A 59-year-old Chinese man was admitted to the hospital for vomiting blood. He has a history of hepatitis C and is a smoker, drinker, and former drug user. Physical examination found abdominal distension with fluid thrill and shifting dullness. Testing showed signs of liver dysfunction. The provisional diagnosis is esophageal varices secondary to liver disease, likely cirrhosis. Esophageal varices form as a result of portal hypertension in liver disease and can bleed, potentially severely. Treatment focuses on stopping the bleeding and lowering portal pressure through various medical and procedural options.
Choledocholithiasis is one of the main causes for Obstructive Jaundice.In this ppt presentation, I have discussed the etiology, clinical features, complications, investigations and management of Choledocholithiasis. I have also included a mindmap and 2 algorithms for Choledocholithiasis. I hope you will find it very useful and interesting.
Approach to Management of Upper Gastrointestinal (GI) BleedingArun Vasireddy
Upper gastrointestinal bleeding is gastrointestinal bleeding in the upper gastrointestinal tract, commonly defined as bleeding arising from the esophagus, stomach, or duodenum. Blood may be observed in vomit (hematemesis) or in altered form in the stool (melena). Depending on the severity of the blood loss, there may be symptoms of insufficient circulating blood volume and shock. As a result, upper gastrointestinal bleeding is considered a medical emergency and typically requires hospital care for urgent diagnosis and treatment. Upper gastrointestinal bleeding can be caused by peptic ulcers, gastric erosions, esophageal varices, and some rarer causes such as gastric cancer.
The initial assessment includes measurement of the blood pressure and heart rate, as well as blood tests to determine hemoglobin concentration. In significant bleeding, fluid replacement is often required, as well as blood transfusion, before the source of bleeding can be determined by endoscopy of the upper digestive tract with an esophagogastroduodenoscopy. Depending on the source, endoscopic therapy can be applied to reduce rebleeding risk. Specific medical treatments (such as proton pump inhibitors for peptic ulcer disease) or procedures (such as TIPS for variceal hemorrhage) may be used. Recurrent or refractory bleeding may lead to need for surgery, although this has become uncommon as a result of improved endoscopic and medical treatment.
esophageal varices are the second most common cause of upper GI bleed after PUD.These are actually the dilated veins which occur secondary to increase in the pressure in the portal circulation called as Portal Hypertension..
CASE PRESENTATION ONCIRRHOSIS OF LIVER WITH PORTAL HYPERTENSION, HEPATIC EN...Akhil Joseph
A DETAIL CASE PRESENTATION ON CIRRHOSIS OF LIVER WITH PORTAL HYPERTENSION, HEPATIC ENCEPHALOPATHY AND GRADE II OESOPHAGEAL VARICES WITH CONGESTIVE GASTROPATHY. LIVER CIRRHOSIS AND ALL ITS COMPLICATION IN A PATIENT.
Today I have uploaded a video on one more cause for Obstructive Jaundice- Pancreatic Carcinoma. Only cancer in head of pancreas cause Obstructive Jaundice. I have talked about cancer in body and tail of pancreas as well. I have discussed the risk factors, pathology, clinical features, investigations, treatment and complications of pancreatic carcinoma. I have included a mind map and two algorithms. I hope you will enjoy this video. You can watch all my surgical teaching video casts in the following link.
Surgicaleducator.blogspot.com
Thank you for your support.
LOWER GI HEMORRHAGE- PLAYLIST OF 6 VIDEOS
Dear Viewers,
Greetings from “Surgical Educator”.
I have made a playlist for Lower GI Hemorrhage which consists of six videos on various causes of Lower GI Hemorrhage. They are Introduction, diverticular disease, haemorrhoids, fissure-in-ano, colorectal carcinoma and inflammatory bowel disease. If you watch all these videos together you will become confident to tackle the clinical problem of Lower GI Hemorrhage. You can watch these videos in the following link: https://www.youtube.com/playlist…
Thank you for watching the videos.
Choledocholithiasis is one of the main causes for Obstructive Jaundice.In this ppt presentation, I have discussed the etiology, clinical features, complications, investigations and management of Choledocholithiasis. I have also included a mindmap and 2 algorithms for Choledocholithiasis. I hope you will find it very useful and interesting.
