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chronic kidney disease, diagnosis, management, prognosis, complications, renal replacement therapy, when to initiate hemodialysis, complication of hemodialysis, mortality and morbility.
Renal Replacement Therapy: modes and evidenceMohd Saif Khan
Renal replacement therapy is a supportive care often required in critically ill patients who develop acute renal failure and its complications. Complexity arises when such patients become hemodynamically unstable and pose special challenge to critical care clinicians in ICU to carefully choose dialytic modality to tackle volume and solute overload. This presentation is about short description of modalities of RRT and current evidence regarding initiation, dose and type of modality.
chronic kidney disease, diagnosis, management, prognosis, complications, renal replacement therapy, when to initiate hemodialysis, complication of hemodialysis, mortality and morbility.
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title; hypotension and causes of hypotension
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Tom Selleck, an enduring figure in Hollywood. has captivated audiences for decades with his rugged charm, iconic moustache. and memorable roles in television and film. From his breakout role as Thomas Magnum in Magnum P.I. to his current portrayal of Frank Reagan in Blue Bloods. Selleck's career has spanned over 50 years. But beyond his professional achievements. fans have often been curious about Tom Selleck Health. especially as he has aged in the public eye.
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Introduction
Many have been interested in Tom Selleck health. not only because of his enduring presence on screen but also because of the challenges. and lifestyle choices he has faced and made over the years. This article delves into the various aspects of Tom Selleck health. exploring his fitness regimen, diet, mental health. and the challenges he has encountered as he ages. We'll look at how he maintains his well-being. the health issues he has faced, and his approach to ageing .
Early Life and Career
Childhood and Athletic Beginnings
Tom Selleck was born on January 29, 1945, in Detroit, Michigan, and grew up in Sherman Oaks, California. From an early age, he was involved in sports, particularly basketball. which played a significant role in his physical development. His athletic pursuits continued into college. where he attended the University of Southern California (USC) on a basketball scholarship. This early involvement in sports laid a strong foundation for his physical health and disciplined lifestyle.
Transition to Acting
Selleck's transition from an athlete to an actor came with its physical demands. His first significant role in "Magnum P.I." required him to perform various stunts and maintain a fit appearance. This role, which he played from 1980 to 1988. necessitated a rigorous fitness routine to meet the show's demands. setting the stage for his long-term commitment to health and wellness.
Fitness Regimen
Workout Routine
Tom Selleck health and fitness regimen has evolved. adapting to his changing roles and age. During his "Magnum, P.I." days. Selleck's workouts were intense and focused on building and maintaining muscle mass. His routine included weightlifting, cardiovascular exercises. and specific training for the stunts he performed on the show.
Selleck adjusted his fitness routine as he aged to suit his body's needs. Today, his workouts focus on maintaining flexibility, strength, and cardiovascular health. He incorporates low-impact exercises such as swimming, walking, and light weightlifting. This balanced approach helps him stay fit without putting undue strain on his joints and muscles.
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Stay informed, stay safe, and get your flu shot today!
Title: Sense of Smell
Presenter: Dr. Faiza, Assistant Professor of Physiology
Qualifications:
MBBS (Best Graduate, AIMC Lahore)
FCPS Physiology
ICMT, CHPE, DHPE (STMU)
MPH (GC University, Faisalabad)
MBA (Virtual University of Pakistan)
Learning Objectives:
Describe the primary categories of smells and the concept of odor blindness.
Explain the structure and location of the olfactory membrane and mucosa, including the types and roles of cells involved in olfaction.
Describe the pathway and mechanisms of olfactory signal transmission from the olfactory receptors to the brain.
Illustrate the biochemical cascade triggered by odorant binding to olfactory receptors, including the role of G-proteins and second messengers in generating an action potential.
Identify different types of olfactory disorders such as anosmia, hyposmia, hyperosmia, and dysosmia, including their potential causes.
Key Topics:
Olfactory Genes:
3% of the human genome accounts for olfactory genes.
400 genes for odorant receptors.
Olfactory Membrane:
Located in the superior part of the nasal cavity.
Medially: Folds downward along the superior septum.
Laterally: Folds over the superior turbinate and upper surface of the middle turbinate.
Total surface area: 5-10 square centimeters.
Olfactory Mucosa:
Olfactory Cells: Bipolar nerve cells derived from the CNS (100 million), with 4-25 olfactory cilia per cell.
Sustentacular Cells: Produce mucus and maintain ionic and molecular environment.
