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Responsesm To Metabolic Gi and Liver Alterations
Responsesm To Metabolic Gi and Liver Alterations
METABOLIC-GI
AND LIVER
ALTERATIONS
SHARED BY:
MICHAEL P. TUYAY
GENERAL ASSESSMENT
*Assess patient’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
GENERAL ASSESSMENT
*Assess patient’s physical & psychological statuses & interpret lab data;
A. Altered Gastrointestinal Function
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
GENERAL ASSESSMENT
*Assess patient’s physical & psychological statuses & interpret lab data;
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
GENERAL ASSESSMENT
*Assess patient’s physical & psychological statuses & interpret lab data;
B. Focused Assessment of Clients with Hepato-Biliary & Pancreatic Disorders
1. Health History
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
Antiseizure meds – phenytoin, valproic acid
TB drugs – isoniazid, pyrazinamide
PHYSICAL ASSESSMENT
*Patient lies supine, knees flexed, slightly for inspection, auscultation, percussion & palpation of
the abdomen
PHYSICAL ASSESSMENT
1. Inspection
- Performed first noting any skin changes, nodules, skin lesions, scarring and/or
discolorations - Lesions
are of particular importance because GI diseases 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
PHYSICAL ASSESSMENT
2. Auscultation
- Always precedes percussion & palpation because 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)
PHYSICAL ASSESSMENT
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
DIAGNOSTIC ASSESSMENT
A. NON-INVASIVE
1. GUAIAC TEST (STOOL FOR OCCULT BLOOD): Detect GI bleeding (GI cancer)
2. HEPATOBILIARY SCAN: Radioactive materials=size and shape of liver
tissue/visualize replacement of liver tissue with scars, cysts and tumor
3. Radionuclide Imaging or Cholecystography : images of the gallbladder and biliary tract
4. Barium Swallow (Upper GIT study/series): drinks barium sulfate (BaSO4)=to visualize
the esophagus, stomach, duodenum and jejunum
5. Lower GI study/series (Barium enema): detecting bowel obstruction and cause of
diarrhea and constipation
6. Capillary Blood Glucose Monitoring: monitoring blood glucose patterns
Normal blood is sugar is defined as: (1) An FBS < 100 mg/dL (5.6 mmol/L), or (2) Random/casual blood glucose < 140
mg/dl (7.7mmol/L), or (3) 2-hr blood sugar in the 75gm OGTT < 140 mg/dl (7.7mmol/L) [Level 2, Grade B].
DIAGNOSTIC ASSESSMENT
B. INVASIVE
1. ESOPHAGOGASTRODUODENOSCOPY (EGD): Upper GI fibroscopy
2.ENDOSCOPIC RETROGRADE CHOLANGIOPANCREATOGRAPHY (ERCP):
Endoscopic visualization of common bile, pancreatic, and hepatic ducts
3. PERCUTANEOUS TRANSHEPATIC CHOLANGIOGRAPHY (PTC): 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
4. LIVER BIOPSY: Sampling liver tissue by needle aspiration for histologic analysis
5. SERUM BLOOD STUDIES: Liver function tests, Serum Proteins, Pigment Studies,
Serum Ammonia, Blood Coagulation Studies (PT, INR, PTT)
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
PLANNING
Administering Volume Replacement
Controlling bleeding
Maintaining surveillance for complications
Administering fluids, insulin, and electrolytes
Monitor Response to therapy
Normalize body temperature
Patient education
METABOLIC-
GI AND LIVER
ALTERATIONS
SHARED BY:
MICHAEL P. TUYAY
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
74-100% of critically ill patients 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
Coffee-ground emesis
Caused when blood is mixed w/ digestive juices
Usually indicates that the bleeding has slowed/stopped
o Melena
Black, tarry stool w/ a characteristic foul order
Usually indicates upper GI bleeding sources (Because 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
CLINICAL PRESENTATION
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
TAKE NOTE:
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 treatment: 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
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)
TREATMENT
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
TREATMENT
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 o All critically ill patients should be considered
at risk for stress ulcers and therefore GI
MANAGEMENT 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
Intra-abdominal Hypertension and Abdominal
Compartment Syndrome
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
patients
Intra-abdominal Hypertension and Abdominal
Compartment Syndrome
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
intraabdominal 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
Possibly caused by bacterial translocation additional release of cytokines perpetuates the
positive feedback loop
o Combination results in increasing IAP and hypoxia
Pain is usually the main symptoms in pancreatitis and is aggravated when lying down
o N/V worsen with oral intake and does not relieve the pain
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
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
o Increase serum lipase, amylase levels
Although in most cases, both are elevated w/in 24H of the onset of symptoms
SL: Remain elevated for a longer period, often days longer than amylase
o Hyperglycemia
Important to closely monitor blood glucose levels in patients w/ pancreatitis because of the malfunction in the insulin
production
o Hypocalcemia
Morphine sulfate can cause spasms in the sphincter of Oddi thereby increasing bowel obstruction & exacerbating the
condition
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 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 treatment & is universally recommended for patients
w/ acute pancreatitis
o Peritoneal lavage
o Cholecystectomy after acute pancreatitis is resolved
NURSING MANAGEMENT
o Administer pain management as ordered
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
Acute pancreatitis can cause decrease urine output w/c results from the renal failure that sometimes
accompanies this condition
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
Acetaminophen toxicity
o Antidote:
o Bec of this, jaundice is typically evident when bilirubin exceeds 2-3 mg/dL
o Neurological status requires vigilant assessment because hepatic encephalopathy, cerebral edema, & increased ICP can rapidly progress
into brain & death)
o Hypokalemia may occur from inadequate oral intake potassium loss from vomiting
LIVER FAILURE
o Clinical Manifestation:
Melena
Ascites
o Accumulation of fluid in the stomach due to a lot of factors
Portal hypotension, hypoalbuminemia, inactivation ofRAA 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
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
Observe for signs of dehydration, 2ndary infection, neurologic disturbances, edema, jaundice
Provide adequate diet with high proteins, CHO, and vitamins (carefully monitor this in encephalopathy)
Pulmonary complications – mechanical ventilation may berequired esp for mgmt. of cerebral edema & acute respiratory
distress syndrome
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, andcerebral perfusion pressure above 50-60 mmHg
o Judicious administration of sedation and analgesia for patientsexperiencing agitation during certain stages of Hepatic
encephalopathy.
Treatment would focus on resolution of LF, decreasing ammonia lvl, & monitoring ICP w/ interventions to decrease cerebral
edema
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 patients 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)
HYPERGLYCEMIA
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)
o Fatigue, blurred vision, slurring of speech
HYPERGLYCEMIA
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 patient 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
HYPERGLYCEMIA
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
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 infection
Release of cortisol due to stress decreases production of insulin. Thus, increasing risk of DKA
DIABETIC KETOACIDOSIS
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, patient will exhibit Kussmaul’s respiration/breathing
Deep, labored, fast breathing
Happens when body tries to remove Co2 & acid from the body by quickly breathing it out
Implementation:
o Similar treatment with DKA
o Includes fluid replacement, correction of
electrolyte imbalances
o Hypokalemia
Administer KCL & insulin
administration
HYPERGLYCEMIC-HYPEROSMOLAR
NONKETOTIC SYNDROME (HHNS/HONKS)
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