Approach to Management of Upper Gastrointestinal (GI) BleedingArun Vasireddy
Upper gastrointestinal bleeding is gastrointestinal bleeding in the upper gastrointestinal tract, commonly defined as bleeding arising from the esophagus, stomach, or duodenum. Blood may be observed in vomit (hematemesis) or in altered form in the stool (melena). Depending on the severity of the blood loss, there may be symptoms of insufficient circulating blood volume and shock. As a result, upper gastrointestinal bleeding is considered a medical emergency and typically requires hospital care for urgent diagnosis and treatment. Upper gastrointestinal bleeding can be caused by peptic ulcers, gastric erosions, esophageal varices, and some rarer causes such as gastric cancer.
The initial assessment includes measurement of the blood pressure and heart rate, as well as blood tests to determine hemoglobin concentration. In significant bleeding, fluid replacement is often required, as well as blood transfusion, before the source of bleeding can be determined by endoscopy of the upper digestive tract with an esophagogastroduodenoscopy. Depending on the source, endoscopic therapy can be applied to reduce rebleeding risk. Specific medical treatments (such as proton pump inhibitors for peptic ulcer disease) or procedures (such as TIPS for variceal hemorrhage) may be used. Recurrent or refractory bleeding may lead to need for surgery, although this has become uncommon as a result of improved endoscopic and medical treatment.
esophageal varices are the second most common cause of upper GI bleed after PUD.These are actually the dilated veins which occur secondary to increase in the pressure in the portal circulation called as Portal Hypertension..
CASE PRESENTATION ONCIRRHOSIS OF LIVER WITH PORTAL HYPERTENSION, HEPATIC EN...Akhil Joseph
A DETAIL CASE PRESENTATION ON CIRRHOSIS OF LIVER WITH PORTAL HYPERTENSION, HEPATIC ENCEPHALOPATHY AND GRADE II OESOPHAGEAL VARICES WITH CONGESTIVE GASTROPATHY. LIVER CIRRHOSIS AND ALL ITS COMPLICATION IN A PATIENT.
Today I have uploaded a video on one more cause for Obstructive Jaundice- Pancreatic Carcinoma. Only cancer in head of pancreas cause Obstructive Jaundice. I have talked about cancer in body and tail of pancreas as well. I have discussed the risk factors, pathology, clinical features, investigations, treatment and complications of pancreatic carcinoma. I have included a mind map and two algorithms. I hope you will enjoy this video. You can watch all my surgical teaching video casts in the following link.
Surgicaleducator.blogspot.com
Thank you for your support.
LOWER GI HEMORRHAGE- PLAYLIST OF 6 VIDEOS
Dear Viewers,
Greetings from “Surgical Educator”.
I have made a playlist for Lower GI Hemorrhage which consists of six videos on various causes of Lower GI Hemorrhage. They are Introduction, diverticular disease, haemorrhoids, fissure-in-ano, colorectal carcinoma and inflammatory bowel disease. If you watch all these videos together you will become confident to tackle the clinical problem of Lower GI Hemorrhage. You can watch these videos in the following link: https://www.youtube.com/playlist…
Thank you for watching the videos.
FISSURE-IN-ANO – Lower GI Hemorrhage
Dear Viewers,
Greetings from “Surgical Educator”
Today in this episode, I have talked about yet another cause for lower GI haemorrhage- “Fissure-in-Ano”. Unlike other causes of lower GI haemorrhage, fissure-in-ano present with painful bleeding per rectum. I am talking on etiology, types, clinical features and treatment of fissure-in-ano. I have also included a mind map, a diagnostic algorithm and a treatment algorithm. You can watch this video in the following links:
surgicaleducator.blogspot.com
youtube.com/c/surgicaleducator
Thank you for watching the video.
POST-OPERATIVE WOUND COMPLICATIONS
Dear Viewers,
Greetings from “Surgical Educator”.
Today I have uploaded a video on “POST-OPERATIVE WOUND COMPLICATIONS”. I have discussed about seroma,hematoma,wound infection,wound dehiscence,entero-cutaneous fistula and necrotizing fasciitis- about which all surgeon’s must have a working knowledge. I have restricted my discussion to the essential minimum an undergraduate medical student must know. You can watch all my surgical teaching video casts in the following link:
Surgicaleducator.blogspot.com
Thank you for your support.
In this PPT presentation I try to teach many causes of Abdominal pain in various quadrants of the abdomen. Since it is individual case based teaching i concentrate only in the essential minimum an undergraduate medical student should know and you will have immersive learning experience.
PATIENT INFORMATIONName Mr. W.S.Age 65-year-oldSex Male.docxJUST36
PATIENT INFORMATION
Name: Mr. W.S.
Age: 65-year-old
Sex: Male
Source: Patient
Allergies: None
Current Medications: Atorvastatin tab 20 mg, 1-tab PO at bedtime
PMH: Hypercholesterolemia
Immunizations: Influenza last 2018-year, tetanus, and hepatitis A and B 4 years ago.
