INTERNAL ASSESSMENT ( PRACTICAL)
CASE REPORT :
60 Years Old Male Who is a Resident of Iskilla(Village) ; Ramannapet ( Mandal ); Yadadri ( District) Who Works in Nursery Came with chief Complaints of
Both Lower Limb swelling Since 7 day
Decreased Urine Output Since 3 days
Shortness Of Breath Since 3 Days
Fever since 3 days
Unable to walk since 3 days
HISTORY OF PRESENT ILLNESS :
Patient Was apparently Asymptomatic 2 years Back , then he developed pain in both Knee joints insidious in onset, non - progressive since 2 Years ,he managed to do his Job who works in Government Nursery since 4 years which is near by his house & goes to Job by walk & he is able to do his routine works but since 1 year due to increased intensity of pain he Used to take pain killer Injection ( IM) once in Week / 10days and also used oral NSAIDS . He use to feel comfortable for 2 to 3 days after injection and then again he will have pain with activity , not associated with early morning stiffness.
He was fine till 1 week back , he noticed swelling of both lower limbs , Intially started in both Foot & progressed upto bilateral knees .
At home he had he had 1 episode of vomiting on last saturday which was non bilious , non - projectile ,containing food particles associated with mild abdominal discomfort and nausea.
Breathlessness since 3 days , insidious onset , non progressive of grade 1 to 2 according to mmrc associated with rapid and shallow breathing ,not associated with chest pain, sweating, giddiness , blackout,orthopnea or PND
Decreased urine output since 3 days
Knee pain Increased Since last 3 days & so he had difficulty in walking & unable to go to Work
Fever since 3 days which is high grade, Intermittent , associated with chills & rigor , Not associated with cough or burning micturation
No history of narrow stream of urine, hesistency , suprapubic pain
PAST HISTORY:
N/K/C/O DM ; HTN ; TB ; Epilepsy; Asthma
No H/o any Past Surgeries
Personal History:
Marriage at the age of 20 years
He Had 2 daughter's & 2 son's each of them studied Upto 3rd & 4th Class & stopped education due to financial problems. All of them were married and he had grand sons and daughters
He wake up at 5 am in the morning , do his morning activities like going to washroom and brushing , gets ready for his job and eats Rice with the curry cooked along with it some tea in the morning. Goes to his job by walk , at his workplace : he waters the plants and remove the weed plants and other works told by his superiors,will have a chutta ( atleast 2-3/ day ) at afternoon again he eats rice with curry and he returns home by 4pm . He will take a nap and at night again he will have some rice and curry
No fruits are included in his diet
Since 1 year he stopped talking non veg also as someone told him that knee pains aggrevates on taking non vegetarian
Decreased appetite since 1 year
Decreased urine output since 3 days
Sleep : Normal
No bowel disturbances
No high risk behaviour
Addictions :
Alcoholic Since 20 years of Age & Drinks 90-180ml Once in Every 7-10days stopped since 1 year ( As someone told him that alcohol will aggrevates knee pains )
Smoker Since 20 years of Age - Smokes 2-3 Beedis Per Day
Family history :
He was born 2nd in the family to non consangeous parents , 1 elder brother , 1 younger brother and 3 younger sisters
Elder brother diagnosed with renal failure 5 years back and was on dialysis since 5 years ( causes and indication for dialysis were not known as patient attenders doesnot have good terms with them and they doesn't shown any interest to know the reason for his renal failure though i insist for it . All others are normal .
Timeline Events :
Worked as farmer since age of 13 years , used to go to farm daily , sits on his knees ( in squatting position) for removal of weeds daily from 9am to 5pm
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Got married at age of 20
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Had 2 son's and 2 daughter's , educated them only upto 3rd class and they stopped due to financial crises. |
Since age of 20 he started drinking alcohol and smoking ( but stopped taking alcohol since 2 years ).
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Since 4 years working in Nursery |
Since 2 years he had bilateral knee pains
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Increased in pain intensity since 1 year started taking Pain killers
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Decreased appetite since 1 year
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Since 7 days he had pedal odema ,since 3 days breathlessness, decreased urine output , unable to walk due to Severe pain in bilateral knees
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Admitted in our hospital 3 days back
GENERAL EXAMINATION :
Patient was conscious, coherent and co-operative
In Supine Position
Pulse - 94 bpm, regular, normal volume, condition of vessel wall - normal, no radio-radial or radio-femoral delay. All peripheral pulses were normal.
