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RENAL PROTECTION IN PEDIATRIC CARDIAC SURGERY. BY DR/ WASEEM Z. AZIZ LECTURER OF ANAESTHESIA AND INTENSIVE CARE AIN SHAMS UNIVERSITY MARCH 2009. QUESTIONS. 1. The risk of development of acute renal failure after cardiac surgery is highest in: a. Neonates. b. Infants. c. Children.

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Renal protection in pediatric cardiac surgery

RENAL PROTECTION IN PEDIATRIC CARDIAC SURGERY

BY

DR/ WASEEM Z. AZIZ

LECTURER OF ANAESTHESIA AND INTENSIVE CARE

AIN SHAMS UNIVERSITY

MARCH 2009


Questions

QUESTIONS

1. The risk of development of acute renal failure after cardiac surgery is highest in:

a. Neonates.

b. Infants.

c. Children.

d. Adults.


Questions1

QUESTIONS

2. Which of the following causes vasodilation of the cortical vasculature?

a. Mannitol. c. Both.

b. Furosemide. d. Neither.


Questions2

QUESTIONS

3. Clinical settings in which mannitol has definitely been shown to be effective in preventing the deterioration of renal function is:

a. During and after cardiopulmonary bypass.

b. During and after aortic cross-clamping.

c. During and after hypovolemic shock.

d. Before the administration of cisplatin.

e. None of the above.


Questions3

QUESTIONS

4. Which of the following statements is least accurate regarding acute renal failure?

a. Adults with no underlying renal disease who develop acute renal failure have a worse prognosis compared with children.

b. Following cardiac surgery, the incidence of acute renal failure is higher in children than in adults.

c. Children over the age of 2 years with acute renal failure have a much better outlook with meticulous medical care.

d. Spontaneous recovery from acute renal failure is likely to begin 1–3 weeks after onset.

e. The mortality rate for children with acute renal failure is much higher than in adults


Questions4

QUESTIONS

5. Which of the following statements is true regarding management of suspected acute renal failure?

a. In euvolemic patients, the rapid intravenous administration of mannitol should result in a urine output greater than 0.5 mL/kg within 1 hour if a prerenaletiology dominates.

b. The vasodilatory and natriuretic properties of furosemide are beneficial when administered early in the course of acute renal failure.

c. In euvolemic patients, furosemide in an incremental dose of up to 10 mg/kg may be used.

d. If there is no response to a fluid challenge, low dose dopamine could be added.

e. All of the above


Questions5

QUESTIONS

6. In a patient who has just been admitted to the pediatric intensive care unit with new onset of acute renal failure, which of the following pathophysiological changes is least likely to occur?

a. Blood urea nitrogen (BUN) and creatinine will rise at 10 and 0.5 mg/dL/day, respectively.

b. Serum HCO3 decreases by 2 mEq/L/day because of release of tissue phosphate.

c. Serum K+ increases by 0.3–0.5 mEq/L/day.

d. Hypernatremia is commonly observed.

e. Hypophosphatemia and associated hypocalcemia may develop rapidly after the onset of acute renal failure


Incidence of postoperative renal dysfunction

Incidence of postoperative renal dysfunction

  • Postop. renal failure (more in pediatrics) is associated with mortality rates of 60–90% (more in adults than pediatrics).

  • The incidence of renal impairment varies between 4 and 24% because there is no rigid definition of renal dysfunction.

  • In cardiac surgery Postoperative ARF

    sepsis

    ↑ ICU stay

    ↑ length of ↑ GI ↑ requiring

    hospital stay bleeding infection


Renal unit anatomy

RENAL UNIT ANATOMY


Renal physiology

RENAL PHYSIOLOGY

  • RBF = 20% of resting CO ↓ by

    atherosclerosis ↓ CO α- adrenergic ++

    (↓ RBF inspite of

    maintain BP)

  • Intraglomerular blood pressure =the difference between the pressures in the efferent and afferent arterioles)

  • GFR=100-200ml/min


Renal physiology1

RENAL PHYSIOLOGY

Linear ↑

  • GFR autoregulated across wide range of ABP but urine output is not. ( UOP with arterial BP.

    e.g 100mmHg 200 7 times ↑ in UOP

    ˂50mmHg stop of UOP

    due to slight rise in GFR but ↑ peritubular vascular pr.

