Presentation on the common manifestation of difficulty with swallowing and causes of bleeding in the gut.

1. DYSPHAGIA and
GASTROINTESTINAL
BLEEDING
Siteki Arnold
MBChB 4

2. Case scenario
• A 73-year-old man presented to his gastroenterologist for evaluation of dysphagia that had begun 6 months
previously. He reported progressively worsening intermittent solid food dysphagia with difficulty initiating
swallows. He denied dysphagia with ingestion of liquids, nasal regurgitation, abdominal pain, weight loss,
voice changes, aspiration, or choking episodes.
• His medical history was notable for prostate cancer treated with radiation therapy, type 2 diabetes mellitus,
and well-controlled gastroesophageal reflux disease (GERD). His current medications included metformin,
amlodipine, omeprazole, and glipizide. Other than a recent cataract operation on his right eye, he had had no
previous surgical procedures. He had a remote history of alcohol and tobacco use but had quit using both
substances more than 10 years previously. He lived in the Virgin Islands.
• Physical examination revealed no muscle fatigability or vision issues, such as diplopia or ptosis. He was able
to lift his arms above his head and rise from a seated position without difficulty. He had no difficulty
swallowing water. The remainder of his examination findings were unremarkable. Results of laboratory
studies, including complete blood cell count, electrolyte panel, thyroid-stimulating hormone level, and
evaluation of kidney function, were unremarkable.

3. • In this patient, which one of the following features is most helpful in
determining the location of his dysphagia?
• a.Dysphagia to solids
• b.Progressively worsening clinical course
• c.History of GERD
• d.Lack of weight loss
• e.Difficulty initiating swallows

4. • The medical history is key in the evaluation of dysphagia. In most cases, an
accurate diagnosis can be obtained on the basis of the history alone. Dysphagia
occurring only with solid foods suggests an obstructive lesion such as a stricture,
ring, web, or tumor, all of which rarely pose a barrier to liquids.
• The location of dysphagia is best determined by the history as well.
Oropharyngeal dysphagia is caused by disorders affecting swallowing function
above the level of the esophagus, and esophageal dysphagia is caused by disorders
affecting the body of the esophagus.
• The patient had difficulty initiating swallows, indicating possible oropharyngeal
dysfunction.

5. INTRODUCTION
• Definition: Dysphagia is difficulty in swallowing.
Dysphagia can be a serious health threat because of the risk of
aspiration pneumonia, malnutrition, dehydration, weight loss and airway
obstruction.
• Aphagia: Inability to swallow.
• Odynophagia: Pain on swallowing. Odynophagia is also a feature of
infective oesophagitis and may be particularly severe in chemical
injury.

6. CLASSIFICATION
• Dysphagia can be acute due to foreign body impaction or acute infection
or chronic due to causes like stricture or carcinoma.
• It can also be classified as oropharyngeal or oesophageal depending on
the cause.
• Dysphagia may be due to pathology in voluntary/pharyngeal phase of the
swallowing in which the patient also develops cough while swallowing.
Dysphagia due to problem in oesophageal involuntary phase of
swallowing is specified by food getting stuck in the pathway.
• It can be progressive or intermittent.

7. FUNCTIONALANATOMY

11. ETIOLOGY
• Causes of dysphagia can be classified as motility-related and
structural.
• They occur at the oropharyngeal level and esophageal level.

12. Oropharyngeal dysphagia
Motility-related dysphagia
• Neurological disorders:
o Stroke
o Neurodegenerative diseases
o Parkinson disease
o Brain tumor
o Traumatic brain injury
o Cerebral palsy
o Guillain-Barreˊ syndrome
o Other (e.g., iatrogenic nerve damage,
post-polio syndrome)
Structural dysphagia
• Mucosal disorders:
o Local infection (e.g., epiglottitis, acute tonsillitis)
o Corrosive injury (e.g., thermal or chemical burn)
o Zenker diverticulum
o Mucositis (e.g., caused by radiation therapy or
chemotherapy)
o Oropharyngeal cancer
o Head and neck surgery

