Transcript Renal Emergencies: Fluids and Electrolytes

Caroline Straatmann, MD
¼ Plasma
(Intravascular)
1/3 ECF
¾ Interstitial
Fluid
0.6 x weight
2/3 ICF
Intracellular (mEq/L)
Extracellular (mEq/L)
Na
20
135-145
K
150
3-5
____
Cl
98-110
HCO₃
10
20-25
PO₄
110-115
5
Protein
75
10
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A 12 year old boy with chronic renal
insufficiency secondary to obstructive
uropathy is admitted for pancreatitis. He
cannot tolerate enteral feeds and is on
TPN. He complains of his legs feeling
weak. Labs show
144
7.4
120
15
60
4.7
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What do you do first?
EKG
EKG shows peaked T waves
What do you do next?
Give calcium gluconate
Stop his TPN, which has K in it!
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In addition to this treatment, which one of
the following would be the most effective
therapy for his hyperkalemia?
 Subcutaneous insulin and slow infusion of
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glucose
Intravenous beta – 2 agonist
Intravenous insulin
Intravenous sodium bicarbonate
Oral sodium polystyrene sulfonate
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Growing child requires 1-2 mEq/kg/day
 Avoid potassium deficiency
 Cellular growth
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Serum potassium concentration does not
reflect total body potassium content
 Ex: Diabetic ketoacidosis
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Disturbance in serum K⁺ can affect cell
membrane resting potential
 Muscle paralysis
 Ventricular arrhythmias
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Serum K >5 mmol/L (5 meq/L)
Kidney failure is the leading cause
Can be life-threatening due to risk of
ventricular arrhythmias
Normal renal response to hyperkalemia
 Stimulate aldosterone secretion which then
stimulates urinary potassium excretion
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Symptoms
 Skeletal muscle weakness
 Paralysis
 Parasthesias
 Respiratory failure
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Decreased renal excretion
 Reduced GFR
 Reduced tubular secretion
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Increased intake
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Transcellular shifts
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Common Drugs
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 Metabolic acidosis
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 Tumor Lysis Syndrome
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 Rhabdomyolysis
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Aldosterone deficiency or
resistance
Amiloride
Spironolactone
Cyclosporine/Tacrolimus
Heparin
ACE inhibitors/ARBs
Pentamidine
TrimethoprimSulfamethoxazole
3 Na
ECF
ICF
Na= 150 mmol/L
K=4 mmol/L
Na= 10 mmol/L
K=140 mmol/L
2K
Reason for K to have shifted outside the cells?
K shift to outside the cell after the blood was collected?
 Hemolysis
 Tissue hypoxia distal to tourniquet
 Heel stick
 Are the kidneys excreting K appropriately?
 GFR
 Drugs
 Aldosterone
 Excessive dietary K intake contributing to the problem?
 IVFs and TPN!!!
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Repeat serum K
EKG stat
If EKG shows changes, start treatment
immediately
 Progression of changes
 Peaked T waves-Prolonged PR interval-ST
depression-Widened QRS-Ventricular
fibrillation
 Peaked T waves
 Loss of P wave
 Widening of QRS
 ST depression
 Prolonged PR interval
 Ventricular
dysrhythmias
 Cardiac arrest
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Eliminate source of potassium intake or
offending drugs
K⁺ < 6 mEq/L
 Low potassium diet
 Diuretics
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K⁺ > 6 mEq/L
 Cation exchange resin: SPS
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EKG changes = EMERGENCY
Stabilize myocardium
 IV calcium chloride or calcium gluconate (10%)
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Shift potassium into cells
 Beta agonists, insulin/glucose, sodium
bicarbonate
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Remove excess potassium from the body
 Sodium polystyrene sulfonate (SPS)
 Furosemide
 Hemodialysis
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Weakness or paralysis
Ileus
Cardiac dysrhythmias
 Delayed depolarization
 Flat/absent T waves
 U waves
U WAVES
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BMP
 Hypernatremia
 Alkalosis
 Bartter’s
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Renin
Aldosterone
Cortisol
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If > 2.0 mEq/L and no EKG changes, treat orally
with KCl, minimum 2 mEq/kg/day
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If < 2.0 and/or EKG changes, treat intravenously,
with KCl 40 mEq/L into IV fluids
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“Potassium runs”: not recommended unless
cardiac/ICU patient
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Monitor potassium values until normal value is
established
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A 7 yo male with cystic fibrosis and
obstructive lung disease is admitted for a 2
week h/o progressive lethargy. He is
obtunded.
Labs: Na=105, K=4, Cl=72, HCO3=21
Plasma osmolality= 222mOsm/kg H20
Urine osmolality= 604 mOsm/kg H20
Urine Na= 78 mEq/L
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What is the most likely diagnosis?
 Pseudohyponatremia
 SIADH
 Psychogenic polydipsia
 Hypoaldosteronism
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How would you raise the plasma sodium
concentration?
