23 year old female with fever 🤒

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23 year old female completed degree and is taking police training since 1year, came with c/o fever since 5days

Patient was apparently asymptomatic 5days back, c/o fever since 5days, rise of temperature in the afternoon and night time. Rise of temperature associated with chills and rigors followed by profuse sweating and fall of temperature,associated with generalised body pains. 

Outside report 4days back showed smear for MP positive and she was put on T. Monocef and T. PCM. 4 days back she had 2episodes of vomiting, food as content and 2episodes of vomiting 2days back food as content.

C/o 1episode of black coloured stool 3days back

No h/o rashes, cold, cough, SOB,loose stools

H/o dengue 1year back for which she was admitted and managed medically

H/o chicken pox 5months back, did not use any medications, subsided in 9days spontaneously

Not a k/c/o DM, HTN, CAD, CVA, TB, asthma, epilepsy

Menstrual history: 5/35,normal flow, no clots, dysmenorrhoea,LMP:9/9/20

O/E:pt c/c

Pallor+  , icterus -ve , clubbing -ve , cyanosis -ve , koilonychia -ve , bilateral sub mandibular non tender lymph nodes palpable , no edema

Temp:101.5 - 99.5F. 

PR:120/min,BP:100/80mmhg,RR:22cycles/min

SpO2:97% on RA

GRBS:101mg/dl

Cvs:S1 s2+, no murmurs

RS:BAE+, NVBS

P/A:soft, non tender, no organomegaly

CNS:no FND

Fever under evaluation (? Clinical malaria) 

Anemia under evaluation 

Hypoalbuminemia 

Hb:7.9gm/dl

TLC:6,000cells/cumm 

plt:1.8lak/cumm

MCV:65.3 fl

MCH:22.3 pg

MCHC:34.2%

 PCV:1.8 vol%

Microcytic,hypochromic with anisopoikilocytosis tear drop cells and pencil forms present

Outside report USG abdomen:right Renal caliculi(2.3,2.8mm without HUN) 

RFT

Urea:27mg/dl

Creat:0.9mg/dl

Uric acid:3.0mg/dl

Ca+:9.9 mg/dl

Po4-:1.9 mg/dl

Na:134 meq/l

K:4.4 meq/l

Cl:101 meq/l

MP:strip negative 

Smear negative

LFT:

TB 1.2mg/dl

DB 0.34mg/dl

Sgot 119 IU/L

Sgpt 139 IU/L

Alp 224 IU / L

Alb 2.7 gm/dl

Dengue

NS1:negative

IgG:negative

IgM:negative

CUE alb 1+,pus cells:3-4,rbc:3-4

Day 1:-

OE pt c/c

Temp:104F at 10 30 am(T. PCM 650mg given, ice packs, tepid sponging done) 

BP 110/70mmhg

PR:102/min

Spo2:94%on RA

Cvs:s1 s2+

Rs:BAE+, NVBS

P/A soft, non tender

CNS :no FND

Rectic count:2.1%

Corrected retic count :1%

RPI:0.5

S/o hypoproliferative anemia

Serum iron:50mcg/dl

Serum ferritin - 203.7ng/dl

CBP today:

Hb 7.5 gm/dl

TLC 5,600 cells /cumm

Plt 1.5L/cumm

X ray :-

Urine culture

Day 2:-

COMPLAINTS OF FEVER SPIKES,DRY COUGH,AND SHORTNESS OF BREATH AND DID NOT PASS STOOLS SINCE YESTERDAY.

TEMP 104F.

O/e - inspection normal

         Palpation Normal

         Percussion - dull notes present in 

                                 Right                        Left

                          Infrascapular area.      Infrascapular area

                          Infra auxiliary area

                                                          Rt >lt

       Auscultation - 

                                                        Right                           Left

Vocal fremitus  decreased in   rt infrascapular area.     Lt suprascapular area

Whispering pectoriloquy in rt infrascapular area.       Lt suprascapular area

Bronchophony                       in lt suprascapular area

SHE WAS GIVEN 

    TAB PCM 650MG,

    INJNEOMOL 100IV,

    INJ CEFTRIAXONE 1GM /IV BD, and

    FIRST DOSE OF INJ FALCIGO 120MG/IV STAT WAS        GIVEN.

