Disorders of Lower GIT system Ppt (3).ppt
- 1. Management of patient with gastrointestinal disorders Learning objectives At the end of the session you will able to describe disorders; features ;diagnosis and management of: Gastrointestinal reflex disease Gastritis Pelvic inflammatory disease Intestinal obstruction Liver cirrhosis Hemorrhoids 1
- 2. Gastrointestinal (GI) Tract The GI tract is basically a hollow tube that takes food from your mouth, down your throat (esophagus), into your stomach, and on to the intestines. Along the way, your body extracts nutrients from the food and turns them into the fuel you need to walk, talk, think, read, play, and everything else you do. After that, the GI tract takes what’s left over and moves it down to your rectum where it eventually leaves your body as feces. 2
- 3. Gastro-esophageal Reflux Disease (GERD) GERD is not a disease Is a syndrome produced by conditions that result in reflux (back-flow) of gastric or duodenal secretions in to the esophagus. Gastroesophageal reflux is the involuntary movement of gastric contents to the esophagus Gastroesophageal reflux is a normal physiological process that occurs several times a day without symptoms or damage of the esophageal mucosa in most otherwise healthy individuals. Gastroesophageal reflux disease (GERD) is a condition in which reflux of gastric contents into the esophagus produces frequent or severe symptoms that negatively affect the individual’s quality of life or result in damage to esophagus, pharynx, or the respiratory tract. 3
- 4. 4 Fig Gastro esophageal reflex diseases
- 5. GERD--Predisposing conditions Incompetent LES Conditions resulting in gastric contents near the GEJ Bending down Hiatal hernia Decreased gastric emptying Certain drugs that interfere LES function gastric pressure Dietary habits Fatty foods Chocolate Caffeinated Carbonated beverages Ingestion of alcohol Tobacco smoking Pyloric stenosis 5
- 6. Complications Esophagitis, Esophageal strictures, Barrett’s esophagus Esophageal irritation and inflammation Corrosion to the esophagus Scar tissue formation and decreased dispensability of secondary to inflammation and irritation Aspiration 6
- 7. Clinical manifestations Pyrosis Dyspepsia (indigestion) Regurgitation Dysphagia Odynophagia Hypersalivation Esophagitis 7
- 8. Diagnosis Barium swallow-determine if there is protrusion of the gastric cardia Esophagoscopy- determine the incompetence of the LES and the extent of inflammation, potential scarring, and strictures Biopsy and cytologic analysis pH monitoring Motility (manometry) studies Bilirubin monitoring 8
- 9. Common suggestions to help alleviate the symptoms of esophageal reflux: Avoid foods that increase gastric acidity. Avoid foods that decrease lower esophageal sphincter pressure. Avoid foods that affect peristalsis. Avoid foods that slow gastric emptying. Avoid large meals. Avoid smoking. Avoid lying down after meals. Elevate the head of the bed. 9
- 10. Management A. Patient education Low-fat diet To avoid caffeine, tobacco, beer, milk, foods containing peppermint or spearmint, and carbonated beverages which increase gastric secretion Eating or drinking 2 hours before bedtime To maintain normal body weight To avoid tight-fitting clothes To elevate the head of the bed on 15- to 20-cm blocks 10
- 11. GERD-- Mgt Cont’d… B. Drugs Antacids- 1 to 2 hrs after meals and at bed time Histamine receptor blockers Proton pump inhibitors like omeprazole Cholinergics (e.g. bethanechol) Metoclopramide 11
- 12. Gastritis 12
- 13. Gastritis Definition Is an inflammation of the gastric or stomach mucosa Is the result of a breakdown in the normal gastric barrier (mucosa), which normally protects the stomach tissue from auto-digestion by acid Types 1. Acute Gastritis 2. Chronic Gastritis In gastritis, the gastric mucous membrane becomes edematous and hyperemic (congested with fluid and blood) and undergoes Superficial erosion . It secretes a scanty amount of gastric juice, containing very little acid but much mucus. Superficial ulceration may occur and can lead to hemorrhage. 13
- 14. Type A Chronic gastritis Referred autoimmune gastritis and occurs in the fund us (body of stomach). Diagnosed by Endoscopy, Upper gastrointestinal (GI) x-ray examination, and Gastric aspirate analysis. Type A gastritis is often asymptomatic. Patients usually do not secrete enough intrinsic factor from their stomach cells and have difficulty absorbing vitamin B12, 14
- 15. Type B chronic gastritis Type B chronic gastritis affects the ant rum and pylorus (lower end of the stomach near the duodenum) and is associated with helicobacter pylori bacterial infection. Is the most common type of chronic gastritis. Signs and symptoms Poor appetite, Heartburn after eating, Belching, a sour taste in the mouth, and nausea and vomiting. Diagnosed by Endoscopy, Upper gastrointestinal x-ray examination, and Gastric aspirate analysis. H. pylori infection is treated with antibiotics. 15
- 16. Etiology-- Chronic Gastritis Repeated episodes of acute gastritis Benign or malignant ulcers of the stomach Bacteria helicobacter pylori Autoimmune diseases such as pernicious anemia Dietary factors such as caffeine Use of medications, like NSAIDs Chronic alcohol abuse Smoking Reflux of intestinal contents into the stomach 16
- 17. Etiology --Acute Gastritis Drugs: Steroidal & NSAIDs Alcohol Radiation Helicobacter pylori Staphylococcus organisms Bile and pancreatic secretions Physiology stress: shock, sepsis, burns Psychologic stress Spicy, irritating foods Ingestion of strong acid or alkali Trauma: naso-gastric suction, large hiatal hernia, endoscopic techniques 17
- 18. PP Chronic Inflammation chronic alterations in the protective mucosal barrier Progressive gastric atrophy Eventual death of chief and parietal cells Decreased number of acid-secreting parietal cells 18 Hypochlorhydria Or Achlorhydria
- 19. Clinical Manifestation Acute gastritis Anorexia, nausea and vomiting, hiccupping, Epigastric tenderness Feeling of fullness and abdominal discomfort Hemorrhage associated with alcohol abuse Headache, lassitude Usually self-limited lasting from a few hours to a few days 19
- 20. C/Ms Cont’d… Chronic gastritis S/S are similar to that of acute gastritis Anemia because of atrophy of cells producing intrinsic factor 20
