Transcript Metabolic Abnormalities - Rutgers New Jersey Medical School

Metabolic Abnormalities
Asha Bale, MD
Surgical Fundamentals Lecture #6
Overview
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Symptoms, Etiology, Treatment
Sodium
Potassium
Magnesium
Calcium
Glucose abnormalities
Arrhythmias
Hyponatremia Na<136
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Most Common causes are Iatrogenic or SIADH
Sx: CNS (increased ICP)
Sx usually don’t occur until Na<120
Causes:
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Na depletion (extracellular volume deficit)
Na dilution (Excess extracellular water)
Excess solute relative to free water (ie: hyperglycemia)
Pseudohyponatremia
Na depletion
• Decreased intake
– Low sodium diet
– Enteral feeds
• Loss of Na containing fluids
– GI losses (vomiting, NGT, diarrhea)
– Renal losses (diuretics or primary renal disease)
Na Dilution
• Excess extracellular water/Excess
extracellular volume
– Iatrogenic (IVF, free water)
– High ADH (increases reabsorption of free
water, causing increase in volume and hypoNa)
• SIADH- low serum Na, high Urine Na and U Osm
– Drugs causing water retention
• Antipsychotics, tricylcic antidepressants, ACE
inhibitors
Excess solute causing HypoNa
• Excess solute relative to free water can
cause hyponatremia
– Untreated hyperglycemia
• Glucose causes an osmotic force, shifting water
from the Intracellular compartment to the
Extracellular compartment (like dilutional hypoNa)
• For every 100mg/dl increase in Glu, plasma Na
decreased by 1.6
– Mannitol
Pseudohyponatremia
• Extreme elevations in plasma lipids and
proteins
• No true decrease in extracellular sodium
relative to water
Hyponatremia Algorithm
• Symptomatic or Asymptomatic?
• Asymptomatic
– Hypotonic (POsm<280)
• Hypervolemic- water restriction, diuresis
• Hypovolemic- isotonic saline
• Isovolemic- water restriction
– Isotonic (POsm 280-285, hyperlipidemia)
• Correct underlying disorder
– Hypertonic (POsm>280, hyperglycemia, hypertonic infusions like
mannitol)
• Correct underlying disorder
• Symptomatic (treat aggressively)
– 3% NaCl
– Don’t correct fast!
– Stop when Na 120-125
Treatment of Hyponatremia
• Water deficit(L) = (serumNa-140 / 140) x TBW
– TBW estimated as 50% of lean body mass in men and
40% in women
• Don’t correct faster than 1mEq/h and 12mEq/d, avoids
cerebral edema and herniation
• Frequent neurologic exams
Treatment of Hyponatremia
• Most cases- Free water restriction, if severeadminister sodium
• If Neuro Sx, then use 3% NS to increase Na
by no more than 1mEq/L per hour until Na
level reaches 130, or Neuro Sx are inproved
• Rapid correction causes pontine myelinosis,
seizures, death
Hypernatremia Na>144 mEq/L
• Caused by loss of water or a gain in Na in excess
of water (hypervolemic, isovolemic, hypovolemic)
• Can be assoc with increased, normal or decreased
extracellular volume
• Water shifts from ICF to ECF, causing cellular
dehydration
• Sx (neurologic): restlessness, irritability, seizures,
coma, death
Hypervolemic Hypernatremia
(Gain of water and salt)
• Iatrogenic
– Administration of Na containing fluids, including Na
bicarb
• Mineralocorticoid excess
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U Na>20meq/L, Uosm>300mOsm/L
Hyperaldosteronism
Cushing’s Syndrome
Congenital Adrenal Hyperplasia
Normovolemic Hypernatremia
(Loss of water)
• Nonrenal Causes of water loss
– GI
– Skin
• Renal Causes of water loss
– Diabetes Insipidus
– Diuretics
– Renal Disease
Hypovolemic Hypernatremia
(Loss of water and salt)
• Renal water loss
– DI (Low ADH) (high Serum Na, dilute urine, low U Na
and U Osm)
– Osmotic diuretics
– Adrenal failure
– Renal tubular diseases (UNa<20, UOsm<300-400)
• Nonrenal water loss (GI, Skin)
– UNa<15, UOsm >400)
Hypernatremia Algorithm
• History, physical, electrolytes, BUN/Creatinine, Urine Na,
UOsmolarity
• Assess extracellular volume status
– Hypovolemic (Loss of water and Na)
• Restore extracellular volume, calculate water deficit
• Isotonic saline until euvolemic, then hypotonic saline or D5W to correct
HyperNa
– Isovolemic (Loss of water)
• D5W IV or water p.o.
