CASE
I've been given these three cases data here
https://alekyatummala.blogspot.com/2020/09/45-yr-female-with-anasarca.html?m
This may develop my competency
a) reading and comprehending clinical data related to the case including history, clinical findings, investigation
b) come up with a diagnosis such as
- 1) Anatomical location of the root cause
- 2) Physiological functional disability
- 3) Biochemical abnormalities that could be a root cause at a molecular lev
- 4) Pathology that could reflect the root cause at a cellular lev
c) a treatment plan for each of these patients of paraparesis that can have a pharmacological and non pharmacological componency
d) learning the scientific basis of diagnostic and therapeutic approach in terms of past collective experiences and experiments (aka evidence based medicin
The first step to developing these competencies after reading and comprehending each patient data will be :
a) create a problem list for each patient in order of the patient's perceived priori
b) Discuss the root causes for the problem as described above in terms of anatomy, biochemistry and pathology, microbiology
c) discuss possible solutions to tackle these root causes from upstream (soil from which the roots begin) or downstream (to treating the stem and branches aka palliation) in terms of pharmacological (medicinal) and non pharmacological (such as prosthetics, implants) both in historical terms (past dominant treatments for the same cause and it's current evolution) as well as recent advances ( ongoing trials and innovative approaches even at a hypothetical stage
1) What is your complete anatomic and etiologic diagnosis from the data available in the patient's online record linked above? (ignore the provisional diagnosis on admission mentioned in the case report)
Ans- Anatomic diagnosis: acute kidney injury at glomerulus, mesangial thickening could be the pathoanatomic change with nodular sclerosis AKA kimmelstein Winston lesion
Etiologic diagnosis: diabetic nephropathy
2) What are the reasons for her Azotemia?
Ans- reduced GFR results in reduced excretion of nitrogenous wastes leading to azotemia
Anemia
Erythropoietin deficiency
Hypoalbuminemia
Increased glomerular capillary permeability due
Acidosis
reduction in GFR leads to reduced H+, and other organic acids excretion leading to acidosis. metabolic acidosis increased anion gap
3) What was the rationale for her treatment plan detailed day wise in the record?
Day1
HCO3 was given to treat acidosis - target HCO3 22meq
potassium was given to counteract hypookalemia
Day2
insulin was given to correct hyperglycemia
pantoprazole was given to prevent curling ulcer
Vitamin B9 or Folic Acid, iron was given to reat anaem
furocemide was given to reduce fluid overload (evidenced by pulmonary edem
Day3
furcemide - reduce fluid overload
spirinolactone - reduce potassium loss from furosemide
Vitamin B9 or Folic Acid, iron was given to reat anaem
nicardipine - to achieve target BP of 130/
erythropoietin to treat underlying cause of anemia
calcium and vitamin d3 - reduce renal osteodystrophy
tab sodium bicarbonate - reduce/prevent metabolic acidos
potassium was given to counteract hypokalemia
renal replacement there
Day4
lactulose to reduce encephalopathy
protien to counteract protien low
ceftrioxone to prevent infection as a risk of renal replacement thera
Particularly mention rationale and efficacy for some of the drugs administered such as oral and iv bicarbonate? When is iv or oral bicarbonate indicated and why is it contraindicated in certain situations?
Metabolic acidosis in patients with chronic kidney disease: Oral (off-label): Note: KDIGO guidelines suggest oral replacement when plasma HCO3- concentrations are <22 mEq/L (KDIGO 2013
Initial: 15.4 to 23.1 mEq/day in divided doses (eg, 650 mg tablet 2 to 3 times daily); titrate to normal serum bicarbonate concentrations (eg, 23 to 29 mEq/L) or up to 5850 mg/day; baking soda may be used as an alternative in patients who cannot take tablets (Chen 2014; KDIGO 2013; Kovesdy 2009; Raphael 2016). Avoid exceeding serum bicarbonate concentrations >32 mEq/L since this has been associated with increased mortality in patients with CKD (Navaneethan 2011
https://www.uptodate.com/contents/sodium-bicarbonate-drug-information?topicRef=127552&source=see_li
https://reference.medscape.com/drug/sodium-bicarbonate-3423
4) What was the indication for dialysing her and what was the crucial factor that led to the decision to dialyze her on the third day of admission?
"Intractable dependent oedema resistant to diuretic
Pulmonary oedema
Severe hypertension
Potassium resistant to dietary control and medical intervention
Uraemic syndrome including anorexia, nausea, lethargy etc. (generally not until eGFR < 10 mL/min/1.73 m2
Chronic acidosis resistant to bicarbonate therapy
Intractable anemia despite erythropoietin and iron
Hyperphosphatemia despite binder
(Reference: davidson 23rd edition table 15.)
