GI

CRITICAL CARE NURSING OF PATIENTS WITH GASTROINTESTINAL DISORDERS

Distinguish between upper and lower GI bleeds

  • Upper: esophagus, stomach, duodenum 

    • Upper GI bleed could be caused by peptic ulcer, esophageal varices rupture, esophagitis, mallory wise tear, erosive gastritis, AV malformations 

  • Lower: below the treitz ligament (most common is colon) 

  • The major issue in GI bleed is loss of circulating blood volume 

  • Hematemesis- blood in vomit 

  • Hematochezia - blood in stool

  • Melena - black stool 

  • Loss of 30% of blood volume

    •  s/s of hypovolemic shock occur

Upper GI Bleed 

  • Symptoms: 

    • Hematemesis

    • Melena

    • Hematochezia

    • Syncope or pre-syncope

    • Pain from an ulcer or esophagitis

    • Dyspepsia

    • epigastric pain

    • Heartburn 

    • Diffuse abdominal pain

    • Dysphagia

    • Unable to eat/vomiting a lot = weight loss

    • Digested blood = jaundice

    • Jaundice r/t esophageal varices

  • Treatments 

    • Fluid replacement (crystalloids)

      • Loss of blood volume 

    • May also need blood products 

    • Antacids (H2 blockers, PPIs) - know how & when they're given, & how long before/after they eat should they be taken, what interactions occur with other meds

    • Endoscopic tx 

    • Surgical repair if the viscera is perforated, if there is massive life-threatening unresponsive bleeding, or if bleeding continues after other tx are attempted, or if this is the second hospitalization

Nursing measures 

  • Upper : 

    • Airway (always comes first) 

    • Loss of circulating blood volume - blood pressure (+orthostatic)

      • So you know how the patient is doing circulatory wise  

    • 2 large bore IVs 

    • CBC, CMP, Amylase/lipase, type & crossmatch

      • For blood 

    • Accurate I&Os 

Gastric Lavage 

  • Not used often anymore

  • Risks often outweigh benefits 

  • May help identify high risk lesion in the upper GI tract (prone to rebleeding, which is associated with increased morality) 

  • IV erythromycin instead - expedites the contents from the stomach, also used to increase motility along with being an ABX 

  • Better visualization for endoscopy if they do gastric lavage first 

  • Studies that compared IV erythromycin vs gastric lavage had no evidence that doing gastric lavage decreased mortality or length of stay in hospital or need to transfuse

    •  (no clinical difference) 

  • Pts cited NG tube placement as worse than fx reduction, intubation, abscess drainage, or urethral catheterization (really unpleasant)

  • contraindications 

    • Lavage is contraindicated when airway is compromised or unprotected 

    • Pts at risk for GI hemorrhage due to perforation 

    • Sometimes used in poisoning, but contraindicated when poisoning is due to erosive substance (strong acid or strong base) or if the poison was a hydrocarbon, or if drugs have effective antidotes

    • aluminum phosphate poisoning 

  • Can be used as tx for GI hemorrhage from PUD from ruptured esophageal or gastric varices, but oyster tx are preferred 

  • If it is gonna be performed: a large bore single or double lumen tube is placed into the left nare (assuming its patent), then irrigating fluid is instilled (250 mL), then withdrawal after 30 seconds, position pt on left side with HOB at 15 degrees

    •  measure I&O, monitor VS & cardiac rhythm, NEVER leave patient alone 

  • Complications : 

    • Perforation

    • Aspiration

    • water intoxication

    • Hyponatremia

    • hypochloremia (can draw off hydrochloric acid from stomach) 

  • Lower GI bleed

  • After the ligament of treitz 

  • Causes 

    • Diverticulitis

    • angiodysplasias (abnormal growth of blood vessels)

    • IBD

    • Crohn's

    • UC

    • Neoplasm

    •  Polyps

    • Hemorrhoids

    • infection in the colon or GI tract (Salmonella) 

  • s/s: 

    • Hematochezia

    • maroon stools

    •  Melena

    •  asymptomatic other than bleeding slowly (unnoticed)