Surgical History: Appendectomy 47 years ago.
Family History: Father- died 81 does not report information
Mother-alive, 88 years old, Diabetes Mellitus, HTN
Daughter-alive, 34 years old, healthy
Social Hx: No smoking history or illicit drug use, occasional alcoholic beverage consumption on social celebrations. Retired, widow, he lives alone.
SUBJECTIVE:
Chief complain: “headaches” that started two weeks ago
Symptom analysis/HPI:
The patient is 65 years old male who complaining of episodes of headaches and on 3 different occasions blood pressure was measured, which was high (159/100, 158/98 and 160/100 respectively). Patient noticed the problem started two weeks ago and sometimes it is accompanied by dizziness. He states that he has been under stress in his workplace for the last month.
Patient denies chest pain, palpitation, shortness of breath, nausea or vomiting.
ROS:
CONSTITUTIONAL: Denies fever or chills. Denies weakness or weight loss. NEUROLOGIC: Headache and dizzeness as describe above. Denies changes in LOC. Denies history of tremors or seizures.
HEENT: HEAD: Denies any head injury, or change in LOC. Eyes: Denies any changes in vision, diplopia or blurred vision. Ear: Denies pain in the ears. Denies loss of hearing or drainage. Nose: Denies nasal drainage, congestion. THROAT: Denies throat or neck pain, hoarseness, difficulty swallowing.
Respiratory: Patient denies shortness of breath, cough or hemoptysis.
Cardiovascular: No chest pain, tachycardia. No orthopnea or paroxysmal nocturnal
dyspnea.
Gastrointestinal: Denies abdominal pain or discomfort. Denies flatulence, nausea, vomiting or
diarrhea.
Genitourinary: Denies hematuria, dysuria or change in urinary frequency. Denies difficulty starting/stopping stream of urine or incontinence.
MUSCULOSKELETAL: Denies falls or pain. Denies hearing a clicking or snapping sound.
Skin: No change of coloration such as cyanosis or jaundice, no rashes or pruritus.
Objective Data
CONSTITUTIONAL: Vital signs: Temperature: 98.5 °F, Pulse: 87, BP: 159/92 mmhg, RR 20, PO2-98% on room air, Ht- 6’4”, Wt 200 lb, BMI 25. Report pain 0/10.
General appearance: The patient is alert and oriented x 3. No acute distress noted. NEUROLOGIC: Alert, CNII-XII grossly intact, oriented to person, place, and time. Sensation intact to bilateral upper and lower extremities. Bilateral UE/LE strength 5/5.
HEENT: Head: Normocephalic, atraumatic, symmetric, non-tender. Maxillary sinuses no tenderness. Eyes: No conjunctival injection, no icterus, visual acuity and extraocular eye movements intact. No nystagmus noted. Ears: Bilateral canals patent without erythema, edema, or exudate. Bilateral tympanic membrane.
Case Report : Integrating Review Inflammation and Commorbid diseasesSoroy Lardo
Diabetes is associated with atherosclerosis and COPD contributed to the chronic inflammation within the systemic vascular. Management of CVI with diabetes and COPD requires multi-disciplinary approach
Ethanol (CH3CH2OH), or beverage alcohol, is a two-carbon alcohol
that is rapidly distributed in the body and brain. Ethanol alters many
neurochemical systems and has rewarding and addictive properties. It
is the oldest recreational drug and likely contributes to more morbidity,
mortality, and public health costs than all illicit drugs combined. The
5th edition of the Diagnostic and Statistical Manual of Mental Disorders
(DSM-5) integrates alcohol abuse and alcohol dependence into a single
disorder called alcohol use disorder (AUD), with mild, moderate,
and severe subclassifications (American Psychiatric Association, 2013).
In the DSM-5, all types of substance abuse and dependence have been
combined into a single substance use disorder (SUD) on a continuum
from mild to severe. A diagnosis of AUD requires that at least two of
the 11 DSM-5 behaviors be present within a 12-month period (mild
AUD: 2–3 criteria; moderate AUD: 4–5 criteria; severe AUD: 6–11 criteria).
The four main behavioral effects of AUD are impaired control over
drinking, negative social consequences, risky use, and altered physiological
effects (tolerance, withdrawal). This chapter presents an overview
of the prevalence and harmful consequences of AUD in the U.S.,
the systemic nature of the disease, neurocircuitry and stages of AUD,
comorbidities, fetal alcohol spectrum disorders, genetic risk factors, and
pharmacotherapies for AUD.
