GI Alterations - Dr. Wiles Lecture PDF

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GI Alterations  

GI Bleed, Intra-abdominal Hypertension, Pancreatitis, Liver Failure GI Review o GI Function  Convert ingested nutrients into simpler forms that can be transported from the GI tract to the portal circulation and then used in metabolic processes  Detoxify the body by eliminating bacteria, viruses, chemical toxins, and drugs o Stomach pH 1.0  When mixed with food can rise to 2-3 o “Yellow feed the fellow”  Yellow colored enzymes are produced by the duodenum & are required for nutrient digestion  When seen in the NGT, patient is generally ready to eat o “Green obstruction is seen”  Don’t have the bile salts, means there’s an obstruction GI BLEEDING

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A medical emergency characterized by bleeding anywhere in the GI tract o Most cases are upper GI bleeding which is more life threatening o Lower GI bleeding is generally oozing in the colon Acuity ranges from out pt. treatment to ICU admission with maximal intervention Key to survival is prevention o Best treated when diagnosed early 3 main causes in ICU o Peptic ulcer disease, Stress related erosion, & esophageal varices Higher incidence of death occurs when 1+ co-factors exist o > 55 years old o Disease in 3+ organs o Transfusion of 5+ units o Lung (oxygenation) or liver (clotting factors) disease o Recent major surgery o Immunosuppression o Shock Left untreated, GI bleed results in hypovolemic shock, the initiation of the shock response, and the development of MODS The most common cause of death is NOT retractable hypovolemic shock but EXACERBATION of the underlying disease process GI Bleeding: Peptic Ulcer Disease (PUD) o Result from breakdown of gastric and duodenal mucosal lining o Leading cause of upper GI bleed in ICU o Causes  NSAIDS  Ibuprofen (Motrin, Advil), naproxen sodium (Aleve), etc.  Helicobacter pylori bacteria  Decreased mucosal blood flow o Gastric & duodenal ulcers  In addition to the “normal causes” in the ICU the normal protective mechanisms of the GI tract cease to function if there is not adequate GI mucosal blood flow GI Bleeding: Stress Related Mucosal Disease o Acute erosive gastritis o Second leading cause of ICU GI bleed—20% o High Risk Patients o Prophylaxis / pH testing  Pharmacologic gastric acid neutralization to maintain pH > 4.0 o Guiac tests  Checking for occult blood in stool o Range from superficial oozing to erosive disease

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GI Bleed: Stress Related Mucosal Disease (cont’d) o Cause  ↑ acid production d/t stress coupled with ↓ mucosal blood flow which degenerates stomach protective lining o Happens within hours of ICU admission o Can be prevented by prophylaxis o High Risk  Burns, CHI with coma, trauma, liver failure, shock sepsis GI Bleeding: Esophageal Varices o Engorged and distended blood vessels of the esophagus and proximal stomach o Develop from portal HTN secondary to hepatic cirrhosis o Third leading cause of GI bleed o Highest mortality rate—40-70%  Rupture and hemorrhage occurs 30% of the time and has a 40-70% mortality secondary to hypovolemic shock, SIRS, MODS & DIC  Co-morbid factors o With liver disease pressures are higher in the liver and the blood flow gets backed up causing varicesall of which have the potential to bleed o The usual pressure is 3 mm Hg; they will intervene with TIPS procedure at 10 mm Hg to shunt/decompress the pressure o The pt will have ascites due to all the albumin that seeps out in this space & can get splenomegaly o Caput Medusae  Veins are covered on the abdomen GI Bleeding Assessment o Terms  Hematemesis  Bright red or coffee ground emesis UGIB- generally the duodenal-jejunal junction (allows for reverse peristalsis) BRB vs. coffee ground o Related to length of time in contact with stomach acid  Hematochezia  Bright red stool  Massive lower GI hemorrhage (could be a rapid massive upper GI as well)  BRBPR – bright red blood per rectum  Melena  Black, tarry or dark red stools  Digestion of blood from upper GIB Signs & Symptoms  Abdominal pain  May or may not complain of abd pain  Nausea / Vomiting  Blood-tinged? How much?  Change in LOC  S/S of shock Labs  H&H  Poor indicators of severity or rapidity of blood loss o Horrible acute indicator  Blood and plasma are lost in the same proportion therefore the H&H stays the same (it is a percentage) o HCT of 45 before = HCT of 45 directly after  It may take long as 72 hours for the redistribution of plasma from the extravascular space to the intravascular space and cause the drop in HCT so watch the patient s/s as much as the labs  Giving IVF also changes the mix & makes H&H inaccurate  Hemoglobin-Hematocrit relationship is 1:3 o If Hgb is 10, Hct should be 30 o Consider IVF dilution if off  Transfusions  

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Expect HGB to increase by 1 and HCT by 3 for each unit, all else aside

