LRA peri-operatória Flashcards

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1
Q

Peri-operative acute kidney injury is common, accounting for 30–40% of all in-hospital cases of acute kidney injury.
It is associated with clinically significant morbidity and mortality

A

accumulation of waste products, electrolytes, and fluid, but also less obvious effects, including reduced immunity and dysfunction of non-renal organs

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2
Q
KDIGO definition and classification of AKI
Stage 1
Increased sCr × 1.5–1.9 that is known or
presumed to have occurred within the
preceding 7 days or sCr increase ≥0.3 mg
dl−1 within 48 h
or
urine output <0.5 ml kg−1 h−1 for 6–12 h
A

Stage 2
Increased sCr × 2–2.9
or
urine output <0.5 ml kg−1 h−1 for ≥12 h

Stage 3
Increased sCr × 3
or sCr ≥4 mg dl−1
or initiation of RRT
or GFR decrease to <35 ml min−1 (1.73 m)−2
in patients <18 yr old
or
urine output <0.3 ml kg−1 h−1 for ≥24 h or
anuria for ≥12 h
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3
Q

Limitações

  • Administration of drugs which interfere with tubular secretion of creatinine (i.e. cimetidine, trimethoprim)
  • Reduced production of creatinine (i.e. muscle wasting, liver disease, sepsis)
  • Ingestion of substances which lead to increased generation of creatinine independent of renal function (i.e. creatin, cooked meat)
  • Obesity
A
  • Conditions associated with physiologically increased GFR (i.e. pregnancy)
  • Interference with analytical measurement of creatinine
    (i. e. 5-fluorocytosine, cefoxitin, bilirubin)
  • Fluid resuscitation and overload
  • Progressive CKD with gradual rise in serum creatinine
  • Extrinsic creatinine administration as a buffer in medications (i.e. in dexamethasone, azasetron)
  • Oliguria due to acute temporary release of ADH post-operatively, nausea, pain) enhanced by maximal sodium reabsorption in the setting of volume/salt depletion
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4
Q

Etiologia LRA PRÉ RENAL
Redução do volume intravascular efectivo
-Hipovolémia( Hemorragia, Perda de volume:GI, pele,
respiratório) 3º espaço

A

-Insuficiência Cardíaca
-Vasodilatação sistémica (Sépsis, Cirrose, Anafilaxia
Anestesia)

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5
Q
Alteração da autorregulação renal
-Vasoconstrição pré-glomerular
(arteríola aferente)
Hipercalcémia
Síndrome hepato-renal
Fármacos: AINE’s, CsA, adrenalina
A

-Vasoconstrição pós glomerular
(arteríola eferente)
IECA
ARA II

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6
Q

LRA RENAL

  • Oclusão das artérias renais
  • Oclusão das veias renais

-Glomérulos
Glomerulonefrite aguda
GNRP

A

-Vasos
SHU/PTT
HTA maligna
Ateroembolismo

-Túbulos
NTA isquémica
NTA tóxica

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7
Q

-Interstício
Nefrite intersticial aguda

-Obstrução intratubular
Mieloma múltiplo
Cristais

A
Etiologias peri-operatórias 
PRE RENAL
Preoperative
-Hypovolaemia (Gastrointestinal loses, Haemorrhage,Third spacing)
-Sepsis
-cardiac failure
-Increased intra-abdominal pressure
-Cirrhosis, hepatorenal syndrome
-Drugs-non-steroidal anti-inflammatory drugs, angiotensin-converting enzyme
inhibitors, norepinephrine, diuretics.
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8
Q

Intraoperative
-Hypovolaemia(Insensible loses, Haemorrhage, Over diuresis)
-Hypotension due to low systemic vascular
resistance (anaesthesia induced)
- Low cardiac output (heart failure,
anaesthesia and Cadiopulmonarbypass induced)
- Increased intra-abdominal pressure
- Aortic cross-clamp
-Drugs-non-steroidal anti-inflammatory drugs, angiotensin-converting enzyme
inhibitors, norepinephrine, diuretics