13. Cont…
Motility-related dysphagia
• Muscular disorders:
o Myasthenia gravis
o Progressive muscular dystrophies
o Paraneoplastic syndrome
o Sarcoidosis
o Mixed connective tissue disorders (e.g., systemic
sclerosis, CREST syndrome, Sjogren syndrome)
o Inflammatory myopathies e.g., polymyositis,
dermatomyositis, inclusion body myositis)
Structural dysphagia
• Extramural disorders:
oDeep neck infection
oCricopharyngeal muscle spasm
oOsteophytes
oThyroglossal duct cyst

14. Esophageal dysphagia
Motility-related dysphagia
• Achalasia
• Gastro-esophageal reflux disease
(GERD)
• Esophageal hypermotility disorders
• Mixed connective tissue diseases
Structural dysphagia
• Intraluminal disorders of which are either impacted
foreign body or food bolus
• Mucosal disorders (intrinsic narrowing)
o Esophagitis (e.g., infectious esophagitis, eosinophilic
esophagitis, corrosive esophagitis or secondary to
chemotherapy or radiotherapy)
o Esophageal webs (e.g., in Plummer-Vinson syndrome)
o Esophageal rings (e.g., Schatzki ring)
o Esophageal cancer
o Esophageal diverticulum
o Autoimmune conditions (e.g., Crohn disease, Behcet
disease, pemphigus syndromes)

15. Cont…
• Extrinsic compression:
Thyromegaly, substernal thyroid
Hilar lymphadenopathy
Neoplasia (e.g., mediastinal tumor, thyroid tumor)
Cardiac dysphagia
o Includes vascular ring anomalies (e.g., double aortic arch), dysphagia lusoria (abnormal
right subclavian artery), severe atherosclerosis and aneurysms.
o Dysphagia megalatriensis: compression of the esophagus by a giant left atrium, most
commonly caused by mitral stenosis due to rheumatic heart disease and a left atrial
myxoma.
Hiatal hernia

18. Approach
• History:
The History can be used to differentiate structural from functional causes of
dysphagia.
Dysphagia that is episodic and occurs with both liquids and solids from the outset
suggests a motor disorder, whereas when the dysphagia is initially for solids and
then progresses with time to semisolids and liquids suggests a structural cause (e.g.,
stricture).
Rapid progress with associated significant weight loss suggests malignancy.
Patients complain that foods or liquids are no longer being swallowed easily and
there is a sensation of food sticking.

19. • Physical Examination:
Complete head and neck examination
Inspection of oral cavity
Dentition
Oropharynx
Nasolaryngoscopy
Cranial nerve examination (Absent gag reflex and facial asymmetry
indicate cranial nerve palsies e.g., due to stroke)

20. Characterization of dysphagia

21. Cont…

22. Diagnosis
• Haematocrit
• Chest X-ray often shows mediastinal mass lesion/foreign body
• Oesophagoscopy
• Modified barium swallow
oPreferred test for suspected oropharyngeal dysphagia. Provides functional
evaluation of swallowing and can be used to assess the risk of aspiration.
• CT scan chest is very useful method to identify the anatomical location of the
cause (nodes/tumour/aorta/cardiac cause/congenital). Extent, spread, nodal
status, size and operability of tumour also assessed.

23. • Endoscopy:
Structural assessment
Functional assessment
• High resolution oesophageal manometry in achalasia cardia or
Gastroesophageal reflux disease (GERD)
• Consider an esophagogastroduodenoscopy (EGD) to rule out an esophageal
etiology for dysphagia in patients in whom an oropharyngeal etiology has
been ruled out.
• 24 hour pH monitoring for GERD by use of a transnasal catheter under
manometry guidance.

24. • Endosonography and abdominal ultrasound to assess site, layers of the
esophagus, nodes and spread as well as liver and ascites.
• Magnetic Resonance Imaging (MRI)

25. Differential diagnosis
• Achalasia
• Dermatomyositis
• Myasthenia Gravis
• Parkinson Disease
• Paediatric poliomyelitis
• Polymyositis
• Syphilis

26. Complications
• Esophageal bolus impaction
• Aspiration pneumonia: common complication of oropharyngeal
dysphagia
• Malnutrition.

27. Treatment
• Depends on cause
• The goals of treatment are to maintain adequate nutritional intake for
the patient and to maximize airway protection
• In adults:
oDirect techniques include modifications of food consistency
oIndirect techniques include stimulation of the oropharyngeal structures
and the adoption of behavioral techniques.

