Two similar cases yet very different

                                                    

Case of a 45 year old female with Acute Kidney Injury

                                                      Submitted by: Simran Dash

                                                     MBBS: IV | Roll number: 153

I have been given this case 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 link:

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

This is the 1st case.  

My analysis for this patient is as folows:-

Age: 45 years

Sex: Female

Occupation: Housewife

Chief complaints:

• Pedal edema since 5 days
• Oliguria since 3 days

Analysis of each complaint in detail-

   1) Pedal edema:

• Onset- Insidious
• Duration- 6 months
• Progression- Gradually Progressive 
• Type- Pitting
• Aggravated on- Walking
• Relieved on- Rest
• Associated complaints-
• Facial puffiness mainly periorbital edema
• Abdominal distension
• Dyspnea (Initially Grade 3 later, Grade 4 according to NYHA)
• Intermittent Palpitations
• Right sided Chest pain, non- radiating

Etiology for pedal edema:

• Renal
• Cardiac
• Hepatic

   2) Oliguria:

• Onset- Sudden
• Duration- 3 days
• Progression- Progressed from oliguria to anuria in the last 3 days

But since there is oliguria too, this could be either renal or cardiac etiology. Considering the associated complaints, it is more likely to be Congestive Heart Failure leading to Renal Failure.

Past Medical And Surgical History: Known case of Type 2 Diabetes Mellitus since 5 years and Hypertension since 1 year.

From the history, Possible causes for her complaints could be-

• Congestive heart failure 
• Malignant Hypertension causing Hypertensive Nephropathy
• Diabetic Nephropathy

On Examination, she has pallor and generalised edema i.e. Anasarca. She also has dependant ulcer on her right sole.

Per Abdomen Examination: Distended abdomen (could be ascites but there is no shifting dullness hence rules it out.)

Vitals:

 

          BP- 180/80 mm Hg

          RR- 20cpm

Investigations done on her and their respective findings on a daily analysis can be found in the following link:

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

The rationale behind detailed day wise recording of her treatment plan is as follows:-

• Gives a better idea of all the treatment options received by her.
• Also helps in better monitoring of the patient.
• We can understand if the patient is responding to the specific treatment regime or not, depending upon which either the drugs or their dosages can be changed.
• This rationale makes the data more organized.

Following investigations were done-

1) CBP:

 

 

                                                   Microcytic Hypochromic Anemia

2) CUE:

                                          There is Grade 4 Proteinuria.

3) RFT: 

                                  Elevated levels of serum creatinine and Urea.

                                  The ratio of Blood Urea Nitrogen to Serum Creatinine is less than 20:1, Then the possible pathology could be in the kidneys. It could be a renal cause.

4) ABG:

 

            There is metabolic acidosis as evidenced by the decrease in ph and serum bicarbonate levels.

5) Random Blood Sugar and HbA1c levels:

   Normal blood glucose levels.

Elevated HbA1c levels.

 6) APTT: 

                                              Normal APTT reflecting no hypercoagulability.

7) Prothrombin Time:

                                     Normal prothrombin time also rules out hypercoagulabilty.

8) Serum albumin:

                                                          There is Hypoalbuminemia.

9) Urine protein/Creatinine Ratio:                                           

                                                Normal Urine protein and creatinine ratio.

10) Serum Iron:

                                                                   Normal values.

11) Venous Doppler Ultrasound of bilateral kidneys:

                  Normal Venous Doppler of bilateral kidneys, thereby rules out Renal Vein thrombosis.

12) Colour Doppler 2D ECHO:

                Heart Failure with preserved ejection fraction i.e., Diastolic dysfunction.

13) Chest X-Ray:

 

                       There is a left sided pleural effusion with mediastinal shift to the right side.

14) ECG: 

                                                                        Normal ECG 

15) Ultraonography of abdomen:

Normal size and shape of bilateral kidneys.

16) 24 hours urinary protein:

                                                           There is massive Proteinuria.

