Bimonthly assessment for the month of march
Submission of bimonthly assessment for the month of march
Question 1:1) Please go through the patient data in the links below and answer the following questions:
https://ashakiran923.blogspot.com/2021/03/60-years-old-male-fever-under-evaluation.html?m=1
a). What is the problem representation of this patient and what is the anatomical localization for his current problem based on the clinical findings?How specific is his dilated superficial Abdominal vein in making diagnosis?
Answer --
Problem presentation:
From history :
⏩High Grade Fever intermittent since 15 days reliving with medication not associated with chills rigor
⏩SOB (grade 2-3 ) progressed to grade 4 occurring even on rest since 3 days
⏩Pain in abdomen + (didn't mention the duration)
⏩on and off Facial puffiness +( progression not being mentioned)
⏩Chronic smoker and Chronic alcoholic (duration not being mentioned)
, ⏩apthous ulcers
Examination findings:
Pallor +
Cvs-apex beat in 6th ICS- pointing displaced apex beat may be because of ventricular hypertrophy
P/a- Abdomen distended +
Guarding +
Shifting dullness+
Localisation of lesion :
From history and examination--
1) As the patient is a chronic smoker and chronic alcoholic
🔽
Possibility of pathological changes occuring in the liver and lung (of course other organs being affected too)
Examination of par abdomen - since there is no organomegaly --
🔽
LIKELY POSSIBILITY OF SHRUNKEN LIVER ( CIRROHOTIC LIVER) or normal liver
2)High grade fever intermittent not associated with chills rigor ruling out the possibility of an abscess in the body
3) Pain in abdomen +(duration,diffuse or localized??H/O vomting or h/O constipation, H/o any abdominal surgery not being mentioned)
🔽
D/d
1)Intestinal obstruction (as bowel sounds are not heard o/e)
2) Diseases of liver - hepatitis, cirrhosis ( guarding+, shifting dullness+ due to gross ascites which is around 500-1000ml )
Based on the above findings I attribute this to a liver problem
1 answer-
Dilated superficial veins----
Chronic alcoholic
🔽
risk factor to develop portal hypertension
🔽
Presents with superficial abdominal veins and varices
Other differentials include:
Caput medusae due to portal hypertension
Dilated veins in IVC
Congenital
Obstruction of IVC
b) What is the etiology of the current problem and how would you as a member of the treating team arrive at a diagnosis? What is the cause of his hypoalbuminemia?Why is the SAAG low?
Etiology :
1) cirrhosis of liver
2) Hepatitis
3) Chronic malnutrition from protein losing enteropathy such as ulcerative collitis
4) Intestinal obstruction
Cause of his hypoalbuminemia-
Binge drinking
🔽
Alcoholic hepatitis resulting from chemical injury because of acetaldehyde
🔽
Swelling of hepatocytes with formation of Mai Lory bodies
🔽
Presents with painful hepatomegaly
🔽
Cirrhosis long term complication due to fibrosis mediated by TGF from stellate cells
🔽
Cf -
Portal hypertension
Ascites
Splenomegaly
Hypoalbuminemia (as albumin is synthesized in the liver)
Mental status changes
1c) SAAG- SERUM ASCITIC ALBUMIN GRADIENT
Measured as saag =(serum albumin -ascitic albumin)
His saag is low because as the patient is having hypoalbuminemia due to liver cirrhosis
🔽
Decrease oncotic pressure with increasing hydrostatic pressure
🔽
Thus the fluid moves into the peritoneum causing ascites
🔽
Albumin being a heavier molecule on the other side stays in the blood vessel
Source
https://en.wikipedia.org/wiki/Serum-ascites_albumin_gradient
c)Will PT,INR derangement preceed hypoalbuminemia in liver dysfunction??Share reference articles if any!
Yes,
⏩PT is a measure of extrinsic and common pathways
Liver dysfunction
🔽
Decreased synthesis of clotting factors
🔽
⬇activation of vitamin k by epoxide reducatase
Source
https://www.medscape.com/answers/177354-36077/what-is-the-role-of-prothrombin-time-pt-in-the-evaluation-of-acute-liver-failure
d)What is the etiology of his fever and pancytopenia?
e)Can there be conditions with severe hypoalbuminemia but no pedal edema? Can one have hereditary analbuminemia and yet have minimal edema? Please go this article https://www.frontiersin.org/articles/10.3389/fgene.2019.00336/full and answer the question
Yes
Inflammation and infection
Albumin is considered a negative acute phase reactant, which means that as inflammation and other acute physiologic processes occur, its levels decrease
In liver disease:Albumin is synthesized in the liver, and low serum albumin can be indicative of liver failure or diseases such as cirrhosis and chronic hepatitis. If present, hypoalbuminemia is generally considered to be a sign of advanced hepatic cirrhosis, or irreversible damage to the liver
Malnutrition or malabsorption
Low albumin levels can also indicate chronic malnutrition from protein losing enteropathy.[3] This is often caused or exacerbated by ulcerative colitis,[10] but can also be seen in cardiac disease and systemic lupus erythematosus
F) What is the efficacy of each of the drugs listed in his current treatment plan
1) Tamsulosin efficacy
Source
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1477608/
2) Nitrofurantoin efficacy
https://academic.oup.com/jac/article/70/9/2456/721364
3) Ecospirin
www.ncbi.nlm.nih.gov › NBK548900
Web results
Aspirin - LiverTox - NCBI Bookshelf
4) Atrovas
www.ncbi.nlm.nih.gov › articles › P...
