Fluid and Electrolyte Management

WU Xing,MBBS,MMed,Associate Professor, Affiliated Hospital of Hainan Medical College

The recognition and management of fluid, electrolyte, and related acidbase problems are common challenges on the surgical service.
Lawrence, Essentials of General Surgery

Goals
Introduce concept of total body fluids Introduce types of crystalloids Intrduce electrolytes disturbances & their

treatment strategies.

Body Fluids
Intercellular Intravascular Interstitial

40%
4%

Body Water = 60% of a patients body weight

Fluid Requirements
typically 35 mL/kg/day insensible loss = 700 mL/day or 0.2

cc/kg/day for every 1 C > 37 1-10 kg = 100 mL/kg/day {4mL/kg/hr} 11-20 kg = 50 mL/kg/day {2mL/kg/hr} > 21 kg = 20 mL/kg/day {1mL/kg/hr}
Trick for hourly maintenance = 40 + weight (kg)

Serum Values of Electrolytes

Cations
Sodium Potassium Calcium Magnesium Concentration, mEq/L 135 - 145 3.5 - 4.5 4.0 - 5.5 1.5 - 2.5 95 - 105 24 - 30 2.5 - 4.5

Anions
Chloride CO2 Phosphate

Electrolyte in body fluid

ECF: Na+Cl- HCO3-, mainly

maintained by Na+.
ICF: K + Mg2 + HPO42-

Pr-,

mainly maintained by K+.

Composition of Fluids
plasma interstitial 146 4 3 1 104 27 1 2 5 intracellular 12 150 10 7 3 10 116 40

Cations Na K Ca Mg
Anions Cl HCO SO4 HPO4 Protein

140 4 5 2 103 24 1 2 16

Daily Requirements for Electrolytes

Sodium: 1-2 mEq/kg/d Potassium: 0.5-1 mEq/kg/d Calcium: 800 - 1200 mg/d Magnesium: 300 - 400 mg/d Phosphorus: 800 - 1200 mg/d

Interstitial fluid
Interstitial fluid (or

tissue fluid, or intercellular fluid) is a solution which bathes and surrounds the cells of multicellular animals. It is the main component of the extracellular fluid , which also includes plasma and transcellular fluid.

How to differentiate function and nonfunction interstitial fluids

Function: Taking part in modulating

the balance of body fluids. Non-function: Fluids in cavity in normal status.Including cerebrospinal , joint, pericardium and abdominal cavity fluids.

Third Space
Definition:

Pathophysiologically, relatively nonfunctional extra-cellular fluid. Mainly for the change of quantity of functional and nonfunctional ECF.

Third Space
Distribution:

exudates in burns; ascites; soft tissue injuries. bowel wall; peritoneum; infected lesions.
Attention:

not confused with the nonfunctioning components from interstitial fluid.

Control of Volume
Kidneys maintain constant volume and composition of body fluids
Filtration and reabsorption of Na Regulation of water excretion in response to ADH (antidiuretic hormone)

Water is freely diffusible

Movement of certain ions and proteins between compartments restricted

The Concept of Osmotic Pressure

Fluid Pressures (Starlings Law)

ECF and ICF fluid shifts occur related to

changes in pressure within the compartments Fluid flows only when there is a difference in pressure 3 types of body fluids
Isotonic Hypotonic Hypertonic

Osmotic pressure
Osmotic pressure is the

hydrostatic pressure produced by a solution on a space, separated from a solvent, by a semipermeable membrane due to a differential in the concentrations of solute. Osmoregulation is the homeostasis mechanism of an organism to reach balance in osmotic pressure.

 Pressure leading to the shift of water

through semi-permeable membrane

Semi-permeable membrane

water
water

Anion and Cation as well as non-electrolyte particles

Osmotic potential
Osmotic potential is the opposite of water potential with

the former meaning the degree to which a solvent (usually water) would want to stay in a liquid. Hypertonicity is a solution that causes cells to shrink. It may or may not have a higher osmotic pressure than the cell interior since the rate of water entry will depend upon the permeability of the cell membrane. Hypotonicity is a solution that causes cells to swell. It may or may not have a lower osmotic pressure than the cell interior.since the rate of water entry will depend upon the permeability of the cell membrane. Isotonic is a solution that produces no change in cell volume.

The Concept of Osmotic Pressure

Definition

the number of osmotically active particles

or ions per unit volume.

