Signs & Symptoms of the Gastrointestinal Tract PDF

Signs and Symptoms of the Gastrointestinal tract Dr. Konstantinos Ekmektzoglou Assistant Professor School of Medicine European University Cyprus JANUARY 2024 DYSPHAGIA - DYSPEPSIA – NAUSEA & VOMITING ABDOMINAL PAIN SIGNS AND SYMPTOMS OF THE GI TRACT CONSTIPATION - DIARRHEA FECAL INCONTINCE – INTESTI...

Signs and Symptoms of the Gastrointestinal tract Dr. Konstantinos Ekmektzoglou Assistant Professor School of Medicine European University Cyprus JANUARY 2024 DYSPHAGIA - DYSPEPSIA – NAUSEA & VOMITING ABDOMINAL PAIN SIGNS AND SYMPTOMS OF THE GI TRACT CONSTIPATION - DIARRHEA FECAL INCONTINCE – INTESTINAL GAS GASTROINTESTINAL BLEEDING JAUNDICE Dyspepsia Lecture Outline Definitions Epidemiology Signs and Symptoms Differential Diagnosis Causes of Dyspepsia Approach to Uninvestigated Dyspepsia Treatment Dyspepsia Predominant epigastric pain lasting at least 1 month ± Post prandial fullness Nausea and Vomiting Early satiety Belching Upper abdominal bloating Heartburn and regurgitation Moayyedi P NJ, et al Am J Gastroenterology 2017 Dyspepsia – Rome IV Must fulfill both the following criteria for the last 3 months with symptom onset ≥6 months ago: ≥1 of the following: Bothersome postprandial fullness Bothersome early satiation Bothersome epigastric pain Bothersome epigastric burning No evidence of organic, systemic, metabolic or structural disease (including on upper endoscopy) that is likely to explain the symptoms Dyspepsia – Symptoms definitions Epigastric pain subjective, unpleasant sensation; some patients may feel that tissue damage is occurring Epigastric burning unpleasant subjective sensation of heat Postprandial fullness unpleasant sensation perceived persistence of food in the stomach as the prolonged Early satiation feeling that the stomach is overfilled soon after starting to eat, so that the meal cannot be finished Epidemiology Common disease 20% of the population Incidence 1%-6% per year More common in women, smokers, NSAIDs Significant burden Negative impact on QoL 2–5% having time off work because of symptoms 18 billion $ per year (U.S. health care system) Societal costs are likely to be double Differential Diagnosis Dyspepsia Differential Diagnosis Peptic Ulcer Disease Intestinal parasites (giardia) Gastroesophageal Reflux Disease Medication-induced injury (ASS, NSAIDs, antibiotics, iron) Gastroparesis Diabetes Gastric tumors Thyroid/parathyroid disorders Cholelolithiasis Connective tissue disease Choledocholithiasis Pancreatic cancer Pancreatitis (acute/chronic) Ischemic bowel disease Carbohydrate Malabsorption (lactose, etc) Pregnancy Causes Helicobacter pylori infection Peptic Ulcer Disease GERD Gastric/esophageal cancer Pancreatic/Biliary disorders Intolerance to food or drugs Causes 2% 20% 50% 15% Functional Dyspepsia Peptic Ulcer Disease GERD Gastric and Esophageal Malignancy Causes Organic causes HP infection, PUD, GERD, Cancer, HPB disorders, Intolerances Functional Dyspepsia The presence of 1 or more dyspepsia symptoms that are considered to originate from the gastroduodenal region, in the absence of any organic, systemic, or metabolic disease that is likely to explain the symptoms Functional Dyspepsia Accounts for 50-60% of all dyspepsia 40 to 60 % of patients with dyspepsia evaluated via EGD will have normal findings Often chronic and intermittent symptoms > 75% of patients have aggravation of symptoms after meals Talley NJ et al Gastroenterology 1998 Functional Dyspepsia Dominant symptoms Tack J et al Gastroenterology 2004 Functional Dyspepsia Phenotypes Post-prandial Distress Syndrome One or both: Bothersome postprandial fullness, occurring after ordinary size meals, at least several times a week Early satiety, preventing finishing a regular meal that occurs at least several times a week Epigastric Pain Syndrome All of the following: Pain/burning in epigastrium of moderate severity at least once a week Pain is intermittent Not generalized or localized to other abdominal or chest regions Not relieved by defecation or passage of flatus No structural disease to explain Not fulfilling criteria for symptoms gallbladder or Sphincter of Oddi disorders All criteria must be fulfilled for the last 3 months with symptom onset at least 6 months before diagnosis Pathophysiologic Mechanisms in Functional Dyspepsia Pathophysiologic Mechanisms Functional Dyspepsia Psychosocial factors Altered vagal output Gastric dysrhythmia Symptoms Visceral hypersensitivity: central or peripheral via vagal or DRG/spinal pathways Impaired accommodation or compliance Delayed gastric emptying H. pylori infection Small intestinal dysmotility Dyspepsia PUD 5-15% of patients with dyspepsia Declining in prevalence Risk Factors Age, NSAIDs, H. pylori H pylori and NSAID - synergistic role in PUD Serious ulcer related complications in 1-4% of NSAIDs users 5-15 %of patients with FD have similar symptoms Symptoms not predictive of organic disease H pylori present in 30 - 60 % of FD pts Dyspepsia GERD Approximately 20% of dyspeptic patients 15-20% of patients with dyspepsia have erosive esophagitis 20% of patients have endoscopy negative GERD (NERD) Dyspepsia Malignancy ~1% of dyspeptic pts (gastric and esophageal cancer) Declining incidence of gastric