Blood Pressure - 160/90 mmHg - RIGHT ARM , supine posture .
Temperature - 99 F
Respiratory Rate - 28 cycles per minute , shallow and deep breathing + ,abdomino thorasic type
Spo2: 98% on Room Air
GRBS : 169 mg/dl
Pallor - present
Pedal odema present upto bilateral knees ( pitting type )
No icterus ,clubbing ,cyanosis , lymphadenopathy , facial puffiness
JVP - Not elevated
Picture below showing pitting type of pedal odema :
GENERAL CONDITION - Moderately built and Moderately nourished
HAIR - Greying of Hari +
EYES - Palpebral conjuctiva pallor +,Cataract + ( In both eyes ),No conjunctival chemosis or injection, No redness or corneal lesions. No icterus.
SKIN - hyper-pigmented skin associated with mild odema over right side of neck over 2cms clavicle, sternum secondary to central line insertion. no local rise of temperature ,No skin lesions at other sites of the body .
ORAL CAVITY - No ulcers currently
FINGERS AND NAILS - No clubbing or cyanosis ,
GENERAL HEAD NECK AND ENT EXAMINATION - No abnormalities. No lymph node enlargement.
AXIAL - No apparent spinal deformities
LOCAL EXAMINATION OF BOTH KNEES :
RIGHT LEFT
1) Skin : Normal Normal
2) Swelling : Present on Medical aspect of both knees
3) Tenderness: Present on lateral aspect of both knees
4) Crepitus : Absent on both sides
5) Restriction of Movement : Present on both sides
6) Distal pulses : Present on both sides
PROVISIONAL DIAGNOSIS:
Pedal odema, Breathlessness secondary to ? Heart failure, ? Acute Renal failure secondary to sepsis or NSAID abuse or post renal cause on CKD
Less likely of liver failure , No abdominal distension
Anaemia secondary to renal failure or Nutritional or Iron deficiency secondary to NSAID use
Bilateral knee pains secondary to ? osteoporosis
? Synovitis
SYSTEMIC EXAMINATION:
As Patient is tachypnic , with history of pedal odema and breathlessness , i initially would like to ruleout the cardiovascular cause ( Heart failure )
Cardiovascular System :
Inspection :
JVP : Normal
No visible Apex beat
No scars , sinus, dialted veins
Palpation :
Apex beat : 5 th Intercoastal space 1cm medical to midclavicular line
No parasternal haeve , No palpable heart sounds
Percussion : Normal
Ascultation : S1,S2 + , No murmurs
RESPIRATORY SYSTEM:
UPPER RESPIRATORY TRACT:
No Halitosis, oral hygiene, oral thrush, postnasal drip, pharyngeal deposits, tonsils, dental caries, deviated nasal septum with turbinate hypertrophy, nasal polyps, sinus tenderness
LOWER RESPIRATORY TRACT:
INSPECTION:
Chest : Barrel shape
Trachea – midline
Apical Impulse - Not visible
Movement with respiration equal on both sides
No Drooping of shoulders, supraclavicular or infraclavicular hallowing ,no intercostal fullness/indrawing/retractions
No Sinuses, scars, dilated veins, nodules
PALPATION:
Trachea – midline
Chest movement : Equal on both sides
Measurement of Chest :
AP : 24 cms
Transverse : 29 cms
Ratio : 0.8
Vocal Fremitus : Equal on both sides
PERCUSSION : Normal
AUSCULTATION: bilateral infraaxillary and infrascapular fine crepts +
Normal Vesicular Breath sounds
