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NSG 478 > Nursing mgmt of the patient with an acute GI disorder > Flashcards

Nursing mgmt of the patient with an acute GI disorder Flashcards

1
Q

Ingestion

A

Food is taken into the oral cavity

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2
Q

Digestion

A
  • Starts with chewing, food is broken down into small particles that. can be swallowed and mixed with digestive enzymes (Salivary amylase) also known as chyme
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3
Q

Absorption

A
  • Small nutrient molecules produced by digestion
  • Occurs in SI jejunum
  • Accomplished by active transport and diffusion across the intestinal wall into circulation
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4
Q

Elimination

A

Undigested, unabsorbed food and other waste products

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5
Q

Salivary amylase

A
  • Digestive enzyme that is for chewing and swallowing saliva
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6
Q

Hydrochloric acid

A
  • Secretion used in digestion that breaks down chyme into absorbable molecules
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7
Q

Pepsin

A

Secreted by the stomach for protein digestion

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8
Q

Bile

A
  • Produced by the liver, emulsifies fats
  • Stored in the gallbladder
  • Secreted into the small intestine for fat emulsion
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9
Q

Amylase

A
  • Produced by the pancreas, with its active site being in the small intestine
  • Digest carbs and starches
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10
Q

Lipase

A
  • Produced in the pancreas with its active site being in the small intestine
  • Digestion of fats
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11
Q

Trypsin

A
  • Produced in the pancreas with its active site being in the small intestine
  • Supports the digestion of proteins
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12
Q

Sphincter of Oddi

A
  • Second portion of duodenum
  • Regulates the flow of bile and pancreatic enzymes into the small intestine
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13
Q

Exocrine functions of the pancreas

A
  • Secretes externally through excretory ducts through pancreatic duct
  • Secretes: Amylase, trypsin, lipase
  • Secretions contain bicarb to neutralize acid from gastric fluids
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14
Q

Endocrine functions of pancreas

A

Secretion directly into the bloodstream
* Islets of langerhans
* Beta (Insulin)
* Alpha (Glucagon)
* Delta cells (Somatostatin)

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15
Q

Leading GI cause of hospitalization in the US

A

Acute pancreatitis

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16
Q

Main causes of Acute pancreatitis

A
  • Gallstones
  • Chronic alc use disorder
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17
Q

Prognosis of Acute pancreatitis for alc

A

Poor

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18
Q

Prognosis of Acute pancreatitis for Gallstones

A

Better, you can directly fix the cause which makes it easier to treat

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19
Q

Acute Pancreatitis

A
  • Acute, inflammatory condition caused by dmg to the acinar cells
  • Classified and diagnosed via Atlanta criteria
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20
Q

Diagnosis of acute pancreatitis

A

Diagnosis requires 2 of the following
* Abdominal pain
* Increase in serum amylase or lipase levels to 3x of the upper limit of normal
* Radiographic evidence of disease

Chronic pancreatitis is often undetected, slower process until the person has acute pancreatitis and shows the dmg that has been done

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21
Q

Types of Pancreatitis: Acute interstitial edematous pancreatitis

A
  • Enlargement of pancreas from inflammatory edema
  • 80% of cases
  • Very treatable
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22
Q

Types of acute pancreatitis: Necrotizing pancreatitis with necrosis of the pancreatic parenchyma

A
  • Destruction of the pancreas and local blood vessels by its own digestive enzymes
  • Essentially digestive enzymes leak out and digest their own tissue
  • Involves the cells of the pancreas, causing inflammation to the pancreas and the surrounding tissue
  • More severe and a higher mortality
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23
Q

Atlanta classification for acute pancreatitis: Mild

A
  • No organ failure
  • No local or systemic complications
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24
Q

Atlanta classification for acute pancreatitis: Moderately severe

A
  • Organ failure that resolves within 48 hours (Transient organ failure)
  • Local or systemic complications without persistent organ failure
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25
Q

Atlanta classification for acute pancreatitis: Severe

A
  • Persistent organ failure (>48 hours)
  • Single or multi organ failure
  • High mortality rate
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26
Q

Acute pancreatitis path

A
  • Autodigestion of pancreas by prematurely activated enzymes
  • Inciting factor -> Inflammation –> Ductal obstruction -> increased pressure and duct rupture -> Release of pancreatic enzymes into pancreatic tissue -> intense inflammation
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27
Q

Chronic pancreatitis

A
  • May not know you have it until an acute exasperation
  • Progressive destructive, inflammation and fibrosis
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28
Q