    ↓ reabsorption of

    filterate.


Renal physiology2

RENAL PHYSIOLOGY

RBF=20% of CO ≈50 ml/min→

O2 delivery≈50ml/min/100gm tissue

Distribution is not uniform→≈90% to cortex

O2 utilization only 10% low A-V O2 content

of total body utilization difference in kidney

adequate oxygen reserve

?? Why kidney is highly sensitive to hypoperfusion??

?? Why ARF is frequent complication of hypotension?

PARADOX???


Renal protection in pediatric cardiac surgery

Due to physiological gradient of intra-renal oxygenation with the renal medulla able to function at ambient oxygen tensions of 2–3 Kpa

This low oxygen tension results from the high oxygen requirement for tubular reabsorptive activity of sodium and chloride.

Although

a high percentage of the medullary region has a blood goes to cortex far smaller blood flow

NEED

only about 18% of total about 79% of the delivered oxygen oxygen delivered to it

(heterogeneity of flow and oxygen requirement)


Mediators affect medullary blood flow

MEDIATORS AFFECT MEDULLARY BLOOD FLOW


Pharmacological control of rbf

PHARMACOLOGICAL CONTROL OF RBF

kidney is largely devoid of β2 receptors

++ α1

so CA

++ reninangiotensin system

So, ischemia→ ++ CA→ renal cortical VC

try to redistribute blood flow to the renal medulla


Renal protection in pediatric cardiac surgery

THE IMMATURE KIDNEYChildren undergoing heart surgery are more vulnerable to postoperative renal dysfunction relative to adults


The problematic definition of acute kidney injury aki

The Problematic Definition of Acute Kidney injury(AKI)

The Conceptual Definition of Acute Kidney injury (instead of ARF):

“Sudden loss of renal function resulting in the loss of the kidneys’ ability to regulate electrolyte and fluid homeostasis”


The problematic definition of acute kidney injury aki1

The Problematic Definition of Acute Kidney injury(AKI)

  • Pediatric AKI definition: a moving target

  • Infants

    • Cr in the first few weeks of life may reflect maternal values

  • Children

    • Low baseline Cr makes 0.2-0.3 changes in Cr significant

    • Varying muscle mass

  • Adolescents

    • Similar to adults


The problematic definition of acute kidney injury aki2

The Problematic Definition of Acute Kidney injury(AKI)

  • Over 30 published ARF definitions

    • All based on increased serum creatinine levels

    • Despite extensive adult hospitalized patient study over the past 50 years

  • Widely varying spectrum dependent upon study aims and hypothesis

    • Severe (ARF requiring dialysis)

    • Modest (serum creatinine increase of 0.3 mg/dl)


The problematic definition of acute kidney injury aki3

The Problematic Definition of Acute Kidney injury(AKI)

Diagnostic criteria for acute kidney injury

http://ccforum.com/content/11/2/R31

An abrupt (within 48 hours) reduction in kidney function currently defined as an absolute increase in serum creatinine of more than or equal to 0.3 mg/dl (≥ 26.4 μmol/l), a percentage increase in serum creatinine of more than or equal to 50% (1.5-fold from baseline), or a reduction in urine output (documented oliguria of less than 0.5 ml/kg per hour for more than six hours).

NB: - 2 cr levels within 48hrs.

- adequate hydration

- variation of serum creatinine with modern analyzers is relatively small and therefore increments of 0.3 mg/dl (25 μmol/l) are unlikely to be due to assay variation


Classification staging system for acute kidney injury

Classification/staging system for acute kidney injury

RIFLE MODIFIED


Rifle classification of aki

RIFLE classification of AKI

http://ccforum.com/content/11/2/R31


Modified from rifle

Modified from RIFLE

http://ccforum.com/content/11/2/R31


Difference between two classifications

Difference between two classifications


Aetiology of postoperative renal dysfunction risk factors in general

Aetiology of postoperative renal dysfunctionRisk Factors (In General)

PREOPERATIVE

ARTERIOPATHY

  • Pre-existing renal disease.

  • IDDM

  • Age ˃65ys or ˂2ys

  • Major vascular disease.