Unit :

milliosmoles per liter mOsm / L

Plasma Osmotic Pressure

cation Na K Ca Mg mmol/L 142 5 2.5 1.5 anion HCO3 Cl HPO3 SO3 Orgnic acid Protein Total mmol/L 27 103 1 0.5 6 0.8 138.3

Total

151

Normal Range =290~310mOsm/L

Relation between Osmotic pressure and distribution of body fluid

Osmotic Pressure

Crystal OP and Colloid OP

Plasma Crystal OP :

[Na+] contributes to a major portion of OP

Relation between Osmotic pressure and distribution of body fluid

Plasmatic Colloid OP

Plasma protein contributes a force leading to distribution of ECF

Interstitial Crystal OP

Contributes to the shift of extracellular and intracellular water

Na+

Crystal OP Plasma Colloid OP Plasmatic protein

ECF

Crystal OP

Interstitial Fluid

Semi-permeable membrane ICF

Colloid OP Crystal OP

The Regulation of Body Fluid Balance

Maintaining normal osmotic pressure Maintaining normal concentration &

Integral dose of natrium

Maintaining normal Volume (Blood-volume)

The Regulation of Body Fluid Balance

Maintaining osmotic pressure
hypothalamus osmotic pressure posterior hypophysis Distal renal tubules & collecting tubules

receptor

ADH

Sensitivity ECF Osmotic pressure 12 6 mOsmRelease of ADH

The Regulation of Body Fluid Balance

Maintaining the concentration & Integral

dose of natrium
Distarenal tuble macular densa renin angiotonin adrenal ortex

aldosterone

Increased Nareabsorption &

eliminating KDecreased removing HCO3- acid urine

The Regulation of Body Fluid Balance

Volume regulation (Blood-volume)

Glomerulus paracell+

renin angiotonin

adrenal cortex aldosterone

Assaying CVPAP& PAWP

Classification of body fluid change ( Four Types )

Volume Changes(ECF)

Volume Deficit
Volume Excess
Concentration Changes

Hyponatremia Hypernatremia

Classification of body fluid change( Four Types )

Mixed volume and Concentration

Abnormalities ECF Deficit and Excess with Hyponatremia

ECF Deficit and Excess with Hypernatremia

Classification of body fluid change( Four Types )

Composition Changes

Acid-base disturbances Potassium, Calcium, Magnesium abnormalities

Volume Changes
Isotonic ECF deficit (Na+=135-145mmol/l )

Etiologies ( Acute )
External-losses:

gastrointestinal fluids due to vomiting, nasogastric suction, diarrhea, and digestive tract fistula

Etiologies ( Acute )
Internal-losses : sequestration

(Third Space

Soft tissue injuries and infection, burns

Intra-abdominal and retroperitoneal inflammation

intestinal obstruction, bowel wall, peritonitis

Clinical Manifestations
Moderate CNS Sleepiness, apathy, slow responses, anorexia Cessation of usual activity Progressive decrease in food consumption Serve Decrease tendon reflexes Anesthesia of distal extremities Stupor Coma Nausea, Vomiting Refusal to eat Silent ileus and distention Cutaneous lividity Hypotension Distant heart sounds Cold extremities

GI

CV

Orthostatic hypotension Tachycardia Collapsed veins Collapsing pulse

Clinical Manifestations
moderate
Tissue signs Soft,small tongue longitudinal wrinkling Decreased skin Temperature

serve
Atonic muscles Sunken eyes

Metabolism

Temperature

Diagnosis
Etiology Clinical manifestation : Seeing Table Laboratory

Increased RBC,WBC,PLT and plasma protein Increased HCT Normal serum sodium & chloride hyperbaric urine

Fluid & electrolyte therapy

To eliminate etiologies Quality of Solution Isotonic sodium solution Lactated Ringers solution Quantity hydropenic quantity+continuous losses quantity+physiological quantity Rate and Goal To moderate BP & Pulse rate Urinary Output 30 50 ml / hr

Isotonic ECF excess

Etiology
Iatrogenic
Major operation Retention of sodium & water Renal vascular constriction Increased ADH & Aldosterone

Severe trauma
Infection

Secondary to renal insufficiency

Clinical manifestations
Circulatory overload

Basilar rales
Heart failure
Tissue signs

Subcutaneous pitting edema

Fluid & electrolyte therapy

Restriction of water & sodium Colloid + Diuretics Hypertonic diuresis:

relieve cerebro-edema 20% mannitol

Mixed volume and Concentration Abnormalities

Hypotonic ECF deficit (Na+<135mmol/l )

Etiologies (Secondary)
Continues to drink water while losing large

volumes of gastrointestinal fluids. The loss of a large amount of salt, such as via sweat, and kidney. In the postoperative period when gastrointestinal losses are replaced with only hypotonic sodium solution.

