CASE DISCUSSION 5 : Case study of a 45yr old women with anasarca

 K.mounika

Roll no: 86

I have been given this case to solve in an attempt to understand the topic of patient clinical data analysis and to develop competency in reading & comprehending clinical data including history,clinical findings,investigations & come up with a diagnosis & treatment plan

The entire analysis of this case is found in the link below

https://alekyatummala.blogspot.com/2020/09/45-yr-female-with-anasarca.html?m=1

Cheif complaints :-

1.PEDAL EDEMA - 5months back which is 

     Gradually progressive

     Pitting type

     Aggravated on walking

     Relieved on rest

Associated with abdominal distension,facial puffiness and decreased urine output

2. SHORTNESS OF BREATH - 5days back

 even at rest 

3.CHEST PAIN - 5days back on right side ,non radiating with intermittent palpitations

4.ANURIA - since 3 days

No associated complaints like fever, burning micturition,hematuria and  frothy urine.

Personal history -

Mixed diet

Appetite-normal

Sleep-adequate

Bowel-constipation since 3days,

Anuria since 3days

Habbit of tobacco chewing since 8yrs

Past history - history of pedal edema nd SOB grade 3 6months back

O/E:-

pt is conscious, coherent and cooperative

pallor is present,

no signs of icterus, cyanosis, clubbing,koilonychia and lymphadenopathy.

ulcer noticed on right sole. 

vitals - afebrile

             bp-180/80mmhg,

             pr-84bpm

             rr-13cpm

CVS -S1S2 heard,no murmurs

RS-BAE present,NVBS

P/A- distended,

CNS - 

 pt is conscious and well oriented to time,place and person

speech-normal

motor and sensory system-normal

cranial nerves - intact

cerebellar functions-normal

INVESTIGATIONS:

1) What is your complete anatomic and etiologic diagnosis of the patient?

Based on above investigations,history and clinical examonation this might be a case of diabetic nephropathy with nephrotic syndrome

The pathology may be due to injury at :

Endothelium

Mechanism of injury - Decreased NO synthesis, increased susceptibility to vasoconstriction, hypoxia

Increased VEGF/VEGFR, ET-1

ROS overproduction

Endothelial-to-mesenchymal transition

TUbule

Mechanism of injury - increased O2 utilization

Hypoxia, increased HIF-1α

Mitochondrial dysfunction (MIOXupregulation)

P53 activation

Destabilizing podocyte slit-diaphragm

Activation of fibrotic pathway

Epithelial-to-mesenchymal transition

Decreased autophagy

Podocyte

ROS overproduction

Podocyte loss, FPE

Inflammation

Lipid accumulation

Restoration of slit diaphragm protein

Epithelial-to-mesenchymal transition

Decreased autophagy

Non cell specific type

Unbalanced glomerular hemodynamics, hyperfiltration, albuminuria

ROS overproduction

ECM deposition

Inflammation

Activation of fibrotic pathway

Mitochondrial dysfunction

2)what are the reasons for her

Azotemia

Azotemia is an elevation of blood urea nitrogen (BUN) and serum creatinine levels. The reference range for BUN is 8-20 mg/dL.

The azotemia in this case may be pre renal or intrarenal

Pre renal azotemia

Prerenal azotemia refers to elevations in BUN and creatinine levels resulting from problems in the systemic circulation that decrease flow to the kidneys. The decreased renal flow stimulates salt and water retention to restore volume and pressure.

Intrarenal azotemia

Also known as acute kidney injury (AKI), renal-renal azotemia, and (in the past) acute renal failure (ARF), refers to elevations in BUN and creatinine resulting from problems in the kidney itself. There are several definitions, including a rise in serum creatinine levels of about 30% from baseline or a sudden decline in output below 500 mL/day. If output is preserved, AKI is nonoliguric; if output falls below 500 mL/day, AKI is oliguric. Any form of AKI may be so severe that it virtually stops formation; this condition is called anuria (< 100 mL/day).