INTRAOPERATIVE

  • Hypovolemia→ neurohormonal effects

    Sympatho- aldosterone

    adrenal ADH

    Angiotensin

    glucocortcoids

    VC

    2. nephrotoxins:→intrarenal VC

    →↑ osmotic load


Renal protection in pediatric cardiac surgery

3. Renal ischemia: by concurrent use of ACEI

4.Inflammation: gut ischemia→ endotoxemia→ cytokines

5.Genetic predisposition:

certain gene deletion

→↑% of inflamm. response.

→↑ IL6, IL10→↑% of renal

dysfunction

this deletion is more with same congenital heart disease


The etiology of renal dysfunction in cardiac surgery

The etiology of renal dysfunction incardiac surgery


More risk in children

More Risk in children

  • Immature kidney

  • More dependent of reninangiotensin system for perfusion.

  • Risk factors are

    as adults +

    • Neonatal age group

    • Cyanotic heart disease

    • CPB duration

    • Low CO

    • Perioperative hypotension


In cyanotic heart disease

In cyanotic heart disease

  • Still most imp risk factor is low CO.

  • Associated pre existing renal anomalies: eg.

    • Trisomy 21 (down syn)

    • Trisomy 18 (Edward syn)

    • Trisomy 13 (Patausyn)

    • VATER association

    • 22q11 microdeletion

  • chronically→ cyanotic ht dis → chronic hypoxia

    3 stages

    ectasia of glomerullarcapillaries→benignproteinurea (early sign

    5 ys age of renal dysfunction)

    mesangial proliferation with destruction changes of capillary wall

    2nd decade

    glomerular sclerosis


  • What to do

    WHAT TO DO?

    EARLY IDENTIFICATION EARLY

    RENAL INJURY PREVENTIVE

    (MARKERS) MEASUERS


    Identification of renal injury

    IDENTIFICATION OF RENAL INJURY

    Renal function tests

    available for

    clinical use


    Identification of renal injury classic methods

    IDENTIFICATION OF RENAL INJURYClassic methods

    Serum creatinine

    Easy measurement

    Proportional to GFR in steady state (not in acute injury)

    Affected by GFR in addition to tubular secretion, generation and elimination of creatinine.

    Varies with intravascular volume muscle mass, age, and sex, and it is affected by muscle trauma, fever, liver disease, and immobilization.

    50% of the function of the kidney can be lost without an increase in sCr.

    Change with age. eg. sCr of 1.5 mg/dL corresponded to a GFR of approximately 77 mL/min in a 20 year-old black male, it corresponded to merely 36 mL/min in a 80 year-old white female.


    Renal protection in pediatric cardiac surgery

    CASE

    A 10-day-old male infant weighing 950 g was scheduled for ligation of patent ductusarteriosus (PDA).

    He was born at 29 weeks gestation and was intubatedimmediately after delivery because of respiratory distress. His condition improved over the following 4 days. However, on the fifth day of his life the respiratory distress worsened and a murmur was heard over his chest. Medical treatment for PDA was attempted unsuccessfully. His blood pressure was 60/40 mm Hg, heart rate 150 beats/minute. The laboratory data were as follows: white blood cells (WBCs), 17,000/L; hemoglobin, 11 g/dL; hematocrit, 34%; urine specific gravity, 1.005; protein 1+; sugar 1+; serum calcium 6.0 mg/dL; blood glucose 60mg/dl, S creatinine 1.6mg/dl ; and arterial blood gases: pH, 7.30; PaCO2, 45 mm Hg, PaO2, 60 mm Hg on FIO2 50%; inspiratory pressure, 30/4 cm H2O; and ventilation rate, 25 breaths/minute.


    Renal protection in pediatric cardiac surgery

    The creatinine levels of term infants at birth are 0.6 to 1.2 mg/dL, but within 1 month fall to levels of 0.1 to 0.2 mg/dL. Preterm infants have relatively high serum creatinine levels compared with term infants. They are 0.8 to 1.8 mg/dL at birth and fall to 0.2 to 0.8 mg/dL in 1 month.

    The normal BUN level is 10 to 20 mg/dL in term infants, whereas it is 16 to 28 mg/dL in preterm infants.

    In infants weighing 1,000 to 3,300 g, the normal urine-specific gravity is 1.005 to 1.010. A urine specific gravity of more than 1.020 suggests dehydration.

