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    Manifestations Of Gastrointestinal Diseases   Copy Manifestations Of Gastrointestinal Diseases Copy Presentation Transcript

    • Manifestations of Gastrointestinal Diseases
      • Celso M. Fidel MD,FPSGS,FPCS
      • Diplomate Philippine Board of Surgery
    • What are These Manifestations?
      • 1. PAIN
      • 2. FEVER
      • 3. ANOREXIA
      • 4. HEARTBURN and DYSPEPSIA
      • 5. DYSPHAGIA
      • 6. NAUSEA and VOMITING
      • 7. ABDOMINAL DISTENTION,
      • ERUCTATION and FLATULENCE
      • 8. CONSTIPATION
      • 9. DIARRHEA
    • What are These Manifestations?
      • 10. ILEUS
      • 11. INTESTINAL OBSTRUCTION
      • a. Partial Obstruction and Pseudo-obstruction
      • b. Mechanical Obstruction
      • c. Closed Loop Obstruction
      • d. Colon Obstruction
      • 12. GASTROINTESTINAL BLEEDING
      • a. Upper GI Bleeding
      • b. Lower GI Bleeding
      • 13. JAUNDICE
    •  
    • I Pain
      • Most common symptom of GIT disease
      • Three kinds have been described in gen.
      • 1. Superficial or Cutaneous pain
      • 2. Deep pain from:
      • Muscles
      • Tendons
      • Joints
      • Fascia
      • 3. Visceral pain
    • I Pain
      • Two Types of Pain
      • 1. Somatic Pain 2. Visceral Pain
      • Pathway:  A-delta fibers  Autonomic C-type fibers
      • Receptor:  Parietal, Muscle  Visceral
      • and Skin
      • Specific  Well localized  Poorly localized
      • Description  Sharp  Cramping, Gnawing
      • Stimulus:  Inflammation,  Distention, Traction
      • Pressure
    • Pain
      • Un-referred Visceral Pain
      • ANS innervations:
      • bilateral hence pain is midline except:
      • Kidneys
      • Ureters
      • Cecum
      • Ascending colon
      • Descending colon
      • Sigmoid colon
    • Pain
      • Un-referred Visceral Pain
      •  Midline location is the result of embryologic development of Gut
      •  Epigastric - Foregut:
      • Oropharynx
      • 2 nd portion of duodenum
      • Liver
      • Spleen
      • Pancreas
    • Pain
      • Un-referred Visceral Pain
      •  Periumbilical- Midgut:
      • Distal duodenum
      • Jejunum
      • Ileum
      • Appendix
      • Ascending colon
      • Proximal transverse colon
      •  Hypogastric- Remainder of Hindgut= Colon
      • down to c loaca
    • Pain
      •  REFERRED PAIN
      • Result of afferent neurons that innervate two entirely separate anatomically distinct structures that have a common embryologic
      • origin
    • Pain
      •  REFERRED PAIN
      • 4 th Cervical Nerve Route
      • 1. Parietal peritoneum of the
      • diaphragm
      • 2. Area around the shoulder
      • 3. Supraclavicular hollow
      • e.g. Kehr sign = Pain underneath the diaphragm felt at the tip of the shoulder
    • Pain
      •  REFERRED PAIN
      •  Thoracic Afferents T6-T8
      • Innervates :
      • 1. Right sub-scapular area
      • 2. Biliary tree
      • 3. Liver
      • 4. Peri-pancreatic area
    • Pain
      •  REFERRED PAIN
      •  10 th Thoracic Nerve Route
      • Irritation to the kidney or ureter
      • e.g. In male= Flank and genital
      • pain classically testicular pain
      • In females this is referred to the
      • labia
    • Acute Abdominal Pain
      • Clinical Manifestations
      • Sudden Onset =more likely surgical
      • Gradual Onset= inflammatory process
      • or slower progressive obstruction
      • Nausea and Vomiting 6-12 hours after
      • onset of pain=Obstruction lower GIT
    • Acute Abdominal Pain
      • Clinical Manifestations
      • Foregut and Midgut inflammation
      • often followed by:
      • Anorexia
      • Nausea
      • vomiting
      • Sensory afferents carried by Vagal fibers
    • Acute Abdominal Pain
      • Physical Examination
      • Inspection
      • Scaphoid = Normal
      • Distention= Abnormal
      • Thin Individuals= bowel loops seen
    • Acute Abdominal Pain
      • Auscultation
      • Absent =No bowel sound in a minute
      • 1. Ileus
      • 2. Hypokalemia
      • 3. Peritonitis
      • 4. Hypomagnesemia
      • 5. Mesenteric thrombosis
      • 6. Narcotic Overdose
    • Acute Abdominal Pain