    •  Fever

    • abd cramping

    • dehydration

  • Worry is loss of blood volume 

  • Give crystalloids or colloids

  • May have to transfuse 

  • May have to administer meds to increase blood pressure (ensure you have good circulating volume first) 

  • Goal is to locate and halt the source of bleeding 

    • Endoscopically 

    • Tagging RBCs and infusing them back into the patient, will light up and you can see where they are escaping the vasculature 

    • Open surgery 

      • Go in an search for bleed

    • Surgical intervention - segmentic resection or subtotal colectomy 

    • Massive bleeds have up to 20% mortality rate, and rebleeds are common

Vasopressin : synthetic ADH 

  • Effective in blood vessels

  • Synthetic ADH is rapidly metabolized and destroyed by liver & kidneys

  • Has a 10 minute half life - quickly takes and loses effect 

    • Treats DI, nocturnal enuresis (bed wetting) 

    • Von Wildebrants disease - some forms 

    • GI Hemorrhage - off label use, slows or stops bleeding, 70% rebleed occur, not shown as effective on mortality in an upper GI bleed 

      • Lower GI bleed : buys time until OR 

    • Vasodilatory shock 

  • Can be given IM, SUBQ, IV

  • DDAVP - intranasally (for diabetes insipidus)

  • Acts on kidneys by promoting reabsorption of water 

  • Acts on blood vessels (off label use) to constrict them - especially arteriales, venules, and capillaries 

  • Can raise BP and slow bleeding 

Pancreatitis : 

  • Very serious, possibly life-threatening

  • Inflammation of the pancreas  

  • Up to 60% mortality rate with necrosis or hemorrhage 

  • Pancreatic enzymes activate prematurely (before intestinal system) and they begin to digest their own cells 

  • Severity depends on extent of inflammation and tissue damage

  • 4 physiological processes : 

    • Lipolysis - lipase digests fat, in addition to the damage to the cell itself, calcium begins to get used up (digestion of fat)

    • Proteinlysis : protein gets digested by amylase, wind up with clotting, thrombosis, and gangrene 

    • Necrosis of little blood vessels : bleeding, vasodilation 

    • Inflammation & pus formation 

  • s/s: 

    • Jaundice

    • Boring pain (working its way through you)

      •  intense in the midepigastric or LUQ area worsening in supine position

      • Patients with this condition tend to lie in the lateral position because that is the most comfortable (fetal position)

    •  N/V

    •  weight loss

    •  grey/blue flank/abd discoloration (Turner’s sign = discoloration of the flank, Cullen’s sign = discoloration of the abdomen, umbilicus). These signs represent ecchymotic bleeding & are severe signs with a higher mortality rate

    • absent or decreased bowel sounds 

  • Complications of pancreatitis 

    • Caused by bile duct obstruction (jaundice from bile backing up into the liver)

    • Type 1 diabetes

    • Left lung pleural effusions

    • Pancreatitis is one of the major causes of ARDS and MODS

    • coag defect

    • DIC

    • Shock

    • acute renal failure

  • Diagnosis : 

    • Elevated serum levels of amylase and lipase 

    • Rise in serum bilirubin 

    • Rise in alkaline phosphatase

    • Rise in ALT 

    • CBC to see infection & inflammation

    • ESR & CRP to see inflammation 

    • Calcium, magnesium, BMP

    • Triglycerides 

    • Serum total protein & albumin level

    • CT of abdomen (to see necrosis or hemorrhage) 

Ranson’s criteria : way to gauge severity of pancreatitis & likelihood of mortality 

  • Present on admission 

    • Age greater than 55

    • WBC greater than 16,000

    • BG greater than 200

    • Serum LDH > 350 I.U/L

    • AST > 250 I.U/L

  • Developing during the first 48 hours : 

    • Hematocrit fall >10% 

    • BUN Increase >8

    • Serum calcium <8 

    • Arterial o2 saturation <60 mm Hg

    • Base deficit >4 

    • Estimated fluid sequestration

  • Pts earn one point for each criteria 

  • Greater than 5 points = associated with more than 50% mortality 

Acute pancreatitis treatment : 

  • Make pt NPO (don’t want to make pancreas work to make digestive enzymes)