Causes and risks of acute pancreatitis

A
  • Gallstones
  • Alc use
  • Cigarette smoking and alc use together have increased risk (Positive correlation based on pack years)
  • ERCP, endoscopic retrograde cholangiopancreatography or GI surgery (Inflammation)
  • Hypertriglyceridemia (Triglycerides at like 1000)
  • Genetics
  • Medications
  • Idiopathic, no known cause
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29
Q

Clinical presentation: Acute pancreatitis

A
  • Pain
  • N+V
  • Abdominal distension, hypoactive bowel sounds, tender abdomen
  • Warm, moist skin, fruity breath
  • Fever
  • Weight loss (If it goes on for any period of time)
  • Jaundice
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30
Q

Pain: Acute pancreatitis

A
  • Sudden acute, onset of severe, boring pain in mid epigastrium ( below Sternum)
  • May radiate to back, left flank or left shoulder (Diaphragm aggravation)
  • Worse with lying down
  • Relieved some sitting upright or bending forward
  • Begins 24-48 hours after a heavy meal or alc ingestion
  • Unrelieved by antacids
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31
Q

Why do you have fruity breath with acute pancreatitis

A
  • Acute pancreatitis is inflammation of the pancreas, which produces insulin, if you can’t produce/release insulin you’re going to have hyperglycemia which causes the breakdown of ketones like DKA
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32
Q

Severe S+S pancreatitis

A
  • Fever
  • Tachypnea
  • Tachycardia
  • Hypoxemia
  • Hypotension
  • Confusion
  • Agitation
  • Dyspnea from diahragmatic inflammation
  • Pleural effusion from acities
  • ARDS
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33
Q

S+S Acute pancreatitis

A
  • Severe signs
  • Seepage of blood stained exudates into tissue (Grey turners, cullen’s sign)
  • Ascites
  • Hypocalcemia/Tetany (Trousseau, Chvostek ), twitching and cramping are first tho
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34
Q

Hypercalcemia and pancreatitis

A
  • May be present initially or even a possible cause of acute pancreatitis however with disease progression hypocalcemia is much more common
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35
Q

Trousseau’s sign

A
  • Italian hand
  • Hand spasm with BP cuff inflation, twitching indicates hypocalcemia
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36
Q

Chvostek’s Sign

A
  • Facial twitching when facial nerve is tapped
  • Indicates hypocalcemia
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37
Q

Grey turners sign

A

Flank ecchymosis (Bruising), indication of acute pancreatitis

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38
Q

Cullen’s sign

A
  • Bluish gray periumbilical discoloration
  • Indication of acute pancreatitis
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39
Q

Key points for history with a patient with acute pancreatitis

A
  • History or symptoms of gallstones
  • Amount and pattern of alc use (5 years of heavy consumptoms, of greater than 4 drinks a day)
  • Medications (Prescription or non, new? immunotherapy for cancer)
  • Smoking history
  • Family history of pancreatitis
  • Unexplained weight loss
  • New onset diabetes
  • Prior history of surgery (Abdominal /ERCP)
  • Hypertriglyceridemia
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40
Q

Lab test for acute pancreatitis: Elevated

A
  • Amylase: INcreased with 24 hours and for 2-3 days
  • Lipase: Increases slowly, and will stay elevated longer than amylase (3x ULN)
  • Urine amylase: INcreased for a week
  • Liver enzymes and bilirubin: Increased if associated with biliary dysfunction
  • WBC: Increased due to infection/ inflammation
  • Blood glucose: Increased due to decreased insulin
  • Inflammatory markers: Increased (ESR, CRP)
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41
Q

Labs for acute pancreatitis: Decreased

A
  • Calcium and Magnesium: Decreased due to fat necrosis
    1. Mg must be corrected before calcium
  • Hemoglobin and hematocrit: Can vary depending on bleeding
  • Plt: Decreased
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42
Q

Diagnostic test : Acute Pancreatitis

A
  • CT of the abdomen
  • MRI (Less Nephrotoxic)
  • Abdominal ultrasound (Typically done in the ER)
  • Endoscopic Ultrasound
  • Magnetic resonance cholangiopancreatogram (MRCP)
  • X-rays, chest and abdomen to rule out other cause
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43
Q

Medical complications of Acute pancreatitis

A
  • Necrosis of pancreatic tissue
  • Peripancreatic fluid collections or abscess (Sterile or infected)
  • Pseudocyst (Fluid collection around the gland
  • Pancreatic fistula formation
  • Hemorrhage
  • Hypovolemia and shock
  • Fluid and electrolyte imbalances
  • Acute renal failure
  • Type 1 Diabetes
  • Pleural effusion, Atelectasis, ARDS
  • Pericardial effusion, arrhythmias
  • Coagulation defects: Microvascular dysfunction, DIC
  • Systemic inflammatory system (SIRS)/ Sepsis -> Multi organ failure (MSOF) -> death
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44
Q

