Mellss yr4 anaest icu management
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Transcript of Mellss yr4 anaest icu management
Renal disorders
Electrolytes disorder
Hypo and hypernatremia
Hypo and hyper kalemia
Hypo and hyper magnesimea
Hypo and hyper phosphatemia
Hypo and hyper calcemia
CONTENTS
Renal dysfunction that occurs in critically i l l patients
Statistics of ICU patients:
70% have some degree of renal dysfunction
5% require renal replacement
Mortality rate of patients who require hemodialysis 50–70%
Diagnostic criteria :
RIFLE criteria
AKIN criteria
ACUTE KIDNEY INJURY
Acute Dialysis QualityInitiative (ADQI) in 2002.
5 categories consist of:
3 severity
2 clinical outcome
Limitations:i. No defined e period for change
in serum creatinine
ii. Minimum change in serum creatinine required for the diagnosis of AKI is considered too large.
I. RIFLE CRITERIA
Revised criteria by Acute Kidney Injury Network (AKIN)
which have:
a smaller change in creatinine (≥0.3 mg/dL)
a time limit of 48 hours on the change in serum creatinine.
II. AKIN CRITERIA
Based on location of the insult:Prerenal disorders (30–40% )
Decrease in renal blood flow
Renal disorders Acute Tubular Necrosis (50%)
Result of renal hypoperfusion, inflammatory injury in epithelial lining tubules by tubuloglomerular feedback
Severe sepsis and septic shock, radiocontrast dye, nephrotoxic drugs
Acute Interstitial Nephritis
Inflammatory injury in the renal interstitium
Postrenal obstruction(10% ) Obstruction distal to the renal
parenchyma
Distal portion of the renal collecting ducts (papillary necrosis),
The ureters (extraluminal obstruction from a retroperitoneal mass),
Urethra (strictures)
CATEGORIES OF ACUTE KIDNEY INJURY
Sepsis (50%)
Major surgery, particularly cardiopulmonary bypass
Major trauma victims (30%)
Rhabdomyolysis (30% )
Nephrotoxic drugs and radiocontrast (20% )
Increased abdominal pressure
COMMON CAUSES
USG (postrenal obstruction)
To determine prerenal disorder or renal disorder
EVALUATION
Volume infusion to promote
renal blood flow
Fluid challenge when prerenal
causes is ruled out
Discontinuing any
nephrotoxic drugs
LIST OF NEPHROTOXIC
DRUGS
Treating any conditions that
predispose to AKI
Examples:
Contrast- induced renal injury: IV
hydration, high-dose N-
acetylcysteine
AIN : re-solves spontaneously
after discontinueing offending
INITIAL MANAGEMENT
70% of patients with acute renal failure will require some form of renal replacement
therapy (RRT).
Indications :
a) Volume overload
b) Life threatening hyperkalemia or metabolic acidosis
c) Removal of toxins
RENAL REPLACEMENT THERAPY
Hemodialysis
Diffusion
Countercurrent exchangetechnique
Advantages:
Rapid clearance of small solutes.
Disavantages
Limited removal of large molecules
Risk of hypotension as need to maintain a blood flow of 200–300 ml/min through the dialysis chamber
Hemofiltration
TECHNIQUES
Convection
Continuous arteriovenous
hemofiltration (CAVH) or continuous
venovenous hemofiltration (CVVH)
Advantages
Allows more gradual fluid removal
Removes larger molecules than
hemodialysis
Disadvantage
Slow solute removal
25% of ICU patients.
Can be due to :
Loss of sodium and water ( hypotonic fluid loss)
Free water loss
Gain of sodium and free water (gain of hypertonic fluid)
Causes increase in the effective osmolality of the extracellular fluid (hypertonicity)
HYPERNATREMIC ENCEPHALOPATHY
Mechanisms : shrinkage of neuronal cell bodies and osmotic demyelination
Mortality rate as high as 50% (9)
1.HYPERNATREMIA
<135 mEq/L
in 40–50% of ICU patients.
Condition can present as :
Hypotonic
Isotonic
Eg.Pseudohyponatremia
(plasma lipid level > 1,500 mg/dL or the plasma protein levels >12–15 g/dL)
Hypertonic
Eg.Non ketotic hypergycemia
2.HYPONATREMIA
PREDISPOSING FACTORS
Pharmacotherapy to
be considered:
Demelocycline
Vasopressin antagonist
Conivaptan
Tolvaptan
Distribution Sodium-potassium exchange pump 3:2 ratio
Total body potassium: 50–55 meq per kg body weight
98% intracellular (350meq)
2% extracellular (70 meq)
0.4% plasma (15meq)
Excretion Stool (5–10 mEq/day)
Sweat (0–10 mEq/day)
Urine (40–120mEq/day)
POTASSIUM
Serum K+ <3.5 meq/L
Can be due to : Transcellular shift
Β2 adrenergic receptors stimulation,
alkalosis, hypothermia, insulin.
