Lowers blood sugar levels
o Diabetes Mellitus (Mild-non insulin dependent)
 Preparation:
 Gather and wash young leaves very well.
 Chop.
 Boil 6 tablespoons in two glassfuls of water for 15 minutes under low fire.
 Do not cover pot.
 Cool and strain.
 Take one third cup 3 times a day after meals
VIII. CLIENT EDUCATION
IX. EVALUATION OF OUTCOME OF CARE
X. REPORTING AND DOCUMENTATION OF CARE

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