case I:
1) What is the reason for this patient's ascites?
Ans: excessive chronic alcohol use can cause chronic liver disease, alcholic fatty liver, alcoholic hepatitis, alcoholic cirrhosis..
In absence of inflammation Or necrosis alcohol use can produce Fibrosis..
The clinical manifestations of cirrhosis include ascites, pedal edema, pain, fever, nausea, development of jaundice( scleral icterus) , upper gi hemorrhage..
In cirrhosis increase in portal hypertension causes sphlancnic vasodilation results in increase portal venous flow... Both these cause increased production of splanchnic lymph.. These hemodynamic changes result in sodium retention by causing activation of RAAS pathway with increase in aldosterone..
Sodium retention causes fluid accumulation and expansion of ecf results in edema and 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: 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) causing ? immune suppression leading to secondary infections hence cellulitis and non healing of wound.
3) What was the reason for his asterixis and constructional apraxia and what was done by the treating team to address that?
Ans:Asterixis is a clinical sign that describes the inability to maintain sustained posture with subsequent brief, shock-like, involuntary movements. This motor disorder is myoclonus characterized by muscular inhibition (whereas muscle contractions produce positive myoclonus).Initially described in 1949 by James Foley and Raymond Adams to describe the flapping tremor they observed in liver disease, 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/
the treating team gave
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.
https://www.ncbi.nlm.nih.gov/books/NBK536930/
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
Second case :
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:: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5366108/
His att was stopped due to altered bilirubin metabolism and increased liver enzymes .. He was sympotomatic for ATT induced hepatitis include yellow skin and eyes (jaundice), nausea, abdominal pain, fatigue and fever.
https://clinicaltrials.gov/ct2/show/study/NCT01395654
This clinical trial suggests that It could also be hazardous Reintroducing after att induced hepatitis
2) What were the investigational findings confirming the diagnosis of pulmonary TB in this man?
Ans:: He started having abdominal tightness(after taking spicy foods ),pedal edema - pitting type (on and off) shortness of breath, all symptoms from 1 month for which he was referred to govt hospital where he was diagnosed as sputum positive TB and started ATT
3) What was the cause of his ascites?
Ans: High saag and low ascitic protein Suggestive of cirrhosis is casue for ascites
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.
Third case ::
1) What will be your further approach toward managing this patient of nephrotic syndrome? How will you establish the cause for his nephrotic syndrome?
Ans:By renal biopsy.....subjected to light , immunofloroscence and electron microscopy... If it is diabetic nephropathy, there is capillary basement membrane thickening with Diffuse glomerulosclerosis as most common finding.. Nodular or intercapillary glomerulosclerosis ( kimmelstein Wilson disease) is the most specific finding... If it is membranous nephropathy there is immune complex deposition giving the appearance of Spike and dome on electron microscopy.. If it is FSGS.. There is focal segmental sclerotic areas because of deposition of IgM and C3 ...but hall mark of FSGS is Visceral epithelial cell damage with diffuse effacement of foot process of viscera epithelial cells on E/M. In fibrillary immunotactoid glomerulopathy fibrillar or microtubular deposits of oligoclonal or oligotypic immunoglobulins and complements appear in the mesangium and along the glomerular capillary wall... In Light chain deposit disease.. The light chain deposits are not fibrillar and don't stain with Congo red, but easily detected with anti light chain antibody using immunofluorescence or granular deposits on 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?
Ans::
PROS of renal biopsy :
1)Gives a specific diagnosis, reflect the disease activity, provide information to allow decisions and planned treatment..
2)It remains a valuable clinical tool and of particular benefit when other investigations fail to diagnose...
CONS:
1) Dull ache pain around the needle entry site...
2)Sometimes perirenal haematoma forms leading to severe loin pain...
3)The mean decrease in Hb after biopsy is approximately 1g/dl...
4)Visible hematuria in 3.5% ,Need for blood transfusion in 0.9% and need for intervention to control bleeding in 0.7% and Death in 0.02 %....
5)Rare complications include infection, damage to blood vessels or other organs or urine leak... Sometimes development of arteriovenous fistula.