Potassium depletion
3. HYPOKALEMIA
Clinical features
Asymptomatic
Severe (<2.5 meq/L)
Muscle weakness
ECG abnormalities
Prominent U waves ,
Flattening and inversion of T waves,
QT interval prolongation
Management
Eliminate any condition that
promotes transcellular potassium
shifts
If due to K+ depletion :
20 mEq of K+ and 100 mL of
isotonic saline IV, infuse over 1 hour
at maximum rate of 20 mEq/hr
Serum K+ >5.5 mEq/L,
Can be the result of :
Potassium release from cells (transcellular shift)
High urine K+ (>30 meq/L)
Acidosis, rhabdomyolysis, tumor lysis syndrome,
Impaired renal excretion of potassium
Low urine K+ (<30 meq/L)
4.HYPERKALEMIA
Heart block and cardiac arrest.
ECG changes
Appear at 7 meq/L
Tall T wave , P wave amplitude
decreases, PR interval lengthens
P waves disappear and the QRS
complex widens.
Ventricular fibrillation
CLINICAL CONSEQUENCES
Hemodialysis
release of energy from ATP
functioning of the Na+-K+
exchange pump
regulates the movement of
calcium into smooth muscle
cells
MAGNESIUM
67% ionized (active) form,
19% bound to plasma proteins
14% chelated with divalent anions such as phosphate and sulfate
65% of patients in ICU’s
5.HYPOMAGNESIMEA
b
5% of hospitalized patients.
Predisposing factors :
Renal insufficiency
Hemolysis
Other conditions like diabetic
ketoacidosis (transient), adrenal
insufficiency, hyperparathyroid-
ism
Clinical features
6. MAGNESIUM EXCESS
Hemodialysis .
Intravenous calcium gluconate (1 g IV over 2 to 3 minutes)
to antagonize the cardiovascular effects of hypermagnesemia temporarily
MANAGEMENT
In blood coagulation, neuromuscular transmission, and smooth muscle contraction
Most abundant electrolyte in the human body with 99% bone
In the soft tissues, 10,000 times more concentrated than in the extracellular fluids
Plasma calcium in: Ionized (biologically active)
Complexed (biologically inactive)
80% bound to albumin,
20% to plasma anions such as proteins and sulfates.
CALCIUM
causes
7. HYPOCALCEMIA
Major consequences :
enhanced cardiac and neuromuscular excitability,
reduced contractile force in cardiac muscle and vascular smooth muscle.
Neuromuscular
tetany ,hyperreflexia, paresthesias, and seizures
Cardiovascular
hypotension, decreased cardiac output, and ventricular ectopic activity.
CLINICAL MANIFESTATIONS
Dosing Regimen
bolus 200 mg elemental calcium (diluted in 100 mL isotonic saline and given over 5–10
minutes)
continuous infusion at a rate of 1–2 mg/kg/hr (elemental calcium) for at least 6 hours.
Maintenance Therapy
Daily dose of calcium is 2–4 g in adults
Oral calcium carbonate or calcium gluconate tablets
MANAGEMENT
Clinical Manifestations
Gastrointestinal: nausea, vomiting, constipation, ileus, and pancreatitis
Cardiovascular: hypovolemia, hypotension, and shortened QT interval
Renal: polyuria and nephrocalcinosis
Neurologic: confusion and depressed consciousness, including coma
evident when total serum calcium is >12 mg/dL and almost always present when
the serum calcium is >14 mg/dL
8.HYPERCALCEMIA
serum PO4 <2.5 mg/dL or <0.8 mmol/L
Can be the result of
an intracellular shift of phosphorus
an increase in the renal excretion of phosphorus
a decrease in phosphorus absorption from the GI tract.
Predisposing factors : Glucose loading, prolonged hyperglycemia, respiratory alkalosis,
beta-receptor agonist
9.HYPOPHOSPHATEMIA
Energy Metabolism
Cardiac Output: impair myocardial contractility and reduce cardiac output.
Erythrocytes: hemolytic anemia
Oxyhemoglobin Dissociation: shifts the oxyhemoglobin dissociation curve to the left
Energy Availability: impeding the production of high-energy phosphate compounds (ATP).
Muscle Weakness
CLINICAL MANIFESTATIONS
Phosphate Replacement
Recommended for all
patients with
Severe hypophosphatemia
Hypophosphatemia of any
degree who also have
cardiac dysfunction,
respiratory failure, muscle
weakness, or impaired
tissue oxygenation.
Daily maintenance
therapy
1,200 mg if given orally
IV at 800 mg/day,
MANAGEMENT
Result of impaired PO4
excretion from renal
insufficiency, or PO 4
release from disrupted cells
(e.G., Rhabdomyolysis or
tumor lysis).
Clinical manifestations
The formation of insoluble
calcium–phosphate complexes
(with deposition into soft
tissues),
Acute hypocalcemia (with
tetany)
Management
There are two approaches to
hyperphosphatemia.
promote PO4 binding in the upper
GI tract, which can lower serum
PO4 levels :
Sucralfate or aluminum-containing
antacids can be used for this purpose.
Enhance PO4 clearance with
hemodialysis.
for patients with renal failure
10.HYPERPHOSPHATEMIA
REFERENCE