Indication in this case -
severe shortness of breath - pulmonary edema
metabolic acidosis and refractory anuria
5) What are the other factors other than diabetes and hypertension that led to her current condition?
Failure of secondary prevention that is failure to seak medical help in eary stage of disea
6) What are the expected outcomes in this patient? Compare the outcomes of similar patients globally and share your summary with reference links.
kaplan - Meier survival rate of diabetic CKD is 37%
5year survival is 4
diabetes, low serum albumin, low socioeconomic status of this patient predict poor prognos
FGF-23 levels is a novel marker for mortali
7) How and when would you evaluate her further for cardio renal HFpEF and what are the mechanisms of HFpEF in diabetic renal failure patients
"The complications of CKD result in increased cardiac workload due to hypertension, volume overload, and anemia. Patients with CKD may also have accelerated rates of atherosclerosis and vascular calcification resulting in vessel stiffness
these factors contribute to development left ventricular hypertrophy and left ventricular failu
(Reference: CMDT 2020, topic on chronic kidney diseases)
Frequency of echocardiograph
at time of starting od renal replacement therapy
after 1 month of starting renal replacement therapy
after 3 months of starting or renal replacement therapy
then annually after starting of renal replacement thera
any time if patient's symptoms change
reference: https://pubmed.ncbi.nlm.nih.gov/1580650
8) What are the efficacies over placebo for the available therapeutic options being provided to her for her anemia
"There was an improvement in haemoglobin (MD 1.90 gm/L, 95% CI -2.34 to -1.47) and haematocrit (MD 9.85%, 95% CI 8.35 to 11.34) with treatment and a decrease in the number of patients requiring blood transfusions (RR 0.32, 95% CI 0.12 to 0.83)
ref: https://pubmed.ncbi.nlm.nih.gov/2679013
9) What is the utility of tools like the CKD-AQ that assess the frequency, severity, and impact on daily activities of symptoms of anemia of CKD? Is Telugu among the 68 languages in which it is translated
There are many studies which prove questionares efficatious and lead to early recognition of symptoms and prompt treatmen
https://doi.org/10.1016/j.jval.2018.09.23
10) What is the contribution of protein energy malnutrition to her severe hypoalbuminemia? What is the utility of tools such as SGA subjective global assessment in the evaluation of malnutrition in CRF patient
"subjective global assessment can be used effectively by providers from different disciplines, such as nursing, dietitians, and physicians; and in some studies has beenfound to be reproducible, valid, and reliable
reference:
2) A similar patient data as above with diabetes and renal failure with metabolic acidosis and hypoalbuminemia logged by intern Dr Bhavya here
https://bhavyayammanuru.blogspot.com/2020/09/aki-secondary-to-uti.html?m
Please comment on the differences in the diagnosis, therapy and outcomes in both these two patient
case 1: chronic kidney disea
The aims of management in CKD are to
• monitor renal functio
• prevent or slow further renal damag
• limit complications of renal failur
• treat risk factors for cardiovascular diseas
• prepare for RRT, if appropria
Case 2: acute kidney inju
•fluid stat
If hypovolaemic: optimise systemic haemodynamic sta
If fluid-overloaded, prescribe diuret
•correct hyperkalaemia if K+ > 6.5 mmol
•correct acidosis if H+ is > 100 nmol/L (pH < 7.0) - administer bicarbona
• Discontinue potentially nephrotoxic drugs and reduce doses of therapeutic dru
• nutritional suppor
•proton pump inhibitors to reduce curling ulce
• Screen for infections and tre
• In case of urinary tract obstruction, drain lower or upper urinary tract as necessa
Would you agree with the provisional diagnosis shared for this 58 M in the online case report linked abov
yes, there was no symptoms suggesting of pre renal AKI like Volume depletion (vomiting, diarrhoea, burns, haemorrhage) Drugs (diuretics, ACE inhibitors, ARBs, NSAIDs, iodinated contrast) Liver disea
and symptoms like "Decreased urinary stream since 3days not passing urine since 1 day Pain abdomen since 1day." suggest a post renal A
What are the findings in the ultrasound of both kidneys? How do you explain those findings? Would it explain the etiology for his renal failure?