Basal Cells: Replace worn-out olfactory cells with an average lifespan of 1-2 months.
Bowman’s Gland: Secretes mucus.
Stimulation of Olfactory Cells:
Odorant dissolves in mucus and attaches to receptors on olfactory cilia.
Involves a cascade effect through G-proteins and second messengers, leading to depolarization and action potential generation in the olfactory nerve.
Quality of a Good Odorant:
Small (3-20 Carbon atoms), volatile, water-soluble, and lipid-soluble.
Facilitated by odorant-binding proteins in mucus.
Membrane Potential and Action Potential:
Resting membrane potential: -55mV.
Action potential frequency in the olfactory nerve increases with odorant strength.
Adaptation Towards the Sense of Smell:
Rapid adaptation within the first second, with further slow adaptation.
Psychological adaptation greater than receptor adaptation, involving feedback inhibition from the central nervous system.
Primary Sensations of Smell:
Camphoraceous, Musky, Floral, Pepperminty, Ethereal, Pungent, Putrid.
Odor Detection Threshold:
Examples: Hydrogen sulfide (0.0005 ppm), Methyl-mercaptan (0.002 ppm).
Some toxic substances are odorless at lethal concentrations.
Characteristics of Smell:
Odor blindness for single substances due to lack of appropriate receptor protein.
Behavioral and emotional influences of smell.
Transmission of Olfactory Signals:
From olfactory cells to glomeruli in the olfactory bulb, involving lateral inhibition.
Primitive, less old, and new olfactory systems with different path
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2. Acute kidney injury (AKI), previously known
as acute renal failure, is characterized by the
sudden impairment of kidney function
resulting in the retention of nitrogenous and
other waste products normally cleared by the
kidneys .
Sudden decrease in GFR over a period of hours
to days resulting in the failure of the kidney to
maintain fluid and electrolyte homeostasis.
3. Acute kidney injury (AKI), is not a single disease but
a heterogeneous group of conditions that share
common diagnostic features: specifically,
an increase in the blood urea nitrogen (BUN)
concentration and/or
an increase in the plasma or serum creatinine (SCr)
concentration
associated with a reduction in urine volume.
4. Anuria – no urine output or less than 100ml/24
hours
Oliguria - <400ml urine output/24 hours or
<16ml/hour
Polyuria - >2.5L urine output/24 hours
5. Prerenal
Renal hypoperfusion - no structural damage to the
kidneys, Creatinine normalizes in 24-72 hours with
correction of hypoperfused state.
Post-renal
Obstruction to the urine flow, either
unilateral/bilateral- intra-ureteral or extra-ureteral
or obstruction to bladder neck or renal-pelvis .
Intrinsic-renal
Damage or inflammation within the kidney, may be
of primary renal origin or part of systemic disease.
6. The prerenal sources of oliguria are located proximal to
the kidneys and are characterized by a decrease in
renovascular flow.
The disorders in this category include
low cardiac output from
hypovolemia,
mechanical ventilation,
aortic stenosis, and
end-stage cardiomyopathy,
as well as drugs that impair renal autoregulation
(e.g.angiotensin-converting enzyme inhibitors).
7. Prerenal disorders are responsible for about 30
to 40% of cases of oliguria in the ICU.
The oliguria in these conditions can usually be
corrected by correcting the underlying
disorder, but prolonged or severe prerenal
conditions can lead to renal injury and oliguric
renal failure.
9. Increased ECV with
Arterial underfilling
Reduced Cardiac
Output
Cardiogenic shock, MI, PE
Tamponade, constrictive
Pericarditis ,
Peripheral Vasoldilatation
Sepsis, anaphylaxis,
anaesthesia,
Cirrhosis, other liver
diseases.
10.
11. These medications cause ARF by inhibiting
angiotensin particularly in certain cases where
angiotensin is playing a major crucial
protective role in maintaining GFR by
constricting the glomerular efferent arteriole.
Volume Depletion
B/L Renal artery stenosis
Congestive Heart Failure
Diuretic use
Cirrhosis .
12. Exacerbated in the presence of conditions with
increased renal vasoconstrictor activity like
Congestive heart failure (CHF)
Cirrhosis
Nephrotic Syndrome,
Sepsis, Volume depletion, HTN, CKD.
NSAIDS induced ARF is not seen in Euvolemic
conditions with normal kidney, liver and cardiac
functions.
