CCRN/PCCN Certification Review Gastrointestinal

CCRN/PCCN Certification Review Gastrointestinal

What’s on the Test? CCRN and PCCN CCRN only
GI hemorrhage: Upper and Lower Pancreatitis Hepatic failure/coma: Portal HTN, Cirrhosis, Esophogeal Varicies, Biliary Atresia Bowel infarction/ Obstruction/ Perforation: Mesenteric Ischemia Malnutrition/ Malabsorption GI Reflux CCRN only GI surgeries Acute abdominal trauma PCCN only GI infections GI functional disorders: Obstruction, Ileus, Diabetic Gastroparesis Review what’s on the test.

GI TEST PLAN GI is combined with endocrine, hematology, and renal to make up 18% or the PCCN exam. GI is combined with endocrine/hematology/renal and integumentary to make up 20% of the CCRN exam (total 30 questions all together) Integumentary is included in PCCN – it is in the multisystem lecture That is where we will cover it during this course

Acute GI Bleeding: Upper and Lower
Loss of old or new blood from the GI System 85% of all GI Bleeds are UGI: Stomach or Small Intestine Duodenal ulcer: 27% Erosive Gastritis 23% Varicies 14% Account for approx 2% of all admissions Death can result from circulatory failure/ Shock

UPPER GASTROINESTINAL BLEEDING
Bleeding that originates from any GI site proximal to duodenal jejunal juncture (Ligament of Treitz) Extensive vasculature in this area Common and can be lethal Ligament of Treitz is the suspensory muscle of the duodenum that connects the duodenum to the diaphragm. This is the duodenal landmark of the duodenojejunal junction UPPER GI BLEED: BLEED FROM STOMACH OR SMALL INTESTINE

ETIOLOGY OF UPPER GI BLEEDING
Peptic ulcers Esophageal varices Stress related mucosal disease ** Mallory-Weiss tear ** Diffuse gastritis Esophagitis Gastric-duodenal tumors H. pylori infection ** Mallory Weiss tear is a tear in the mucosa of the esophageal gastric junction caused by forceful vomiting and retching. Critical care patients are at greater risk for upper gi bleed due to the development of stress related mucosal disease. Ulcerations in the stomach and duodenum can occur within hours of a severe injury or surgery. Highest incidences of stress related are with burn and brain injured patients as well as mechanical ventilation, trauma, sepsis, hypotension and shock states, hepatic and renal failure and administration of steroids. Hypotension or shock states shunts blood away from GI system. The reduced gastric blood flow diminishes the protective mucus secretions. There is also increased acid production during stress periods. Colonization of stomach with H. pylori can result in chronic gastritis at the site of infection. H. plyori causes inflammation and allows stomach acid and the digestive enzyme pepsin to overwhelm the mechanisms that protect the stomach and duodenal membrane.

UPPER GI BLEED PRESENTATION/ MANAGEMENT
Hematemesis Vomiting of fresh blood. Melena Black, tarry stool Initial evaluation involves an assessment of hemodynamic stability and resuscitation. Diagnostic Studies follow with the goal of diagnosis and treatment of the specific disorder. Mouth, esophagus, stomach and duodenum are common sites Prior to hematemesis, patient has recurring abdominal pain which is gnawing and located just below xiphoid process, or in right upper quadrant of stomach. Pain is relieved by drinking milk or eating antacids; worse with alcohol, aspirin, caffeine, and spicy foods Bleeding of more than two units of blood (20% of blood volume) is usually associated with shock. Approx 1500ml of blood loss = patient exhibits signs of shock Anorexia, weight loss, and chronic anemia= cancer A slow bleed may produce only weakness, fatigue, and pallor

DIAGNOSIS OF UPPER GI BLEED
Tagged red blood cell study Hemoglobin and Hematocrit WBC’s elevated NG drainage and stool guaiac positive for blood BUN and creatinine elevated (RBC breakdown) Calcium decreased (blood transfusions) H.pylori culture positive Gastric aspiration Endoscopy Preferred method Can do intervention Barium study Identify site of bleed Angiographic exam Need to diagnose probable site of a bleed NG aspiration – can help assess severity of bleed: bright red indicates more recent and severe as opposed to coffee ground Tagged red blood cell study: uses small amount of radioactive material to mark RBC; this can be done by removing your own blood, mixing it with radioactive material, and then reinjecting OR injects the radioactive material directly. Scan is done afterwards to see the cells and track how they move through the body. Citrate in blood products bind calcium

TREATMENT OF UPPER GI BLEED
Assessment and monitoring of vital signs: Maintain Hemodynamic Stability Large bore intravenous access Patient is NPO NG tube placement and lavage with room temperature fluids Manage with resuscitation with blood, blood products, and crystalloid Medications: IV PPI Endoscopic or angiographic coagulation or embolization of ulcer Maintain blood pressure and circulating volume Keep an eye on organ perfusion (look at vital signs and urine output) Should start an intravenous PPI (pantoprazole or omeprazole)

Treatment of GI Hemorrhage Invasive
Laser Photocoagulation Endoscopic sclerotherapy Electrocauterization

SURGICAL TREATMENT Oversew of bleeding site
Vagotomy to interrupt acid production Pyloroplasty to promote gastric emptying Subtotal or total gastrectomy Watch for dumping syndrome where food is dumped rapidly into the small intestine. Patient has abdominal cramping, nausea, vomiting, sweating, diarrhea, light headedness, rapid heart rate. Avoid foods high in sugar, avoid eating solids and drinking liquids during same meal, eat six small meals/day, stop eating when you feel full, eat complex carbs such as vegetables instead of simple carbs like bread

ASSESS FOR PERFORATION
Sudden, severe, generalized abdominal pain Rebound tenderness Abdominal rigidity Fever Leukocytosis Tachycardia PERFORATION IS A SURGICAL EMERGENCY Placement of patch Oversew perforation Colostomy/diverting ostomy There are other causes for perforation.

