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Metabolic Abnormalities. Surgical Fundamentals Lecture Asha Bale, MD 8/06/10. Overview. Symptoms, Etiology, Treatment Sodium Potassium Magnesium Calcium Glucose abnormalities Arrhythmias. Hyponatremia Na
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Metabolic Abnormalities
Surgical Fundamentals Lecture
Asha Bale, MD
8/06/10
Overview
• Symptoms, Etiology, Treatment
• Sodium
• Potassium
• Magnesium
• Calcium
• Glucose abnormalities
• Arrhythmias
Hyponatremia Na<136
• Most Common causes are Iatrogenic or SIADH• Sx: CNS (increased ICP)• Sx usually don’t occur until Na<120• Causes:
– 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 (vomitting, 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 severe- administer 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– 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
– Peaked t waves– Flattened p wave– Prolonged PR interval– Widened QRS complex– Sine wave formation– V-fib
Hyperkalemia EKG Peaked t waves
Flattened p waveProlonged PR interval
Widened QRS complexSine 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, vomiting, 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)
– 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:
– Prolonged QT and PR intervals– ST segment depression– Flattened or inversion of p waves– Torsades de pointes– arrhythmias
Torsades de Pointes- hypomagnesemia
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
• Most cases due to malignancy, if not check PTH level– PTH high hyperparathyroidism– PTH normal or low w/u for malignancy
• Treatment is supportive, treat underlying cause
• Tx when symptomatic (Hypercalcemic crisis) (serum level >12mg/dL)
• 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
• 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:– Need to give 200 to 300mg of Calcium– 20-30mL 10% Ca Gluconate OR– 5-10mL 10% Ca Chloride– Give slowly over several minutes– Can worsen HTN or Dig toxicity– Correct associated deficits in magnesium, potassium and pH
HyperphosphatemiaSerum Phos >5mg/dL
• 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
Hypophsphatemia
• 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
Arrythmias
• 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
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