Metabolic Abnormalities

Asha Bale, MD

Surgical Fundamentals Lecture #6

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 (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 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, 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)

– 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– arrythmias

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%CaChloride– 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

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

• 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