After investigations, I can confirm that our patient has Nephrotic syndrome causing Acute Kidney Injury as evidenced by-

• Oliguria
• Hypoalbminenia
• Proteinuria
• Pedal edema progressing to periorbital edema

Risk Factors for Nephrotic Syndrome in this case which could have led to her current condition are:

• Diabetes Mellitus
• Hypertension
• Anemia
• Malnutrition because of excessive proteinuria (which is masked by the anasarca)

Mainly the causes for Nephrotic syndrome in this case could be:

• Diabetes mellitus causing Diabetic Nephropathy.
• Congestive Heart Failure 
• Hypertensive nephropathy

Complications of Nephrotic syndrome in this case are:

• Acute Kidney Injury
• Malnutrition
• Malignant Hypertension because of damage to glomeruli and the resulting buildup of excess body fluids.

After history,examination and investigations, 

Anatomical diagnosis is pre-renal or intrinsic Acute Kidney Injury.

Etiology behind it are:

1. Pre-renal AKI: Congestive Heart Failure causing impaired cardiac output leading to renal dysfunction i.e. Cardiorenal syndrome
2. Intrinsic AKI: Malignant Hypertension

Pathophysiology behind this:

1) Cardiorenal Syndrome-

2) Malignant hypertension-

In order to confirm these etiologies additional investigations needed are:

• Fundoscopy to check hypertensive retinopathy or diabetic retionopathy.
• To rule out Cardiorenal syndrome, additional investigations needed are-

• Cardiac troponins: Rule out Myocardial Infarction.
• Creatine kinase
• LDH levels
• Brain Natriuretic Peptide

• Early biomarkers to confirm Acute Kidney Injury are:

• Neutrophil Gelatinase associated lipocalin (NAGL)
• N Acetyl B-D- Glucosaminidase (NAG)
• Cystatin C
• Kidney Injury Molecule-1 (KIM-1)

• Tests to confirm the suspected Pleural effusion:

• Thoracic Ultrasound
• Contrast Enhanced CT scan
• Pleural tap can be done to find out whether the effusion is exudative or transudative.

After investigations, we found out that the patient has Azotemia, Anemia, Hypoalbuminemia and Acidosis. The reasons for which are cited below-

1) Azotemia: AKI which could be renal or pre-renal.

So in order to correct this, the patient underwent Hemodialysis on day 4. The main indications for hemodialyis in this patient are:

• Severe Proteinuria
• Metabolic Acidosis refractory to treatment with bicarbonate.
• Acute pulmonary oedema
• Oliguria

2) Anemia: 

Possible causes behind Anemia in this case could be:

• Erythropoeitin deficiency
• Uremia induced inhibitors of erythropoeisis
• Shortened RBC survival
• Disordered iron hemostasis which could be because of hepcidin excess.

For the treatment of Anemia, she received:

1) Day 2 : Tab. OROFER xt BD  

2) Day 3: As there was no improvement in the Hemoglobin level

• Tab. OROFER xt
• Inj. Erythropoeitin S.C. twice weekly 

3) Day 4: Blood transfusion-1 unit of blood (450 ml)

After Blood Transfusion, her Hemoglobin level increased from 6.6 gm/dl to 8.4 gm/dl.

Various studies were conducted for the purpose of seeing the efficacy of erythropoeitin over placebo in the treatment of Anemia induced by CKD. One such study is being discussed here as follows-

"Of the 67 enrolled patients, all received at least one dose of epoetin alfa and were included in the efficacy and safety analyses. Fifty patients completed all visits through week 28; 17 patients withdrew from the study. Reasons for early withdrawals are presented in Figure 1. There were no withdrawals as a result of treatment failure."

"Hb response (defined as achievement of the target Hb range of 11 to 12 g/dl for at least 2 consecutive weeks) was achieved in 59 (88.1%; 95% CI 77.8 to 94.7) of 67 patients by week 28. Twenty-two (32.8%) patients had a Hb response by week 5, and 44 (65.7%) patients had a Hb response by week 9. Of the eight patients who did not reach the Hb target of 11 to 12 g/dl by week 28, five had withdrawn early, two had a rapid rise in Hb and numerous dosage holds, and one had a baseline Hb value of 7.9 g/dl and a final value of 9.6 g/dl. There were no treatment failures."

"Mean time to the first 1- and 2-g/dl rise in Hb was 4.2 ± 3.1 and 7.7 ± 4.8 wk, respectively. Figure 3 presents the proportion of patients with a 1- and 2-g/dl increase in Hb from baseline by weeks 5, 9, and 28."