Couples presenting to the infertility clinic- Do they really have infertility...Sujoy Dasgupta
Dr Sujoy Dasgupta presented the study on "Couples presenting to the infertility clinic- Do they really have infertility? – The unexplored stories of non-consummation" in the 13th Congress of the Asia Pacific Initiative on Reproduction (ASPIRE 2024) at Manila on 24 May, 2024.
MANAGEMENT OF ATRIOVENTRICULAR CONDUCTION BLOCK.pdfJim Jacob Roy
Cardiac conduction defects can occur due to various causes.
Atrioventricular conduction blocks ( AV blocks ) are classified into 3 types.
This document describes the acute management of AV block.
TEST BANK for Operations Management, 14th Edition by William J. Stevenson, Ve...kevinkariuki227
TEST BANK for Operations Management, 14th Edition by William J. Stevenson, Verified Chapters 1 - 19, Complete Newest Version.pdf
TEST BANK for Operations Management, 14th Edition by William J. Stevenson, Verified Chapters 1 - 19, Complete Newest Version.pdf
These lecture slides, by Dr Sidra Arshad, offer a quick overview of physiological basis of a normal electrocardiogram.
Learning objectives:
1. Define an electrocardiogram (ECG) and electrocardiography
2. Describe how dipoles generated by the heart produce the waveforms of the ECG
3. Describe the components of a normal electrocardiogram of a typical bipolar leads (limb II)
4. Differentiate between intervals and segments
5. Enlist some common indications for obtaining an ECG
Study Resources:
1. Chapter 11, Guyton and Hall Textbook of Medical Physiology, 14th edition
2. Chapter 9, Human Physiology - From Cells to Systems, Lauralee Sherwood, 9th edition
3. Chapter 29, Ganong’s Review of Medical Physiology, 26th edition
4. Electrocardiogram, StatPearls - https://www.ncbi.nlm.nih.gov/books/NBK549803/
5. ECG in Medical Practice by ABM Abdullah, 4th edition
6. ECG Basics, http://www.nataliescasebook.com/tag/e-c-g-basics
Ozempic: Preoperative Management of Patients on GLP-1 Receptor Agonists Saeid Safari
Preoperative Management of Patients on GLP-1 Receptor Agonists like Ozempic and Semiglutide
ASA GUIDELINE
NYSORA Guideline
2 Case Reports of Gastric Ultrasound
Title: Sense of Taste
Presenter: Dr. Faiza, Assistant Professor of Physiology
Qualifications:
MBBS (Best Graduate, AIMC Lahore)
FCPS Physiology
ICMT, CHPE, DHPE (STMU)
MPH (GC University, Faisalabad)
MBA (Virtual University of Pakistan)
Learning Objectives:
Describe the structure and function of taste buds.
Describe the relationship between the taste threshold and taste index of common substances.
Explain the chemical basis and signal transduction of taste perception for each type of primary taste sensation.
Recognize different abnormalities of taste perception and their causes.
Key Topics:
Significance of Taste Sensation:
Differentiation between pleasant and harmful food
Influence on behavior
Selection of food based on metabolic needs
Receptors of Taste:
Taste buds on the tongue
Influence of sense of smell, texture of food, and pain stimulation (e.g., by pepper)
Primary and Secondary Taste Sensations:
Primary taste sensations: Sweet, Sour, Salty, Bitter, Umami
Chemical basis and signal transduction mechanisms for each taste
Taste Threshold and Index:
Taste threshold values for Sweet (sucrose), Salty (NaCl), Sour (HCl), and Bitter (Quinine)
Taste index relationship: Inversely proportional to taste threshold
Taste Blindness:
Inability to taste certain substances, particularly thiourea compounds
Example: Phenylthiocarbamide
Structure and Function of Taste Buds:
Composition: Epithelial cells, Sustentacular/Supporting cells, Taste cells, Basal cells
Features: Taste pores, Taste hairs/microvilli, and Taste nerve fibers
Location of Taste Buds:
Found in papillae of the tongue (Fungiform, Circumvallate, Foliate)
Also present on the palate, tonsillar pillars, epiglottis, and proximal esophagus
Mechanism of Taste Stimulation:
Interaction of taste substances with receptors on microvilli
Signal transduction pathways for Umami, Sweet, Bitter, Sour, and Salty tastes
Taste Sensitivity and Adaptation:
Decrease in sensitivity with age
Rapid adaptation of taste sensation
Role of Saliva in Taste:
Dissolution of tastants to reach receptors
Washing away the stimulus
Taste Preferences and Aversions:
Mechanisms behind taste preference and aversion
Influence of receptors and neural pathways
Impact of Sensory Nerve Damage:
Degeneration of taste buds if the sensory nerve fiber is cut
Abnormalities of Taste Detection:
Conditions: Ageusia, Hypogeusia, Dysgeusia (parageusia)
Causes: Nerve damage, neurological disorders, infections, poor oral hygiene, adverse drug effects, deficiencies, aging, tobacco use, altered neurotransmitter levels
Neurotransmitters and Taste Threshold:
Effects of serotonin (5-HT) and norepinephrine (NE) on taste sensitivity
Supertasters:
25% of the population with heightened sensitivity to taste, especially bitterness
Increased number of fungiform papillae
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2. PATIENT’S IDENTIFICATION
Name: Phuah Eng Tea
Age: 59 years old
Gender: Male
Race: Chinese
Religion: Christian
Address: Klang Utama
Occupation: Retired lorry driver
Marital status: Married
Registration No: 1564813
Ward: 4A
Bed: 24
Informant: Wife
4. HISTORY OF PRESENTING ILLNESS
Mr Phuah , 59 years old Chinese gentleman
came to the Emergency Department
complaining of vomiting blood
(hematemesis) which is red in colour and 1
small cup full(approximately 100ml), on
same day of admission. It was sudden and
this was the second episode of hematemesis.