- 21. Diagnosis Endoscopic examination with biopsy Complete blood count (CBC) Stool exam for occult blood Serologic test for H. pylori 21
- 22. Management The gastric mucosa is capable of repairing itself after a bout of gastritis, in about 1 day Acute Gastritis Bed rest Refraining from alcohol and food until symptoms subside Parentral fluid—if symptoms persist Neutralization Antiacids like aluminum hydroxide -- if caused by ingestion of strong acids Diluted lemon juice or diluted vinegar --if caused by strong alkali 22
- 23. Mgt Acute Gastritis Cont’d… Antiemetis for nausea and vomiting Antiacids H2 antagonists Blood transfusion and fluid replacement if gastritis is hemorrhage 23
- 24. Mgt: Chronic Gastritis Dietary & lifestyles modification Reducing stress Promoting rest Initiating pharmacotherapy Antibiotics -- to treat H. pylori Proton pump inhibitor Bismuth salts Regular injections of VitB12—for patients with pernicious anemia 24
- 25. Emphysematous gastritis Is a rare disease related to infection of the gastric wall. It is caused by gas-forming pathogens including enterobacter species, clostridium perfringens and others. Clinically present with symptoms similar to acute abdomen Alcoholism was identified as a risk factor Diabetes mellitus, ulcerative colitis and use of nonsteroidal anti-inflammatory agents were found to be associated with EG 25
- 26. 26
- 27. Peptic Ulcer Disease Gastric andDuodenal Ulcers 27
- 28. Definition PUD is an excavation (hollowed-out area) that forms in the mucosal wall of the stomach, in the pylorus, duodenum, or in the esophagus Results from the digestive action of HCl & pepsin More common in people b/n 40 & 60 years Incidence Is relatively uncommon in women of childbearing age Is almost equal to that in men after menopause Can occur without excessive acid secretion Ulcers are defined as breaks in the mucosal surface >5 mm in size, with depth to the submucosa 28
- 29. Damage of gastric mucosa from irritants 29
- 30. Types of PUD Depending on the degree of mucosal involvement i. Acute PUD Associated with superficial erosion and minimal inflammation ii. Chronic PUD Is of long duration, eroding through the muscular wall with the formation of fibrous tissue Present continuously for many months or intermittently throughout the person’s lifetime Is at least four times as common as acute erosion Depending on the location of erosion a. Gastric ulcer (GU) b. Duodenal ulcer (DU) 30
- 32. Cause Infection with H. pylori Excessive secretion of HCl in the stomach because of: Psychological stress (e.g., anxiety) and physiological stress (like in case of burn, shock, surgery) Ingestion of milk and caffeinated beverages Ingestion of hot, rough, or spicy foods Alcohol Smoking 32
- 33. Cause Cont’d… Ulcerogenic drugs Tumors, like in case of Zollinger-Ellison syndrome (ZES)– produce excessive amounts of the hormone gastrin GERD- resulting esophageal ulcer Familial tendency-genetic link– those with blood type O Pregnancy appears to protect women from the developing ulcers 33
- 34. Pathophysiology 34 Acids, bile salts, aspirin, ischemia, H. pylori Breakdown of gastric mucosal barrier Acid back-diffusion into mucosa Destruction of mucosal cells Acid & Pepsin release Further mucosal erosion Destruction of B/Vs Bleeding Histamine release from damaged mucosa Vasodilation Capillary permeability Loss of plasma proteins into gastric lumen Mucosal edema ULCERATION
- 35. Clinical Manifestations Symptoms may last for a few days, weeks, or months and may disappear only to reappear, often without an identifiable cause 35
- 36. C/Ms Cont’d… Sharply localized tenderness Around the epigastrium or Slightly to the right of the midline Pyrosis (heartburn) Emesis often containing undigested food eaten many hours earlier Bleeding– melana (tarry stools) Epigastric tenderness Abdominal distention 36
- 37. C/Ms Cont’d… Pain of duodenal ulcer origin Burning” or “cramping” Often located in the mid- epigastrium region beneath the xyphoid process Back pain Usually relieved by eating Pain of gastric ulcer origin Located high in the epigastrium Occurs about 1 to 2 hours after meals Can be burning” or “gaseous” 37 Dull, gnawing pain or a burning sensation in the mid- epigastrium or in the back
- 38. Emergency Complications 3 major emergency complications 1. Hemorrhage 2. Perforation 3. Gastric outlet obstruction 38
- 39. Complications Cont’d… 1. Hemorrhage Is the most common observed Cause Erosion of the ulcer through a major blood vessels 39
- 40. Complications Cont’d… 2. Perforation The 2nd most common complication Commonly seen in large penetrating DUs Occurs with ulcer penetrating the serosal surface, with spillage of either gastric or duodenal contents in to the peritoneal cavity S/S Sudden, severe upper abdominal pain that quickly spread throughout the abdomen Shallow and rapid respiration Usually absent bowel sounds Nausea and vomiting 40
- 41. Complications Cont’d… 3. Gastric outlet obstruction Is the least common ulcer-related complication Cause Inflammation and edema in the peripyloric region S/s Long history of ulcer pain Pain Short duration or completely absent More generalized upper abdominal discomfort that becomes worse towards the end of the day as the fills and dilates May be relieved by belching or by self-induced vomiting 41
- 42. Complications Cont’d… S/s of Gastric outlet obstruction Vomiting- which is very common and often projectile Constipation- as result of dehydration Swelling in the upper abdomen as a result of dilation of stomach Loud peristalsis may be heard 42
- 43. Duodenal vs Gastric Ulcers 43 Duodenal Ulcer Gastric Ulcer Lesion Superficial; smooth margins; round, oval, or cone shaped Penetrating Incidence Age 30–60 Male: female 2–3:1 80% of peptic ulcers Usually 50 and over Male: female 1:1 15% of peptic ulcers Risk Factors H. pylori, alcohol, smoking, stress H. pylori, gastritis, alcohol, smoking, use of NSAIDs, stress
- 44. GUs Vs DUs Cont’d… 44 Signs, Symptoms, and Clinical Findings Hypersecretion of HCl May have weight gain Pain occurs 2-3 hrs after a meal Often awakened b/n 1-2 AM Ingestion of food relieves pain Vomiting is uncommon Hemorrhage less likely Melena more common than hematemesis More likely to perforate Normal—hyposecretion of HCl Weight loss may occur Pain 1⁄2 -1 hr after a meal Rarely occurs at night May be relieved by vomiting Ingestion of food does not help Vomiting common Hemorrhage more likely Hematemesis more common than melena Malignancy Possibility Rare Occasionally Duodenal Ulcer Gastric Ulcer
