This lecture was conducted during the Nephrology Unit
Grand Ground by Medical Student rotated under Nephrology
Division under the supervision and administration of Prof.
Jamal Al Wakeel, Head of Nephrology Unit, Department of
Medicine and Dr. Abdulkareem Al Suwaida, Chairman of the
Department of Medicine. Nephrology Division is not
responsible for the content of the presentation for it is
intended for learning and /or education purpose only.
Critical Care Issues in Nephrology
Presented by:
Waleed Alharbi
Medical Student
June 2008
Lessons I have learned during my
Nephrology Rotation Training
1. Knowledge
2. Behavior
3. Excellent Brain Workout!
4. Meet superb & sincere persons like
Dr.Iqbal
Knowledge…
• Renal, acid-base & electrolyte complications
are common in ICU.
• Only selected topics…
• Dialysis issues in ICU…
• I wish if I had more consultation exposure…
Acute Renal failure
• ARF in ICU is alarming why?!
• Mortality 78% in those who require dialysis
• 1/3 will require chronic dialysis
• ARF development in ICU is marked by poor
prognosis & ↑ long-term complications
Protecting the Kidney…
How to prevent ARF in ICU?
• NSAIDs + ACEIs + ARBs
• Alter intrarenal hemodynamics
• Common causes of acute renal dysfunction
in patients who have associated volume
depletion
How to prevent ARF in ICU?
• Crush injuries
• Associated with severe rhabdomyolysis &
myoglobinuric renal failure
• To reduce risk of ARF development:
• Aggressive volume repletion with solution that includes
HCO3 for urinary alkalinzation why?!
• To ↓ myoglobin precipitation in tubules
• Mannitol to ↓ myoglobin precipitation + provides free
radical scavenging
How to prevent ARF in ICU?
•
•
Amphotericin B
High risk are:
1.
2.
3.
4.
5.
>60mg/day
In ICU
On cyclosporin
Baseline renal insufficiency
Diuretic use
•
Pretreatment with NS which suppresses the vasoconstrictive
effect of the tubuloglomerular feedback mechanism
•
Lipid formulations 30-50% risk reduction
•
Infusion over 24hrs rather than 4 hrs 60% less
How to prevent ARF in ICU?
• Aminoglycosides
• 10-15% cause ARF
• Most important intervention is
MONITORING of levels
• Single dosing daily has 13-26% risk
reduction
Prevention of ARF in the ICU
•
Prevention of contrast nephropathy
•
Predisposing factors:
1.
2.
3.
DM
Baseline renal dysfunction
Presence of volume depletion
•
Patients with renal impairement exposure to dye results in
ARF in up to 30% of cases
•
Measures:
1.
2.
3.
NAC
NaHCO3 + Hydration
Low-osmolality contrast
ARF – Making the Dx
• Clinical
• Biochemical
• RIFLE Criteria… Crit Care Journal 2004
presented by Prof.Al-Wakeel
Clinical Approach to the Patient
Work-Up of ARF
Diagnostic Approach to ARF
• Review of Medications
Diagnostic Approach to ARF
•
Rule out Obstruction
•
Urinanalysis & microscopy
•
RBC casts – Dysmorphic RBCs = GN – Vasculitis
•
WBC casts – Sterile pyuria = Interstitial nephritis
•
Muddy brown – pigmented casts = ATN
•
Hyaline casts = PRA
•
Eosinophiluria?!!
• Limited specifity it can be seen in:
•
•
•
•
GN
atheroembolic renal disease
Pyelonephritis
Prostatis
• Need special staining
Most Interesting Topic in Dx of ARF is
differentiating between PRA & ATN
• Assessing volume status?!
• Best is the use of urinary indices
Differentiating between PRA &
ATN
• FENa = [U/P]Na : [U/P]Cr x 100
• If nonoliguric?! There will be greater
overlap
• If on diuretics?! FEUrea*
*Cavernouis et al. FE urea in ARF.Kidney International Journal.Vol 16; 2223-2229: 2002
Specific Therapeutic interventions in ARF
• Diuretics
• Dopamine
Diuretics
• Loop diuretics alone or in combination with
thiazides are often used in an attempt to
convert oliguric ARF into non-oliguric ARF
• Does it make the recovery of renal function
faster?
• Does it improve mortality?
Diuretics
• Diuretics should continue to be used in an
attempt to ↑ UOP in oliguric pts ONLY after
careful correction of volume status
• Trial should be short in duration (good idea
of response can be obtained in 4 to 6 hrs)
• Must not cause delay in the institution of RRT
Renal-Dose Dopamine
• ↑ Renal blood flow
• Short-lived diuretic activity
• Does it improve mortality?
• Does it improve time to recovery of renal function?
• Need of Dialysis?
• Several studies have analyzed the use of renal dose
DA in the prevention & treatment of multiple clinical
conditions related to ARF
Renal-Dose Dopamine
• Randomized double-blind trial*
• 328 pts who had early RF in the setting of
SIRS
• DA had no effect on the:
• severity of RF (Cr 245 DA vs. 249 placebo)
• Need for dialysis (22% DA vs. 25% placebo)
• In-hospital mortality (43% DA vs. 40% placebo)
* Bellomo et al. Low-dose dopamine in pts with early renal dysfunction. ANZICS trial.
Lancet2000;356:2139-43.
Renal-Dose Dopamine