cancer Presence of symptoms usually indicative of advanced disease (32%) Alarm features and age limited predictive value Dyspepsia – Malignancy – Risk Factors Gastric cancer Esophageal Adenocarcinomna Male Male >50 years old Smoking Smoking Alcohol Alcohol Barrett Esophagus H. pylori Atrophic gastritis Inherited syndromes History of gastrectomy Dyspepsia – HBP Diseases Despite common believes, cholelithiasis is not associated with “classic” dyspepsia symptoms Pancreatic disorders may be found in some patients with unexplained dyspepsia Sahai AV et al Gastrointest Endosc 2000 Kraag, et al, Scand J Gastroenterol, 1995 Dyspepsia – Food/drug Intolerance Ingestion of foods such as spices, coffee or alcohol or excess food is, usually, not associated with dyspepsia Effect related to sensorimotor responses to food Common side effect of many medications Dyspepsia – Common medications Acarbose ASA Colchicine Digitalis Estrogens Ethanol Gemfibrozil Glucocorticoids Iron Levodopa Niacin Narcotics Nitrates Orlistat Potassium chloride Quinidine Sildenafil Theophylline Dyspepsia – NSAIDs Chronic use of NSAIDS and/or ASA 20% dyspeptic symptoms If dyspepsia present poorly correlated with presence of ulcer Higher dosing → Worse dyspepsia NSAIDS + PPI (66% RR) vs. NSAID COX 2 vs. NSAID (12% RR) Dyspepsia – Thinking out of the box! Infectious ( Strongyloides stercoralis, TB, syphilis, fungal) Inflammatory Diseases Infiltrative Diseases Ischemia Pregnancy Hyperparathyroidism Dyspepsia - Management 45 years old man complaining of persisting postprandial heartburn since 4 years 35 years old woman complaining of epigastric pain since 7 weeks. She also reports early satiety especially after dinner 65 years old man complaining of epigastric pain since a couple of days. He also reports loss of weight (5kg in the last 4 weeks) and difficulties to swallow Uninvestigated Dyspepsia Dyspeptic symptoms in persons in whom no diagnostic investigations have yet been performed and in whom a specific diagnosis that explains the dyspeptic symptoms has not been determined History – Physical Examination Nature of symptoms Chronicity Relationship with meals Onset (recent infections?) Other systemic disorders Medications Allergies Family History Alarm features Abdominal pain Abdominal mass Organomegaly Ascites FOB Heartburn vs. Dyspepsia Heartburn burning feeling confined to epigastrium 304 pts / 24 hour pH monitoring Heartburn (68% vs 48%) and acid regurgitation (60% vs 48%) correlated with GERD ( pH monitoring) High specificity (89% and 95%, respectively) Low sensitivity (38% and 6%) Klauser et al Heartburn vs. Dyspepsia Considerable overlap noted b/w GERD and Dyspepsia Up to 27 % of pts with GERD have associated dyspepsia Patients suffering from both GERD and Dyspepsia had higher symptom intensity scores PPI treatment could be the first step for these patients Lee et al : Digestion 2009 Piessevaux et al : Neurogastrenterol Motility 2009 Alarm features Weight loss (>10%) Overt Bleeding Anemia dysphagia Odynophagia Previous PUD Persistent vomiting Lymphadenopathy Abdominal Mass FH of UGI malignancy History of gastric surgery Jaundice Alarm features Meta analysis of 15 studies 57,363 pts / 458 with malignancy Low positive predictive value (60 Alarm features Yes EGD Consider biopsies to exclude HP No Non invasive test for HP HP + Treatment HP - PPI Prokinetics TCA Take home message Dyspepsia: predominant epigastric pain Heartburn, early satiety, belching, nausea, vomiting, postprandial fullness may coexist Plethora of causes FD in the majority of the cases Each patient will describe it differently Try to solve the puzzle!! History and physical examination (!!!) Search for alarm signs Evaluate and treat accordingly Nausea and Vomiting Definitions Vomiting: forceful expulsion of stomach contents from the mouth due to involuntary contractions of the abdominal, thoracic and GI (smooth) muscles spontaneous provocative Nausea: feeling of wanting to vomit, often associated with autonomic effects like salivation, pallor, sweating frequently precedes actual vomiting vomiting does not follow necessarily Retching: a strong, involuntary, unproductive effort to vomit associated with abdominal muscle contraction but without expulsion of gastric contents through the mouth 40 Vomiting process Complex process CNS ANS Vomiting center and chemoreceptors Neurotransmitters Acetylcholine Histamine Dopamine Noradrenaline Serotonin Visceral efferent fibers 41 Triggers causing nausea and vomiting Chemotherapeutics Digoxin - L-Dopa Uremia Toxins - Drugs Visceral pain Visceral obstruction Pregnancy Stress Travelers' nausea 4th ventricle chemoreceptors Mucosal chemoreceptors Vagus nerve Vomiting center Vagus nerve Vomiting center Unknown 4 The process of vomiting CTZ stimulation Motor nervous system Parasympathetic nervous system Sympathetic nervous system Heaving or retching before actual vomiting increased salivation Deep breathing preceding the actual vomiting to protect lungs from aspiration Relaxation of the pyloric sphincter that guards the lower end of the stomach to bring up content from the gut Abdominal pressure rises and thoracic pressure lowers The abdominal muscles contract to expel the contents of the stomach Activation of the sympathetic