Nursing mgmt of the patient with an acute GI disorder Flashcards
1
Q
Ingestion
A
Food is taken into the oral cavity
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
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
4
Q
Elimination
A
Undigested, unabsorbed food and other waste products
5
Q
Salivary amylase
A
- Digestive enzyme that is for chewing and swallowing saliva
6
Q
Hydrochloric acid
A
- Secretion used in digestion that breaks down chyme into absorbable molecules
7
Q
Pepsin
A
Secreted by the stomach for protein digestion
8
Q
Bile
A
- Produced by the liver, emulsifies fats
- Stored in the gallbladder
- Secreted into the small intestine for fat emulsion
9
Q
Amylase
A
- Produced by the pancreas, with its active site being in the small intestine
- Digest carbs and starches
10
Q
Lipase
A
- Produced in the pancreas with its active site being in the small intestine
- Digestion of fats
11
Q
Trypsin
A
- Produced in the pancreas with its active site being in the small intestine
- Supports the digestion of proteins
12
Q
Sphincter of Oddi
A
- Second portion of duodenum
- Regulates the flow of bile and pancreatic enzymes into the small intestine
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
14
Q
Endocrine functions of pancreas
A
Secretion directly into the bloodstream
* Islets of langerhans
* Beta (Insulin)
* Alpha (Glucagon)
* Delta cells (Somatostatin)
15
Q
Leading GI cause of hospitalization in the US
A
Acute pancreatitis
16
Q
Main causes of Acute pancreatitis
A
- Gallstones
- Chronic alc use disorder
17
Q
Prognosis of Acute pancreatitis for alc
A
Poor
18
Q
Prognosis of Acute pancreatitis for Gallstones
A
Better, you can directly fix the cause which makes it easier to treat
19
Q
Acute Pancreatitis
A
- Acute, inflammatory condition caused by dmg to the acinar cells
- Classified and diagnosed via Atlanta criteria
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
21
Q
Types of Pancreatitis: Acute interstitial edematous pancreatitis
A
- Enlargement of pancreas from inflammatory edema
- 80% of cases
- Very treatable
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
23
Q
Atlanta classification for acute pancreatitis: Mild
A
- No organ failure
- No local or systemic complications
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
25
Atlanta classification for acute pancreatitis: Severe
* Persistent organ failure (>48 hours)
* Single or multi organ failure
* High mortality rate
26
Acute pancreatitis path
* 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**
27
Chronic pancreatitis
* May not know you have it until an acute exasperation
* Progressive destructive, inflammation and fibrosis
28
Causes and risks of acute pancreatitis
* **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
29
Clinical presentation: Acute pancreatitis
* 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
30
Pain: Acute pancreatitis
* 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**
31
Why do you have fruity breath with acute pancreatitis
* 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
32
Severe S+S pancreatitis
* Fever
* Tachypnea
* Tachycardia
* Hypoxemia
* Hypotension
* Confusion
* Agitation
* Dyspnea from diahragmatic inflammation
* Pleural effusion from acities
* ARDS
33
S+S Acute pancreatitis
* 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
34
Hypercalcemia and pancreatitis
* May be present initially or even a possible cause of acute pancreatitis however with disease progression hypocalcemia is much more common
35
Trousseau's sign
* Italian hand
* Hand spasm with BP cuff inflation, twitching indicates hypocalcemia
36
Chvostek's Sign
* Facial twitching when facial nerve is tapped
* Indicates hypocalcemia
37
Grey turners sign
Flank ecchymosis (Bruising), indication of acute pancreatitis
38
Cullen's sign
* Bluish gray periumbilical discoloration
* Indication of acute pancreatitis
39
Key points for history with a patient with acute pancreatitis
* 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
40
Lab test for acute pancreatitis: Elevated
* 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)
41
Labs for acute pancreatitis: Decreased
* 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
42
Diagnostic test : Acute Pancreatitis
* **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
43
Medical complications of Acute pancreatitis
* **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
44
Nursing problems Acute pancreatitis
* 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)