Nursing problems Acute pancreatitis

A
  • Acuity of patient: ICU or floor
  • Fluid and electrolyte imbalance (Replace F+E after fluid shift)
  • Impaired breathing (Need good resp care)
  • Impaired perfusion (Decreased BV)
  • Acute Pain
  • Impaired nutrition status (NPO initially)
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45
Q

Mgmt of acute pancreatitis: Relieve symptoms and prevent and treat complications

A
  • Rapid and accurate diagnosis
  • Severity determination (Ranson, APACHE II, Atlantic) If determined to be severe, they go to ICU
  • ABC
  • Monitor electrolytes. BUN/ creat, lactate, WBC, Hgb/HCT liver function amylase, lipase
  • Replace electrolytes: K, Mg, Ca
  • Type and screen: Transfuse of hemorrhaging
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46
Q

Mgmt of acute pancreatitis: Aggressive fluid resuscitation

A
  • LR or NS, albumin or blood products (Usually not blood until they are stable)
  • Monitor for Fluid overload
    1. Frequent cardiac and resp assessment
    2. Intra-abdominal hypertension, pressure monitoring
    3. Strict I+O
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47
Q

Mgmt of acute pancreatitis: Resp

A
  • Aggressive resp care
    1. Elevation of diaphragm
    2. Pulmonary infiltrates
    3. Pleural effusion
    4. Atelectasis
  • Oxygen and mechanical vent if hypoxemic
  • ABG
  • Cough and deep breathing, reposition every 2 hours, semi fowlers (15-45 degrees)
  • May be vented
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48
Q

Mgmt of acute pancreatitis: Cardiac

A
  • Hemodynamic monitoring in ICU
    1. CVP
    2. PA cath
    3. MAP
    4. HR (Stroke volume, CO)
  • Tele monitoring changes for arrhythmias, EKG changes (ST elevations) which can indicate MI
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49
Q

Mgmt of acute pancreatitis: GI

A
  • Abdominal assessment
  • NG suction: Not a standard of care unless ileus or severe vomiting
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50
Q

Mgmt of acute pancreatitis: Biliary drains and stents

A
  • Document output
  • May improve pain control, allowing flow
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51
Q

Mgmt of acute pancreatitis: Hyperglycemia

A
  • IV insulin, insulin drip during acute phase if uncontrolled
  • Long acting subQ
  • Premeal and sliding scale
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52
Q

Mgmt of acute pancreatitis: Nutrition

A
  • early enteral nutrition recommended within 72 hours of admission via NG/NJ
    • Prevents dmg to intestinal mucosa and gut barrier to decrease risk for gut bacterial translocation
    • Reduced risk of infectious peripancreatic necrosis or SIRS
    • Reduced length of stay
    • Bowel motility Repletes caloric losses
  • Parenteral nutrition is ONLY used for ileus or bowel obstruction
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53
Q

Mild acute pancreatitis: diet

A
  • NPO initially to rest the bowels
  • Low residue, low fat diet as tolerated
  • Low residue diet limits fiber, and restricts other foods that can stimulate bowel activity
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54
Q

Limit of fiber for low residue diet

A

<10-15 g per day

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55
Q

Do you give morphine for acute pancreatitis

A
  • Nah its best to avoid due to causing sphincter of oddi dysfunction
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56
Q

Acute pancreatitis: Pain mgmt

A
  • Opioids: Fentanyl, Hydromorphone
  • Nsaids: Ketorolac (Tordol)
  • Epidural analgesia
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57
Q

Caution with ketorolac

A
  • Toradol
  • Avoid in kidney disease or acute kidney injury, GI ulceration, GI bleeding
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58
Q

Nursing mgmt of Acute pancreatitis pain

A
  • Assure the effectiveness of pain medication, Use a pain scale
  • Side effects of opioids: Resp depression, N+V, Constipation
  • Monitor for ileus due to opiods
  • Bowel regimen
  • Position patient for comfort, reposition Q 2 hrs
  • Bedrest then increase mobility as tolerated
  • Anti emetics
  • Non pharm: Relaxation, guided imagery, focused breathing
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59
Q

