Bimonthly internal assessment

Case 1:

Q1 What is the Reason for this patients ascites ?

      The most common cause of Ascites is

      Cirrhosis of liver 

      risk factors in this patient : 

     1. Chronic alcoholism since 40 years 

     2. Truncal obesity leading to metabolic syndrome causing NAFLD leading to cirrhosis

          https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6092576/

Altered echo texture of liver due to Cirrhosis causes portal hypertension leading to increased hydrostatic pressure causing fluid accumulation hence Ascites 

Q2 Bilateral pedal oedema which is of pitting type is due to decrease in the albumin level trends due to course of the disease and long standing cirrhosis causing decrease in the production of proteins causing decrease in the oncotic pressure leading to accumulation of fluid.

as per the given clinical data due to chronic liver disease there was increasing trend of INR which was as high as 4.7 causing bleeding manifestations ( bleeding gums, hematoma formation )

ulcerations are due his limited self practising manoeuvres done in inappropriate conditions such as 

improper dressing of the wound, not maintaining aseptic conditions , indescriminate use of steroids (self medication) to quote from history (Patient attenders were giving history of multiple self medications whenever patient developed fever or shortness of breath they used to take decadron injections, larigo tablets,monocef and pantop over 4 months intermittently )  causing ? immune suppression leading to secondary infections hence cellulitis and non healing of wound. 

Q3 Reason for Asterexis and constructional apraxia 

Asterixis is a clinical sign that describes the inability to maintain sustained posture with subsequent brief, shock-like, involuntary movements.

this clinical sign is not pathognomonic for any condition. However, it may indicate a serious underlying disease process. 

https://www.ncbi.nlm.nih.gov/books/NBK535445/

West haven criteria is being used for HE

In hepatic encephalopathy (due to cirrhosis of liver ) damage occurs to brain cells due to the impaired metabolism of ammonia is predominantly related to the development of asterixis in hepatic encephalopathy,

pathophysiology of HE

1 role of neurotoxins, 

2.impaired neurotransmission due to metabolic changes in liver failure, changes in brain energy metabolism, systemic inflammatory response and alterations of the blood brain barrier which produces a wide spectrum of nonspecific neurological and psychiatric manifestations. 

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5421503

lactulose and rifaximin

underlying mechanism of Giving lactulose

The human small intestinal mucosa does not have the enzymes to split lactulose, and hence lactulose reaches the large bowel unchanged. 

basically three mechanisms have been described on usage of lactulose 

1.First, the colonic metabolism of sugars causes a laxative effect via an increase in intraluminal gas formation and osmolality which leads to a reduction in transit time and intraluminal pH. This laxative effect is also beneficial for constipation.

2. lactulose promotes increased uptake of ammonia by colonic bacteria which utilize the trapped colonic ammonia as a nitrogen source for protein synthesis. The reduction of intestinal pH facilitates this process, which favors the conversion of ammonia (NH3) produced by the gut bacteria, to ammonium (NH4+), an ionized form of the molecule, unable to cross biological membranes. 

3. lactulose also causes a reduction in intestinal production of ammonia. The acidic pH destroys urease-producing bacteria involved in the production of ammonia.  The unabsorbed disaccharide also inhibits intestinal glutaminase activity, which blocks the intestinal uptake of glutamine, and its metabolism to ammonia


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 further prevent bleeding manifestions
 
8. Syp lactulose 15ml/PO/BD for hepatic encephalopathy 

9. Tab udiliv 300mg/PO/BD contain Ursodeoxycholic acid as an active ingredient. It is used to dissolve gall stones in various liver-related disorders such as cirrhosis

10.syp hepameiz 15 ml/PO/OD

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

CASE 3:

1. As per the available clinical data nephrotic syndrome have been established 

  1.Initial management should focus on investigating the cause,
       Primary ( idiopathic )
       Secondary glomerular pathology
  
