Final Grand Rounds.pptx

1
Moderator: Dr. Roy Diamond Arco
Presentor: Dr. Wilfredo T. Mata Jr.
02  22  2022
ACE Dumaguete Doctors, Inc.
DEPARTMENT OF INTERNAL MEDICINE
GRAND ROUNDS

OBJECTIVES
A C E D u m a g u e t e D o c t o r s , I n c .
D E P A R T M E N T O F I N T E R N A L M E D I C I N E
1. To be able to discuss a case of AKI
2. To be able to discuss the definition & prevalence of AKI
3. To be able to discuss the most common etiologies of AKI and its respective
pathophysiology
4. To be able to discuss the clinical presentation and diagnostic approach in AKI
5. To be able to discuss the different management principles
6. To be able to elucidate the appropriate timing of RRT especially in critically ill pxs

CASE
77/F, came in due to hypogastric pain with
anorexia.
OPD labs: Mild anemia (Hgb:10), leukocytosis (WBC:
10,700) w/ neutrophilic predominance, elevated serum
crea (2.5, CrCl:19ml/min), alk phos and tot cholesterol.

CASE
Awake, alert, w/ signs of dehydration
VS: T:36.4, BP: 90/70, PR: 94, RR:20, O2sat: 97%
Abd: NABS, tympanitic, no tenderness, no mass
DRE: unremarkable
 NPO, Ceftriaxone, D5LR 1 L @ 30 gtts/min

CASE
32.2
10.9
7.88
282
N – 81
L – 12
M – 7
E -0
B - 0
BUN – 58.3 (H)
Uric Acid – 7.6 (H)
Chronic Kidney DIsease

Case
700
600
400
1,700
1,200 1,220
1,500
1,000
80
0
0
200
400
600
800
1000
1200
1400
1600
1800
HD 1 HD 2 HD 3 HD 4 HD 5 HD 6 HD 7 HD 8 HD 9 HD 10
Urine Output

Case
700
600
400
1,700
1,200 1,220
1,500
1,000
80
0
0
200
400
600
800
1000
1200
1400
1600
1800
Urine Output
HD2
 Gen liquids
 Improving anemia (Hgb 11.4) & crea (1.1)
 Hypokalemia (3.2)

Case
700
600
400
1,700
1,200 1,220
1,500
1,000
80
0
0
200
400
600
800
1000
1200
1400
1600
1800
Urine Output
HD3
 (+) abd distention
 NGT inserted

Case
700
600
400
1,700
1,200 1,220
1,500
1,000
80
0
0
200
400
600
800
1000
1200
1400
1600
1800
Urine Output
HD4
 Inc UO

Case
700
600
400
1,700
1,200 1,220
1,500
1,000
80
0
0
200
400
600
800
1000
1200
1400
1600
1800
Urine Output
HD5
 CT scan WA: malignancy, ascending colon
 Crea: 0.9
 Referred to Gastro

Case
700
600
400
1,700
1,200 1,220
1,500
1,000
80
0
0
200
400
600
800
1000
1200
1400
1600
1800
Urine Output
HD6
 S/P Colonoscopy w/ Biopsy
 Referred to GS for possible R, Hemicolectomy

700
600
400
1,700
1,200 1,220
1,500
1,000
80
0
0
200
400
600
800
1000
1200
1400
1600
1800
Urine Output
Case
HD9
 S/P Exlap w/ R Hemicolectomy (2 hrs, 300 cc blood
loss)
 Noted Hypotension intraop  fluid resu + PRBC
Transfusion X 2 + Double Inotropes (Dopa & Norepi)
 On mech vent in ICU
 ABG: metabolic acidosis (HCO3 – 8.2)  NaHCO3
50 meqs + HCO3 Drip
 (+) Hypotension, (+) Hypothermia, (+) Respiratory
distress
 ABG: Metabolic acidosis (HCO3 – 6.2)
 CBC: septic WBC count (59.01) w/ mild anemia
(Hgb: 12.3) & thrombocytopenia (Plt:94)

700
600
400
1,700
1,200 1,220
1,500
1,000
80
0
0
200
400
600
800
1000
1200
1400
1600
1800
Urine Output
Case
HD10
 Severe anemia (Hgb 7) w/ thrombocytopenia (63)
 Elevated Crea – 1.4
 ABG: Metabolic Acidosis (HCO3 -5.7)  NaHCO3
100 mg IVTT x 2 doses
 Anuria
 (+) Bradycardia  Atropine and Dobutamine drip
 Expired