MEDICATIONS Histamine blockers Block gastric acid secretion
- Rantidine (Zantac) -Famotidine (Pepcid) Proton pump inhibitors - Omeprazole (Prilosec) - Pantoprazole (Protonix) Antacids Neutralize acids - Mylanta - Amphojel Histamine receptor anatagonists promote ulcer healing, prevent reoccurrence; side effect is thrombocytopenia and higher incidence of nosocomial pneumonia Proton pump inhibitors inhibit gastric acid; have higher incidence of diarrhea and an association with C diff Antacids raise low gastric ph

MEDICATIONS Antibiotics for H.Pylori - Amoxicillin - Ampicillin
- Metronidazole Mucosal barrier enhancers -- Sucralfate Vasopressin infusion Constricts arterioles: Watch for cardiac dysfunction Sulcralfate forms a physical barrier to gastric acids Vasopressin infusion prevents bleeding. Can be given intra-arterially or peripherally

LOWER GI BLEEDING CAUSES
Diverticulosis Angiodysplasia (AVM) Neoplasm Polyps/benign growths Ischemic colitis/ bowel infarction Upper GI sources

SIGNS OF LOWER VS UPPER GI BLEEDS
Lower GI bleed Hematemesis (coffee ground or bloody) Melena stools (dark, tarry odorous) Elevated BUN (Normal creatinine): Greater absorption of protein in the stomach and duodenum Decreased hemoglobin and hematocrit No hematemesis Bloody stools Normal BUN Decreased hemoglobin and hematocrit Maroon color stool can be lower or upper GI bleeding

DIAGNOSIS OF LOWER GI BLEED
Colonoscopy (gold standard) Plain radiographic film Labs are the same ones used with upper GI bleeding Interventions the same as with upper GI bleeding, but using colonoscopy Surgery the same as UGI, but may require colostomy Blood in the terminal ileocecal valve indicates bleeding is in the small bowel.

Pancreatitis An acute inflammatory autodigestive process of the pancreas. Thought to be from activated pancreatic enzymes acinar cells into nearby tissues

PATHOPHYSIOLOGY OF ACUTE PANCREATITIS
Premature activation of exocrine enzymes (trypsin, lipase, amylase) prior to transport into the duodenum Events begin with the acinar cells and ducts Massive autodigestion of the pancreas occurs Reflux of duodenal juices, leakage of enzymes Systematic inflammatory response occurs Enzymes, oxygen free radicals, inflammatory mediators (cytokines) are released Enzymes are activated in the pancreas itself; normally pancrease secretes the enzymes in an inactive form, and they are activated by fluids present in the duodenum.

CAUSES OF ACUTE PANCREATITIS
Cholelithiasis ** Alcoholism Infection Abdominal surgery Hypercalcemic states Lipid abnormalities Medications such as thiazides, oral contraceptives, NSAIDS Idiopathic Cholelithiasis is the most common cause; alcoholism is the second. GALLSTONES BLOCK OFF PANCREATIC DUCT Alcohol increases protein content of pancreatic juice, causing plugging in the ducts; alcohol may also cause spasm of the sphincter of ODDI, increasing the pressure in the pancreatic ductal system, and injuring the pancreas.

PRESENTATION OF ACUTE PANCREATITIS
Severe, epigastric, abdominal, and back pain Diffuse abdominal tenderness and rebound, guarding Low grade fever Nausea and vomiting Glucose elevation Jaundice Ileus Circulatory instability Cullen’s sign (perumbilical ecchymosis) Grey Turner’s sign (ecchymosis of groin, flank, and thigh) Bibasilar crackles Weight loss Epigastric pain is the hallmark sign accompanied by nausea and vomiting Pain is severe, knife-like; usually in upper abdomen and radiates to the back Patient goes into the knee-chest position to relieve the pain; supine positions exacerbate the pain Ecchymotic signs like Cullen’s and grey turners are usually not seen on admission Circulatory instability is hypotension, tachycardia.

CULLEN’S SIGN

RANSON’S CRITERIA AT ADMISSION Age greater than 55 years
Leukocytosis greater than 16,000 LDH > 350 IU/L AST greater than 250 U/L Glucose greater than 200 mg/dl without history of diabetes DURING INITIAL 48 HOURS Hematocrit decreases > 10% BUN increases > 5 mg/dL Calcium < 8 mg/dL Phosphorous < 60 mm Hg Base deficit > 4 mg/dL Fluid sequestration > 6 Liters Means to prognosticate mortality risk. Mortality risk increases with 4 (6%); 5-6 (40%), greater than 6 (100%) Presence of three of the five Ranson criteria on admission is considered severe pancreatitis Done at hospital admission and 48 hours later.