This is associated with loose black
stool(melena), abdominal pain, dizziness,
fatigue and loss of appetite. The review of
other systems were unremarkable.
5. PERSONALAND SOCIAL HISTORY
Mr Phuah is a retired lorry driver. He is married
with no children and lives in a single-storey house
with his wife with basic amenities. He smokes 5-6
pieces of cigarette per day since 20 years old, he
also consumes 2-3 cans of beer everyday for more
than 30 years and he is a heroin drug user. He
takes a normal chinese diet and undergoes
sedentary lifestyle.
FAMILY HISTORY
There is no chronic illness or malignancies
running in his family.
6. PAST MEDICAL HISTORY and
DRUG HISTORY
He has hypertension.
He was admitted 2 twice before due to
drug abuse and altered mental status.
He was diagnosed with Hepatitis C in
2013.
Currently, he is taking Covapril for his
HTN.
He is also a heroin drug user since young.
8. PHYSICAL EXAMINATION
General Examination
Patient was lying comfortably on bed in supine
position supported with one pillow. The patient
was alert, conscious and well-oriented to time,
place and person. The patient was not in pain and
respiratory distress. There was an ID tag on his
right hand and branula attached on his dorsum of
right hand which is attached to IV Metronidazole.
He is moderately build, with adequate nutritional
status.
9. Hands
Hands were warm and dry
No clubbing, koilonychia or leukonychia
No peripheral cyanosis
No palmar erythema
Eyes
Has conjunctival pallor
No jaundice
Oral cavity
Tongue is coated
No central cyanosis
No mouth ulcers
Moderate oral hygiene
Neck
No swelling observed
Legs
No pitting edema
10. Vital signs
Blood pressure : 144/77 mmHg
Pulse rate : 77 beats per minute
Respiratory rate : 18 breaths per minute
Temperature : 37.0 ᵒC
11. Local Examination Of The Abdomen
On Inspection
The abdomen was distended. The umbilicus was
centrally located and inverted. There were no
surgical scars or discoloration of the skin. All
quadrants of the abdomen moved symmetrically
during respiration.
On palpation
On superficial and deep palpation, there were no
rigidity, guarding and tenderness of abdomen. The
liver and spleen were not palpable.
12. On percussion
The liver span is normal at 10cm.
There was positive fluid thrill and shifting
dullness
On auscultation
Normal bowel sound was heard(3 times per
minute).
13. SUMMARY
A 59 years old Chinese man was admitted
to hospital due to hematemesis associated
with loose black stool(melena), dizziness,
fatigue, abdominal pain and loss of
appetite.
On physical examination the abdomen was
distended. There was positive fluid thrill
and shifting dullness.