Primary causes include

FSGS
membranous glomerular nephropathy
minimal change 
MPGN

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2394708/


Secondary causes of nephrotic syndrome

Other diseases

  • Diabetes mellitus

  • Systemic lupus erythematosus

  • Amyloidosis

Cancer

  • Myeloma and lymphoma

Drugs

  • Gold

  • Antimicrobial agents

  • Non-steroidal anti-inflammatory drugs

  • Penicillamine

  • Captopril

  • Tamoxifen

  • Lithium

Infections

  • HIV

  • Hepatitis B and C

  • Mycoplasma

  • Syphilis

  • Malaria

  • Schistosomiasis

  • Filariasis

  • Toxoplasmosis

Congenital causes

  • Alport’s syndrome

  • Congenital nephrotic syndrome of the Finnish type

  • Pierson’s syndrome

  • Nail-patella syndrome

  • Denys-Drash syndrome

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2394708/


     2. Identifying complications such as 
         thromboembolism
         Infections
         hyperlipidemia
         acute renal failure

     3. Managing the symptoms of the disease such as protein loss, pedal oedema, 
         and hyper coagulable state which still did not manifested in this patient or need not be in many     
        cases.

    I would start with Low dose steroids as initial management which also rules out steroid resistant nephrotic syndrome in future course of treatment, and slowly taper according to the need.

A renal biopsy would be helpful in establishing the cause of which type of glomerular pathology is causing the nephrotic syndrome. however if the nephrotic syndrome is secondary to other above mentioned cases ruling out that gives a better picture rather than going straight away for biopsy .

2. As per my limited clinical knowledge and ICU rounds. I don't see any pros in getting renal biopsy done for that patient as it would only provide which type of glomerular pathology given already established he has nephrotic syndrome. instead look for the other causes leading to nephrotic syndrome 

CONS 

1. Time and expenditure ( knowing the affordability of the patient ) instead of that relying more on history taking would be reliable.

2. May be Post biopsy complications 

I wouldn't agree that this actually meets his actual requirement and his road to recovery.


CASE 2

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

Q1 May be ATT were stopped because of his concomitant Chronic liver disease secondary to ? chronic alcoholism as, the ATT first line drugs such as isoniazid and rifampicin are hepatic toxic

LFT is deranged 
TB raised 
ALP raised 

low serum albumin ( synthesis is affected ).

 history of watery diarrhoea since 20 days might be due to ?GI infection or
 ?Rifampicin induced (pseudomembranous colitis) was noticed although not specific to usage of   rifampicin. 

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3363060/

Usage of ATT induced hepatotoxicity increased 14-fold in patients with chronic liver diseases (CLD) and liver cirrhosis, more so in those with decompensated disease, probably due to the cirrhosis-associated immune dysfunction syndrome, and case-fatality rates are high.

If hepatotoxicity develops in those with liver cirrhosis, particularly decompensated cirrhosis, the risk of severe liver failure is markedly increased. 

Currently, there are no established guidelines for anti-tuberculosis therapy (ATT) in CLD and liver cirrhosis although the need for such guidelines is self-evident. 

1. It is proposed that ATT should include no more than 2 hepatotoxic drugs (RIF and INH) in patients with CLD or liver cirrhosis and stable liver function [Child-Turcotte-Pugh (CTP) ≤7], 

2. only a single hepatotoxic drug (RIF or INH) in those with advanced liver dysfunction (CTP 8–10) and 

3. no hepatotoxic drugs with very advanced liver dysfunction. 
recommended dose of 15–30 mg/kg has significantly less risk of hepatotoxicity. The frequency of hepatotoxicity in patients who received PZA in doses of 25–35 mg/kg along with RIF and INH was found to be similar to those who received only RIF and INH.

Treatment regimens of anti-tuberculosis therapy in patient with chronic liver disease.

A. Regimens with only two potentially hepatotoxic drug:
 (i) Regimens without INH
 (ii) Regimens without PZA
B. Regimens with only one potentially hepatotoxic drug.
C. Regimens with no potentially hepatotoxic drugs.

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3940527/

Q2. Bilateral Infiltrations of lung fields noted in CXR PA view
    consolidations
    ?cavitiy in right lung.

Q3. Chronic decompensated liver disease leading to ?portal hypertension
    as the tap was transudative based on Lights criteria 
    although serum albumin was low 

Q4.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 - - --> TID

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

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

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

Temp BP PR monitoring 4th hourly

IVF - 1 DNS @50ml/hr for hydration

Nebulisation with salbutamol







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