Manifestations Of Gastrointestinal Diseases Copy

Manifestations Manifestations of of

GastrointestinGastrointestinal Diseasesal Diseases

Celso M. Fidel MD,FPSGS,FPCSCelso M. Fidel MD,FPSGS,FPCS

Diplomate Philippine Board of Diplomate Philippine Board of SurgerySurgery

What are These Manifestations?What are These Manifestations? 1. PAIN1. PAIN

2. FEVER2. FEVER

3. ANOREXIA3. ANOREXIA

4. HEARTBURN and DYSPEPSIA4. HEARTBURN and DYSPEPSIA

5. DYSPHAGIA5. DYSPHAGIA

6. NAUSEA and VOMITING6. NAUSEA and VOMITING

7. ABDOMINAL DISTENTION, 7. ABDOMINAL DISTENTION,

ERUCTATION and FLATULENCEERUCTATION and FLATULENCE

8. CONSTIPATION8. CONSTIPATION

9. DIARRHEA9. DIARRHEA

What are These Manifestations?What are These Manifestations? 10. ILEUS 10. ILEUS

11. INTESTINAL OBSTRUCTION11. INTESTINAL OBSTRUCTION

a. Partial Obstruction and Pseudo-obstructiona. Partial Obstruction and Pseudo-obstruction

b. Mechanical Obstructionb. Mechanical Obstruction

c. Closed Loop Obstructionc. Closed Loop Obstruction

d. Colon Obstructiond. Colon Obstruction

12. GASTROINTESTINAL BLEEDING12. GASTROINTESTINAL BLEEDING

a. Upper GI Bleedinga. Upper GI Bleeding

b. Lower GI Bleedingb. Lower GI Bleeding

13. JAUNDICE 13. JAUNDICE

I PainI Pain

Most common symptom of GIT diseaseMost common symptom of GIT disease

Three kinds have been described in gen.Three kinds have been described in gen.

1. Superficial or Cutaneous pain1. Superficial or Cutaneous pain

2. Deep pain from:2. Deep pain from:

MusclesMuscles

TendonsTendons

JointsJoints

FasciaFascia

3. Visceral pain3. Visceral pain

I PainI Pain Two Types of PainTwo Types of Pain

1. Somatic Pain 2. Visceral Pain1. Somatic Pain 2. Visceral Pain

Pathway: Pathway: A-delta fibers A-delta fibers Autonomic C-type fibers Autonomic C-type fibers

Receptor: Receptor: Parietal, Muscle Parietal, Muscle Visceral Visceral and Skinand Skin

Specific Specific Well localized Well localized Poorly localized Poorly localized

Description Description Sharp Sharp Cramping, Gnawing Cramping, Gnawing

Stimulus: Stimulus: Inflammation, Inflammation, Distention, Traction Distention, Traction PressurePressure

PainPain Un-referred Visceral PainUn-referred Visceral Pain

ANSANS innervations:innervations: bilateral hence pain is midline bilateral hence pain is midline

except:except: Kidneys Kidneys Ureters Ureters Cecum Cecum Ascending colonAscending colon Descending colonDescending colon Sigmoid colonSigmoid colon

PainPain Un-referred Visceral PainUn-referred Visceral Pain Midline location is the result of Midline location is the result of

embryologic development of Gut embryologic development of Gut EpigastricEpigastric- Foregut:- Foregut: OropharynxOropharynx 22ndnd portion of duodenum portion of duodenum Liver Liver SpleenSpleen PancreasPancreas

PainPain Un-referred Visceral PainUn-referred Visceral Pain Periumbilical- Midgut:Periumbilical- Midgut: Distal duodenumDistal duodenum JejunumJejunum IleumIleum AppendixAppendix Ascending colonAscending colon Proximal transverse colonProximal transverse colon

Hypogastric- Remainder of Hindgut= Colon Hypogastric- Remainder of Hindgut= Colon

down to down to ccloacaloaca

PainPain

REFERRED PAINREFERRED PAIN Result of afferent neurons that Result of afferent neurons that

innervate two entirely separate innervate two entirely separate anatomically distinct structures anatomically distinct structures that have a that have a common embryologiccommon embryologic

originorigin

PainPain

REFERRED PAINREFERRED PAIN

44thth Cervical Nerve RouteCervical Nerve Route

1. Parietal peritoneum of the 1. Parietal peritoneum of the

diaphragmdiaphragm

2. Area around the shoulder2. Area around the shoulder

3. Supraclavicular hollow3. Supraclavicular hollow

e.g. e.g. Kehr signKehr sign= Pain underneath the = Pain underneath the diaphragm felt at the tip of the diaphragm felt at the tip of the shouldershoulder