Clinical manifestations
CNS signs increased intracranial pressure

& secondary hypertension Tissue signs excessive intracellular water Digestive system: Vomiting, Nausea Shock:Progressing to oliguric renal failure promptly Asymptomatic Untill the serum sodium falls below 120 mmol/L

Clinical manifestations
One important exception

Closed head injury, in which mild hyponatremia may be extremely deleterious

Diagnosis
Etiology

Laboratory

Serum sodium concentration < 135 mmol/L Decreased urinary sodium and Hypobaric urine< 1.010

Increased HCT and serum BUN & NPN

Diagnosis
Clinical Manifestation

Clinic manifestation Mild Symptomless Moderate Increased ICP (compensated) Severe Increased ICP (decompensated)

Serum sodium NaCl deficit (mmol/L) ( g/kg ) 131~135 0.5 130~121 0.5~0.75 <120 0.75~1.25

Mild or moderate hyponatremia Fluid & electrolyte therapy

Eliminating etiologies

Quality of solution: NS5%GNS and or

5%NaCl

Severe hyponatremia Fluid & electrolyte therapy

TBW (liters) =Body weight ( kg )0.6 (female 0.5) Sodium deficit (mmol)= Serum sodium (standard

actual)TBW
Total Amount:Half of sodium deficit + Requisite

amount per day

Severe hyponatremia Fluid & electrolyte therapy

Quality:

5%sodium chloride solution (2/3) + Isotonic sodium chloride (1/3)

Shock

colloid: crystalloid=1:2~3
Convulsions or coma

5%NaCl 100 ~ 250 ml

Severe hyponatremia Fluid & electrolyte therapy

Rate of increment of sodium

is 0.5~1mmol/L/h; and no more than 12 mmol/L within 24hs

Complication:

Osmotic Demyelination Syndrome(ODS). Pontine demyelination

Management of severe acute and chronic hyponatremia

EFW: electrolyte free water

Therapy for Severe Acute hyponatremia

Aim:

Shrink the size of brain cells with hypertonic saline

Na+<120mmol/L

having seizures. To raise the plasma [Na+] by 5 mmol/L during the next hour
Raising [Na + ]

to 130mmol/L at 1~2mmol/L/h; and <12mmol/L within 24h

Therapy for Severe Acute hyponatremia

How to calculate the amount of 10NaCl

per hour Raising [Na + /h] Kg 0.6(0.5)= the amount of mmol of NaCl

Therapy for Severe Chronic hyponatremia

Convulsion or Coma:

PNa rise <5mmol/L in 2-3 hours

No convulsion:

PNa rise <8mmol/L/day Restrict water Think ICF K+

Water intoxication (Dilutus hyponatremia)

Retention of water in the body
[Na+] is decreased Intracranial pressure is increased highly

Management

Stopping infusion of water Diuresis Negative balance of water

Hypertonic ECF deficit (Na+>150 mmol/l )

Etiology(Primary)
Restricted water intake in circumstances:

Sweat Burn Diabetic coma

Clinical manifestations
Central nerve system

restless,weakness,delirium,maniacal

behevior, coma Tissue signs -dry and thirsty, sticky mucous membranes Dehydration fever Tachycardia Oliguria

Diagnosis
Etiology Laboratory

Increased sodium ( >150mmol/L) & HCT Hyperbaric urine Clinical Manifestation Extremely thirsty High fever Oliguria

Fluid & electrolyte therapy

Principles

-Adopting 5 GS , 0.45% NaCl , water via intestine -Half of volume deficit Requisite amount per day

Fluid & electrolyte therapy

Measures

with loss 1% body weightinfusing 400500ml supplemental quantities (ml) = [actual serum sodium normal serum sodium (mmol/L)]body weight (kg) 4

Classification of ECF changes

ECF deficit Isotonic hypotonic hypertonic normal Na+ hyponatrium hypernatrium ECF excess normal Na+ hyponatrium hypernatrium

Composition Changes
Hypokelamia(<3.5mmol/L)

Common cause
Excessive excretion:

Kidney ; Digestive tract (Vomiting, Diarrhea, Gastric suction, Intestinal fistula) Less in-take: Less dietary intake ; potassium-free parenteral fluids Redistribution The transfer of extracellular potassium into cells Alkalosis

+ 3K

+ 2Na

Cell 2Na+
+ 1H

+ 1H + 3K

H++HCO3- =H2O+CO2

Clinical manifestations
General:

Anorexia,Nausea,Vomiting Skeletal muscles (Diminished to absent tendon reflexes, respiratory hypoventilation) Smooth muscles(Paralytic ileus ) Cardiac muscles (Hypotension) Muscular weakness Flaccid paralysis ( k + < 2.5mmol / L

Clinical manifestations
CNSSerum potassium2.0mmol/L

MorbusObnubilationdisorientation Cardiovascular ECG:

ST segment depression, decreased T wave, Increased U wave, T<U
Premature ventricular and aterial contractions ventricular and aterial tachyarrhythmias

Arrhythmia:

Diagnosis
History Clinical symptoms Serum potassium3.5 mmol/L EKG

Treatment
The quantities of supplemental potassium

Serum potassium3mmol/L. To replace 200400mmolMay be increased by 1mmol/L Serum potassium 33.5mmol/L To replace 100200mmol May be increased by 1mmol/L The rate of administration (intravenous) Should not exceed 20 mmol K+ / hr

Treatment
Attention

Therapy of shock
Urine output arrive at 40 ml/hr, and

potassium infused No more than 40 mmol K+added to 1 liter (0.03%) of IV fluids via peripheral vein infused Calcium not infused

Hyperkelamia(>5.5mmol/L)

Common causes
Excessive potassium entered into blood

circulation
Iatrogenicity , Infusion of excessive potassium Infusion of a vast reserve of blood

Renal excretion decreased

Abnormal distribution
Acidosis Acute tumor lysis, burn, Acute intravascular hemolysis

Clinical manifestations
Gastrointestinal Nausea & vomiting Intermittent colic & diarrhea Paresthesia & Weakness Cardiovascular Bradycardia Microcirculatory dysfunction ( Be cold, cyanosis, pale and hypotension)

Clinical manifestations
EKG Shortening of QT interval and high peaked T wave Widened QRS , PR interval prolongation disappearance of P wave degeneration of the QRS to a sine wave pattern Ventricular asystole or fibrillation

Diagnosis
Any inexplicable symptoms ECG Serum potassium ion > 5.5mmol/L

Treatment
Withholding of exogenously administered

potassium
Correction of the underlying cause Anti- arrhythmia

- 10% Calcium gluconate infused

Treatment
Lowering of serum potassium

Transfer potassium into cells5% NaHCO3;11.2% Sodium lactate, GI Diuretics Cation-exchange resins (oral ; maintaining clysis) Peritoneal dialysis, or hemodialysis, hemofiltration

Hyperkelamia EKG change yes Effect in 10min calcium gluconate V. Removec cause Urinary systerm urine potassium low Increase egest: Mineralocorticoid no gastroin testinal Decrease oral ion exchange resin, coloclysis

Aversilon intracell Insulin NaHCO3

hemodialysis

NaHCO3 Acetazolamide

Disturbances of Calcium Hypocalcemia(<2.0mmol/L)

Hypocalcemia
Causes: acute pancreatitis; renal failure; intestinal fistula;

Infusion of a vast reserve of blood; blood purification Manifestation Symptoms:numbness; tingling;Apnea; Tetany Signs: Hyperactive tendon reflexes; Chvosteks Signs

Treatments:10%calcium gluconate;5%Calcium Chloride

Hypercalcemia(>4.0mmol/L)
Causes:

hyperparathyroidism; Bony Metastasis Manifestations: Fatigue; Vomiting Treatment: EDTA; Na2SO4; Calcitonin

Magnesium deficiency(<0.7mmol/L)
Causes:

intaking /absorption Manifestations: Pale /excited /Fret Treatment: 25%MgSO4

Hypophosphatemia (<0.96mmol/L)
Causes:

Burn/Pancreatitis Manifestations: Emotional disturbance Treatment: Glycophosphate

Acid-base imbalance
Buffer system A weak acid or base & the salt of that acid or base
Intracellular B.Protein/H.Protein Extracellular B.HCO3/H2CO3 Red cell B.Hb/HHb

B2HPO4/ BH2PO4

B.HbO2/HHbO2

Anion Gap=[Na+][Cl-+HCO3-]

The important role of potassium

Assumption:

pre- existing potassium depletion

Outcome:

