Focus on Upper Gastrointestinal Problems

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1 Focus on Upper Gastrointestinal Problems Chapter 42, Nursing Management: Upper Gastrointestinal Problems Revised for Voice Thread Nursing 246 Gastroesophageal Reflux Disease GERD (a syndrome if with tissue damage) Reflux of gastric secretions into esophagus. Predisposing conditions: Results in: - irritation pyrosis (heartburn) - inflammation - esophogitis, - difficulty swallowing dysphagia GERD Etiology and Pathophysiology Fig

2 GERD-Diagnosis Barium swallow Upper GI Esophageal endoscopy X-Ray Contrast and Nuclear Medicine Studies Barium Swallow UGI Series Barium Swallow Outlines the esophagus Contrast is INGESTED Barium Gastrografin (water soluble contrast) 2

desired patient will also ingest some carbonated

3 Upper GI Series Esophagus, stomach, duodenum Also uses barium sulfate milkshake If air contrast is desired patient will also ingest some carbonated powder Exam usually 30 Longer if waits to see small bowel 3

4 4

Patient Education (GERD) Lifestyle changes time of meals, clothing, smoking Dietary changes fat, alcohol, spices, chocolate, caffeine Medications- antacids (maalox, tums), H2 blockers (Tagamet,

5 Patient Education (GERD) Lifestyle changes time of meals, clothing, smoking Dietary changes fat, alcohol, spices, chocolate, caffeine Medications- antacids (maalox, tums), H2 blockers (Tagamet, Pepcid), proton pump inhibitors (Protonix, Nexium), prokinetic meds (metaclopromide) Hiatal Hernia bulging upwards of a portion of stomach through diaphragmatic opening Acid from stomach spills into esophagus 5

Procedure: fundoplication Can be preformed via

6 Surgical Therapy (Hiatal Hernia) Objective is to reduce reflux by enhancing integrity of LES LES = Procedure: fundoplication Can be preformed via laparoscope Prevents reflux in 90% of patients. Relapse common 6

Peptic Ulcer Disease Ulceration occurs mostly in: Antrum (lesser curvature) Duodenum Mucosal Defensive System is impaired MUCUS BICARBONATE SUFFICIENT BLOOD FLOW PROSTAGLANDINS More Physiology of PUD

7 Peptic Ulcer Disease Ulceration occurs mostly in: Antrum (lesser curvature) Duodenum Mucosal Defensive System is impaired MUCUS BICARBONATE SUFFICIENT BLOOD FLOW PROSTAGLANDINS More Physiology of PUD Ulcer will not form in absence of acid Rarely gastric acid alone causes There must be something else disrupting the mucosa H. pylori Inadequate blood flow Smoking NSAIDs H. pylori is a gram-negative, microoerophilic, spiral bacillus originally cultured in 1982 from gastric biopsy specimens in patients with documented gastritis. 7

8 Dr. Marshall's stomach biopsy taken 8 days after he drank a culture of H. pylori Even shallow ulcers can erode near a blood vessel and cause an acute upper GI hemorrhage 8

9 Duodenal ulcer of the posterior wall penetrating into the head of the pancreas resulting in walled-off perforation. H. Pylori Helicobacter pylori bacterium Promotes peptic ulcer formation Treatment: triple therapy More Physiology of PUD Ulcer will not form in absence of acid BUT rarely gastric acid alone causes There must be something else disrupting the mucosa H. pylori Inadequate blood flow Smoking NSAIDs 9

Stress Ulcers Erosive gastritis caused by transient GI ischemia (low blood supply) - shock, burns, surgery imbalance of acid and mucus barrier Prevention: prophylactic meds: Antacids, H2

10 Stress Ulcers Erosive gastritis caused by transient GI ischemia (low blood supply) - shock, burns, surgery imbalance of acid and mucus barrier Prevention: prophylactic meds: Antacids, H2 blockers, PPIs How to Treat For Specific Causes of PUD H. pylori Antibiotics and acid suppression NSAIDS Avoid If must use Cytotec (Misoprostel) Replaces endogenous prostaglandins PPI 10

Systemic Acid Blockers Histamine 2 Take any time of day with no food restrictions Usually twice daily Zantac, Tagamet, Pepcid = IV and PO Tagamet = oldest one and lots of drug interactions not for