FINAL DIAGNOSES
1.1. COLONIC MASS PROBABLY
MALIGNANT RIGHT ASCENDING COLON
2.2. COMPLETE BOWEL OBSTRUCTION
SECONDARY TO #1
3.3. S/P RIGHT HEMICOLECTOMY (6/25/21)
4.4. SEPSIS SECONDARY TO
INTRAABDOMINAL INFECTION
5.5. AKI SECONDARY TO #4

 AKI as defined by KDIGO
a) Increase in serum crea by  0.3 mg/dl within 48
hours; or
b) Increase in serum crea to  1.5 times baseline, within
the prior 7 days; or
c) Urine volume < 0.5 ml/kg/h for 6 hours
Definition

 AKI staging according to severity
Definition

What is the prevalence of AKI
among critically ill patients admitted
in the ICU?
a. 10%
b. 20%
c. 30%
d. 50%

What is the prevalence of AKI
among critically ill patients admitted
in the ICU?
a. 10%
b. 20%
c. 30%
d. 50%
C. 30%

 AKI complicates:
 Acute care – 5-7%
 ICU – 30%
Prevalence

 AKI complicates:
 Acute care – 5-7%
 ICU – 30%
Prevalence
Worldwide: 30-70% (5% had RRT)
Mortality: 50%

 AKI affects:
 Hospital inpatients – 7 and 18%
 Community – 20 to 200 per million
population
Prevalence

 AKI affects:
 Hospital inpatients – 7 and 18%
Prevalence
 Elderly
 Sepsis, surgery, heart or liver failure,
nephrotoxic medication

 AKI affects:
 Community – 20 to 200 per million population
Prevalence
 Younger and healthier
 Hypovolemia, heart failure,
medications, urinary tract
obstruction, malignancy

Prevalence

 Divided into three categories:
 Prerenal azotemia
 Intrinsic renal parenchymal disease
 Postrenal obstruction.
Etiologies & Pathophysiology

 Divided into three categories:
 Prerenal azotemia
 Intrinsic renal parenchymal disease
 Postrenal obstruction.
Etiologies

 PRERENAL azotemia
 Rise in crea and BUN d/t inadequate renal
plasma flow & intraglomerular
hydrostatic pressure to support normal
filtration.
 Most common form of AKI
 No parechnymal damage & rapidly
reversible
Etiologies

 INTRINSIC AKI
 Acute Tubular Necrosis
(ATN)
 Inflammation, apoptosis and
altered regional perfusion
Etiologies

 INTRINSIC AKI
 SEPSIS- associated AKI
Etiologies SEPSIS
Cytokine production Toxins
Upregulated Nitric
Oxide Synthase
Generalized Arterialized
Vasodilation
Excessive Arteriole
Vasodilation
↓ Glomerular
Hydrostatic Pressure
↓ GFR
Injury to renal
tubular cells

 INTRINSIC AKI
 ISCHEMIA- associated AKI
 Occurs in limited
renal reserve /
coexisting insults
Etiologies ISCHEMIA
Enhanced Leukocyte-
endothelial interactions
Inflammation and reduced blood flow
in S3 segment of proximal tubule
Proximal Tubule Injury
Deranged solute secretion
Enhanced Delivery of solute to MD
↓ GFR
Preglomerular Vasoconstriction
Activates Tubuloglomerular feedback

 INTRINSIC AKI
 ISCHEMIA- associated AKI
 NSAID & ACEi/ARBs
Etiologies
ACEi/ARBs
NSAIDS
Inhibits Prostaglandin
Production
Loss of vasodilatory
mechanism
↑ Afferent Resistance
↓ Glomerular capillary pressure
↓ GFR
Inhibits production
of Angiotensin II
Loss of
vasoconstriction
mechanism
↓ in Efferent Resistance

 INTRINSIC AKI
 NEPHROTOXIC- associated AKI
 Contrast Induced
• ↑ crea at 1-2 days
after exposure,
peak at 3-5 days,
resolve in 1 week
Etiologies
CI - AKI
Hypoxia d/t perturbations in renal
microcirculation and occlusion of
small vessels
Cytotoxic damage to the tubules
Transient tubule obstruction d/t precipitation

 INTRINSIC AKI
 NEPHROTOXIC- associated AKI
 Drug Induced
Etiologies Vancomycin, Aminoglycosides,
Amphotericin B, Penicillins,
Cephalosporins, Quinolones,
Sulfonamides, Rifampin
Cisplatin, Ifosfamide,
Bevacizumab, Mitomycin C,
Gemcitabine
Acyclovir, Foscarnet,
Pentamidine, Tenofovir, Cidofovir