nervous system: sweating, palpitation and rapid heart rate 5 Causes of acute nausea and vomiting in adults Infections Acute hepatitis Acute gastroenteritis Ovarian Torsion Peritonitis Acute Appendicitis Renal colic Acute abdominal pain Biliary colic Acute Pancreatitis Acute Cholecystitis 44 Causes of acute nausea and vomiting in adults Intestinal ileus Ileus Paralytic ileus Volvulus Acute glaucoma Sigmoid torsion Meningitis CNS Diseases CNS tumors Medications Drugs 45 Causes of chronic nausea and vomiting in adults GI Diseases Metabolic Diseases Peptic Ulcer Disease Uremia Pyloric Stenosis Hypercalcemia Gastric/Pancreas Cancer Diabetic gastroparesis Chronic Pancreatitis Diabetic ketoacidosis Superior Mesenteric Artery Syndrome Hyperthyroidism Gastrectomy -> Bile Reflux Gastritis Addison Disease 46 Causes of chronic nausea and vomiting in adults Neuropsychological Diseases Other Migraine Malignant hypertension Labyrinth Diseases Labyrinth Diseases Psychogenic Vomiting Pregnancy Anorexia nervosa Radiotherapy Bulimia nervosa Idiopathic cycling vomiting 47 Vomiting as a Side Effect Medications where vomiting has been reported as a SE in >5% of the cases Cytostatic and chemotherapeutic agents Opioids Hormones Corticosteroids, estrogen Antiasthmatic Antibiotics Theophylline Macrolides, Vancomycin, Sulfonamides, Tetracycline, Isoniazid, Rifabicin Meds used in neurology Amphetamines, L-Dopa Meds used in cardiology B-blockers, digoxin, spironolactone, Ca channel blockers Meds used in gastroenterology (!!!) Sulfasalazine Meds used very often (!!!) ASS, NSAIDs 48 Hyperemesis (excessive vomiting) clinical consequences Syndrome Mallory-Weiss Syndrome Boerhaave Electrolyte and metabolic disorders Hypovolemia Hypochloremic metabolic alkalosis Significant weight loss 49 Work-up History Physical examination Signs and Symptoms Lab tests Imaging 50 History How long? Relationship to meals? Contents of vomitus? Diabetes? Other chronic diseases? Psychiatric disease? Medications? When was last menstrual period? Any previous surgeries? Alcohol / drugs? Relationship to meals Early morning vomiting Pregnancy Alcoholism Before or during meals Psychogenic vomiting After the meals GI disease (e.g. stomach) 52 Associated symptoms Vertigo, dizziness, headache, focal neurological symptoms Chest or abdominal pain Fever, myalgias Diarrhea Jaundice Weight loss, anorexia 53 Physical Examination Abdominal exam Rectal exam Cardiopulmonary exam Neurological exam including funduscopic exam (papilledema) Vital signs BP and pulse tilt test Emesis content and odor Food, blood, bile, feces 54 Laboratory studies Electrolytes, glucose, BUN/creatinine Calcium, albumin, total serum proteins CBC LFTs Pregnancy test Urinalysis Serum lipase  amylase 55 Additional studies Tumor markers Hormones Ophthalmology exam ECG 56 Imaging Plain abdominal films Imaging Plain abdominal films Imaging Abdominal ultrasonography or CT if pain is key feature Imaging EGD Gastric outlet obstruction / duodenal obstruction Peptic ulcer disease Gastroparesis Imaging Radiopaque marker emptying studies or radionuclide scintigraphy Diabetic gastroparesis Abdominal Pain Lecture Outline Causes of abdominal pain Location of abdominal pain Types of abdominal pain Acute abdominal pain Chronic abdominal pain Abdominal Pain One of the most common reasons for outpatient and ER visits A plethora of diseases may present with abdominal pain as the main symptom An organized approach is needed Abdominal causes of abdominal pain Esophagitis / GERD Esophageal spasm PUD Gastric outlet obstruction Bowel obstruction Intussusception Bowel perforation Cancer CD / UC Gastroenteritis Appendicitis Cholecystitis Choledocholithiasis Pancreatitis Cholangitis Mesenteric ischemia AAA rupture Diverticulitis Ectopic pregnancy Pelvic inflammatory disease Incarcerated Hernia Hepatitis Splenic infarct/abscess IBS Other causes of abdominal pain Systemic Infectious –DKA Thoracic –Strep pharyngitis –Alcoholic ketoacidosis – Myocardial (more often in infarction/ Unstable –Uremia children) angina –Sickle cell disease –Rocky Mountain –Pneumonia –Porphyria Spotted Fever –Pulmonary embolism –SLE –Mononucleosis –Herniated thoracic –Vasculitis Abdominal wall disc (neuralgia) –Glaucoma –Muscle spasm Genitourinary –Hyperthyroidism –Muscle hematoma –Nephrolithiasis / UTI Toxic –Herpes zoster –Testicular torsion –Methanol poisoning –Renal colic –Heavy metal toxicity –Scorpion bite –Black widow spider bite Abdominal Pain Location Types of Abdominal Pain Visceral –Crampy, achy, diffuse –Poorly localized Somatic –Sharp, cutting, stabbing –Well localized Referred –Distant from site of generation –Symptoms, but no signs Visceral Pain Stretching of nerve fibers of walls or capsules of organs Crampy – Dull - Achy Often unable to lie still Bilateral innervation Foregut organs (stomach, duodenum, biliary tract) produce pain in the epigastric region Midgut organs (most small bowel, appendix, cecum) cause periumbilical pain Hindgut organs (most of colon, including sigmoid) as well as the intraperitoneal portions of the genitourinary tract cause pain initially in the suprapubic or hypogastric area. Parietal Pain Irritation of fibers that innervate the parietal peritoneum Usually anterior abdominal wall Localised to the