14. Provisional Diagnosis
Diagnosis Points to support
Esophageal Varices 2⁰
to Liver Disease
- Age (> 60 years old)
- Past history of hematemesis and melena
- History of Hepatitis C (known history of
liver disease)
- Intravenous drug user
- Alcohol consumer and smoker
- Abdominal pain
- Loss of appetite
- Unknown loss of weight
- Loose stool (diarrhea)
- Weakness & Fatigue
15. Differential Diagnosis
DIAGNOSIS POINTS TO SUPPORT POINTS AGAINST
Peptic Ulcer Disease - Nausea & vomiting
- Unknown weight loss
- Loss of appetite
- Melena & hematemesis
(severe case)
- Smoking
- No abdominal bloating
- No burning pain before
or after meal
- No heartburn
- No indigestion
Esophageal Carcinoma - Gender - male
- Unknown weight loss
- Melena
- Hematemesis
- Vomiting
- Smoking
- Age (usually >65yrs)
- No persistent cough
- No hoarseness
- No indigestion
- No dyspepsia
- No heartburn
- No dysphagia
- No chest or back pain
16. Gastric Carcinoma - Age (common in elderly)
- Nausea or vomiting
- Loss of appetite
- Melena
- Hematemesis
- Weight loss
- Diarrhea
- Weakness and fatigue
- No indigestion
- No dysphagia
- No postprandial
fullness
- No palpable mass on
abdomen
- No heartburn
- No bloated feeling
after eating
DIAGNOSIS POINTS TO SUPPORT POINTS AGAINST
17. Investigations
Self revised Done by hospital
Full Blood Count Haemotological Test
Liver Function Test Renal Function Test
Renal Function Test Liver Function Test
Endoscopy (OGDS) Arterial Blood Gases
Coagulation Profile Chest X-Ray
Chest X-Ray Abdominal X-Ray
Abdominal X-Ray HIV Test
Hepatitis C Screening Hepatitis C Screening
Hepatitis B Screening
Rapid Plasma Reagin
18. 1) Haemotological Test
Test Patient’s Result Unit Normal Range Interpretation
RBC 2.68 10^6/uL 4.5 – 6.5 Low
WBC 19.6 10^3/uL 4 - 11 High
HGB 8.1 g/dL 13 - 18 Low
HCT 23.9 % 40 – 54 Low
MCV 89.2 fL 76 – 96 Normal
MCH 30.2 pg 27 – 32 Normal
PLT 207 10^3/uL 150 - 400 Normal
.
19. 2) Renal Function Test
Test Result Unit Range Interpretation
Urea 15.4 mmol/L 2.8 – 7.2 High
Sodium 140 mmol/L 136 – 145 Normal
Potassium 4.6 mmol/L 3.5 – 5.1 Normal
Chloride 104 mmol/L 98 – 107 Normal
Creatinine 95 umol/L 45 - 84 Normal
20. 3) Liver Function Test
Test
Patient’s
Result
Unit
Normal
Range
Interpretation
Total Protein 59 g/L 66 – 83 Low
Albumin 28 g/L 35 – 52 Low
Globulin 31 g/L 25 – 39 Normal
A/G Ratio 0.9 0:9 – 1:8 Normal
ALP 53 IU/L 30 – 120 Normal
ALT 79 IU/L 0 – 50 High
Total
Bilirubin
20.1 umol/L 5 - 21 Normal
21. 4) Arterial Blood Gas
Test Result Unit Range
pH 7.382 - 7.350 – 7.450
pCO2 37.1 mmHg 35.0 – 48.0
pO2 21.3 mmHg 83.0 - 108
5) HIV Test & Rapid Plasma Reagin
Test Result
HIV Ag/Ab Non-Reactive
Syphilis Reagin Ab Non-Reactive
22. 6) Hepatitis B Screening
Test Result
Hepatitis B e Ab Reactive
Hepatitis B e Ag Non-Reactive
Hepatitis B s Ag Non-Reactive
7) Hepatitis C Screening
Test Result
Anti HCV Reactive
HCV particle Agglutination Detected
25. CHILD-PUGH-SCORE (SEVERITY OF CIRRHOSIS)
CATEGORY 1 2 3
ENCEPHALOPATHY 0 I/II III/IV
ASCITES ABSENT MILD-MODERATE SEVERE
BILIRUBIN
(umol/L)
<34 34 – 51 >51
ALBUMIN(g/L) >35 28 – 35 <28
INR <1.3 1.3 – 1.5 >1.5
Score A : 6 or less
Score B : 7-9
Score C : 10 and greater
Encephalopathy
Grade I : confusion, altered mood and behaviour
Grade II : drowsy, inappropriate behaviour
Grade III : stuporous but obeys simple commands, slurred speech, marked confusion
Grade IV : unarousable coma
26. CATEGORY RESULT SCORE
ENCEPHALOPATHY No 1
ASCITES Mild 2
BILIRUBIN (umol/L) 20 1
ALBUMIN(g/L) 28 2
INR 1.7 3
Total score : 9
Grade : Child Pugh B
27. RESUSCITATION
• Vitals are monitored (pulse, BP, cardiac monitor, urine output)
• Assessment of haemodynamic stability – severity of blood loss
• IV Route - Fluid resuscitation such as normal saline
• Oxygen support to prevent hypoxia of tissues – nasal cannula
or facemask.