    • It is going to make the pancreas digest itself 

  • NG or OG tube (OG are usually more comfortable) to suction saliva 

  • Pain management (opioids)

  • IV fluids 

  • Calcium and magnesium replacement 

  • H2 antagonists & PPIs 

  • ABX is sometimes given 

  • Insulin because the pancreas is not puting out insulin 

Hepatic Failure : 

  • Number 1 cause is cirrhosis which is defined as widespread fibrosis due to inflammation and extensive degeneration and destruction of hepatocytes 

  • Cirrhosis is permanent scarring, usually chronic, following necrosis and reduced to the liver - liver cells are damaged or destroyed leading to necrosis and reduced blood flow to the liver which scars over, any time scar forms in the body it never performs to the same function of the original cell

  • Major cause of cirrhosis: 

    • hepatitis C

    • Alcoholism

    • biliary obstruction

    • Usually fatal 

  • Complications of hepatic failure :

    •  portal HTN

    •  Ascites

    • esophageal varices

    •  coagulation defects

    •  Jaundice

    • hepatic encephalopathy

    •  hepatorenal syndrome

Hepatitis Review : 

  • Hepatitis is inflammation of the liver cells

  • Viral is the most common form 

    • Hep A-Hep E

    • Know how each is contracted 

  • Toxins can cause hepatitis (alcohol, acetaminophen) 

  • Other industrial toxins

  • Secondary infections (CMV, varicella, herpes simplex virus) 

  • Classified as acute or chronic 

  • May be symptom-free and still contagious 

  • s/s: 

    • Flu-like symptoms (fatigue, anorexia, nausea, abdominal pain, joint pain)

    •  Fever

    • Vomiting

    • dark urine (liver isn’t doing its job in converting bilirubin)

    •  clay colored stools (no bile production) 

  • Chronic hepatitis : Hep B, C, D

    • Increases risk for liver cancer 

    • Fulminating hepatitis - symptoms progress quickly (hours or days) to severe liver failure 

    • Prevention is key : education on transmission, vaccines, PPE, hand washing, food prep & travel to countries that may have hepatitis

      • Hep A and Hep B

    • Risk for contracting hepatitis: blood transfusion prior to 1992, patients with hemodialysis, percutaneous exposure (needles, tattoos, piercings), unprotected sex (multiple partners or anal sex), food prep by someone with hepatitis, crowded living consitions 

Hepatitis Viral Testing 

  • Hepatitis B 

  • HBsAG- surface antigen infectious

  • Anti-HBs- surface antibody recovery and immunity

  • Anti-HBc- core antibody previous or ongoing infection

  • IgM anti-HBc- core antigen acute infection

  • HBeAg- e antigen- replication occurring

  • Anti-Hbe- predicts long-term clearance

Hepatitis Review - Vaccines & treatment 

  • Vaccines for Hepatitis A, given at 1 year and then 6 months later (18 months), available as part of toddler vaccine, can be given as post-exposure vaccine or immunoglobulin 

  • Hepatitis B vaccine is a series of 3, first one is given at birth, second one at 1-2 months, then third at 6 months, need to be 6 months between the first and third. Someone who doesn’t get the vaccine at birth can still receive the vaccine, and it remains a 3 dose series 1 month between the first and second and 6 months between the 1st and third. 

    • Immune globulin is also available for Hep B and can be given to infants who are born to infected mothers. 

    • Supportive care for acute infection (rest, diet, no further liver injury, antivirals for chronic Hep B) 

  • No vaccine for hep C, antivirals are available (peg interferon and riboviron)(usually given in combination), cure is possible 

  • Hep D is similar to B and only occurs in tandem with Hep B (co-infection), and can't have Hep D without Hep B. No vaccine available. 