dermatome superficial to the site of painful stimulus Pain evolution Visceral Parietal Non specific Localised tenderness Guarding Rigidity Rebound Referred Pain Pain or discomfort perceived at a site distant from the affected organ because of overlapping transmission pathways Reflects embryologic origin Referred Pain subdiaphragmatic irritation ipsilateral supraclavicular or shoulder pain gynecologic pathology back or proximal lower extremity pain biliary tract disease right infra-scapular pain myocardial ischemia mid-epigastric, neck, jaw, or upper extremity pain ureteral obstruction ipsilateral testicular pain Acute abdominal pain Less than a couple weeks Usually present since days to hours Don’t forget about the chronic pain that has acutely worsened Usually immediate attention is required Surgical vs. nonsurgical Chronic abdominal pain Present for months to years Usually not life threatening Outpatient work-up Constipation, IBS, dyspepsia the most common causes… Diagnosis easily in younger patients, but pay attention in patients >55 years old Approach to the patient History: of PARAMOUNT importance Location, quality, severity, radiation, exacerbating or alleviating factors, associated symptoms Medical history including sexual and menstrual Social history including alcohol, drugs, domestic abuse, stressors, travel etc. Family history IBD, cancers, etc Medication Chronic and recent History: what to ask for O: P: Q: R: S: T: onset provocation /palliation quality/quantity region/radiation severity/scale timing/time of onset History: associated symptoms Gastro – intestinal Nausea Vomiting Dyspepsia Change in bowels Genitourinary Gynaecologic Weight loss Bleeding History: complementary elements Medical History DM HT Liver Disease Renal Disease Sexually Transmitted Infections Surgical History Abdominal Surgery Pregnancies Deliveries/ Abortions/ Ectopic Trauma Consultations/ Presentations Meds NSAIDs Steroids OCP/ Fertility Drugs Narcotics Immunosuppressant Chemotherapy agent Allergies Contrast Analgesic Physical examination Vitals (incl postural) -> always document!!! General appearance Systematic physical examination Jaundice, signs of chronic liver disease Costovertebral angle tenderness Abdominal exam FIRST Look, THEN listen, THEN feel Digital Recta Examination Pelvic exam, Genito-Urinary examination Musculoskeletal examination Physical examination Lots of bedside information Distressed vs. non distressed Lying still -> peritonitis Writhing -> renal Colic Murphy’s sign Associated with acute cholecystitis Examiner’s hand at the middle inferior border of the liver Patient is asked to breath deeply If positive: patient will experience pain and stop short of inspiration McBurney’s sign Associated with acute appendicitis Palpate the point over the right side of the abdomen (one-third of the distance from the anterior superior iliac spine to the umbilicus) If positive: patient will experience pain Rovsing’s sign Associated with acute appendicitis Palpate the left lower quadrant of the abdomen If positive: patient feel pain in the right lower quadrant Cullen sign Associated with acute necrotizing pancreatitis Periumbilical ecchymosis Tracking of blood from the retroperitoneum to the umbilicus and then subsequently to subcutaneous umbilical tissues Grey-Turner sign Associated with acute necrotizing pancreatitis High mortality Hemorrhagic fluid spreading from the posterior pararenal space to the lateral edge of the quadratus lumborum muscle and thereafter to the subcutaneous tissues by means of a defect in the fascia of the flank Laboratory tests Labs CBC, electrolytes, BUN, Cr, coagulation Amylase and lipase, LFTs Urine analysis B-Human chorionic gonadotropin Lactate Toxin-drug screen H. pylori serology FOBT ECG anyone with upper abdominal pain or elderly Imaging Imaging Plain films Computer tomography Ultrasound MRI Angiography Endoscopy EGD Colonoscopy ERCP/EUS Radiology Plain film Exclude perforation Exclude small bowel obstruction Radiology Plain film Useful for renal stones, but CT is the primary investigation modality Abdominal Ultrasound Biliary Disease Gynecologic complaints Rule out ectopic pregnancy Appendicitis in children No radiation Computer tomography CT is accurate for: Renal colic Appendicitis Diverticulitis AAA Intra-abdominal abscesses Mesenteric Ischaemia Bowel Obstruction Avoid repeated CT scans Limit use in younger patients Avoid where possible in pregnant females Acute (surgical) abdomen The first thing to be considered in acute abdominal pain Early identification is very important prognosis worsens rapidly with delay Important to get surgeons involved early if this is even mildly suspected This is a clinical diagnosis Presentation is usually bad Fevers, tachycardia, hypotension Tender abdomen, possibly rigid Presentation can vary with other demographic and medical factors Advanced age Immunosuppression Acute abdomen Most common causes Acute appendicitis Acute cholecystitis Acute pancreatitis Diverticulitis Acute peritonitis rupture of a hollow viscus or as a complication of inflammatory bowel disease or malignancy Mesenteric ischemia Ruptured abdominal aortic aneurysm Ruptured ectopic pregnancy Ovarian torsion Ureteral colic -pyelonephritis Small bowel obstruction