- 45. Diagnosis Fiberoptic endoscopy To visualize inflammatory changes, ulcers, and lesions To obtain a biopsy of the gastric mucosa Upper GI barium-contrast study Gastric secretory studies CBC – determine anemia secondary to bleeding Liver enzyme studies Stool tests – for the presence of blood Serologic test for antibodies to the H. pylori 45
- 46. Management Aim of the treatment 1.To decrease the amount of gastric acidity 2.To enhance mucosal defense mechanisms 3.To minimize the harmful effects on the mucosa 46
- 47. Mgt Cont’d… Conservative management/minimum medical treatments Adequate rest Dietary interventions Medications Elimination of smoking Long-term follow-up care 47
- 48. Mgt Cont’d… Lifestyle modifications Adequate physical and emotional rest A quite, calm environment Elimination of stress Moderate in daily activity 48
- 49. Mgt Cont’d… Nutritional Management Avoiding irritant foods and beverages Hot, spicy foods and pepper Alcohol Carbonated beverages Tea and coffee Foods high in roughage, such as raw fruits, salads, and vegetables may irritate an inflamed mucosa Proteins Best neutralizing food Stimulates HCl secretion Carbohydrates and fats The least to stimulate HCl secretion Don’t neutralize well 49
- 50. Nutritional Mgt Cont’d… Milk Milk proteins and calcium are stimulant to gastric acid production Can neutralize gastric acidity Contains prostaglandins and growth factors which protect the GI mucosa from injury NB i. No specific diet seems totally appropriate in the treatment of ulcer disease ii. Each patient should be instructed to eat and drink foods and fluids that do not cause and distressing or harmful side effects 50
- 51. Mgt Cont’d… Pharmacologic Therapy 1. Neutralizing agents – Antiacids Are the initial drugs of choice Decrease gastric acidity and the acid content of chyme reaching the duodenum Block the conversion of pepesinogen to pepsin by raising the pH to above 3.5 Some (like Al(OH)3) can bind to bile salts and decrease their effects on the gastric mucosa Examples: Aluminum hydroxide and magnesium trisilcates 51
- 52. Pharmacologic Mgt Cont’d… II. Antisecretory a. Histamine H2-receptor antagonists Inhibit the action of histamine at histamine H2 receptor cells to reduce the secretion of gastric acid and total pepsin output Ex: cimetidine, famotidine, nizatidine, ranitidine b. Proton pump inhibitors (H+, K+-ATPase inhibitors) Inhibit the H+, K+-ATPase enzyme system Block the last step of acid production Ex: Omeprazole, Lansoprazole, Rabeprazole 52
- 53. Pharmacologic Mgt Cont’d… III. Cytoprotective Sucralfate Accelerate healing Doesn’t have acid neutralizing effect Should be given at least 30 minutes before or after an antiacid Misoprostol Is a synthetic prostaglandin Protects the gastric mucosa s mucus production and bicarbonate levels Bismuth subsalicylate Suppresses H. pylori bacteria 53
- 54. Pharmacologic Mgt Cont’d… IV. Antibiotics for H. pylori Tetracycline + proton pump inhibitor + bismuth salts Amoxicillin + clarithromycin + proton pump inhibitor Metronidazole + clarithromycin + proton pump inhibitor Clarithromycin + proton pump inhibitor + amoxicillin 54
- 55. PUD Rx-- DACA-Ethiopia I. PUD only First Line Ranitidine 150 mg P.O. BID OR 300 mg at bedtime for 4-6 weeks Maintenance therapy: 150 mg at bedtime. Alternatives Cimetidine 400 mg P.O. BID, with breakfast and at night, OR 800 mg at night for 4 - 6 weeks OR Famotidine, 40 mg, P.O. at night for 4-6 weeks OR Omeprazole 20 mg P.O. QD for 4 weeks (DU) or 8 weeks (GU) 55
- 56. Pharmacologic Mgt Cont’d… II. PUD associated with H. pylori First Line Amoxicillin, 1g, P.O. BID PLUS Clarithromycin, 500mg P.O. BID PLUS Omeprazole, 20mg P.O. BID (OR 40mg QD) All for 7 - 14 days Alternative Amoxicillin, 1g, P.O. BID PLUS Metronidazole, 500mg, P.O. BID PLUS Omeprazole, 20mg P.O. BID OR 40mg QD for 7-14 days 56
- 57. Mgt Cont’d… Surgical Management Usually recommended for: Patients with intractable ulcers Those that fail to heal after 12 to 16 weeks of medical treatment Life-threatening hemorrhage, perforation, or obstruction Those with ZES not responding to medications Types 1. Pyloroplasty- the pylorus, is cut and resutured, to relax the muscle and widen the opening into the intestine. 2. Vagotomy 57
- 58. Mgt Cont’d… 3. Antrectomy- surgical removal, of antrum which is the lower third of the stomach Antrum produces gastrin, which is a hormone that stimulates the production of stomach acid Removal of the lower portion of the antrum of the stomach as well as a small portion of the duodenum and pylorus. The remaining segment is anastomosed to the duodenum- Gastroduodenostomy (Billroth I) or to the jejunum-Gastrojejunostomy (Billroth II) 58
- 59. 59
- 61. Appendicitis 61
- 62. Introduction The Appendix A small, finger-like appendage about 10 cm (4 inch) long Attached to the cecum just below the ileocecal valve Fills with food and empties regularly into the cecum Because it empties inefficiently and its lumen is small, the appendix is prone to obstruction and is particularly vulnerable to infection organ may have an immunoprotective function and acts as a lymphoid organ, especially in the younger person. Other theories contend that the appendix acts as a storage vessel for "good" colonic bacteria. 62
- 63. Definition Appendicitis- is an inflammation of the vermiform appendix Etiology Obstruction of the lumen by: A fecalith (accumulated feces) Foreign bodies Worms (e.g., Pinworms, ascaris) Intramural thickening caused by lymphoid hyperplasia Tumors of the cecum or appendix 63
- 64. PP Obstruction Distension Venous engorgement Accumulation of mucus and bacteria (pus) Gangrene Perforation 64
- 65. Clinical classification A. Simple (non-perforated): ◦ Inflamed appendix, ◦ Absence of gangrene, perforation, or abscess around the appendix; B Complex (gangrenous or perforated) inflammation perforated or gangrenous appendicitis or the presence of periappendicular abscess 65
- 66. Catarrhal appendicitis: Acute appendicitis characterized by distension of the appendix and vascular congestion Phlegmonous appendicitis: If catarrhal appendicitis progresses causes appendiceal edema and vascular congestion become pronounced with the formation of multiple abscesses in the wall and purulent fluid on the serosal surface. Gangrenous appendicitis. Causes local circulatory dysfunction, infarction opposite to the junction between the mesoappendix and appendix, where the blood supply is inadequate. The appendix becomes congested dark red with black necrotic areas 66