16. Large and Medium size vessels
Renal artery thrombosis or emboli
Renal vein thrombosis
Polyarterial nodosa
Small vessel disease
Atheroembolic phenomenon
Microangiopathies like TTP, HUS, HELLP and
malignant HTN.
17. Nephritis
Hematuria
Proteinuria (1-2gm/d)
ARF
May present as Rapidly
progressive
Glomerulonephritis
Renal Biopsy to
diagnose
Nephrosis
Massive
proteinuria(>3gm/d)
Minimal hematuria
May present as ARF
Renal Biopsy needed to
diagnose.
18. Focal/diffuse edema and infiltration of the renal
interstitium with inflammatory cells.
Acute
Interstitial
Nephritis
Drugs
Antibiotics, NSAIDs,
Phenytoin,
allopurinol,
diuretics etc.,
Systemic
Diseases
SLE etc.,
Infections
Staph, Strepto, CMV,
EBV, TB etc.,
19. Ischemia induced
Shock
Hemorrhage
Sepsis
Trauma
Pancreatitis
Nephrotoxin induced
Drugs like IV contrast,
Aminoglycosides,
Ampho B, pentamidine,
Acyclovir, Ethylene
Glycol etc.,
Endogenous Toxins in
the case of
Rhabdomyolysis,
Hemolysis, uric acid
nephropathy
20. Ischemia-associated AKI is a serious complication in
the postoperative period, especially after major
operations involving significant blood loss and
intraoperative hypotension.
The procedures most commonly associated with AKI
are
Cardiac surgery with cardiopulmonary bypass
(particularly for combined valve and bypass
procedures),
vascular procedures with aortic cross clamping, and
intraperitoneal procedures.
21. Severe AKI requiring dialysis occurs in
approximately 1% of cardiac and vascular
surgery procedures.
Longer duration of cardiopulmonary bypass is
a risk factor for AKI.
22. Community acquired ARF seen in 1% of all
hospitalized patients on admission - 50% of
those patients have underlying CKD.
Development of ARF in hospitalized patients is
common and carries independent mortality
risk.
In patients with normal renal function, the
incidence of ARF is about 5%.
In patients with underlying CKD, the incidence
is about 16%.
23. ICU associated ARF along with respiratory
failure requiring hemodialysis, the mortality is
>90%.
ICU associated ARF with out respiratory
failure or hemodialysis, it is 72%
Non-ICU renal failure associated mortality is
around 32%.
24. Retention of nitrogenous waste products
Nausea, vomiting, diarrhea, hiccups, foul taste, dry
crusted mouth, itching,
Drowsiness, clouding of consciousness, neuropathy,
pericarditis, GI bleeding,
Coma
Retention of salt and water
Pulmonary edema, peripheral edema, ascites, pleural
effusion
25. Retention of potassium
Weakness, lassitude, paralysis, EKG changes with
tenting T waves, widening of QRS complex,
increased PR interval, sine wave pattern, cardiac
arrest, VT
Retention of acid
Kussmaul respiration, hyperreflexia, hypotension
27. Differentiate acute or chronic renal failure
Distinguishing between acute and chronic renal
failure is important, as the approach to these
patients differs greatly.
28. Factors that suggest chronicity :
Long duration of symptoms,
Absence of acute illness, anaemia,
hyperphosphatemia, and hypocalcaemia,
Previous Serum creatinine measurements
Small kidneys on ultrasound (except for in -
Diabetes, PCKD, Urinary Tract Obstruction)
29. Careful History and tabulation of data
including urinary output, weight, vitals,
medications etc.
Physical Examination findings including signs
of volume depletion ,
Urinalysis
Urinary indices(Urine sodium, creatinine,
FeNa, FeUrea )
31. Easiest and least expensive diagnostic procedure.
The presence of tubular epithelial cells abundant
with epithelial cell casts is virtually pathognomonic
of ATN.
The presence of white cell casts identifies an
interstitial nephritis, and the presence of pigmented
casts identifies myoglobinuria.
32. UA positive for heme and proteinuria seen in
Glomerular and Interstitial renal failure.
Urine eosinophils are seen in AIN,
Atheroembolic disease .
Urine sediment positive for red cell casts seen
in Glomerulonephritis.
33. Normal S.Creatinine is 0.6-1.2mg/dl and is
the most commonly used parameter to
assess renal function.
Unfortunately the correlation between
S.Creatinine concentration and GFR may be
confounded by several factors.