28. Pharmacologic Treatment:
• Proton pump inhibitors (PPIs) for Gastroesophageal reflux disease (GERD).
• Smooth muscle relaxants for esophageal motility disorders.
• Aerosolized steroids for eosinophilic esophagitis.
Endoscopic intervention:
• Botulinum toxin injections (Botox) to control hypertonia.
• Dilation: for etiologies that cause significant narrowing (e.g., achalasia,
esophageal rings or webs, strictures).
• Diverticulotomy: for esophageal diverticula.

29. Surgery:
• Myotomy: considered for refractory esophageal hypermotility disorders.
• Curative or palliative tumor resection (e.g., in pharyngeal cancer or esophageal
cancer).
• Surgical resection of refractory rings and/or strictures.
Supportive therapy: Optimize nutrition of patients with dysphagia refractory to
therapy.
Diet modification as needed (e.g., pureeing solid food, taking small bites, chewing
carefully).
Consider temporary nasogastric tube feeding (e.g., in patients with acute stroke).

30. • Food bolus impaction: Prompt endoscopic removal of the bolus.
Intravenous glucagon for esophageal relaxation.
Complete obstruction: emergency endoscopy.
Incomplete obstruction: urgent endoscopy, ideally within 24 hours
The esophageal mucosa should be evaluated to determine if an
underlying structural pathology triggered the impaction. If no structural
pathology is identified, multilevel biopsies should be obtained to assess
for eosinophilic esophagitis.

31. GASTROINTESTINAL
BLEEDING

32. Case scenario
• A 70-year-old woman presents with a chief complaint of having a large,
bloody bowel movement? Earlier in the day, the patient experienced the
urge to defecate and then passed a large quantity of blood. She had no
nausea, vomiting, abdominal pain, tarry stool or lightheadedness.
• Although she appeared pale in the ER, she was alert and talkative. Her pulse
was 110/min and regular. Her blood pressure, in a supine position was
150/70 mmHg, which fell to 130/60 when she sat up. The examination of
the abdomen revealed normal active bowel sounds and no tenderness,
masses or organomegaly. Rectal exam revealed large external hemorrhoids
but no masses. Stool was grossly bloody.

33. • The hematocrit was 27%, WBC was 10,500 cells/mm3 without a left
shift.
• Platelets were 347,000/mm3. Prothrombin time was 10.2 seconds.
BUN and creatinine were 12 mg/dL and 0.6 mg/dL respectively. The
initial workup was negative for a specific bleeding site.
• During hospitalization the stool was negative for blood; however, she
passed a bloody stool on the fourth hospital day.

34. • What is the clinical problem?
• Develop a differential diagnosis by listing diseases which may present
with this problem, especially in an elderly person.
• What is your diagnosis?

35. 1. What is the clinical problem?
Bright red blood per rectum. Hematochezia.
2. Develop a differential diagnosis by listing diseases which may present with this
problem, especially in an elderly person?
Generally indicates lower GI tract hemorrhage from the colon or distal ileum.
Small volume Hematochezia
• anorectal disease
• colitis (ischemic)
• polyps or neoplasm
Large volume Hematochezia
• diverticulosis
• arteriovenous malformation

36. 3. What is your diagnosis?
• Arteriovenous malformation.

37. Definition
• Gastrointestinal bleeding or gastrointestinal hemorrhage describes every form of hemorrhage (loss of blood)
in the gastrointestinal tract. It occurs anywhere along the alimentary canal from the pharynx to the rectum.
• It may be divided into:
o Upper gastrointestinal bleeding – Bleeding from a source located above the ligament of Treitz and it occurs in
approximately 80% of hospitalized patients due to gastrointestinal bleeding.
o Lower gastrointestinal bleeding – Bleeding from a source located below the ligament of Treitz which occurs
in approximately 20% of patients hospitalized due to gastrointestinal bleeding.
Gastrointestinal bleeding can also be divided into:
o Overt gastrointestinal bleeding - Bleeding that is visible, such as hematemesis (bloody or coffee – ground
emesis), hematochezia (presence of blood and blood clots in feces), or melena (black tarry stools)
o Occult gastrointestinal bleeding – Bleeding which is not overt (e.g., detected through occult blood testing or
confirmed only after investigations for iron-deficiency anemia.

