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Approach To Abdominal Pain Dr. Nahla A Azzam MRCP,FACP Assistant Professor &Consultant Gastroenterology.

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Presentation on theme: "Approach To Abdominal Pain Dr. Nahla A Azzam MRCP,FACP Assistant Professor &Consultant Gastroenterology."— Presentation transcript:

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2 Approach To Abdominal Pain Dr. Nahla A Azzam MRCP,FACP Assistant Professor &Consultant Gastroenterology

3 One of the most common causes for OP & ER visits Multiple abd and non-abd pathologies can cause abd pain, therefore an organized approach is essential Some pathologies require immediate attention Abdominal pain

4 Introduction Abdominal pain is an unpleasant experience commonly associated with tissue injury. The sensation of pain represents an interplay of pathophysiologic and psychosocial factors.

5 ANATOMIC BASIS OF PAIN Sensory neuroreceptors in abdominal organs are located within the mucosa and muscularis of hollow viscera, on serosal structures such as the peritoneum, and within the mesentery..

6 two distinct types of afferent nerve fibers: myelinated A-delta fibers and unmyelinated C fibers. A-delta fibers are distributed principally to skin and muscle and mediate the sharp, sudden, well-localized pain that follows an acute injury.

7 C fibers are found in muscle, periosteum, mesentery, peritoneum, and viscera. Most nociception from abdominal viscera is conveyed by this type of fiber and tends to be dull, burning, poorly localized

8 The abdominal pain receptors are directly activated by substances released in response to: local mechanical injury Inflammation Tissue ischemia and necrosis Thermal or radiation injury.

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10 Definitions Acute abdominal pain with recent onset within hours-days Chronic abdominal pain is intermittent or continuous abdominal pain or discomfort for longer than 3 to 6 months. Abdominal Pain

11 Acute abdominal pain Surgical –Appendicitis –Cholecystitis –Bowel obstruction –Acute mesenteric ischemia –Perforation –Trauma –Peritonitis Medical –Cholangitis –Pancreatitis –Choledocholithiasis –Diverticulitis –PUD –Gastroenteritis –Nonabdominal causes Abdominal Pain

12 Onset Character Location Severity Duration Abdominal Pain History

13 Eating Drinking Drugs Body position Defecation Abdominal Pain History Aggravating and alleviating factors

14 Anorexia Weight loss Nausea/vomiting Bloating Constipation Diarrhea Hemorrhage Jaundice Dysurea Menstruation Abdominal Pain History Associated symptoms

15 PMH: Similar episodes in past Other relevant medical problems Systemic illnesses such as scleroderma, lupus, nephrotic syndrome, porphyrias, and sickle cell disease often have abdominal pain as a manifestation of their illness. PSH: Adhesions, hernias, tumors, trauma Drugs: ASA, NSAIDS, antisecretory, antibiotics, etc GYN: LMP, bleeding, discharge Social: Nicotin, ethanol, drugs, stress Family: IBD, cancer, ect Abdominal Pain History

16 Physical Exam Abdominal Pain General appearance Ambulant Healthy or sick In pain or discomfort Stigmata of CLD Vital signs

17 Physical Exam- Abdomen Abdominal Pain Inspection Distention, scars, bruises, hernia Palpation Tenderness Guarding Rebound Masses Auscultation Abd sounds: present, hyper, or absent

18 CBC Liver profile Amylase Glucose Urine dipsticks Pregnancy test Laboratory Testing Abdominal Pain

19 Plain films Ultrasonography Computed Tomography Imaging Abdominal Pain

20 Endoscopy EGD Colonoscopy ERCP/EUS Abdominal Pain

21 Approach Abdominal pain Acute Chronic Surgical nonsurgical Abdominal Pain

22 RUQ-PAIN Cholecystitis Cholangitis Hepatitis RLL pneumonia Subdiaphragmatic abscess Abdominal Pain

23 LUQ- PAIN Splenic infarct Splenic abscess Gastritis/PUD Abdominal Pain

24 RLQ-PAIN Appendicitis Inguinal hernia Nephrolithiasis IBD Salpingitis Ectopic pregnancy Ovarian pathology Abdominal Pain