• Diabetes Insipidus- Vasopressin
– Hypervolemic (Gain of Na and water)
• Lasix and D5W or D51/4 NS
• If renal failure dialysis
Hyperkalemia
• Normal K = 3.5 to 5.0 meq/L
• History, physical, EKG, chemistry, ABG
• Sx: GI (n/v, diarrhea), neuromuscular (weakness),
cardiovascular (EKG changes, arrhythmias)
• EKG changes
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Peaked t waves
Flattened p wave
Prolonged PR interval
Widened QRS complex
Sine wave formation
V-fib
Hyperkalemia EKG
Peaked t waves
Flattened p wave
Prolonged PR interval
Widened QRS complex
Sine wave formation
V-fib
Hyperkalemia
• Excess Potassium Intake
– Oral, iv, blood transfusion
• Increased Release of K+ from cells
– Cell destruction/breakdown
– Hemolysis, rhabdomyolysis, crush injuries, gi
hemorrhage, acidosis
• Impaired excretion by kidneys
– Meds: K+ sparing diuretics, ACE Inhibitors, NSAIDs
– Renal Insufficiency, Renal Failure
Treatment of Hyperkalemia
• Reduce total body K
– Stop exogenous sources of K+
– Kayexalate
• (Cation-exchange resin, binds K in exchange for Na)
• PO or PR
– Dialysis
• Shift K from extracellular to intracellular
– Glucose/Insulin, bicarbonate
– Albuterol
• Protect cells from effects of increased K
– When EKG changes present, use Calcium chloride or calcium
gluconate (5-10mL of 10% solution)
• Use cautiously in patients on Digoxin- can cause Dig toxicity
Hyperkalemia Algorithm
• History, PE, EKG, Chemistry, ABG
• K+<6.5, no EKG changes
– Stop supplemental K+ and repeat K+
• K+<6.5, EKG changes
– Stop K+, Kayexalate or Lasix, look for underlying cause
• K+>6.5 or EKG changes
– Calcium gluconate, Glucose & Insulin, NaHCO3, Kayexalate,
Lasix, Dialysis
Hypokalemia
• K+<3.5 mg/L
• Sx
– Ileus, constipation
– Weakness, fatigue
– Cardiovascular
• EKG changes: u waves,
t wave flattening, ST
segment changes,
arrhythmias
Etiology-Hypokalemia
• Inadequate intake
– Dietary, K+ free IVF, TPN with inadequate K+
• Excessive Renal Excretion
– Hyperaldosteronism (waste K+)
– Meds
• Diuretics which increase K+ excretion
• Penicillin (promotes renal tubular loss of K+)
• Loss in GI Secretions
– Diarrhea, vomitting, high NGT outputs
Etiology- Hypokalemia
• Intracellular shifts
– Metabolic Alkalosis
• K+ decreases by 0.3 meq/L for every 0.1 increase in pH above
normal
– Insulin therapy
• Drugs causing Magnesium depletion will cause
K+ depletion as well
– Amphotericin, aminoglycosides, foscarnet, cisplatin
– Replace Magnesium!
Treatment of Hypokalemia
• Check K+, electrolytes, renal function and urine output
• Estimate for every 10 meQ K+ replaced, the serum
potassium will increase by 0.1 mg/L
• Potassium repletion
• Oral (functioning GI tract, & mild, asymptomatic patients)
– KCl, K-dur
• IV (Nonfunctioning GI tract, or severe hypokalemia)
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No more than 20meq/H in an unmonitored setting
Can be up to 40meq/h replacement in monitored setting
Caution in patients with impaired renal function
Repeat K+ levels
KCl, KPhos
Magnesium Abnormalities
• Magnesium found in the intracellular
compartment
• Of that found in the extracellular space, 1/3
is bound to albumin
• Normal 1.3 to 2.1 meQ/L
Hypermagnesemia Mg >2.2 mEq/L
• Rare
• Impaired renal function, excess intake with TPN,
Excess use of laxatives or antacids
• Sx: n/v, weakness, lethargy, hypotension
• EKG changes: (similar to hyperkalemia)
– Increase PR interval, widened QRS complex, elevated
t-waves
• Tx: Ca 100-200mg IV over 5-10 mins., Dialysis,
Remove Magnesium source
Hypomagnesemia
• Renal excretion
– Alcoholism, diuretics, amphotericin B
• GI Losses
– Diarrhea, malabsorption, acute pancreatitis,
DKA, primary hyperaldosteronism
• Poor p.o. intake
– Starvation, alcoholism, prolonged use of IVF,
TPN
HypoMagnesemia
• Sx: neuromuscular and CNS hyperactivity,
tremors, delerium, seizures
• Sx similar to hypercalcemia
• Associated with hypokalemia
• EKG:
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Prolonged QT and PR intervals
ST segment depression
Flattened or inversion of p waves
Torsades de pointes
arrythmias
Torsades de Pointeshypomagnesemia
Treatment of Hypomagnesemia
• Oral replacement if mild or asymptomatic
– Magnesium Oxide
• IV replacement if severe (<1.0 mEq/L) or
symptomatic
– 2g Magnesium sulfate IV over 5 minutes followed by
10g during the next 24 hours (if renal function is
normal)
• If Torsades, give over 2 mins.