Per abdomen :
Abdomen is scapoid
Soft, No terderness , No organomegaly or free fluid
Bowel sounds present
Central Nervous system: Normal
No neck stiffness
Brudzinski : Negative
Kernig's : Couldn't be ellicted properly as patient is having severe knee pains
HMF : Normal
Memory : Intact
Speech : Normal
Motor :
TONE : Normal
POWER upper limb lower limb
Right 5/5 4+/5
Left 5/5 4+/5
REFLEXES :
Biceps Triceps Supinator Knee Ankle
R : 1+ 1+ 1+ 1+ 1+
L : 1+ 1+ 1+ 1+ 1+
Plantar : withdrawal on both sides
Sensory and Cerebellum : Normal
Gait video :
https://youtube.com/shorts/AfX-y5E8kfQ?feature=share
INVESTIGATIONS :
COMPLETE BLOOD PICTURE :-
Hb:- 9.5 gm/dl
TLC:- 15,600 (19/4)-----> 13,800 (On admission)
Neutrophils :- 78%
Lymphocytes :- 11%
Monocytes :- 9%
Eosinophils:- 2%
PCV:-28.9%
MCV:- 84.3 fl
MCH:- 27.7 pg
MCHC:- 32.9 %
RBC:- 3.43 million/cumm
PLATELETS:- 1.20 lakhs /cu mm
Peripheral smear : Normocytic Normochromic anaemia , Leucocytosis with Mild thrombocytopenia
Retic count : 0.5
Absolute Reticulocyte count : 0.3
Reticulocyte Index : 0.23 ( Hypoproliferative Marrow )
Serum Iron : 69
COMPLETE URINE EXAMINATION:-
Pus cells- 3-4
Epithelial cells :- 2-3
Albumin :- 2+
Sugars :- Nil
No RBC , No casts
RBS : 169 mg/dl
Hba 1C : 6.7
Urine protein/ Creatinine ratio:-
Spot urine protein:-5.45
Spot urine creatinine : 18.9
Ratio:- 0.28
RFT :- (19/4)-------------------> On admission
Urea:- 225 mg/dl
Creatinine:- 8.4 mg/dl -----> 9.7 mg/dl
Uric acid :- 9.9 mg/dl
Calcium:- 7.4 mg/dl
Corrected calcium :7.88 [ total ca + 0.8 ( 4 - Serum albumin )
Phosphorus :- 3.1 mg/dl
Sodium:- 138 mEq/L
Potassium:- 3.4 mEq/L
Chloride :- 103 mEq/L
Urinary Electrolytes
Sodium : 169 mmol/L
Pottasium : 5.98 mmol/L
Chloride : 147 mmol/L
LFT:-
Total Bilirubin :- 0.52 mg/dl
Direct Bilirubin:- 0.16 mg/dl
AST:- 11 IU/L
ALT:- 13 IU/L
Alkaline phosphatase:- 742 IU/L
Total proteins :- 5.5 gm/dl
Albumin :- 3.4 gm/dl
A/G ratio:- 1.64
ESR : 50 mm /1 st hour
Serology :- NEGATIVE
ABG :(on admission)
PH : 7.11
PCO2 : 12.6
PaO2 : 83.4
HCO3 : 3.9
Spo2 : 95.2
Anion gap :26.6
ABG at presentation : High anion gap metabolic acidosis with fully compensated respiratory alkalosis
ECG :
showing Normal sinus rythm
Heart Rate of 83 beats per minute
Normal Axis
PR interval : 0.16 sec
QTc : 513 msec ( Prolonged secondary to ? hypocalcaemia )
LVH +
Chest xray :
Chest xray PA view
Hyperinflatted lungs + ( Increased spaced between the ribs )
ULTRASOUND :
Impression :-
1) Bilateral Raised echogenicity of kidneys
Size : Right : 9.5*4.5 , Left : 8.6 *3.9
CMD +, PCS : Normal
2) Grade 1 prostatomegaly ( size : 33 cms )
2D ECHO:
Impression:-
EF:- 55%
Concentric LVH , Dialted LV
RVSP:- 35 mmhg
Sclerotic AV , Mild AR
TRIVIAL TR+/ MR+
NO RWMA , NO AS/MS
Good LV Systolic Functions
Diastolic Dysfunction +
NO PAH/PE
Xray bilateral knees AP and Lateral view :
L- S spine AP and Lateral
Final Diagnosis:
1. AKI ( ? Renal , Creatinine clearance:6ml/min )secondary to NSAID use or metabolic syndrome with Metabolic acidosis On CKD ( Stage 5, egfr :6ml/min/1.73 m2 ,On haemodialysis )