- 67. Clinical Manifestations Vague epigastric or per umbilical pain Progressing to RLQ May be accompanied by: A low-grade fever: A temperature of ≥38oC is not common and may be present when perforation has occurred Nausea and vomiting: Vomiting before onset of pain – this can occur in patients with retrocecal appendices, inflammation of the appendix can cause irritation of the duodenum causing vomiting and nausea before pain occurs in the RLQ Diarrhoea –often the stools are soft, of small volume and frequent rather than watery in true diarrhoea Loss of appetite Local tenderness is elicited at McBurney’s point when pressure is applied 67
- 68. If perforation has already occurred present with: Generalised abdominal pain High heart rate Temperature over 38oC 68
- 69. 69
- 70. McBurney’s point and test of Rovsing’s sign 70
- 71. C/Ms Cont’d… a. Blumberg’s sign: is positive (the pain elicited by steadily increasing pressure at the site of tenderness increases on abrupt release of the pressure) ---Rebound tenderness : b. Rovsing’s sign Elicited by palpating the LLQ; this paradoxically causes pain to be felt in the RLQ c. Positive Psoas Sign Feeling pain in the RLQ while applying resistance to the right knee as the patient tries to lift the right thigh while lying down d. Dunphy's sign -increased abdominal pain with coughing 71
- 72. Appendicitis-- Psoas Sign Cont’d… 72
- 73. C/Ms Cont’d… d. Positive Obturator Sign Flex the patient’s right thigh at the hip, with the knee bent, and rotate the leg internally at the hip This maneuver stretches the internal obturator muscle Positive obturator sign Suggests irritation of the obturator muscle by an inflamed appendix If the appendix has ruptured The pain becomes more diffuse Abdominal distention develops The patient’s condition worsens 73
- 74. C/Ms Obturator Sign Cont’d… 74
- 75. C/Ms Cont’d… The extent of tenderness depends on the location of the inflamed appendix Pain on defecation suggests that the tip of the appendix is resting against the rectum. Pain in urination suggest that the tip is near to the bladder If tip is in the pelvis can be elicited only on rectal examination. 75
- 76. Acute Complications a. Perforation The most common and generally occurs 24 hours after the onset of pain b. Peritonitis c. Postoperative abscesses, hematomas, and wound complications 76
- 77. Diagnosis History Complete physical examination Lab tests CBC—ed WBCs (neutrophils >75%) Serum electrolyte profile Abdominal x-ray films, ultrasound studies, and CT scans 77
- 78. Management The gold-standard treatment for acute appendicitis is to perform an appendectomy. Laparoscopic appendectomy is preferred over the open approach. Most uncomplicated appendectomies are performed laparoscopic ally. In cases where there is an abscess or advanced infection, the open approach may be needed. The laparoscopic approach affords less pain, quicker recovery, and the ability to explore most of the abdomen through small incisions Appendectomy 78
- 79. Antibiotics and intravenous fluids To correct or prevent fluid and electrolyte imbalance and dehydration, until surgery is performed Used for 6 to 8 hrs before the appendectomy If the appendix has ruptured and there is evidence of peritonitis or an abscess Analgesics after diagnosis 79
- 80. 80
- 81. Nursing Management Patient preparation for surgery IV infusion to replace fluid loss and promote adequate renal function Antibiotic therapy to prevent infection Enema is not administered Avoid self-treatment like the use of laxatives and enema to prevent perforation Cold compress to the RLQ to decrease blood flow to the area and impend the inflammatory process Heat is never used because it may cause the appendix to rupture 81
- 82. Nsg Mgt Cont’d… Postoperative care Placing the patient in a semi-Fowler position: This position relaxes the abdominal muscles and reduces pain. Opioid, usually morphine sulfate Oral fluids as tolerated Food is provided as desired and tolerated on the day of surgery Ambulation begins the day of surgery or the first postoperative day Discharge on the first or second postoperative day Normal activities are resumed 2 to 3 weeks after surgery 82
- 83. 83
- 84. Differential Diagnosis Crohn ileitis, Mesenteric adenitis, Ruptured ovarian cyst, Ectopic pregnancy, Tubal-ovarian abscess, Musculoskeletal disorders, Endometriosis, Pelvic inflammatory disease, Gastroenteritis, Renal colic, kidney stones, irritable bowel disease, testicular torsion, ovarian torsion, round ligament syndrome, epididymitis, and other nondescript gastroenterological issues. 84
- 85. A Sample case scenarios A 24-year-old female who presented to the emergency department with a four-hour history of right lower quadrant (RLQ) abdominal pain. The pain originated in the umbilical region, radiating diffusely across the lower abdomen and subsequently localized to the RLQ. The pain was of sudden onset, sharp and colicky with progressing intensity. Over the counter, analgesic was taken before presenting to E, which did not alleviate the pain. The pain was exacerbated by lifting the right leg and relieved by leaning forwards. The case most likely? 85
- 86. Peritonitis Peritoneum is: Double-layered, semipermeable sac Lines the abdominal cavity and covers some of the abdominal organs Peritoneal organs: 1.Liver 2.Stomach 3.Gallbladder 4.Spleen 5.Jejunum, ileum 6.Transverse and sigmoid colon 7.Cecum 8.Appendix 86
- 87. Definition Is an inflammation of the peritoneum Causes The most common causative organisms: Escherichia coli Klebsiella Proteus Pseudomonas Others organisims: Streptococci spp Staphylococci Pneumococci 87
- 88. Cause Peritonitis Cont’d… It can result from Diseases of the GI tract From the internal reproductive organs (females) External sources Injury or trauma (e.g. gunshot wound, stab wound) Extension from the inflammation of retroperitoneal organs like the kidneys Appendicitis Perforated ulcer Diverticulitis Bowel perforation Abdominal surgical procedures and peritoneal dialysis 88