Peritonitis Peritonitis Often signals an intraabdominal catastrophe Perforation, big abscess, severe bleeding Patient usually appears ill Exam findings Rebound, rigidity, tender to percussion or light palpation, pain with shaking bed Blumberg's sign or rebound tenderness indicative of peritonitis pain upon removal of pressure rather than application of pressure to the abdomen Acute abdomen Work-up Start with stat labs Surgical abdominal series (plain films) Consider stat CT if readily available Sometimes patients go straight to surgery Surgeons should get involved early guidance and early intervention Special populations Elderly May lack physical findings despite serious pathology Reduced diagnostic accuracy Risk of Vascular Catastrophes Assume surgical cause until proven otherwise 30-40% of elderly with acute abdominal pain need surgery Biliary Disease is the commonest cause Special Populations Women of Childbearing Age PREGNANCY should be always included in DD B-Human chorionic gonadotropin in all women of childbearing age and acute abdominal pain Lactate Atypical clinical presentations due to gravid uterus that displaces intra-abdominal organs Pregnant women still get common surgical abdominal conditions Cholecystitis Choledocholithiasis - cholangitis Abdominal Pain What to avoid Incomplete physical examination Always perform: rectal, pelvic and genital examination… Incomplete histories Ask about medications and drugs… Missing abnormal vitals Relying only on labs Relying only on imaging Not performing serial exams Elderly, the young, the pregnant, altered or psychiatric patients “IBS” - “Constipation” - “GERD” - “Gastroenteritis” -“UTI” Constipation 100 Definitions Constipation infrequent, difficult passage of stool with the sensation of incomplete bowel emptying Prevalence 14% in the general population 30% more common in non-white population more common in women (3:1) 101 Classification By course Acute By etiology Primary (functional) Poor diet and insufficient exercise Slow transit time Bowel obstruction Chronic Secondary Mechanical Drugs Endocrine Neurological Connective tissue disorders IBS 3 Secondary constipation Mechanical Drugs Endocrine/Metabolic Neurological CRC, diverticulosis, strictures, volvulus hemorrhoids, colonic opiates , iron supplements, antacids, anticholinergics, antidepressants, CCB hypothyroidism, DM hypokalemia, hyperparathyroidism Multiple sclerosis, diabetic neuropathy, stroke, Hirschsprung, Parkinson, Chagas (megacolon), botulism Connective Tissue Disorders scleroderma, amyloidosis IBS 4 Constipation Assessment History dietary habits medication use Mobility stool character and frequency problems with defecation anorectal pain In children delayed passage of meconium?? (e.g., Hirschsprung disease) voluntary withholding of stool (e.g., squatting, crying, crossing ankles, hiding) fecal (overflow) incontinence Functional Constipation (Rome IV criteria) At least two of the following must have occurred in ≥ 1/4 of defecations during the past 12 weeks with onset of symptoms ≥ 6 months ago: Passage of stool < 3 times/week Passage of hard or lumpy stool Sensation of anorectal obstruction/blockage Manual aid to evacuate stool Straining during attempts to defecate Sensation of incomplete evacuation 105 Constipation Physical Examination Inspect the anorectal area Fissures Hemorrhoids Anal wink reflex Anal contraction when a cotton pad runs along all 4 quadrants around anus Absence suggestive of pathology (sacral nerve injury) Digital rectal examination Mass (CRC?, fecal impaction?) Sphincter tone (pelvic floor dysfunction) 106 Constipation Further Investigation Laboratory Electrolytes (exclude hypokalemia) Hormones (TSH, hypothyroidism) Glucose (diabetes) Imaging X-ray, radiopaque markers for slow transit constipation Colonoscopy Especially if alarm symptoms, age >50, acute onset 107 Constipation Alarm Features Family history (e.g. CRC, IBD) Iron deficiency anemia Blood in stool Palpable abdominal mass Reduced stool caliber Rectal prolapse Significant unexplained weight loss Sudden onset of new change in bowel habit Persistent constipation, despite treatment > 50 years of age and no previous screening for colorectal cancer108 Constipation Treatment Diagnose and treat any underlying conditions. Adults (step-up approach) Lifestyle changes high-fiber diet (psyllium seed husk, wheat bran) increased fluid intake exercise Administer osmotic laxatives Stimulant laxatives Biofeedback training helpful in treating disturbances in defecation DIARRHEA 110 Definition Diarrhea is defined as painless loose or watery stools during ≥75% of defecations for the prior 3 months, with symptom onset at least 6 months prior to diagnosis Stool volume may increase to >200 g in 24 hours. However … Collecting and weighing stools is neither practical nor required except in a clinical research setting A good working definition is three or more loose or watery stools per day A definite decrease in consistency and increase in frequency based upon an individual baseline Acute (30 days) Duration? Key questions during history Acute diarrhea up to 2 weeks / Chronic diarrhea lasting 4 weeks or more Characteristics? volume, frequency, consistency Presence of mucus, pus, or blood? Associated tenesmus? a