    Glucosuria 1+ normally presents in 13% of preterm infants who are less than 34 weeks gestational age because the preterm infant has a decreased renal tubular reabsorption for glucose. After 34 weeks of gestational age, glucosuria is usually associated with hyperglycemia.

    Albumin is normally filtered by the glomerulus and is completely reabsorbed. However, because of tubular immaturity, 16% to 21% of preterm infants have proteinuria.


    Identification of renal injury classic methods1

    IDENTIFICATION OF RENAL INJURYClassic methods

    Creatinine clearance (ClCr)= (urine Cr × urine volume)/ serum creatinine ≈ GFR

    Cockcroft-Gault formula:

    CrCl= ([140 - age] X weight)/(72 X Scr)

    (multiplied by 0.85 if female sex)

    overestimates GFR because tubular secretion of creatinine is ignored

    FENa is another measure to assess kidney function

    FEs =(Us × V) / Ps FE =the fractional excretion, s =any substance

    GFR Us =the urinary concentration of the substance

    Ps = the plasma concentration, and V =the urine flow rate.

    renal failure index (RFI) = UNa

    Ucr/PCr

    Both RFI and FENa diff. bet renal and prerenal impairment

    Also modified by diuretics


    Identification of renal injury biomarkers

    IDENTIFICATION OF RENAL INJURYBIOMARKERS

    • Are urinary kidney-specific proteins.

    • Ideally AKI would have a biomarkers like myocardial infarction (i.e. troponin-1)

    • Currently no Troponin-I like marker to identify the site or severity of injury, although various markers are being evaluated


    Identification of renal injury biomarkers1

    IDENTIFICATION OF RENAL INJURYBIOMARKERS


    Identification of renal injury biomarkers2

    IDENTIFICATION OF RENAL INJURYBIOMARKERS


    Identification of renal injury biomarkers3

    IDENTIFICATION OF RENAL INJURYBIOMARKERS

    Current status of promising acute kidney injury (AKI) biomarkers in various clinical situations


    Identification of renal injury biomarkers4

    IDENTIFICATION OF RENAL INJURYBIOMARKERS

    Example :

    Cystatin C

    • Cysteineproteinase inhibitor.

    • Not depend on muscle mass, sex, and age

    • Not affected by inflammation, fever, and extrinsic substances

    • Allow earlier detection of renal impairment than sCr.


    Kidney specific proteins and cardiac surgery

    KIDNEY-SPECIFIC PROTEINS AND CARDIAC SURGERY

    all original studies from 1990 to 2005 in which kidney-specific proteins were measured in patients undergoing cardiac surgery were reviewed…………..but:

    • Mostly are observational studies.

    • Small no. of patients.

    • Pt population are wide (off- and on-pump surgery, CABG surgery, valve surgery, and even children with correction of congenital heart disease).

    • The period of studying varied from 1 hour to 40 days after surgery.

    • The conventional measures for detecting kidney injury varied widely; some used CrCl, others used sCr or UOP.

    • No common definition for AKI.

    • No long term kidney function followup.

      So we need more specific studies


    Prevention of renal dysfunction and renal protection in cardiac surgery

    Prevention of renal dysfunction and renal protection in cardiac surgery

    The superior doctor prevents sickness;

    The mediocre doctor attends to impending sickness;

    The inferior doctor treats actual sickness;

    Chinese proverb


    Strategies of renal protection

    Strategies of Renal Protection

    1. Maintain adequate oxygen delivery—by ensuring adequate cardiac output, adequate oxygen carrying capacity, and proper haemoglobin saturation.

    2. Suppression of renovascular constriction—by ensuring adequate volume preload, use of infusions of mannitol, calcium entry block, and angiotensin converting enzyme inhibitors.

    3. Renal vasodilation—by dopaminergic agents, prostaglandins, and atrialnatriuretic peptide.

    4. Maintain renal tubular flow—by loop diuretics and mannitol (which may act to prevent tubular obstruction which can cause cellular swelling, ischaemia and death).