 POST RENAL AKI
 ↑ retrograde hydrostatic
pressure
Etiologies

DIAGNOSIS
CLINICAL PRESENTATION

 Four phases of AKI
Diagnosis / Clinical Presentation
PHASES Duration Findings
ONSET Onset of
injury
a) Renal flow at 25% of normal
b) Oxygenation to the tissue at 25% of normal
c) UO at ≤ 30 ml/hr or ≤ 0.5 ml/kg/hr
d) Urine sodium excretion ≥40 mEq/L
e) Reversing the damage can be achieved during this pre renal failure
onset phase
OLIGURIC/
ANURIC
8-14 days a) Great reduction in the GFR (UO ≤ 400 cc/day)
b) ↑ in BUN and Creatinine levels
c) Electrolyte imbalances
d) Metabolic acidosis
e) Fluid overload from kidneys
DIURETIC 7-14 days a) Increase in GFR
b) UO as high as 2-4 L/day
c) Passive loss of electrolytes
d) Electrolyte depletion were also noted due to osmotic effects of high
BUN
RECOVERY Months to
a year
a) edema decreases, renal tubules begin to function adequately and
fluid and electrolyte balance are restored
b) GFR: return to 70-80% of normal

Diagnosis / Clinical Presentation
 Suggestive of CKD
Clues suggestive of CKD
Radiologic studies •Renal UTZ: small shrunken kidneys w/
cortical thinning
•Xray: Renal osteodystophy
Laboratories •Normocytic anemia
•Secondary hyperparathyroidism w/
hyperphosphatemia and hypocalcemia

Diagnosis or Clinical Presentation
Urinary Obstruction?
Renal hypoperfusion?
Drug induced AKI?

 Depends on the phase, degree of azotemia and
degree of metabolic acidosis
 Presentation consistent with AKI
Oliguria Edema Uremia
pruritus, neurological manifestations,
nausea and vomiting, diarrhea, loss of
appetite with anorexia, cardiac
arrhythmia, and insomnia.

 Laboratory findings in AKI
  BUN and creatinine
 Electrolyte imbalances (K, Na, PO4)
 Metabolic acidosis
 Reduced GFR
 Anemia
 Thrombocytopenia

 Novel BIOMARKERS
 Kidney Injury Molecule – 1 (KIM-1)
 Present shortly after ischemic/nephrotoxic
injury in urine

 Neutrophil gelatinase associated lipocalin (NGAL,
also known as lipocalin 2 or Siderocalin).
 Present after inflammation and kidney injury,
detected in the plasma and urine within 2 hrs

 Insulin-like growth factor binding protein 7
(IGFBP7) and tissue inhibitor of
metalloproteinase-2 (TIMP-2)
 predictive of higher risk of development of
moderate to severe AKI in critically ill patients.

 Cystatin C
 Early marker for CI-AKI
 increase concentration of > 10% at 24 hours
after contrast media exposure

Management
 PREVENTION
Px at risk is identified
Window of opportunity to act
Effective preventative
interventions

Management
 PREVENTION
 Risk Factors
Px Related Factors
•Older age
•Higher baseline creatinine/CKD
•Diabetes mellitus
•Heart failure
•Hypertension

Management
 PREVENTION
 Risk Factors
Situational
Risk Factors
•Presence of sepsis/SIRS
•Higher severity of disease scores
•Use of vasopressors/inotropes
•Use of “nephrotoxic” drugs
•High-risk surgery
•Emergency surgery
•Use of IABP in cardiothoracic patients
•Longer time in cardiopulmonary bypass pump in cardiothoracic patients

Management & Prevention
 Principles in the management
1. Optimization of systemic and renal hemodynamics
through volume resuscitation and judicious use of
vasopressors
2. Elimination of nephrotoxic agents
3. Initiation of renal replacement therapy when
indicated.
4. Management of electrolyte derangements

 Optimization of systemic and renal hemodynamics through volume resuscitation and
judicious use of vasopressors
 Ischemia and Sepsis induce AKI
 Replace fluids
 PRBCs – severe acute blood loss
 Isotonic crystalloid and/or colloid – less severe
hemorrhage or plasma loss (eg burns or pancreastitis)

 Crystalloids over colloids
 Less expensive but equally effective
 Hydroxyethyl starch solution (HES)– inc risk of severe
AKI in critically ill pxs d/t osmotic nephrosis

 Isotonic in severe hypovolemia
 Hypotonic (0.45 %) in less severe hypovolemia &
hypernatremic pxs

 Isotonic
 Inc risk of AKI d/t its chloride rich, non buffered
solutions  hyperchloremic metabolic acidosis,
↓ renal blood flow & renal vasocontriction

 Isotonic vs Balanced crystalloids (RL, Hartmanns, Plasma lyte)
 SPLIT trial: No difference in primary outcome (AKI /
need of Kidney Renal Therapy, mortality)

