BIMONTHLY INTERNAL ASSESSMENT - MARCH 2021


QUESTION 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?

60 year old male chronic smoker & alcoholic  non diabetic & non hypertensive

c/o fever since 15 days associated with burning micturition, on & off facial puffiness , abdominal distention , SOB Grade -2 which progressed to Grade -4 , aphthous ulcers & dysphagia.

O/E: Distended abdomen with dilated superficial abdominal vein

Shifting dullness +

Localization: Cirrhosis of liver with portal hypertension

UTI

AKI on CKD


    


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?

The etiology of the disease in this patient could be a chronic history of alcoholism.

Based on his history & clinical findings : chronic alcoholism ----> cirrhosis of liver ----> portal HTN

Cirrhosis of liver ----> reduced protein synthesis  ----> decreased serum albumin ----> hypoalbuminemia. 

Hypoalbuminemia can also be due to either increased excretion of protein in urine - nephrotic syndrome (Low SAAG) 

Or a long standing infectious etiology causing cachexia and hypoproteinemia (malnutrition / negative acute phase reactant)

Chronic smoking may be the cause of his apthous ulcers. 

Low SAAG is because this patient may have exudative pathology.


   


c)Will PT,INR derangement preceed hypoalbuminemia in liver dysfunction??Share reference articles if any!

The liver plays a central role in the clotting process, and acute and chronic liver diseases are invariably associated with coagulation disorders due to multiple causes: decreased synthesis of clotting and inhibitor factors, decreased clearance of activated factors, quantitative and qualitative platelet defects, hyperfibrinolysis, and accelerated intravascular coagulation.

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?

1) May be bone marrow tuberculosis because ascites is low SAAG ( exudative : ?TB) and same tuberculus bacillus may be invading the bone marrow

2) May be liver dysfunction causing haematological abnormalities like anemia and thrombocytopenia


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. 

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, but can also be seen in cardiac disease and systemic lupus erythematosus. 

Conditions with severe hypoalbuminemia and no pedal edema- There can be a compensatory synthesis of protiens (globulins) other than albumin and thereby maintain the oncotic pressure in the intravascular compartment and preventing the extravasation of fluid. This could also be possible if there is a hypovolemic state in the same patient with hypoalbuminemia so that the pressures are again maintained and there is no fluid accumulation. 

It is possible for one with hereditary analbuminemia to not have pedal edema. Since it is a chronic and hereditary disease there can be compensatory synthesis of other plasma proteins. 


f) What is the efficacy of each of the drugs listed in his current treatment plan

Tamsulosin :

1.α1-Adrenergic receptor antagonists are used by 80% of physicians as the first agent to treat patients with benign prostatic hyperplasia (BPH) presenting with lower urinary tract symptoms (LUTS); 27 of 30 clinical trials have confirmed that α-blockers are effective for BPH treatment.

2.Tamsulosin's α1A subtype adrenergic receptor selectivity is considered to be responsible for its low cardiovascular side effects and lack of interaction with antihypertensives.

3.A 4-year extension, multicenter, open-label, phase IIIB clinical study evaluated long-term efficacy, safety, and tolerability of tamsulosin for up to 6 years; the study found a consistent statistically significant improvement in AUA symptom scores over 6 years, and most patients showed improvement during the first year that was sustained over 6 years.

4.The low incidence of acute urinary retention in patients treated with tamsulosin for up to 6 years suggests that tamsulosin may reduce the risk of AUR in patients with BPH.

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1477608/

Nitrofurantoin




comparing 3 days of nitrofurantoin with placebo in young women with symptoms of UTI and pyuria found clinical cure rates of 70% versus 42%, respectively, 7 days after the start of therapy.

The prevalence of participants with side effects attributed to nitrofurantoin in the 17 studies generally ranged from 5% to 16%; nausea, abdominal discomfort and headaches were described. An exception was an open-label randomized controlled trial whose primary outcome was quality of life.




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?

1.Abdominal distension since 2years

2.shortness of breath 

3.pedal edema since 2 months

4.cachexia_malnourishment

Anatomical localisation:

1.abdominal distension : causes: fluid , fetus , flatus , fat , faeces , fatal tumors

Here in this case:

O/E: flank fullness and fluid thrill is present - indicates distension is because of fluid - ASCITIS

In this case the pattern is ascites followed by pedal edema _clinically it indicates problem is in liver.

2.shortness of breath and dull note in right side _ IAA,ISA,IMA and decreased breath sounds on right side indicates pleural effusion - hepatic hydrothorax

3.Cachexia - is due to her loss of appetite which in turn because of massive ascites .

Overall the major problem in this case - refractory ascites since 2 years.


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?

Sodium water retention due to underfill theory 

Increased portal pressure ( high SAAG) causing splanchnic vasodilation

And overfill theory is causing refractory ascites and hepatic hydrothorax is responsible for pleural effusion 

CAUSES OF REFRACTORY ASCITES:

1.Non compliance to treatment
2.Tumor_hepatoma
3.Renal failure
4.spotaneous bacterial peritonitis
5.Portal vein thrombosis
6.NSAIDS
7.Infection
8.GI Bleeding


c) Approach to a patient with ascites?Clinically is there any way to differentiate pre hepatic, post hepatic and hepatic causes

Approach to a patient with ascites


Hepatic : patient has cirrhosis of liver ( shrunken nodular on usg) with liver failure symptoms and signs splenomegaly varices

Pre hepatic : dilated veins and congenital umbilical webs

Post hepatic : raised jvp with heart failure features


   


d) Causes of budd chiari syndrome?Why did the patient undergo bone biopsy?