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Normal=280-295 mOsm/kg
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Osmotic equilibrium tightly regulated
between ECF and ICF compartments
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Water moves between compartments in
response to alterations in osmolality of
either compartment
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2 [Na⁺] + [BUN] + [Glucose]
2.8
18
• Serum osmolality is tightly regulated
• Sodium is the major determinant of serum
osmolality
• Sodium balance is regulated by the kidney
• Serum sodium does not reflect total body
sodium content
• Na requirements in growing child
• 2-3 mEq/kg/day
Drawn from an indwelling catheter
Hyperlipidemia
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Normal plasma Osm
Hyperglycemia
 Drives water into extracellular space, diluting
the Na concentration
▪ Plasma osm will be high
▪ Na decreases 1.6 mEq/L for each 100 mg/dL rise in
glucose
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Serum Na < 130 mEq/L
Loss of sodium
Gain of water
Most common cause is intravascular
volume depletion from gastroenteritis
 After volume expansion, will be able to regulate
free water excretion
Lose more salt relative to water but still
hypovolemic
 Hyponatremic dehydration
 GI losses (prolonged AGE/hypotonic intake)
 Renal losses
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 Chronic diuretic therapy
 Salt wasting nephropathy
 Adrenal insufficiency
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Skin losses
 Cystic fibrosis (hyponatremic/hypochloremic)
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Hypervolemia
Fluid overload
 Congestive heart failure
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Water intoxication
 Diluted formula
 Hypotonic fluids
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SIADH
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History and Physical
 Determine volume status
 Estimate sodium intake and output
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If hypovolemic:
 Renal or Extrarenal losses?
 Urine Na⁺
 Does kidney respond appropriately to
hypovolemia?
 Urine specific gravity
 Urine osmolality
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Correct underlying cause
 Hyponatremic dehydration
 SIADH
▪ Fluid restriction (insensible water losses) until Na levels normalize
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Rate of correction depends on how quickly it developed
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Acute hyponatremia is more dangerous
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Increased risk of herniation or apnea from increased ICP from rapid,
unbalanced water movement into brain cells
In general, correction with hypertonic saline in
unnecessary unless there are neurological
manifestations of hyponatremia
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Sodium deficit (mEq) = Fluid deficit (L) X
0.6 X [Na⁺] in ECF (mEq/L) PLUS
 Excess sodium deficit =
(Desired Na⁺ - Actual Na⁺) X (0.6 L/kg) X Wt (kg)
 Desired Na⁺ is 135 mEq/L
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Maintenance and ongoing losses
Replace over 24 hours
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As sOsm falls, water moves into cells, and risk of
cerebral edema
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If severe (<120 mEq/L), may observe seizures,
altered mental status, vomiting
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For Na⁺ < 120 mEq/L, raise Na⁺ to 125 mEq/L by
giving 3% saline
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Rapid correction of hyponatremia : central
pontine myelinolysis
EARLY
ADVANCED
Headache
 Nausea and vomiting
 Lethargy
 Weakness
 Confusion
 Altered consciousness
 Agitation
 Gait disturbances
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Seizures
 Coma
 Apnea
 Pulmonary edema
 Decorticate posturing
 Dilated pupils
 Anisocoria
 Papilledema
 Cardiac arrhythmias
 Central diabetes insipidus
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2 ml/kg bolus of 3% NaCl, max 100 ml over
10 min
Repeat 1-2 times until symptoms improve
Goal of correction is 5-6 mEq/L in first 1-2
hours
Recheck sNa q 2 hours
Moritz et al. Pediatr Nephrol (2010) 25:
1225-1238
Insufficient Correction
Cerebral Edema
Too aggressive Correction
Demyelination
•Acute hyponatremia=Most dangerous
•Symptomatic hyponatremia = Medical Emergency
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A 9 yr old boy who has cerebral palsy is admitted to
CHNOLA following 4 days of diarrhea. His initial
serum Na level is 174mEq/L. Once circulatory
volume is restored, the primary focus of the fluid
management must be to provide appropriate
amounts of:
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Chloride
Free water
Glucose
Phosphate
Potassium
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Serum sodium >150 mEq/L
Always abnormal and should be evaluated
Free water deficit
Increased sodium intake/retention
Increased serum Osm
Does not imply total body sodium overload
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Rarely develops in those who have access
to free water
Most often from inability to access free
water
At risk
 Ineffective breastfeeding
 Critically ill patients
 Infants
 Neurologically impaired
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Children who have hypernatremic
dehydration often appear minimally
dehydrated on exam. This is due to
maintenance of:
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Extracellular fluid volume
Intracellular fluid volume
Total body glucose
Total body sodium concentration
Total body water balance
Water Deficit
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Renal loss
 Diuretic use
 Nephropathy with renal concentrating defect
 Diabetes insipidus
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Extrarenal loss
 Vomiting/Diarrhea
 Skin losses
Increased Sodium Intake/Retention
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Salt poisoning
Exogenous sodium
 Hypertonic feeding/saline
 NaHCO3 administration
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Mineralcorticoid excess
Hyperaldosteronism
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Determine volume status
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Blood pressure
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Renal water loss
 Kidney does not appropriately respond to hypovolemia
 Low urine s.g and osmolality
 High urine Na⁺
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Extrarenal water loss
 Kidney responds appropriately to hypovolemia
 High urine s.g.