      •  Auscultation
      • Hypoactive
      • 1. Hypokalemia
      • 2. Inflammation
      • 3. Ischemic bowel disease
    • Acute Abdominal Pain
      • Auscultation
      •  Hyperactive
      • 1. Early small bowel obstruction
      • 2. Diverticulitis
      • Percussion
      • Palpation
    • Acute Abdominal Pain
      • Laboratory Evaluation
      • CBC
      • Urinalysis
      • Blood Chemistry e.g. Amylase; Liver
      • function test
      • Pregnancy Test
      • ECG
    • Acute Abdominal Pain
      •  Radiologic Examination
      • 1. Pneumoperitoneum
      • 2. Calculi
      • 3. Ileus
      • 4. Air fluid level
      • 5. Aerobilia
      • 6. Fat lines
    • Acute Abdominal Pain
      • Ultrasound
      • 1. Suspected Pancreatic
      • 2. Hepatobiliary disease
      • 3. Phlegmon
      • 4. Abscess
      • 5. Pseudocyst
      • 6. Gynecologic Problem that mimics GIT
      • disease
    • Acute Abdominal Pain
      •  Ultrasound
      • (F.A.S.T.) detecting Hemoperitoneum
      • in Blunt Trauma
      • 1. Sensitivity of 93.4%
      • 2. Specificity of 98.7%
      • 3. Accuracy of 97.5%
    • Acute Abdominal Pain
      •  Surgical Decision Making
      • 1. Usually made by History
      • 2. Physical Examination is confirmatory
      • 3. Laboratory tests are focused on the
      • suspected diagnosis
    • Acute Abdominal Pain
      • Nature of Surgical Decision Making in
      • Acute Abdomen does not require
      • specific diagnosis, but
      • 1. Plan of action
      • 2. Indication for the operation
      • 3. Timing and Approach
    • Intermittent and Recurrent Abdominal Pain
      • 1. Various Hematologic disorders produce
      • abdominal pain
      • 2. Clinical Manifestations relate to the
      • occurrence of crisis; anemia; jaundice;
      • splenomegaly; and cholelithiasis
      • 3. Due to disturbed gastrointestinal motility
      • or alternating areas of spasm and
      • dilatation
    • Chronic Abdominal Pain
      • If persistent-- is a clear pathophysiologic
      • abnormality such as:
      • 1. Chronic pancreatitis
      • 2. Pancreatic Malignancy
      • 3. Colonic Malignancy
      • May arise from the abdominal wall
      • 1. Iatrogenic peripheral nerve injuries
      • 2. Hernias
      • 3. Myofascial Pain Syndrome
    • Intractable Abdominal Pain
      • 1. Challenging and sometimes a frustrating
      • problem
      • 2. Opiate Analgesics, if given in sufficient
      • dosage, usually can control abdominal
      • pain, however risk of addiction is always
      • there undermining patient’s ability to
      • function effectively
      • 3. In Properly selected patients, interruption
      • of pain pathway (Splanchnicectomy) is
      • suggested
    • II FEVER
      • Not dangerous unless it is unusually high
      • Often a postoperative event often:
      • 1. A Thermostat reset
      • 2. Response to intraoperative body cooling
      • 3. Result of Normal Cytokine Activation
    • II FEVER
      • Indication of Illness such as:
      • 1. Infection
      • 2. Inflammation
      • 3. Autoimmune Disease
      • 4. Neoplasia
      •  If persistent, indicative of infectious complication
    • II FEVER
      • Pathophysiology
      • Inflammatory Response activates Cytokines
      • that are locally released in the brain or into
      • the bloodstream peripherally acting on the
      • hypothalamus in Endocrine fashion
    • II FEVER
      •  Pathophysiology
      • Activated Macrophages also liberates pyrogens
      • 1. Interleukin
      • 2. TNF
      • 3. Interferon
      • Upward resetting of a thermoregulatory
      • Apparatus,triggering 2 physiologic mechanisms:
      • 1. Vasoconstriction
      • 2. Increase Heat production by shivering
    • II FEVER
      • Clinical Manifestation
      • Those of GIT origin=Infection in the
      • Abdominal Cavity
      • Monomicrobial infections include:
      • 1. Biliary Tract Infection
      • 2. Spontaneous or Primary Peritonitis
    • II FEVER
      • Clinical Manifestation
      • Intraabdominal Sepsis > polymicrobial
      • Fever of reactivated Crohn’s disease
      • Established Infection postop 10-20%
      • 20% of unknown origin 2ndary to CA.