This single-arm, open-label, multicenter study demonstrated that initiation of therapy with epoetin alfa at a dosing interval of 20,000 IU every 2 wk was effective for patients with anemia of CKD-NOD.

https://cjasn.asnjournals.org/content/2/2/215

Further for the treatment of anemia, administration of Iron and Erythropoeisis Stimulating Agents reduced the risk for RBC transfusion compared with iron therapy alone in patients undergoing cardiac and non cardiac surgery.

s://link.springer.com/article/10.1007/s12630-019-01351-6

 "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. It also has the potential to improve patients’ HRQoL (Health related Quality of life).The patient-centered approach utilized to develop the CKD-AQ is an important feature because it ensures that the symptoms most relevant to patients with anemia of CKD were included."

But despite of the above advanatages, it has certain limitations which are as follows-

• First, not all questions were asked of all participants because interview time was limited. 
• However, not all concepts were relevant to every participant, especially if certain symptoms were not initially reported. 
• Participants with comorbid conditions could also affect the results because symptoms of another condition could be attributed to anemia of CKD.

https://jpro.springeropen.com/articles/10.1186/s41687-020-00215-8#:~:text=The%20final%20CKD%20and%20Anemia,use%20in%20global%20clinical%20trials.

Despite the above limitations no other measures include assessments of both severity and frequency of all the relevant symptoms and impacts identified together in a single questionnaire.

3) Hypoalbuminemia:

It is associated with AKI because of a combination of reduced synthesis and increased degradation of albumin resulting in proteinuria. This altered albumin homeostasis in AKI patients is caused by a synthetic inflammatory state which is closely related with mortality. This is further aggravated by protein calorie malnutrition which decreases the albumin synthesis.

So for the treatment of this, she received Protinex powder 2 tbsp in 1 glass milk BD. 

She can also receive Albumin in this case which increases the intravascular oncotic pressure to transfer the extravascular fluid into the intravascular compartment for ultrafiltration in order to mobilize the edema fluid.

https://www.karger.com/Article/Abstract/90185

4) Metabolic 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.
• It could be because of Congestive Heart Failure impairing the excretion of organic acids leading to accumulation of these acids.

In order to correct it, the treatment received by her are-

1) Day 1: Inj. NaHCO3 100 mEq/I.V./stat in 100 ml NS

2) Day 2: Continued with it.

3) Day 3: Continued it till day 6. And the bicarbonate levels rose from 6.7 mmol/L to 15.7 mmol/L. This was associated with an increase in the ph from 7.19 to 7.33.

Indications of I.V. sodium bicarbonate:

• Cardiac arrest
• Adjunct to adavanced cardiovascualar life support during CPR.
• Severe metabolic acidosis.
• Less urgent metabolic acidosis
• Urine alkalinization
• Antacid
• Hyperkalemia

Contraindications of I.V. Sodium bicarbonate are:

• 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 Sodium bicarbonate are:

• To relieve heart burn or sour stomach
• Alkalinization of urine

Contraindications of oral Sodium bicarbonate are:

• 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

Efficacy of sodium bicarbonate in the treatment of metabolic acidosis is discussed in the following studies-

"Sodium bicarbonate administration usually, although not always, corrects the acidosis, rising serum bicarbonate concentration, serum pH, and the partial pressure of carbon dioxide, but evidence for clinical benefit derived from this effect is not conclusive. Therapy of such situations should be focused on the cause of the acidosis. Recent studies have suggested that metabolic acidosis might contribute to worsening kidney disease and sodium bicarbonate supplementation has been proposed as a renoprotective strategy. However, limitations of these studies prevent reaching definite conclusions and further investigations are required in order to ensure the validity of this therapeutic approach."

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4227445/#:~:text=Sodium%20bicarbonate%20infusion%20reduces%20plasma,level%20in%20serum%20%5B96%5D.

Three recent studies on 150 patients with metabolic acidemia (pH ≤ 7.35) and increased lactate concentrations (serum lactate > 2.45 or 5 mmol/L) failed to prove sodium bicarbonate offered a limited benefit on mortality and hemodynamic variables.

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6538112/

Factors which could have led to her current condition are-

1. Diabetes mellitus
2. Hypertension
3. Anemia
4. Malnutrition

The pathophysiology by which the first 3 led to Acute Kidney injury has been well described in detail in the text above.