11 Systemic Acid Blockers Histamine 2 Take any time of day with no food restrictions Usually twice daily Zantac, Tagamet, Pepcid = IV and PO Tagamet = oldest one and lots of drug interactions not for elderly Axid = PO only Proton Pump Inhibitors Take in AM before breakfast (30 ) Usually once a day Prilosec, Prevacid, Protonix, Aciphex Nexium + Protonix= PO, IV form Prilosec not indicated for those on Coumadin Complications of Chronic Ulcer Disease Hemorrhage more common with duodenal ulcers Perforation most lethal complication (PERITONITIS) Gastric outlet obstruction-scaring scaring and atrophy of pylorus. 11

Surgical Interventions (Cancer or Ulcer Disease) Procedures: gastrectomy: billroth I or II Partial or total resection of stomach vagotomy: cutting vagus nerve to decrease gastric acid secretion

12 Surgical Interventions (Cancer or Ulcer Disease) Procedures: gastrectomy: billroth I or II Partial or total resection of stomach vagotomy: cutting vagus nerve to decrease gastric acid secretion pyloroplasty: pyloric dilatation For ulcer disease, all are rarely performed now Question(s) What is it the vagus nerves does to the stomach? Hint: Vagal stimulation occurs with the sight and smell of food 12

Total gastrectomy for stomach cancer (total gastrectomy with esophagojejunostomy) Nursing interventions Post-Op Care If NG tube present, maintain patency *do not reinsert if it comes out!

13 Total gastrectomy for stomach cancer (total gastrectomy with esophagojejunostomy) Nursing interventions Post-Op Care If NG tube present, maintain patency *do not reinsert if it comes out!! LOCATION LOCATION LOCATION! Patient may have abdominal incision(s) AND chest tube(s) Teaching about dietary needs is ongoing throughout post-op op time Continues to discharge Peptic Ulcer Disease Surgical Therapy for PUD Postoperative care NG Tube Aspirate observed for Color Bright red at first with darkening within first 24 hours Color changes yellow-green within 36 to 48 hours Amount Odor 13

14 Peptic Ulcer Disease Surgical Therapy for PUD Postoperative care (cont d) NG suction must be in working order and patency maintained Observe for signs of peristalsis and lower abdominal discomfort Intestinal obstruction Peptic Ulcer Disease Surgical Therapy for PUD Postop care (cont d) Accurate I/O essential Vital signs every 4 hours Frequent position changes IV therapy Observe for signs of infection Long-term complication pernicious pernicious anemia Dumping Syndrome Cause is reduced gastric capacity Symptoms occur min. after a meal, feelings of weakness, sweating, palpitations, dizziness Due to large bolus of hypertonic fluid entering intestine and fluid is drawn into the bowel, causes distention of bowel. Advise patient to lie down, it will pass. 14

15 Dietary Measures 6 small feedings per day Avoid fluids with meals minutes before or after Avoid concentrated sweets High protein diet and include some fat with each meal Nutritional Interventions Eliminate drinking fluids with meals Dry foods with low carbohydrate content (avoid high sugar diet) Rest after meals Focus on Nausea and Vomiting Chapter 42, Nursing Management: Upper Gastrointestinal Problems revised 15

16 Nausea and Vomiting Most common manifestations of GI diseases Nausea and Vomiting Etiology and Pathophysiology Occurs from GI disorders Pregnancy Infectious diseases CNS disorders Cardiovascular problems Metabolic disorders Side effects of drugs Psychologic factors Nausea and Vomiting Etiology and Pathophysiology Vomiting also can occur when the GI tract becomes irritated, excited, or distended Vomiting can be a protective mechanism 16

17 Nausea and Vomiting Clinical Manifestations Nausea Subjective complaint Usually accompanied by anorexia Vomiting Dehydration can rapidly occur when prolonged Water and essential electrolytes are lost Nausea and Vomiting Clinical Manifestations Metabolic alkalosis from loss of gastric HCl Metabolic acidosis from loss of bicarbonate if the contents from the small intestine are vomited Nausea and Vomiting Collaborative Care Fecal odor and bile indicates a lower obstruction Color of emesis aids in determining presence and source, if bleeding Time of day occurring 17

18 Nausea and Vomiting Collaborative Care Nondrug therapy Acupuncture Acupressure Botanicals Ginger Peppermint oil Breathing exercises Nausea and Vomiting Collaborative Care Nutritional therapy IV fluids to replace fluid and electrolytes, glucose NG tube suction to decompress stomach Nausea and Vomiting Collaborative Care Nutritional therapy (cont d) Clear liquids started first 5 to 15 ml fluid every 15 to 20 minutes No extremely hot/cold liquids Room-temp carbonated beverages without carbonation okay Warm tea May advance to dry toast, crackers 18