Comfortable positions for acute pancreatitis

A
  • Sitting up/leaning forward
  • Side lying
  • Fetal
  • HOB up

NOT on their back

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60
Q

Should you give a patient with a sterile abscess antibiotics

A

No it isn’t infected it wont do anything

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61
Q

Med mgmt of acute pancreatitis: Antimicrobials

A
  • Culture is taken to see what bacteria
  • Imipenem (Beta-lactam) is go to due to its effect on Gram+/-
  • No need for sterile pancreatic necrosis
  • No role for prophylactic antibiotics to prevent infection

Nursing actions are to monitor temp and S+S infection

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62
Q

mgmt of acute pancreatitis: Wound care

A
  • Patients can have multiple drains
  • Primary intention: Wound edges approximated, sewed shut by surgery
  • Secondary intention: Left open by surgery, requires wound packing
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63
Q

Surgical mgmt of acute pancreatitis, Obstructive etiologies

A
  • ERCP to open the sphincter of Oddi if due to gallstones
  • Cholecystectomy: Due to cholecystitis and gallstones
    • Sphincterotomy: To enlarge pancreatic duct sphincter

Goal is to remove necrotic tissue causing inflammation

64
Q

Surgical mgmt of acute pancreatitis: Refractory necrotizing pancreatitis

A
  • Step up approach: Minimally invasive
    1. Percutaneous drains
    2. Video assisted retroperitoneoscopic debridement (Through back)
    3. Endoscopic pancreatic necrosectomy to remove necrotic tissue (Orally)
65
Q

Nursing teaching and discharge: Acute pancreatitis

A
  • Prevent complications (Cholecystectomy, diabetes, pancreatic exocrine insufficiency) by engaging in follow up care
  • Call for fever, pain, feeding intolerance -Risk for infected peripancreatic fluid collections, PEI, recurrence
  • Referral for home care or rehab
  • Involve other professions
  • Lifestyle changes, modifiable risk factors
    • Alc cessation or rehab
    • Weight reduction
    • Smoking cessation
    • Avoid heavy metals in food
    • Avoid caffeine/ spicy/ fatty foods
  • Pain meds
66
Q

Hypertriglyceridemia mgmt

A
  • Fibrates
  • Statins
  • Niacin
  • Omega 3 fatty acids
67
Q

Pancrelipase

A
  • Creon
  • Pancreatic enzymes, aids digestion of fats and proteins, take with each meal and snack
  • Used for pancreatic enzyme insufficiency (PEI)
  • Depends on degree of pancreatic destruction the need for this
    *
68
Q

Pancreatic enzyme insufficiency (PEI)

A
  • Causes fatty stools
  • Pancreas doesn’t make enough enzymes to properly break down lipids
69
Q

Liver

A
  • Very vascular organ that gets blood from GI tract via the Portal vein(Deoxy) and the aorta via hepatic artery (Oxy)
70
Q

Responsibilities of the Liver

A
  • Conversion of Ammonia into urea
  • Detoxifies
  • GLucose metabolism and regulation of serum concentration
  • Protein metabolism
  • Fat metabolism
  • Bile formation
  • Drug metabolism
71
Q

Hepatic dysfunction

A
  • Due to dmg to liver parenchymal cells
    • Directly from primary liver diseases (Hepatitis/cirrosis)
    • Indirectly from either obstruction of bile flow or alterations in hepatic circulation
  • When severe the liver is unable to remove toxins from the blood
72
Q

Hepatic Encephalopathy (HE)

A
  • Complication of acute liver failure (ALF) or chronic liver failure (CLF)
  • Continuum of symptoms from normal cognition/subtle changes to confusion, stupor and coma
  • Can be episodic recurrent or persistent
  • Cardinal life threatening symptoms of cerebral edema leads to brain herniation and death
73
Q

HE Patho

A
  1. Liver is unable to convert the ammonia to urea
  2. Ammonia crosses the blood brain barrier leading to swelling of astrocytes
  3. Cerebral edema and increased ICP hypertension
74
Q

Astrocytes

A

Brain cells

75
Q

Hepatic insufficiency

A
  • Liver does not work well enough to detoxify by products of metabolism
  • Liver cannot process all the poison that’s going through it
76
Q

Portosystemic shunting

A
  • Development of collateral vessels, allowing toxic blood to bypass the liver entering systemic circulation
77
Q

2 main causes of HE

A
  • Hepatic insufficiency
  • Portosystemic shunting
78
Q

Chronic liver failure + HE

A
  • Symptoms are less severe and occur insidiously
  • Dementia like symptoms
79
Q