45
Mgmt of acute pancreatitis: **Relieve symptoms and prevent and treat complications**
* 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
46
Mgmt of acute pancreatitis: **Aggressive fluid resuscitation**
* 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
47
Mgmt of acute pancreatitis: Resp
* 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
48
Mgmt of acute pancreatitis: Cardiac
* 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
49
Mgmt of acute pancreatitis: GI
* Abdominal assessment
* NG suction: **Not a standard of care** unless ileus or severe vomiting
50
Mgmt of acute pancreatitis: Biliary drains and stents
* Document output
* May improve pain control, allowing flow
51
Mgmt of acute pancreatitis: Hyperglycemia
* IV insulin, insulin drip during acute phase if uncontrolled
* Long acting subQ
* Premeal and sliding scale
52
Mgmt of acute pancreatitis: Nutrition
* **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
53
Mild acute pancreatitis: diet
* 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
54
Limit of fiber for low residue diet
<10-15 g per day
55
Do you give morphine for acute pancreatitis
* Nah its best to avoid due to causing sphincter of oddi dysfunction
56
Acute pancreatitis: Pain mgmt
* Opioids: Fentanyl, Hydromorphone
* Nsaids: Ketorolac (Tordol)
* Epidural analgesia
57
Caution with ketorolac
* Toradol
* Avoid in kidney disease or acute kidney injury, GI ulceration, GI bleeding
58
Nursing mgmt of Acute pancreatitis pain
* 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
59
Comfortable positions for acute pancreatitis
* Sitting up/leaning forward
* Side lying
* Fetal
* HOB up
NOT on their back
60
Should you give a patient with a sterile abscess antibiotics
No it isn't infected it wont do anything
61
Med mgmt of acute pancreatitis: Antimicrobials
* 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
62
mgmt of acute pancreatitis: Wound care
* Patients can have multiple drains
* Primary intention: Wound edges approximated, sewed shut by surgery
* Secondary intention: Left open by surgery, requires wound packing
63
Surgical mgmt of acute pancreatitis, Obstructive etiologies
* 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
Surgical mgmt of acute pancreatitis: Refractory necrotizing pancreatitis
* 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
Nursing teaching and discharge: Acute pancreatitis
* 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
Hypertriglyceridemia mgmt
* Fibrates
* Statins
* Niacin
* Omega 3 fatty acids
67
Pancrelipase
* 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
Pancreatic enzyme insufficiency (PEI)
* Causes fatty stools
* Pancreas doesn't make enough enzymes to properly break down lipids
69
Liver
* Very vascular organ that gets blood from GI tract via the **Portal vein**(Deoxy) and the aorta via **hepatic artery** (Oxy)
70
Responsibilities of the Liver
* **Conversion of Ammonia into urea**
* **Detoxifies**
* GLucose metabolism and regulation of serum concentration
* Protein metabolism
* Fat metabolism
* Bile formation
* Drug metabolism
71
Hepatic dysfunction
* 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
Hepatic Encephalopathy (HE)
* 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
HE Patho
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
Astrocytes
Brain cells
75
Hepatic insufficiency
* Liver does not work well enough to detoxify by products of metabolism
* Liver cannot process all the poison that's going through it
76
Portosystemic shunting
* Development of collateral vessels, allowing toxic blood to bypass the liver entering systemic circulation
77
2 main causes of HE
* Hepatic insufficiency
* Portosystemic shunting
78
Chronic liver failure + HE
* Symptoms are less severe and occur insidiously
* Dementia like symptoms
79
Acute liver failure + HE
* Poor prognosis of untreated and may need a liver transplant
80
Causes of HE: Type A
Due to Acute liver failure
* Viral hepatitis
* Ischemic hepatitis
* Ingestion of hepatic toxic chemicals
81
Causes of HE: Type B
* Associated with portosystemic shunt, without structural liver disease (Shunt occurring without dmg)
* No cirrhosis or liver disease
* Congenital
* Trauma
* Invasive procedure
82
Causes of HE: Type C
* Patients with cirrhosis/CLF and portal hypertension
83
HE, and pre existing cirrhosis
* 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
Grades of hepatic encephalopathy
* Western haven criteria