LAB DIAGNOSIS OF ACUTE PANCREATITIS
Elevated serum amylase: After 1st 24hrs, only about 2 days elevated Lipase: Within 24-48hrs: 5-7 days Elevated urine amylase Liver function tests may be elevated Elevated White Blood Cell count Hgb and Hct may be elevated or decreased Both amylase and lipase elevate rapidly (within 3 – 6 hours) following onset of pancreatitis. Amylase rises first within 24 hours after symptoms Lipase has a longer half life and hangs around longer The degree of the elevation has no prognostic value Elevated Hct can indicate a leaking of fluids (third spacing) and is defined as a Hct greater than 44% on admission Severely affected individuals have hypocalcemia, anemia, leukocytosis, hypoxemia, hypoalbuinemia, and hyperglycemia

RADIOLOGIC DIAGNOSIS OF ACUTE PANCREATITIS
CXR and abdominal films Abdominal CT scan with IV contrast (gold standard) ** MRI Ultrasound Endoscopic retrograde cholangio-pancreatography (ERCP) MRI not used as much but advantage is not having to use gadolinium with its renal toxicity Ultrasound can look for the presence of gall stones (not accurate for identifying necrosis or inflammation of pancreas) ERCP can look at biliary duct for strictures or stones Ultrasound can identify gallstones and compromise to biliary tree as well as fluid collections. Has limited visualization of pancreas itself Can do CT scan without iv contrast – contrast gives better visualization, but can cause renal injury and aspiration MRI can identify which lesion Is drainable and which is solid – difficult to do with sick patient

MANAGEMENT OF ACUTE PANCREATITIS
Volume resuscitation: Prevent/ Control Shock Pain management NPO Parenteral nutrition or jejunostomy feedings Electrolyte replacement ----Hypocalcemia, hypokalemia, hypomagnesemia ----Monitor ECG, Chvostek’s and Trousseau’s signs NG tube of vomiting or abdominal distention Chvostek’s sign – spasm of facial muscle when tapping Trousseau’s sign – hand spasms with pressure GOAL: MAINTAIN PERFUSION AND LIMIT PANCREATIC INJURY Inadequate fluid replacement can cause intestinal ischemia with translocation of bacteria into the pancreas (infected necrosis) as well as distal organ hypoperfusion. Early resuscitation reduces the incidence of systemic inflammatory response syndrome (SIRS) and multisystem organ failure. Target for fluid resuscitation is to correct concentrated hematocrit and maintain adequate urine output. Lactated ringers may be used to prevent hyperchloremic acidosis which occurs with large volumes of 0.9% of NaCL administration. NPO rests pancreas and prevents release of digestive enzymes. Give feedings past duodenum so pancreas is not stimulated. If amylase/lipase increases with enteral feedings, then TPN should be used

MANAGEMENT CONTINUED Insulin if hyperglycemic
Supress Pancreatic Stimulation: Somatostatin (Octreotide) to inhibit pancreatic secretion: Controversial Histamine blockers or Proton Pump Inhibitors Monitor for hypovolemic shock, renal failure, hemorrhage, respiratory failure Monitor for sepsis May need surgical interventions (cholecystectomy, pancreatic resection, drainage of pseudocyst, drainage of abscess) Somatostatin decreases production of gastrin and cholecystokinin and reduces secretion of the pancreas. Controversial Prevent and Control Shock: Hypovolemic: Kinins, N&V, Hemorrhage Relieve Pain Supress Pancreatic Stimulation Complications: Pancreatic Abcess: High Fever, Palpable mass, abdominal tenderness, N&V, Leukocytosis, Hyperglycemia: Requires Surgery/ IR Rad Pancreatic Pseudocyst: Abdominal Pain/ Fever/ N&V >1 week, WBC or amylase remains elevated

EXAM QUESTION A patient in the ICU begins vomiting blood and becomes hemodynamically unstable. His heart rate increased to 120 bpm, BP decreased to 90/54, and oxygen saturations decreased to 90% on 40% facemask. Which of the following is the priority of care at this time? A. Assist with placement of a central venous catheter B. Intubate and place on mechanical ventilation C. Assist with endoscopy to localize source of bleeding D. Type and cross for two units of red blood cells

QUESTION A patient with colorectal cancer was admitted to the PCU one week after the last chemotherapy treatment. On admission, the patient complained of fatigue and was pale with a blood pressure of 110/70 and a pulse of 88 beats/minute. The BP is now 130/84, the pulse is 110 beats/minute, and the patient is passing dark, tarry stools. The nurse’s plan of care will center on this patient’s most immediate needs related to: A. Malnutrition B. Gastrointestinal bleeding C. Anemia D. Immunosuppression

QUESTION A patient with colorectal cancer was admitted to the PCU one week after the last chemotherapy treatment. On admission, the patient complained of fatigue and was pale with a blood pressure of 110/70 and a pulse of 88 beats/minute. The BP is now 130/84, the pulse is 110 beats/minute, and the patient is passing dark, tarry stools. The nurse’s plan of care will center on this patient’s most immediate needs related to: A. Malnutrition B. Gastrointestinal bleeding C. Anemia D. Immunosuppression Anemia is probable, but not the most pressing thing at this time