    5. Decrease oxygen demand—by use of loop diuretics and mild cooling.

    6. Attenuate ischaemic reperfusion injury—as a result of the release of oxygen free radicals and calcium ions.


    Prevention of renal dysfunction and renal protection in cardiac surgery1

    Prevention of renal dysfunction and renal protection in cardiac surgery


    Hydration

    HYDRATION

    • Studies for crystalloids vs colloids (no difference)

    • Type: ?? NS, LR,…….Hetastarch,albumin…

    • Amount:??controversy

      • Target CVP of at least 14-16mmHg

      • Fill till signs of overfill just manifest

        • CVP>16mmHg

        • Drop in PO2/FO2 ratio

        • Bilateral crackles

        • S3

        • Loss of stroke volume variation


    Prevention cpb

    PREVENTION CPB


    Inflammation in cpb

    Inflammation in CPB


    Renal protection in pediatric cardiac surgery

    Glomerulus from group A anesthetized and heparinized only. Well-filled capillaries with clear definition of glomerular anatomy. AA afferent arteriole; EA efferent arteriole; GC glomerular capillaries; PD polar diameter

    PATHI ET AL

    RENAL MICROCIRCULATION AND CARDIOPULMONARY BYPASS

    Ann ThoracSurg1998;65:993–8


    Renal protection in pediatric cardiac surgery

    Glomerulus from group B (cardiopulmonary bypass at 28°C, for 30 minutes) Smaller glomerulus with narrowedcapillaries suggesting diversion of flow through alternative channels

    PATHI ET AL

    RENAL MICROCIRCULATION AND CARDIOPULMONARY BYPASS

    Ann ThoracSurg1998;65:993–8


    Renal protection in pediatric cardiac surgery

    Glomerulus from group C (cardiopulmonary bypass at 28°C, for 120 minutes) Severe reduction in size of glomerulus with complete loss of functional unit. These act as shunts between afferent and efferent arteriolar systems

    PATHI ET AL

    RENAL MICROCIRCULATION AND CARDIOPULMONARY BYPASS

    Ann ThoracSurg1998;65:993–8


    Renal protection in pediatric cardiac surgery

    Glomerulus from group D (cardiopulmonary bypass at 28°C, 120 minutes; an 30 minutes of normothermic perfusion at theend)Some recovery of anatomy of the functional unit, although shunting of blood past the nephrons is still evident. Narrowing of the capillaries and increase in intercapillary spaces suggest interstitial edema

    PATHI ET AL

    RENAL MICROCIRCULATION AND CARDIOPULMONARY BYPASS

    Ann ThoracSurg1998;65:993–8


    Renal protection in pediatric cardiac surgery

    CARDIOPULMONARY BYPASS PROCEDURAL FACTORSclinically, although there are multiple experimental and clinical studies suggesting that various procedural aspects of CPB may be detrimental to the kidney, there is no clear consensus that CPB per se causes renal failure.


    Hemodilution

    HEMODILUTION

    2 opposing effects

    As O2 carrying capacity α HCTHemodilution

    ↓ afterload ↓ viscosity

    Hemodilution

    ↑ CO ↑ bl. flow in ↓RBCs oxygenation

    microcirculation at postcapillary

    ↓ O2 transportvenules

    ↑ O2 Delivery

    the net effect is ↑ O2delivery


    Hemodilution1

    HEMODILUTION

    From the figure:

    the most suitable Hct is 28-30%

    blood priming for pediatric population

    Hint H. The pharmacology of dextran and the physiological background for the clinical use of Rheomacrodex and Macrodex. ActaAnaesthBelg 1968;19:119–138


    Hypothermia

    HYPOTHERMIA

    • ↓ metabolic rate

    • ↑ intracellular PH

    • ?? Controversy about:

      • Warm cardioplegia

      • Warm Ht surgery ( normothermic bypass)

  • But studies→ less evidence of protective effects of hypothermia on kidneys.


  • Pulsatile perfusion

    PULSATILE PERFUSION

    • More physiologic

    • Improve microcirculation

    • But no evidence that is superior to non pulsatile perfusion in renal protection.


    Oxygenators and filters

    OXYGENATORS AND FILTERS

    • When bubble oxygenators was used → multiple emboli was found in brain, heart and kidneys → less with membrane oxygenators and arterial filters.

    • But in pediatric units → only 30% of centers use filters because large amount of volume required to prime the filters.


    Prevention drug therapy

    PREVENTIONDRUG THERAPY


    Dopamine

    DOPAMINE

    • ↓ Activity of Na+/K+ATPase.

