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.
Complete details regarding the case are in the mentioned link above.
ANSWERS TO CASE 2 :
Question 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. The patient is a chronic alcoholic with alcohol dependence issues, is a previously diagnosed case of acute liver injury, chronic pancreatitis, cholelithiasis with DM and HTN.
Liver is the main organ for drug metabolism and de-toxification.
“During treatment of latent TB infection (LTBI) ala- nine aminotransferase (ALT) monitoring is recommended for those who chronically consume alcohol, take concomitant hepatotoxic drugs, have viral hepatitis or other preexisting liver disease or ab- normal baseline ALT”
“Treatment should be interrupted and, generally, a modified or alternative regimen used for those with ALT elevation more than three times the upper limit of normal (ULN) in the presence of hepatitis symptoms and/or jaundice, or five times the ULN in the absence of symptoms”
His symptoms were loose stools and vomiting, w/o pain abdomen or fever. Which are normal side-effects to any antibiotic treatment (because of altered gut flora). On examination, icterus with pedal edema are present. And, as the jaundice was present, the treatment was stopped.
His ALT values have been normal throughout, with mild elevation in AST. And almost >2x elevation in Alkaline Phosphatase.
But, even after stopping the ATT, the Total Bilirubin, AST, ALT (though still in normal limit) and Alkaline Phosphatase continued to rise. Only Direct bilirubin has decreased.
More over, the following is the inclusion and exclusion criteria for for stopping ATT in pt’s presencting with Hepato-toxicity.
“Inclusion
Patients with a diagnosis of antituberculosis drug-induced hepatotoxicity, as defined by the following criteria:
1) an increase 5 times the upper limit of the normal levels (50 IU/l) of serum AST and/or ALT on 1 occasion, or >3 times the upper limit of normal (>150 IU/l) on 3 consecutive occasions;
2) an increase in serum total bilirubin >1.5 mg/dl;
3) any increase in serum AST and or ALT level above pretreatment values together with anorexia, nausea, vomiting, and jaundice;
4) absence of serological evidence of infection with hepatitis A, B, C, or E virus; and
5) improvement in liver function test results (serum bilirubin level <1 mg/dl; AST and ALT level <100 IU/l) after withdrawal of antituberculosis drugs
Drug-induced hepatotoxicity was diagnosed if criteria 1, 2, or 3 were present in combination with criteria 4 and 5
Patients of either sex
Patients who were 16-65 years of age
Initial antituberculosis regimen: not explicitly stated, but appeared to include some or all of isoniazid, rifampicin, and pyrazinamide
Exclusion
1.Serological evidence of acute viral hepatitis
2.Ultrasonographic evidence of chronic liver disease
3.HIV infection
4.Long-term alcoholism, defined as consumption of >48g of alcohol per day for at least 1 year
5.Concomitant consumption of other potentially hepatotoxic drugs (e.g. methotrexate, phenytoin, valproate, and fluconazole Pregnancy”
1. The pt does not full-fill the inclusion criteria as, inspite of him having jaundice, the Total bilirubin and Transaminase values continue to increase after withdrawing ATT.
2. He full-fills the exclusion criteria as
- USG evidence of Chronic Liver Disease is present
- Long term alcoholism
Question 2) What were the investigational findings confirming the diagnosis of pulmonary TB in this man?
Ans.
- CXR - showing opacities in the B/L Lower Lobes
- CT -
- Plueral Thickening with interlobular septal thickening in RT lower lobe
- Fibro-cavitary changes in medial basal segment of RT lower lobe
In history - Fever and cough, more at night
On Examination - Inspiratory Crepts Present in right and left mammary,infra mammary,left axillary and infra axillary areas.
Question 3) What was the cause of his ascites?
Ans. 1. Hypoproyeinemia (hypoalbuminemia)
2. Portal HTN (presence of vascular collaterals, Decreased caliber of rt branch of portal vein, chronic thrombus in rt branch of portal vein, reduced caliber of hepatic vein on CT )
Question 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.
Ans.
1. Actrapid human insulin instead of OHAs to counter stable serum levels of insulin
“HbA1c levels remained relatively stable over the 6 months treatment with Actrapid, insulin human”
“major hypoglycaemic events occurred less frequently in type 2 diabetic patients”
2. ATT with-held for sometime, later re-started
3. Nutritional Supplementation - he is malnourished
4. Salbutamol (short acting B2 agonist) + Mucomyst nebulization - this is done to clear the mucus and dilate the airway , so as to facilitate ease of breathing and reducing risk of mucus accumulation which might get infected and cause further complications
5.Antibiotic cover with IV Fluids
6.Strict I/O charting and vitals monitoring
ANSWERS TO CASE 3 :
Question 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. The Pt has Total Protein >2.5 and and SAAG <1.1, with increased TLC
- Malignancy has been rules out
- Ascitic ADA is in normal range, TB Peritonium can be ruled out ?
- IVC Obstruction above the level of Renal vein - MRA can be done (Dye can be problematic in pt’s with bad renal condition)
- H/o Eliticing consumption of anabolic steroids / NSAIDs/ D- penicillamine ?
- VDRL to rule out syphillis
- Sickle Cell Trait has been associated in CKD in Few - Sickling test could be done to rule out SCT
“ Although SCT largely has been considered a benign condition, renal manifestations are the most commonly reported complications and include impaired urinary concentration, asymptomatic hematuria, and papillary necrosis.”
- ANA in serum - to rule out SLE
- Rheaumatoid Factor - to rule out Rheumatoid Arthritis
- CXR shows enlarged Lymph Nodes at the root of the Lung, it could indicate sarcoidosis (very very rare) - Urine Calcium and serum calcium may be looked for to rule out sarcoidosis
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:
- Histopathological and immunohistochemical (In case there is anti-phospholipase A2 receptor antibody) confirmation of etiology of nephrotic syndrome
- Imaging studies like MRA / Radionucleiotide studies are non invasive, but they might not give a sure-shot etiology, and can be economically draining to the family income of the patient.
- During a pandemic, any sort of invasive procedure is not recommended unless life threatening and pt has resources to bear the consequences
- Risk of a clot ,colic and obstruction
- Rarely, bleeding into kidney requiring surgery/ angiography
If the patient can handle the financial demands of the previously mentioned non-invasive tests, he should go by them if the treating physician agrees upon them too.
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