19 Nausea and Vomiting Collaborative Care Use Gatorade, broth with caution because of Advance to high carbohydrates, low fat next since easier to digest Baked potato, plain gelatin, cereal with milk Eat slowly and in small amounts Nausea and Vomiting Collaborative Care Nutritional therapy (cont d) Fluids between meals instead of with meals to avoid overdistention Dietitian may be helpful with appropriate food with adequate nutritional value Nursing Management Nursing Diagnoses Nausea Deficient fluid volume Imbalanced nutrition: Less than body requirements 19

20 Nursing Management Gerontologic Considerations More likely to have cardiac or renal insufficiency Increased risk for life-threatening fluid/electrolyte imbalances Increased susceptibility to CNS side effects of antiemetic drugs Nursing Management Gerontologic Considerations Caution with fluid replacement in patients with HF Alteration in LOC greater risk for aspiration Anti-Emetics Prokinetic Serotonin Receptor Agonists Dopamine Antagonists Glucocorticoids Cannabinoids Benzodiazepines Motion Sickness Drugs 20

21 Key Points AntiEmetics It s s easier to prevent nausea than treat it! Give prophylactically! Most cause sedation Special precaution during pregnancy Thalidomide tragedy 1957 to 1962 in UK, Canada, Germany, Japan - not FDA approved prevented morning sickness 12,000 babies who survived, with phocomelia (flipper-like arms or legs) Prokinetic Drug - Reglan AKA Metoclopramide Dopamine and serotonin receptor blocker BUT also increases UPPER GI motility Used for post-op op Nausea/Vomiting Limitation = sedation Good for diabetic gastroparesis Since has serotonin effects see next slides regarding extrapyramidal side effects 21

22 Serotonin Receptor Agonists Basically these three EXPENSIVE Drugs Zofran Kytril Anzemet Used for: CINV Chemotherapy Induced N/V Helps with induction of anesthesia Dopamine Antagonists also famous for Extrapyramidal Phenothiazines Phenergan (prochlorperazine) Compazine Thorazine Butyrophenones Haldol (haloperidol) Inapsine (droperidol) Extrapyramidal Reactions Repetitive Movements Oral-buccal buccal-lingual lingual (Tardive Dyskinesia) Limb, neck, and trunk (Parkinsonian-like) Can occur within the 1 st few days or not for weeks Or appear months and years after use Also associated with the antipsychotics 22

ANOTHER OF MODERN MEDICINE S HORROR STORIES: TARDIVE

com/report IV Phenergan Induced Promethazine IV, IM Can be

tissue IV use has the highest risk of severe tissue damage Use

23 ANOTHER OF MODERN MEDICINE S HORROR STORIES: TARDIVE DYSKINESIA IV Phenergan Induced Promethazine IV, IM Can be highly caustic to the lining of blood vessels and surrounding tissue IV use has the highest risk of severe tissue damage Use at lower doses (6.25 to 12.5 mg) Are really just as effective Dilute with 10 ml Normal Saline 23

24 Glucocorticoids SoluMedrol Decadron Useful to prevent post-op op nausea and vomiting Given prior to induction of anesthesia Cannabinoids Marinol Can cause subjective effects similar to those caused by smoking marijuana However Slow onset Did not generate much street interest 24

Benzodiazepines Ativan Is really the only one useful for N/V More Specific for Motion Sickness Scopolamine patch Apply evening before surgery or 4 hours before the end of surgery Antihistamines

25 Benzodiazepines Ativan Is really the only one useful for N/V More Specific for Motion Sickness Scopolamine patch Apply evening before surgery or 4 hours before the end of surgery Antihistamines Dramamine Antivert All can cause the triad of: blurred, dry, urinary /constipation the patch should be kept in place for 24 hours following surgery at which time it should be removed and discarded. 25

Mortality rate 6% to 10% for past 40 years Increased

26 Emesis Basins Most Important Not To Be Without 150,000 to 200,000 hospital admissions each year for UGI bleeding Mortality rate 6% to 10% for past 40 years Increased incidence of UGI bleeding in older adults, especially women, and use of NSAIDs 26

