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kidney The HEART of icu
1.
2. KIDNEY
The HEART of ICU
Dr Nirmal Jaiswal MD(med)
ICU director and Chief Intensivist
Wockhardt multispeciality and
Suretech Hospital
Nagpur India
3. DEFINATION of Acute Renal Failure
BOB2017
Abrupt
Decrease in
kidney function
Retention of Urea
and nitro waste
Dysregulation of
ECV and
electrolyte
ARF
AKI : Reflecting the recognition of
MINOR CHANGES in the markers of
renal function to the requirement of
Renal Replacement Therapy
4. BOB2017
• ARF has been reported to affect from 1% to 25%
of ICU patients
• Mortality rates :15–60%
• Epidemiological evidence supports the notion that even
mild / reversible AKI has important clinical consequences,
including increased risk of death
16. BOB2017
Markers of
glom function :
Creatinine
Cystatin C
Hepcidine
Markers of Repair
and Inflm :
Calprotectin
IL-18,HGL
Encephalin
Markers of
tubular and
damage and
repair :
AAP,ALP
Alpha-GST
Hepcidine
KIM 1,
Micro RNA
a1/beta2 -
microglob,
NGAL
NAG
NECTIN1
RBP
TIM2
Markers of AKI
17. Question
• Which is the best indicator for AKI ?
A. Creatinine
B. Urine output
C.Signs and symptoms
D.Newer biomarkers
18. BOB2017
Clinical History
Exam
Clinical Test
LAB Value
AKI STAGING
AKI
OBSTRUCTION
?
CO
CONTINUE TO MONITOR
IF HIGH RISK
OBSTRUCTION
RENAL VASO -
CONSTRICTION
HYPOVOL
KIDNEY
PERFUSION
USG
NO
NO
YES
YES
21. Evaluation
• History
• Physical examination
• Biochemical parameters
• To distinguish between PRE RENAL and RENAL AKI
• Importance of Urine-R and Renal biopsy
23. Volume-Responsive and
Volume-Unresponsive AKI
• Volume-responsive AKI describes a functional
impairment that can be improved by fluid
administration
• Many patients with volume-responsive AKI and
overall lesser severity of illness may be managed in
a standard clinical setting
• Optimal method to determine a patient’s fluid-
responsiveness remains a matter of debate
Clin J Am Soc Nephrol 3: 962–967, 20
24. IMPORTANT TIPS
• Volume resuscitation can correct prerenal conditions
resulting from absolute or relative hypovolemia
• Renal hypoperfusion resulting from low cardiac output
(e.g., end-stage congestive heart failure) and reduced renal
perfusion pressure (e.g., sepsis, or liver failure) cannot
always be corrected by fluid administration
25. In non-critically
ill patients
without cardiac
disease, there is
proportionately
less risk
associated with
initial vigorous
volume therapy
At the extreme
end of the
spectrum is the
patient with AKI
and multiorgan
dysfunction
syndrome,
including acute
lung injury
27. First because hypotension results in
decreased renal perfusion and, if
severe or sustained, may result in
kidney injury
Second, the injured kidney loses
autoregulation of blood flow
Careful titration of fluids and
vasoactive medications
28. Which fluid
• In the absence of hemorrhagic shock- isotonic
crystalloids or iso-osmotic fluid rather than colloids
(albumin or starches) as initial management
• Saline vs. Albumin Fluid Evaluation (SAFE) study- safe
but no more efffective
• Almost two-fold increased risk of AKI with HES
compared to crystalloids
• Use vasopressors in conjunction with fluids in patients
with vasomotor shock
29. PROTOCOLIZED HEMODYNAMIC
MANAGEMENT
• Based upon achieving specific physiologic end-points
within 6 hours of hospital admission has been termed
Early Goal-Directed Therapy (EGDT)
• Protocolized strategy, consisting of fluids, vasoactive
medication, and blood transfusions targeting
physiological parameters
30. • The physiologic goals are:
i) return of mean arterial blood pressure to >65mm Hg
ii) central venous pressure between 8–12mm Hg
iii) improvement in blood lactate levels
iv) central venous oxygen saturation (ScvO2) 70%
v) a urine output of >0.5 ml/kg/h
33. General supportive management
• Insulin therapy targeting plasma glucose 110–149 mg/dl
• NUTRITIONAL ASPECTS
– A total energy intake of 20–30 kcal/kg/d
– No restriction of protein intake
– 0.8–1.0 g/kg/d of protein in noncatabolic AKI patients without
need for dialysis
– 1.0–1.5 g/kg/d in patients with AKI on RRT
– Up to a maximum of 1.7 g/kg/d in patients on continuous renal
replacement therapy (CRRT) and in hypercatabolic patients
– Providing nutrition preferentially via the enteral route
34. Diuretics in AKI
• Recommend not to use diuretics to prevent AKI
except in the management of volume overload
• No Mannitol
35. NO Vasodilator therapy
• Dopamine
• Fenoldopam, - pure dopamine type-1 receptor agonist
• Natriuretic peptides- Atrial natriuretic peptide, Urodilatin,
Nesiritide (brain natriuretic peptide)
• No trials support or shown any benefit
36. Growth factor intervention
• Recommend not using recombinant human (rh)IGF-1 to
prevent or treat AKI
• Erythropoietin
• Adenosine receptor antagonists- Theophylline
37. Timing of renal replacement therapy
in AKI
• When life-threatening changes in fluid, electrolyte, and acid-
base balance exist
• Consider the broader clinical context, the presence of
conditions that can be modified with RRT, and trends of
laboratory tests
• Other factors that might influence the decision of when to start
RRT are
– the severity of the underlying disease (affecting the
likelihood of recovery of kidney function),
– the degree of dysfunction in other organs (affecting the
tolerance to e.g., fluid overload),
– the prevalent or expected solute burden (e.g., in tumor
lysis syndrome), and
– the need for fluid input related to nutrition or drug therapy
38. • Indications for dialysis (RRT ) in patients :
– Volume OVERLOAD that cannot be managed with
diuretics
– Refractory Hyperkalemia
– Refractory severe acid-base Disturbances
– Severe azotemia (BUN >80-100)
– Uremia
39. Points to be remember for
prevention of AKI
• The evaluation and initial management of patients with
acute kidney injury (AKI) should include:
– an assessment of the contributing causes of the
kidney injury,
– an assessment of the clinical course including
comorbidities,
– a careful assessment of volume status, and
– the institution of appropriate therapeutic measures
designed to reverse or prevent worsening of
functional or structural kidney abnormalities
Clin J Am Soc Nephrol 3: 962–967, 2
40. Future
• Agents designed to increase large vessel kidney blood
flow
• Improve kidney microvascular blood flow, attenuate
inflammation
• Limit renal tubular epithelial cell injury, necrosis and
apoptosis
• Enhance renal tubular epithelial cell recovery after acute
injury
• Cell therapies using renal progenitor cells and/or
mesenchymal stem cells to promote recovery or replace
damaged renal tubular epithelia
41. Points to Remebered
• Immediate management of Hypovolemia or offending
cause
• Try to improve Cardiac function
• Management to carried out under Hemodynamic
monitoring
• Find out the cause of AKI
• DO NOT USE DIURETICS IN Rx OF AKI
• STOP ACE AND ARB’S before giving contrast
• ONLY the Adequate volume can prevent the CI-AKI and
the other agents and avoi hemodialysis unless staging
warrents
• Adjust the doses of medication as per Creat cl
• Avoid Aminoglycosides
BOB2017