QUESTION A patient presenting with severe abdominal pain and vomiting is diagnosed with pancreatitis. Which of the following findings on admission would most predict an increased severity of pancreatitis? A. Hematocrit 45% B. Amylase greater than 140 U/L C. Lipase greater than 70 U/L D. Potassium 4.5 mEq/L Normal amylase level is 23 – 85 U/L (some lab results go up to 140 U/L Normal lipase levels are 0 – 160 U/L

QUESTION A patient presenting with severe abdominal pain and vomiting is diagnosed with pancreatitis. Which of the following findings on admission would most predict an increased severity of pancreatitis? A. Hematocrit 45% B. Amylase greater than 140 U/L C. Lipase greater than 70 U/L D. Potassium 4.5 mEq/L A concentrated hematocrit in a pancreatitis patient indicates third spacing of fluids demonstrating a more severe episode of pancreatitis. Amylase and lipase levels are elevated in pancreatitis, but the degree of elevation does not indicate the severity of pancreatitis. Potassium levels typically decrease in pancreatitis

GI Inflammation & Infections
Clostridium difficile colitis Inflammation Esophagitis Gastritis Colitis Crohn’s Disease

GI Infections Clostridium difficile colitis ~Pseudomembranous colitis C-Diff Organism that is responsible for antibiotic colitis. C.diff colonizes and over-grows GI tract after the normal flora has been altered by antibiotic therapy. Two endotoxins (proteins) toxin A and toxin B These endotoxins cause injury and inflammation As bacteria grow, they release these endotoxins Besides antibiotics, other risk factors are surgery of GI tract, weakened immune system, previous infection, 65 or older, colonic diseases such as inflammatory bowel disease, proton pump inhibitors

C-Diff Assessment: Fever, abdominal cramping/pain, heme-positive stool, and diarrhea (profuse +10 liquid fouls stools a day) in a patient currently or recently receiving antibiotics & possible antibiotic therapy Abdominal distention, colonic bleeding, fecal leukocytes

C-Diff Management- Includes
Supportive Care: correction of fluid & electrolytes Discontinuation of antibiotics when possible Avoidance of antiperistaltic agents Patient placed in contact isolation Appropriate antibiotic therapy Metronidazole – Oral is recommended first line agent Vancomycin – Alternative first line drug is oral Vanco Relapses- repeat treatment (5% to 50%) Hand washing in isolation

Gastroesophageal Reflux- GERD
Chronic condition in which gastric contents enter into and remain within the lower esophagus because of impaired esophageal function. GERD is a systematic condition or histological alteration that results from episodes of reflux that may produce inflammation of the esophagus.

Assessment: Hallmark system: heartburn described as substernal sensation Regurgitation dysphagia hemorrhage Belching fullness early in the meal Atypical Symptoms

Lab Findings / Tests: Clinical history most useful tool Barium swallow Endoscpoy 24 hour pH monitoring Esophageal manometry Esophageal manometry is a tube that gets passed down the nose to esophagus that tells whether esophagus is working properly. Tells whether lower sphincters are closing properly 24 hour PH: tube is passed through nose, down esophagus and secured to face with tape. It is attached to a portable recorder that patient wears. Patient pushes button on recorder when they eat, drink, and lay down

Management: Treatment in Phases based on assessment Phase I- HOB elevation, diet changes, avoidance of foods impacting LES pressure, avoidance of foods impacting mucosa, increase protein intake, weight reduction and other diet/lifestyle modifications. Addition of OTC H2 blockers, use of antacids as needed Phase II – Continuation of Phase I plus add prescription dose of H2 blocker, prokinetic agents and/or mucosal agents

Phase III –Increase the dosage of initial drug or add a second drug like a PPI. Step up or step down therapy as needed and based on patient condition Phase IV – Surgical intervention- Failed management or complications have developed

IBS Chronic condition with long term management
Only a small number of people with irritable bowel syndrome have severe signs and symptoms. Some people can control their symptoms by managing diet, lifestyle and stress. Others will need medication and counseling.

INTESTINAL OBSTRUCTION
Blockage of the lumen of the intestine due to partial or complete occlusion of the lumen or inadequate propulsive motility. Necrosis with toxicity and possible perforation may occur with strangulation. Obstruction is the Most common indication for abdominal surgery

ETIOLOGY OF OBSTRUCTION/INFARCTION
CAUSES OF OBSTRUCTIONS Adhesions ** Hernias Malignancies Volvulus twisting of the bowel upon itself Abscess Inflammatory diseases Decreased blood flow (can cause infarction) ----Vasopressor medications ----Hypovolemia ----Decreased cardiac output Adhesions from previous surgery is a common cause

DIAGNOSIS Abdominal pain sometimes out of proportion to physical findings Tenderness Distension Fever Decreased or absent bowel sounds Elevated WBC Elevated BUN and signs of hemoconcentration Obstruction series Presentation depends on where the obstruction is. If in small intestine, you see vomiting and crampy epigastric pain. If it is distal, it can be vague, crampy of diffuse abdominal pain. Signs of hemoconcentration occur from the vomiting, patients not taking in fluids, and fluid gets trapped in intestinal loops X-rays show dilated small bowel loops; can also use ultrasound to diagnose