 Isotonic vs Balanced crystalloids (RL, Hartmanns, Plasma lyte)
 SMART trial: low adverse kidney events at 30 days
(MAKE30) when using balanced crystalloids; No
difference in preventing AKI

 Restriction of Fluid volumes in oliguric/anuric AKI
 strong association bet excess fluid accumulation & inc
mortality
 FACT Trial: less need of KRT in pxs w/ acute lung injury
who received conservative fluid management; no
difference in mortality rate

 Individualization
 Judicious & individualized approach to fluid
resuscitation, avoiding excessive fluid accumulation

 Diuretics
 Not advocated by KDIGO, unless known beneficial
 Risks: overly exuberant UO resulting to volume
depletion, increases neurohormonal mediators via TGF
mechanism  worsen cardiac function, unique
toxicities (ototoxicity in loop diuretics)

 Intraoperative blood pressure
 INPRESS Trial: reduction in postop organ dysfunction in
high risk pxs maintained with norepi for SBP within
10% of preop value intraoperatively & 4 hours
postoperatively

 Sepsis - associated AKI
 Treating the infection and hemodynamic support

 Elimination of nephrotoxic agents
 Avoid Renalism w/ careful assessment of risks & benefits of
these agents
 Appropriate dosing of meds
 Contrast Induced AKI
 PREHYDRATION as prevention
 Minimizing contrast volume

 Elimination of nephrotoxic agents
 Avoid Renalism w/ careful assessment of risks & benefits of these
agents
 Appropriate dosing of meds
 Contrast Induced AKI
 PRESERVE trial: no role for IV bicarb or NAC

 Initiation of renal replacement therapy when indicated.
 Timing is still controversial

 Management of electrolyte derangements
 Hyponatremia
 Restriction of water intake, minimize use of hypotonic solns
 Hypertonic saline RARELY necessary, vasopressin antagonists not
needed

 Hyperkalemia
 Restriction of dietary K+ intake
 DC of K-sparing diuretics, ACEi, ARBs, NSAIDS
 Loop diuretics
 K binding ion-exchange resin (Sodium polystyrene sulfonate)
 Insulin (10 u R) + glucose (50 cc of D50W)
 Inhaled B-agonist
 Calcium gluconate or calcium chloride (1g)

 Metabolic Acidosis
 NaHCO3 (if pH <7.2 to keep serum HCO3 > 15 mmol/L)
 Use of other bases (eg THAM)
 RRT
 Hyperphosphatemia
 Diet restriction
 Phosphate binding agents (Ca acetate, sevelamer, Al Hydroxide)

 Hypocalcemia
 Ca Carbonate / Ca gluconate
 Hypermagnesemia
 DC Mg2+ containing antacids
 Hyperuricemia
 Acute tx usually not indicated except in Tumor Lysis Syndrome
 Nutrition
 20-30 kcal/kg/day to avoid negative nitrogen balance

Outcome & Prognosis
 AKI
 Inc risk of in-hospital and long term mortality, longer length of stay,
and increased costs
 Prerenal and Postrenal – better prognosis vs Intrinsic AKI
 Kidney injuries may recover even after severe, dialysis requiring AKI
 High risk for CKD progression & ESRD (10%)

Journal Update

Journal Update
 Population and Method
 Total of 3,019 critically ill patients with severe AKI
 1,465 were in the accelerated strategy group (in
which renal replacement therapy was initiated w/in
12 hrs)
 1,462 in the standard strategy group (in which RRT
was discouraged unless conventional indications
developed or AKI persisted for > 72 hours).

Journal Update
 Outcome
 At 90 days, death occurred in 43.9% of accelerated-
strategy group and 43.7% in the standard-strategy
group
 Survivors: continued dependence on RRT in 10.4% of
the accelerated strategy group and 6.0% in the
standard-strategy group
 Adverse events: 23.0% in the accelerated-strategy
group and 16.5% in the standard-strategy group

Journal Update
 Outcome
Among critically ill patients with acute kidney injury,
an accelerated renal-replacement strategy was
not associated with a lower risk of death at 90
days than a standard strategy.

Key Concepts
 AKI
 Increasing prevalence but unrecognized yet
 Establish AKI and determine its cause then appropriately manage afterwards
 Prevention involves identifying pxs at risk
 Individualization is advised in terms of fluid resuscitation or restriction
 Crsytalloids are favored over colloids in fluid resuscitation
 Use of diuretics in the tx of AKI is not advocated
 HCO3 & NAC has no role in CI-AKI
 Accelerated renal-replacement strategy in critically ill pxs was not associated
with a lower risk of death at 90 days than a standard strategy.

87
ACE Dumaguete Doctors, Inc.
DEPARTMENT OF INTERNAL MEDICINE
THANK YOU

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Editor's Notes