  • Hepatitis E - no vaccine available, supportive care only (rest, fluids, proper diet, don’t ruin liver with Tylenol or alcohol) 

Cirrhosis: 

  • Normal liver tissue is replaced by tissue or scarring, which lacks function and often affects portal and periportal areas, which can block bile flow & cause other circulation problems

  • Post-necrotic cirrhosis: scarring 

  • Laennic cirrhosis: alcohol related 

  • Biliary cirrhosis: blocked bile tract 

  • s/s: 

    • Fatigue

    •  weight loss

    • abdominal pain and distention

    •  Pruritus

    • Confusion

    • personality changes

    • changes in mentation

    •  emotional lability

    • cognitive changes

    •  altered sleep

    •  Depression,

    • GI bleed

    •  Ascites

    •  Jaundice

    •  Icteris

    •  Petechiae

    •  nose bleeds

    •  Hematemesis

    •  Melena

    • palmar erythema

    •  Spiderangiomas

    •  dependent peripheral edema

    •  Asterixis (flapping tremor)

    • Fetter hepaticus (weird musty/fruity odor on breath) 

  • Cirrhosis complications : 

    • Portal hypertension : blockage of blood flow through the portal vein usually from scarring happening around it, blood seeks lower pressure channels and finds them in the spleen, esophagus, stomach, intestines abdomen, rectum, etc 

      • Blood backs up into these veins, but they have fragile and thin walls, if they’re in the esophagus they become distended and tortuous (bendy) and they may bleed - bleeding potential is related to size, bleeding esophageal varices is a life-threatening emergency (shock, LOC - may be lost before you are even aware of the bleeding) (distal esophagus) 

      • Esophageal varices bleeding may be spontaneous or occur with a trigger (heavy lifting, vigorous exercise, chest trauma, dry or hard food) 

    • Ascites: free fluid (plasma protein) in the peritoneal cavity secondary to increased hydrostatic pressure from portal hypertension, which causes reduced circulating proteins in the blood, fluid escapes into the periphery plus the liver fails to produce albumin, resulting in low serum colloid levels (hypovolemia & edema at the same time - puffy ankles but not enough blood in vessels) 

    • Splenomegaly: backup of blood into the spleen which causes the spleen to begin destroying platelets which contributes to the possibility of a massive bleed that doesn't stop 

    • Coag defects : biliary obstruction causes decreased production of bile and if the bile is not produced we have a problem absorbing vitamin k, so clotting factors 2,7,9,10 are not produced in sufficient quantities so they are susceptible to easy bleeding and bruising 

      • Prolonged PT & PTT and PLT count is decreased (recipe for disaster) In end stage liver failure

    • Hepatic encephalopathy : when the liver is not detoxifying the blood we have a rise of levels of ammonia in the blood. 

      • Early recognition and treatment may reverse encephalopathy

      • Symptoms

      •  sleep/mood disturbances

      •  changes in mental status

      •  speech problems due to altered LOC

      •  neuromuscular problems

      •  metabolic abnormalities.

      •  High protein diet, infection, drugs, GI bleed, bulimia, hypokalemia are all factors that can predispose the patient to developing hepatic encephalopathy

    • Hepato-renal syndrome: carries with it a very poor prognosis, usually fatal unless liver transplant.

    • Symptoms 

      •  sudden onset of oliguria (low urine output)

      •  increased BUN & creatinine

      •  decreased sodium excretion

      • increase urine osmolality

      • histology of liver cells are compromised

      •  normal kidney cells caused by altered blood flow to kidneys.

      •  Triggers include 

        • infection and GI bleed

        •  aggressive diuretic use

        •  taking off too much fluid during paracentesis (body has become accustomed to that fluid)

        •  early recognition of who is at risk is important.

        •  Kidney and liver dialysis can be done, liver dialysis is when we give a dialysate solution to help rid the body of substances which is just before transplantation (TREATMENT)

Diagnostics: LIVER FAILURE AND CIRROSIS

  • Hepatitis panel 

  • AST, ALT 

  • LDH (lactate dehydrogenase) 

  • Serum alkaline phosphatase

  • Bilirubin (total, direct, indirect) 

