AN INTERESTING CASE

OF ACUTE KIDNEY
INJURY
Presented by-
Dr. Moni Sankar Bhattacharjee
Postgraduate trainee
R.G.Kar Medical College and Hospital
 PART-1
CASE SCENEARIO
 PRESENTATION AT EMERGENCY…

 A 58-year old female presented with altered sensorium and

breathlessness at emergency
- for last 18-24 hour
- without any history of Trauma
- without any history of vomiting or diarrhea

 she had history of fever for last 5 days along with

decreased urine output for last 2 days as per her family
members.
 CHECKING VITALS…
 On rapid assessment patient had-
 Altered sensorium
 Glasgow coma scale score – E2 V3
M4(9/15)
 Pulse- 96/min, low-volume
 BP- 90/64 mm Hg
 Capillary blood Glucose- 226 mg/dl
 Temperature- 100.5oF
 Respiratory Rate- 22/min
 Saturation- 98% with nasal prongs
 EMERGENCY INVESTIGATIONS…

 ECG- No significant changes noted.

 NCCT Brain- No significant changes noted.
 Arterial Blood Gas Analysis-
 pH- 7.00 (7.35-7.45)

 pO2- 92 mmHg (75-100 mmHg)

 pCO2- 29 mmHg ( 35-45 mmHg)
 Bicarbonate- 7 mmol/L (22-26 mmol/L)
 Lactate- 12 mmol/L (0.5-2.5 mmol/L)
 Sodium- 132 mmol/L (135-145 mmol/L)
 Potassium- 5.4 mmol/L (3.5-5 mmol/L)
 CONTD.

 Foleys catherization done at emergency and around 30 ml

urine collected in bag.
 There is absence of ketone bodies in urinary dipstick

 She had cold, clammy extremities with signs of poor

hydration without any features of volume overload.
 CONTD.

 EMERGENCY LABORATORY EVALUTION-

 Hemoglobin- 10.7 gm%
 Total leucocyte count- 18,200 cells/microliter
 Differential count- N88% L07% E3%
 Platelet- 175,000/microliter
 Urea- 230 mg/dl
 Creatinine- 6.2 mg/dl
 IMPRESSION

SEPTIC SHOCK WITH ACUTE KIDNEY

INJURY(AKI)
 What is the Definition of AKI (Manisankar) and What are the Stages of AKI -Manishankar

 how does AKI differ from AKD or acute on CKD (sakuja)

 What the risk factors of AkI or what are the causes of AKI (Purbasha with One Slide )

 How kidney Maintains homeostasis ( Himadri with one Slide)

 How AKI affects Homeostasis ( Manali)

 PART-2
DETAILED HISTORY AND
EXAMINATIONS
 SALIENT POINTS FROM HISTORY-

 COMPLAINTS:(Before Admission in Hospital)

 Fever for last 5 days
 Lower abdominal pain for last 3 days
 Decreased urine output for last 2 days
 CONTD.
 HISTORY OF PRESENT ILLNESS:
 Patient complained of fever for last 5 days before
admission
 High-grade, intermittent fever
 Associated with chills, anorexia and generalized malaise
 Temperature subsided with sweating
 Not associated with vomiting or diarrhoea
 Not associated with headache, chest pain, arthralgia or
skin rash
 CONTD.
 HISTORY OF PRESENT ILLNESS:
 Also complained with lower abdominal pain aggravated on
passing urine
 Pricking in nature, also radiating to flank
 Associated with urgency and dysuria
 But not associated with haematuria

 And for last 2 days patient also noticed decreased urine

output but not associated with facial puffiness or pedal
oedema.
 CONTD.

 PAST HISTORY:
 Patient is known Diabetic , non-hypertensive
 On regular oral hypoglycemic medications
 No other co-morbidities
 Had no history of underlying kidney disease.
 DETAILED EXAMINATION:

 GENERAL EXAMINATION:
 Higher function status- Altered level of
consciousness( Glasgow coma scale-E2V3M4)
 Built- Average
 Nutrition- Not adequate
 Weight- 62kgs
 Clinically no pallor or cyanosis or icterus
 Clinically no Pedal edema or facial puffiness
 Costovertebral tenderness present
 No Lymphadenopathy
 CONTD.

 SYSTEMIC EXAMINATION:
 Respiratory System- Bi-lateral vesicular breath sound
present
 Cardio-Vascular System- Both S1 and S2 present.
 Gastro-intestinal System- No organomegaly found
 Neurological System- normal
 PART-3
INVESTIGATIONS AND
MANAGEMENT
 INITIAL MANAGEMENT
 Patient was shifted to medicine ward and fluid challenge with
crystalloid solutions( 0.9% Normal saline) done over 1 hour.
Simultaneously-

 Oxygen support was given

 Initial empirical Anti-biotics support was given
 Correction of electrolytes.
 Urine output was monitored
 Marinating intake-output chart
 Monitoring vitals
 Monitoring volume status
 Particularly look for any features of volume overload
 RENAL FUNCTION TESTS REPEATED…

AFTER 12 HOUR AFTER 24 HOUR

UREA (mg/dl) 236 270

CREATININE (mg/dl) 6.4 6.8

SODIUM (mmol/l) 130 128

POTASSIUM (mmol/l) 5.8 6.2

 Serum creatinine and GFR are related?(Mahesh)

 How you will differentiate between functional impairment vs Structural injury.