41. UPPER GI BLEEDING CAUSES

42. UPPER GASTROINTESTINAL
BLEEDING
• Upper gastrointestinal bleeding remains a major medical problem with an incidence over 100/100000
per year in Western practice that increases with increasing age.
• Associated with NSAID use.
• Causes include:
o Esophageal varices: Sudden onset, painless large volumes, dark or bright red blood, history of liver
disease, other features of portal hypertension e.g., ascites, dilated abdominal veins.
o Reflux esophagitis: Small volumes of bright red blood, associated with regurgitation of acidic gastric
contents.
o Esophageal cancer
o Esophageal ulcer
o Mallory Weiss tear: Longitudinal mucosal tears at the gastro-oesophageal junction due to repetitive and
strenuous. Usually bleeding stops spontaneously.

43. Cont…
• Gastric causes include:
o Gastric ulcer: Often larger sized bleed, painful, possible preceding smaller bleeds,
accompanied by altered blood that looks like ground coffee, history of PUD
o Gastric neoplasms: Rarely large bleed, anaemia more common, associated weight
loss, anorexia, dyspeptic symptoms
o Gastritis: Small volumes, bright red, may follow alcohol or NSAID intake, history
of dyspepsia
o Gastric varices
o Gastric antral vascular ectasia
o Dieulafoy’s lesions: Gastric arteriovenous malformations

44. Cont…
• Duodenal causes:
Duodenal ulcers: Past history of duodenal ulcer, melaena is prominent,
symptoms of back pain, hunger pains, NSAID use.
Duodenitis: Small volumes, bright red, may follow alcohol or NSAID
use, history of dyspepsia.

45. Clinical presentation
• Haematemesis
• Melaena
• Hematochezia
• Epigastric pain or diffuse abdominal pain
• Weakness, dizziness, syncope or presyncope
• Dyspepsia
• Dysphagia
• Jaundice
• Weight loss

46. Evaluation
• History:
Important information to obtain includes potential comorbid conditions,
medication history, potential toxic exposures as well as the severity,
timing, duration and volume of bleeding.
• Physical Examination:
Aims at evaluating for shock and blood loss and assessing the patient
for hemodynamic instability and clinical signs of poor perfusion.

47. Severe GI Bleeding
• Gastrointestinal bleeding accompanied by shock or orthostatic
hypotension and a decrease in the hematocrit value by at least 6% or a
decrease in hemoglobin of at least 2g/dl or transfusion of at least two
units of packed RBC.

48. INVESTIGATIONS
• Full haemogram: Iron deficiency anaemia in carcinoma, reflux oesophagitis
• Liver function tests
• Coagulation profile: Bleeding diatheses
• Endoscopy: Investigation of choice. High diagnostic accuracy, allows
therapeutic manoeuvres (varices: injection or banding; ulcers: injection)
• Test for H.pylori infection
• Angiography (CT Angiography: rare duodenal causes, obscure recurrent
bleeds).

49. • Ulcers are generally characterized by the Forrest classification, which reliably predicts the
likelihood of rebleeding:
• – Class I: Active spurting bleeding (Ia) or active oozing bleeding (Ib).
• – Class IIa: Visible nonbleeding vessel.
• – Class IIb: Adherent clot at the ulcer base.
• – Class IIc: Flat pigmented spot at the ulcer base.
• – Class III: Clean (white) ulcer base.
• Classes Ia, Ib, and IIa are associated with high risk for rebleeding and are usually treated
endoscopically in combination with injection therapy, coagulation, or clips. Class IIb lesions
warrant targeted irrigation to attempt to dislodge the clot and then treat the underlying lesion.
Classes IIc and III usually do not require endoscopic therapy, as they are associated with low
risk for rebleeding.

50. LOWER GASTROINTESTINAL
BLEEDING
• It encompasses a wide spectrum of symptoms, ranging from
hematochezia to massive hemorrhage with shock.
• Acute lower gastrointestinal bleeding is bleeding that is of recent
duration, originates beyond the ligament of Treitz, results in instability
of vital signs and is associated with signs of anaemia with or without
need for blood transfusion.

