BIMONTHLY ASSESSMENT ( February)

 Questions:

1)50 year man, he presented with the complaints of

Frequently walking into objects along with frequent falls since 1.5 years

Drooping of eyelids since 1.5 years

Involuntary movements of hands since 1.5 years 

Talking to self since 1.5 years 

https://archanareddy07.blogspot.com/2021/02/50m-with-parkinsonism.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?

A)chronic smoker and  tobacco chewer

H/o left lower limb fracture 2 years back

Started 15 years ago, initially chewed 1 or 2 packs/day & gradually increased to 3-4/day and even 5-7 on a few days. Abruptly stopped consuming both alcohol & khaini after the RTA in June, 2018. Son has offered khaini several times after, but the patient was very reluctant eversince.

Now presenting complaints are frequently walking into objects along with frequent falls since, Drooping of eyelids(progressing as the day passes) and ,involuntary movements of hands ,Talking to self since 1.5 years . previously aggressive and now not expressing emotions,and also thin urine stream since 1year,chronic hypokalemia,Anatomical location :Basal ganglia

b) What is the etiology of the current problem and how would you as a member of the treating team arrive at a diagnosis? Please chart out the sequence of events timeline between the manifestations of each of his problems and current outcomes. 

1) Reduced arm span 

2) progressive ptosis 

 c)chat is the efficacy of each of the drugs listed in his current treatment plan 

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3228622/

2) Patient was apparently asymptomatic 2 years back then he developed weakness in the right upper and lower limb, loss of speech.

 https://ashfaqtaj098.blogspot.com/2021/02/60-year-old-male-patient-with-hrref.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?

A)progressive sob from grade 2 to 4 since 2 months

orthopnea,pnd

b/l pedal edema upto knee since 2 months

Generalised weakness since 2 months

H/o cva (rt hemiparesis recovered) with persistent loss of speech since 2 years.

anatomical localisation

Based on history:pnd ,sob with orthopnea suggest left heart failure

based on examination:

shift of apex to 6th ics,presence of thrill palpable at apex(?s1), nature of the apex not mentioned

presence of loud p2 ,dilated veins ,pedal edema,s3 in both apical and left parasternal areas.

(?biventricular failure)

b) What is the etiology of the current problem and how would you as a member of the treating team arrive at a diagnosis? Please chart out the sequence of events timeline between the manifestations of each of his problems and current outcomes. 

Etiology:

CAD

Ecg showing 

1)normal axis

2)pathological Q waves from v1 to v6

3)poor R wave progression

suggest a CAD probably involving LAD and LCX territory 

confirmed with finding on the echo leading to heart failure

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

1)salt and fluid restriction

https://pubmed.ncbi.nlm.nih.gov/23787719/#:~:text=Conclusion%3A%20Individualized%20salt%20and%20fluid,Quality%20of%20life%3B%20Salt%20restriction.

Ninety-seven stable patients in NYHA class II-IV, on optimal medication, with previous signs of fluid retention, treated with either >40 mg (NYHA III-IV) or >80 mg (NYHA II-IV) of furosemide daily were randomized to either individualized salt and fluid restriction or information given by the nurse-led heart failure clinics, e.g. be aware not to drink too much and use salt with caution, and followed for 12 weeks. Fluid was restricted to 1.5 L and salt to 5 g daily, and individualized dietary advice and support was given.

Results After 12 weeks, significantly more patients in the intervention than in the control group improved on the composite endpoint (51% vs. 16%; P < 0.001), mostly owing to improved NYHA class and leg oedema. No negative effects were seen on thirst, appetite, or QoL

2)benfomet as thiamine replacement in alcoholic pts

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4550087/

3)aldactone(spironolactone)

https://www.aafp.org/afp/2001/1015/p1393.html

Based on earlier work suggesting a benefit of therapy,2 the Randomized Aldactone Evaluation Study (RALES) was undertaken to evaluate the role of spironolactone when used in addition to standard therapy for CHF. Standard therapy in this study did not include beta blockers

 S-The investigators prospectively enrolled 1,663 patients with severe (New York Heart Association [NYHA] class IV) CHF (Table 1).4 Most of the enrolled patients were white men averaging 65 years of age. These patients had a left ventricular ejection fraction of 35 percent or less and marked physical limitations related to CHF. Patients were excluded if they had unstable angina or moderate renal failure, and if they were hyperkalemic.