34. There is abrupt drop in GFR but the S.Cr. does not start going up for
24 or 36 hours after the acute insult .
40
80
0
GFR
(mL/min)
0 7 14 21 28
4
Days
2
0
6
Serum
Creatinine
(mg/dL)
Relationship between GFR and serum creatinine in
ARF
35. Cystatin C –protein:
Produced by nucleated cells
Filtered and completely reabsorbed
Changes in serum levels occur sooner in this
protein.
Other Newer biomarkers are IL-8, NGAL-
neutrophil gelatinase associated lipocalin
36. Peripheral eosinophilia is seen in AIN,
Atheroembolic disease.
Hypocomplementemia seen in SLE, MPGN,
Atheroembolic disease .
Elevated ESR seen in Atheroembolic disease.
Serologies like ANA, ANCA, Anti GBM, HIV may
be positive in glomerular diseases.
Elevated LDH seen in Renal Vein Thrombosis
(RVT).
37. Thrombocytopenia with microangiopathic
hemolysis seen in Thrombotic thrombocytopenic
purpura(TTP),Haemolytic uremic syndrome( HUS).
Low Haptoglobin, High reticulocyte count seen in
microangiopathic states.
CPK and uric acid levels, to evaluate for
rhabdomyolysis, uric acid nephropathy.
Evidence of hepatic insufficiency is useful in
diagnosing hepatorenal syndrome.
38. Ultrasound
Useful in Post renal ARF.
Early obstruction may not show significant
hydronephrosis.
External obstruction encasing the whole
urinary system may not show hydronephrosis,
for e.g., retroperitoneal fibrosis.
U/S doppler is useful in diagnosing Renal
vein thrombosis.
39. CT scan
Useful for detecting stones, location of the
obstruction, Tumours .
Isotope renography
To evaluate the function significance of
obstruction.
Done with lasix and Mag3 isotope for
evaluating obstruction.
40. Cystoscopy and Retrograde
Pyelography
To evaluate patients with high clinical
suspicion of obstruction especially in unique
cases of calculi, pyogenic debris, blood clots,
bladder cancer .
Renal Angiography
In emergent cases of anuria with suspicion of
renal embolization.
41. Done only in patients with no clear etiology.
In patients with active urinary sediment (RBCs,
red cell casts ).
RPGN (rapidly progressive
glomerulonephritis).
Refractory ATN with out recovery despite no
further renal insults.
Acute Interstitial nephritis.
42.
43.
44. Fluid resuscitation and the use of vasopressor
therapy- are universally emphasized in the
prevention and treatment of ARF.
The controversy regarding crystalloid versus
colloid still contiues.
The prompt and adequate correction of
hypovolemia and hypotension is much more
important than the type of fluid used.
45. Volume repletion with isotonic fluids to
improve renal perfusion pressures should be
done in prerenal failure-CVP/ PAWP
monitoring.
Colloidal substances like blood products in
hemorrhagic shock.
Management of heart failure by improving
cardiac output.
Supportive measures for sepsis with
vasopressors .
46. Use of vasopressors in ARF
Concern has been expressed in usage of
vasopressors because renal vasoconstriction
may be increased and the situation exacerbated.
Overall effect of using norepinephrine in septic
patients is to increase the GFR and urinary
output.
Lower mortality rates were observed in a
prospective observational trial of almost 100
septic patients who were treated with
norepinephrine .
47. The use of dopamine to either treat or prevent ARF
is not supported by the literature now.
Despite several years of use as a renal vasodilator,
low-dose dopamine (2μg/kg/min) has shown no
evidence of benefit in patients with acute oliguric
renal failure
48. Convertion of oliguric to nonoliguric ARF with
the use of diuretics is not advised and
mortality rates and dialysis requirements are
not changed by this practice.
Furosemide – loop diuretic used in oliguric
renal failure.
If furosemide is used in an attempt to promote
urine flow,it is preferred to be given by
continuous infusion
49. Drugs need to be dosed according to the renal
clearance.
Electrolyte and acid base correction.
Foley catheterization –in case of bladder neck
obstruction/prostatic obstruction
Diuretics- used in overt fluid overload states.
50. Use of Mannitol has been shown to be associated
with improved renal outcome
Forced alkaline diuresis together with mannitol is
generally accepted as preventing acute tubular
necrosis in severe crush injury
N-acetylcysteine- a reactive oxygen metabolite
scavenger, has been advocated as a renal protection
agent specifically in contrast-mediated
nephropathy.