IN VIEW OF FALL INSATURATION OF 88% ON ROOM AIR, SHE WAS PUT ON 4-6 LITRES OXYGEN.IV FLUIDSWERE GIVEN.

Day 3:- 

COMPLAINTS OF FEVER SPIKES, COUGH AND SHORTNESS OF BREATH.

O/e - inspection normal

         Palpation Normal

         Percussion - dull notes present in 

                                 Right.                          Left

                          Infrascapular area. Infrascapular area

                          Infra auxiliary area

                                              Rt >lt

       Auscultation - 

                                                        Right                        Left

Vocal fremitus decreased in rt infrascapular area. Lt suprascapular area

Whispering pectoriloquy in rt infrascapular area. Lt suprascapular area

Bronchophony in lt suprascapular area

ABG

PH   - 7.46 

PCO2   - 26.6 mmhg

 PO2  - 67.4  mmhg

HCO3   - 18.7 mmol/l

 St.HCO320.9  mmol/l

BEB-4.0 mmol/l

 BEecf-4.5 mmol/l

TCO2  - 39.2

 O2 Sat   - 86.1%

 O2 Count - 10.4

TEMP -100F.

X ray :

DECREASED BREATH SOUNDS IN RIGHT ISA,IAA AND LEFT ISA.

 INJ NEOMAL GIVEN.

INJCEFTRIAXONE 1GM/IV AND

TAB ZINCOVIT OD AND 

TAB LIMCEE WAS GIVEN.

SECOND DOSE OF INJ FALCIGO 120MG/IV STAT GIVEN.

His peripheral smear

Target cells , pencil cells , teardrop cells were seen

End posting exam

 1)Anatomical diagnosis -? Glomerulosclerosis Etiological diagnosis - ?? Nephrotic syndrome secondary to the diabetic nephropathy or CKD.   

  2)Reasons for I) Azotemia : impaired renal excretion of urea and creatinine secondary to CKD.

 II) Anemia : decreased erythropoietin. 

III) Hypoalbunemia: capillary basement membrane and podocytes damage.

 IV) acidosis: acidification of urine is lost.                                      

3) Rationale : syp potchlor was given because of the hypokalemia.. Inj. NaHCO3 was given because of metabolic acidosis ..Insulin and antihypertensives are given because known case of DM and HTN. Orofer XT was given because of anemia.. Inj. Lasix was given to decrease her volume overload. Spironolactone was given it was a potassium sparing diuretic.Calcium was given to the patient because of hypocalcemia secondary to CKD. Indications of NaHCO3:metabolic acidosis in cardiac arrest, Tricyclic antidepressants, aspirin and phenobarbitone overdoses, Hyperkalemia, Crush injuries, C/I in certain conditions because of adverse reactions like Hypernatremia, metabolic alkalosis, cellulitis, seizures, Tetany, sodium retention, peripheral edema.             

4) indication of dialysis in this pt: worsening of SOB secondary to metabolic acidosis with Anuria not resolved with high ceiling diuretics...Crucial factor: pt became symptomatic on 3rd day....          

5) Causes of same condition : primary : Minimal change disease, Focal segmental glomerulosclerosis, Membranous nephropathy. Secondary : DM, SLE, HIV , Viral hepatitis, malaria, amyloidosis, Sarcoidosis, Drugs : Nsaids, gold, pencillamine Cancer: Hodgkin's and non Hodgkin's, solid tumours of GIT, RCC and lung.

