Biweekly internal assesment assessment

Case 1

https://swathibogari158.blogspot.com/2020/09/chronic-decompensated-liver-disease.html

Q1 Reason for this patients ascites 

Might be due to liver cirrhosis 

1.reduced albumin synthesis causes decreased oncotic pressure and transudation of fluid

2.reduced aldosterone metabolism causing 

no aldosterone in circulation activating RAAS  ,

salt and water retension causing ascites

2) Why did the patient develop bipedal lymphedema? What was the reason for the recurrent blebs and ulcerations and cellulitis in his lower limbs?  

A) underfilling of circulation due to hypoalbuminemia and salt water retention causes splancnic vasodilation that increases splanchnic arterial pressure and increases permeabilty which increases lymph accumulation

Ulcers might be due to 

Lymph stasis causes thickening of skin due to protein crosslinking which might cause inadequate circulation gradually ischemia and he mighy have developed ulcers

3) What was the reason for his asterixis and constructional apraxia and what was done by the treating team to address that?  

A) due  to liver dysfunction  

Ammonia is not metabolized in liver it bypasses liver and crosses blood brain barrier  probably due to interruption of posture pathway in rostral reticular formation and abnormal joint proprioception causing asterixsis and constructional apraxia 

Lactulose is given as it acts as osmotic purgative.in colon,lactulose is catabolized to lactic acid and acetic acid which lowers the colonic ph andhelps in conversion of ammonia into non absorbable ammonium ion which helps in excreting ammonia 

Rifaximin is antibiotic that reduces ammonia production by removing ammonia producing bacteria 

4) What was the efficacy of each treatment intervention used for this patient? Identify the over and under diagnosis and over and under treatment issues in the management of this patient. 

efficacy of treatment intervention given

high protein diet (2eggs / day) for decreased albumin synthesis

1. Air or water bed to prevent pressure bed sores in the dependent areas

2. Fluid restriction <1.5litres/day so as to decrease of fluid dissemination into the extra vascular space

Salt restriction <2.4gms/day to prevent retention of water due to osmotic gradient as sodium causes retention

3. Inj augmentin 1.2gm IV/BD to prevent secondary bacterial infections 

4. Inj pan 40 mg IV/OD

5. Inj zofer 4mg IV/BD

6. Tab lasilactone (20/50)mg BD ( combination of furosemide and aldactone to decrease pedal oedema
If SBP <90mmhg - to avoid excessive loss of fluid

7. Inj vit k 10mg IM/ STAT ( as vitamin K causes coagulation to prevent further bleeding manifestions)

 
8. Syp lactulose 15ml/PO/BD for hepatic encephalopathy 

9. Tab udiliv 300mg/PO/BD contain urodeoxycolic acid .UDCA has a choleretic effect, increasing hepatocellular bile acid excretion, as well as cytoprotective, antiapoptotic, and immunomodulatory properties. 

UDCA has been shown to delay development of gastroesophageal varices and progression to cirrhosis as well as to improve long-term survival in patients with primary biliary cirrhosis

10.syp hepameiz 15 ml/PO/OD as it has hepatoprotection properties 

11.IVF 1 NS slowly at 30ml/hr to maintain hydration

12. Inj thiamine 100mg in 100mlNS /IV/TID as thiamine deficiency's occur in chronic alcoholics

13.strict BP/PR/TEMP/Spo2 CHARTING HOURLY 

14.strict I/O charting 

15.GRBS 6th hourly

16.protein x powder in glass of milk TID for protein supplementation and muscle wasting which commonly occurs in cirrhosis patients 

17. 2FFP and 1PRBC transfusion to support coagulation pathways 

18 .ASD DONE for wound infections and ulcer

Case2 :

https://sainiharika469.blogspot.com/2020/09/hello-everyone.html?m=1

1) Why were his antitubercular therapy stopped soon after his current admission? Was he symptomatic for ATT induced hepatitis? Was the method planned for restarting antitubercular therapy after a gap of few days appropriate? What evidence is this approach supported by?

 

A)his medications were stopped due to his chronic liver disease(alchoholic since 35 years)as ATT drugs are hepatotoxic and cane deteriorate his condition .