    • III Anorexia
      • Complicates many diseases
      • Indicates a significant degree of
      • inflammation
      • Common in liver disease, through CNS
      • mechanism, probably mediated at least
      • in part by Ammonia & Neuropeptide Y.
    • III Anorexia
      • Common cause is Carcinoma, usually
      • with significant tumor burden
      • Postoperatively associated with loss of
      • taste, especially in diarrhea whose zinc
      • stores are chronically low. Give 220 mgs
      • daily and taste returns in 10 days to 3 weeks.
    • III Anorexia
      • Pathophysiology
      • Complex and Multifaceted. In Animals
      • independent variables alter food intake:
      • 1. Changes in glucose utilization rate
      • 2. Changes in rate of lipid metabolism
      • 3. Alteration in brain & peripheral peptides.
      • 4. Imbalance in plasma & brain amino profiles
      • 5. Increase & decrease neurotransmitter activity
      • 6. Alteration in Cytokine levels
    • III Anorexia
      • Pathophysiology
      • Hypothalamus is feeding center of the brain
      • Lateral area lesions = anorexia
      • Ventro-medial region lesions causes
      • hyperphagia and obesity
      • Vagal afferents , important in communicating
      • peripheral nutrition related information from
      • the GIT or from Glucose sensitive cells in the
      • liver
    • III Anorexia
      • Pathophysiology
      • Galanin located in several brain regions appear to selectively stimulate fat intake
      • According to Glucostatic hypothesis of feeding,
      • increased use of glucose signal satiety, and
      • decreased glucose metabolism is associated
      • with hunger
    • III Anorexia
      • Pathophysiology
      • The discovery of obese gene protein( leptin)
      • provides a proposed mechanism for modula-
      • tion of food intake and body weight that is
      • directly related to adipose tissue mass. Level
      • of circulating leptin increase as the amount
      • of adipose tissue increases
    • III Anorexia
      • Pathophysiology
      • Elevated activity in Serotonin neurons
      • also inhibit feeding; reducing serotonin
      • levels usually increases the amount of
      • feeding elicited by orexigenic agents
    • III Anorexia
      • Pathophysiology
      • Carbohydrate intake appears to be under
      • Neuropeptide Y control
      • Adrenalectomy reduces feeding elicited
      • by intrahypothalamic Neuropeptide Y
      • or nor epinephrine
    • III Anorexia
      • CANCER Anorexia
      • Results from tumor-induced aberrations
      • of neurochemical mechanisms that
      • normally control hunger and satiety
      • Weight loss & Cachexia have significant
      • negative prognostic implications
    • III Anorexia
      • CANCER Anorexia
      • Weight loss of 10-15 % during 3 to 4
      • months is one of two prime indicators
      • that a patient may be nutritionally or
      • immunologically impaired
    • IV HEARTBURN AND DYSPEPSIA
      • Substernal burning associated w/ bitter taste
      • Normal individuals experience this when lying
      • down or bending over after overeating &