Acute liver failure + HE

A
  • Poor prognosis of untreated and may need a liver transplant
80
Q

Causes of HE: Type A

A

Due to Acute liver failure
* Viral hepatitis
* Ischemic hepatitis
* Ingestion of hepatic toxic chemicals

81
Q

Causes of HE: Type B

A
  • Associated with portosystemic shunt, without structural liver disease (Shunt occurring without dmg)
  • No cirrhosis or liver disease
  • Congenital
  • Trauma
  • Invasive procedure
82
Q

Causes of HE: Type C

A
  • Patients with cirrhosis/CLF and portal hypertension
83
Q

HE, and pre existing cirrhosis

A
  • HE can be precipitated
  • By infection, electrolyte imbalance, GI bleeding, meds, renal failure, hypovolemia, hypoxia, constipation, thrombosis
  • Need to determine the underlying cause
  • Diagnosis of exclusion
84
Q

Grades of hepatic encephalopathy

A
  • Western haven criteria
  • Overt and covert
  • Graded 1-4
  • MHE minimal hepatic encephalopathy, may need psychometric testing to determine
85
Q

Grades of hepatic encephalopathy: Grade 1

A
  • Covert
  • Inattention
  • Euphoria/anxiety
  • Altered sleep pattern
  • Decreased attention span

More energy

86
Q

Grades of hepatic encephalopathy: Grade 2

A

Overt
* Lethargy
* time disorientation
* asterixis
* Behavior changes
* Personality changes
* Hypoactive DTR

Asterixis

87
Q

Asterixis

A

Symptoms of HE, hand flapping

88
Q

Grades of hepatic encephalopathy: Grade 3

A

Overt
* Somnolence to semi stupor
* Responsive to stimuli, time and place… not much else
* Disorientation
* asterixis
* Hyperactive DTR

DTR go from hypo to hyper, LOC goes from alert to borderline coma

89
Q

Grades of hepatic encephalopathy: Grade 4

A

Coma

90
Q

Covert vs overt

A
  • Covert is grades 0-1 HE
    • Minimal HE
  • Overt has changes in activity and lethargy grades 3-4
91
Q

Assessments and clinical findings: HE

A
  • Take a good history; depending on level of confusion you may need family help
    • Meds, high risk lifestyle, exposures, alc , toxins
  • Changes in LOC and motor function, subtle to obvious
    • Decreased attention, reaction time and memory
    • Mood changes, disorientation, inappropriate behavior, confusion, stupor
    • Slurred speech, ataxia, hyperactive/absent DTR, nystagmus
    • Seizures
    • Psychometric test: Test psychomotor performance/speed and visual constructive ability
  • Sleep disturbances, insomnia/hypersomnia
  • Fetor hepaticus, asterixis, N+V, ascites, edema, jaundice, easy bleeding (Coagulation issues) bruising, pruritus, melena
  • Abdominal pain if Acute liver failure
  • Muscle wasting, sarcopenia, palmar erythema,spider telangiectasias
92
Q

Normal ammonia level

A

15-45 µ/dL

93
Q

Diagnostics for HE: CBC and plt

A
  • Altered coagulation due to liver dmg
  • Elevated PT/INR due to the liver producing proteins in the coagulation array
94
Q

Diagnostics for HE: Complete metabolic panel (CMP)

A
  • Electrolytes, glucose, liver function, BUN, Creatine, protein , albumin, bilirubin, total protein, albumin
95
Q

Diagnostics for HE: Ammonia level

A
  • Elevated
  • Normal is 15-45
96
Q

Diagnostics for HE: Liver function test

A
  • Bilirubin
  • Ast
  • ALT
97
Q

Diagnostics for HE: Hepatitis panel

A

Test for hep B/C

98
Q

Diagnostics for HE: CT or MRI of the brain

A
  • Rule out other causes of S+S (Stroke)
  • Evaluate for cerebral edema
99
Q

Diagnostics for HE: CT of liver /abdomen

A

Done to see liver enlargement and other issues, can get an ultrasound of liver as well

100
Q

Medical mgmt of HE

A
  • ICU vs floor vs home care
  • Need to identify and correct underlying condition
    • GI bleeding, infection, hypokalemia, metabolic alkalosis, renal failure, hypovolemia, hypoxia, holding sedatives or tranq, hypoglycemia, constipation
    • Hypokalemia correction is essential, hypokalemia causes increased renal ammonia production making HE worse
  • Nutritional support: once able to eat, don’t restrict protein, they are losing a lot of weight
  • Adequate hydration and electrolyte correction
  • Discontinue sedatives , analgesics, and tranquilizers and any other meds or supplements that can affect liver function
101
Q