constant urgency to defecate, accompanied by pain, cramping, and involuntary straining Does diarrhea occur at night? Are the stools greasy or oily? Frothy? Foul-smelling? Floating on the surface? Medications? Recent travel? Diet patterns? Baseline bowel habits? Risk factors for immunocompromise? Small bowel vs. colon Small bowel watery diarrhea large volume abdominal cramping bloating, gas, weight loss Rarely fever No blood or inflammatory cells Colon frequent and regular small volume often painful bowel fever may be present bloody or mucoid stools Acute diarrhea Diarrhea = increased water content of the stool impaired water absorption active water secretion by the bowel In severe infectious diarrhea, > 20 / day defecation occurring every 20 or 30 minutes Total daily volume of stool may > 2 liters volume depletion and hypokalemia Most patients with acute diarrhea 3 - 7 movements per day stool volume < 1 liter / day Etiology Most cases of acute infectious gastroenteritis are probably viral stool culture has been positive in only 1.5 to 5.6% In contrast, bacterial causes are responsible for most cases of severe diarrhea Protozoa are less commonly identified as the etiologic agents of acute gastrointestinal illness Etiology Infectious origin Bacteria Salmonella Campylobacter Shigella Escherichia coli 0157:H7 Clostridium difficile Non- infectious origin Virus Norovirus Adenovirus Rotavirus Protozoa Cryptosporidium Giardia Cyclospora Entamoeba histolytica Drugs Food allergies IBD Thyrotoxicosis Carcinoid syndrome Acute Diarrhea – General Approach Careful history to determine symptoms’ duration Frequency and stool characteristics Signs of extracellular volume depletion decreased skin turgor, orthostatic hypotension Fever and peritoneal signs invasive enteric pathogen Acute Diarrhea - Further Evaluation? Profuse watery diarrhea with signs of hypovolemia Small volume stools with blood and mucus Bloody diarrhea Fever Six unformed stools per day; illness duration >48h Severe abdominal pain Recent use of antibiotics or hospitalized patients Elderly (70 years of age) or immunocompromised Responsible pathogens per site Small Bowel Colon Bacteria Salmonella Escherichia coli Clostridium perfringens Staphylococcus aureus Aeromonas hydrophila Bacillus cereus Vibrio cholera Campylobacter Shigella Clostridium difficile Yersinia Vibrio parahaemolyticus Enteroinvasive E. coli Plesiomonas shigelloides Viruses Rotovirus Norovirus Cytomegalovirus* Adenovirus Herpes simplex virus Protozoa Cryptosporidium* Microsporidium* Isospora Cyclospora Giardia lamblia Entamoeba histolytica Foodborne acute diarrhea Timing Symptoms that begin within six hours suggest ingestion of a preformed toxin of Staphylococcus aureus or Bacillus cereus Symptoms that begin at 8 to 16 hours suggest infection with Clostridium perfringens Symptoms that begin at more than 16 hours can result from viral or bacterial infection Food contamination with enterotoxigenic or enterohemorrhagic E. coli Recent antibiotic use Search for Clostridium difficile Diagnostic Approach Blood and white cells in stool Low sensitivity, suggestive of invasive bacteria (?) Stool cultures Immunocompromised patients, severe, inflammatory diarrhea underlying IBD Ova and Parasite studies Persistent diarrhea +/- travel to special region Persistent diarrhea with exposure to infants in daycare centers MSM, patients with AIDS Community waterborne outbreak Bloody diarrhea with few or no fecal leukocytes intestinal amebiasis Diagnostic Approach Endoscopy is usually NOT needed IBD vs. infectious diarrhea -> biopsies Diagnosing C. difficile infection (pseudomembranes) in patients who are toxic and tissue culture assays results pend Decreased need for endoscopy due to ELISA for C. difficile toxins A and B In immunocompromised patients (eg CMV) Suspicion of ischemic colitis with unclear diagnosis after clinical and radiologic assessment Treatment Oral rehydration solutions Empiric antibiotic therapy Symptomatic Treatment Antibiotic Treatment Indications moderate to severe travelers' diarrhea (>4 stools /d, fever, blood, pus, or mucus in the stool) > 8 stools / day, volume depletion, symptoms > 1 week Immunocompromised bacterial diarrhea with fever, bloody diarrhea NO for suspected EHEC empiric therapy: oral fluoroquinolone E.g. ciprofloxacin 500 mg twice daily, 3-5 days Symptomatic Treatment Loperamide (Imodium): symptomatic treatment of patients with acute diarrhea when NO fever and NO bloody stools 4 mg) initially, then 2 mg after each unformed stool Maximum 16 mg/day for 2 days. Dietary Recommendations Adequate nutrition is important enterocyte renewal Short period of consuming only liquids Boiled starches and cereals (eg, potatoes, noodles, rice, wheat, and oat) Gradual reinsertion of all foods Approach To The Patient with Chronic Diarrhea Sub-types of Diarrhea Osmotic Secretory Motility Induced Chronic diarrhea Osmotic Diarrhea: Unusually large amounts of poorly absorbed osmotically active solutes Carbohydrates, laxatives Secretory Diarrhea: Defects in ion absorption Cl-/HCO3- or NA+/H+ exchange Abnormal mediators: cAMP, cGMP, etc Motility induced Diarrhea Rapid transit leads to decreased absorption Inflammatory Diarrhea Inflammation and ulceration compromise the mucosal