• Correction of coagulopathy and thrombocytopenia
• Urine output (through an indwelling catheter)
• Blood transfusion is administered to patients who are shocked
and are actively bleeding.
Management
28. • Pharmacological therapy : vasoconstrictors to arrest the
bleeding (terlipressin, octreotide, vasopressin, somatostatin)
• Banding
• Sclerotherapy
• Non-selective ß-adrenergic antagonists such as propranolol
and nadolol to prevent rebleeding.
• Transjugular Intrahepatic Portosystemic Shunt (TIPS)
• Distal Splenorenal Shunt (DSRS).
• Liver transplant
• Devascularization
• Esophageal transection
Management
31. a) Currently, no treatment can prevent the development of esophageal
varices in people with liver disease.
b) While beta blocker drugs are effective in preventing bleeding in
many people who have esophageal varices, they do not keep
esophageal varices from forming.
c) If one have been diagnosed with liver disease, strategies to avoid
liver disease complications should be taken.
- Don't drink alcohol.
- Eat a healthy diet.
- Reduce your risk of hepatitis.
Prevention
32. Discussion
• Portal venous pressure = portal venous flow x portal venous
resistance
• Hepatic venous pressure gradient (HVPG) is the difference in
pressure between the portal vein (wedged hepatic venous
pressure) and free hepatic vein pressure.
• HVPG = surrogate for portal pressure
• Increased HVPG > 5mmHg = Portal Hypertension
• Clinical manifestation of portal hypertension are many
included Esophageal Varices.
33. Increased portal pressure
(HVPG > 10mmHg)
Formation of varices
Dilatation of varices
Rupture of varices
(HVPG > 12mmHg)
Natural History
34.
35. Anatomy of esophagus
• The esophagus is a 25-cm long muscular tube that connects the
pharynx to the stomach.
• The esophagus extends from the lower border of the cricoid cartilage
(at the level of the 6th cervical vertebra) to the cardiac orifice of the
stomach at the side of the body of the 11th thoracic vertebra.
• The esophagus has 3 constrictions in its vertical course.
• These measurements are clinically important for endoscopy and
endoscopic surgeries of the esophagus.
• The esophagus has been subdivided into 3 portions:
a) Cervical
b) Thoracic
c) Abdominal
• Histologically, the esophagus has 4 concentric layers. (Mucosa,
Submucosa, Muscular, Adventitia)
36.
37. Blood supply
• Cervical portion : inferior thyroid artery
• Thoracic portion : bronchial and esophageal branches of the
thoracic aorta
• Abdominal portion : ascending branches of the left phrenic and left
gastric arteries.
Venous drainage
• Venous blood from the esophagus drains into a submucosal plexus.
From this plexus, blood drains to the periesophageal venous plexus.
Esophageal veins arise from this plexus and drain in a segmental
way similar to the arterial supply, as follows:
• From the cervical esophagus, veins drain into the inferior thyroid
vein
• From the thoracic esophagus, veins drain into the azygos veins,
hemiazygos, intercostal, and bronchial veins
• From the abdominal portion, esophagus veins drain into the left
gastric vein; the left gastric vein is a tributary of the portal system.
38. Risk Factors
• High portal vein pressure. The risk of bleeding increases with the
amount of pressure in the portal vein (portal hypertension).
• Large varices. The larger the varices, the more likely they are to
bleed.
• Red marks on the varices. When viewed through an endoscope
passed down your throat, some varices show long, red streaks or
red spots. These marks indicate a high risk of bleeding.
• Severe cirrhosis or liver failure. Most often, the more severe your
liver disease, the more likely varices are to bleed.
• Continued alcohol use. Your risk of variceal bleeding is far greater if
you continue to drink than if you stop, especially if your disease is
alcohol related.