25 LLQ-PAIN Diverticulitis Inguinal hernia Nephrolithiasis IBD Salpingitis Ectopic pregnancy Ovarian pathology Abdominal Pain

26 Epigastric-Pain PUD Gastritis GERD Pancreatitis Cardiac (MI, pericarditis, etc) Abdominal Pain

27 Periumbelical-Pain Pancreatitis Obstruction Early appendicitis Small bowel pathology Gastroenteritis Abdominal Pain

28 Pelvic-Pain UTI Prostatitis Bladder outlet obstruction PID Uterine pathology Abdominal Pain

29 Diffuse Pain Gastroenteritis Ischemia Obstruction DKA IBS Others –FMF –AIP –Vitamin D deficiency –Adrenal insufficiency Abdominal Pain

30 Chronic abd pain approach History Intermittentcontinuous biliary intest. obstruction Intst. angina endometriosis porphoryea IBS metastasis Intest. tumor pancreatic disorder pelvic inflammation Addison dis functional disorder Alarm symptoms IDA Hematochezia Endoscopy Cholestasis US/CT ERCP Fever C&S CT Weight loss Endoscopy CT Abdominal Pain

31 Take Home Points Good history and physical exam is important ( History is the most important step of the diagnostic approach ) Lab studies limitations. Imaging studies selection (appropriate for presentation and location). Alarm symptoms oriented investigations Early referral of sick patients Treatment initiation Abdominal Pain

32 Irritable bowel syndrome (IBS) is an intestinal disorder that causes abdominal pain or discomfort, cramping or bloating, and diarrhea or constipation. Irritable bowel syndrome is a long-term but manageable condition. What Is IBS

33 First described in 1771. 50% of patients present <35 years old. 70% of sufferers are symptom free after 5 years. GPs will diagnose one new case per week. GPs will see 4-5 patients a week with IBS. 32 Introduction

34 It is estimated that between 10% and 15% of the population of North America, or approximately 45 million people, have irritable bowel syndrome. only about 30% of them will consult a doctor about their symptoms. IBS tends to be more common in In women, IBS is 2 to 3 times more common than in men. Who Gets IBS?

35 Rome III Diagnostic criteria. Manning’s Criteria. 34 Diagnostic Criteria

36 The positive predictive value (PPV) of the Manning criteria for the diagnosis of IBS has ranged between 65 and 75%, 35

37 At least 12 weeks history, which need not be consecutive in the last 12 months of abdominal discomfort or pain that has 2 or more of the following: –Relieved by defecation. –Onset associated with change in stool frequency. –Onset associated with change in form of the stool. 36 Rome III Diagnostic Criteria.

38 Supportive symptoms. –Constipation predominant: one or more of: BM less than 3 times a week. Hard or lumpy stools. Straining during a bowel movement. –Diarrhoea predominant: one or more of: More than 3 bowel movements per day. Loose [mushy] or watery stools. Urgency. 37 Rome IlI Diagnostic Criteria.

39 –General: Feeling of incomplete evacuation. Passing mucus per rectum. Abdominal fullness, bloating or swelling. 38 Rome IlI Diagnostic Criteria.

40 Diarrhoea predominant. Constipation predominant. Pain predominant. 39 Subtypes

41 In people with IBS in hospital OPD. –25% have depression. –25% have anxiety. Patients with IBS symptoms who do not consult doctors [population surveys] have identical psychological health to general population. In one study30 % of women IBS sufferers have fibromyalgia 40 Associated Symptoms

42 IBS Pathophysiology Heredity; nature vs nurture Dysmotility, “ spasm ” Visceral Hypersensitivity Altered CNS perception of visceral events Psychopathology Infection/Inflammation Altered Gut Flora

43 Immune Activation Mast Cell Activation Luminal Flora A New Paradigm

44 Immune Activation Mast Cell Activation Luminal Flora STRESS INFECTION ALTERED MICROBIOTA

45 Immune Activation Mast Cell Activation Luminal Flora

46 Systemic Immune Compartment in IBS Serum Cytokines Dinan, et al. Gastroenterology. 2006. * IL-6 IBSControls 65432106543210 IL-6 (pg/ml) * sIL-6r IBSControls 0 50000 100000 150000 sIL-6r