MANAGEMENT OF BOWEL OBSTRUCTION
Intravenous fluids Correct fluid and electrolyte losses NG suction NPO Status Analgesia Surgery, lysis of adhesions, resection, strangulation- emergent surgery Rectal tube for decompression of cecum Miller-Abbot/Cantor tube – stimulate peristalsis NG suction helps decompress the stomach and improve comfort level ½ to ¾ need surgery to correct problem Miller Abbot Cantor tube is to treat obstructions. Has two lumens with a small balloon near the end of the tube. One lumen is for aspiration and irrigation; the other is used to inflate balloon . Goes down to small intestine Cantor tube is a single lumen that does the same thing – decompresses the intestine. Both are 10 feet long

EXAM QUESTION Choose the intervention that is most important to perform before a patient undergoes surgery to correct a complete small bowel obstruction: A. Ensure proper fluid and electrolyte replacement B. Teach the patient about ileostomy care C. Obtained informed consent for the procedure D. Begin total parenteral nutrition (TPN)

EXAM QUESTION Choose the intervention that is most important to perform before a patient undergoes surgery to correct a complete small bowel obstruction: A. Ensure proper fluid an electrolyte replacement B. Teach the patient about ileostomy care C. Obtained informed consent for the procedure D. Begin total parenteral nutrition (TPN) Small bowel obstruction can lead to vomiting, which leads to fluid and electrolyte problems. There is no indication that an ileostomy needs to be done. They physician get consent, not the nurse. TPN will most likely be used later, but is not as important as preventing shock from fluid loss or electrolyte depletion

ILEUS Is a condition where there is a neurogenic failure or loss of peristalsis in the absence of any obstruction.

CAUSES OF ILEUS Postoperative (delay in GI motility beyond 3 days)
Anesthesia: “Sleepy bowel” “Not moving” after surgery Narcotic induced Intra-abdominal process (abscesses) **Again, remember it is NOT an obstruction

Ileus Assessment: Nausea Vomiting Bloating Sense of fullness
Abdominal distension Tympany Bowel sound abnormalities / Bowel movement abnormalities

Ileus Diagnostics Electrolytes Xrays: Obstruction Series
Barium Swallow CT Scan

Ileus Care of the patient / Possible Complications
Non narcotic interventions for pain Feedings as tolerated: May need NPO Progressive ambulation (needs more study) Fluid and electrolyte replacement Nasogastric tube to suction Treat underlying causes

GASTROPARESIS: CAUSES
Delayed gastric emptying: Post Op (13%) Consequence of systemic conditions such as diabetes (29%) Idiopathic (36%) Unknown prevalence

GASTROPARESIS SIGNS AND SYMPTOMS
Nausea, vomiting Early satiety Abdominal discomfort Distention Bloating Anorexia

MANAGEMENT OF GASTROPARESIS
Suspect and exclude mechanical obstruction Assess GI motility Hydration Electrolyte repletion Nutritional supplementation Metoclopramide (Reglan) – prokinetic Erythromycin – accelerates gastric emptying Octreotide, antiemetics, antibiotics

EXAM QUESTION Abdominal distention, a tympanic percussion note and rushes of high-pitched tinkling sounds that coincide with abdominal cramping indicate which of the following? A. Rapid GI transit time B. Intestinal obstruction C. Celiac artery infarction D. Superior mesenteric artery occlusion

GASTRIC BYPASS SURGERY
Vertical banded gastroplasty (lap band) Infection, obstruction, band slippage, esophageal dilation Roux-en-Y: proximal gastric pouch whose outlet is a limb of small bowel Atelectasis, pulmonary infection and embolus Wound disruption,rhabdomyolysis Anastomotic leak, DVT, Dumping syndrome

EXAM QUESTION After ambulating following gastric bypass surgery, a patient becomes tachycardic, tachypneic, diaphoretic, and febrile. Assessment reveals a clean, dry, closed abdominal staple line, and a large firm tender abdomen. The most likely cause for these acute changes would be: A. Pulmonary emboli B. Routine postoperative pain C. Anastomosis leak D. Acute cholelithiasis

EXAM QUESTION After ambulating following gastric bypass surgery, a patient becomes tachycardic, tachypneic, diaphoretic, and febrile. Assessment reveals a clean, dry, closed abdominal staple line, and a large firm tender abdomen. The most likely cause for these acute changes would be: A. Pulmonary emboli B. Routine postoperative pain C. Anastomosis leak D. Acute cholelithiasis Pain, fever, firm tender abdomen are classic for peritonitis. PE would have more pulmonary symptoms, pain would not explain the fever and firm abdomen, and gallstones typically cause nausea and do not develop immediately after surgery

Whipple Procedure Surgical treatment for benign and malignant tumors of the pancreas and bile ducts Removal of distal portion of stomach, duodenum, head of pancreas, distal common bile duct with anastomosis of all structures to jejunum

Whipple Procedure Care of the patient / possible complication
Surgery and treatment (radiation/chemotherapy) Bleeding Infection Insulin resistance Pain Anastomotic breakdown Risk versus benefits Psychosocial issues

Esophagogastrectomy Surgical procedure for cancer of the esophagus
Removal of involved digestive tract and 10 cm on either side of tumor and insertion of a conduit to replace the esophagus (usually the stomach)

PATIENT MANAGEMENT Pain management
Prevent respiratory complications (most common) Monitoring for dysrhythmias (atrial) Monitoring for anastomotic leak Nutritional requirements **Surgery is performed in conjunction with chemotherapy and radiation therapy**