• Bacterial infection - schistosomiasis
39. Sign & Symptoms
1) Vomiting blood (in large amount) can cause
- Dizziness
- Loss consciousness
- Pallor
- Anaemia
2) Some patient bleed in smaller amount over a longer period, they
swallow the blood rather than vomit it, so they may have :
- Black, tarry or bloody stools
3) Shock and sepsis(in severe cases)
4) Low blood pressure (hypotension)
5) Rapid heart rate (tachycardia)
6) Abdominal pain
7) Confusion secondary to encephalopathy
40. Signs of liver disease :
1) Jaundice (yellow discoloration)
2) Spider nevi (cluster of tiny blood vessels shaped like spider)
3) Palmar erythema (Reddening on palm)
4) Splenomegaly
5) Hand deformity known as Dupuytren’s contracture
6) Testicular atrophy
7) Ascites (fluid build up)
8) Gynaecomastia
9) Hair Loss
10) Pruritus
11) Muscle loss
41. • Encephalopathy (sometimes called hepatic encephalopathy)
• Esophageal stricture after surgery or endoscopic therapy
• Hypovolemic shock
• Infection (pneumonia, bloodstream infection, peritonitis)
• Rebleeding after treatment
• Kidney failure
Possible Complications
42. References
• Bailey & Love's Short Practice of Surgery, 25th
edn
• http://www.hopkinsmedicine.org
• http://www.slideshare.net
• http://www.nlm.nih.gov
• http://emedicine.medscape.com
Video Capsule Endoscopy (VCE) may be an alternative
Coagulation profile : prothrombin time with activated partial thromboplastin time and an international normalised ratio (INR), fibrinogen level.
-consumptive coagulopathy may occur with UGIB. This ass with thrombocytopenia. Platelet count < than 50 with active bleeding
1. Assessment of severity of blood loss :- An orthostatic decrease of 20 mm Hg in systolic blood pressure or increases in the pulse of 20 beats / min. indicate – 10% blood loss, if pt is pulsless and in shock- > 20% loss.
2. Fluid resuscitation is done by crystalloids such as normal saline or RL if hypoalbuminemia is detected use colloids.
3. Blood is also transfused when the haemoglobin concentration is less than 100 g/l
Optimum resuscitation must be done before endoscopy is undertaken. Endoscopy is dangerous in the haemodynamically compromised or hypoxic patient.
-Banding. A small rubber bands placed directly over the varices. This will stop the bleeding and get rid of the varices.
-Sclerotherapy. The varices are directly injected with a blood-clotting solution instead of banding them.
-TIPS A stent (a tubular device) is placed in the middle of the liver. The stent connects the hepatic vein with the portal vein. This procedure is done by placing a catheter through a vein in the neck. It is done to relieve the high BP that has built up in the liver.
Distal Splenorenal Shunt (DSRS). A surgical procedure that connects the splenic vein to the left kidney vein in order to reduce pressure in the varices and control bleeding.
Liver transplant This can be done in cases of end-stage liver disease.
Devascularization. procedure of removing the bleeding varices. This is done when a TIPS or a surgical shunt isn't possible or unsuccessful in controlling the bleeding.
Esophageal transection. A surgical procedure in which the esophagus is cut through and then stapled back together after the varicies have been tied off. Sometimes there is bleeding at the staple line
Don't drink alcohol. Since alcohol is processed by the liver. Drinking alcohol may stress an already vulnerable liver.
Eat a healthy diet. Choose a plant-based diet, whole grains and lean sources of protein. Reduce the amount of fatty and fried foods.
Maintain a healthy weight. An excess amount of body fat can damage liver. Obesity is associated with a greater risk of complications of cirrhosis. Lose weight if obese or overweight.
Reduce your risk of hepatitis. Sharing needles and having unprotected sex can increase your risk of hepatitis B and C.
CONSTRICTIONS
1st : At 15 cm from the upper incisor teeth, where the esophagus commences at the cricopharyngeal sphincter; this is the narrowest portion of the esophagus and approximately corresponds to the sixth cervical vertebra.
2nd : At 23 cm from the upper incisor teeth, where it is crossed by the aortic arch and left main bronchus
3rd : At 40 cm from the upper incisor teeth, where it pierces the diaphragm; the lower esophageal sphincter (LES) is situated at this level.
PORTIONS
The cervical portion extends from the cricopharyngeus to the suprasternal notch
The thoracic portion extends from the suprasternal notch to the diaphragm
The abdominal portion extends from the diaphragm to the cardiac portion of the stomach.
The upper esophageal sphincter (UES) is a bundle of muscles at the top of the esophagus. The muscles of the UES are under conscious control, used when breathing, eating, belching, and vomiting. They keep food and secretions from going down the windpipe.
The lower esophageal sphincter (LES) is a bundle of muscles at the low end of the esophagus, where it meets the stomach. When the LES is closed, it prevents acid and stomach contents from traveling backwards from the stomach. The LES muscles are not under voluntary control.
Although many people with advanced liver disease develop esophageal varices, most won't experience bleeding. Varices are more likely to bleed if you have:
EV usually don’t cause S&S unless they bleed.
Patient maybe suspect varices if they have any signs of liver disease :