GI Bleeding Assessment (cont’d) o Labs (cont’d)  PT / INR / PTT  DIC screen  To make sure patient is not using up all of their clotting factors o Diagnosis  Urgent fiber-optic endoscopy  Vasopressin/DDAVP  Octreotide (Sandostatin)  Epinephrine  During the scope, often use injection therapy and cautery to treat the bleed as well90% success rate when scoped within 12 hours of the bleed  Vasopressin & Sandostatin o Decreases splanchnic blood flow thus decreasing portal pressure  They can inject intraarterial vasopressin, embolizing agents like gelfoam, stainless steel coils, and polyvinyl alcohol particles.  Angiography  Angiograms are done if they can’t visualize the site due to the copious amounts of blood present GI Bleeding: Nursing Diagnosis o Fluid volume deficit o Decreased cardiac output o Impaired tissue perfusion o Altered nutrition: Less than body requirements o Risk for aspiration o Powerlessness o Ineffective family coping o Knowledge deficit GI Bleeding: Treatment Goals o Priorities: control bleeding & restore lost volume o Hemodynamic stability  If not, risk kidney failure (pre-renal) o Therapeutic procedures to control or stop bleeding o Meds GI Bleed Medications o Basically you want to buffer the stomach, reduce the amount of gastric secretions, provide a protective cover to the stomach, or inactivate the acid pump o Antacids  Buffer stomach and raise gastric pH  Maalox / Mylanta  Remember to clamp NGT after administration o H2 Antagonist  Reduce volume and concentration of gastric secretions  Tagamet  Zantac  Pepcid o Gastric mucosal agents  Coats & protects the ulcer  Carafate  Not something we use prophylactically  For known ulcer o Proton Pump Inhibitors  Inactivates acid pump blocking the release of HCl  Prilosec  Prevacid  Nexium  Aciphex  Protonix

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Will see a lot in the ICU because it can be given IV

GI Bleed Medications (cont’d) o Anticoagulation Reversal  Reverse coagulopathies that may be contributing to the GIB  Protamine Sulfate (heparin)  Vitamin K (Coumadin) GI Bleeding: Therapeutic Management o Treatment  Gastric lavage  NG tube lavage with NS or water until return is clear o When placing NGT: chin down to chest, swallow  Room temperature fluid  Gastric pH measurement  Goal: pH > 4  PPI  Generally Protonix drip o Fluid Resuscitation/ Volume Replacement  Volume replacement: crystalloids and blood 2 large bore IVs  Replace with PRBCs  Don’t forget to replace clotting factors  Crystalloids  Normal Saline to remain in vascular space  Blood and blood products  Emergent transfusion  Universal Donor (O-) o Males can receive O+ Blood Transfusions o Informed Consent o Patient ID  Double check  Blood products checked by 2 nurses o VS  Before, during, after  Within 15 minutes, then the next 15, then hourly  Temperature most important  Fever is the first sign of a transfusion reaction  Patients already febrile need a special order o Hanging Blood  NS with Y tubing  Transfuse within 4 hours  1 unit = 4 hours; 2 units = 8 hours; etc.  Can transfuse 1 unit of blood as fast as 1-3 minutes if patient is unstable o Transfusion Requirements in CC study (1999) set new guidelines for transfusion from trigger of 10/30 to Hgb of 7-9  Mortality rates were similar in both groups but those in the restrictive trigger group (7-9) had less complications that the traditional trigger group o If whole blood is lost rather than just volume depletion, blood products need to be considered to replace hgb. o Generally replace with PRBCs & save plasma to be used for other needed components  Can transfuse those PRN o National Patient Safety Goal: eliminate transfusion errors related to patient misidentification Transfusion Reactions o Allergic  Allergen in donor blood  Prevent by pre-medicating with Benadryl pre-transfusion, close observation  Treatment  Epinephrine and steroids PRN  Signs & Symptoms of Anaphylaxis  Dyspnea, hives/swelling, hoarse voice, NVD, abd pain