LIVER Dysfunctions Functions Produces bile to emulsify fats
Synthesizes proteins Stores Vitamin B Absorption of Vitamin K Produces coagulation factors Steatorrhea, malnutrition, decreased absorption of fat soluble vitamins Hypoalbuminemia, third spacing, ascites Peripheral nerve degeneration, nystagmus Coagulopathy Thrombocytopenia Liver is the largest organ in the body Approximately 1500 cc of blood enters the liver each minute, making the liver one of the most vascular organ Steatorrhea is the presence of excess fat in feces. Stool has oily appearance and is foul smelling

LIVER Functions Dysfunctions
Removes activated clotting factors from blood Conjugates bilirubin Detoxifies substances Elevated prothrombin time (PT) Jaundice, dark foamy urine, elevated bilirubin levels, pruritus Elevated estrogen, spider angiomas, gynecomastia, elevated ammonia, elevated ADH and aldosterone, palmar erythema, sodium and water retention, elevated cortisol Elevated estrogen also leads to testicular atrophy, impotence Elevated ADH and aldosterone leads to increased circulating blood volume, loss of potassium through kidney, increased ascites, edema Elevated cortisol leads to moon face The liver removes bilirubin (by product of breakdown of red blood cells), from the blood via urine and feces Liver gets rid of old red blood cells, detoxifies drugs, vitamins and hormones. Breaks down carbohydrates and stores glycogen Breaks down protein (forms urea from ammonia so it can be eliminated from blood)

HEPATIC FAILURE CLINICAL INDICATORS
Bilirubin concentrations >10mg/dL Serum albumin < 2.5 mg/dL Prothrombin time > 5 seconds beyond control Incapacitating hepatic encephalopathy Recurrent variceal bleeding Intractable ascites Recurrent spontaneous bacterial peritonitis

CAUSES OF HEPATIC FAILURE
Hepatitis A Oral-fecal route; self limiting Hepatitis B, C Contact with blood, body fluids, needles Cirrhosis Chronic Disease: diffuse damage of hepatocytes Laennec’s (alcoholic) Biliary Cardiac Postnecrotic (late result of acute hepatitis)

SIGNS AND SYMPTOMS OF HEPATITIS
Flulike symptoms Low grade fever Anorexia Jaundice Urticaria Dark urine Presence of antibodies May be asymptomatic

CLINICAL SIGNS AND SYMPTOMS OF HEPATIC FAILURE
Jaundice Urticaria Fever Nausea Abdominal discomfort Petechiae Anemia Can’t synthesize plasma proteins of the coagulation factors: easy bruising, petechiae, anemia

DIAGNOSIS OF HEPATIC FAILURE (END STAGE LIVER DISEASE)
Transaminases (AST and ALT) Direct and total bilirubin Protein and albumin levels Coagulation studies Ultrasound and CT scan Liver biopsy (gold standard) Can’t synthesize plasma proteins: Albumin and coagulation factors are proteins; they become deficient

COMPLICATIONS OF HEPATIC FAILURE
Portal hypertension (esophageal varices/ascites) Hepatic encephalopathy Hepatorenal Syndrome Hepatopulmonary Syndrome Hepatorenal: development of acute renal failure as a result of poor renal perfusion.

PORTAL HYPERTENSION

PORTAL HTN: ESOPHAGEAL VARICES
Causes increased pressure in esophageal veins The veins become fragile, distended and easily rupture Diagnose: esophagogastroduodenoscopy (EGD) Prevent rupture Beta blockers and nitrates Endoscopic variceal ligation (banding) Treatment of rupture Balloon tamponade Endoscopic banding Esophageal varices are dilated, engorged, tortuous veins usually seen in mid to distal esophagus Result from increased pressure in the portal veins (veins that drain the stomach and the small and large intestine) Blood can no longer pass through fibrotic liver and finds alternate pathways. Vasopressin can be used to reduce portal venous pressure. Can use vasopressin with nitrates Somatostatin inhibits the release of vasodilator hormones; Octreotide is the long acting anolog of somatostatin Besides banding sclerotherapy can also be used. Sclerotherapy is injecting a fibrosing agent into the bleeding vein

TIPS PROCEDURE (TRANSJUGULAR INTRAHEPATIC PORTOSYSTEMIC SHUNT)
Shunt is place between portal and hepatic vein through a catheter in a non-surgical procedure. Stent redirects some of the portal blood directly into the hepatic vein, thus decreasing portal pressure and decompression of varices Also have spleenorenal shunt , portacaval shunt, mesocaval shunt Greater risk of encephalopathy with blood being shunted around liver Watch for bleeding, infection, allergy to dye, new onset encephalopathy, puncture or surrounding areas

Has three ports: Gastric aspiration, gastric balloon, and esophageal balloon
There is also a Minnesota tube or Linton tube Used to stop acute bleeding Balloon is in the upper portion of the stomach and esophagus to place pressure on the bleeding veings Watch for aspiration of blood, occlusion of the airway, esophageal necrosis, and esophageal rupture Watch for signs of asphyxiation or aspiration. Suction mouth frequently If no breath sounds are heard, the tube slipped and is occluding the trachea. Cut across the tube and remove it.