barrier Mucous, protein, blood released into the lumen absorption diminished Osmotic Diarrhea Lactose-Dairy products Sorbitol-Sugar free gum, fruits Fructose-Soft drinks, fruit Magnesium-Antacids Laxatives-Citrate, NaSulfate Osmotic Diarrhea History Ask about ingestion pf: Laxatives, unabsorbed carbohydrates, magnesium containing products Can be watery or loose No blood, minimal cramping, no fever! Diarrhea stops when patient fasts! Stool analysis Osmotic gap > 125 Osmotic Diarrhea Workup Stool electrolytes (Na+ and K+) Stool osmolality pH NOT FEASIBLE in everyday clinical practice HISTORY is the key! Remove potential etiology factor Secretory Diarrhea History Diarrhea is usually watery Non-bloody Persistent during fast Non-cramping Secretory Diarrhea Causes Causes of Secretory Diarrhea Villous adenoma Carcinoid tumor Medullary thyroid CA Bile acid malabsorbtion Stimulant laxatives Intestinal lymphoma Zollinger-Ellison syndrome VIPoma Lymphocytic colitis Hyperthyroidism Collagenous colitis Sprue Dysmotility Diarrhea Causes of Dysmotility Diarrhea Irritable bowel syndrome Carcinoid syndrome Resection of the ileo-cecal valve Hyperthyroidism Post gastrectomy syndromes Constipation Constipation as cause of Dysmotility Diarrhea “Overflow” diarrhea Extremely common! Often in elderly with fecal incontinence Fiber enriched diet, fleet Colon cancer Partial obstruction due to mass Recent alteration in bowel habits, lower abd pain >55 years Modern Sub-types of Diarrhea Inflammatory IBD, parasitic infections, fungal, TB, viral, Sprue(?), rare bacteria Watery Secretory, osmotic and some motility types Fatty Pancreatic insufficiency, sprue, bacterial overgrowth, large small bowel resections Inflammatory Diarrhea Inflammatory bowel disease Celiac Disease Chronic infections Amoeba C. Difficile, aeromonas Other parasites HIV, CMV, TB, Inflammatory Diarrhea History Bloody diarrhea Tenesmus, cramping Fever, malaise, weight loss Family History of IBD? Recent Travel abroad? Watery Diarrhea Osmotic Diarrhea Secretory Diarrhea Fatty Diarrhea Malabsorption pancreatic disease bacterial overgrowths Sprue Greasy, floating stools Measure 24 hour fecal fat > 5g per day = fat malabsorption Chronic Diarrhea General Approach History Inflammatory, watery or fatty? Are there any obvious associations? Foods (lactose!), candies, medications, travel, stress, medications Is the patient constipated? Is there any weight loss or abdominal pain? Are there any night time symptoms? Family history? IBD, IBS Are there any other medical conditions? Thyroid, DM, Collagen vascular Chronic Diarrhea Physical Examination Vital Signs, general appearance Abdomen – tenderness, masses, organomegaly Rectal exam – Sphincter tone and squeeze Skin – rashes, flushing, Thyroid mass?? Edema? Chronic Diarrhea Work-up (Initial) Address any obvious causes!!! Labs CBC, Chemistry, Stool analysis Wt., Na+, K+, osm, pH, Fat assessment (sudan) O&P, C Diff. stool? WBC? Chronic Diarrhea Work-up (Further) If subtype not clear… Stool elastase, TTG, Anti-EMA Colonoscopy/FS and EGD with SB biopsy CT Scan, SBFT etc When to Refer a Patient? Inflammatory Watery Fatty Refer to GI Wait labs Refer to GI Secretory Treat infection Treat IBS Osmotic Stop offending agent However … Consider fecal incontinence Consider constipation Consider IBS Minimal work-up. Intestinal Gas 149 Volume and Composition 100-200ml during fasting – 65% increase after meal ingestion Input Swallowing, chemical reactions, bacterial fermentation, diffusion from blood Output Belching, bacterial consumption, absorption into blood, anal evacuation >99%: N2, O2, CO2, H2 and CH4 150 Gas excretion 151 Odoriferous Gases None of the quantitatively important gases has an odor The unpleasant odor of feces is due to gases present in trace quantities (hydrogen sulfide and methanethiol) Extremely toxic! – Metabolised to thiosulfate to protect colonisc mucosa – Negligible quantities enter the – Not excreted in the breath. Abdominal bloating and Distension Definitions Among the most frequently encountered GI complaints Bloating: the sensation of increased abdominal pressure Abdominal distention: an objective increase in abdominal girth – Distention usually develops following meals or at the end of the day and resolves after an overnight rest Abdominal bloating and Distension Pathophysiology IBS: increased gas production caused by SIBO or malabsorption – not supported by other well-designed studies – similar net production and content of intestinal gas – impaired handling of the infused gas – disturbances in gas propulsion may lead to localized gas accumulations that cause symptoms in the hypersensitive intestines of patients with bloating – sensation of distention is associated with an increase in the anteroposterior diameter of the abdomen and a significant diaphragmatic descent but only a modest increment in intestinal gas content Abdominal bloating and Distension Treatment Nonpharmacological therapies – Dietary manipulations to reduce gas production – Treatment of constipation with low-fiber and low-residue diets reduces bulking and improves bloating – Probiotics may reduce symptoms – Hypnosis has been reported to reduce symptoms of IBS Pharmacologic therapies – Rifaximin can reduce symptoms of IBS, IBS may