- 89. It may be localized or generalized, and is thought to pass through three phases: 1. Firstly, a phase of rapid removal of contaminants from the peritoneal cavity into the systemic circulation; 2. Secondly, a phase of synergistic interactions between aerobes and anaerobes; and 3. Thirdly, an attempt by host defenses to localize infection. The two main types of peritonitis are: Primary spontaneous peritonitis, an infection that develops in the peritoneum; and Secondary peritonitis, which usually develops when an injury or infection in the abdominal cavity allows infectious organisms into the peritoneum. Both types of peritonitis are life-threatening. 89
- 90. Clinical Manifestations Symptoms depend on the location and extent of the inflammation S/S include: Pain At first diffuse type Tends to become constant, localized, and more intense near the site of the inflammation. Usually aggravated by movement 90
- 91. C/Ms Cont’d… The affected area of the abdomen becomes extremely tender and distended, and the muscles become rigid Ascites is found but virtually always predates infection Rebound tenderness Nausea and vomiting Peristalsis is diminished Increased temperature and pulse rate Almost always an elevated leukocyte count 91
- 92. Diagnosis Lab tests Increased leukocyte count ed Hemoglobin and hematocrit blood loss Serum electrolyte studies Abdominal x-ray- air or fluid level CT scan of the abdomen- abscess Peritoneal aspiration and culture 92
- 93. Complications 1. Sepsis-- the major cause of death 2. Shock bcs of septicemia or hypovolemia 3. Intestinal obstruction with bowel adhesion as a result of the inflammatory process 4. Wound dehiscence and abscess formation S/S Tender or painful abdomen Feeling as if something just gave way 93
- 94. Management Administration of several liters of an isotonic solution Analgesics Antiemetics Intestinal intubation and suction Oxygen therapy by nasal cannula or mask 94
- 95. Mgt Cont’d… Large doses of IV broad-spectrum antibiotic until the specific organism causing the infection is identified Third-generation cephalosporins Cefotaxime (2 g q8h, IV) Ceftriaxone (2 g q24h IV) Patients with primary bacterial peritonitis (PBP) usually respond within 72 hours to appropriate antibiotic therapy Administered for as little as 5 days and can be extended to 2 weeks course 95
- 96. Mgt Cont’d… Surgery To remove the infected material and correct the cause Includes: Excision (i.e., appendix) Resection with or without anastomosis (i.e., intestine) Repair (i.e. perforation) Drainage (i.e. abscess) 96
- 97. Case study A 42 year-old male presented to wollega university referral Hospital for evaluation of worsening abdominal pain, nausea and vomiting starting 3 days prior to presentation. On admission, he denied any constipation, or associated hematemesis, fevers, chills or urinary symptoms. On examination he was febrile, with a heart rate of 120 beats/min, blood pressure 135/78 mmHg and respiratory rate of 22/min. Abdominal examination revealed mild distension with generalized guarding and marked rebound tenderness in the epigastrium. There were no palpable masses and bowel sounds were absent. The case most likely? 97
- 99. Intestinal Obstruction A partial or complete blockage of the bowel that prevents the normal flow of intestinal contents through the intestinal tract. Two types: Mechanical obstruction Functional obstruction 99
- 100. Types of Intestinal Obstruction Cont’d… A. Mechanical Obstruction Mechanical (dynamic) obstruction there is a physical obstruction of the bowel lumen associated with increased peristalsis in an attempt to overcome the blockage Cause: Intra-luminal obstruction or Obstruction from pressure on the intestinal walls Accounts for 90% of intestinal obstructions Examples: 1. Adhesions (50%) Loops of intestine become adherent to areas that heal slowly or scar after abdominal surgery May produce a kinking of an intestinal loop 100
- 101. Types of Intestinal Obstruction Cont’d… 2. Hernias (15%) Protrusion of intestine through a weakened area in the abdominal muscle or wall May result in complete obstruction of intestinal lumen and obstruction of blood flow to the area 3. Intussusception One part of the intestine slips into another part located below it Results in narrowing of intestinal lumen 101
- 102. Hernia (inguinal) Intussusception Types of Intestinal Obstruction Cont’d… 102
- 103. Types of Intestinal Obstruction Cont’d… 4. Volvulus Bowel twists and turns on itself Results in obstruction to intestinal lumen and accumulation of gas and fluid in the trapped bowel 5. Others include: Neoplasms (15%) Stenosis Strictures Abscesses 103
- 104. Volvulus of the sigmoid colon Types of Intestinal Obstruction Cont’d… 104
- 105. Types of Intestinal Obstruction Cont’d… B. Functional Obstruction Intestinal musculature cannot propel the contents along the bowel as result of neuromuscular or vascular disorders In adynamic obstruction there is reduced or absent peristalsis due to a disturbance of the neuromuscular transmission of the parasympathetic innervation to the bowel. Examples: Paralytic/adynamic ilues (the most common) Amyloidosis Muscular dystrophy Endocrine disorders such as diabetes mellitus Neurologic disorders such as Parkinson's disease 105
- 106. Causes of Nonmechanical Obstruction • Abdominal surgery and trauma • Pneumonia • Spinal injuries • Hypokalemia • Myocardial infarction • Peritonitis 106
- 107. Small Intestine Obstruction Accumulate of fluid, gas & intestinal contents proximal to the obstruction Abdominal distention and retention of fluid Reduced absorption of fluids and stimulation of more gastric secretions Increased fluid in the lumen Increased intraluminal pressure Increased capillary permeability 107 Circulating blood Hypovolemic Shock Edema, congestion, necrosis Perforation of the intestinal wall Peritonitis Fluid and electrolyte extravasation to the peritoneal cavity
- 108. Clinical Manifestations The cardinal features of obstruction are abdominal pain, vomiting, distension and absolute constipation Crampy pain that is wavelike and colicky Severe, steady pain strangulation((signs of which may include tachycardia, tenderness, fever and leucocytosis) In the absence of strangulation, the abdomen is not tender Passing blood & mucus, with no fecal matter & no flatus Unmistakable signs of dehydration Abdominal distension Nausea and vomiting 108