EXAM QUESTION A patient with end stage liver failure, ascites, and bleeding esophageal varices is treated with a Sengstaken-Blakemore tube, a vasopressin infusion at 0.5 units/minute and normal saline at 150 mL/hour. The patient is agitated, restless, and appears cyanotic. The nurses’ priority is to: A. Call for the respiratory therapist to intubate B. Apply oxygen via non rebreather and get an ABG C. Cut the balloon lumens with scissors D. Being CPR and administer 1 mg intravenous epinephrine

Ascites: Free fluid within the peritoneal cavity
Ascites is due to inappropriate renal sodium and water retention, increased lymph production and increased capillary membrane permeability Liver can’t detoxify sex hormones, ammonia, mineralcorticoids (aldosterone), glucocorticoids (cortisol) and numerous drugs. Ascites is due to: low albumin level, portal hypertension which causes fluid to leak into peritoneal cavity, abnormal renal responses in cirrhosis which lead to more fluid retention.

ASCITES Inappropriate renal sodium and water retention, increased lymph production and increased capillary membrane permeability Sodium and fluid restriction K-sparing diuretics (Aldactone) Albumin Paracentesis Peritoneal-venous shunt

HEPATIC ENCEPHALOPATHY
Liver unable to convert ammonia to urea Ammonia crosses blood brain barrier Clinical presentation: Constructional apraxia Deterioration in handwriting Asterixis Flapping tremor of hands Fetor hepaticus Manage: lactulose and neomycin, moderate protein intake, eliminate hepatotoxins, liver transplantation Patients present with subtle mental status change such as mild confusion all the way to coma Asterixis is abnormal flapping of the hands Constructional apraxia: can’t build, assemble, or draw objects Lactulose and neomycin change the bacterial flora of the colon, thus decreasing the production of potentially toxic agents like ammonia that are absorbed into the blood stream. Goal of lactulose: three soft stools/day

OTHER Hepatorenal Syndrome: Renal failure unresponsive to fluid administration of diuretics; may need hemodialysis or CRRT Hepatopulmonary Syndrome: Deterioration of the pulmonary system with ESLD. See worsening hypoxemia requiring mechanical ventilation Fulminant hepatic failure (Acute Liver Failure): Sudden and severe impairment of hepatic function. Requires urgent liver transplant Causes include infection, toxins, drug,metabolic disorders Acute liver failure = most common cause is acetaminophen overdose Summary for liver failure: Check neuro status, give lactulose and neomycin to decrease ammonia levels, nutritional intervention – just watch increasing protein intake, check for bleeding, monitor fluid status, avoid toxins

EXAM QUESTION A 38 year old man is admitted to the ICU with a diagnosis of hepatic coma. She’s lethargic and responds only to painful stimuli. Which therapy would probably be used to lower her serum ammonia level? A. High protein diet, and increase fluid intake B. Administer lactulose and neomycin C. Administer opioid analgesics and sedatives D. Administer Lanoxin (Digoxin) and Furosemide (Lasix)

EXAM QUESTION A 38 year old man is admitted to the ICU with a diagnosis of hepatic coma. She’s lethargic and responds only to painful stimuli. Which therapy would probably be used to lower her serum ammonia level? A. High protein diet, and increase fluid intake B. Administer lactulose and neomycin C. Administer opioid analgesics and sedatives D. Administer Lanoxin (Digoxin) and Furosemide (Lasix) Neomycin kills bacteria in the intestine to diminish protein breakdown; lactulose eliminates protein from the GI tract. Appropriate therapy includes low protein diet and fluid restrictions.

EXAM QUESTION In a patient with cirrhosis and ascites who develops fever and generalized abdominal pain, the nurse needs to assess for additional evidence of: A. Acute appendicitis B. Spontaneous bacterial peritonitis C. Small bowel obstruction D. Acute pancreatitis

EXAM QUESTION In a patient with cirrhosis and ascites who develops fever and generalized abdominal pain, the nurse needs to assess for additional evidence of: A. Acute appendicitis B. Spontaneous bacterial peritonitis C. Small bowel obstruction D. Acute pancreatitis Spontaneous bacterial peritonitis is the infection of ascites fluid and is a common complication of decompensated cirrhosis. Acute appendicitis presents as a vague midline abdominal pain accompanied with nausea, vomiting, lack of appetite that slowly migrates to the right lower quadrant over 24 hours. A small bowel obstruction presents with nausea, vomiting, and severe cramping abdominal pain that comes in waves. Acute pancreatitis presents with severe upper abdominal pain, nausea, vomiting, and fever.