first appear after antibiotic therapy More data needed – Neostigmine (prokinetic agent) reduces abdominal symptoms – Smooth muscle relaxants are superior to placebo in the management of symptoms, specifically abdominal pain and – Drugs with antinociceptive action may also be useful Repetitive Eructation Pathophysiology Occasional belch expels gas swallowed with ingested solids or liquids Repetitive eructation: inadvertent aspiration of air into the hypopharynx entering the stomach – Emotional stress Episodes of continuous post meal belching – underlying dyspeptic-type postprandial symptoms that patients misinterpret as excessive gas in the stomach – If swallowed air enters the stomach, discomfort may increase – Eructation produces partial relief and reinforces the false impression of the patient, and a vicious cycle develops Chronic eructation is almost always a behavioral disorder – No radiologic and endoscopic evaluation needed – In patients with aerophagia, swallowed air may pass into the intestine bloating sensation Repetitive Eructation Treatment Provide a clear-cut pathophysiologic explanation for the patient’s repetitive belching “Air swallowing rather than gas production in the GI tract is the problem” Understanding the benign nature of chronic eructation Patients should be instructed to refrain from belching – Holding a pencil between the teeth during episodes of repetitive belching may help a patient become aware of swallowing and stop the cycle Treat underlying dyspeptic syndromes Flatulence Pathophysiology Secondary to air swallowing – associated in most instances with other GI symptoms; abdominal bloating Patients with functional GI symptoms have increased colonic and rectal perception (visceral hypersensitivity -> functional flatulence) – the lower tolerance for and more efficient evacuation of gas arriving into the rectum More frequent passages of smaller volumes could be a behavioral response to rectal gas sensation Unusually due to carbohydrate malabsorption (lactose malabsorption, celiac disease) Flatulence - Treatment First step: daily record of gas passages – > 20 passages / day: abnormal If carbohydrate malabsorption: treat the underlying condition Functional flatulence (no demonstrable intestinal absorptive defect) – low-flatulogenic diet – improvement in subjective flatulence and abdominal symptoms Lack of data concerning the effect of diet on anal gas evacuation – Legumes, Brussels sprouts, onions, celery, carrots, raisins, bananas, fermentable fiber, and complex starches (wheat, potatoes) – Diets low in fermentable oligosaccharides, disaccharides, monosaccharides, and polyols (FODMAPs, little evidence Activated charcoal has been reported to reduce breath H2excretion (???) Rifaximin may reduce intestinal gas production – decreased rectal gas excretion has not been demonstrated Pre- and probiotics influence the composition of colonic flora – no direct evidence Fecal Incontinence 160 Definitions Fecal incontinence recurrent frequent uncontrolled leakage of stool and/or stool staining for more than 1 month Incidence 1,4-18% higher in middle-aged women, elderly and nursing patients Gas – soft or liquid stool – solid stool Passive or with awareness Mild - moderate - severe 161 Pathophysiology Abnormal Anorectal or Pelvic Floor Structures – – – – – Anal sphincter muscles Puborectalis muscle Pudendal nerve NS, ANS, spina cord Rectum Abnormal Anorectal or Pelvic Floor Function – Impaired anorectal sensation – Fecal impaction Altered Stool Characteristics – Increase volume, loose consistency, hard stools, retention Miscellaneous – Physical mobility, cognitive function – Drugs, psychosis – Food intolerance 162 Fecal Incontinence Assessment History – Onset, precipitating factors – Duration, severity, timing – Co-existing medical illnesses – Obstetric or surgery history – Medication Physical examination – DRE Examinations – Anal manometry – Anorectal ultrasound – Colonoscopy Bowel diary Fecal Incontinence History – Onset, precipitating factors – Duration, severity, timing – Co-existing medical illnesses – Obstetric or surgery history – Medication Physical examination – DRE Examinations – Anal manometry – Anorectal ultrasound – Colonoscopy Bowel diary Bio-feedback the most effective treatment GASTROINTESTINAL BLEEDING Gastrointestinal Bleeding UPPER vs LOWER GI BLEEDING UPPER GI bleeding LOWER GI bleeding Causes Upper gastrointestinal hemorrhage Non-variceal peptic ulcers (28-59%) - (duodenal ulcer 17-37% and gastric ulcer 11-24%) mucosal erosive disease of the esophagus/stomach/duodenum (1%–47%) Mallory–Weiss syndrome (4-7%) upper GI tract malignancy (2-4%) other diagnosis (2-7%) no exact cause identified (7-25%) Variceal Causes Risk stratification for UGIH Treatment Preendoscopic Endoscopic Postendoscopic Pre-endoscopic management - UGIH HEMODYNAMIC RESUSCITATION hemoglobin between 7-9g/dL STOP/REVERT ANTICOAGULANTS AND ANTIPLATELETS vitamin K, prothrombin complex concentrate (PCC), fresh frozen plasma (FFP) (INR) < 2.5 before performing endoscopy PHARMACOLOGICAL THERAPY high dose intravenous proton pump inhibitors (PPIs) GASTRIC LAVAGE – NO ET INTUBATION – NO (only in ongoing active hematemesis, encephalopathy, or agitation) Endoscopy - UGIH early (≤24 hours) very early (