Web results
Use of Statins in Patients with Chronic Liver Disease and Cirrhosis: Current ...
5) clopidogrel
www.ncbi.nlm.nih.gov › NBK547946
Web results
Clopidogrel - LiverTox - NCBI Bookshelf
QUESTION 2
45year old female with abdominal distension
A). What is the problem representation of this patient and what is the anatomical localization for her current problem based on the clinical findings?
Problem presentation
⏩abdominal distension since 2 years, insidious in onset rapidly progressed since last year troubling her in doing her daily activities like eating, drinking even though she has a fair amount of appetite
⏩ pedal edema since 2 months
⏩k/c/O Diabetic since 6 years took medicines and stopped for 6 months
Anatomical localisation
Based on history
As edema developed first in the abdomen
Cause likely is in the liver
On examination
Malnourished, clubbing +
P/a -ovoid distension of abdomen, slit like umbilicus
Fluid thrill + (implies around 1000-2000ml fluid is present in the abdominal cavity)
All the above indicate a liver pathology
b) What is the etiology of her refractory ascites and pleural effusion? and how would you as a member of the treating team arrive at a diagnosis?
Refractory ascites is defined as ascites that does not recede or that recurs shortly after therapeutic paracentesis, despite sodium restriction and diuretic treatment. To date, there is no approved medical therapy specifically for refractory ascitis
The diagnostic criteria of refractory ascites consist of ascites that cannot be mobilized with early recurrence within 4 weeks of abdominal paracentesis and lack of response to maximal doses of diuretic (spironolactone 400 mg/d and furosemide 160 mg/d) for at least 1 week.
Etiolgy of refractory ascites
Right sided pleural effusion being more common because there are connections from the bare of liver to lung through the diaphragm
Hepatic hydrothorax
c) Approach to a patient with ascites?Clinically is there any way to differentiate pre hepatic, post hepatic and hepatic causes?
Approach to pt with ascites

Source
Doctorlib.info
Ascites - Common Patient Presentations - Harrisons Manual of ...




source
www.ncbi.nlm.nih.gov › articles › P...
ABC of diseases of liver, pancreas, and biliary system: Investigation of liver ...
d)Causes of budd chiari syndrome?Why did the patient undergo bone biopsy?
Causes of budd chiari syndrome are
D)The pt underwent Bone marrow biopsy because suspecting a Primary Budd-Chiari syndrome which is characterized by a blocked hepatic venous outflow tract at various levels from small hepatic veins to inferior vena cava, resulting from thrombosis or its fibrous sequellae. This rare disease affects mainly young adults. Multiple risk factors have been identified and are often combined in the same patient. Myeloproliferative diseases of atypical presentation account for nearly 50% of patients; their diagnosis can be made by showing the V617F mutation in Janus tyrosine kinase-2 gene of peripheral blood granulocytes and, should this mutation be absent, by showing clusters of dystrophic megacaryocytes at bone marrow biopsy.
Source
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4147117/
D)Management strategies for refractory ascites and Budd chiari syndrome? Share the potential advantages and disadvantages of Peritoneal dialysis catheter placement in refractory ascites?
Management of refractory ascites
Source
Clinical Gastroenterology and Hepatology
Cirrhosis With Refractory Ascites: Serial Large Volume ...
Management of budd chiari syndrome-
Source
Postgraduate Medical Journal - The BMJ
Budd–Chiari syndrome: investigation, treatment and outcomes ...
emedicine.medscape.com
Budd-Chiari Syndrome Treatment & Management: Approach ...
⏩Advantages, Disadvantages of peritoneal dialysis
Source
https://www.researchgate.net/figure/Advantages-and-disadvantages-of-peritoneal-dialysis-in-patients-with-chronic-kidney_tbl1_51842873
pubmed.ncbi.nlm.nih.gov › ...
[Peritoneal dialysis in cirrhotic patients] - Pub Med
E) What is the efficacy of each of the drugs listed in his current treatment plan
1- fluid, salt restrictions
Source
www.ncbi.nlm.nih.gov › articles › P...
Web results
Sodium restriction in patients with cirrhotic ascites: a protocol for a ...
2) Lasix
Source
www.medscape.com › answers › wh...
Web results
What is the role of furosemide in the treatment of ascites and cirrhosis?
3) spironolactone
Source
Diagnosis and therapy of ascites in liver cirrhosis
www.medscape.com › answers › wh...
What is the role of furosemide in the treatment of ascites and cirrhosis?
f)What is the current outcome?and what could be the etiology of her current outcome?