47 Mucosal Compartment Frank inflammation Immune Activation – ↑ IEL’s – ↑ CD3 +, CD25 + Chadwick et al, 2002 Decreased IgA+ B Cells Forshammar et al, 2008 Altered expression of genes involved in mucosal immunity Aerssens et al, 2008

48 10-14% incidence following confirmed bacterial gastroenteritis Dunlop, et al. 2003. Mearin, et al. 2005. Risk factors –Female –Severe illness –Pre-morbid psyche Depression –Persistent inflammation EC cells T lymphocytes Post-Infectious IBS Dunlop, et al. 2003. 300 200 100 0 PI-IBS Patient Controls Volunteers Lamina Propria T Lymphocytes Per hpf ** 75 50 25 0 PI-IBS Patient Controls Volunteers EC Cells Per hpf **

49 Lessons from PI-IBS Disturbed Flora Susceptible Host Inflammatory Response Myo-Neural Dysfunction SYMPTOMS

50 Inflammatory bowel disease. Cancer. Diverticulosis. Endometriosis. Celiac disease 49 Differential Diagnosis

51 50

52 Blood test for IBS Current best evidence does not support the routine use of blood tests to exclude organic gastrointestinal disease in patients who present with typical IBS symptoms without alarm symptoms.

53 Reasons to Refer  Age > 45 years at onset.  Family history of bowel cancer.  Failure of primary care management.  Uncertainty of diagnosis.  Abnormality on examination or investigation. 52

54 Urgent Referral  Constant abdominal pain.  Constant diarrhoea.  Constant distension.  Rectal bleeding.  Weight loss or malaise. 53

55 Treatment Patients’ concerns. Explanation. Treatment approaches. 54

56 Usually very concerned about a serious cause for their symptoms. Take time to explore the patients agenda. Remember that investigations may heighten anxiety. 55 Patients’ Concerns.

57 Placebo effect of up to 70% in all IBS treatments. Treatment should depend on symptom sub-type. Often considerable overlap between sub-groups. 56 Treatment Approaches.

58 Antispasmodics will help 66%. Mebeverine is probably first choice. Hyoscine 10mg qid can be added. 57 Pain Predominant.

59 Smooth Muscle Relaxants Some patients improve particularly those whose symptoms are induced by meals Most studies that have looked at these medications have been poorly designed, poorly controlled, and have not shown significant benefits above placebo

60 A data from meta-analysis of 22 studies involving 1778 patients and 12 different antispasmodic agents demonstrated modest improvements in global IBS symptoms and abdominal pain However, up to 68% of patients suffered side effects when given the high dose required to improve abdominal pain Page and Dirnberger, 1981

61 Poor evidence for efficacy. Better evidence for tricyclics and SSRIs. 60 Antidepressants

62 Tricyclic Antidepressants  TCAs likely modulate pain both centrally and peripherally  The best data supporting the use of TCAs in the treatment of IBS is from a large placebo-controlled study evaluating desipramine.  This highlights the fact that if a patient can tolerate some of the side effects of a TCA, then he or she is more likely to note an improvement in chronic abdominal pain compared with a patient treated with placebo  [Drossman et al. 2003]

63 Selective Serotonin Reuptake Inhibitors (SSRIs Six studies have been conducted to date, two each involving fluoxetine, paroxetine and citalopram Talley et al. 2008; Tack et al. 2006; Vahedi et al. 2005; Tabas et al. 2004; Kuiken et al. 2003; Masand et al. 2002]. Most patients noted an improvement in overall wellbeing, although none of the studies showed any benefit with regards to bowel habits, and abdominal pain was generally not improved

64 Only one trial has provided a head-to-head comparison between a TCA (imipramine 50 mg) and an SSRI (citalopram 40 mg), Although neither drug demonstrated significant improvements in global IBS symptoms over placebo Talley et al. 2008

65 Constipation  Lifestyle Modifications  Bowel Training and Education  Fibre  Twelve randomized controlled trials have been performed to date evaluating the efficacy of fiber in the treatment of IBS. Four of these studies noted an improvement in stool frequency (polycarbophil and ispaghula husk), while one noted an improvement in stool evacuation  Toskes et al. 1993; Jalihal and Kurian, 1990; Prior and Whorwell, 1987; Longstreth et al. 1981].  No improvement in abdominal pain  30-50% of patients treated with a fiber product will have a significant increase in gas

66 Over-the-counter Medications PEG Lactulose Tegaserod stimulate gastrointestinal peristalsis, increase intestinal fluid secretion and reduce visceral sensation 5 HT agonist FDA approved for chronic constipation in women.