Abdominal Trauma Blunt vs Penetrating Diagnosis: FAST/ DPL/ CT Scans
Liver/ Spleen: Grading Operative vs Non Operative Management

ASSESSMENT OF ABDOMINAL TRAUMA
Cullen’s sign: purplish discoloration of umbilicus (blood in abdominal wall) Grey-Turner’s sign: ecchymosis of flank, groin (retroperitoneal bleeding or injury to pancreas) Kehr’s sign: referred pain to left shoulder (ruptured spleen) Hematoma in flank (renal injury, major vessel or pancreatic injury) Blunt; MVC, Falls, Assaults Penetrating: Knives/guns

EXAM QUESTION A patient was admitted after a motor vehicle accident, in which he was the driver and now complains of severe left shoulder pain when lying supine. There are bruises across the abdomen and chest from the seat belts. Vital signs are: BP 120/80, HR 112 bpm, RR 18 breaths/minute. The nurse is assessing the patient. Which of the following findings should the nurse interpret as an emergency situation? A. Abdominal distention with absent bowel sounds B. Epigastric pain with belching C. Decreased breath sounds bilaterally D. Pain and burning with hematuria

ABDOMINAL COMPARTMENT SYNDROME
Tissue edema of free fluid collects in abdominal cavity Causes of fluid include fluid resuscitation, multiple trauma, retroperitoneal/abdominal wall bleeding Intra-abdominal hypertension: A IAP> 12 mmHg without obvious organ failure Abdominal compartment syndrome: A IAP > 20 mmHg with at least one organ dysfunction or failure Treatment: Varies depending on evidence of organ dysfunction and result. Optimize fluid management Paracentesis Decompress GI tract(NG tube, enema, rectal tube Surgery

MALNUTRITION IN HOSPITALIZED PATIENTS
Malnutrition present in >50% of inpatients Can be due to abnormal intake, impaired digestion, malabsorption, or abnormal metabolism or excretion of a nutrient Nutrition assessment PPN/TPN if necessary

EXAM QUESTION Mr. J is at postoperative day 3 after popliteal bypass surgery. His protein intake was inadequate and nutritional consult was obtained. His prealbumin level was 7.4 g/dL and he had an albumin level of 1.6 g/dL. He has lost 10 pounds and demonstrates muscle weakness. Which of the following is the best assessment of this patient’s protein malnutrition? A. Muscle weakness B. Weight loss C. Albumin D. Prealbumin

EXAM QUESTION Mr. J is at postoperative day 3 after popliteal bypass surgery. His protein intake was inadequate and nutritional consult was obtained. His prealbumin level was 7.4 g/dL and he had an albumin level of 1.6 g/dL. He has lost 10 pounds and demonstrates muscle weakness. Which of the following is the best assessment of this patient’s protein malnutrition? A. Muscle weakness B. Weight loss C. Albumin D. Prealbumin Prealbumin levels have a shorter half life and so have been found to be a greater predictor of protein malnutrition and outcomes. Their half life is 2 days compared to 20 day half life of albumin. Weight loss and weakness are not specific

EXAM QUESTION When caring for a patient with acute pancreatitis, you should be alert for: A. Hypercalcemia B. Acute respiratory distress syndrome (ARDS) C. Pericarditis D. Diabetes insipidus

EXAM QUESTION When caring for a patient with acute pancreatitis, you should be alert for: A. Hypercalcemia B. Acute respiratory distress syndrome (ARDS) C. Pericarditis D. Diabetes insipidus ARDS occurs as a result of hypoperfusion and shock. Hypocalcemia and diabetes mellitus (not hypercalcemia and diabetes insipidus) occurs. Pericarditis is not associated with pancreatitis.

EXAM QUESTION A patient with hepatitis C is admitted to the Intensive Care Unit with shallow, labored respirations and severe ascites. Choose the intervention that best relieves respiratory distress caused by ascites: A. Nasopharyngeal suction B. Placing the patient in a supine position C. Administering diuretics and maintaining sodium restriction D. Maintaining a low protein and fat restricted diet

EXAM QUESTION A patient with hepatitis C is admitted to the Intensive Care Unit with shallow, labored respirations and severe ascites. Choose the intervention that best relieves respiratory distress caused by ascites: A. Nasopharyngeal suction B. Placing the patient in a supine position C. Administering diuretics and maintaining sodium restriction D. Maintaining a low protein and fat restricted diet A low protein and fat-restricted diet is appropriate for hepatic failure, but does not affect ascites.

EXAM QUESTION A patient involved in a farm accident that resulted in blunt trauma to the chest and abdomen delayed coming to the hospital for 24 hours until he began experiencing acute abdominal pain. On examination, the nurse notes periumbilical ecchymosis. This may represent: A. Diaphragmatic injury B. Retroperitoneal hemorrhage C. Gastric injury D. Intestinal perforation

EXAM QUESTION A patient involved in a farm accident that resulted in blunt trauma to the chest and abdomen delayed coming to the hospital for 24 hours until he began experiencing acute abdominal pain. On examination, the nurse notes periumbilical ecchymosis. This may represent: A. Diaphragmatic injury B. Retroperitoneal hemorrhage C. Gastric injury D. Intestinal perforation Cullen’s sign is an indication of retroperitoneal bleeding and may be accompanied by ecchymosis and swelling in the flank areas (Grey-Turner’s sign) if bleeding is renal. Cullen’s sign is seen with necrotic pancreatitis, but can also occur from blunt abdominal trauma. It is not seen immediately after the trauma, but usually within a few hours up to 24 – 48 hours after.

EXAM QUESTION A 96 year old man with a history of long-standing esophageal reflux is admitted to the surgical ICU post esophagogastrectomy. His vital signs are: T 99.F BP 146/76 P 122 bpm Incisional pain 8/10 Which of the following interventions would be key to reducing this patient’s risk of mortality and morbidity? A. Pulmonary care B. Pain management C. Administration of large amounts of IV fluids D. Immediate institution of tube feedings

CCRN/PCCN Certification Review Gastrointestinal

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