Med mgmt of HE: Agitation

A

Haloperidol is safer than benzo

Avoid meds that depress CNS function

102
Q

Med mgmt of HE: Lactulose

A

Also lactitol
* Decrease absorption of ammonia from GI tract, allowing it to be excreted
* Dose is divided into 2-4 doses per day
* Can be given rectally via enema if not tolerate PO
* Titrate dose so pt has 2-3 loose stools a day
* S/E are abdominal cramping diarrhea, flatulence, F/E, N+V
* Risk of hyponatremia, and dehydration if stools are watery and exceed 5 per day
* Continues after recovery

103
Q

Med mgmt of HE: Rifaximin

A
  • Eliminates ammonia producing bacteria in the colon, lowering blood ammonia levels
  • Given if there is no improvement on lactulose within 48 hours or the pt is unable to take lactulose
  • Usually given with lactulose
  • Taken 2-3 times a day
  • Well tolerated

Can kill good bacteria

104
Q

Med mgmt of HE: Spironolactone

A

Aldactone, given if ascites present
K sparing

105
Q

Med mgmt of HE: Lasix

A

Furosemide
Given if ascites present

106
Q

Med mgmt of HE: Vitamins

A
  • B1 (Thiamine)
  • B2 (Riboflavin)
  • B6 Pyridoxine
  • Folic acid

Routinely given for pt with alc abuse, banana bag

107
Q

Nursing interventions HE: Bleeding

A
  • Assess for GI bleeding, bleeding gums, epistaxis, petechiae (PT/INR)
  • Safety, use an electric razor and soft toothbrush
108
Q

HE nursing interventions: Fluid and electrolyte

A
  • Strict I+O
  • Daily weights
  • Monitor for edema and ascites (Resp difficulty)
  • Measure abdominal girth
  • Admin diuretics
109
Q

Diet with HE

A
  • Consult dietician for best considerations
  • High carb
  • Protein amount and sources for daily intake
110
Q

Upper GI bleed (UGIB)

A
  • Occurs 5-6 more than LGIB
  • More unstable than LGIB
  • Can have rapid bleeding leading to hypovolemia
  • Area of bleed
    • Esophagus, somach, and duodenum
111
Q

Ligament of treitz

A

area of small intestine used to measure where a bleed is upper or lower

112
Q

Causes of UGIB

A
  • Peptic ulcers (62%)
  • Gastritis and duodenitis
  • Gastroesophageal varices of all UGIB
    • 50% are cases with a cirrhotic patient
    • Most fatal complication in this subset
  • Esophagitis
  • Mallory-weiss tear
  • Upper GI tract malignancy
  • Unknown cause
113
Q

Mallory weiss tear

A

Tear of the GI tract due to forceful coughing or vomiting, leading to bleeding

114
Q

Patho UGIB:Chronic Peptic ulcer disease

A
  • H pylori degrades the gastric mucosa through bacterial enzymes and direct gastric inflammation
  • Nsaids causes direct irritations to the GI mucosa and inhibit prostaglandin synthesis
115
Q

Patho UGIB: Stress related ulcers

A
  • Occurs when hospitalized patients due to decreased defence and repair mechanisms due to overwhelming stress response and mucosal ischemia
116
Q

Patho UGIB: Variceal bleeding

A
  • Due to cirrhosis (Toxic ingestions alcoholism, NAFLD, chronic hepatitis)
    • Liver become fibrotic, increasing portal pressure which causes varices to develop as a result of the pressure
    • Varices rupture with persistent increase in pressure, flow and size of varices
117
Q

Lower GI bleed

A
  • Bleeding source below the ligament of treitz
  • Jejunum, ileum, colon, rectum
  • Bright red bleeding typically
118
Q

Causes of LGIB

A
  • Diverticular disease (40%)
  • Inflammatory bowel disease (Crohn’s/UC)
  • Ischemic colitis
  • Angiodysplasia (Tortuous/swollen blood vessels in mucosal and submucosal layers)
  • Hemorrhoids and anal fissures
  • Recent polypectomy
  • Infectious colitis (C. Diff)
  • Colorectal cancer
119
Q

Risk factors for GI bleeding

A
  • H. Pylori
  • Chronic Nsaid use (ASA, Cox2) antiplt and anticoagulant, steroids, ssri,SNRI
  • Advancing age
  • Smoking , SUD, Alc
  • Known peptic ulcer disease, caricies, cirrhosis , diverticular disease, hemorrhoids, IBD (Duh)
  • Size of Varices, degree of portal pressure and cirrhosis
  • Comorbidities (CVD/ASD, renal disease, DM)
  • Mechanical vent over 48 hours
  • Coagulopathies, (plt <50K, INR >2.5 or PTT >2x control
  • Recent colonoscopy or sigmoidoscopy
  • Constipation/ straining
120
Q