6)expected outcomes of ckd patients depend upon age,genes,associated co morbidities This patients condition may deteriorate due to pleural effusion

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5261605/

                               

7)association of ckd with hrpef

Activation of raas system

Anemia 

Hypercalcemia 

Hyperphosphatemia

Uremic toxins .these critically discuss the potentail contribution to coronary dysfunction, left ventricular stiffening and delayed left ventricular relaxation

8)mean Hemoglobin levels,before and after study,in rhuepo group we’re 8.85+ or - 1.01g/do and 9.90+ or - 0.29 g/dl,respectively(p less than 0.001) and in control group were,9.00+ or -g/dl and 7.81 + or - g/dl,respectively

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4293514/

9)Anaemia contributes to the impairment of health-related quality of life (HRQoL) in patients with CKD [7]. Its impact on patients’ HRQoL burden is exacerbated by reduced physical capacity and energy levels among these patients.

10)Malnutrition is an important complication in CRI patients and ESRD patients on dialysis. SGA is a reliable method of assessing nutritional status. Most important is the fact that it can detect the changing trend of nutritional status, which may be missed by one-time anthropometry and biochemical methods.

11)this 58M had history of fever with cought and elevated tlc with indiacates renal acute kidney injury.As well there is no albuminuria,no edema

In 45M had had pedal edema ,facial piffiness,abdominal distention,anuria with clearly indicates nephrotic nephritic syndrome.and investigations showed that there is microalbuminuria,micro haematuria.Therapy in is patient  

Etilogy of renal failure in 58M could be fever associated with cough which might have increased leucocyte count and caused renal aki

48 year old man with diabetes since 15 years and pedal edema since four months

This is an online E log book to discuss our patient's de-identified health data shared after taking his/her/guardian's signed informed consent. 

Here we discuss our individual patient's problems through series of inputs from available global online community of experts with an aim to solve those patient's clinical problems with collective current best evidence based inputs. 

This E log book also reflects my patient-centered online learning portfolio and your valuable inputs on the comment box is welcome.

49year old male patient

K/c/o CKD on MHD since 4months

K/c/o type 2DM since 15years

K/c/o HTN since 1year

Driver by occupation.

Patient was apparently asymptomatic 1year back when he developed on and off fever and hematuria for which he was admitted in our hospital and was managed medically  (no records available with the patient), after that he was on medication and later he discontinued medication for one month .

4months ago he started developing bilateral pedal edema which was insidious onset, gradually progressed upto knees, associated with h/o dyspnoea grade 3,No h/o decreased urine output.patient was taken to ****** hospital where he was diagnosed with CKD and the serum creatinine was 21. He was put on dialysis there. 14sessions of dialysis in 2months.Due to covid pandemic it became difficult for them to go to that hospital and was admitted here.

At admission..... 

O/E

Pt conscious coherent 

Cvs :s1s2+

Rs:BAE+, crepts + in B/L IAA, ISA

P/A soft, NT

CNS :no FND

BGT -- AB +Ve

                                    09/08/2020

                                        USG

01/09/2020

04/09/2020

                                       ECG

He underwent 10sessions of dialysis in july and 10 sessions of dialysis in august, 1 dialysis this month (September)

In between he developed flash pulmonary edema which was managed medically by inj lasix and inj NTG

                           X ray of pulmonary edema

2 Inj of EPO and 1inj  of iron given 

2pint PRBC transfusion were done

28 year old man with Shortness of breath

This is an online E log book to discuss our patient's de-identified health data shared after taking his/her/guardian's signed informed consent. 

Here we discuss our individual patient's problems through series of inputs from available global online community of experts with an aim to solve those patient's clinical problems with collective current best evidence based inputs. 

This E log book also reflects my patient-centered online learning portfolio and your valuable inputs on the comment box is welcome.

Here is a case i have seen

28 year old man, hypertensive since 6 months, non diabetic, non alcoholic, non smoker, unmarried, constructor worker from Nalgonda who was apparently alright, busy working daily at construction sites one day an year back developed high grade fever along with body pains for which he was taken to a RMP and he was given ' tablets for fever ' as the attendant describes it, which got subsided temporarily.  By night he again developed fever for which he was taken to Nalgonda Hospital and was admitted for a few days and was discharged. 

