Bimonthly blended assessment
Submitted by: Simran Dash
MBBS- IV | Roll number- 153
I have been given the following cases to solve in an attempt to understand the topic of "Patient clinical data analysis" to develop my competency in reading and comprehending clinical data including history, clinical findings, investigations and diagnosis and come up with a treatment plan.
The entire real patient clinical problem is presented in the following three links for three different patients.
1st case: https://swathibogari158.blogspot.com/2020/09/chronic-decompensated-liver-disease.html
2nd case: https://sainiharika469.blogspot.com/2020/09/hello-everyone.html?m=1
3rd case: https://sushma29.blogspot.com/2020/09/ascites-secondary-to-nephrotic-syndrome.html?m=1
The questions asked with respect to these cases is represented by the following link-
https://medicinedepartment.blogspot.com/2020/09/medicine-paper-for-october-2020-first.html?m=1
Coming to the 1st case,
Answers to the questions are given as follows-
1) Causes of ascites in this patient could be-
- Liver disease
- Heart disease
- Hypoalbuminemia (There is albuminuria)
I came to this conclusion on the basis of the following findings in history, examination and investigations-
A) Findings supportive of Liver disease are-
i) History:
- Gross abdominal obesity
- Bilateral pedal edema
- Bleeding gums
- Black stools
- Generalised weakness
- Mental confusion
- Shortness of breath
ii) Examination:
- Icterus
- Pedal edema
- Asterixis
iii) Investigations:
- Elevated total bilirubin
- Elevated direct bilirubin
- USG revealed moderate hepatosplenomegaly and enlarged liver with nodular contour and coarse echotexture.
- Stool for occult blood positive.
These findings are suggestive of-
- Cirrhosis causing Hepatic encephalopathy( Type C)
This is further supported by the patient being a chronic alcoholic since 40 years taking 180 ml whiskey daily.
B) Findings supportive of congestive heart failure:
- Shortness of breath
- Pedal edema
I rhink the cause for Ascites in this case is Alcoholic cirrhosis leading to hepatic encephalopathy.
2) The reason for bipedal lymphedema is because of the following reasons-
3) The reason for his asterixis and constructional apraxia seems to be Hepatic Encephalopathy which is caused by accumulation of ammonia in the blood which is generally removed by liver.
Treatment received by the patient for it-
- Lactulose
- Rifaximin
- Protein powder
- Hepamerz
4) Efficacy of the treatment received by him:-
i) Lactulose
"Seventy-five cirrhotic patients with hyperammonemia in the past or at the time of the study were randomly divided into two groups (treated with lactulose or nontreated) in 14 hospitals in Japan. Thirty-six cirrhotic patients were diagnosed as having subclinical hepatic encephalopathy (SHE), and 39 were diagnosed as non-SHE.Twenty-two of the SHE patients were treated with lactulose (45 mL/d) for 8 weeks, and the other 14 SHE patients did not receive lactulose. The SHE had disappeared in 10 (50%) of the 20 treated patients at week 8, but it persisted in 11 (85%) of the untreated 13 patients. We concluded that lactulose treatment in cirrhotic patients with SHE is effective with respect to psychometric tests."
ii) Rifaximin
"A number of retrospective studies have indicated that long-term treatment with rifaximin is safe and possibly beneficial, high quality trials are needed to further clarify efficacy and safety of long-term treatment with rifaximin and evaluate effects of combination therapy with lactulose and branched-chain amino acids for patients with liver cirrhosis and hepatic encephalopathy."
iii) Hepamerz (L-ornithine- L- Aspartate)
"L-ornithinine-L-Aspartate has demonstrated beneficial therapeutic effects in several clinical studies either per oral or intravenous administration, compared to placebo administration."
2nd Case:
1) Yes this patient is symptomatic for Drug induced hepatitis, in this case it is Anti-Tuberular Treatment. Hence the ATT was stopped in the 3rd day of his admission.
Findings supportive of ATT induced Hepatitis are as follows:
- Fever
- Generalised weakness
- Elevated bilirubin levels
- Abnormal Coagulation profile
"Once withdrawn, anti-TB treatment should be withheld ideally until the liver tests normalize. Considering that first line anti-TB drugs are highly effective and relatively inexpensive, benefits of re-challenge must outweigh its risks; it is unwise to discard these drugs from the regimen. Therefore, it is acceptable to attempt reintroduction of these medications. In 11%–24% of patients, re-exposure to the same drug regimen leads to recurrence of DILI and positive re-challenge is not affected by the degree of initial injury. A study randomized 175 patients with hepatotoxicity into these 3 reintroduction regimens and found no difference in the frequency of recurrent DILI. On the contrary a small randomized controlled trial of 45 patients with hepatotoxicity compared restarting of all drugs simultaneously with sequential reintroduction regimen without pyrazinamide showed safety of the latter regimen."
(DILI- Drug Induced Liver Injury)
2) Findings confirming the diagnosis of pulmonary TB in this man are:-
- Chest X ray showing the characteristic findings bilaterally as given below-
- Consolidation
- Pleural effusion
- CT Scan showing-
- Fibro-cavitatory changes are noted involving the medial basal segments of right lower lobe.
- Pleural thickening with inter-lobular septal thickening noted involving right lower lobe.
Additional investigations which are needed are:-
- Sputum for AFB
- Tuberculin skin test
- Molecuar methods such as CBNAAT, Line Probe Assay, Xpert MTB
3) Cause of Ascites in this pateint is Chronic Pancreatitis which can be attributed to his chronic alcoholism and gall stones. It is also responsible for the pleural effusion in this patient.