It is normal in si
corticomedullary differentiation norm
pelvi calyceal saperation norm
in pre renal aki there is less perfusion to kidney and kidney is structurally norma
doppler imaging would help in confirming less perfusi
loss of cortico medullary differintation is seen in CKD which helps in rulling out the conditi
pelvi calyceal sustem is dilated in post renal AKI which helps in rulling out the condition I've been given these three cases data her
https://alekyatummala.blogspot.com/2020/09/45-yr-female-with-anasarca.html?m
This may develop my competency
a) reading and comprehending clinical data related to the case including history, clinical findings, investigati
b) come up with a diagnosis such a
1) Anatomical location of the root cau
2) Physiological functional disabili
3) Biochemical abnormalities that could be a root cause at a molecular lev
4) Pathology that could reflect the root cause at a cellular lev
c) a treatment plan for each of these patients of paraparesis that can have a pharmacological and non pharmacological componen
A
d) learning the scientific basis of diagnostic and therapeutic approach in terms of past collective experiences and experiments (aka evidence based medicin
The first step to developing these competencies after reading and comprehending each patient data will be
a) create a problem list for each patient in order of the patient's perceived priori
b) Discuss the root causes for the problem as described above in terms of anatomy, biochemistry and pathology, microbiolo
a
c) discuss possible solutions to tackle these root causes from upstream (soil from which the roots begin) or downstream (to treating the stem and branches aka palliation) in terms of pharmacological (medicinal) and non pharmacological (such as prosthetics, implants) both in historical terms (past dominant treatments for the same cause and it's current evolution) as well as recent advances ( ongoing trials and innovative approaches even at a hypothetical stage
1) What is your complete anatomic and etiologic diagnosis from the data available in the patient's online record linked above? (ignore the provisional diagnosis on admission mentioned in the case repo
Anatomic diagnosis: acute kidney injury at glomerulus, mesangial thickning could be the pathoanatomic change with nodular sclerosis AKA kimmelstein Winston lesio
Etiologic diagnosis: diabetic nephropat
2) What are the reasons for her
Azotemi
reduced GFR results in reduced excretion of nitrogenous wastes leading to azothem
Anemi
Erythropoietin defecien
Hypoalbuminemi
Increased glomerular capillary permeability due
Acidosi
reduction in GFR leads to reduced H+, and other organic acids excretion leading to acidosis. metabolic acidosis increased anion g
3) What was the rationale for her treatment plan detailed day wise in the record?
Day
HCO3 was given to treat acidosis - target HCO3 22meq
potassium was given to counteract hypookalemi
Day
insulin was given to correct hyperglycem
pantoprazole was given to prevent curling ulc
Vitamin B9 or Folic Acid, iron was given to reat anaem
furocemide was given to reuce fluid overload (evidenced by pulmonary edem
Day
furcemide - reduce fluid overlo
spirinolactone - reduce potasium loss from furocemi
Vitamin B9 or Folic Acid, iron was given to reat anaem
nicardipine - to achieve target BP of 130/
eruthropoietin to treart underlying cause of anaem
calcium and vitamin d3 - reuce renal osteodystrop
tab sodium bicarbonate - reduce/prevent metabolic acidos
potassium was given to counteract hypookalemi
renal replacement ther
Day
lactulose to reduce encephalopat
protien to counteract protien lo
ceftrioxone to prevent infection as a risk of renal replacement thera
Particularly mention rationale and efficacy for some of the drugs administered such as oral and iv bicarbonate? When is iv or oral bicarbonate indicated and why is it contraindicated in certain situations?
Metabolic acidosis in patients with chronic kidney disease: Oral (off-label): Note: KDIGO guidelines suggest oral replacement when plasma HCO3- concentrations are <22 mEq/L (KDIGO 2013
Initial: 15.4 to 23.1 mEq/day in divided doses (eg, 650 mg tablet 2 to 3 times daily); titrate to normal serum bicarbonate concentrations (eg, 23 to 29 mEq/L) or up to 5850 mg/day; baking soda may be used as an alternative in patients who cannot take tablets (Chen 2014; KDIGO 2013; Kovesdy 2009; Raphael 2016). Avoid exceeding serum bicarbonate concentrations >32 mEq/L since this has been associated with increased mortality in patients with CKD (Navaneethan 2011
https://www.uptodate.com/contents/sodium-bicarbonate-drug-information?topicRef=127552&source=see_li
https://reference.medscape.com/drug/sodium-bicarbonate-3423
4) What was the indication for dialysing her and what was the crucial factor that led to the decision to dialyze her on the third day of admission?
"Intractable dependent oedema resistant to diureti
Pulmonary oedem
Severe hypertensi
Potassium resistant to dietary control and medical interventio
Uraemic syndrome including anorexia, nausea, lethargy etc. (generally not until eGFR < 10 mL/min/1.73 m2
Chronic acidosis resistant to bicarbonate therap
Intractable anaemia despite erythropoietin and iro
Hyperphosphataemia despite binder
Reference: davidson 23rd edition table 15.
Indication in this case
severe shortness of breath - pulmonary ede
metabolic acidosis and refractory anur
5) What are the other factors other than diabetes and hypertension that led to her current condition?