.hepatotoxicity due to anti-TB drug treatment was defined as the following criteria: 1) serum aspartate aminotransferase (AST) and/or alanine aminotransferase (ALT) levels >5 times the upper limit of normal (ULN; 40 IU/L) or >3×ULN, with clinical symptoms such as nausea, vomiting, abdominal pain 

He doesnot match with any criteria so he is not symptomatic for att induced hepatotoxicity 

.yes he can take att provided using drugs which are not potentially hepatotoxic as main concern is primary focus 

2) What were the investigational findings confirming the diagnosis of pulmonary TB in this man? 

Ans. In history he mentioned he was positive for spitum

Bilateral infiltration of lung fields noted in chest X-Ray (PA view) 

3) What was the cause of his ascites?

A) as saag ratio is 1.2 it is non inflammatory cause most likely portal hypertension

4) What are the efficacy of each intervention mentioned in his treatment plan and identify the over and under diagnosis as well as over and under treatment issues?

A)Inj  Human Actrapid Insulin s/c 8am - 2pm  - 8pm for diabetic management

Inj  PAN 40 mg IV/OD

Inj optineuron 1 amp in 100 ml NS Iv/bd for nutritional supplementation such as Vit B12

ATT to be with held for hepatoxicity although should be used based on CTP score mentioned above 

Syp lactulose 15ml HS to prevent hepatic encephalopathy 

Protein powder 3 to 4 scoops in 1 glass of milk or water QID for protein supplementation

Stop all OHA s

Grbs charting 6th hrly

Strict I/0 charting

High protein diet 4eggs daily for protein supplementation 

ORS sachets in 1 litre of water to compensate electrolytes lost due to diarrhoea 

Bp charting hourly

Inj PIPTAZ 4.5gm/IV/bd  stat 

Vit k 10 mg Iv OD for 5 days to prevent bleeding manifestations

Temp BP PR monitoring 4th hourly

IVF - 1 DNS @50ml/hr for hydration

Nebulisation with salbutamol and mucomist 12th hourly. for ?cough

Inj thiamine 100 mg in 100 ml NS IV TID. for chronic alcoholism.

Case3

https://sushma29.blogspot.com/2020/09/ascites-secondary-to-nephrotic-syndrome.html?m=1

1) What will be your further approach toward managing this patient of nephrotic syndrome? How will you establish the cause for his nephrotic syndrome?

A) 1.symptomactic treatment as we dont the cause of nepheotic sundrome

Salt restriction , protein diet 

Lasix and aldactone for edema 

Steroids starting from low dose can be started 

Coagulation factors (antithrombin) might be lost in urine so prophylactic anticoagulany therapy can be started 

Lipid abnormalities may be present in future hmgcoa reductase inhibitors can be useful 

Loss of igs can cause sepsis which is major cause of death so prophylactic vaccines can be advised 

Approach to the case:

Primary idiopathic glomerular disease 

Membranous glomerulopathy 

Minimal change disease 

Focal segmental glomerulosclerosis 

Iga nephropathy 

Membranoproliferative glomerulonephtitis

Mesangial proliferative 

-renal biopsy would help ifthis is the cause 

Infections like malaria ,infective endocarditis  hepatitis Band C ,hiv whick are unlikely

Systemic diseases 

Dm which he doesnt have 

Amyloidosis to rule out electrophoresis must be done

SLE but he doent fit for criteria 

Polyarteritis nodosa but mostly visceral involvement will be more 

Wegeners granulomatosis for which patients will have hematuria which is not present in this case 

Drugs and toxins 

Pemcillamine  street heroin ,captopril 

Malignancy 

Carcinoma of lung and colon

Melanoma unlikely 

Hodgkins disease - it may develop due to immune complex deposition in kidneys 

CLL there is no lympocytosis so its not the cause 

2) What are the pros and cons of getting a renal biopsy for him? Will it really meet his actual requirements that can put him on the road to recovery?

1.pros 

It would help to know the cause of his situation if it is glomerulus pathology

Cons - expensive 

Post biopsy complications like blood in urine,pain at site ,