27 Etiology and Pathophysiology Types of UGI bleeding Obvious bleeding Hematemesis Bloody vomitus» Appears fresh, bright red blood or coffee grounds Melena Black, tarry stools» Caused by digestion of blood in GI tract» Black appearance iron Etiology and Pathophysiology Types of UGI bleeding (cont d) Occult bleeding Small amounts of blood in gastric secretions, vomitus, or stools Undetectable by appearance Detectable by guaiac test Etiology and Pathophysiology Bleeding from arterial source profuse bright red The bright red color = blood has not been in contact with the stomach s s acid secretions 27

28 Etiology and Pathophysiology Coffee ground vomitus reveals that the blood has been in the stomach for some time and has been changed by gastric secretions Melena: Slow bleeding from an upper GI source Etiology and Pathophysiology Longer the passage of blood through intestines, the darker the stool color due to breakdown of Hb release of iron Cause of bleeding is not always easy Variety of areas in GI tract may be involved Common Causes of UGI Bleeding Esophageal origin Stomach and duodenal origin Drug-induced origin Systemic disease origin 28

Common Causes of Bleeding Esophageal Origin Chronic esophagitis GERD Mucosa-irritating drugs Alcohol Cigarettes Common Causes of Bleeding Esophageal Origin Mallory-Weiss tear Tear in mucosa near

29 Common Causes of Bleeding Esophageal Origin Chronic esophagitis GERD Mucosa-irritating drugs Alcohol Cigarettes Common Causes of Bleeding Esophageal Origin Mallory-Weiss tear Tear in mucosa near esophagogastric junction Related to severe retching/vomiting Linear and longitudinal tears in the esophagus at the EG junction Are believed to be the consequence of severe retching... Mallory Weiss tear at the Gastroesophageal Junction GEJ Are encountered most commonly in alcoholics, attributed to episodes of excessive vomiting and reflux of gastric contents in the setting of an alcoholic stupor... 29

30 Common Causes of Bleeding Esophageal Origin Esophageal varices Usually occurs secondary to cirrhosis of liver due to high pressure secondary to portal hypertension Anything that increases pressure (, ) or causes irritation ( ) may cause massive bleeding 30

31 Common Causes of Bleeding Stomach and Duodenal Origin Gastric cancer Steady blood loss as it grows and ulcerates Hemorrhagic gastritis Peptic ulcer disease Bleeding ulcers account for 50% of UGI bleeding cases Related to H. pylori or drug use (NSAIDs) Common Causes of Bleeding Stomach and Duodenal Origin Polyps Stress-related related mucosal disease 31

32 Peptic Ulcers Fig Common Causes of Bleeding Drug-Induced Origin OTC or prescribed drugs: Major cause of UGI bleeding Irritate and disrupt gastric mucosal barrier Aspirin Excedrin Alka-Seltzer NSAIDs Ibuprofen Corticosteroids Careful history of all commonly used drugs required Emergency Assessment & Management 80% to 85% of patients who have massive hemorrhage spontaneously stop bleeding Cause still must be identified and treatment initiated 32

33 Emergency Assessment & Management Immediate physical examination with emphasis on BP Rate and character of pulse Peripheral perfusion with capillary refill Observation of neck vein distention Emergency Assessment & Management VS every 15 to 30 minutes Signs and symptoms of shock evaluated Abdominal exam Tense, rigid abdomen may indicate perforation and peritonitis Emergency Assessment & Management Once immediate interventions have started Complete history of events leading to bleeding episode Previous bleeding episodes Weight loss Received blood transfusion Other illnesses (liver disease, cirrhosis) Medication use Religious preferences regarding blood or blood product usage 33

34 Emergency Assessment & Management Laboratory studies Emergency Assessment & Management Laboratory tests (cont d) Liver enzymes ABGs Type/cross-match for possible blood transfusions Emergency Assessment & Management Other laboratory studies Vomitus/stools Tested for the presence of gross and occult blood Urinalysis Specific gravity: Indication of the patient s hydration status 34

35 Emergency Assessment & Management Fluid replacement IV lines Should be established for fluid and blood replacement Preferably two IVs 16 or 18 gauge Generally best to begin with an isotonic crystalloid solution (lactated Ringer s solution) Emergency Assessment & Management Blood replacement Whole blood, packed RBCs and fresh frozen plasma Used for replacement of lost volume in massive hemorrhage Packed RBC are preferred over whole blood because of fluid overload and immune reactions Emergency Assessment & Management Blood replacement (cont d) Hb and Hct provide baseline for further treatment Initial Hct may be normal and not reflect loss until 4 to 6 hours after fluid replacement Initially loss of plasma and RBC is equal 35