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Transfusion Reactions (cont’d) o Febrile  Less common with leuko poor (irradiated / washed) blood  Treatment  Tylenol, antihistamines, steroids  Signs & Symptoms  Temp 104, chills , HA, flushing, palpitations, CP, flank pain, back pain o Hemolytic  ABO or Rh incompatibility; incorrect cross match  Treatment  Shock with fluids & pressors, lots of labs, monitor for DIC  Signs & Symptoms  CP, SOB, shock, fever, chills, flank pain, flushing, impending doom (feel like you’re going to die) o No matter what reaction, STOP THE BLOOD  Unhook from the hub  Get fresh line, fresh tubing, fresh saline Cultural Considerations o Religious groups  Jehovah’s Witness  Old testament passage can’t consume blood / get blood interferes with their eternal life- correcting the medical problem on earth isn’t as important as eternal life  Jewish faith  Believe same passage, but believe that saving a life is a commandment- AKA thou shalt not kill  Muslims  The body and parts (such as blood) are sacred- blood is impure but if the medicine is needed an effective and there is no there cure some are willing to receive it- they do not believe in selling blood or blood products o Never assume—always ask o Remain nonjudgmental o Be supportive o Provide alternatives  Plasma expanders, albumin, etc. (problem is that they don’t have O2 carrying capacity) Massive Blood Transfusion Protocol o Rapid and effective restoration of an adequate blood volume  For those emergently bleeding out o Maintain blood composition within safe limits  Hemostasis  Oxygen carrying capacity  Oncotic pressure o Why  To restore volume and O2 carrying capacity o Who  Patients who have lost their total blood volume in < 24 hours  Adults losing 50% of their total blood volume in < 3 hours o What  PRBC, FFP and platelets  5:5:1, in that order  Giving PRBCs, FFP, and platelets restores multiple blood components  FFP contains the labile as well as stable components of the coagulation, fibrinolytic and complement systems; the proteins that maintain oncotic pressure and modulate immunity; and other proteins that have diverse activities

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Massive Transfusion Complications o Coagulopathy  Clotting defects  Anticoagulants in stored blood products  Disseminated Intravascular Coagulation (DIC)  Overstimulation of the normal coagulation process  Shock, hypothermia, & acidosis contribute  Patients get dilutional thrombocytopenia  Need to transfuse with clotting factors (FFP) and platelets o Hypothermia  Transfusion of cold blood  Exacerbates coagulopathies  Warming needed, use a warmer (makes room/body temp)  Reduces citrate and lactate metabolism which results in hypocalcemia and metabolic acidosis  Cardiac dysrhythmias may occur & may exacerbate coagulopathy o Hypocalcemia  Presence of citrate (anticoagulant) in transfused blood  Citrate binds the calcium and the patient becomes hypocalcemic  Treat with IV calcium  When giving mass transfusions you also have to give them calcium o Hyperkalemia  Plasma concentration of potassium in blood increases during storage  Potassium in blood is about 4 mEq per unit- with 10 units that’s 40 mEq  Need to consider how rapidly it is being given o Acid Base Imbalance  Acidosis followed by alkalosis  Acid-Base balance can be seen after massive transfusion however patients will become alkalotic  Patients may initially be acidotic because the blood load itself is acidic and there may be a prevailing lactic acidosis from hypoperfusion  However, once normal perfusion is restored, any metabolic acidosis resolves and the citrate and lactate are then converted to bicarbonate in the liver o Acute Respiratory Distress Syndrome  Due to under and over transfusion  Antigen/antibody reactions that can cause fluid shifts  Risk minimized if perfusion & oxygenation are maintained GI Bleeding: Therapeutic Management o Esophagogastric Balloon Tamponade Tubes  Blakemore tube (brand)  Used in extreme cases when bleeding is out of control  Large NGT/OGT that applies direct pressure against the bleeding vessels and decompresses the stomach with a balloon pulled tight  Allows decompression, drainage, and puts pressure on bleeding vessels  Balloon is placed in the gastro-esophageal junction  Effective short term / temporizing measure / adjunct prior to a definitive fix  50% of all patients rebleed after the tube is removed  Risk of it deflating and migrating, blocking the airway o Blakemore tube  Has gastric and esophageal balloons that are left inflated to control bleeding  Often secured with a football helmet  Tube left in for 24-48 hours  Must deflate balloon for 15 minutes every 4 hours to prevent tissue necrosis  Helmet serves as an anchor to decrease the chances of migration into the airway o Nursing Management of Blakemore Tubes  Monitoring for rebleeding  Observe for complications  Pulmonary aspiration  Esophageal rupture  Nasal necrosis  Need to consider emptying the stomach and intubating prior to Blakemore insertion  Minimizes the risk of aspiration