• Also correct hypocalcemia, frequently associated
Hypercalcemia
Ca>10.5
• Serum Ca above normal range of 8.5 to 10.5
mEq/L, or an increase in the ionized
calcium level above 4.2 to 4.8 mg/dL
• Primary hyperparathyroidism (outpatient)
• Malignancy (inpatient)
• Sx: Neuro (confusion, depression), Musc
(weakness, back pain), gi (n/v/ abd pain),
cardiac, EKG changes
Hypocalcemia prolongs the QT interval by stretching out the ST segment.
Hypercalcemia decreases the QT interval by shortening the ST segment so that the T wave
seems to take off from the QRS complex
Treatment of Hypercalcemia
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Most cases due to malignancy, if not check PTH level
– PTH high hyperparathyroidism
– PTH normal or low w/u for malignancy
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Treatment is supportive, treat underlying cause
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Tx when symptomatic (Hypercalcemic crisis)(serum level >12mg/dL)
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Replete volume deficit, then brisk diuresis with normal saline and Lasix
– 1-2L NS over 1-2h, followed by 200-400mL/h with Lasix 20-80mg IV over 2-3h
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Etidronate, phosphate, mithramycin, steroids, calcitonin, Dialysis
Hypocalcemia
• Etiologies: pancreatitis, massive soft tissue infections,
renal failure, pancreatic and SB fistulas,
hypoparathyroidism, Magnesium abnormalities, tumor
lysis syndrome
• Transiently after removal of a parathyroid adenoma
• Malignancies assoc w/ increased osteoclastic activity
• Massive blood transfusions (precipitation with citrate)
• Sx: parasthesias, muscle cramps, stridor, tetany, seizures
Treatment of hypocalcemia
• Check albumin, check for abnormalities of Phos and Mag
• Asymptomatic- give po or iv
• Chronic
– Add Calcium to IVF
– Calcium p.o. (1500 to 3000mg per day, plus vitamin D)
• Acute symptomatic:
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Need to give 200 to 300mg of Calcium
20-30mL 10% Ca Gluconate OR
5-10mL 10%CaChloride
Give slowly over several minutes
Can worsen HTN or Dig toxicity
Correct associated deficits in magnesium, potassium and pH
Hyperphosphatemia
Serum Phos >5mg/dL
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Normal 2.7 to 4.5 mg/dL
Mostly seen in pt with renal failure
Hypoparathyroidism
Tx
– Chronic- Low Phos diet, aluminum binding
antacids
– Acute- Dialysis
Hypophosphatemia
• Decreased intake
• Intracellular shift of phosphorus
– alkalosis, insulin therapy
• Increased phosphorus excretion
• Sx: muscle weakness (important for vent
dependent pts)
• PO- Nutraphos
• IV- NaPhos, KPhos
Arrhythmias
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Ask Desk Clerk to CALL Senior Resident and/or Attending!
Symptomatic or Asymptomatic?
ABC’s
Code Cart into room, call Anesthesia if needed
Vital signs, O2 Sat
Quick History/Physical Exam
EKG/Rhythm strip- Recognize the Arrhythmia
Place on a monitor, Supplemental Oxygen
ACLS Protocol- Stabilize Patient
ABG or ABE, electrolytes, cardiac enzymes
Treat Underlying Cause
Arrhythmia
Arrhythmia
Arrhythmia= A-Fib
Arrhythmia
Arrhythmia = SVT
Arrhythmia
Arrhythmia= V-Tach
Arrhythmia
Arrhythmia