1.a-pain in the epigastric region - associated with nausea,constipation ,abdominal distension- acute onset
possible differentials would be
Intestinal obstruction
Acute pancreatitis
Ascites
In this case usg showed evidence of pancreatic inflammation ,serum and ascitic fluid analysis showed high amylase levels -all the clinical,biochemical and radiological findings are consistent with acute pancreatitis
- decreased urine output -could be due to obstruction ,pre renal AKI ,Renal pathology
As usg showed normal sized kidneys -it could be an acute event that lead to decreased urine output
no post voidal residue and no bladder distension -hence obstruction is excluded .
Possible mechanism of renal failure in this patient are -acute pancreatitis causing third space fluid loss and precipitating acute kidney injury
Release of toxins,free radicals directly damage glomeural structure
Hypovolemia,hypotension,hypoxia ,inflammation,-all these contribute to pathogenesis of AKI in acute pancreatitis
https://cjasn.asnjournals.org/content/14/7/1106
Cytokines may contribute to the pathogenesis of AKI. TNF-α acts directly on glomeruli and tubular capillaries, leading to ischemia and tubular necrosis. It also stimulates release of other cytokines, such as IL-1β, IL-8, and IL-6, which act on endothelial cells leading to kidney ischemia, thrombosis, and release of oxygen free radicals. Inflammatory mediators may increase mucosal permeability leading to translocation of endotoxin and bacteria from the colon. Endotoxins contribute to the development of AKI by increasing endothelin level, which causes vasoconstriction, decreased kidney blood flow, and tubular necrosis (19). Also, oxygen free radicals may react with proteins and enzymes, leading to lipid peroxidation of the cell and organellar membranes, protein denaturation and increased capillary permeability, ischemia, and direct kidney cell membrane injury
In the background of chronic smoking and also clinical ,radiological findings suggestive of atherosclerotic changes -PERIPHERAL ARTERIAL DISEASE can be considered .
Time line chart :
Acute pancreatitis —-renal failure -AKI——-central line catheterisation ,hemodialysis(inj.vancomycin was added for CRBSI) —Resolution of pain abdomen (Started on oral feeds )
B- NBM and IV fluids And other supportive treatment were given as a part of management of acute pancreatitis .
According to recent guidelines vancomycin is preferred empirically for treatment of catheter based infections in patients undergoing hemodialysis .
Class -2A EVIDENCE
Vancomycin is recommended for empirical therapy in heath care settings with an elevated prevalence of methicillin-resistant Staphylococcus aureus(MRSA); for institutions in which the preponderance of MRSA isolates have vancomycin minimum inhibitory concentration (MIC) values >2 μg/mL, alternative agents, such as daptomycin, should be used (A-II).
2-with the history of cough,low grade fever ,loss of appetite , weight loss for more than a year - intermittently suggesting chronic Course of the disease.The possible etiologies In this patient are :
Infections/Tumor
As India is endemic to TUBERCULOSIS - the m/c/c to be considered here would be TB ,even the
ZN stain and CT CHEST are in favor for tuberculosis .
Going with age of patient and history of chronic anemia and generalized myalgia - neoplasm is another differential .
With osteolytic skull lesions,plasma cells in bone marrow , M spike in protein electrophoresis- possible diagnosis would be MULTIPLE MYELOMA
So if we consider Multiple Myeloma as primary cause -the hypothesis is —as MM is associated with hypogammaglobulinemia -they are more prone to infections than normal population .So the patient here would have contracted Tuberculosis .
-Hypercalcemia,hyperuricemia,hyperphoshpatemia ,renal failure all these features -explaining high turn over of Malignant cells and thus lead to TUMOR LYSIS SYNDROME.
Renal failure is seen in nearly 25% of MM patient's ,and the m/c/c is hypercalcemia
Glomerular deposits of amyloid ,hyperuricemia ,recurrent infections,use of NSAId for bone pains ,all these can contribute to renal failure
Tubular damage is also seen bcz of excretion of light chains .Damage can be directly from light chain toxins or indirectly from intracellular lysosomal enzymes .
Earliest manifestation of this tubular damage is Adult FANCONI SYNDROME - TYPE 2 PROXIMAL RTA .
Management of MM
3- patient presented with gradually progressive pedal edema associated with shortness of breath
He also reports similar complaints 2 months back.
—-edema-
As patient used preload reducing agents before he was brought to hospital JVP was not elevated ,although there was significant pedal edema
Given the history of DM,HTN ,HFPEF WITH RWMA ,AF,echo suggestive of reduced ejection fraction the most probable cause of bilateral pedeal edema is congestive cardiac failure
Etiology of CCF -in this particular case Could be Atherosclerotic CORONARY ARTERY DISEASE .[secondary to metabolic syndrome ]
Timeline ; DM,HTN,SMOKING,ALCOHOLISM ——- CVA,AF,HFPEF ———-HFREF
B- non pharmacological interventions include salt and water restriction -so as to prevent excess preload on heart .
Pharmacological -
Lasix- to decrease preload by inducing diuresis
Metxl- metoprolol - by decreasing the heart rate decreases the o2 consumption of cardiac muscles,hence decrease workload on the heart .
The rationale to use β-blockers is based on the markedly increased sympathetic activity in patients with CHF. The positive inotropic effect of this sympathetic activation is far outweighed by its adverse effects, which include myocardial ischemia, arrhythmogenicitiy, sodium retention, hypokalemia, and myocardial cell death and apoptosis
- Multicenter, double-blinded, parallel-group, randomized, placebo-controlled trial
- N=3,991
- Metoprolol XL (n=1,990)
- Placebo (n=2,001)
- Setting: 313 centers in US and Europe
- Enrollment: February 1997 to April 1998
- Mean follow-up: 1 year
- Analysis: Intention- To treat
4-
A-history of palpitations ,pedal edema ,PND,shortness of breath on exertions -would indicate cardiac origin.
With Background history of chronic alcoholism and no other comorbidities - BERI BERI [high output cardiac failure ] can be considered as the cause of heart failure .
Thiamine acts as cofactors in Various energy producing Pathways ,deficiency of thiamine leads to accumulation of pyruvate and lactate -both can cause vasodilatation -peripheral pooling of blood and thus increase in sympathetic activity [activation of RAAS ] to maintain high cardiac output .it acts as viscious cycle and if thaimine is not replaced at appropriate time,patient may land up in decompensated heart failure .
History of pins and needles ,slippage of footwear,sensory deficit on examination - a sensory motor polyneuropathy - all these can be manifestation of DRY BERI BERI .
B- non pharmacological interventions include fluid and salt restriction- So as to decrease preload On heart
Lasix to induce diuresis and decrease preload
Thaimine to replenish the stores and for active management of high output cardiac failure
Normal thiamine requirement per day is 1.4 gm ,and humans can not synthesis thaimine.but they can store 30-50 mg in skeletal ms and cardiac muscle .
Without dietary intake ,stores usually deplete within 18 days .
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