  • Urine bilinogen 

  • Fecal urobilinogen 

  • Serum total protein

  • Serum albumin 

  • Serum globulin 

  • Serum ammonia 

  • PT/INR

  • US/KUB/CT/MRI

  • Upper GI 

  • Percutaneous biopsy 

Liver biopsy : most definitive diagnostic test for dx of cirrhosis

  • Possible to identify scope of infection or damage that has occurred 

  • Need informed consent 

  • Pts should be NPO at least 2 hours prior 

  • Pre procedure meds

  • Position supine with RUQ exposed

  • Talk them through exhaling and holding their breath for 10 seconds during needle insertion (highly vascular area, don’t want any mistakes), pt can resume breathing after needle is withdrawn 

  • Put pressure on site afterwards and post procedure they need to lie on their right side for several hours after

  • monitor VS, check for abd pain, continuously assess site for bleeding

Treatments : 

  • Rest - not the time to increase activity level

  • Nutrition therapy - small frequent meals, high carb, high calorie, low fat/protein/sodium, vitamin supplements (folate and multivitamin)

  • May need to give diuretics

  • Be careful not to spur on hepatorenal syndrome

  • Often give beta blockers to prevent HTN (GI bleed, esophageal bleed)

  • ABX (cipro, fluoroquinolones, IV ceftriaxone) 

  • Vasoactive drug (vasopressin) to raise pressure and stop bleeding 

  • Many drugs will be used sparingly

    • Because alot of drugs are digested in the liver 

  • Reduction of ammonia levels: lactulose, flagyl, neomycin sulfate 

  • Paracentesis - relieves ascites 

    • Consent 

    • Watch VS 

    • Void ahead of time 

    • Supine with HOB up (use gravity to drop fluid down) 

    • Dressing over puncture site 

    • Label specimen 

    • Before & after weights 

  • Endoscopy treatment - sclerotherapy, variceal ligation, balloon tamponades to stop active bleed, TIPS procedure (trans jugular intrahepatic portal systemic shunt - shunting portal blood that’s under too high of pressure into the system) 

  • Surgical bypass - last resort, ascites is shunted to the SVC

  • Liver transplant - end of the road of tx for liver failure, not available to everybody (severe heart/lung disease, metastatic liver cancer, actively abusing alcohol will not qualify) 

Lactulose : used in cirrhosis patients who have hepatic encephalopathy (Heptalac) 

  • Laxative with other uses 

  • Draws water and ammonia into the colon and can be given PO/rectally (enema), used to treat constipation but also to decrease ammonia levels in the body via intestinal excretion 

  • Usual dose is 15 mLs PO QD 

  • Hepatic encephalopathy - 30 mL TID or 300 mL and 700 mL of water in normal saline as an enema (have patient retain for 30-60 minutes if possible) every 4-6 hours until desired effect 

  • Maintenance dose for hepatic encephalopathy is 30-45 mL PO TID 

  • SE : GI disturbances, electrolyte disturbances (hypokalemia, hypernatremia, hyperchloremia) 

  • Extra benefit seen in tandem with miralax in hepatic encephalopathy

  • Know TSP and TBSP for lactulose question

    • 1 tsp= 5 mL

    • 1 tbsp= 15 mL

Transplant: done for a pt in end stage liver failure when there is no alternative

  • Sources for transplant include a living donor or a trauma victim 

    • Family members donating to each other is common

    • Liver is regenerative; the donor’s liver will rebuild 

    • The transplanted liver will regenerate and grow based on the individual's needs

  • Exclusion criteria: severe CV & respiratory disease, metastatic malignant liver cancer, persistent alcohol and drug abuse (clean for 6 months)

  • Pts will be in the ICU after transplant

    • Watch for infection & graft rejection (tachycardia, fever, RUQ pain, change in bile color or increased jaundice, increasing AST or ALT levels) 

    • T-Tube in place after surgery that needs to be kept in a dependent position, needs to be emptied frequently, & record the amount of drainage 

    • After surgery, immunosuppressants will be administered to prevent rejection (immunosuppressant teaching) 

    • Transplants cause the trading of one problem for another 

    • Diet after transplant: low-fat, low-cholesterol, low-sodium, low-sugar, increase fiber, avoid grapefruit & alcohol on cyclosporines, teach increase in activity (low-impact), teach that they MAY be permitted to play contact sports again due to its regenerative nature, teaching surrounds infection and rejection & signs that something is going on with the liver (jaundice, pain, increased HR)