"Approximately 95% of cases of pancreatic ascites are associated with chronic pancreatitis. The leak manifests upstream of a stricture or stone, and the point of least resistance for the pancreatic juice to flow is into the belly cavity rather than the duodenum, where it belongs."
4) The different treatment modalities which have been received by this patient are:-
- For Diabetes Mellitus: Inj. Human Actrapid Insulin
- Hyponatremia: ORS Sachets and DNS
3rd case:
1) Additional investigations needed in this case to find out the cause of Nephrotic syndrome are:
- Renal biopsy
- Anti neutrophil antibody: to rule out auto-immune diseases like Sjogren's syndrome, SLE
- Serum electrophoresis: to rule out multiple myeloma
Depending upon the cause, the additional treatment which could be received by the patient is as follows:
- Statins such as Atorvastatin should be given for Hyperlipidemia.
- Low Molecular Weight Heparin can be given as a prophylactic to prevent Thromboembolism.
- Corticosteroids such as Prednisolone can be prescribed to-
- Decreases proteinuria
- Risk of infection
- Resolution of edema
- Immunosuppressors such as Cyclophosphamide are prescribed if they are tolerant to corticosteroids.
2) Pros and cons of getting renal biopsy in this patient:
- Could help in knowing the actual cause of nephrotic syndrome in this patient which could be-
- Focal segmental Glomerulsclerosis
- Membranous nephropathy
- Multiple myeloma
- Malignancy
- Minimal Change Disease
Although there are evidences suggesting that the prognosis for renal function and remission solely dependent on the responsiveness to steroids given on an alternate day basis for a period of 2 months.
But still if the patient does not respond to the steroid therapy, there is good evidence that giving more intensive immunosuppression with alternate months of prednisolone and chlorambucil is of benefit in inducing a remission and slowing down the rate of progression in a patient with membranous nephropathy. So in order to start such a toxic treatment, the diagnosis should be made certain with renal biopsy.
"A striking
feature of that particular study was that 50% of all
patients with a nephrotic syndrome had membranous
nephropathy. If one assumes that a further 25% had
minimal-change nephropathy then the case for blind
treatment with steroids is persuasive. However, in most
other studies membranous nephropathy accounts for
only 20% of all cases of the nephrotic syndrome in
adults. Further, two other controlled studies showed no benefit of steroids in membranous nephropathy and the balance of evidence is that
steroids are ineffective in this disorder. A further point
that is often overlooked is that the nephrotic syndrome
in adults with minimal-change nephropathy responds
to steroids slightly less often than in children and also
more slowly. Only 60% of adults with minimal-change
nephropathy are in remission at 8 weeks and this rises
to 76% at 16 weeks. There is thus good reason to
conclude that in these patients, 8 weeks of alternate day steroids may not lead to remission of the nephrotic
syndrome."
"LM, IF, and EM should be done routinely in all biopsies. Kidney biopsy, appropriately processed and interpreted, will yield the correct clinicopathologic diagnosis, leading to the appropriate therapeutic strategy while, at the same time, providing key prognostic information."
So getting a renal biopsy will be beneficial in this patient.
References:
2) https://www.mayoclinic.org/diseases-conditions/cirrhosis/symptoms-causes/syc-20351487
7) https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3099317/
8) https://watermark.silverchair.com/11-1-12.pdf?token=AQECAHi208BE49Ooan9kkhW_Ercy7Dm3ZL_9Cf3qfKAc485ysgAAApwwggKYBgkqhkiG9w0BBwagggKJMIIChQIBADCCAn4GCSqGSIb3DQEHATAeBglghkgBZQMEAS4wEQQMjvxf_S7fTAUeLBPGAgEQgIICT1VSxZ-fEPMjDoW5tWx0afuHi4Le-OVzT7WGY0JtahYRlUeDrXd9L0SYrDHHqS9SkPzttK2unI0Hn-1wMX2ZPtG__djwwbTPax43FgktOfq746SshuTE-aEmpgJkF0S3HJtFB-JPxfkOqf3uKriTKm3guYKptwY5Vv5XRaat6Tx1C1qYlbHj7kIhZbFcBe0O_a8AZzKV8z-pUOROyRpMBk4qFTdjua9bPSzE7NgMGleUEIOqtZ2npuMmxb74uzzkRC1w_f_F3UoJ0jtjR0FjmiJsea2znZEiPfMN-g7riE6C98eq3OUInvJ1S1ajAk10e6XBSvBeJoStj8N5-UBNSyk2JmTIhfRciKAVsyjbcvqSyxC4mc8t8jFgcorwEM4YVSNuIVuazfoYHeW-7UrIKkiS4Y3CdxiluyaZ2niJ9no74B4OzcHxp4Gf28llZ4SvnrTA3zikViltCQamD75dLd3SrJ37tVCx_HrCCGZlqkJhUuSEy6InbZkBaK8XON9YrPpmcAbBxkf_TWPqaxxf3IGcveFN2uAw6OMQL9z6V5pB9D03GCKWqAPYXHJXEcR97X6d5TO8WO_LS9OvzOeUWUQooCr1bA6l93sTK09_vVUkDVupkEBM124KpL26_vG9NNFcjB7ofuekUPxdAVtwstHGiLisOyKCmmyFzZMLevu_5D1CMOaX-EtNw62LCHksGcw0bJKS2Y_wStwQ80DgYwVpQScXRppGFO0aW9ZIaJBCOFZJ5MXQJH57-0DxDLG2O6-dGbNpYLERkw83HfJU4g
9) https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3741965/
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