Nursing Management of Blakemore Tubes (cont’d)  Balloon migration  Potentially life-threatening- can obstruct airway  If respiratory distress develops, needs to be deflated and removed immediately! o Deflate esophageal one first! Managing Portal Hypertension o Transjugular Intrahepatic Portosystemic Shunt (TIPS) (p.782)  This is used in severe cases particularly bleeding in the portal system/varices  Puts a shunt beyond the blockage so blood can keep moving forward and stop backing up  They go in the Right IJ, a shunt is created through the liver parenchyma between one of the three main hepatic veins. This bypasses the increases liver resistance that the patient has in conjunction with their disease. Portal HTN will reoccur in 90% of these patients, however.  It can be done by an interventionist radiologist, vascular surgeon, or gastroenterologist. Preferred that they are intubated, because the patient has to lie perfectly still for hours, needs to be cooperative, and the equipment takes up so much space that if the person were to need emergency intubation, they wouldn’t be able to get to them.  Post procedure  Monitor for bleeding  Overt bleeding o IJ bleeding  Covert bleeding o Intrahepatic GI Bleeding: Surgical Interventions o Again surgeries are becoming less and less common. They will do the endoscopies at the bedside in the critical care unit. They can do injection therapy with endoscopy, they can cauterize the bleed and this is done w/ a 90-95% accuracy rate. o PUD  Vagotomy or pyloroplasty  Sever vagus nerve which will stop acid production, hopefully stops ulcers  Also slows gastric emptying  Vagus nerve in the stomach is severed which eliminates the gastric cell production of HCl acidsince the vagus nerve also stimulates motility the pyloroplasty is performed to provide for gastric emptying o SRES  Total gastrectomy  Ulcer over sew  Total gastrectomy for generalized bleeding- esophagus anastomosed to the jejunum for oversew the bleeding vessel if ligated & the ulcer crater closed o Varices  Hepatic shunting  Banding  Shunt. More to come… o Banding  Applying metal bands or clips around the circumference of the bleeding varicies to induce venous obstruction and control bleeding  After 1-2 days there is tissue sloughing and scar formation  This can be done weekly for 1-4 weeks until all varicies are gone GI Bleeding: Therapeutic Management o Teaching  Etiology & precipitating factor modification  Taking meds  Take Prednisone with food because it can cause ulcers  Lifestyle changes  Smoking and alcohol cessation  Diet modification  Stress management o

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INTRA-ABDOMINAL HYPERTENSION       

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Occurs in 50% of ICU patients Can occur in trauma patients Patients who received fluid resuscitation then third spaced Patients who had abdominal surgery with closure Progresses to abdominal compartment syndrome Your patient’s weight is up… o Where do 5+ liters of fluid go in the human body? Into the gut! Elevated Abdominal Pressure o Normal: 5-7 mm Hg o HTN: > 12 mm Hg o Severe: > 15 mm Hg  Associated with organ system dysfunction o Abdominal Compartment Syndrome  Pressure > 20 mm Hg Intra-Abdominal Hypertension: Categories o Primary or Acute  Occurs when intra-abdominal pathology is directly responsible for the compartment syndrome o Secondary  Occurs when no visible intra-abdominal injury is present but injuries outside the abdomen cause fluid accumulation in the abdomen (e.g. sepsis) o Chronic  Occurs in the presence of cirrhosis and ascites or related disease states, often in the later stages of the disease Intra-Abdominal Hypertension: Presentation o ↑ abdominal girth o ↑ TF residuals o ↓ bowel sounds o Difficulty breathing o ↓ urine output (gut isn’t perfused, kidneys aren’t being perfused) o Nausea & vomiting o ↓ BP; ↑ HR Intra-Abdominal Hypertension: Diagnostics o CT scan o Intra-abdominal pressure monitoring  Bladder pressures  IAP can be easily monitored by measuring bladder pressure.  Measurement of intraluminal bladder pressure consists of instilling about 50 mL of saline into the urinary bladder through the Foley catheter. The tubing of the collecting bag is clamped, and a needle is inserted into the specimen-collecting port of the tubing proximal to the clamp and is attached to a manometer.  Bladder pressure (measured in mm Hg) is the height at which the level of the saline column stabilizes with the symphysis pubis as the zero point. Intra-Abdominal Hypertension: Treatment o Improve abdominal wall compliance  Decompressive laparotomy  Decompressive lap- trying to prevent dead gut o Blue Towel Closure to Wound Vac Intra-Abdominal Hypertension: Treatment o HOB > 20°  Avoid prone position; consider Trendelenburg o NG and rectal tubes to decompress / evacuate contents o DC enteral nutrition o Anything to relieve pressure… o Open up their gut Patient Presentation 43 YO male c/o epigastric pain n/v after weekend of heavy drinking. Patient rocking back and forth. Tender belly. VS T 101.8, HR 122, RR 24, BP 92/54. What do you think is wrong with this patient?

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Pancreatitis

PANCREATITIS Normal role of pancreas o Digestive organ  Secretes digestive enzymes o Endocrine function  Alpha cells secrete glucagon  Beta cells secrete insulin Mortality approaches 60% when accompanied with necrosis or hemorrhage Most Common Causes of Pancreatitis o Biliary disease / Gallstones o Alcoholism Other Causes of Pancreatitis o Trauma o Drug Induced  Sulfas, cyclosporine, diuretics o Idiopathic Pancreatitis: Pathophysiology o Digestive enzymes (primarily trypsin) activate prematurely and auto-digests tissue  Causes inflammation & swelling  Release of elastase causes hemorrhage o Fluid extravasation  fluid shifts  hypovolemia  shock o Auto-digestion causes parenchymal and adipose tissue necrosis o Results in inflammation and sw...