• Meta-analysis till 2000*
• 17 randomized trials
• 854 pts
• Had similar findings
*Kellum et al. Use of dopamine in ARF: a meta-analysis. Crit Care Med 2001;29:1526-31.
Renal dose Dopamine
• Renal-dose dopamine can be used as diuretic
agent in ARF if synergistic diuretic schemes
are needed
• But there is no support for its use in the Rx of
ARF
• Better to be avoided becoz of unpredictable
levels of plasma clearance between pts
Selected Issues in Electrolyte
disorders
• New causes & novel approaches to
hyponatremia
• Hypernatremia: Important balance in the
quality of ICU care
• K-Mg interactions in critical care
• Important aspects of hypophosphatemia to
the nephrologist
New Causes & Novel approaches to
Hyponatremia
•
Classic approach…
•
SIADH is the most common cause of hyponatremia in hospitalized
pts
•
SIADH:
•
1.
2.
3.
4.
Clinical euvolemia
↑Na urine >20
↑urinary osmolality >100
↓Na
Clinical exam has poor sensitivity & specifity in the setting of
hyponatremia when compared with the urine Na conc.*
* Chung et al. Clinical assessment of extracellular fluid volume in hyponatremia. Am J Med 1987; 83:905-8.
SIADH
•
Caused by multiple mechanisms in critically ill pts:
1.
2.
3.
4.
5.
6.
Malignancy – lung, brain
Primary brain disorders-hemorrhages
Lungs disorders- acute infections, respiratory failure
Postop pain & nausea
Hypotonic postop fluid replacement
Drugs
a)
b)
c)
d)
Vasopressin analogs – desmopressin, oxytocin
Enhance vasopressin release – opiates, TCA, carbamazepine
Potentiate renal vasopressin activity – cyclo, NSAIDs
Unkown mechanism – Haloperidol, SSRI
Treatment Hyponatremia
• Untreated severe hyponatremia is
marked by a risk of:
• Respiratory compromise
• Anoxic encephalopathy
• Frequent monitoring of serum Na is
essential to prevent overshoot
Hypernatremia: Important Balance
in the quality of ICU care
• 6% in pts in the ICU
• Development of ↑Na during ICU stay
associated with greater mortality 32% than
the presence of ↑Na on admission 20%*
• Development of ↑Na in critically ill pts
results from combination of lack of access to
water & excessive loss of hypotonic fluids
*Palvesky et al. Hypernatremia in hospitalized pts. Ann Intern Med 1996; 124:197-203.
Hypernatremia
Hypernatremia
• Evaluation of ↑Na is straightforward
• It is always associated with net state of water defeciency regardless of
extracellular volume status
• Aquapenia or Hypoaquemia!!
• Management is focused on the correction of possible underlying
mechansims & replacement of water losses
• We have to understand that replacement of previous & ongoing losses
is necessary to correct serum osmolality
*Polderman et al. Hypernatremia in the ICU: an indicator of quality of care? Crit Care Med 1999; 27:1105-8.
Value of the AG in the ICU
Value of AG in the ICU
•
Two valuable factors are often overlooked
in the assessment of the AG in the ICU
1.
Need to acount for the degree of
hypoalbuminemia → false underestimation of
the AG
•
2.
Figge formula: Adjusted AG = observed AG + [0.25 x
(4 – albumin)
Use of the measured not corrected serum Na
when calculating the AG in the setting of
hyperglycemia → overestimate the AG when
using corrected Na
K-Mg Interactions in critical care
• K & Mg defeciency are often coexistent
in critically ill pts why?!
• Causes of ↓K are also causes of ↓Mg
• Diarrhea
• Diuretics
• Post-ATN diuresis
• any state of aldesterone excess
K-Mg Interactions in critical care
• ↓Mg is cause of ↓K in its own how?!
• Current evidence suggests that Mg leads to
↓ATP activity → ↑ activity of ATP-inhibitable
luminal K channels*
• Only aggressive replacement of Mg will
allow successful K repletion
* Agus ZS. Hypomagnesemia. J Am Soc Nephrol 1999; 10:1616-22.
Important aspects of Hypophosphatemia
to the nephrologist
•
Can be caused by multiple mechanisms in the ICU:
1.
Transcellular shifts





2.
↓ Intestinal absorption


3.
4.
Respiratory alkalosis
Dextrose therapy
Insulin
Refeeding
Sepsis
Vit D defeciency
Antacids
Prolonged decreased intake
↑ renal losses




Osmotic diuresis
Glycosuria
Chronic alcoholism
hyperparathyroidism
Hypophsphatemia
• Severe hypophosphatemia promotes significant
morbidity in pts in the ICU
• Even moderate degrees of phosphate depletion leads
to impaired diaphragmatic contractility & impair
weaning from MV*
• Associated with impaired myocardial contractility#
*Aubier et al. Effect of hypophosphatemia on diaphragmatic contractility in pts with acute respiratory failure.
NEJM 1985; 313:420-4
#Vered et al. LV function in pts with chronic hypophosphatemia. Am Heart J 1984; 107:796-8.
“The practice of medicine is an art, not a trade; a
calling, not a business; a calling in which your heart
will be exercised equally with your head.”
William Osler