* Overt and covert
* Graded 1-4
* MHE minimal hepatic encephalopathy, may need psychometric testing to determine
85
Grades of hepatic encephalopathy: Grade 1
* Covert
* Inattention
* Euphoria/anxiety
* **Altered sleep pattern**
* Decreased attention span
| More energy
86
Grades of hepatic encephalopathy: Grade 2
Overt
* Lethargy
* time disorientation
* **asterixis**
* Behavior changes
* Personality changes
* **Hypoactive DTR**
| Asterixis
87
Asterixis
Symptoms of HE, hand flapping
88
Grades of hepatic encephalopathy: Grade 3
Overt
* **Somnolence** to semi stupor
* Responsive to stimuli, time and place... not much else
* Disorientation
* asterixis
* **Hyperactive DTR**
## Footnote
DTR go from hypo to hyper, LOC goes from alert to borderline coma
89
Grades of hepatic encephalopathy: Grade 4
**Coma**
90
Covert vs overt
* Covert is grades 0-1 HE
* Minimal HE
* Overt has changes in activity and lethargy grades 3-4
91
Assessments and clinical findings: HE
* 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
Normal ammonia level
15-45 µ/dL
93
Diagnostics for HE: CBC and plt
* Altered coagulation due to liver dmg
* **Elevated PT/INR** due to the liver producing proteins in the coagulation array
94
Diagnostics for HE: Complete metabolic panel (CMP)
* **Electrolytes**, glucose, liver function, BUN, Creatine, protein , albumin, bilirubin, total protein, albumin
95
Diagnostics for HE: **Ammonia level**
* Elevated
* Normal is 15-45
96
Diagnostics for HE: **Liver function test**
* Bilirubin
* Ast
* ALT
97
Diagnostics for HE: Hepatitis panel
Test for hep B/C
98
Diagnostics for HE: **CT or MRI of the brain**
* Rule out other causes of S+S (Stroke)
* Evaluate for cerebral edema
99
Diagnostics for HE: **CT of liver /abdomen**
Done to see liver enlargement and other issues, can get an ultrasound of liver as well
100
Medical mgmt of HE
* 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
Med mgmt of HE: Agitation
Haloperidol is safer than benzo
## Footnote
**Avoid meds that depress CNS function**
102
Med mgmt of HE: Lactulose
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
Med mgmt of HE: Rifaximin
* 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
Med mgmt of HE: Spironolactone
Aldactone, given if ascites present
K sparing
105
Med mgmt of HE: Lasix
Furosemide
Given if ascites present
106
Med mgmt of HE: Vitamins
* B1 (Thiamine)
* B2 (Riboflavin)
* B6 Pyridoxine
* Folic acid
| Routinely given for pt with alc abuse, banana bag
107
Nursing interventions HE: Bleeding
* Assess for GI bleeding, bleeding gums, epistaxis, petechiae (PT/INR)
* Safety, use an electric razor and soft toothbrush
108
HE nursing interventions: Fluid and electrolyte
* Strict I+O
* Daily weights
* Monitor for edema and ascites (Resp difficulty)
* Measure abdominal girth
* Admin diuretics
109
Diet with HE
* Consult dietician for best considerations
* High carb
* Protein amount and sources for daily intake
110
Upper GI bleed (UGIB)
* 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
Ligament of treitz
area of small intestine used to measure where a bleed is upper or lower
112
Causes of UGIB
* **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
Mallory weiss tear
Tear of the GI tract due to forceful coughing or vomiting, leading to bleeding
114
Patho UGIB:Chronic Peptic ulcer disease
* 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
Patho UGIB: Stress related ulcers
* Occurs when hospitalized patients due to decreased defence and repair mechanisms due to overwhelming stress response and mucosal ischemia
116
Patho UGIB: Variceal bleeding
* 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
Lower GI bleed
* Bleeding source below the ligament of treitz
* Jejunum, ileum, colon, rectum
* Bright red bleeding typically
118
Causes of LGIB
* **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
Risk factors for GI bleeding
* 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
Melena
Black tarry stools
121
Hematemesis
Vomiting bright red or coffee grounds
122
Hematochezia
Bright red or maroon color mixed with stool
123
UGIB presentation
* Hematemesis
* Melena
| Can have hematochezia with massive UGI hemorrhage
124
LGIB presentation
Hematochezia/ can also have pure blood or bloody diarrhea
125
S+S Acute GIB/ Impending Hypovolemic Shock: General
* Fatigue
* Conjunctival pallor
* Acute abdominal pain
* **Fever if perforation or ischemic colitis**
126
S+S Acute GIB/ Impending Hypovolemic Shock: Neuro