PainPain


Thoracic Afferents T6-T8Thoracic Afferents T6-T8

Innervates :Innervates :

1. Right sub-scapular area1. Right sub-scapular area

2. Biliary tree2. Biliary tree

3. Liver 3. Liver

4. Peri-pancreatic area 4. Peri-pancreatic area

PainPain


1010thth Thoracic Nerve Route Thoracic Nerve Route

Irritation to the kidney or ureterIrritation to the kidney or ureter

e.g. In male= Flank and genital e.g. In male= Flank and genital

pain classically testicular painpain classically testicular pain

In females this is referred to the In females this is referred to the labia labia

Acute Abdominal PainAcute Abdominal Pain Clinical ManifestationsClinical Manifestations

Sudden Onset =more likely surgicalSudden Onset =more likely surgical

Gradual Onset= inflammatory processGradual Onset= inflammatory process

or slower progressive obstructionor slower progressive obstruction

Nausea and Vomiting 6-12 hours afterNausea and Vomiting 6-12 hours after

onset of pain=Obstruction lower GITonset of pain=Obstruction lower GIT

Acute Abdominal PainAcute Abdominal Pain Clinical ManifestationsClinical Manifestations

ForegutForegut and and MidgutMidgut inflammation inflammation

often followed by: often followed by:

AnorexiaAnorexia

Nausea Nausea

vomitingvomiting

Sensory afferents carried by Vagal fibers Sensory afferents carried by Vagal fibers

Acute Abdominal Pain Acute Abdominal Pain Physical ExaminationPhysical Examination

InspectionInspection

Scaphoid = NormalScaphoid = Normal

Distention= AbnormalDistention= Abnormal

Thin Individuals= bowel loops seenThin Individuals= bowel loops seen

Acute Abdominal Pain Acute Abdominal Pain

AuscultationAuscultation

Absent =No bowel sound in a minuteAbsent =No bowel sound in a minute

1. Ileus 1. Ileus

2. Hypokalemia2. Hypokalemia

3. Peritonitis 3. Peritonitis

4. Hypomagnesemia4. Hypomagnesemia

5. Mesenteric thrombosis5. Mesenteric thrombosis

6. Narcotic Overdose6. Narcotic Overdose

Acute Abdominal PainAcute Abdominal Pain


HypoactiveHypoactive

1. Hypokalemia 1. Hypokalemia

2. Inflammation2. Inflammation

3. Ischemic bowel disease3. Ischemic bowel disease



HyperactiveHyperactive

1. Early small bowel obstruction 1. Early small bowel obstruction

2. Diverticulitis2. Diverticulitis

PercussionPercussion

PalpationPalpation

Acute Abdominal PainAcute Abdominal Pain Laboratory EvaluationLaboratory Evaluation

CBCCBC

UrinalysisUrinalysis

Blood Chemistry e.g. Amylase; Liver Blood Chemistry e.g. Amylase; Liver

function testfunction test

Pregnancy TestPregnancy Test

ECGECG


Radiologic Examination Radiologic Examination

1. Pneumoperitoneum1. Pneumoperitoneum

2. Calculi 2. Calculi

3. Ileus3. Ileus

4. Air fluid level4. Air fluid level

5. Aerobilia5. Aerobilia

6. Fat lines6. Fat lines

Acute Abdominal PainAcute Abdominal Pain UltrasoundUltrasound 1. Suspected Pancreatic 1. Suspected Pancreatic 2. Hepatobiliary disease2. Hepatobiliary disease 3. Phlegmon3. Phlegmon 4. Abscess4. Abscess 5. Pseudocyst5. Pseudocyst 6. Gynecologic Problem that mimics GIT6. Gynecologic Problem that mimics GIT diseasedisease

Acute Abdominal PainAcute Abdominal Pain UltrasoundUltrasound (F.A.S.T.) detecting Hemoperitoneum(F.A.S.T.) detecting Hemoperitoneum in Blunt Traumain Blunt Trauma 1. Sensitivity of 93.4%1. Sensitivity of 93.4%

2. Specificity of 98.7%2. Specificity of 98.7%

3. Accuracy of 97.5%3. Accuracy of 97.5%

Acute Abdominal PainAcute Abdominal Pain Surgical Decision MakingSurgical Decision Making

1. Usually made by History1. Usually made by History

2. Physical Examination is confirmatory2. Physical Examination is confirmatory

3. Laboratory tests are focused on the 3. Laboratory tests are focused on the

suspected diagnosissuspected diagnosis

Acute Abdominal PainAcute Abdominal Pain Nature of Surgical Decision Making inNature of Surgical Decision Making in