Failure of secondary prevention that is failure to seak medical help in eary stage of disea
6) What are the expected outcomes in this patient? Compare the outcomes of similar patients globally and share your summary with reference links.
kaplan - Meier survival rate of diabetic CKD is 37%
5year survival is 4
diabetes, low serum albumin, low socioeconomic status of this patient predict poor prognos
FGF-23 levels is a novel marker for mortali
7) How and when would you evaluate her further for cardio renal HFpEF and what are the mechanisms of HFpEF in diabetic renal failure patients
"The complications of CKD result in increased cardiac workload due to hypertension, volume overload, and anemia. Patients with CKD may also have accelerated rates of atherosclerosis and vascular calcification resulting in vessel stiffness
these factors contribute to development left ventricular hypertrophy and left ventricular failu
Reference: CMDT 2020, topic on chronic kidney diseas
Frequency of echocardiograph
at time of starting od renal replacement therap
after 1 month of starting renal replacement thera
after 3 months of starting or renal replacement thera
then annually after starting of renal replacement thera
any time if patient's symptoms change
reference: https://pubmed.ncbi.nlm.nih.gov/1580650
8) What are the efficacies over placebo for the available therapeutic options being provided to her for her anemia
"There was an improvement in haemoglobin (MD 1.90 gm/L, 95% CI -2.34 to -1.47) and haematocrit (MD 9.85%, 95% CI 8.35 to 11.34) with treatment and a decrease in the number of patients requiring blood transfusions (RR 0.32, 95% CI 0.12 to 0.83)
ref: https://pubmed.ncbi.nlm.nih.gov/2679013
9) What is the utility of tools like the CKD-AQ that assess the frequency, severity, and impact on daily activities of symptoms of anemia of CKD? Is Telugu among the 68 languages in which it is translated
There are many studies which prove questionares efficatious and lead to early recognition of symptoms and prompt treatmen
https://doi.org/10.1016/j.jval.2018.09.23
10) What is the contribution of protein energy malnutrition to her severe hypoalbuminemia? What is the utility of tools such as SGA subjective global assessment in the evaluation of malnutrition in CRF patient
"subjective global assessment can be used effectively by providers from different disciplines, such as nursing, dietitians, and physicians; and in some studies has beenfound to be reproducible, valid, and reliable
reference:
https://www.researchgate.net/publication/8232450_Subjective_Global_Assessment_in_chronic_kidney_disease_a_revie
2) A similar patient data as above with diabetes and renal failure with metabolic acidosis and hypoalbuminemia logged by intern Dr Bhavya here
https://bhavyayammanuru.blogspot.com/2020/09/aki-secondary-to-uti.html?m
Please comment on the differences in the diagnosis, therapy and outcomes in both these two patient
case 1: chronic kidney disea
The aims of management in CKD are to
• monitor renal functio
• prevent or slow further renal damag
• limit complications of renal failur
• treat risk factors for cardiovascular diseas
• prepare for RRT, if appropria
Case 2: acute kidney inju
•fluid stat
If hypovolaemic: optimise systemic haemodynamic sta
If fluid-overloaded, prescribe diuret
•correct hyperkalaemia if K+ > 6.5 mmol
•correct acidosis if H+ is > 100 nmol/L (pH < 7.0) - administer bicarbona
• Discontinue potentially nephrotoxic drugs and reduce doses of therapeutic dru
• nutritional suppor
•proton pump inhibitors to reduce curling ulce
• Screen for infections and tre
• In case of urinary tract obstruction, drain lower or upper urinary tract as necessa
Would you agree with the provisional diagnosis shared for this 58 M in the online case report linked abov
yes, there was no symptoms suggesting of pre renal AKI like Volume depletion (vomiting, diarrhoea, burns, haemorrhage) Drugs (diuretics, ACE inhibitors, ARBs, NSAIDs, iodinated contrast) Liver disea
and symptoms like "Decreased urinary stream since 3days not passing urine since 1 day Pain abdomen since 1day." suggest a post renal A
What are the findings in the ultrasound of both kidneys? How do you explain those findings? Would it explain the etiology for his renal failure?
It is normal in si
corticomedullary differentiation norm
pelvi calyceal saperation norm
in pre renal aki there is less perfusion to kidney and kidney is structurally norma
doppler imaging would help in confirming less perfusi
loss of cortico medullary differintation is seen in CKD which helps in rulling out the conditi
pelvi calyceal sustem is dilated in post renal AKI which helps in rulling out the condition ononl alalze KIsee?ryatrst gste/Lictuusrytee e e n : ses. =1
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."s?21t.? 5/."? 2/ pypypyy y
e.re."?
tyis0%,
se
iama
35s"n y ) n ona cs
05nk).).
pysshy 5apya ishyia80iadead 3a)iaeria 2a /l 1
aps toa cya iaa :
hyns
rt)).ndgytytoe)ndt.eleltyses:onsin =1kidney is structurally normal
doppler imaging would help in confirming less perfusion
loss of cortico medullary differintation is seen in CKD which helps in rulling out the condition
pelvi calyceal sustem is dilated in post renal AKI which helps in rulling out the condition
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