      • gastric capacity is exceeded
    • IV HEARTBURN AND DYSPEPSIA
      • Esophagus is normally protected by:
      • 1. Competent Lower esophageal sphincter
      • 2. Rapid Esophageal clearing of reflux material
      • 3. Neutralization of refluxed acid by bicarbonate
      • rich saliva
      • 4. Intact mucosal diffusion barrier
      • Most common clinical abnormality of
      • esophageal motility is incompetence of LES
    • IV HEARTBURN AND DYSPEPSIA
      • Dyspepsia is a non specific term given
      • to a collection of symptoms involving:
      • 1. Esophagus
      • 2. Stomach
      • 3. Duodenum
      • 4. Biliary Tree
      • 5. Pancreas
    • IV HEARTBURN AND DYSPEPSIA
      • It is a postprandial complaint involving:
      • 1. Substernal pressure
      • 2. Epigastric distress
      • 3. Nausea
      • 4. Bloating
      • Three (3%) of these patients have angina
    • IV HEARTBURN AND DYSPEPSIA
      • Work-up should include:
      • 1. Cineflouroscopy
      • 2. Contrast Radiography
      • 3. Upper GI series
      • 4. Endoscopy and Biopsy
    • IV HEARTBURN AND DYSPEPSIA
      • Manometry if esophageal spasm is
      • suspected
      • Relationship of symptoms to eating and
      • other activities may give clues to the
      • diagnosis
    • V DYSPHAGIA
      • Disturbances in swallowing can be
      • categorized according to the etiologies:
      • 1. Degenerative
      • 2. Functional
      • 3. Inflammatory
      • 4. Mechanical
      • 5. Autoimmune
      • 6. Neoplastic
      • Odynophagia= Painful swallowing
    • VI NAUSEA AND VOMITING
      • 1. May be related or unrelated to diseases
      • of the gastrointestinal tract
      • 2. Vomiting may result whenever any part
      • of the GIT excessively irritated, over-
      • distended, or excitable
      • 3. Duodenal distention is a particularly
      • potent stimulus for vomiting
      • 4. Vagal and Sympathetic afferents carry
      • impulses from the GIT to the bilateral
      • vomiting center in the medulla
    • VI NAUSEA AND VOMITING
      • Rapidly changing directions of motion
      • stimulate receptors in the labyrinthine
      • apparatus, impulses are carried into the
      • vestibular nuclei into the cerebellum to
      • vomiting center
    • VI NAUSEA AND VOMITING
      • Ischemia to the vomiting center in:
      • 1. Increased intracranial pressure
      • 2. Anemia
      • 3. Vascular occlusion
      • 4. Shock
      • 5. Severe pain
    • VI NAUSEA AND VOMITING
      • A variety of antibiotics directly affecting
      • the GIT may cause nausea & vomiting:
      • 1. Erythromycin
      • 2. Bactrim
      • 3. Neomycin
    • VI NAUSEA AND VOMITING
      • Acute Nausea and Vomiting due to:
      • 1. Inflammation or infectious agents
      • affecting the GIT
      • 2. Neoplastic disease
      • 3. Mechanical obstruction at any level
    • VII ABDOMINAL DISTENTION,ERUCTATION AND FLATULENCE
      • Most of these patient’s are Aerophagics;
      • they swallow too much Air when they
      • eat too quickly or talk too much when
      • they eat. Hyperactive bowel sounds is
      • the rule.