    • Renal V.D.(D1 receptors in low dose

      0.5-2.5 µg/Kg/min).

    • ↑ CO (β1 receptors ˃ 5-10 µg/Kg/min).

    • Studies → controversy → ?? Diuretic

      → ++ ↑ CO


    Dopexamine

    DOPEXAMINE

    • Sympathomimetic agent.

    • Mainly on β2 agonist→

      • +veinotropic

      • +vechronotopic

      • ??↓ vascular resistance

  • In animals (not in human)→DA1 agonist →↑ renal bl. flow→ diuresis

  • But human→ diuresis only by ↑ CO.


  • Loop diuretics furosemide

    LOOP DIURETICSFUROSEMIDE

    Renal V.D.

    ?? Dose: 0.5mg/kg/min. for 48hrs

    ?? Effective prophylaxis (only pigment nephropathy)

    High-dose furosemide has been shown to decrease the duration of oliguria and need for dialysis in patients with ARF, but has no effect on mortality.


    Mannitol

    MANNITOL

    • Mech:

      • Osmotic diuretic.

      • Renal V.D. by ↑ PG production.

      • Free radical scavenger→↓ ischemic reperfusion injury.

    • AGAIN?????? Clinical trials failed to prove evidence


    Calcium channel blockers

    Calcium Channel Blockers

    eg: verapamil, diltiazim

    Mech:↑cytoplasmic Ca+ blocked arteriolar vc

    by CCB


    Ace i

    ACE I

    Pretreatment with ACEI→↓ the increase of renal vascular resistance associated with cross clamping.

    But →?? May ↑ postop. Renal dysfunction


    Atrial natriuretic peptide anp urodilatin

    AtrialNatriuretic peptide (ANP)(Urodilatin)

    ANP produced due to stretch by volume overload

    VD of afferent arterioles.

    ↑GFR

    VC of efferent arterioles.

    Anaritide, a synthetic analogue of ANP, there was improved mortality in treated patients with oliguria.

    administration of urodilatin (a natriuretic peptide found in human urine) is beneficial in oliguric patients after cardiac surgery and significantly reduces mortality and the need for dialysis.

    In comparison with circulating ANP, urodilatin exerts greater diuretic properties. Its method of action is thought to involve both improving renal blood flow and acting upon the distal collecting system


    Other possible thereapies

    OTHER POSSIBLE THEREAPIES

    1-ET Antagonist

    ET1→ V.C

    We need either→ ET receptor antagonist

    OR→ ET antibodies

    2- Prostaglandins E1

    Endogenous renal V.D


    3 dopaminergic drugs fenoldopam

    3-DOPAMINERGIC DRUGS FENOLDOPAM

    Selective DA1 agonist.

    Introduced mainly as an antihypertensive agent.

    It ↓ blood pressure in a dose-dependent manner while preserving RBF and GFR.

    Dose: 0.03-0.05 ng/kg/min


    3 fenoldopam

    3-FENOLDOPAM

    Mech1: DA1agonist→VD→↑ RBF.

    No effect on myocardial contractility as dopamine(no β effect)→ less arrhythmogenic and no tachycardia.

    Mech2: -- of Na+ transport in the mTAL

    region →↓ O2 utilization.


    3 fenoldopam1

    3-FENOLDOPAM

    "When we looked at the results, there was no difference between the fenoldopam group and those treated with standard therapy," says Landoni (Continuous Improvement in Cardiac Surgery Program )(CICPS).

    Bove T et al Circulation 2005; 111:3230-3235


    Renal protection in pediatric cardiac surgery

    Continuous Improvement in Cardiac Surgery Program (CICPS)concluded thatat high risk patients (eg. CABG)ARF depends on factors linked to poor cardiac performance and advanced atherosclerotic vascular diseasenot to vasodilatory effectsso, in pediatric populationneed more studies


    4 clonidine

    4-CLONIDINE

    • α-adrenergic (α1 and α2) agoniost.

    • Mech:

      • inhibits ADH production (central α1 effect).

      • Inhibits reabsorption of Na and H2O

        ( peripheral α2 effect).

      • block adrenergic VC stimuli to surgical stress

        →↓ renal hypoperfusion.