* Dizziness
* Weakness
* Syncope
* Restlessness
* Agitation
* Confusion
127
S+S Acute GIB/ Impending Hypovolemic Shock: Resp
* SOB
* Tachypnea
* Hypoxia
* Crackles in lungs
128
S+S Acute GIB/ Impending Hypovolemic Shock: CV
* Decreased BP (SBP <100 mmHg)
* Narrowing pulse pressure (Normal is ~60 mmHg)
* Tachycardia
* Palpitations
* CP (Underlying CAD)
* EKG changes (ST changes)
129
S+S Acute GIB/ Impending Hypovolemic Shock: Extremities
* Cold and clammy
* decreased cap refill
* Mottled skin
130
S+S Acute GIB/ Impending Hypovolemic Shock: Abdomen
* Hyper/hypo/absent (Can develop paralytic ileus)
* Basically anything
* Board like abdomen= peritonitis/ perforation
131
S+S Acute GIB/ Impending Hypovolemic Shock: GU
* Decreased or no urine output, increased BUN and creatinine
132
Labs Acute GIB: **CBC**
* 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
Normocytic
Reduced number, normal size
134
Microcytic
Smaller rbc than normal
135
Important labs for Acute GIB
* CBC
* PT/PTT/ INR
* CMP
* Lactate level
* Type and screen (Blood type)
* Stool and blood cultures if infectious source is suspected
136
Diagnostics Acute GIB
* **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
Nursing interventions acute GIB
* 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
Medical and treatment of Acute GIB
* **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
Medical and treatment of acute GIB: cardio and resp
* 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
Can you give vasopressors with no blood in circulation
* No you can't raise an empty tank, you need to fill it with fluids before they work
141
Medical treatment of acute GIB: Medications
* Somatostatin/**Octreotide**: stops hemorrhage of varices
* Vasopressin
* Proton pump inhibitor (Decrease acid in stomach)
* Prokinetics prior to EGD to improve gastric visualization
142
Medical treatment of acute GIB: Blood thinners and thrombolytics
* Hold Warfarin, anti Xa thrombin/factor Xa inhibitors, plt inhibitors (Plavix)
143
Acute GIB Tubes: NG tube
* Used to check gastric content
* provide gastric lavage
* Paralytic ileus (suc)
* distention (suc)
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Acute GIB tubes: Sengstaken-Blakemore tube
* 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**
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Minnesota tube
Same as sengstaken blakemore tube but it has a 4th port to pull gastric secretion from
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Potential complications of balloon tamponade
* Aspiration/ asphyxiation
* Rebleeding upon removal
* Esophageal rupture
* Mediastinitis or peritonitis
* mucosal ulcers
| Always keep scissors at the bedside to quickly deflate balloon
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Hemostatic treatments in acute UGIB: Endoscopy/ Colonoscopy
* 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 a noncontact form of electrocautery that uses ionized argon gas (plasma)
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Hemostatic treatments in acute UGIB: Vascular
Embolization
Transjugular intrahepatic portosystemic shunt (TIPS): Diverts portal blood flow away from the liver when endoscopic and pharm treatment fail in varices
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UGIB: Surgery
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
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Acute GIB meds: Proton pump inhibitors
* 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
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Acute GIB meds: Vasoconstrictors
* 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
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Acute GIB meds: Beta blockers
* Used long term in variceal pt to lower pressure
* Nadolol, propranolol
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Acute GIB meds: Prokinetic agents
* Metoclopramide (reglan)
* Given prior to endoscopy to clear GI for better visualization
* Used for N+V, gastroparesis
* SE are **tardive dyskinesia** and extrapyramidal symptoms
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Acute GIB meds: Mucosal barrier
* Forms a protective barrier that adhere to an ulcer
* Given 4x a day before meals and at bedtime
* Sucralfate (Carafate)
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Acute GIB meds: Antacids
* Magnesium hydroxide (MOM)
* Aluminum hydroxide + Magnesium or Calcium (Mylanta, Maalox)
* Calcium carbonate (TUMS)