    • VII ABDOMINAL DISTENTION,ERUCTATION AND FLATULENCE
      • Chronic Eructation may be an indication
      • of chronic pathology
      • Lactase deficiency can result in Eructation
      • and Flatulence
    •  
    • VIII CONSTIPATION
      • Most often Mechanical in origin
      • In trauma with retroperitoneal hematoma
      • Can be a result of:
      • 1. Psychologic factor
      • Improper training
      • 2. Dietary constituents
      • 3. Laxatives & drugs
    • VIII CONSTIPATION
      • Can be a result of:
      • 4. Neurogenic causes
      • a. Tabes Dorsalis
      • b. Multiple Sclerosis
      • c. Spinal Cord Tumor
      • 5. Decreased skeleto-muscular power
    • IX DIARRHEA
      • Pathophysiological Mechanisms
      • 1. Luminal secretion of solute or water
      • 2. Exudation or the loss of protein, blood and
      • mucus
      • 3. Osmotic retention of water
      • 4. Abnormal or disordered contact between
      • chyme and the absorptive surface of bowel
      • History is important in ascertaining whether
      • this is new, chronic, or recurrent problem
    • X ILEUS
      • Three Types
      • 1. Adynamic or inhibition ileus
      • a. Most Common
      • b. Inhibition of normal neuromuscular activity
      • 2. Spastic Ileus with a tightly contracted bowel
      • without propulsive activity
      • 3. Ischemic Ileus from either low flow( non-
      • occlusive ischemia) or vascular occlusion
      • Coordinated motility is impossible because
      • of dying musculature
    • X ILEUS
      • Adynamic ileus occurs after a variety of
      • abdominal operations
      • 1. Gastric ileus last approximately 2 days
      • 2. Colonic ileus last for approximately 3-4 days
      • 3. In the normal postoperative course, the small
      • bowel continues to function
    • X ILEUS
      • If ileus is prolonged possible causes includes:
      • 1. Metabolic
      • 2. septic
      • 3. Mechanical or inflammatory
    • XI INTESTINAL OBSTRUCTION
      • Classification
      • 1. Extra luminal( including adhesions and
      • Neoplastic Disease
      • 2. Intra luminal( such as gallstone ileus & stricture
      • 3. Intra mural( such as crohn’s disease
      • Small bowel obstruction secondary to adhesion
      • constitutes 60-80%
      • Hernia constitutes 15-20%
      • Colonic Obstruction due to CA is 60%
    • XI INTESTINAL OBSTRUCTION
      • Partial Obstruction and Pseudo-obstruction
      • Chronic Nausea and Vomiting
      • When intestinal, bowel sounds reflect amphoric
      • fluid filled bowel loops
      • Succussion spasm when pylorus & duodenum
      • are obstructed
    • XI INTESTINAL OBSTRUCTION
      • Partial Obstruction and Pseudo-obstruction
      • Chronic intestinal pseudo-obstruction involves
      • abnormalities in:
      • Intestinal muscle( myopathic)
      • Nervous system( myenteric) e.g. Chagas’
      • disease and infiltrative diseases
    • XI INTESTINAL OBSTRUCTION
      • Partial Obstruction and Pseudo-obstruction
      • 1. Pseudo-obstruction postop is most dangerous
      • Vagotomized patients
      • Intestinal Operation
      • 2. Early recognition of Pseudo-obstruction is
      • critical to proper therapy
      • a. Biopsy of intestine may or may not reveal
      • loss of myenteric plexi
      • b. Full thickness rectal biopsy( Hirschsprung’s
      • Disease) is suspected
    • XI INTESTINAL OBSTRUCTION
      • Mechanical Obstruction
      • 1. Physiologic derangement if intact blood supply
      • a. Accumulation of fluid and Gas above the
      • point of obstruction
      • b. Altered bowel motility leading to systemic
      • derangement
      • 2. Gamble showed that mortality in simple type
      • was due to:
      • a. Loss of fluid and electrolytes by vomiting
      • b. Sequestration of fluid in obstructed bowel
    • XI INTESTINAL OBSTRUCTION
      • Mechanical Obstruction
      • 3. After 48 hours, rate of entry of water into the
      • intestinal lumen increases as a consequence
      • of blood to lumen flux
      • 4. Prostaglandin release in response to bowel