Current outcome - Death of the patient
Etiology could possibly be because of liver failure
Sequence of events
Shrunken right lobe of liver with hypertrophy of left lobe
🔽
Hypoalbuminemia, unable to detoxifiy of toxins , refractory ascites, mental status changes( hepatic encephalopathy)
Disturbance in coagulation resulting in Microvascular clots and DIC
🔽
End stage Liver failure
🔽
Death
QUESTION 3
55year old male with SOB and abdominal distension,orthopnea
https://jayanth1802.blogspot.com/2021/02/55-year-old-farmer-with-sob-abdominal.html?m=1
A) What is the problem representation of this patient and what is the anatomical localization for his current problem based on the clinical findings?
Problem representation -
Abdominal distention with scrotal swelling since 1 week
SOB grade IV since 4 days
SOB on lying down since 3days
Pedal edema since 3 days
O/e increased JVP upto angle of mandible
Pansystolic murmur +
Anatomical Localization
Features like Pedal edema, Ascites, Orthopnea suggest Heart problem (Right heart failure)
His current problem
Cor Pulmonale with severe PAH Grade III with AKI, Congestive hepatomegaly & gross ascites.
Above symptoms have aggravated since 1 week associated with constipation since 1 week, relieved on taking medication.
Decreased urine output intermittently, facial puffiness and anasarca relieved on medication.
Symptoms increased on intake of alcohol, non adherence to diet.
B) What is the etiology of his ascites? and how would you as a member of the treating team arrive at a diagnosis?Chart out the sequence of events!
Etiology of ascites in this case is due to CARDIAC CIRROHOSIS
Events
History
Chronic smoker and alcoholic
🔽
Copd changes in the lung,
Cirrohotic changes in the liver
Superimposed with severe tricuspid regurgitation in the patient
🔽
Resulting in Pulmonary arterial hypertension
🔽
Increase preload
🔽
Increase back pressure to hepatic veins
🔽
Resulting in Congestive hepatomegaly
🔽
Decreased perfusion of oxygen, hemorrhagic injury, modification of hepatic architecture
🔽
Chronic congestion can lead to hastening of liver cirrhosis (also occuring due to alcohol)
Source
https://www.ncbi.nlm.nih.gov/books/NBK431053/
Source
CJASN
Pulmonary Hypertension, Right Ventricular Failure, and Kidney ...
c)What is the efficacy of each of the drugs listed in his treatment plan?
1) fluid and salt restriction
Source
⏩Sodium Restriction in Heart Failure: Benefit or Harm? - NCBI - NIH
⏩www.medscape.com › viewarticle
Sodium Restriction in Heart Failure - Medscape
⏩trialsjournal.biomedcentral.com
Web results
Effect of fluid and dietary sodium restriction in the management of ...
2) Lasix in heart failure
Source
⏩www.medscape.com › answers › wh...
What is the role of diuretics in the management of pulmonary arterial ...
3) Salbutamol beta blocker
⏩Source
www.ahajournals.org
Web results
Use of β-Blockers in Pulmonary Hypertension | Circulation: Heart Failure
⏩www.sciencedirect.com › article › pii
Web results
Heart Failure and Chronic Obstructive Pulmonary Disease: The Quandary of ...
⏩
thorax.bmj.com › content
Web results
β-Blockers, heart disease and COPD: current controversies and ...
4) Hydrocortisone
As it improves oxygenation
Source
ResearchGate
PDF) Hydrocortisone Improves Oxygenation Index and Systolic Blood ...
d)What are his current outcomes ?
Immediate cause of Death due to cardiopulmonary arrest
Because of
Acute exacerbation of copd with cor pulmonale grade 3
Pre renal AKI
QUESTION 4
4)Please go through the thesis presentation below and answer the questions below by also discussing them with the presenter
https://youtu.be/QlPrb1BSHGE
a)What was the research question in the above thesis presentation?
-Role of SAAG in diagnosing the etiology of ascitis.
b) What was the researcher's hypothesis?
41/F, with retro virus positive, c/o : abdominal distension (duration ?) , fever— was diagnosed as ascitis secondary to Chronic liver disease.
First they thought the ascitis maybe secondary to TB (TUBERCULAR PERITONITIS) .
🔽
Peritoneal Paracentesis is performed, SAAG was expected to be low, but the result of SAAG, took a 360 degree turn in diagnosing the patient.
🔽
SAAG RESULT came out HIGH, after which they suspected ART (anti retro-viral therapy) INJURY TO HEPATOCYTES leading to CHRONIC LIVER DISEASE
c)What is the current available sensitivity and specificity of SAAG in diagnosis of etiology of ascites
When using the SAAG cut-off value 11 g/L, its sensitivity and specificity were 100.00% and 85.19% with an accuracy of 94.37%.
https://diagnosticpathology.biomedcentral.com/articles/10.1186/1746-1596-8-143#:~:text=When%20using%20the%20SAAG%20cut,%25%2C%20P%3C0.01).
Comments
Post a Comment