Since then he was on regular NSAID use for fever and body pains.

After 4 months he again developed fever and he was taken to NIMS where they performed a Renal biopsy and told them his kidneys got affected because of overuse of painkillers. 

Biopsy report

2 months later he developed Dyspnea at rest, reduced urine output, non productive cough, he developed even pedal edema which slowly crawled up to his abdomen cause its distension along with facial puffiness. Upon examination they were told that he had hypertension and was started on antihypertensives and that he needed hemodialysis. 

During his stay in the hospital a pleural tap was done and his sputum cultures were sent too. They were negative for tuberculosis. 

On examination, pallor is present

flat nails are present

Jvp raised

PR - 92 bpm, regular

Bp - 150/8

Afebrile 

chest wall retraction are present with a respiratory rate of 20 cpm

Abdomen is distended and umbilicus is everted

Inspiratory crackles present in Bilateral iAA, ISA

Apex beat present in 6th intercostal space

ECG shows

sinus tachycardia and Left ventricular hypertrophy

During his hospital stay, his blood pressure has always been on the higher end and he has been going into Pulmonary edema on and off for which he been put on the following medications :

7am - T Nicardia 20mg

Arkamine 0.1mg

Met XL 50mg

Lasix 80mg

Spironolactone 25mg 

At 1:30 - 2pmish 

T Arkamine 0.1mg

Nicardia 20mg

6pm

T Lasix 80mg

8pm

T Arkamine 0.1mg

Met XL 50

Lasix 80mg

Spironolactone 25mg

Nicardia 20mg

He has also been started on emperical ATT even though his sputum turned out to be negative because of the long standing history of fever, cough and around 10 kgs of weight loss in 7 months. 

After initiating ATT, his blood pressure couldn't be under control. 

On reviewing this literature as suggested by one of my senior PGs,a decision was made to put Rifampicin on hold

Link to the article : 

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5015508/

24 patients enrolled had controlled hypertension (BP ≤140/90 mmHg) with stable anti-HT drug requirement for ≥4 weeks before recruitment. All patients were receiving regular thrice-weekly MHD. Patients were excluded if they were receiving concomitant drugs which could influence CYP450 metabolism; had a current history of smoking or alcohol abuse; were inadequately dialyzed; had fluid overload, or were poorly compliant to treatment. 

A Single-center, prospective observational cohort study conducted at a tertiary care hospital in India between September 2012 and December 2013.

Serum levels of amlodipine besylate, metoprolol succinate, and prazosin hydrochloride were measured using high-performance liquid chromatography (HPLC) technique. Blood samples for estimation were drawn at baseline (day 0) and days 3, 7, 10, and 14 days after starting rifampicin. 

All 24 patients in the study had worsening of hypertension after rifampicin and 83.3% required increase in drugs to maintain BP <140/90 mmHg. Serial amlodipine levels were estimated in 16 patients; metoprolol and prazosin in four patients each. Drug levels declined by >50% in all patients and became undetectable in 50-75%. Drug requirement increased from 4.5 ± 3.6 to 8.5 ± 6.4 units (P < 0.0001). Mean time to first increase in dose was 6.5 ± 3.6 days. Eleven (46%) patients experienced a hypertensive crisis at 9.1 ± 3.8 days. Three of them had a hypertensive emergency with acute pulmonary edema. In two patients, rifampicin had to be discontinued to achieve BP control. In conclusion, rifampicin caused a significant decrease in blood levels of commonly used anti hypertensives. This decrease in levels correlated well with worsening of hypertension. 

Rifampicin, a first-line antitubercular drug, exhibits pharmacokinetic interactions with numerous drugs. It is a potent inducer of cytochrome P450 (CYP)