- 109. C/Ms Cont’d… Vomiting Bilious rapid projectile vomiting obstruction located high in the small bowel Vomiting of fecal material Obstruction below the proximal colon or in the ileum Progression of the vomiting Vomiting the Stomach contents Then the bile-stained contents of the duodenum & the jejunum Finally, with each paroxysm of pain, the darker, fecal-like contents of the ileum 109
- 110. Diagnosis History and physical examination Abdominal x-ray studies CT-scan Ultrasound Biopsy Laboratory studies CBC ed WBCs Strangulation or perforation ed hemoglobin or hematocrit Bleeding from neoplasm or strangulation with necrosis Serum electrolyte profile 110
- 111. Management Medical Management Conservative management ‘drip and suck’, which is the foundation of conservative management Decompression of the bowel through a naso-gastric or small bowel Surgical intervention A commonly quoted surgical aphorism is: "never let the sun rise”. IV therapy before surgery to replace the depleted water, sodium, chloride, and potassium Include: Repairing the hernia Dividing the adhesion Removing the portion of affected bowel and anastomosis 111
- 112. Large Bowel Obstruction Attributes to15% of intestinal obstructions Commonly occur in the sigmoid colon The most common causes: Carcinoma Diverticulitis Impaction of feces Benign tumors 112
- 113. Clinical Manifestations Unlike small intestine symptoms develop and progress relatively slowly Obstruction in the sigmoid colon or the rectum Constipation in patients Distention of the abdomen Visible outlining of loops of large bowel through the abdominal wall Crampy lower abdominal pain Fecal vomiting Symptoms of shock may occur 113
- 114. Diagnosis History and physical examination Abdominal x-ray studies CT-scan Ultrasound Biopsy Laboratory studies CBC Serum electrolyte profile Barium enema To locate large intestinal obstruction Not used if perforation is suspected 114
- 115. Management Colonoscopy Inspection of the interior surface of the colon To untwist and decompress the bowel. Cecostomy To make a surgical opening into the cecum for patients Who are poor surgical risks In need of urgent relief from the obstruction Temporary or permanent colostomy Ileoanal anastomosis To remove the entire large colon Rectal tube To decompress an area that is lower in the bowel 115
- 116. Case study A 59-year-old woman with a medical history of cerebral palsy due to birth hypoxia, was brought to the hospital by her husband , with a 3- day history of complete constipation and feculent vomiting. She had no other medical or surgical history. On examination, her abdomen was distended and mildly tender in the right iliac fossa, but there was no guarding. Observations revealed sinus tachycardia at a rate of 115 bpm, blood pressure 139/102 mm/Hg, respiratory rate 18 bpm, temperature 37.1°C and saturation 98% on room air. 116
- 117. 117 Abdominal hernia
- 118. Abdominal hernia A protrusion of a biological tissue, structure, or part of an organ through the muscular tissue or the biological membrane Causes Condition that increases the pressure of the abdominal cavity Obesity Heavy lifting Coughing Straining Fluid in abdominal cavity 118
- 119. Types of hernias Inguinal hernia Most common hernias (up to 75%). For more understanding of inguinal hernias, much insight is needed in the anatomy of the inguinal canal. Inguinal hernias divided into: Indirect inguinal hernia Direct inguinal hernia 119
- 120. Types of hernias cont’d… Indirect inguinal hernia Affects only men. A loop of intestine passes down the canal from where a testis descends early in childhood into the scrotum. Increase progressively in size causing the scrotum to expand grossly. Direct inguinal hernia: Affects both sexes. The intestinal loop forms a swelling in the inner part of the fold of the groin. 120
- 121. 121
- 122. Types of hernias cont’d… Femoral hernia: Affects both sexes, although most often women. An intestinal loop passes down the canal containing the major blood vessels to and from the leg. Umbilical hernia Umbilical hernias are especially common in infants They involve protrusion of intra abdominal contents through a weakness at the site of passage of the Umbilical cord. These hernias often resolve spontaneously. 122
- 123. Types of hernias cont’d… Incisional hernia Occurs when the defect is the result of an incompletely healed surgical wound. These can be the most frustrating and difficult to treat, as the repair utilizes already attenuated tissue. Clinical manifestations Pain and swelling 123
- 124. Hernia cont’d… Complications Inflammation Bowel obstruction Strangulation Management Repairing the weak abdomen part of abdominal wall. 124
- 125. 125 Diseases of the Anorectum
- 126. Diseases of the Ano-rectum Patients seek medical care primarily because of Pain Rectal bleeding Change in bowel habits Protrusion of hemorrhoids Anal discharge Perianal itching and swelling Anal tenderness, stenosis, or ulceration 126
- 127. Anorectal Abscess Is undrained collection of perianal pus Caused by obstruction of an anal gland More prevalent in Immuno-compromised patients or Clients with inflammatory bowel disease (IBD) May occur in and around the rectum The most common causes are Escherichia coli Staphylococci Streptococci Many of these abscesses result in fistulas 127
- 128. Clinical Manifestations Superficial abscess Local pain and swelling Redness Foul-smelling drainage Tenderness Deeper abscess Lower abdominal pain Elevated temperature 128
- 129. Treatment Palliative therapy consisting of sitz baths and analgesics Incising and draining the abscess Packing the wound with gauze impregnated with petroleum jell The packing should be changed every day Moist, hot compress application to the area Avoiding soiling the dressing during urination or defecation Patient education regarding wound care, sitz baths, thorough cleaning after bowel movement, and follow up visit 129
- 130. Anal Fistula Is a tiny, tubular, fibrous tract/tunnel leading out from the anus or rectum extending to: The outside of the skin Vagina Buttocks Usually precedes an anorectal abscess 130
- 131. Causes Inflammation/infection Trauma Fissures Clinical Manifestations Leakage of stool or pus, blood stained drainage constantly from the cutaneous opening Passage of flatus or feces from the vagina or bladder, depending on the fistula tract Systemic infection in untreated fistulas 131