67 Lubiprostone stimulates type 2 chloride channels in epithelial cells of the gastrointestinal tract thereby causing an efflux of chloride into the intestinal lumen It was approved by the FDA for the treatment of adult men and women with chronic constipation in January 2006 Nausia and diarrhea 6-8%

68 Increasing dietary fibre is sensible advice. Fibre varies, 55% of patients will get worse with bran. “Medical fibre” adds to placebo effect. Loperamide may help Diarrhea predominant 67

69 Diarrhea Loperamide inhibiting intestinal secretion and peristalsis, loperamide slows intestinal transit and allows for increased fluid reabsorption, thus improving symptoms of diarrhea

70 Alosetron is 5-HT3 receptor antagonist that slows colonic transit meta-analysis of eight randomized controlled trials involving 4842 patients determined that alosetron provided a significant reduction in the global symptoms of diarrhea, abdominal pain, and bloating in patients with IBS and diarrhea four-fold increased risk for ischemic colitis compared to placebo [Ford et al. 2008

71 RECENT THERAPY Antibiotics PROBIOTICS

72 “Target” Trials 1,260 patients with non-constipation irritable bowel syndrome (IBS) recruited in the US and Canada Rifaximin 550 mg, 3 times daily, for 2 weeks Primary endpoint: –The proportion of subjects who achieved adequate relief of IBS symptoms for at least 2 weeks during the first 4 weeks (weeks 3-6) of the 10-week follow-up phase Also assessed relief of IBS bloating and symptom responses at 12 weeks (10 weeks after end of therapy)

73 EndpointsTarget 1 Rif vs Placebo Target 2 Rif vs Placebo Combined Rif vs Placebo Adequate relief of IBS symptoms 41% vs 31%41% vs 32% Adequate relief of IBS bloating 40% vs 29%41% vs 32%40% vs 30% All p<0.03 Hitting the Target!

74 Probiotics

75 Mode of Action of Probiotics? Competition with, and exclusion, of pathogens Anti-bacterial: –Produce bacteriocins –Destroy toxins Enhance barrier function, motility Enhance host immunity –Immune modulation –Cytokine modulation –IgA production Metabolic functions

76 % Answering “Yes” at Week 4 70 60 50 40 30 80 B. infantis 1x10 6 B. infantis 1X10 10 B. infantis 1X10 8 Placebo P=0.0118 Global Assessment of Symptom Relief

77  Prospective, multicenter, double-blind, placebo- controlled, crossover trial assessing the efficacy and safety of the probiotic, VSL#3  Patients treated with VSL#3 had a significant improvement in the primary endpoint, which was the global relief of IBS symptoms (p < 0.05). Secondary endpoints of abdominal pain (p = 0.05) and bloating (p < 0.001) were also improved.  Guandalini et al. 2008

78 Avoid caffeine. Limit your intake of fatty foods. Fats increase gut sensations, which can make abdominal pain seem worse. If diarrhea is your main symptom, limit dairy products, fruit, or the artificial sweetener sorbitol. Increasing fiber in your diet may help relieve constipation. Avoiding foods such as beans, cabbage, or uncooked cauliflower or broccoli can help relieve bloating or gas. What about diet?

79 Hypnosis. Hypnosis can help some people relax, which may relieve abdominal pain. Relaxation or meditation. Relaxation training and meditation may be helpful in reducing generalized muscle tension and abdominal pain. Biofeedback. Biofeedback training may help relieve pain from intestinal spasms. It also may help improve bowel movement control in people who have severe diarrhea. Alternative Medicine

80 Self-help IBS network, IBS support group Awareness 79

81 THANK YOU 80


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