Acute Abdomen does not require Acute Abdomen does not require

specific diagnosis, butspecific diagnosis, but

1. Plan of action1. Plan of action

2. Indication for the operation2. Indication for the operation

3. Timing and Approach3. Timing and Approach

Intermittent and Recurrent Abdominal PainIntermittent and Recurrent Abdominal Pain

1. Various Hematologic disorders produce 1. Various Hematologic disorders produce

abdominal painabdominal pain

2. Clinical Manifestations relate to the2. Clinical Manifestations relate to the

occurrence of crisis; anemia; jaundice;occurrence of crisis; anemia; jaundice;

splenomegaly; and cholelithiasissplenomegaly; and cholelithiasis

3. Due to disturbed gastrointestinal motility3. Due to disturbed gastrointestinal motility

or alternating areas of spasm andor alternating areas of spasm and

dilatation dilatation

Chronic Abdominal PainChronic Abdominal Pain If persistent-- is a clear pathophysiologicIf persistent-- is a clear pathophysiologic

abnormality such as:abnormality such as:

1. Chronic pancreatitis1. Chronic pancreatitis

2. Pancreatic Malignancy2. Pancreatic Malignancy

3. Colonic Malignancy 3. Colonic Malignancy

May arise from the abdominal wallMay arise from the abdominal wall

1. Iatrogenic peripheral nerve injuries1. Iatrogenic peripheral nerve injuries

2. Hernias 2. Hernias

3. Myofascial Pain Syndrome 3. Myofascial Pain Syndrome

Intractable Abdominal PainIntractable Abdominal Pain

1. Challenging and sometimes a frustrating1. Challenging and sometimes a frustrating

problem problem

2. Opiate Analgesics, if given in sufficient2. Opiate Analgesics, if given in sufficient

dosage, usually can control abdominaldosage, usually can control abdominal

pain, however risk of addiction is pain, however risk of addiction is alwaysalways

there undermining patient’s ability tothere undermining patient’s ability to

function effectivelyfunction effectively

3. In Properly selected patients, 3. In Properly selected patients, interruptioninterruption

of pain pathway (Splanchnicectomy) isof pain pathway (Splanchnicectomy) is

suggested suggested

II FEVERII FEVER

Not dangerous unless it is unusually highNot dangerous unless it is unusually high

Often a postoperative event often:Often a postoperative event often:

1. A Thermostat reset1. A Thermostat reset

2. Response to intraoperative body cooling2. Response to intraoperative body cooling

3. Result of Normal Cytokine Activation3. Result of Normal Cytokine Activation

II FEVERII FEVER

Indication of Illness such as:Indication of Illness such as:

1. Infection1. Infection

2. Inflammation2. Inflammation

3. Autoimmune Disease 3. Autoimmune Disease

4. Neoplasia4. Neoplasia

If persistent, indicative of infectious complicationIf persistent, indicative of infectious complication

II FEVERII FEVER

PathophysiologyPathophysiology

Inflammatory Response activates Inflammatory Response activates Cytokines Cytokines that are locally released in the brain or intothat are locally released in the brain or into the bloodstream the bloodstream peripherally acting on theperipherally acting on the hypothalamus hypothalamus in Endocrine fashion in Endocrine fashion

II FEVERII FEVER

PathophysiologyPathophysiology Activated Macrophages also liberates Activated Macrophages also liberates

pyrogenspyrogens 1. Interleukin 1. Interleukin 2. TNF2. TNF 3. Interferon3. Interferon Upward resetting of a thermoregulatory Upward resetting of a thermoregulatory Apparatus,triggering 2 physiologic Apparatus,triggering 2 physiologic

mechanisms:mechanisms: 1. Vasoconstriction1. Vasoconstriction

2. Increase Heat production by shivering2. Increase Heat production by shivering

II FEVERII FEVER

Clinical ManifestationClinical Manifestation

Those of GIT origin=Infection in the Those of GIT origin=Infection in the

Abdominal CavityAbdominal Cavity

Monomicrobial infections include:Monomicrobial infections include:

1. Biliary Tract Infection1. Biliary Tract Infection

2. Spontaneous or Primary Peritonitis2. Spontaneous or Primary Peritonitis

II FEVERII FEVER

Clinical ManifestationClinical Manifestation

Intraabdominal Sepsis > polymicrobialIntraabdominal Sepsis > polymicrobial

Fever of reactivated Crohn’s diseaseFever of reactivated Crohn’s disease

Established Infection postop 10-20%Established Infection postop 10-20%

20% of unknown origin 2ndary to CA.20% of unknown origin 2ndary to CA.