2. Anemia secondary to ? Iron deficiency ? renal failure
3. Heart failure secondary to congestion ( Renal failure, Anaemia, Metabolic syndrome )
4. Denovo Hypertension and Diabetes ( Hba 1c :6.
7 )
5. Bilateral knee pains secondary to ? Osteoarthritis ? hypocalcaemia ( osteopenia ) due to secondary hyperparathyroidism secondary to CKD ( Evidence of CKD : Anaemia, Hypertension, Diabetes or bilateral knee pains secondary to ?synovitis
6. NSAID abuse since 1 year
7. Grade 1 Prostatomegaly
Treatment Plan :
Control of hypertension and sugar control
Metabolic acidosis and Azotemia
Treatment Given : ( at time of admission )
1)Inj furosemide 40 mg iv/stat
2) Tab Nifedipine 10 mg po/stat
Due to Severe Metabolic acidosis and Azotemia patient has been taken for dialysis within 8 hours of admission
Pre dialysis vitals : Afebrile
PR : 98 bpm
BP :170/90 mm of hg
1st session : Duration :2hours
UF : 1 litre
UF rate : 400ml
Pre dialysis weight :
Post dialysis weight :
Weight loss after 1 st session : 1 kg
Post dialysis vitals :
Pt : c/c/c , Afebrile
PR : 98 bpm
Bp: 160/90 mm of hg
No interdialytic complications like hypotension, hypoglycemia, muscle cramps
ABG :( Post dialysis)
PH : 7.38
PCO2 : 20.3
PaO2 : 87.9
HC03 : 11.8
Serum Cr : 7.2 mg/dl
Serum Urea : 155 mg/dl
BP Monitoring 4 th hrly
Time
5 pm : 160/90 mm of hg ( Tab Nifedipine 10 mg stat given )
9pm : 140 / 80 mm of hg
1am : 150 /80 mm of hg
8am : 140/70 mm of hg
GRBS monitoring 6 th hrly
5pm : 169 mg/dl
8am : 113 mg/dl
2nd Dialysis taken on D4 of admission for 4 hours
Day 5 :
S : Breathlessness decreased from admission
Pedal odema subsided
No fever spikes
O: Patient is conscious coherent and cooperative
pallor - present
No odema, No icterus ,clubbing,cyanosis,lymphadenopathy ,
Vitals :
BP- 140/80 mmhg
PR -94 bpm
RR- 20 cpm
Spo2- 98% on RA
GRBS - 118 mg/dl
Temperature- 99.3 F
I/O Charting:- 1050/900 ml
Cvs: s1,s2 heard ,no Murmurs,jvp not raised
Rs: BAE, No crepts
P/A: soft, non tender ,bowel sounds present
CNS: Normal
A: 1. AKI ( ? Renal ) secondary to NSAID use or metabolic syndrome with Metabolic acidosis On CKD ( On haemodialysis )
2. Anemia secondary to ? Iron deficiency ? renal failure
3.Heart failure secondary to congestion ( Renal failure, Anaemia, Metabolic syndrome
4. Denovo Hypertension and Diabetes ( Hba 1c :6.
7 )
5. Bilateral knee pains secondary to ? Osteoarthritis ? hypocalcaemia ( osteopenia ) due to secondary hyperparathyroidism secondary to CKD ( Evidence of CKD : Anaemia, Hypertension, Diabetes or bilateral knee pains secondary to ?synovitis
6. NSAID use since 1 year
7. Grade 1 Prostatomegaly
P:
-IV FLUIDS URINE OUTPUT+ 30ml/hr
-INJ. LASIX 40 MG IV/ SOS
- TAB. Ultracet 1/2 PO/QID
-TAB. NICARDIA 10 MG PO/TID
- Syrup Potklor 15 ml in glass of water PO/TID
-STRICT I/O CHARTING
- GRBS 6 th hrly
Current reports :
PH : 7.35
PCO2 : 30
PaO2 : 88
HCO3 : 18
Spo2 : 95
Cr :4.8
, urea 101
Na : 138 ,K :2.6 ,cl: 101
Patient received 4 sessions of dialysis and got discharged on D7 of admission , his breathlessness subsided, appetite improved , able to walk ( pain in knees had decreased in intensity)
No pedal odema, fever, breathlessness at time of discharge
Metabolic acidosis resolved at time of discharge ( PH:7.38, PCO2 38, PaO2:88, HCO3 : 20, spo2 :94)
Patient has been asked for follow up after 1 week or so ( if he experience breathlessness, pedal odema, anuria, vomitings, decreased sensorium or any other complaints as early as possible to casualty)
Discussion :
METABOLIC SYNDROME :
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Leads to Insulin resistance ( Important MetS-related etiological factor for CKD)
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Insulin resistance, which is typical of type 2 diabetes, leads to inflammation, oxidative stress and renal insufficiency.