(sakuja)

 How to differentiate between Prerenal azotemia vs Intrinsic AKI .(Mahesh)

 What are the fallacies of Functional Biomarkers and What are the implications
of structural Biomarkers (Sakuja)

 Among the novel biomarkers, which signifies progression of AKI to CKD (Sakuja)

 Role of biopsy in AKI (Mahesh)

 OTHER INVESTIGATIONS…
 URINE ANALYSIS:
 Routine microscopical examination:
o Protein- 2(+)
o RBCs- 1-2/HPF
o Pus cells- 10-12/HPF
o Granular casts were found
 Urine ACR: 250 mg/g
 Urine Culture and sensitivity:
o Culture shows colony count 75,000 CFU/ml of urine sample
o Shows growth of gram negative rods
o Sensitive to meropenem, imipenem, amikacin
 OTHER INVESTIGATIONS…
 RADIOLOGICAL INVESTIGATIONS:
 ULTRASOUND-
o Right Kidney- 10 cm

o Left Kidney- 9.7 cm

o Cortical echogenicity increased

o Though corticomedullary differentiation maintained

o Swollen kidney (left>right) with focal change in echotexture

 Plain CT-Scan-
o Shows diffusely swollen kidney ( left>right)
 OTHER INVESTIGATIONS…
 BLOOD CULTURE:
 Did not reveal any growth

 Fever Profile:
 MPDA- Negative
 Peripheral smear for MP- Not found
 Dengue IgM- Negative
 Leptospira IgM- Negative
 Scrub Typhus IgM- Negative
 CRP- 6.4 mg/dl (Normal range:0.8-1.0 mg/dl)

 DCXR- does not reveal any abnormality.

 AFTER INITIAL MANAGEMENT…
 Even After adequate fluid resuscitation-
 Patient had still poor vitals ( SBP NOT IMPROVING)
 Considered for vasopressor support
 And monitoring vitals parameter closely
 Meropenem with dose modification was started

 On close Monitoring-
 No improvement in her sensorium
 Increasing trend of serum creatinine along with serum potassium
 Urine output is only 350 ml over 24 hours
 And patient showed features of volume overload
 CONSIDERATION OF DIALYSIS…
 Due to development of metabolic and uremic complication-

 Patient was planned for intermittent haemodialysis

 Though it can not started initially due to poor vitals

 After correction of haemodynamic status, haemodialysis

started and given slowly over prolonged period of time with
close monitoring of blood pressure.
 .What is the principle of Stage based Management in AKI ? Sakuja
 What is the problem of overzealous fluid resuscitation? Rafikul
 .What vasopressor is to be used and why in vasodilatory shock? Sakuja
 How to prevent contrast induced nephropathy in AKI? Sakuja
 .What are the common nephrotoxic drugs ? Manishankar
 what is the principle of dose modification? Mahesh
 Indications of RRT in AKI. manishankar
 What are the RRT Modalities preferred in AKI? Sakuja
 how to maintain nutrition in AKI ? Rafikul
 LABORATORY PARAMETERS…
AFTER 48 AFTER 72 AFTER 5 AFTER 7 AFTER 10
HOURS HOURS DAYS DAYS DAYS
TOTAL 18000 16000 12500 11500 8500
LEUKOCYTE
COUNT(cell
s/mcl)
SERUM 332 300 220 176 112
UREA(mg/dl
SERUM 7.5 7.0 6.5 5.4 5.0
CREATININE
(mg/dl)
SERUM 128 130 132 134 140
SODIUM(m
mol/l)
SERUM 6.0 5.8 5.0 4.5 4.6
POTASSIUM
(mmol/l)
 FINAL IMPRESSION

SEPTIC ACUTE TUBULAR

NECROSIS(ATN) DUE TO UROSEPSIS
 PART-4
FOLLOW-UP
(Patient on Dialysis Support)
 CLINICAL FOLLOW-UP…
 Along with improvement of laboratory parameters

 Patient also regained her consciousness gradually after 5 days

 Urine output also increased gradually

 Intermittent Haemodialysis is continued along with monitoring of all

laboratory parameters

 Along with monitor urine output, maintain intake/output chart and

maintain glycaemic control.

 3 weeks after intermittent Haemodialysis patient became clinically

stable and advised to attend Nephrology Department
Thank you
 What are the complications of AKI (Sakuja)

 . In which phase of AKI, arrthymia and uremic complications can arise?

(Sakuja)
 What is the prognosis of AKI ? Rafikul
 newer advances Regarding AKI.