55M obese male with SOB at rest

This is an online E log book to discuss our patient's de-identified health data shared after taking his/her/guardian's signed informed consent. 

Here we discuss our individual patient' problems through series of inputs from available global online community of experts with an aim to solve those patient's clinical problems with collective current best evidence based inputs.

Author : Dr. Chandana, Dr. Sai charan

55 year male 

Hypertensive since 10years

Toddy tree climber by occupation 

6yrs ago patient fell from a tree and after that had low back ache and neck pain,he used to take NSAID s daily for the pains since 6years,stopped using them after coming to our hospital in August 2021 and underwent a cervical spine surgery 6years ago after the injury.

Presented to our hospital for the first time in August 2021 with c/o fever ,burning micturation for 10days,severe pedal edema,grade 3 SOB  

Diagnosed with AKI(creat 4.9) on CKD secondary to left lower limb cellulitis,?UTI.underwent HD 3times in view of AKI at that time and patient was discharged.

Again presented to our hospital in april 2022 with SOB and was started in Maintainence hemodialysis at that time.patient underwent HD 2times and later did not come for HD as patient is afraid of HD.

In the month of May patient came on OPD basis in view of pedal edema and was adviced to continue MHD but patient was not willing and continued using diuretics and anti hypertensives regularly

Yesterday patient came again with increased pedal edema, decreased urine output since 1week and no urine output since 1day

SOB progressed to grade 4 since 2days.

O/E

Obese male

Pt c/c

Bp-130/70mmhg

PR - 120bpm

Spo2 - 90at RA,99%with 2lit o2

RR 20cpm

Cvs s1s2+

RS BAE+ ,B/L basal crepts+

A:1 session of HD done yesterday night in view of fluid overload,SOB

Hb:6.4,after HD 6.0

TLC 10,100

Plt 2.91

Urea 231 -after HD 188

Creat 15.2 ,after HD 13.0

Na 127 after HD 132

K 4.7 after HD 4.3

Cl 96

TB 1.03

DB 0.18

AST 17

ALT 15

ALP 109

TP 5.5

Alb 2.75

A/G 1.0

pH 7.23 after HD 7.36

Pco2 24.3-->24.7

Po2 80.9-->132

Hco3 10.7-->13.8

St.Hco3 12.7-->15.6

O2sat 98.6

CUE

Alb 3+

Pc 4-5

Sugar nil

Bgt B+

DX CKD on MHD secondary to

?NSAID abuse ? hTN

I/O since admission -400/10ml

After 1 HD yesterday night patient SOB decreased

P:USG abdomen,2d echo now

And plan next HD today evening 

Q :cause of albuminuria ? causing hypoalbuminemia

 Alcoholic since the age of 30,used to drink daily 90ml.stopped 4yrs ago

Smoker-30beedis per day, decreased the quantity since 1-2yrs to 1 beedi /day

Discussion : 

[6/17, 11:59 AM] Dr Adithya Sir Gm Kam: Does NSAID abuse cause CKD at all? If so, which NSAIDs are implicated? If they do cause injury, do they cause glomerular damage at all?

[6/17, 12:03 PM] Dr Adithya Sir Gm Kam: What are the 11 well established associated cancers with smoking?

Do you think this patient had chronic glomerular injury causing secondary hypertension?

[6/17, 12:41 PM] Dr Chandana Gm Kam: Classical analgesic nephropathy that is associated with habitual consumption of predominantly combination analgesic products. This disease takes many years to develop and is characterized by a dense interstitial fibrosis and the insidious development of renal failure. Renal papillary necrosis had been classically associated with this illness. 

Second form of analgesic nephropathy is typically an acute renal failure associated with the use of nonsteroidal anti-inflammatory drugs

Analgesics associated with nephropathy are aspirin, acetaminophen, caffeine,salcimide

The 2 main pathologies are 1.renal papillary necrosis and 2.chronic interstitial nephritis 

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2194329/

Hypotensive insult at the cellular level from inhibition of the prostaglandin synthesis pathway. Inhibition of the vasodilatory effect of prostaglandins is the most recognized and accepted mechanism of hypoperfusion-related medullary ischemia, which is generally accompanied by papillary damage in the form of necrosis in the vast majority of cases.The other pathological manifestations include interstitial tubular necrosis and interstitial nephritis.

https://www.ncbi.nlm.nih.gov/books/NBK541101/

[6/17, 12:43 PM] Dr Adithya Sir Gm Kam: Great. Thanks for sharing.

Was your patient using any of those mentioned above?

And clearly there is no evidence that NSAIDs cause glomerular injury?

In fact it is extremely unlikely that you will find a case report of NSAIDs causing CKD after 1982 (not AKI due to interstitial nephritis due to hypersensitivity).

[6/17, 12:43 PM] Dr Chandana Gm Kam: His renal failure developed after hypertension sir.

[6/17, 12:44 PM] Dr Adithya Sir Gm Kam: Classic post hoc bias

[6/17, 12:44 PM] Dr Adithya Sir Gm Kam: Or rather post hoc fallacy. Because renal failure developed after hypertension, the cause of RF is HTN.

What is the incidence of CKD with benign hypertension alone? Also does it cause a glomerular pathology?

[6/17, 12:46 PM] Dr Chandana Gm Kam: They don't have thise medication with them now sir.Dont know which drugs they have used.

Tried searching but dint find any analgesic causing glomerulopathy.its mainly the interstitium and papillae

[6/17, 12:47 PM] Dr Adithya Sir Gm Kam: Yes. Well done and thanks for sharing this crucial point here.

It is unlikely he will have taken Aspirin or Caffeine or Salcimide (never heard before) for pain. He may have taken Diclofenac or Aceclofenac mostly.

[6/17, 12:48 PM] Dr Chandana Gm Kam: Yes sir

[6/17, 12:50 PM] Dr Adithya Sir Gm Kam: Now will you agree if I frame the problem as -

55/M with 10 year history of hypertension and proteinuria / hypoalbuminemia since a few years.

Which common glomerular injuries can progress slowly and indolently over several years and cause hypertension and proteinuria at mild to moderate levels?

[6/17, 12:52 PM] Dr Adithya Sir Gm Kam: Will also be skeptic about the cellulitis he had last August. I mean surgery PGs are notorious to make any leg swelling a cellulitis and also frequently report "bilateral" cellulitis (speaks volumes that there is not one single case report in the world of bilateral cellulitis).

He may have had Venous stasis due to leg edema and consequently may have developed a Venous ulcer.

[6/17, 12:54 PM] Dr Adithya Sir Gm Kam: This looks too old and poorly healing to have happened yesterday. Also notice the darkening of skin and some brawming of the skin, which strongly favors ulcers due to Venous Stasis.

[6/17, 12:56 PM] Dr Adithya Sir Gm Kam: Venous Stasis even more likely. Brawning and brownish discoloration.

Any signs of peripheral neuropathy?

Day 1 soap notes : 

Today's Nephrology update: 

1. Icu bed 2 : 

55M with SOB and Rt lower limb ulcer

http://drkulkarnimd.blogspot.com/2022/06/55m-obese-male-with-sob-at-rest.html

S - C/O SOB at rest decreased compared to yesterday. Rt lower limb ulcer 2to trauma

O - Bp normal with sinus tachy (108) with Spo2 - 96% on 4L oxy. RR - 30. Auscultation mild IAA crepts in both sides

A - SOB at rest may be due to Pulmonary edema/ ?OSA(truncal obesity) / ?COPD

P - shifted for dialysis. General surgery opinion done on Rt lower limb ulcer.