51. CLASSIFICATION OF LOWER
GASTROINTESTINAL BLEEDING
• Massive:
Age: >65 with medical problem
Hematochezia
SBP: =90
Pulse: >100
Low urine output
Hemoglobin: =6 g/dl
• Moderate:
Any age
Hematochezia/melaena
Long term disease
Moderate amount acute or chronic bleeding
• Occult:
Any age
Hypochromic/microcytic anemia
Neoplasm

52. Etiology
• Coagulopathy
• Colitis:
Ulcerative colitis: Blood mixed with mucus, associated with systemic upset,
long history, intermittent course, diarrhea prominent
Infectious colitis – E.coli, Shigella, Salmonella, Campylobacter jejuni
• Hemorrhoids: Bright red bleeding post defecation, stops spontaneously,
perianal irritation
• Angiodysplasia
• Neoplasms – Leiomyoma and lymphoma: rare, intermittent history, often
modest volumes lost

53. Cont…
• Diverticular disease: Spontaneous, painless, large volume of mostly
fresh blood, previous history of constipation.
• Anal fissure: Children and young adults, extreme pain on defecation,
small volumes bright red blood on stool.
• Crohn’s disease
• Mesenteric ischaemia: Elderly, severe abdominal pain, bloody
diarrhea, collapse and shock later.
• Colonic polyps: May be large volume or small, possible associated
change in bowel habit, blood often mixed with stool.

54. Rectum
Carcinoma of the rectum: change in bowel habit
common, rarely large volumes.
Proctitis: bloody mucus, purulent diarrhoea in
infected, perianal irritation common.
Solitary rectal ulcer: bleeding post defaecation,
small volumes, feeling of ‘lump in anus’, mucus
discharge.
LOWER GI BLEEDING

56. 1. FHG: iron deficiency anaemia–tumours/chronic colitis.
2. Coagulation profiles: bleeding diatheses.
3. Proctoscopy: anorectal tumours, prolapse, haemorrhoids,
distal colitis.
4. Abdominal X-ray, ultrasound: intussusception.
5. Flexible sigmoidoscopy: suspected colitis, sigmoid tumours
or diverticular disease.
6. Colonoscopy: diverticular disease, colon tumours,
angiodysplasia.
7. Angiography: angiodysplasia.
INVESTIGATIONS

57. MANAGEMENT
• Management of UGIB in acute phase:
oAssess for airway, breathing, circulation first
oIf not present/or compromised activate rapid response team and restore abc
first
oFluid resuscitation by intravenous colloids/crystalloid transfusion
oMaintenance of vital signs
oBlood transfusion
oPain management
oSedatives can be used, but after determining level of consciousness
oEndoscopy to rule out the actual problem

58. • Treatment of variceal bleeding:
Fluid replacement
Octreotide/vasopressin and nitroglycerine
Endoscopic banding and sclerotherapy (with Beta blockers and nitrates
to stop rebleed)
Balloon tamponade with a Sengstaken Blakemore tube/Minnesota
tube) and Transjugular intrahepatic portosystemic shunt (TIPS).

59. SURGICAL TREATMENT
• Surgical ligation of the bleeding vessel for upper GI
• Lower GI : resection of the affected area as the last resort
• Indications for surgery:
Persistent hypotension
Failure of medical treatment or endoscopic homeostasis
Coexisting condition (perforation, obstruction, malignancy)
Transfusion requirement
Recurrent hospitalizations

60. • The management of LGIB has three components:
oResuscitation and initial assessment
oLocalization of bleeding site
oTherapeutic intervention to stop bleeding at the site

61. Treatment for different LGIB
• Diverticular bleeding: colonoscopy with bipolar probe coagulation,
epinephrine injection or metallic clips.
• Recurrent bleeding: Resection of the affected bowel segment.
• Angiodysplasia: Thermal therapy (e.g., electrocoagulation, argon
plasma coagulation).
• In patients in whom the bleeding site cannot be determined,
vasoconstrictive agents such as vasopressin can be used. If vasopressin
is unsuccessful or contraindicated, superselective embolization is
useful.

62. ROCKALL SCORE
• Used to predict risk of adverse outcome following
acute UGIB
• Score <3: good prognosis
• Score>8: high risk of mortality

63. REFERENCES
• Slideshare.net
• Amboss.com/us/knowledge
• SRB’s Manual of surgery 5th edition Pg788-790
• Bailey and Love’s short practice of surgery 7th edition Pg 1069 and
1070

64. THANK YOU