III AnorexiaIII Anorexia

Complicates many diseasesComplicates many diseases

Indicates a significant degree of Indicates a significant degree of inflammationinflammation

Common in liver disease, through CNS Common in liver disease, through CNS mechanism, probably mediated at leastmechanism, probably mediated at least in part by Ammonia & Neuropeptide Y.in part by Ammonia & Neuropeptide Y.


Common cause is Carcinoma, usually Common cause is Carcinoma, usually with significant tumor burdenwith significant tumor burden

Postoperatively associated with loss of Postoperatively associated with loss of taste, especially in diarrhea whose zinctaste, especially in diarrhea whose zinc stores are chronically low. stores are chronically low. Give 220Give 220 mgs mgs daily and taste returns in 10 days to 3 weeks.daily and taste returns in 10 days to 3 weeks.



Complex and Multifaceted. In AnimalsComplex and Multifaceted. In Animals

independent variables alter food intake:independent variables alter food intake:

1. Changes in glucose utilization rate1. Changes in glucose utilization rate

2. Changes in rate of lipid metabolism2. Changes in rate of lipid metabolism

3. Alteration in 3. Alteration in brain & peripheral peptides.brain & peripheral peptides.

4. Imbalance in plasma & brain amino profiles4. Imbalance in plasma & brain amino profiles

5. Increase & decrease neurotransmitter activity5. Increase & decrease neurotransmitter activity

6. Alteration in Cytokine levels 6. Alteration in Cytokine levels



Hypothalamus is feeding center of the brain Hypothalamus is feeding center of the brain

Lateral area lesions = anorexiaLateral area lesions = anorexia

Ventro-medial region lesions causes Ventro-medial region lesions causes

hyperphagia and obesityhyperphagia and obesity

Vagal afferentsVagal afferents,, important in important in communicatingcommunicating

peripheral nutrition related information fromperipheral nutrition related information from

the GIT or from Glucose sensitive cells in the the GIT or from Glucose sensitive cells in the

liverliver



Galanin located in several brain regions Galanin located in several brain regions appear to selectively stimulate fat intakeappear to selectively stimulate fat intake

According to Glucostatic hypothesis of feeding,According to Glucostatic hypothesis of feeding,

increased use of glucose signal satiety, andincreased use of glucose signal satiety, and

decreased glucose metabolism is associateddecreased glucose metabolism is associated

with hungerwith hunger



The discovery of obese gene protein( leptin)The discovery of obese gene protein( leptin)

provides a proposed mechanism for modula-provides a proposed mechanism for modula-

tion of food intake and body weight that istion of food intake and body weight that is

directly related to adipose tissue mass. Leveldirectly related to adipose tissue mass. Level

of circulating leptin increase as the amount of circulating leptin increase as the amount

of adipose tissue increases of adipose tissue increases



Elevated activity in Serotonin neurons Elevated activity in Serotonin neurons

also inhibit feeding; reducing serotoninalso inhibit feeding; reducing serotonin

levels usually increases the amount oflevels usually increases the amount of

feeding elicited by orexigenic agentsfeeding elicited by orexigenic agents



Carbohydrate intake appears to be underCarbohydrate intake appears to be under

Neuropeptide Y controlNeuropeptide Y control

Adrenalectomy reduces feeding elicited Adrenalectomy reduces feeding elicited

by intrahypothalamic Neuropeptide Yby intrahypothalamic Neuropeptide Y

or nor epinephrine or nor epinephrine


CANCER AnorexiaCANCER Anorexia

Results from tumor-induced aberrationsResults from tumor-induced aberrations

of neurochemical mechanisms thatof neurochemical mechanisms that

normally control hunger and satietynormally control hunger and satiety

Weight loss & Cachexia have significantWeight loss & Cachexia have significant

negative prognostic implicationsnegative prognostic implications


CANCER AnorexiaCANCER Anorexia

Weight loss of Weight loss of 10-15 %10-15 % during 3 to 4 during 3 to 4

months is one of two prime indicatorsmonths is one of two prime indicators

that a patient may be nutritionally orthat a patient may be nutritionally or

immunologically impairedimmunologically impaired

IV HEARTBURN AND DYSPEPSIAIV HEARTBURN AND DYSPEPSIA

Substernal burning associated w/ bitter tasteSubsternal burning associated w/ bitter taste

Normal individuals experience this when lying Normal individuals experience this when lying down or bending over after overeating & down or bending over after overeating & gastric capacity is exceededgastric capacity is exceeded


Esophagus is normally protected by:Esophagus is normally protected by:

1. Competent Lower esophageal sphincter1. Competent Lower esophageal sphincter 2. Rapid Esophageal clearing of reflux material2. Rapid Esophageal clearing of reflux material

3. Neutralization of refluxed acid by bicarbonate3. Neutralization of refluxed acid by bicarbonate rich salivarich saliva 4. Intact mucosal diffusion barrier4. Intact mucosal diffusion barrier

Most common clinical abnormality of Most common clinical abnormality of esophageal motility is incompetence of LESesophageal motility is incompetence of LES


Dyspepsia is a non specific term givenDyspepsia is a non specific term given

to a collection of symptoms involving:to a collection of symptoms involving:

1. Esophagus 1. Esophagus

2. Stomach 2. Stomach

3. Duodenum3. Duodenum

4. Biliary Tree 4. Biliary Tree

5. Pancreas5. Pancreas


It is a postprandial complaint involving:It is a postprandial complaint involving:

1. Substernal pressure1. Substernal pressure

2. Epigastric distress2. Epigastric distress

3. Nausea3. Nausea

4. Bloating4. Bloating

Three (3%) Three (3%) of these patients have anginaof these patients have angina


Work-up should include:Work-up should include:

1. Cineflouroscopy1. Cineflouroscopy

2. Contrast Radiography2. Contrast Radiography

3. Upper GI series3. Upper GI series

4. Endoscopy and Biopsy4. Endoscopy and Biopsy


Manometry if esophageal spasm isManometry if esophageal spasm is

suspectedsuspected

Relationship of symptoms to eating and Relationship of symptoms to eating and

other activities may give clues to theother activities may give clues to the

diagnosisdiagnosis

V DYSPHAGIA V DYSPHAGIA

Disturbances in swallowing can beDisturbances in swallowing can be

categorized according to the etiologies:categorized according to the etiologies:

1. Degenerative1. Degenerative

2. Functional2. Functional

3. Inflammatory3. Inflammatory

4. Mechanical4. Mechanical

5. Autoimmune5. Autoimmune

6. Neoplastic6. Neoplastic

Odynophagia= Painful swallowingOdynophagia= Painful swallowing

VI NAUSEA AND VOMITING VI NAUSEA AND VOMITING

1.1. May be related or unrelated to diseases May be related or unrelated to diseases

of the gastrointestinal tractof the gastrointestinal tract

2. Vomiting may result whenever any part2. Vomiting may result whenever any part

of the GIT excessively irritated, over-of the GIT excessively irritated, over-

distended, or excitabledistended, or excitable

3. Duodenal distention is a particularly 3. Duodenal distention is a particularly

potent potent stimulus for vomitingstimulus for vomiting

4. Vagal and Sympathetic afferents carry4. Vagal and Sympathetic afferents carry

impulses from the GIT to the bilateralimpulses from the GIT to the bilateral

vomiting center in the medullavomiting center in the medulla

VI NAUSEA AND VOMITINGVI NAUSEA AND VOMITING

Rapidly changing directions of motionRapidly changing directions of motion stimulate receptors in the labyrinthinestimulate receptors in the labyrinthine apparatus, impulses are carried into theapparatus, impulses are carried into the vestibular nuclei into the cerebellum tovestibular nuclei into the cerebellum to vomiting center vomiting center


Ischemia to the vomiting center in:Ischemia to the vomiting center in: 1. Increased intracranial pressure1. Increased intracranial pressure 2. Anemia2. Anemia

3. Vascular occlusion3. Vascular occlusion 4. Shock4. Shock

5. Severe pain 5. Severe pain


A variety of antibiotics directly affectingA variety of antibiotics directly affecting

the GIT may cause nausea & vomiting:the GIT may cause nausea & vomiting:

1. Erythromycin1. Erythromycin

2. Bactrim2. Bactrim

3. Neomycin3. Neomycin


Acute Nausea and Vomiting due to:Acute Nausea and Vomiting due to:

1. Inflammation or infectious agents1. Inflammation or infectious agents

affecting the GITaffecting the GIT

2. Neoplastic disease2. Neoplastic disease

3. Mechanical obstruction at any level3. Mechanical obstruction at any level

VII ABDOMINAL DISTENTION,ERUCTATION AND VII ABDOMINAL DISTENTION,ERUCTATION AND FLATULENCEFLATULENCE

Most of these patient’s are Aerophagics;Most of these patient’s are Aerophagics;

they swallow too much Air when theythey swallow too much Air when they

eat too quickly or talk too much wheneat too quickly or talk too much when

they eat. Hyperactive bowel sounds is they eat. Hyperactive bowel sounds is

the rule.the rule.