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Raised insulin levels stimulate insulin-like growth factor 1 (IGF-1) production, which increases connective tissue growth factor, thus causing fibrosis in the diabetic state.
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Obesity may lead to increased secretion by adipose tissue of pro-inflammatory cytokines such as leptin, interleukin-6, and tumor necrosis factor-alpha (TNF-α).
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Leptin may lead to increased intra-renal expression of transforming growth factor-beta (TGF-β), leading to glomerulosclerosis.
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It may also promote type IV collagen production. TNF-α may lead to the production of reactive oxygen species (ROS) that can in turn lead to renal endothelial cell dysfunction, mesangial expansion and fibrosis.
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Anti-inflammatory hormones like adiponectin may be reduced, contributing to insulin resistance as well.
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Adiponectin deficiency is associated with vascular intima thickening and smooth muscle cell proliferation.
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Its vascular effects may even be independent of insulin sensitivity, and so may extend to CKD. Obesity also leads to increased glomerular volume, podocyte hypertrophy, and mesangial matrix expansion preceding CKD.
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Triglycerides and free fatty acids may themselves be nephrotoxic by promoting pro-inflammatory cytokine production.
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In association with hypertension, another MetS component, angiotensin II stimulates ROS production, in turn decreasing nitric oxide synthase production and causing renal microvascular injury, ischemia, and tubulointerstitial damage.
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Dissecting out the relative contribution of insulin resistance, obesity, and hypertension to these findings versus the composite of MetS however is difficult.
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In this regard, the presence of early arterial hyalinosis which is more typical of diabetes but not MetS, may point towards MetS being a distinct risk factor for CKD independent of its individual components.
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One more somewhat provocative hypothesis is that hyperuricemia, not a “traditional” MetS component but associated with MetS, is a promoter of CKD through the inhibition of nitric oxide production or even recurrent nephrolithiasis .
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Another limitation to be pointed is that most mechanistic explanations have been derived from animal models, and so their importance in human patients with MetS and CKD, with their different lifespans and disease profiles remains to be demonstrated.
Approach to Renal failure :
Pathophysiology of NSAIDS induced renal failure:
https://www.ejinme.com/article/S0953-6205%2822%2900172-8/pdf
ABG :
The actual bicarbonate is what one should use when one is assessing the degree of compensation in acid-base disorders using the Boston bedside blood gas rules. Because using the standard bicarbonate value to estimate the effectiveness of compensation can lead one to inaccurate conclusions.
Approach to hypocalcemia:
https://www.researchgate.net/figure/Clinical-approach-to-investigation-of-causes-of-hypocalcemia-CKD-chronic-kidney_fig3_297583173Further Approach to this patient :
After few sessions of dialysis , would like to wait for 1 week ( after his initial symptoms like breathlessness secondary to metabolic acidosis has subsided ) whether he can improve , and further decison of dialysis is made by his clinical condition ,renal parameters
Efficacy of Denosumab in mineral and bone disorder secondary to renal failure
Prior to initiating denosumab, it is important to assess for and optimize CKD–mineral and bone disorders (CKD-MBD). In observational studies and small RCTs, denosumab has been shown to improve bone mineral density and reduce bone turnover in CKD, but there have been no studies focused upon its fracture efficacy
https://link.springer.com/article/10.1007/s11657-021-00971-0
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