Anemia

Diabetic nephropathy (DN) is a leading cause of chronic kidney disease (CKD) in both patients before initiation of dialysis (CKD stages II, III, IV), and those receiving dialysis (CKD stage V). Normochromic normocellular anemia is known to be a frequent complication of CKD, where the primary etiology is decreased production of erythropoietin by the kidney. The severity of anemia is proportional to the stage of CKD, but anemia may be observed before active renal involvement is apparent (i.e., proteinuria, impaired renal function). In addition, anemia in patients with DM and renal disease occurs earlier and in greater severity than in patients with CKD of the same stage but with a different primary renal disease. In addition to iron, vitamin B12 and folic acid deficiency, poor nutrition, secondary hyperparathyroidism, blood loss and malignancy may be involved in the pathogenesis of anemia in DM. Several other, less well known causes and interrelated mechanisms, such as ultrafiltration, proteinuria, chronic inflammation, damage of interstitial kidney tissue, autonomic neuropathy, the uremic toxins, the renin-angiotensin system, increased tubular sodium reabsorption and disorders of erythrocytes are also implicated in the pathogenetic process. This is an overview of the main mechanisms involved in the onset of anemia in these patients.

Hypoalbuminemia

In nephrotic syndrome, the glomeruli are affected by an inflammation or a hyalinization (the formation of a homogenous crystalline material within cells) that allows proteins such as albumin, antithrombin or the immunoglobulins to pass through the cell membrane and appear in urine.

An increase in glomerular permeability leads to albuminuria and eventually to hypoalbuminemia. In turn, hypoalbuminemia lowers the plasma colloid osmotic pressure, causing greater transcapillary filtration of water throughout the body and thus the development of edema.

ACIDOSIS

Causes for Metabolic Acidosis in this patient are-

Because of decrease in the ability of kidneys to excrete acids.

Decrease tubular reabsorption of bicarbonate.

Insufficient production of bicarbonate in relation to amount of acids synthesized in body and ingested with food.

3) What was the rationale for her treatment plan detailed day wise in the record?

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?

Sodium bicarbonate indications i.v:

Cardiac arrest

Adjunct to adavanced cardiovascualar life support during CPR.

Severe metabolic acidosis.

Less urgent metabolic acidosis

Urine alkalinization

Antacid

Hyperkalemia

Contraindications:

Metabolic or respiratory Alkalosis

Hypercarbic acidosis

Hypersensitivity

Hypocalcemia because alkalosis can cause tetany

Excessive Chloride loss from vomiting or G.I. suctioning

Indications of oral NAHCO3:

To relieve heart burn or sour stomach

Alkalinization of urine

Contraindications:

Acute ingestion of strong mineral acids

Sodium bicarbonate should be used with extreme caution in the following patients:

Heart Failure

Renal insufficiency

Any edematous or sodium retaining conditions

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?

severe metabolic acidosis & refractory anuria

5) What are the other factors other than diabetes and hypertension that led to her current condition?

6) What are the expected outcomes in this patient? Compare the outcomes of similar patients globally and share your summary with reference links

 & 7)o How and when would you evaluate her further for cardio renal HFpEF and what are the mechanisms of HFpEF in diabetic renal failure patients?

8) What are the efficacies over placebo for the available therapeutic options being provided to her for her anemia 

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 Telegu among the 68 languages in which it is translated?

The CKD-AQ captures the frequency and severity of the most relevant symptoms and impacts associated with anemia of CKD. It has the potential to assist clinicians in assessing and understanding patients' symptoms due to anemia of CKD as well as to help evaluate treatments for anemia of CKD in clinical trials.

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 patients?

Malnutrition is a common problem in patients with end stage renal disease (ESRD) undergoing hemodialysis that may occur secondary to several factors such as inadequate nutritional intake, increased losses, or to an increase in protein catabolism. The results of malnutrition are various and include increased susceptibility to infection, impaired wound healing, poor rehabilitation, fatigue, malaise, and increased rates of hospitalization, morbidity and mortality 

Subjective global assessment (SGA) is a tool used by health care providers to assess nutritional status and aids in the prediction of nutrition-associated clinical outcomes ; it is inexpensive and rapidly conducted. Moreover, it has been recommended by the National Kidney Foundation (NKF) Kidney Disease/Dialysis Outcomes and Quality Initiative (K/DOQI) for use in nutritional assessment in the adult dialysis population , however, it seems its semi-quantitative scale, consisting of three discrete severity levels, restricts its reliability and precision. In other words, responses to some sections of SGA depends on the patient’s ability to provide accurate data and ability of the physician to conduct detailed, probing interviews . Biochemical parameters like serum albumin levels are extensively used to assess the nutritional status in general population . Nonetheless, it seems they can be influenced by non-nutritional factors such as infection, inflammation, hydration status, peritoneal or urinary protein losses, and acidemia