VII ABDOMINAL DISTENTION,ERUCTATION AND VII ABDOMINAL DISTENTION,ERUCTATION AND FLATULENCEFLATULENCE

Chronic Eructation may be an indicationChronic Eructation may be an indication

of chronic pathologyof chronic pathology

Lactase deficiency can result in Lactase deficiency can result in Eructation Eructation

and Flatulenceand Flatulence

VIII CONSTIPATIONVIII CONSTIPATION Most often Mechanical in originMost often Mechanical in origin In trauma with retroperitoneal hematomaIn trauma with retroperitoneal hematoma Can be a result of:Can be a result of: 1. Psychologic factor1. Psychologic factor Improper trainingImproper training

2. Dietary constituents2. Dietary constituents

3. Laxatives & drugs3. Laxatives & drugs

VIII CONSTIPATIONVIII CONSTIPATION

Can be a result of:Can be a result of: 4. Neurogenic causes4. Neurogenic causes a. Tabes Dorsalis a. Tabes Dorsalis b. Multiple Sclerosisb. Multiple Sclerosis c. Spinal Cord Tumorc. Spinal Cord Tumor

5. Decreased skeleto-muscular power5. Decreased skeleto-muscular power

IX DIARRHEAIX DIARRHEA Pathophysiological MechanismsPathophysiological Mechanisms

1. Luminal secretion of solute or water1. Luminal secretion of solute or water

2. Exudation or the loss of protein, blood and 2. Exudation or the loss of protein, blood and

mucusmucus

3. Osmotic retention of water3. Osmotic retention of water

4. Abnormal or disordered contact between 4. Abnormal or disordered contact between

chyme and the absorptive surface of bowelchyme and the absorptive surface of bowel

History is important in ascertaining whether History is important in ascertaining whether

this is new, chronic, or recurrent problemthis is new, chronic, or recurrent problem

X ILEUSX ILEUS Three TypesThree Types

1. Adynamic or inhibition ileus1. Adynamic or inhibition ileus

a. Most Commona. Most Common

b. Inhibition of normal neuromuscular activityb. Inhibition of normal neuromuscular activity

2. Spastic Ileus with a tightly contracted bowel2. Spastic Ileus with a tightly contracted bowel

without propulsive activitywithout propulsive activity

3. Ischemic Ileus from either low flow( non-3. Ischemic Ileus from either low flow( non-

occlusive ischemia) or vascular occlusionocclusive ischemia) or vascular occlusion

Coordinated motility is impossible becauseCoordinated motility is impossible because

of dying musculatureof dying musculature

X X ILEUSILEUS Adynamic ileus occurs after a variety ofAdynamic ileus occurs after a variety of

abdominal operationsabdominal operations

1. Gastric ileus last approximately 2 days1. Gastric ileus last approximately 2 days

2. Colonic ileus last for approximately 3-4 days2. Colonic ileus last for approximately 3-4 days

3. In the normal postoperative course, the 3. In the normal postoperative course, the smallsmall

bowel continues to functionbowel continues to function

XX ILEUSILEUS

If ileus is prolonged possible causes includes:If ileus is prolonged possible causes includes:

1. Metabolic1. Metabolic

2. septic2. septic

3. Mechanical or inflammatory3. Mechanical or inflammatory

XI INTESTINAL OBSTRUCTIONXI INTESTINAL OBSTRUCTION ClassificationClassification

1. Extra luminal( including adhesions and 1. Extra luminal( including adhesions and

Neoplastic DiseaseNeoplastic Disease

2. Intra luminal( such as gallstone 2. Intra luminal( such as gallstone ileus & strictureileus & stricture

3. Intra mural( such as crohn’s disease3. Intra mural( such as crohn’s disease

Small bowel obstruction secondary to adhesionSmall bowel obstruction secondary to adhesion

constitutes 60-80%constitutes 60-80%

Hernia constitutes 15-20%Hernia constitutes 15-20%

Colonic Obstruction due to CA is 60%Colonic Obstruction due to CA is 60%

XI INTESTINAL OBSTRUCTIONXI INTESTINAL OBSTRUCTION

Partial Obstruction and Pseudo-obstructionPartial Obstruction and Pseudo-obstruction

Chronic Nausea and VomitingChronic Nausea and Vomiting

When intestinal, bowel sounds reflect When intestinal, bowel sounds reflect amphoricamphoric

fluid filled bowel loopsfluid filled bowel loops

Succussion spasm when pylorus & duodenumSuccussion spasm when pylorus & duodenum are obstructedare obstructed