    • Dose: 4µg/kg


    Renal protection in pediatric cardiac surgery

    5-PENTOXIFYLLINE

    • PDE Inhibitor→-- activation of neutrophil by TNFαand IL-1, and TNF-α release by inflammatory cells.

    • No direct effect on kidneys.

      6-STEROIDS

      (DEXAMETHASONE)

    • failed to protect against renal dysfunction after cardiac surgery.

    • A recent study examined the effect of blocking complement activation in patients who underwent CPB


    Renal protection in pediatric cardiac surgery

    7- A single-chain antibody specific for human C5 (pexelizumab)

    C5 → block complement activation→

    ??renal function after CPB

    8- N-acetylcysteine (N-AC)

    • block inflammation and oxidant stress in cardiac surgery patients.

    • studied most extensively in the prevention of radiocontrast induced nephropathy.


    Summary

    SUMMARY

    Renal failure is relative rare complication but associated with a 10-fold increase in surgical mortality.

    Although CPB is a nonphysiologic state that alters renal blood flow and many neuroendocrine responses affecting the kidney, there is little clear-cut evidence that CPB per se is responsible for renal dysfunction.

    Risk factors mainly:→perop→renaldysfunc

    →intraop→infammatory response

    →postop→↓ COP

    Protection mainly to maximize postop. COP to avoid renal hypoperfusion.


    Principles of management of oliguria and acute renal failure

    Principles of management of oliguria and acute renal failure


    Special situation aortic surgery

    SPECIAL SITUATIONAORTIC SURGERY

    • Paraplegia and renal failure are the main determinants in postoperative mortalities.

    • In pediatrics eg. Coarctation, aneurysm (Marfan,..)......

    • Problem: Aortic cross clamp (suprarenal vsinfrarenal)

    • renal protection including:

      • Hypothermic CPB with circulatory arrest.

      • Selective volume and pressure controlled perfusionby: Retrograde aortic perfusion,followed by

        • warm blood visceral perfusion,

        • Cold crystalloids renal arteries perfusion

        • antegrade cold blood visceral perfusion,

        • retrograde cold bloodperfusion, and

        • the perioperative use of a renal protective pharmacologicagent, fenoldopam.

          Perform selective perfusion by 4 branched tubing system connected to extracorporeal circulation with the 4 braches connected to celiac, superior mesenteric and 2 renal arteries.

      • Shunts

        • both temporary and permanent .

        • These included

          • permanent axillo-bifemoral graft ,

          • aorto iliac Gott shunt , axillo-femoral Gott shunt ,

          • temporary axillofemoral graft ,

          • combination of double clamping then temporary perfusion using a Javid shunt.

        • These techniques have the disadvantages of complexity or of incurring significant period of renal ischaemia.


    Aswers

    ASWERS

    1. The risk of development of acute renal failure after cardiac surgery is highest in:

    a. Neonates.

    b. Infants.

    c. Children.

    d. Adults.


    Renal protection in pediatric cardiac surgery

    A

    Kidneys are able to maintain renal blood flow over a wide range of systemic blood pressures by autoregulation of intrarenal vascular resistance. Therefore, hypotension with renal hypoperfusion may or may not produce ischemic renal injury. However, these autoregulatory mechanisms are not well developed in neonates.Neonates have high reninlevels, which in turn, are associated with decreased glomerular filtration rate (GFR) and reduced outer cortical blood flow. The cortical glomeruli are immature and so are their corresponding tubules. This pattern of high renin and reduced outer cortical blood flow makes neonates more vulnerable to renal dysfunction as a result of hypotension of systemic pressures only slightly below the normal range. In animal studies, newborn animals have decreased production of atrialnatriuretic peptide in response to saline challenge. All these factors combined make the incidence of acute renal failure in neonates, after cardiac surgery, higher than in older infants and children. (Nichols DG, et al. Critical Heart Disease in Infants and Children, Mosby 1995; pp. 125, 562.)


    Renal protection in pediatric cardiac surgery

    2. Which of the following causes vasodilation of the cortical vasculature?

    a. Mannitol. c. Both.

    b. Furosemide. d. Neither.