Melena

A

Black tarry stools

121
Q

Hematemesis

A

Vomiting bright red or coffee grounds

122
Q

Hematochezia

A

Bright red or maroon color mixed with stool

123
Q

UGIB presentation

A
  • Hematemesis
  • Melena

Can have hematochezia with massive UGI hemorrhage

124
Q

LGIB presentation

A

Hematochezia/ can also have pure blood or bloody diarrhea

125
Q

S+S Acute GIB/ Impending Hypovolemic Shock: General

A
  • Fatigue
  • Conjunctival pallor
  • Acute abdominal pain
  • Fever if perforation or ischemic colitis
126
Q

S+S Acute GIB/ Impending Hypovolemic Shock: Neuro

A
  • Dizziness
  • Weakness
  • Syncope
  • Restlessness
  • Agitation
  • Confusion
127
Q

S+S Acute GIB/ Impending Hypovolemic Shock: Resp

A
  • SOB
  • Tachypnea
  • Hypoxia
  • Crackles in lungs
128
Q

S+S Acute GIB/ Impending Hypovolemic Shock: CV

A
  • Decreased BP (SBP <100 mmHg)
  • Narrowing pulse pressure (Normal is ~60 mmHg)
  • Tachycardia
  • Palpitations
  • CP (Underlying CAD)
  • EKG changes (ST changes)
129
Q

S+S Acute GIB/ Impending Hypovolemic Shock: Extremities

A
  • Cold and clammy
  • decreased cap refill
  • Mottled skin
130
Q

S+S Acute GIB/ Impending Hypovolemic Shock: Abdomen

A
  • Hyper/hypo/absent (Can develop paralytic ileus)
  • Basically anything
  • Board like abdomen= peritonitis/ perforation
131
Q

S+S Acute GIB/ Impending Hypovolemic Shock: GU

A
  • Decreased or no urine output, increased BUN and creatinine
132
Q

Labs Acute GIB: CBC

A
  • Normocytic RBC= Acute RBC
  • Microcytic RBC or iron deficiency anemia= chronic bleed
  • Hemoglobin and hematocrit (H/H) may be normal initially in acute bleed, then drop due to blood loss and hydration
133
Q

Normocytic

A

Reduced number, normal size

134
Q

Microcytic

A

Smaller rbc than normal

135
Q

Important labs for Acute GIB

A
  • CBC
  • PT/PTT/ INR
  • CMP
  • Lactate level
  • Type and screen (Blood type)
  • Stool and blood cultures if infectious source is suspected
136
Q

Diagnostics Acute GIB

A
  • Need to rule out upper GI bleed first
  • Upper endoscopy (EGD): within 24 hours, 12 hours if varices
  • Colonoscopy: needs bowel prep
  • CT angiography: if unable to tolerate EGD (uses contrast to see bleeding)
  • Angiography based on CTA must be done quickly while the bleed is still ongoing (Thread a cath from femoral artery and see are of bleed from inside)
  • CT or MRI of the abdomen or liver, portal circulation
137
Q

Nursing interventions acute GIB

A
  • Goal of care is fluid resuscitation and improve tissue perfusion and stabilize hemodynamics
  • To make up for blood and fluid loss and keep GI circulation and cellular function intact
  • Maintain safe environment, prevent injury, bleeding and infection
  • admin prescribed treatments and monitor for potential complications
  • Encourage deep breathing and position changes
  • Education and support of patient and family
138
Q

Medical and treatment of Acute GIB

A
  • Rapid assessment and early recognition are key
    • Thorough medical history and exam, labs and diagnostics to determine location and cause of bleeding
    • ICU for severe bleeding
  • Airway breathing circulation, ALWAYS first
  • Volume resuscitation don’t overload them with fluids
    • Central line or 2 peripheral cath
    • IV Fluids (LR/NS)
    • Volume expanders (albumin)
    • Colloid blood products (PRBC, plasma, Plt), not first choice get volume up first
    • Electrolyte replacement
139
Q

Medical and treatment of acute GIB: cardio and resp

A
  • Resp: O2 possible mech ventilation, monitor O2 sats/ABG
  • Cardio: Tele with close monitoring of VS, MAP, EKG
    • Hemodynamic monitoring: Art line, CVP line, pulmonary art cath
    • Notify providers of changes
    • Admin IV vasopressors to maintain BP (Not till you fill the tank)
140
Q