XI INTESTINAL OBSTRUCTIONXI INTESTINAL OBSTRUCTION

Partial Obstruction and Pseudo-obstructionPartial Obstruction and Pseudo-obstruction Chronic intestinal pseudo-obstruction involvesChronic intestinal pseudo-obstruction involves abnormalities in:abnormalities in: Intestinal muscle( myopathic)Intestinal muscle( myopathic)

Nervous system( myenteric) e.g. Chagas’Nervous system( myenteric) e.g. Chagas’ disease and infiltrative diseasesdisease and infiltrative diseases

XI INTESTINAL OBSTRUCTIONXI INTESTINAL OBSTRUCTION Partial Obstruction and Pseudo-obstructionPartial Obstruction and Pseudo-obstruction

1. Pseudo-obstruction postop is most dangerous1. Pseudo-obstruction postop is most dangerous

Vagotomized patientsVagotomized patients

Intestinal OperationIntestinal Operation

2. Early recognition of Pseudo-obstruction is2. Early recognition of Pseudo-obstruction is

critical to proper therapycritical to proper therapy

a. Biopsy of intestine may or may not reveala. Biopsy of intestine may or may not reveal

loss of myenteric plexiloss of myenteric plexi

b. Full thickness rectal biopsy( Hirschsprung’sb. Full thickness rectal biopsy( Hirschsprung’s

Disease) is suspectedDisease) is suspected

XI INTESTINAL OBSTRUCTION XI INTESTINAL OBSTRUCTION Mechanical ObstructionMechanical Obstruction

1. Physiologic derangement if intact blood supply1. Physiologic derangement if intact blood supply

a. Accumulation of fluid and Gas above thea. Accumulation of fluid and Gas above the

point of obstructionpoint of obstruction

b. Altered bowel motility leading to systemicb. Altered bowel motility leading to systemic

derangementderangement

2. Gamble showed that mortality in simple type2. Gamble showed that mortality in simple type

was due to:was due to:

a. Loss of fluid and electrolytes by vomitinga. Loss of fluid and electrolytes by vomiting

b. Sequestration of fluid in obstructed bowelb. Sequestration of fluid in obstructed bowel

XI INTESTINAL OBSTRUCTIONXI INTESTINAL OBSTRUCTION Mechanical ObstructionMechanical Obstruction 3. After 48 hours, rate of entry of water into the3. After 48 hours, rate of entry of water into the intestinal lumen increases as a consequenceintestinal lumen increases as a consequence of blood to lumen fluxof blood to lumen flux 4. Prostaglandin release in response to bowel4. Prostaglandin release in response to bowel distention, increases secretion to obstructeddistention, increases secretion to obstructed loopsloops 5.Interference with the mesenteric blood supply5.Interference with the mesenteric blood supply is the most serious complication of intestinalis the most serious complication of intestinal obstructionobstruction

XI INTESTINAL OBSTRUCTIONXI INTESTINAL OBSTRUCTION Close loop ObstructionClose loop Obstruction 1. Both afferent & efferent limbs are obstructed1. Both afferent & efferent limbs are obstructed

2. Rapid progression of strangulation of blood2. Rapid progression of strangulation of blood supply before manifestations of obstructionsupply before manifestations of obstruction becomes obviousbecomes obvious

3. Abdominal distention does not occur3. Abdominal distention does not occur

XI INTESTINAL OBSTRUCTIONXI INTESTINAL OBSTRUCTION Colon ObstructionColon Obstruction 1. Fluid and Electrolyte sequestration progresses1. Fluid and Electrolyte sequestration progresses more slowlymore slowly

2. Progressive distention is the most dangerous2. Progressive distention is the most dangerous aspect of non-strangulated colon obstructionaspect of non-strangulated colon obstruction

XI INTESTINAL OBSTRUCTIONXI INTESTINAL OBSTRUCTION Clinical ManifestationsClinical ManifestationsThe distance of the obstruction from the The distance of the obstruction from the ligamentligament

of Treitz can be ascertained by:of Treitz can be ascertained by:

1. How long before vomiting takes place after1. How long before vomiting takes place after

the onset of painthe onset of pain

2. The nature of the vomitus2. The nature of the vomitus

XI INTESTINAL OBSTRUCTIONXI INTESTINAL OBSTRUCTION Clinical ManifestationsClinical Manifestations

Cardinal Signs and Symptoms of IntestinalCardinal Signs and Symptoms of Intestinal

Obstruction:Obstruction:

1. Crampy Abdominal Pain 1. Crampy Abdominal Pain

2. Nausea & Vomiting2. Nausea & Vomiting

3. Obstipation 3. Obstipation

4. Abdominal Distention4. Abdominal Distention

XII GASTROINTESTINAL BLEEDINGXII GASTROINTESTINAL BLEEDING

1. 1. Has high morbidity & mortality particularly inHas high morbidity & mortality particularly in the elderlythe elderly

