BIMONTHLY INTERNAL ASSESSMENT - OCTOBER

 

 CASE:1

57 year old man with jaundice, pedal edema and abdominal distension since three years and bleeding gums since three days"

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

1) What is the reason for this patient's ascites? 

ANS:- 

• CHRONIC LIVER DISEASE (ALCOHOL INDUCED LIVER CIRRHOSIS)
• HYPOALBUMINEMIA
• TRUNCAL OBESITY >> METABOLIC SYNDROME >> NAFLD >> CIRRHOSIS

Mechanism:

Cirrhosis >> portal hypertension >> increased hydrostatic pressure >> 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?  

ANS:- Bipedal lymphedema due to FILARIASIS

Recurrent blebs and ulcerations and cellulitis is due to FILARIASIS

CELLULITIS is an acute diffuse inflammation of subcutaneous cellular tissue usually caused by streptococci or staphylococci. In FILARIASIS, acute inflammation of lymphatics and adjacent tissue is caused by DYING ADULT WORMS. It is aggravated by SECONDARY BACTERIAL INFECTIONS – in the lower extremity from the lesions of web spaces of toes or nails and in the scrotum and breast by scratching trauma.

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

ANS:- HEPATIC ENCEPHALOPATHY

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/

SYRUP. HEPAMERZ - It is used for protecting the liver from harmful chemicals or free radicals. L-ornithine- L-aspartate (LOLA), the salt of the natural amino acids ornithine and aspartate acts through the mechanism of substrate activation to detoxify ammonia.

SYRUP. LACTULOSE - Helps to reduce the amount of ammonia in the blood of patients with liver disease. It works by drawing ammonia from the blood into the colon where it is removed from the body. It also reduces enteric production of ammonia.

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. 

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.

TAB.RIFAXIMIN - It is a poorly absorbed antibiotic that is thought to reduce ammonia production by eliminating ammonia-producing colonic bacteria. Many small studies have suggested that rifaximin is effective in treating acute HE and is extremely well tolerated.

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. 

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 used to dissolve gallstones

10.syp hepameiz 15 ml/PO/OD - It is used for protecting the liver from harmful chemicals or free radicals. L-ornithine- L-aspartate (LOLA), the salt of the natural amino acids ornithine and aspartate acts through the mechanism of substrate activation to detoxify ammonia.

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

19. High protein diet (2eggs / day) for decreased albumin synthesis

CASE:2

A 54 year old male with cough,abdominal tightness,pedal edema and diarrhea.

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?

ANS:- His ATT was stopped because of ELEVATED LIVER ENZYMES AND LIVER FAILURE (? ATT INDUCED LIVER DAMAGE)

Patient was SYMPTOMATIC

Starting ATT after few days was appropriate AFTER ACUTE EPISODE OF LIVER FAILURE SUBSIDE.

Method followed was:

ETHAMBUTOL followed by RIFAMPICIN followed by PYRAZINAMIDE followed by ISONIAZID.

Each drug should be started with min dosage and increased to max dosage

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 (CTP ≥11).

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

ANS:- Infiltrates in CHEST X-RAY

Plueral thickening and fibrocavitory changes noted in HRCT.

Sputum positive TB with RIFAMPICIN sensitivity.

3) What was the cause of his ascites?

ANS:- 

• ALCOHOLIC CIRRHOSIS OF LIVER >> PORTAL HYPERTENSION
• LATE BUDD-CHIARI SYNDROME
• HYPOALBUMINEMIA

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 in it. 

High protein diet 4eggs daily for protein supplementation 

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

Inj PIPTAZ 4.5gm for antibiotic cover

Vit k 10 mg Iv OD for 5 days to prevent forthcoming bleeding manifestations as his PT INR APTT are elevated 

IVF - 1 DNS @50ml/hr for hydration

Nebulisation with salbutamol and mucomist 12th hourly for cough and crepts

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

CASE:3

47 year old man with bipedal edema since one year and abdominal distension since one month

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?

Further approach towards managing is:

ACE INHIBITORS and ARB'S : reduce intraglomerular pressure by inhibiting angiotensin II ̶ mediated efferent arteriolar vasoconstriction and thus have proteinuria-reducing effect.

Renoprotective effect of ACE INHIBITORS

• Reduced breakdown of bradykinin (an efferent arteriolar vasodilator)
• Restoration of size and charge selectivity to the GCW
• Reduced production of cytokines that promote glomerulosclerosis and fibrosis, such as transforming growth factor (TGF)–beta.

CALCIUM CHANNEL BLOCKERS

IMMUNOSUPPRESANTS

To establish the cause for his nephrotic syndrome:

Rule out the secondary causes:

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/

AUTOIMMUNE SCREEN to rule out an underlying autoimmune disease is antinuclear antibody (ANA), antidouble stranded DNA antibody (dsDNA), and complement values (C3 and C4)

RENAL BIOPSY and histological preparations for light microscopy, immunofluoresence or immunoperoxidase, electron microscopy.

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?

PROS: 

We may know the cause for his nephrotic syndrome and treat him accordingly some extent.

CONS:

• Bleeding
• Infection
• Injury to other organs in the area
• Inadequate and/or no specimen for interpretation
• Blood loss sufficient to require either surgery or blood transfusion to stop the bleeding. 

It may meet his requirement and cure him to some extent.