Can you give vasopressors with no blood in circulation

A
  • No you can’t raise an empty tank, you need to fill it with fluids before they work
141
Q

Medical treatment of acute GIB: Medications

A
  • Somatostatin/Octreotide: stops hemorrhage of varices
  • Vasopressin
  • Proton pump inhibitor (Decrease acid in stomach)
  • Prokinetics prior to EGD to improve gastric visualization
142
Q

Medical treatment of acute GIB: Blood thinners and thrombolytics

A
  • Hold Warfarin, anti Xa thrombin/factor Xa inhibitors, plt inhibitors (Plavix)
143
Q

Acute GIB Tubes: NG tube

A
  • Used to check gastric content
  • provide gastric lavage
  • Paralytic ileus (suc)
  • distention (suc)
144
Q

Acute GIB tubes: Sengstaken-Blakemore tube

A
  • Used in balloon tamponade to put pressure on esophageal varices
  • 3 lumens, double ballooned, esophageal tube
  • Temp measure for hemostasis in gastric and esophageal varices
  • Airway protection most important, pt NEEDS to be intubated
145
Q

Minnesota tube

A

Same as sengstaken blakemore tube but it has a 4th port to pull gastric secretion from

146
Q

Potential complications of balloon tamponade

A
  • Aspiration/ asphyxiation
  • Rebleeding upon removal
  • Esophageal rupture
  • Mediastinitis or peritonitis
  • mucosal ulcers

Always keep scissors at the bedside to quickly deflate balloon

147
Q

Hemostatic treatments in acute UGIB: Endoscopy/ Colonoscopy

A
  • Sclerotherapy-injecting chemicals into vessel/varices
  • Ligation-band vessel/varices
  • Clip-applied to vessel
  • Cautery, Thermal coagulation (probe, laser)
  • Epinephrine/Adrenaline injection-vasoconstriction
  • Infrared photocoagulation—heat coagulates the vessel in hemorrhoids
  • APC–Argon plasma coagulation is anoncontact form of electrocauterythat uses ionizedargon gas(plasma)
148
Q

Hemostatic treatments in acute UGIB: Vascular

A

Embolization
Transjugular intrahepatic portosystemic shunt (TIPS): Diverts portal blood flow away from the liver when endoscopic and pharm treatment fail in varices

149
Q

UGIB: Surgery

A

Gastric and duodenal ulcers
* Vagotomy-eliminates vagal stimulation to the acid-secreting portion of the stomach
* Partial gastrectomy
* Antrectomy/partial gastrectomy
* Subtotal gastrectomy
* Gastrointestinal reconstruction–necessary following partial gastrectomy to reestablish gastrointestinal continuity
* Billroth I, Billroth II, and Roux-en-Y most common

LGI bleed: Colon resection

150
Q

Acute GIB meds: Proton pump inhibitors

A
  • Standard of therapy in UGIB
  • Suppresses gastric acid secretion and maintains a neutral gastric PH
  • IV then oral for 8 wks
  • Taken orally on an empty stomach 30 min before eating, needs acid to work (Bold and highlighted)
  • Can cause Rebound hypersecretion of acid
  • to prevent rebound hypersecretion of acid you need to be weaned
  • Pantoprazole, omeprazole, esomeprazole
151
Q

Acute GIB meds: Vasoconstrictors

A
  • For esophageal variceal hemorrhage (Controls bleeding)
  • Octreotide : Somatostatin analogues, better tolerated with less side effects
  • Vasopressin: ADH can cause ischemia, arrhythmias, needs to be used with nitro to prevent constriction of coronary arteries
152
Q

Acute GIB meds: Beta blockers

A
  • Used long term in variceal pt to lower pressure
  • Nadolol, propranolol
153
Q

Acute GIB meds: Prokinetic agents

A
  • Metoclopramide (reglan)
  • Given prior to endoscopy to clear GI for better visualization
  • Used for N+V, gastroparesis
  • SE are tardive dyskinesia and extrapyramidal symptoms
154
Q

Acute GIB meds: Mucosal barrier

A
  • Forms a protective barrier that adhere to an ulcer
  • Given 4x a day before meals and at bedtime
  • Sucralfate (Carafate)
155
Q

Acute GIB meds: Antacids

A
  • Magnesium hydroxide (MOM)
  • Aluminum hydroxide + Magnesium or Calcium (Mylanta, Maalox)
  • Calcium carbonate (TUMS)

NSG 478 (23 decks)

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