All patients who could tolerate the drug were given an ACE inhibitor and a loop diuretic, and 70 percent were taking digoxin. Only 10 percent were taking beta blockers. Patients were randomly assigned to receive placebo or 25 mg of spironolactone daily in addition to their current regimen. After eight weeks, if the patient showed worsening CHF and had a stable potassium level, the dosage was increased to 50 mg daily. The dosage was decreased to 25 mg every other day if at any time the patient became hyperkalemic

https://soumya9814.blogspot.com/2021/01/this-is-online-e-log-book-to-discuss.html?m=1

a) What is the problem representation of this patient and what is the anatomical localization?

A)52 year old  male diabetic and hypertensive with complains of SOB, cough ,decrease sleep and appetite since 10 days

Pure vegetarian with hb 5.7,macrocytes on smear suggesting Vit B12 deficiency and electrolyte imbalance

Anatomical location

sob without pedal edema, pnd, orthopnea can be localised to the lung

(sob on exertion grade 2 can also be localised the heart but no history or examination finding of pedal edema or jvp rise rules it out

cough with sputum

b)What is the etiology of the current problem and how would you as a member of the treating team arrive at a diagnosis? Please chart out the sequence of events timeline between the manifestations of each of his problems and current outcomes. 

A)?Sub acute combined degeneration of spinal cord secondary to vit B12 deficiency.

?Diabetic neuropathy

?Hypervolemic hyponatremia secondary to heart failure

?Pseudohyponatremia secondary to uncontrolled sugars

c) What is the efficacy of each of the drugs listed in his current treatment plan especially for his hyponatremia? What is the efficacy of Vaptans over placebo? Can one give both 3% sodium as well as vaptan to the same patient?  

A)https://www.sciencedirect.com/science/article/pii/S0085253815551089

THE INDICATIONS FOR VAPTANS ARE NOT CLEAR

1-First, we do not know how to distinguish between symptoms that are an indication for vaptan and those that are not.

2-Together, we lack information on which degree of severity of hyponatremia should give us reason to consider vaptan treatment.

3-Third, work by Gankam Kengne et al.28 suggested that patients with mild chronic hyponatremia fall to the ground more often than matched normonatremic controls .

We are unable to answer the question of whether elderly patients with chronic mild hyponatremia should be treated, for example, by a vaptan to correct hyponatremia and prevent fractures.

4-Fourth, in terms of indication for vaptan, the area least controversial might appear to be that of severe symptomatic (chronic) hyponatremia. A ‘hyponatremia-naive’ physician is likely to conclude that vaptans if anything should be promising in severe symptomatic hyponatremia. However, there are literally no published data on this. Clinical trials of vaptans have consistently excluded severe symptomatic hyponatremia from study because of ethical concerns (risk of worsening of severe symptoms when receiving placebo)

recent expert panel suggested that in severe symptomatic (chronic) hyponatremia, infusions of hypertonic saline should have priority over vaptan.30 This is an area of significant uncertainty. It has been pointed out that 3% NaCl may correct hyponatremia too quickly,31 or it may occasionally lead to pulmonary edema in SIAD(H). On the other hand, we have personal experience (PAG) that SIAD(H)-related severe symptomatic hyponatremia is a rewarding indication for vaptan. Thus, in the absence of a trial comparing fluid restriction plus 3% saline with vaptans in severe symptomatic hyponatremia, we do not have a database to make specific recommendations for or against vaptans.

4) Please mention your individual learning experiences from this month.

Posted in ICU 

1) Learned about the ventilator settings 

2) Placed 3 central lines 

3) Learned about the heart blocks in CKD pt 

4) MOA of tamsulosin in BPH 

5) Approch to sudden onset of sob in CKD patients

6) CSF analysis

7) Difference between traumatic tap and subarchnoid haemorrhage

8) Management of hyponatremia

9) Done 2 pleural Taps 

10) Learned about the procedure of lung biopsy