           

IN THIS CASE BONE BIOPSY DONE FROM POSTERIOR ILIAC CREST ON LEFT SIDE TO EVALUATE THE OSTEOSCLEROTIC LESIONS IN PELVIS , RIBS, VERTEBRAE .

Patients with myeloproliferative disorders also developed budd chiari 

So to look for any myeloproliferative disorders and for any bone metastasis bone biopsy was done


e) Management strategies for refractory ascites and Budd chiari syndrome? Share the potential advantages and disadvantages of Peritoneal dialysis catheter placement in refractory ascites?

1.Diagnosis of BCS made by clinical features, laboratory and radiological investigations , management of underlying cause

2.Anti coagulant therapy with LMWH and then warfarin aim for INR 2-3

3.Treat the complications of portal hypertension with spirinolactone ,furosemide,and gastroscopy for variceal screening and band ligation

4.consider angioplasty /stenting for venous obstruction

5.consider TIPS if no improvement with anticoagulation , angioplasty, stenting.

6.TIPS fails /no improvement and acute liver failure consider liver transplantation.

7.Monitor chronic BCS for HCC by 6 monthly USG and alpha fetoprotein.

     
       



  



         


f) What is the efficacy of each of the drugs listed in his current treatment plan 

Lasilactone:


Warfarin and LMWH:



g)What is the current outcome?and what could be the etiology of her current outcome

Patient got expired on 14th of march preceded by 1 day h/o vomiting and nausea.

Cause of death was not confirmed, may be because of dislodgement of thrombus leading to pulmonary embolism.



QUESTION 3

55year old male with SOB and abdominal distension,orthopnea


a). What is the problem representation of this patient and what is the anatomical localization for his current problem based on the clinical findings?

55 male chronic smoker & alcoholic k/c/o COPD with RHF (cor pulmonale) since 6 years

C/o abdominal distention & pedal edema since 1 year which aggregated from 1 week associated with SOB grade 3-4 , decreased urine output , on & off facial puffiness & anasarca

Based on the history & clinical findings his problem localization

COPD ----> RHF (corpulmonale) ----> Pre renal AKI (?CRS-1) & ?congestive hepatopathy


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.

COPD ----> RHF (corpulmonale) ----> Pre renal AKI (?CRS-1) & ?Congestive hepatopathy ----> Ascites

SAAG is 1.9 suggestive of portal hypertensive but low asctic protein of 2.1 and one of the important cause of high SAAG low protein is cirrhosis of liver which can be attributed to alcohol but USG abdomen shows normal liver.

So the other differential is heart failure causing ascites (but ascitic protein should be more than 2.5) 


But by going through the events it could be a mixed ascites.



c)What is the efficacy of each of the drugs listed in his treatment plan?

1. LASIX : Mortality: 3 placebo-controlled trials (n=221) reported data; the OR was 0.25 (95% confidence interval, CI: 0.07, 0.84, P=0.03), representing an absolute risk reduction of 8% in mortality in patients treated with diuretics compared to placebo.

Worsening of heart failure: 4 placebo-controlled trials (n=448) and 4 active-controlled trials (n=177) reported data. The OR was 0.31 (95% CI: 0.15, 0.62, P=0.001) for the placebo-controlled trials and 0.34 (95% CI:0.10, 1.21, P=0.10) for the active-controlled trials.

https://www.ncbi.nlm.nih.gov/books/NBK69174/

2. SALT AND FLUID RESTRICTION

https://pubmed.ncbi.nlm.nih.gov/23787719/

Individualized salt and fluid restriction can improve signs and symptoms of CHF with no negative effects on thirst, appetite, or QoL in patients with moderate to severe CHF and previous signs of fluid retention.


d)What are his current outcomes ?

Patient had cardiopulmonary arrest secondary to acute exacerbation of COPD with corpulmonale & severe PAH (Type-3)



QUESTION 4

Please go through the thesis presentation below and answer the questions below by also discussing them with the presenter


a) What was the research question in the above thesis presentation? 

To know the etiology of ascites based on SAAG 


b) What was the researcher's hypothesis? 

SAAG is better for etiological diagnosis of ascites than asctic fluid total protein as a marker


c) What is the current available sensitivity and specificity of SAAG in diagnosis of etiology of ascites

The sensitivity and specificity of SAAG were 100% and 87.8% respectively. Serum ascites albumin gradient is a reliable marker to differentiate ascites into portal hypertensive and non-portal hypertensive etiology. the presence of oesophageal varices is significantly associated with high SAAG levels.

When using the SAAG cut-off value 1.1 g/L, its sensitivity and specificity were 100.00% and 85.19% with an accuracy of 94.37%.




QUESTION 5

5) Journal club questions on Ascites theme 

a) Please identify the study design and outcomes in the article linked here https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6644216/ as well as the thesis linked here https://chandanavishwanatham19.blogspot.com/2021/03/of-thesis-clinical-profileevaluationdia.html

The study design was a prospective study and it showed that liver cirrhosis is the main cause of ascites among the 52 patients included in the study and next most common cause being heart failure and nephrotic syndrome
And the etiology of liver cirrhosis being HCV HBV virus.


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