51. Activated protein C and steroid replacement
(in those patients who demonstrate a steroid
deficiency) have been shown to reduce
mortality in patients with severe sepsis.
Avoid nephrotoxic agents like Contrast dye,
NSAIDs, Aminoglycosides .
Nutritional support with parenteral or enteral
feeding in ICU
52. Volume overload –salt restriction<1-1.5g/d.
water restriction-<1 litre /d
diuretics
Hyponatremia –restriction of oral &
intravenous fluids
Hyperkalemia – K binding resins ,
glucose + insulin
Ca gluconate, Na bicarbonate
Metabolic acidosis – Na bicarb ., if < 15 meq
Hyperphosphatemia – PO4 binders .
53. Renal replacement therapy
Modes of dialysis:
IHD (Intermittent RRT)
Quick removal of solutes over 3-4 hours.
In ICU, hypotensive patients are not the best
candiadtes for this type of HD.
CRRT (Continuous renal replacement therapy).
Modality of choice in critically ill patients.
Peritonial dialysis
54. Peritoneal dialysis uncommonly used for
managing ARF.
It may be used in locations where IHD or
CRRT are not available.
55. Dialysis = diffusion =passive
movement of solutes across a
semi-permeable membrane
down concentration gradient
Good for removal of small
molecules
Ultrafiltration = convection =
solute + fluid removal across
semi-permeable membrane
down a pressure gradient
(solvent drag)
Better for removal of fluid and
medium-size molecules
56. •Miller's Anesthesia, 7th ed. 2009
Hemodialysis -solute passively diffuses down
concentration gradient
Dialysate flows countercurrent to blood flow.
Urea, creatinine, K move from blood to dialysate
Ca and bicarb move from dialysate to blood.
Hemofiltration: uses hydrostatic pressure gradient
to induce filtration of plasma water + solutes across
membrane.
Hemodiafiltration: combination of dialysis and
filtration.
57. 1. Oliguria < 200ml/12 hours
2. Anuria < 50 ml/12 hours
3. Hyperkalemia > 6.5 mmol/L
4. Severe acidemia pH < 7.0
5. BUN > 80meq/L
6. Uraemic complications
7. Dysnatraemias > 160 or < 115meq/L
8. Hyper/(hypo)thermia
9. Drug overdose with dialysable drug
58. •Allows control of intra/extravascular
volume
•Corrects acid-base disturbances
•Corrects uraemia & effectively clears
“toxins”
•Promotes renal recovery
•Improves survival
•Is free of complications
•Clears drugs effectively
60. Oldest and most common technique
Primarily simple diffusive treatment: blood and
dialysate are circulated in countercurrent manner
Some amount of fluid removal occurs by
ultrafiltration due to pressure driving through circuit
Best for removal of small molecules.
A double lumen catheter is placed in the internal
jugular subclavian or femoral vein.
Typically performed for 4 hours 3 times in a wk .
61. Introduced in 1980s
Involves either dialysis (diffusion-based solute
removal) or filtration (convection-based solute
and water removal) treatments in a continuous
mode with slower rate of solute or fluid
removal
CRRT includes continuous hemofiltration,
hemodialysis and hemodiafiltration, all of
which can be performed using arteriovenous or
venovenous extracorporeal circuits.
62. Continuous venovenous hemofiltration (CVVH):
Uses blood pump to remove fluids/solutes by
convection ie along a pressure gradient.
This is the convective flow of water and dissolved
solutes down a pressure gradient caused by
hydrostatic or osmotic forces
It provides better removal of large MW solutes e.g.
B2-microglobulin, improved clearance of low MW
uraemic toxins and better cardiovascular stability
and Bp control than HD.
63. Continuous venovenous hemodialysis
(CVVHD): Uses pump + dialysate run at low
flow rate countercurrent to blood flow.
Continuous venovenous hemodiafiltration
(CVVHDF): combines diffusion for small solute
removal + convection for large solutes.
64. Arteriovenous versions (CAVH, CAVHD and
CAVHDF) are similar to venovenous except
use AV access and blood pump not required.
Diadvantages: requires arterial cannulation (+
venous)
Unreliable flow in patients with ↓ BP or severe PVD
Requires more anticoagulation
VV preferred due to lower risk, and faster/more
reliable flow
65. Used for fluid removal in overloaded CHF
patients
Blood is driven through a highly permeable
filter in a venovenous mode to primarily
remove water, not solute.