36 Emergency Assessment & Management Use of supplemental oxygen may help increase blood oxygen saturation Indwelling urinary catheter Accurate urine volume assessment Central venous pressure line to monitor patient s s fluid volume status Diagnostic Studies Endoscopy Primary tool for diagnosing source of bleeding Before performing May need to lavage for clearer view NG or orogastric tube placed and room- temperature water or saline used Never advance orogastric tube against resistance!! Aspiration of stomach contents through a large-bore tube (Ewald tube) to remove clots Diagnostic Studies Angiography Used to diagnose only when endoscopy cannot be done Invasive procedure May not be appropriate for high-risk or unstable patient 36

Collaborative Care Endoscopic hemostasis therapy Goal: To coagulate or thrombose bleeding artery Useful for gastritis, Mallory-Weiss tear, esophageal and gastric varices, bleeding peptic ulcers, and

37 Collaborative Care Endoscopic hemostasis therapy Goal: To coagulate or thrombose bleeding artery Useful for gastritis, Mallory-Weiss tear, esophageal and gastric varices, bleeding peptic ulcers, and polyps Collaborative Care Several techniques are used including Thermal (heat) probe Electrocoagulation probe Argon plasma coagulation (APC) Neodymium yttrium-aluminum aluminum-garnet (Nd-YAG) laser common and very effective treatment but its effect is transient 37

38 Clip intact, without bleeding Collaborative Care Surgical therapy Indicated when bleeding continues Regardless of therapy provided Site of bleeding identified 38

39 Collaborative Care Surgical therapy (cont d) Site of hemorrhage determines choice of operation Surgeon must consider age of patient Collaborative Care Drug therapy During acute phase used to Bleeding HCl acid secretion Neutralize HCl acid that is present Collaborative Care Drug therapy (cont d) Injection therapy during endoscopy for acute hemostasis Bleeding due to ulceration Epinephrine 39

40 Collaborative Care Drug therapy (cont d) IV or intraarterial vasopressin (Pitressin) For variceal bleeding Somatostatin analog octreotide (Sandostatin) Used with upper GI bleeding Collaborative Care Drug therapy (cont d) Acid reducers Acidic environment can alter platelet function and clot stabilization Histamine-2 2 receptor blockers (H 2 R) PPIs Antacids Neutralize HCl acid Maintains gastric ph above 5.5 Nursing Management Signs/symptoms of shock Low BP Rapid, weak pulse Increased thirst Cold, clammy skin Restlessness 40

41 Peptic Ulcer Disease Surgical Therapy for PUD Preoperative care Laparoscopic or open surgery techniques Surgeon should educate family/patient on surgical procedure Nurse can clarify questions Peptic Ulcer Disease Surgical Therapy for PUD Preoperative care (cont d) Instructions should be given on Comfort measures Pain relief Coughing and deep breathing NG tube IV fluids Peptic Ulcer Disease Surgical Therapy for PUD Postoperative care Similar to postop care after abdominal laparotomy NG tube used to decompress and decrease pressure on suture line 41

42 Peptic Ulcer Disease Surgical Therapy for PUD Postoperative care (cont d) Aspirate observed for Color Bright red at first with darkening within first 24 hours Color changes yellow-green within 36 to 48 hours Amount Odor NG suction must be in working order and patency maintained Peptic Ulcer Disease Surgical Therapy for PUD Postoperative care (cont d) Observe for signs of peristalsis and lower abdominal discomfort Intestinal obstruction Peptic Ulcer Disease Surgical Therapy for PUD Postop care (cont d) Accurate I/O essential Vital signs every 4 hours Frequent position changes IV therapy Observe for signs of infection Long-term complication pernicious pernicious anemia 42

43 QUESTION(s) Your patient has been admitted with acute UGI bleeding She weighs 320 pounds A foley has been placed in the ER What would be the minimum hourly urine output you would expect to indicate adequate renal perfusion? 43

KK College of Nursing Peptic Ulcer Badil D ass Dass, Lecturer 25th July, 2011

KK College of Nursing Peptic Ulcer Badil Dass, Lecturer 25 th July, 2011 Objectives: By the end of this lecture, the students t will be able to: Define peptic pp ulcer Describe the etiology and pathology