A

RENAL Perioperative

  • Inflammation
  • Patient co-morbidities-chronic kidney disease, diabetes mellitus, obesity, atherosclerosis.
  • Drug-induced-Antibiotics, aspirin, phenytoin, furosemide, non-steroidal antinflammatory drugs, clopidogrel, tacrolimus
  • Radio-contrast agents
  • Endogenous nephrotoxins-haemoglobin and myoglobin
  • Acidosis
  • Infection
  • CPB
  • Anaemia
  • Packed red blood cell administration
  • Fluid solutions (hydroxyethyl starch, chloride-rich solutions)
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9
Q
POS RENAL
Preoperative 
-Tumour 
-Prostatic enlargement
-Calculi
-Blood clots
-Neurogenic bladder
A

Intraoperative

-Surgical intervention or damage

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10
Q

Management

Preoperative: Identify patients at risk:

Patient related factors- co-morbidities (obesity, CKD, DM, cardiovascularand hepatobilliary diseases, male sex, obesity, pulmonary disease, steroid use, cancer, ASA score, ICU patients, increased intraabdominal pressure, sepsis, older age and neonates)

Procedure related factors
a.Major surgery (extensive laparotomy
lung resections, transplantations)
b. Emergency surgery
c. Cardiac surgery
d. Use of contrast dye
A

Anemia - Correct anaemia before to surgery when possible according to the patient blood management protocol.

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11
Q

Intraoperative:
Choice of fluid solution
a. Avoid HES solutions when possible.
b. Balanced crystalloid solutions may prove superior to chloride rich solutions in preventing AKI.

A

Fluid management

a. The use of intraoperative urinary output as a guide to fluid administration may not be beneficial.
b. Avoid the use of diuretics unless a need to treat volume overload arises.
c. Use measures during surgery to avoid blood loss and unnecessary PRBC transfusion.

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12
Q

Haemodynamic goals

a. Avoid a low MAP even for relatively short periods of time.
b. Evidence so far do not recommend the use of one vasopressor over the other
c. Low dose dopamine is no longer considered “renoprotective” and is not recommended.

A

General considerations
Avoid the use of aminoglycosides unless no suitable less
nephrotoxic alternative exists.

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13
Q

Haemodynamic goals
The main haemodynamic goal in the perioperative patient is to prevent tissue hypoperfusion and thus organ hypoxia.
indirect measures, such as MAP, heart rate variabil
ity,and lactate concentrations
In the ICU setting, MAP >60–65 mm Hg (>75 mm Hg in patients with chronic hypertension) is recommended to prevent AKI.
The risk of AKI was increased when MAP was <60 mm Hg for >20 min or <55 mm Hg
for >10 min.56

A

Urine output in anaesthetized patients may not
be an adequate indicator of fluid balance and is not predictiveof postoperative AKI in elective surgeries (non-vascular, noncardiac, and non-transplant).

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14
Q

Respiratory
A pragmatic approach in high-risk surgical patients would beto adopt low tidal volume ventilation settings of 5–7ml.kg using optimal PEEP settings as determined
by oxygenation and compliance, together with the
avoidance of hypoxia and hypercarbia

A

volatile anaesthetics are known to activate several
pathways involved in production of cytoprotective and
anti-inflammatory signalling molecules, which may
reduce renal ischaemia–reperfusion injury seen in sur
gical procedures such as organ transplant, cardiac and
vascular surgery

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15
Q
hyperglycaemia may increase the risk of postoperative
AKI 
• Minimise fasting
• Avoid hyperglycaemia /
blood-sugar variability with
close monitoring
• Consider appropriate
intravenous insulin infusions
A

Muscle injury leading to AKI through rhabdomyolysis
classically results from trauma such as following crush
injury, but may also complicate prolonged immobilisation
or compartment syndrome

The breakdown of striated muscle ultimately progressing to myocyte necrosis causes AKI
in approaching 50% of patients with rhabdomyolysis
through renal vasoconstriction, intraluminal cast formationand direct cytotoxicity, induced by haem protein

Lengthy procedures (> 4 h) and high BMI,
together with hypotensive anaesthesia, are significant
risk factors, and tourniquet use has also been associated with rhabdomyolysis.
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