- 132. Management Wearing pad to prevent staining of cloth Fistulectomy An excision of the entire fistulous tract Packing the wound with gauze 132
- 133. Anal Fissure Is a longitudinal tear or ulceration in the lining of the anal canal Cause Passing a large, firm stool Persistent tightening of the anal canal because of stress & anxiety constipation Childbirth Trauma 133
- 134. Clinical Manifestations Extremely painful defecation Burning Bleeding Constipation as result fear of pain 134
- 135. Management Usually heals if treated by conservative measures Stool softeners and bulk agents An increase in water intake Sitz baths Emollient suppositories Suppository combined of an anesthetic with a corticosteroid Anal dilation under anesthesia Surgery, if fissures do not respond to conservative treatment 135
- 136. Hemorrhoids Hemorrhoidal vein: are veins draining the walls of the anal canal and rectum Hemorrhoids are varicose veins in the anal canal. They are caused by an increase in pressure in the veins, often from increased intra-abdominal pressure. Hemorrhoids are dilated portions of veins in the anal canal and are very common conditions Types i. Internal hemorrhoids Those above the internal sphincter ii. External hemorrhoids Appear outside the external sphincter Occur at the anal opening and may hang outside the anus By the age of 50, about 50% of people have hemorrhoids to some extent 136
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- 140. Cause/Risk Factors ed pressure in the hemorrhoidal tissue due to: Pregnancy or giving birth Strain during bowel movements Holding back or waiting a long time before having a bowel movement Lifting heavy weights Sitting for a long time on toilet Overweight Coughing or sneezing a lot Sitting or standing for a long time Having liver disease like cirrhosis 140
- 141. Clinical Manifestations Common reasons for seeking health care: Bleeding Protrusion Anal itching Anal ache or pain, especially while sitting Pain during bowel movements 141
- 142. C/Ms Cont’d… External hemorrhoids are associated with severe pain Internal hemorrhoids are not usually painful until they bleed or prolapse Bright red blood on toilet tissue, stool, or in the toilet bowl One or more hard tender lumps near the anus 142
- 143. Diagnosis History Physical examination Inspection of the perianal region Careful digital examination Anoscopy 143
- 144. Staging The Staging of Hemorrhoids Stage Description of Classification I Enlargement with bleeding II Protrusion with spontaneous reduction III Protrusion requiring manual reduction IV Irreducible protrusion 144
- 145. Management Relieving hemorrhoidal symptoms and discomfort Good personal hygiene Avoiding excessive straining during defecation High-residue diet that contains fruit and bran Increased fluid intake to soften stool Application of ice packs for a few hours, followed by warm compresses Sitz baths Analgesic ointments and suppositories, 145
- 146. Mgt Cont’d… Bed rest T-binder to hold dressing in place Bismuth subgallate, insert one suppository in the rectum bid, or use topical application, bid for five days Hemorrhoidectomy 146
- 147. Management of Patients with Hepatic Disorders 147
- 148. Hepatic Dysfunction Hepatic dysfunction results from damage to the liver’s parenchymal cells by: Directly from primary liver diseases Indirectly from obstruction of bile flow or derangements of hepatic circulation 148
- 149. The most common and significant symptoms of liver disease 1. Jaundice 2. Portal hypertension, ascites, and varices 3. Nutritional deficiencies 4. Hepatic encephalopathy or coma 149
- 150. Jaundice/Icterus Is yellowish-tinged or greenish-yellow discoloration of the body tissues, including the sclerae, mucosa and the skin as result of abnormal elevation of bilirubin concentration in the blood. Is a symptom rather than a disease Becomes clinically evident when the serum bilirubin level exceeds 2.5 mg/dL May result from impairment of: Hepatic uptake Conjugation of bilirubin Excretion of bilirubin into the biliary system 150
- 151. Types of Jaundice 1. Hemolytic 2. Hepatocellular 3. Obstructive 151
- 152. I. Hemolytic/ Prehepatic Jaundice Results from an increased destruction of the red blood cells Flood the plasma with unconjugated bilirubin so rapidly Causes Hemolytic transfusion reactions Sickle cell crisis Hemolytic anemia 152
- 154. Hemolytic Jaundice Cont’d… If prolonged it may result in: The formation of pigment stones in the gallbladder Extremely severe jaundice (>20 to 25 mg/dl) poses a risk for brain stem damage Lab Tests ed fecal and urine urobilinogen Urine is free of bilirubin 154
- 155. II. Hepatocellular/ hepatic Jaundice Caused by the inability of damaged liver cells to: Take up bilirubin from the blood or Conjugate or Excrete normal amount of bilirubin from the blood Cirrhosis Patients may be mildly or severely ill 155
- 156. Hepato-cellular Jaundice Cont’d… Causes of cellular damage Infection by viral hepatitis or other viruses Medication or chemical toxicity or alcohol Hepatic carcinoma Lab Tests: ed unconjugated serum bilirubin ed ALT (Alanine aminotransferase) edAST (aspartate aminotransferase 156
- 157. III. Obstructive / Posthepatic Jaundice Is due to impended or obstructed flow of bile A. Intrahepatic obstruction May involve obstruction of the small bile ducts within the liver Can be caused by Pressure on these channels from inflammatory swelling of the liver Inflammatory exudate within the ducts themselves 157
- 158. Obstructive Jaundice Cont’d… B. Extra-hepatic obstruction Caused by occlusion of the bile duct by a gallstone, an inflammatory process, a tumor, or pressure from an enlarged organ 158
- 159. Obstructive Jaundice Cont’d… Clinical Findings Bile backed up into the liver substance Reabsorbed into the blood Carried throughout the entire body Staining the skin, mucous membranes, and sclera Deep orange and foamy urine Light or clay-colored stool The skin may itch intensely Intolerance to fatty foods 159
- 160. Obstructive Jaundice Cont’d… Lab tests: AST, ALT levels generally rise only moderately, ed conjugated and unconjugated bilirubin ed urine bilirubin ed to no fecal or urinary urobilinogen 160
- 161. Hepatic Cirrhosis Characterized by irreversible chronic injury of the hepatic parenchyma Extensive degeneration and destruction of the liver parenchyma cells and by replacement of liver tissue by fibrous scar tissue. 161