Pathophysiology behind Malnutrition causing AKI in this case is-

In addition to this, the presence of metabolic acidosis in this patient could have led to increased metabolism thereby aggravating her nutritional status.

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6019478/

 For the evaluation of malnutrition in patients with CRF, certain tools have been developed such as-

1) Subjective Global Assay (SGA):

• It is easy to use and consists of only three discrete severity levels but closely correlated with more subjective measures. 
• SGA is a reproducible and useful method for assessing the nutritional status of MHD patients.
• It is inexpensive, can be performed rapidly, requires only brief training and gives a global score of protein energy nutritional status.
• Disadvantages of this method include the fact that visceral protein levels are not included in the assessment; it is focused on nutrient intake and body composition.

"SGA-DMS is a reliable method of assessing nutritional status in hemodialysis patients and useful in recommending nutritional support in these patients. However more comparative and longitudinal studies are needed to confirm the validity of this nutrition scoring system in Indian population."

"There are other several methods of nutritional state evaluation available ranging from anthropometric measurements to more elaborate techniques such as DEXA, Bio Impedance Assay but the reliability of these methods in detecting protein-calorie malnutrition and their practicability as not been proven. Moreover, more elaborate methods are costly and time–consuming, which restricts their use to a few research centers."

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3224408/ 

We have also been given the following case to understand the differences with respect to diagnosis,therapy and outcomes in both these patients with similar findings. The entire real patient clinical problem in the 2nd case is given in the link as follows-

https://bhavyayammanuru.blogspot.com/2020/09/aki-secondary-to-uti.html?m=1

Comparing the two cases which have been assigned to us, the striking differences between them which I have come across are as follows:-

1) After comparing the history in both of these cases, I think that the 2nd case is mainly due to a post-renal cause whereas the 1st case was due to a renal cause. the findings which helped me in reaching to such a conclusion are-

• Dribbling of urine
• Burning micturition
• Fever with cough

So my anatomical diagnosis in this case : Post-renal Acute Kidney Injury

Etiology behind this:

• Urinary Tract Infection
• Neurogenic bladder (Past history of Spine surgery 3 year back)
• Benign Prostatic Hyperplasia (BPH)
• Reflux nephropathy

2) From the ultrasound of both the kidneys in both the cases, there appears to be an asymmetry in the size of kidneys in the 2nd case. The left kidney in this case appears to be a little shrunken.

Causes for unilaterally shrunken kidney are:

• Renal artery stenosis
• Congenital hypoplasia
• Reflux nephropathy
• Obstructive uropathy

These causes can be confirmed with the help of following investigations such as-

• Duplex ultrasonography- B mode and Doppler
• Intravenous Urography
• CT scan
• Computed Tomography Angiography (CTA)
• Magnetic Resonance Angiography
• Renal Scintigraphy
• Micturitating Cystography

Management of this patient: Depends upon the cause

• If it is Reflux nephropathy: Surgery (Ureteral Reimplantation) is needed.
• For her UTI, she is already receiving antibiotics (PIPTAZ)

 

References:

https://www.glowm.com/resources/glowm/cd/pages/drugs/s014.html#:~:text=Orally%20administered%20sodium%20bicarbonate%20is,edematous%20or%20sodium%2Dretaining%20conditions.

https://www.mayoclinic.org/drugs-supplements/sodium-bicarbonate-oral-route-intravenous-route-subcutaneous-route/proper-use/drg-20065950

https://www.kidney-international.org/article/S0085-2538(15)59093-5/pdf

https://en.wikipedia.org/wiki/Cardiorenal_syndrome#:~:text=Cardiorenal%20syndrome%20(CRS)%20is%20an,chronic%20dysfunction%20of%20the%20other%E2%80%9D.

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3169795/

Active learning points from conversation:

[05/09/20, 7:42:15 PM] MBBS 2016 UG: Good evening sir, I was going through the case which you have given us for biweekly assessment.

[05/09/20, 7:42:30 PM] MBBS 2016 UG: Does she have pleural effusion?

[05/09/20, 7:49:29 PM] Post residency PG 1: Possible but will need to be confirmed on Usg. Have they mentioned that report?

[05/09/20, 8:08:55 PM] MBBS 2016 UG: No sir, there is no report of the ultrasound.

[05/09/20, 8:09:17 PM] MBBS 2016 UG: Sir, I have another doubt too.