    Renal protection in pediatric cardiac surgery

    2. C

    Furosemide causes vasodilation of the cortical vasculature by direct action and through release of prostaglandins. Furosemide maintains renal blood flow and tubular blood flow when cardiac output is compromised. Mannitol is also a vasodilator of the cortical vasculature that increases renal blood flow either directly by drawing fluid from extravascularto intravascular space, thus increasing total plasma volume, or by increasing prostaglandin production. Increased plasma volume alone does not fully explain the effects of mannitol, because volume expansion with saline improves renal blood flow without improving GFR. The improvement in GFR seen with mannitol is associated with a decrease in afferent and efferent arteriolar resistance, which is probably mediated by prostaglandins. (Rogers MC, et al. Textbook of Pediatric Intensive Care, 2nd Edition; pp. 1192–1194, 1202.)


    Renal protection in pediatric cardiac surgery

    3. Clinical settings in which mannitol has definitely been shown to be effective in preventing the deterioration of renal function is:

    a. During and after cardiopulmonary bypass.

    b. During and after aortic cross-clamping.

    c. During and after hypovolemic shock.

    d. Before the administration of cisplatin.

    e. None of the above.


    Renal protection in pediatric cardiac surgery

    3. D

    Clinical studies comparing prophylactic administration of mannitol (or furosemide) with maintenance of adequate intravascular volume during cardiopulmonary bypass failed to reduce the incidence of postoperative renal dysfunction. However, there are experimental studies that have shown some beneficial effects of mannitol. Mannitol has been shown to be effective in preventing deterioration of renal function before administration of Amphotericin B and Cis-Platinum. (Rogers MC, et al. Textbook of Pediatric Intensive Care, 2nd Edition; pp. 1194,1195; Nichols DG. Critical Heart Disease in Infants and Children, Mosby 1995; pp. 129,130; Olivero JJ, et al. Br Med J, 1975; 1:550; Hayes D, et al. Cancer, 1977; 39:1372.)


    Renal protection in pediatric cardiac surgery

    4. Which of the following statements is least accurate regarding acute renal failure?

    a. Adults with no underlying renal disease who develop acute renal failure have a worse prognosis compared with children.

    b. Following cardiac surgery, the incidence of acute renal failure is higher in children than in adults.

    c. Children over the age of 2 years with acute renal failure have a much better outlook with meticulous medical care.

    d. Spontaneous recovery from acute renal failure is likely to begin 1–3 weeks after onset.

    e. The mortality rate for children with acute renal failure is much higher than in adults


    Renal protection in pediatric cardiac surgery

    4. E

    Children have a lower mortality compared with adults. (Rogers MC, et al. Textbook of Pediatric Intensive Care, 2nd Edition; pp. 1198–1201.)


    Renal protection in pediatric cardiac surgery

    5. Which of the following statements is true regarding management of suspected acute renal failure?

    a. In euvolemic patients, the rapid intravenous administration of mannitol should result in a urine output greater than 0.5 mL/kg within 1 hour if a prerenaletiology dominates.

    b. The vasodilatory and natriuretic properties of furosemide are beneficial when administered early in the course of acute renal failure.

    c. In euvolemic patients, furosemide in an incremental dose of up to 10 mg/kg may be used.

    d. If there is no response to a fluid challenge, low dose dopamine could be added.

    e. All of the above


    Renal protection in pediatric cardiac surgery

    6. In a patient who has just been admitted to the pediatric intensive care unit with new onset of acute renal failure, which of the following pathophysiological changes is least likely to occur?

    a. Blood urea nitrogen (BUN) and creatinine will rise at 10 and 0.5 mg/dL/day, respectively.

    b. Serum HCO3 decreases by 2 mEq/L/day because of release of tissue phosphate.

    c. Serum K+ increases by 0.3–0.5 mEq/L/day.

    d. Hypernatremia is commonly observed.

    e. Hypophosphatemia and associated hypocalcemia may develop rapidly after the onset of acute renal failure


    Renal protection in pediatric cardiac surgery

    5-6. E, D

    All of the strategies mentioned are appropriate for oliguria in a setting of suspected renal insufficiency. With the onset of acute renal failure, hyponatremia is more commonly seen owing to the dilutional effect of intake of fluid orally, which is mostly hypotonic. (Rogers MC, et al. Textbook of Pediatric Intensive Care, 2nd Edition; p. 1202. Nichols DG. Critical Heart Disease in Infants and Children, Mosby 1995; pp. 128–138.)


    Thank you

    THANK YOU


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