- 162. Types of cirrhosis or scarring of the liver: A. Alcoholic cirrhosis Frequently due to chronic alcoholism for decades, resulting in: Chronic inflammatory Toxic effects on the liver Blocking the normal metabolism of protein, fats, and carbohydrates Scar tissue characteristically surrounds the portal areas Is the most common type of cirrhosis 162
- 163. Types of Cirrhosis Cont’d… B. Postnecrotic cirrhosis There are broad bands of scar tissue as a late result of a previous bout of acute viral hepatitis (hepatitis B or hepatitis C) C. Biliary cirrhosis Scarring occurs in the liver around the bile ducts Is the result of chronic biliary obstruction and infection (cholangitis) Much less common 163
- 164. Clinical manifestation Early manifestation Palpation of liver reveals a firm, lumpy, (nodular), usually enlarged liver. GI disturbance – anorexia, nausea, vomiting… Hepatomegally Pain Late manifestation Ascites, gastro intestinal bleeding from varices Encephalopathy, splenomegally, jaundice, skin lesion, Anemia Sodium and fluid retention 164
- 165. Diagnosis History Physical Exam Diagnostic Studies Liver scans/biopsy- Detects fatty infiltrates, fibrosis, destruction of hepatic tissues, tumors Esophagogastroduodenoscopy (EGD)- demonstrate presence of esophageal varices Electrolytes: Hypokalemia Urine urobilinogen: May/may not be present. Fecal urobilinogen: Decreased. 165
- 166. Dx Increased Serum bilirubin Increased Serum ammonia: because of inability to convert ammonia to urea. Decreased Serum glucose: impaired glycogenesis Decreased Serum albumin CBC: Hb/Hct and RBCs may be decreased because of bleeding Increased BUN: indicates breakdown of blood/protein Increased Liver enzymes 166
- 167. Medical Management Symptomatic management Antacids—to decrease gastric distress and minimize the possibility of GI bleeding. Vitamins and nutritional supplements Potassium-sparing diuretics (spironolactone, triamterene)-- to decrease ascites Avoidance of alcohol 167
- 168. Hepatic Encephalopathy and Coma Hepatic encephalopathy Is a life-threatening complication of liver disease occurring with profound liver failure May result from the accumulation of ammonia and other toxic metabolites in the blood Can occur in any condition in which liver damage causes ammonia to enter the systemic circulation without liver detoxification Hepatic coma represents the most advanced stage of hepatic encephalopathy 168
- 169. Hepatic Encephalopathy cont’d… Normally, the liver converts ammonia in to glutamine, which is stored in the liver and later converted to urea and excreted via the kidneys. Blood ammonia rises when the liver cells are unable to perform this conversion due to liver cell damage and necrosis. C/m From mild mental confusion like, unresponsiveness, forgetfulness, trouble concentrating, or changes in sleep habits to deep coma. Simple tasks, such as handwriting, become difficult 169
- 170. Hepatic Encephalopathy cont’d… Asterixis or “liver flap”. The patient is asked to hold the arm out with the hand held upward (dorsiflexed). Within a few seconds, the hand falls forward involuntarily and then quickly returns to the dorsiflexed position. Dx Lab-results show elevated blood ammonia 170
- 171. Hepatic Encephalopathy cont’d… Medical Management Principles of intervention in hepatic encephalopathy. Reduce protein in the intestine Prevent gastro-intestinal bleeding. Reduce bacterial production of NH3 by neomycin High cleansing enema to decrease bacteria. Eliminate infection. Intravenous administration of glucose to minimize protein breakdown 171
- 172. Cholelithiasis It is the presence/formation of calculi in the gallbladder Usually form in the gallbladder from the solid constituents of bile: Cholesterol Bile salts Bilirubin Calcium Protein They vary greatly in size, shape, and composition 172
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- 174. Types: there are two major types A. Cholesterol stones Predominantly composed of cholesterol Is insoluble in water Its solubility depends on bile acids and lecithin (phospholipids) in bile B. Pigment stones Primarily composed of pigment When unconjugated pigments in the bile precipitate to form stone Account for about one third of cases in the US Cannot be dissolved and must be removed surgically 174
- 175. Risk factors Long –term parenteral nutrition, which results in decrease gal bladder motility. Cirrhosis of the liver. Chronic hemolytic disorders, which result in increased bile pigments Obesity 175
- 176. Clinical Manifestations Gallstones may be silent Pain, tenderness, and rigidity of the upper right abdomen that may radiate to the midsternal area or right shoulder Pain and biliary colic Bleeding tendency as a result of vitamin deficiency Changes in urine and stool color Very dark color urine The urine become foamy when shaken Clay-colored feces Jaundice 176
- 177. Management Nutritional and supportive therapy Rest, intravenous fluids, nasogastric suction, analgesia, and antibiotic agents Low-fat foods High protein and carbohydrates Cooked fruits, rice, lean meats, mashed potatoes, bread, coffee, or tea may be taken Remind the patient that fatty foods may bring on an episode 177
- 178. Mgt Cont’d… Pharmacologic therapy Drugs to dissolve Ursodeoxycholic acid (UDCA) Chenodeoxycholic acid (chenodiol or CDCA) 178
- 179. Mgt Cont’d… Non-surgical managements Dissolving gallstones by infusion of a solvent Lithotripsy- uses repeated shock waves directed at the gallstones in the gallbladder Surgical interventions Cholecystostomy-The gallbladder is surgically opened, the stones and the bile or the purulent drainage are removed Cholecystectomy- The gallbladder is removed through an abdominal incision (usually right sub costal) after the cystic duct and artery are ligated Choledochostomy- involves an incision into the common duct, usually for removal of stones 179
- 180. ` Thanks for your time &attention
- 181. Quiz 10% 1. What is asterix and explain its pathiophysiological mechanism(5%) 2. Discuss type of jaundice (5%) 181
Editor's Notes
- #116: Colostomy: a surgical procedure where a portion of the large intestine is brought through the abdominal wall to carry stool out of the body Colonoscopy: inspection of the interior surface of the colon with a flexible endoscope that is equipped to obtain tissue samples and inserted through the rectum Colectomy: surgical removal of the large bowel