The ultrafiltrate produced during membrane
transit is not replaced so it corresponds to the
fluid loss.
•Miller's Anesthesia, 7th ed. 2009
66. Least useful form of CRRT in the ICU
Blood in capillaries of peritoneal membrane is
exposed to dialysate in abdomen
Continuous or intermittent
Inefficient solute/volume clearance can occur if
unstable or poor intestinal blood flow
Can’t be used if intraabdominal pathology- risk of
peritonitis
Respiratory burden to patient.
67. Also known as Extended daily dialysis (EDD)
or slow continuous dialysis (SCD)
Hybrid therapy: IRRT at lower blood and
dialysate flows for prolonged times (Usually ≥
5 hrs)
Uses conventional dialysis machines
Flexibility of duration and intensity
Major advantages: reduced costs, low or
absent anticoagulation
68. CRRT requires continuous anticoagulation to
prevent clotting in the CRRT circuit
ICU patients often at increased risk of bleeding
and hypercoagulable states.
Many options:
Systemic anticoagulation with heparin (mst
common), LMWH, heparinoids, thrombin
antagonists
Regional citrate anticoagulation (preferred)
Other regional anticoagulation ie heparin/protamine
69. Advantages of early RRT:
Theoretical benefits: may attenuate organ injury
from acidemia, uremia, fluid overload, and
systemic inflammation
Several non-randomized studies have reported
improved outcomes associated with early RRT .
One RCT has compared early and late initiation of
RRT and conclusion was survival at 28 days and
recovery of renal function was equivalent in both
the groups.
70. Earlier initiation of RRT in critically ill patients
with AKI may have a beneficial impact on
survival .
Many studies recommend initiation of RRT
prior to the development of advanced uremic
symptoms, or when the BUN reaches 80 - 100
mg/dL
No known threshold of fluid overload for
initiating RRT
71. Until “evidence of recovery of kidney function”
Improved UOP in oliguria
Decreasing creatinine
Creatinine clearance minimum 20 mL/min.
72. Theoretical benefits to both.
At least 7 RCTs and 3 meta-analyses have not
demonstrated difference in outcome.
A metaanalysis of 9 randomized trials: No effect on
mortality or recovery based on type of RRT used.
Suggestion was that continuous RRT had fewer
episodes of hemodynamic instability and better
control of fluid balance .
73. Specific patient populations who may benefit
from CRRT
Hemodynamic instability
Combined acute renal and hepatic failure
Improved CV instability and intracranial
pressure
Acute brain injury
Vanholder et al. Critical Care 2011, 15:204
74. Practicality and flexibility
Uses same machines as chronic HD
Multiple patients per day
Less expensive than CRRT (by about ½)
Fewer bleeding complications
CRRT requires continuous anticoagulation
Superior solute clearance, more rapid removal
of toxins (due to higher flows)
Vanholder et al. Critical Care 2011, 15:204
75. Specific patient populations benefitting from
IRRT:
High bleeding risk
Ie. after recent surgery
Acute treatment of hyperkalemia, rhabdomyolysis,
poisoning, tumor lysis syndrome
Vanholder et al. Critical Care 2011, 15:204
76. RRT has been proposed as a “Extracorporeal
blood purification therapy (EBPT)” as
adjuvant therapy for SEPSIS/MODS for
removal of harmful inflammatory mediators or
endotoxemia
Very less support from animal models and
small clinical studies
•Miller's Anesthesia, 7th ed. 2009
77. AKI in the ICU is common and associated with
high mortality.
The best time to initiate and stop RRT is
controversial
No good data that CRRT is better than IRRT in
the ICU, except for a few specific situations
Consider CRRT if severely unstable pts, severe
volume overload, combined renal/hepatic failure
IRRT best if there is bleeding risk or acute
hyperkalemia or cases of poisoning.
78. No drugs are Currently available to enhance or
hasten renal recovery once ARF occurs.
There is now clear evidence that ARF is
associated with excess mortality, irrespective of
whether the patient requires renal replacement
therapy.
Hence prevention is the only powerful tool to
improve outcome of AKI
78
79. 79
Identification of patients at high risk to develop
AKI-Elderly, DM, HT. Sepsis
Non Pharmacological Pharmacological
Ensuring adequate
hydration (reversing
dehydration).
Maintenance of
adequate mean
arterial
pressure>65mmHg
Minimizing exposure
to nephrotoxins.
Loop diuretics,
Mannitol,
Vasopressors if
necessory.