This is to discuss, understand and review clinical scenarios so as to improve my clinical competency via online e-logging clinical cases. The cases have been shared after the pt/their guardian signed an informed consent.
Case 1 : https://swathibogari158.blogspot.com/2020/09/chronic-decompensated-liver-disease.html
Complete details regarding the case are in the mentioned link above.
ANSWERS FOR CASE 1
Question 1. What is the reason for this patient's ascites?
Ans - The patient is a chronic alcoholic and alcohol is well known to cause hepatocyte injury.
In the initial stages, due to the immense regenerative property of the hepatic cells, the injury is reversed.
- But in the later stages, as the alcohol consumption reaches chronicity, the injury predominates the regeneration of liver cells.
- The injured liver cells and the Kupffer cells (macrophages of the liver) produce cytokines which activate Stellate cells (which also happen to store Vit A)
- Activation of stellate cells (Which convert to myofibroblasts) starts a process ultimately leading to FIBROSIS OF LIVER TISSUE.
- The fibrosis over time, with continuation of injury, modifies the hepatic architecture, leading to CIRRHOSIS. Where some part of the hepatic parenchyma is functional and some part is not.
- This edificial modification leads to disturbance in hepatic vasculature. Leading to PORTAL HYPERTENSION.
1. DECREASED HEPATIC METABOLISM
2. PORTAL HYPERTENSION
- THERE IS EVIDENCE FROM THE Pt’s HISTORY 3 YRS AGO TO PROVE DECREASED HEPATIC METABOLSIM - RATHER, DECREASED PROTEIN SYNTHESIS
- B/L PEDAL EDEMA UPTO KNEE ( DECREASED ALBUMIN SYNTHESIS)
- BLEEDING FROM GUMS (DECREASED CLOTTING FACTOR SYNTHESIS)
- PORTAL HTN, IS GENERALLY SEEN IN THE END, WHEN ONE COMES ACROSS A VARICEAL BLEEDING. WHICH IS, NOT SEEN IN THIS CASE. BUT THAT DOES NOT RULE OUT THE POSSIBILITY OF PORTAL HTN, AS PORTAL HTN CAN EXIST WITHOUT VARICEAL BLEEDING. ONLY WHEN THE PORTAL PRESSURE IS >12 mmHg, IS THE RISK FOR VARICEAL BLEED HIGHER.
1. Hypoalbuminemia - Due to decreased albumin, the oncotic pressure at the venous end of the capillaries falls, owing to which, the fluid does not shift from interstitium to vascular compartment. And the majority of the fluid, tends to remain in the interstitium.
2. Portal hypertension - leads to splanchnic vasodilation (due to NO released in Portal HTN), And the systemic arterial pressure falls leading to activation of RAAS, which causes sodium and water retention.
This leads to altered intestinal capillary permeability and accumulation of fluid in peritoneum.
“Systemic arterial pressure falls due to pronounced splanchnic vasodilatation as cirrhosis advances. This leads to activation of the renin–angiotensin system with secondary aldosteronism, increased sympathetic nervous activity, increased atrial natriuretic hormone secretion and altered activity of the kallikrein–kinin system (Fig. 22.16). These systems tend to normalise arterial pressure but produce salt and water retention.’’ - Page 863, Davidson Textbook of medicine - 23rd Edition
Question 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 - The B/L pedal edema is due to the same reason as above, hypoalbuminemia leading to decreased oncotic pressure, leading to fluid accumulation in the interstitium of dependent parts.
And, INFERIOR VENACAVAL OBSTRUCTION ?
1. The pt does have a history of lang standing pedal edema. It is possible that, because of the chonicity of pedal edema, the lowers layers of skin on the legs and feet underwent fibrosis and thickened with impaired neuro-vascular supply. Adding, the effect of probable nutritional deficiency (vit a, B12, Folate, Iron) lead to weakened skin, peripheral neuropathy.
2. Due to the long standing pedal edema, the superficial veins dilated, the fluid exits through skin, in the form of blebs. Which, might get infected easily considering the impaired immunity (decresed immunoglobulin systhesis + pt consuming steroids ) and neuro-vascular supply to the lower limbs. These repeated infections might have lead to cellulitis.
The above is my hypothesis, cannot vouch for accuracy. Pls do intimate if it needs any correction.
Question 3. What was the reason for his asterixis and constructional apraxia and what was done by the treating team to address that?
Ans. Liver metabolism of ammonia and urea is impaired. Leading to hepatic encephalopathy.
1. Fluid restriction <1.5litres/day
Salt restriction <2.4gms/day
2. Tab lasilactone (20/50)mg BD
If SBP <90mmhg -avoid
3.syp hepameiz 15 ml/PO/OD
4.IVF 1 NS slowly at 30ml/hr
5.strict I/O charting
Question 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.
Ans. Treatment given is aimed at increasing the fluid wash out with decresed fluid and salt administration and increased protein intake. Antibiotic cover to prevent new and worsening of present infected ulcer. H1-blocker and anti-emetic to prevent the probable side-effects to antibiotics.
1. Diuretics to increase fluid wash out and decrease edema - and to combat the diastolic dysfunction
“Loop diuretics and aldosterone antagonists must be administered to the patients not responding to the previous regimen. Available evidence indicates that aldosterone antagonists are the first-choice drugs, as these substances are more effective than furosemide. Nevertheless, loop diuretics potentiate the effects of aldosterone antagonists. The reduced efficacy of furosemide in these patients, when compared with that of spironolactone, may be related to an impairment of both pharmacodynamics and pharmacokinetics’’ -
2. Vitamin K for decreasing further episodes of internal bleeding. But, cirrhosis can be hypercoagulable or hypocoagulable state. Vit K is given so as to correct PT in cirrhosis patients.
“the practice of vitamin K supplementation in cirrhotic patients is not well defined, and its true value appears questionable.”
3. Hepamerz for hepatic encephalopathy
“L-ornithine-L-aspartate infusions were found to be effective in cirrhotic patients with hepatic encephalopathy.”
4. Udilive - as gall bladder is distended with thickened walls, there could be undetected gall stones in patients with such long lasting liver disease. It has a protective function.
“(1) protection of injured cholangiocytes against toxic effects of bile acids, (2) stimulation of impaired biliary secretion, (3) stimulation of detoxification of hydrophobic bile acids, and (4) inhibition of apoptosis of hepatocytes”
5. Nutritional supplemenatation with thiamine, with strict vitals monitoring and I/O Charting help to proactively prevent Cardiac/Renal Complications or act faster for a better patient outcome.
6. FFP and PRBC transfusion as pt is severely anemic.
With hemodilution and hypervolemia, there is increased stress on heart and lungs.