      • distention, increases secretion to obstructed
      • loops
      • 5.Interference with the mesenteric blood supply
      • is the most serious complication of intestinal
      • obstruction
    • XI INTESTINAL OBSTRUCTION
      • Close loop Obstruction
      • 1. Both afferent & efferent limbs are obstructed
      • 2. Rapid progression of strangulation of blood
      • supply before manifestations of obstruction
      • becomes obvious
      • 3. Abdominal distention does not occur
        
    • XI INTESTINAL OBSTRUCTION
      • Colon Obstruction
      • 1. Fluid and Electrolyte sequestration progresses
      • more slowly
      • 2. Progressive distention is the most dangerous
      • aspect of non-strangulated colon obstruction
        
    • XI INTESTINAL OBSTRUCTION
      • Clinical Manifestations
      • The distance of the obstruction from the ligament
      • of Treitz can be ascertained by:
      • 1. How long before vomiting takes place after
      • the onset of pain
      • 2. The nature of the vomitus
       
    • XI INTESTINAL OBSTRUCTION
      • Clinical Manifestations
      • Cardinal Signs and Symptoms of Intestinal
      • Obstruction:
      • 1. Crampy Abdominal Pain
      • 2. Nausea & Vomiting
      • 3. Obstipation
      • 4. Abdominal Distention
       
    • XII GASTROINTESTINAL BLEEDING
      • 1. Has high morbidity & mortality particularly in
      • the elderly
      • 2. Accurate diagnosis is critical before significant
      • amounts ( 4-6 units) of blood has been lost
      • 3. Bleeding represents the initial symptoms of
      • gastrointestinal disease in more than 1/3 of
      • patients & in 70% there is no history of
      • bleeding episode
    • XII GASTROINTESTINAL BLEEDING
      • 4.Eighty( 80%) will stop spontaneously without
      • intervention
      • 5. Flexible endoscopy and arteriography play an
      • interesting role in the diagnostic & therapeutic
      • management
    • XII GASTROINTESTINAL BLEEDING
      • Terminologies
      • 1. Hematemesis is vomiting of blood , either
      • digested in the stomach or fresh & unaltered
      • 2 . Melena is the per anal passage of stools
      • with altered blood that are black and tarry
      • 3. Hematochezia is the passage of liquid
      • blood or blood clots of varied brightness or
      • color, maroon to bright red
    • XII GASTROINTESTINAL BLEEDING
      • Terminologies
      • As little as 50-60m l of blood produce melena
      • Melena can persist for 5-7 days after a 2-unit
      • (significant) bleed
      • Approximately 10 ml bleeding/ day (Guaiac +)
    • XII GASTROINTESTINAL BLEEDING
      • Upper GI Bleeding
      • Bleeding above the ligament of Treitz
      • include:
      • 1. Esophagitis
      • 2. Esophageal Varices
      • 3. Gastritis
      • 4. Peptic Ulcer
      • 5. Mallory Weiss
      • 6. Gastric Carcinoma
      • 7. Hemobilia
    • XII GASTROINTESTINAL BLEEDING
      • Upper GI Bleeding
      • 8. Stress Ulcer ( Documented Risk Factors)
      • a. Multiple System Trauma
      • b. Hypotension
      • c. Respiratory Failure
      • d. Sepsis
      • e. Jaundice
      • f . Burns
      • g. Renal Failure
      • h . Recent Surgery
    • XII GASTROINTESTINAL BLEEDING
      • Lower GI Bleeding
      • Bleeding below the ligament of Treitz
      • includes:
      • 1. Diverticulitis
      • 2. Angiodysplasia
      • 3. Ulcerative Colitis
      • 4. Malignancy
    • XII GASTROINTESTINAL BLEEDING
      • Lower GI Bleeding
      • Work-up
      • 1. Rectal Examination
      • 2. Proctosigmoidoscopy
      • 3.Technetium 99 scan (Tag RBC)
      • 4. Arteriography
      • 5. Barium Enema
    • XIII JAUNDICE
      • GIT related Causes :
      • 1. Increased pigment production secondary to
      • tissue infarction
      • 2. Inflammatory disease; e.g. spontaneous
      • peritonitis
      • 3. Appendicitis, complicated by coliform organism
      • can give jaundice without pyelephlebiti
      • 4. Ampullary Carcinoma or Carcinoma of the
      • duodenum
    •  
    • THANK YOU!!!