BIMONTHLY ASSESSMENT BYMADDIPATI SRIDEVI
Bimonthly assessment for the month of March 2021
PATIENT WAS APPARENTLY ASYMPTOMATIC BEFORE,
HE DEVELOPED FEVER SINCE 15 DAYS, (HIGH GRADE),INTERMITTENT, NOT ASSOCIATED WITH CHILLS AND, RELIEVED WITH MEDICATION.
NO H/O COUGH, NO SPUTUM, COLD, PAIN ABDOMEN
BURNING MICTURITON +, INTERMITTENTLY SOB +,ON EXCERTION LATER PROGRESSED TO REST ,
NO ORTHOPNEA, NO PND ,NO CHEST PAIN NO PALPITATIONS, NO PEDAL EDEMA.
ON /OFF FACIAL PUFFINESS +
?APTHOUS ULCERS, DIFFICULTY IN SWALLOWING
Problem representation:
A case of 60 year old male with following complaints: fever which is high grade , intermittent in nature since 15 days sob which is intermittent since 3 days , ass with burning micturtion, facial puffiness, aphthous ulcer
No other comorbidities. . However he is a chronic alcoholic and smoker
Anatomical localisation of his current problem::
All these conditions point to liver pathology
About his superficial abdominal veins :
For a long term alcoholic, he could be a risk factor to develop portal hypertension, which may be present with superficial abdominal veins and varices
Other differentials include:
Caput medusae due to portal hypertension
Dilated veins in IVC
Congenital
Obstruction of IVC
Ans:Etiology/causes could be: Alcoholism affecting liver, Smoking affecting his oral cavity causing aphthous ulcers
Patients with advanced cirrhosis almost always have hypoalbuminemia caused both by decreased synthesis by the hepatocytes and water and sodium retention that dilutes the content of albumin in the extracellular space.
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?
e)Can there be conditions with severe hypoalbuminemia but no pedal edema?j 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
Tamsulosin efficacyAns: tamsulosin efficacy in UTI patients
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1477608/
Nitrofurantoin efficay
https://academic.oup.com/jac/article/70/9/2456/721364
Question 2
45year old female with abdominal distension
Following is the link
https://navyamallempalli.blogspot.com/2021/02/dr_6.html
a). What is the problem representation of this patient and what is the anatomical localization for her current problem based on the clinical findings?
A 45 year old female with complaints of abdominal distension since 2 years and pedal edema since 2 months, with increasing distension causing difficulty in eating drinking ,though she has a good appetite and able to fulfill it.
She’s k/c/o DM since one year.Took medicines for 6 months and stopped.
All of the above complaints point to 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.
c) Approach to a patient with ascites?Clinically is there any way to differentiate pre hepatic, post hepatic and hepatic causes?
d)Causes of budd chiari syndrome?Why did the patient undergo bone biopsy?
2d) why did the pt undergo Bone marrow biopsy?Primary Budd-Chiari syndrome 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.
d) Management strategies for refractory ascites and Budd chiari syndrome? Share the potential advantages and disadvantages of Peritoneal dialysis catheter placement in refractory ascites?
Treatment
Treatment of Budd-Chiari syndrome is most successful if the disorder is diagnosed early. There are also various methods of treatment. The use of high doses of the corticosteroid drug, prednisone, may also be administered. Drugs that hinder blood clotting (anticoagulants) such as heparin may be beneficial for treatment of individuals with Budd-Chiari syndrome.
Surgical widening (dilation) of affected veins (angioplasty) may ease high pressure in the vessel walls. In some cases, Budd-Chiari syndrome may be treated surgically by diverting blood flow from one vein to another (shunting). In other cases, a blocked vein may be cleared out and then a slender rod (stent) may be inserted into the vein to maintain blood flow. In serious cases of Budd-Chiari syndrome, liver transplantation may be necessary
.
e) What is the efficacy of each of the drugs listed in his current treatment plan
f)What is the current outcome?and what could be the etiology of her current outcome?
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?
3a
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
Anatomical Localization
Features like Pedal edema, Ascites, Orthopnea suggest Heart (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!
The reason for ascitis in this patient could be RHF. RHF leads to congestive hepatomegaly and thereby derranging the synthetic funtion of the liver to produce albumin. And hypoalbuminemia leads to fluid accumulation.
c)What is the efficacy of each of the drugs listed in his treatment plan?
LASIX (furosemide) - FDA
https://www.google.com/url?sa=t&source=web&rct=j&url=https://www.accessdata.fda.gov/drugsatfda_docs/label/2012/016273s066lbl.pdf&ved=2ahUKEwjO0_fht8PvAhW1yTgGHf32BtwQFjABegQIAxAG&usg=AOvVaw24Pg-DhNjrqyeUwfGu4_aV
diuretics used are furosemide, bumetanide and chlorothiazide. The available data from several small controlled trials show that in patients with CHF, conventional diuretics appear to reduce the risk of death and worsening heart failure when compared to an inactive sugar pill (placebo). About 80 deaths may be avoided for every 1000 people treated. Diuretics also increase the ability to exercise, by about 28% to 33% more than with other active drugs. These conclusions were based on 14 controlled trials (525 people), of which three trials noted deaths in 202 people randomised to receive either diuretic or placebo, and two trials, a total of 169 people, looked at hospitalisation for worsening heart failure. Of the seven trials comparing diuretic treatment with another drug, the effects on exercise were studied in four trials where 91 people were randomised to receive either a diuretic or an ACE inhibitor or digoxin. Most of the trials had small numbers and lasted from 4 to 24 weeks, a short time for a chronic disease. The age of the participants was 59 years, which is relatively young, and the use of diuretic drug was not standardised across the studies. More research would be needed to further confirm the long term benefits of diuretic treatment for CHF patients because these studies were small.”
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6413766/
d)What are his current outcomes ?
- The patient can go in cardiopulmonary arrest.
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).
Question 5 :
5) Journal club questions on Ascites theme
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
STUDY DESIGN
Institution-based cross-sectional study.
THESIS IS ABOUT:
CLINICAL PROFILE,EVALUATION,DIAGNOSIS AND THERAPEUTIC OUTCOMES IN PATIENTS WITH ASCITES
STUDY DESIGN
Prospective study, Qualitative, Non Experimental
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