2. Accurate diagnosis is critical before significant 2. Accurate diagnosis is critical before significant amounts ( 4-6 units) of blood has been lostamounts ( 4-6 units) of blood has been lost

3. Bleeding represents the initial symptoms of3. Bleeding represents the initial symptoms of gastrointestinal disease in more than 1/3 ofgastrointestinal disease in more than 1/3 of patients & in 70% there is no history ofpatients & in 70% there is no history of bleeding episodebleeding episode


4.Eighty( 80%) will stop spontaneously without4.Eighty( 80%) will stop spontaneously without interventionintervention

5. 5. Flexible endoscopy and arteriography play anFlexible endoscopy and arteriography play an interesting role in the diagnostic & therapeuticinteresting role in the diagnostic & therapeutic managementmanagement

XII GASTROINTESTINAL BLEEDINGXII GASTROINTESTINAL BLEEDING TerminologiesTerminologies

1. 1. HematemesisHematemesis is vomiting of bloodis vomiting of blood, , either either

digested digested in the stomach or fresh & unalteredin the stomach or fresh & unaltered

22. . MelenaMelena is the per anal passage of stools is the per anal passage of stools with altered blood that are black and tarrywith altered blood that are black and tarry

3. 3. HematocheziaHematochezia is the passage of liquid is the passage of liquid blood or blood clots of varied brightness or blood or blood clots of varied brightness or color, maroon to bright redcolor, maroon to bright red

XII GASTROINTESTINAL BLEEDINGXII GASTROINTESTINAL BLEEDING TerminologiesTerminologies As little as As little as 50-60m50-60ml of blood produce melenal of blood produce melena

Melena can persist for Melena can persist for 5-7 days 5-7 days after a 2-unitafter a 2-unit (significant) bleed(significant) bleed

Approximately 10 ml bleeding/ day (Guaiac +) Approximately 10 ml bleeding/ day (Guaiac +)

XII GASTROINTESTINAL XII GASTROINTESTINAL BLEEDINGBLEEDING Upper GI Bleeding Upper GI Bleeding Bleeding above the ligament of Treitz Bleeding above the ligament of Treitz include: include: 1. Esophagitis 1. Esophagitis 2. Esophageal Varices2. Esophageal Varices 3. Gastritis 3. Gastritis 4. Peptic Ulcer 4. Peptic Ulcer 5. Mallory Weiss5. Mallory Weiss 6. Gastric Carcinoma 6. Gastric Carcinoma 7. Hemobilia7. Hemobilia

XII GASTROINTESTINAL XII GASTROINTESTINAL BLEEDINGBLEEDING

Upper GI Bleeding Upper GI Bleeding 8. Stress Ulcer ( Documented Risk Factors)8. Stress Ulcer ( Documented Risk Factors) a. Multiple System Trauma a. Multiple System Trauma b. Hypotensionb. Hypotension c. Respiratory Failure c. Respiratory Failure d. Sepsisd. Sepsis e. Jaundice e. Jaundice ff. Burns . Burns g. Renal Failureg. Renal Failure hh. Recent Surgery. Recent Surgery

XII GASTROINTESTINAL BLEEDINGXII GASTROINTESTINAL BLEEDING Lower GI Bleeding Lower GI Bleeding Bleeding below the ligament of Treitz Bleeding below the ligament of Treitz includes:includes: 1. Diverticulitis1. Diverticulitis

2. Angiodysplasia2. Angiodysplasia

3. Ulcerative Colitis3. Ulcerative Colitis

4. Malignancy4. Malignancy


Lower GI Bleeding Lower GI Bleeding Work-upWork-up 1. Rectal Examination1. Rectal Examination 2. Proctosigmoidoscopy2. Proctosigmoidoscopy

3.Technetium 99 scan (Tag RBC)3.Technetium 99 scan (Tag RBC)

4. Arteriography 4. Arteriography 5. Barium Enema 5. Barium Enema

XIII JAUNDICEXIII JAUNDICE GIT related CausesGIT related Causes:: 1. Increased pigment production secondary to1. Increased pigment production secondary to tissue infarctiontissue infarction

2. Inflammatory disease; e.g. spontaneous2. Inflammatory disease; e.g. spontaneous peritonitisperitonitis

3. Appendicitis, complicated by coliform 3. Appendicitis, complicated by coliform organismorganism

can give jaundice without pyelephlebitican give jaundice without pyelephlebiti

4. Ampullary Carcinoma or Carcinoma of the4. Ampullary Carcinoma or Carcinoma of the duodenumduodenum

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