[05/09/20, 8:10:01 PM] Post residency PG 1: Ask Alekya about the missing data. She will upload them.

[05/09/20, 8:10:07 PM] Post residency PG 1: Please share

[05/09/20, 8:10:08 PM] MBBS 2016 UG: She still has very severe metabolic acidosis, even after dialysis.

[05/09/20, 8:10:14 PM] MBBS 2016 UG: why is it like that?

[05/09/20, 8:10:25 PM] MBBS 2016 UG: Okay sir, I will ask ma'am.

[05/09/20, 8:11:46 PM] Post residency PG 1: Will need to be sure that the ABGs are Post dialysis but yes it may take many more sessions to get the stranded H+ ions out

[05/09/20, 8:12:33 PM] MBBS 2016 UG: Okay sir.

[05/09/20, 8:13:44 PM] MBBS 2016 UG: Yes sir, atleast there is more than a 2 fold increase in the bicarbonate level following dialysis.

[05/09/20, 8:24:10 PM] Post residency PG 1: And still the ph didn't normalize?

[05/09/20, 8:41:45 PM] MBBS 2016 UG: The ph has normalized now sir

[05/09/20, 8:41:55 PM] MBBS 2016 UG: but the bicarbonate is still less

[05/09/20, 8:43:44 PM] MBBS 2016 UG: As for the question you asked in the group sir, the child has Eissenmenghar syndrome right sir?

[05/09/20, 8:45:05 PM] Post residency PG 1: What's the current bicarbonate level?

[05/09/20, 8:45:51 PM] Post residency PG 1: Can you share more history about this medical student named Eissenmengers? How did he discover it?

Also what is the primary problem in the child that led to the syndrome?

[05/09/20, 8:46:34 PM] MBBS 2016 UG: Current bicarbonate level is 15.5 mmol/L sir.

[05/09/20, 8:46:40 PM] MBBS 2016 UG: Yes sir I would.

[05/09/20, 8:47:48 PM] Post residency PG 1: 👍

[05/09/20, 8:54:20 PM] MBBS 2016 UG: "The first clinical description originates from the Viennese physician Victor Eisenmengar(29. Jan. 1864 - 11. Dec. 1932). In 1897 he reported on a 32-year-old man with cyanosis and dyspnea since infancy. This patient had a reasonably active life until 3 years before his death, when dyspnea increased and right heart failure began. He succumbed suddenly after massive hemoptysis. Autopsy revealed a nonrestrictive membranous malalignment ventricular septal defect (VSD), marked right ventricular hypertrophy, an overriding aorta, and atheromatosis of the major pulmonary arteries."

[05/09/20, 8:54:22 PM] MBBS 2016 UG:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3083816/

[05/09/20, 8:55:13 PM] MBBS 2016 UG: In her case, it is because of the VSD which led to left-to-right shunt sir.

[05/09/20, 8:55:36 PM] Post residency PG 1: 👍👏👏

[05/09/20, 8:57:55 PM] MBBS 2016 UG: Thank you sir.

[06/09/20, 11:11:19 AM] MBBS 2016 UG: Good morning sir. In the 45 year old female with anasarca, I was a little confused with the ECG findings.

[06/09/20, 11:12:07 AM] MBBS 2016 UG: There is abnormal progression of R wave, so could it possibly be that she developed a silent MI before?

[06/09/20, 11:12:38 AM] MBBS 2016 UG: This is the ECG

[06/09/20, 11:18:04 AM] MBBS 2016 UG: And also the ECG post dialysis looks normal. Could it be due to hypokalemia?

[06/09/20, 11:47:53 AM] MBBS 2016 UG: And sir I have another doubt too. Is it the heart failure which led her to develop AKI or is it vice-versa?

[06/09/20, 1:59:46 PM] Post residency PG 1: What is abnormal about the progression of this R wave?

[06/09/20, 2:00:48 PM] Post residency PG 1: Please share both the EcGs side by side so that we may compare

[06/09/20, 2:01:53 PM] Post residency PG 1: How would heart failure cause AKI? What are her urinary findings that go against pre renal causes and suggest glomerular injury?

[06/09/20, 3:04:33 PM] MBBS 2016 UG: The QRS complex in V4 has a small r wave and a deep S wave sir.