 Low urine Na⁺
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Treat cause
Correct volume disturbance if present
Replace free water deficit
 4mL/kg x (desired change in serum Na (mEq/L))
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Risk of cerebral edema from rapid
correction
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Stones
 Renal calculi
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Bones
 Bone pain
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Moans
 Depression
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Groans
 Constipation
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Symptoms
 Weakness, irritability, abdominal cramping, n/v,
polyuria, polydipsia, renal stones, pancreatitis,
shortened QT interval
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Differential diagnosis
 Hyperparathyroidism, excessive calcium intake,
malignancy, thiazides, prolonged
immobilization, sarcoidosis
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Most hypercalcemic patients are also volume
depleted
Hydration to increase UOP and Ca excretion
 NS with potassium at 2-3x maintenance if renal
function and BP allow
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Forced diuresis
 Furosemide
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Calcitonin
Bisphosphonates
Dialysis
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A 18 month old with ESRD secondary to renal
dysplasia on chronic peritoneal dialysis has a
serum Mg of 3.2. He is asymptomatic. All
other values are normal except his BUN/Cr.
What is your next step in management?
 Change to hemodialysis
 Increase phosphate binders
 Increase vitamin D
 Continue peritoneal dialysis
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Etiologies
 Renal failure
▪ Common in CKD due to decreased
excretion
▪ Levels in AKI parallel potassium and are
derived from the intracellular pool
▪ Rapid cell lysis
 Excessive administration
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Symptoms
 Decreased DTRs, lethargy, confusion
 Hypocalcemia (hypermagnesemia suppresses
PTH)
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Rarely of clinical significance
Treatment
 Stop supplemental Mg
 Diuresis
 Dialysis
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You are called to the floor at 2 am to see a
16 yo orthopedic post-op patient because
his BP is 160/100
What do you do?
A 5 yo boy is brought to the ER because of
new-onset generalized seizure which has
subsided by the time he arrives. He is
postictal with BP of 160/100.
What do you do?
Is this HTN urgency or emergency?
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HTN Emergency is elevated SBP and DBP
with acute end-organ damage
 Stroke (ischemic/hemorrhagic)
 Pulmonary edema
 HTN encephalopathy
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HTN urgency does not have end organ
damage.
 HA, Nausea, Blurred vision
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In children, 75% of cases of HTN emergency
will be secondary to renal or renovascular
causes
What do you need to do before treatment?
Rule out increased ICP as etiology of HTN
Get plasma renin activity level
If the patient is bleeding or coagulopathic,
treat the elevated BP urgently
 Worry about hemorrhagic stroke
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ICU
Don’t lower BP too rapidly
 Lower no more than 20-25% in 1st 8 hours
 Preserve cerebral perfusion
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Acute goal is a mildly elevated BP
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A 5 yo boy is brought to the ER because of
new-onset generalized seizure which has
subsided by the time he arrives. He is
postictal with BP of 160/100.
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What would you start?
What would be your immediate BP goal?
Goal around 130/85 (20% reduction)
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Nitroprusside
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Arterial and venous vasodilator
Very short-acting
Easily titrated
Cyanide toxicity
Don’t use in renal or liver failure
IV Calcium channel blockers
 Nicardipine
 Can cause increased ICP
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IV Labetalol
 Alpha and beta blocker: decreases peripheral
vascular resistance
 Continuous or intermittent dosing
 Do not use in asthmatics, lung disease, CHF,
diabetics
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IV Enalapril (Enalaprilat)
IV hydralazine
 Potent arterial vasodilator
 Infants
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You are called to the floor for a 8 yo child
with PIGN who is seizing. His BP is 155/98
What do you do for immediate treatment?
IV labetalol bolus dose
Transfer to PICU for nicardipine or labetalol
infusion
Goal is to decrease his BP by 20-25% in first
8 hours
What other therapy might be helpful?
Lasix- PIGN is assoc with volume overload
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Severe asymptomatic HTN
 May have headache
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Most commonly due to non-adherence or
ingestion of large amounts of salt
Reduce BP over several hours to days
Oral medications
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Oral medications
 Nifedipine
▪ Short-acting- see effects in 15-20 min
▪ 0.25 mg/kg initial dose
▪ 10 mg capsules
 Isradipine
▪ Short-acting: effects within one hour
▪ 0.05-1 mg/kg/dose
 Labetalol
▪ Heart rate is dose limiting factor