[06/09/20, 3:05:54 PM] MBBS 2016 UG: The first being BUN:Serum creatinine ratio is less than 20:1 sir. That suggests it’s more likely to be Diabetes causing the glomerular injury.

[06/09/20, 3:06:05 PM] MBBS 2016 UG: Hypertension too sir. This is the ECG post dialysis.

[06/09/20, 3:10:44 PM] MBBS 2016 UG: Cardiorenal syndrome sir? Low cardiac output in heart failure patients can result in decreased blood flow to the kidneys which can lead to progressive deterioration of kidney function. As a result, diuresis of these patients will result in hypovolemia and pre-renal azotemia.

[06/09/20, 5:21:33 PM] Post residency PG 1: Sir... In the case... Is the renal failure primarily due to uncontrolled hypertension?

[06/09/20, 5:21:34 PM] Post residency PG 1: Or is it a complication of diabetes sir?

[06/09/20, 5:21:35 PM] Post residency PG 1: Like diabetic nephropathy sir

[06/09/20, 5:21:35 PM] Post residency PG 1: Or is it correct to consider hypertension being a sequelae of renal failure sir

[06/09/20, 5:21:37 PM] Post residency PG 1: Yes the chicken and egg conundrum that plagues most such scenarios. 👍

We expect her renal issues to be multifactorial. Her current glomerular injury manifested in nephrotic proteinuria is surely due to both diabetes and hypertension but what precipitated her current acute renal failure is still grey. Possibly she may have taken pain killers that could have precipited reduced renal perfusion

[06/09/20, 5:25:08 PM] Post residency PG 1: Does this patient demonstrate low cardiac output in terms of her LV ejection fraction?

[06/09/20, 5:27:01 PM] Post residency PG 1: Can this change be due to the lead placement where the leads may not have been placed properly. What you see as V4 in the previous EcG may have been V3 taken twice?

[06/09/20, 5:55:13 PM] MBBS 2016 UG: No sir she has HFpEF.

[06/09/20, 5:55:41 PM] MBBS 2016 UG: Okay sir.

[06/09/20, 5:56:29 PM] MBBS 2016 UG: Yes sir that’s possible. Then her ECG findings are normal right.!

[06/09/20, 5:58:06 PM] Post residency PG 1 : 👍

[05/09/20, 8:12:07 PM] MBBS 2016 UG: I just wanted to ask if there is any ultrasound report of the patient?

[05/09/20, 8:19:40 PM] MBBS 2015 intern: No

[05/09/20, 8:19:49 PM] MBBS 2015 intern: We only did renal Doppler

[05/09/20, 8:19:54 PM] MBBS 2015 intern: But everything's normal

[05/09/20, 8:20:54 PM] MBBS 2016 UG: Okay ma’am. But did she have pleural effusion?

[05/09/20, 8:23:42 PM] MBBS 2015 intern: No

[05/09/20, 8:31:22 PM] MBBS 2016 UG: Okay. Thank you ma'am.

[05/09/20, 8:32:33 PM] MBBS 2016 UG: And ma'am you mentioned in your blog that she had facial puffiness, was it associated with Periorbital edema?

[05/09/20, 8:32:46 PM] MBBS 2015 intern: Yeah

[05/09/20, 8:33:11 PM] MBBS 2016 UG: Thank you ma'am😀

[05/09/20, 9:14:06 PM] MBBS 2016 UG: Ma'am did she have shifting dullness too because of the abdominal distension?

[05/09/20, 9:24:20 PM] MBBS 2015 intern: No

[05/09/20, 9:24:29 PM] MBBS 2015 intern: It's not like ascitis

[05/09/20, 9:24:39 PM] MBBS 2015 intern: Only distension

[05/09/20, 9:29:31 PM] MBBS 2016 UG: Accha okay maam. Thank you.

[06/09/20, 7:14:40 PM] MBBS 2016 UG: Ma'am I wanted to ask how many units of blood did she receive?

[06/09/20, 7:15:08 PM] MBBS 2015 intern: Only 1 till now

[06/09/20, 7:15:15 PM] MBBS 2015 intern: 450ml

[06/09/20, 7:16:23 PM] MBBS 2016 UG :okay ma'am

[06/09/20, 7:16:27 PM] MBBS 2016 UG: Thank you

[06/09/20, 7:16:32 PM] MBBS 2016 UG:  :)