Intracellular (3 K)and extracellular ( 2Na+1 H+ ) exchange

The important role of potassium

Decreased Na+ and K+ exchange, Increased

H+ and Na+ exchange in renal tubule

Paradoxical acid urine

Metabolic alkalosis is aggravated

The important role of the lung

Sensible acids are excreted via the lung

HCINaHCO3

NaCIH2CO3 H2O CO2

The important role of the kidney

Insensible acids excreted by kidney

Inorganic acid anions hydrochloricsulfuric hosphoric acids

with hydrogenH+Na+ exchange ammonium saltsH+ NH3NH4-

organic acid anionslacticketo pyruvic acids

Be metabolized
Some renal excretionwith high levels

Henderson - Hasselbalch equation

BHCO3

pHpKlog H2CO3 27mmol/L

6.1log
1.35mmol/L 20 6.1log 1 6.1 1.3 = 7.4

Bohr

H
HbO2+H++CO2

Hb CO2

+O2

Dissociation curve
Shife lefe
SaO2 normal Shift right

PaO2

Metabolic Acidosis(pH<7.35)
Defects Causes Compensation BHCO3/H2CO3

Retention of Diabetes, Pulmonary(Rapid) <20/1 Fixed acids Starvation :increased rate Anion gap Lactic acid, and depth of Increased Azotemia breathing (numerator)

Metabolic Acidosis(pH<7.35)
Defects
Loss of base bicarbonate (Anion gap normality)

Causes
Diarrhea, Small bowel , pancreatic fistulas

Compensation
Renal slow) : Retention of HCO3-, Excretion of acid salts, ammonia formation, Chloride into RBC

Clinical manifestations
Increased in depth & frequency of

respiration (Kussmaul breathing) Peripheral vessels dilated Circulatory shock, Cerise lip Decreased muscular tension & tendon reflex merged Unconsciousness

Treatments
Principles

Therapy for basic disease Alkali treatment: dose initials 1 / 3 ~ 1 / 2 requisite amount Pre-treatment: serum K+ & Ca++

Treatments
The amount of Alkali necessary

normal CO2-CP - serum CO2-CP TBWKg BE3BWKg normal SB observed SBBW Kg Loss of base mEq

Treatments
Some of alkalescent solution contains HCO 3 1 gm NaHCO312 mmol HCO3 1ml - 11.2%NaC3H5O31 mmol HCO3 1ml - 3.63%THAM0.3 mmol HCO3 -

Respiratory Acidosis(pH<7.35)
Defects Retention of CO2 (Alveolar Ventilation Decreased) Causes Compensation BHCO3/H2CO3

Depression of respiratory center by morphine CNS injury pulmonary disease emphysema pneumonia

Renal <20/1 Retention of (Denominator bicarbonate; increase) excretion of acid salts,increased ammonia formation Chloride shift into red cells

Clinical manifestation
Advanced respiratory insufficiency(Apnea)
Metabolic encephalopathy (headache,

drowsiness, stupor and coma, papilledema) Blood pressure elevated reduced Ventricular fibrillation (hyperkalemia)

Treatment
Treatment of Causes
To improve ventilation Alkalescent solution is harmful !!

Metabolic alkalosis(pH>7.45)
Defects
Loss of fix Acids Gain of base Bicarbonate Potassium, Chloride of Depletion

Causes
vomiting or gastric suction with pyloric obstruction excessive intake of bicarbonate Diuretics

Compensation

BHCO3/H2CO3

Pulmonary (rapid) >20/1 decreased rate (numerate & depth of breath into increase) Renal (slow) excretion bicarbonate retention of acid salts, decreased ammonia formation

Clinical manifestations
Peripheral vessel constricted Mental symptoms: Delirium, Drowsiness Decreased in depth & frequency of

respiration
Tetany & tendon reflex accentuation

Treatment
Therapy for basic disease Correction of the underlying disturbances Loss of gastric fluid replaced with NS or GNS potassium deficit correction of hypokalemia Serum HCO3,4550 mmol/LpH>7.65 0.1 M hydrochloric acid solution IV

Treatment
Hydrochloric acid mmol
[actual serum HCO3-- normal serum HCO 3 mmol/L] BWkg0.4 [normal plasma CI - actual plasma CI mmol] BWkg0.2 0.6

The initial dose of hydrochloric acid:

1 / 2 dose of above mentioned

Respiratory alkalosis(pH>7.45)
Defects Excessive Loss of CO2 Increased Alveolar Ventilation Causes Compensation BHCO3/H2CO3

Hyperventilation Apprehension,Hypomia severe pain, high temperature,assisted ventilation,encephalitis

Renal >20/1 Excretion of (denominator bicarbonate, decreased) acid salts Decreased ammonia formation

Clinical manifestation
A Increased rate and depth of breathing Mental symptom
Paresthesia with Tetany

Treatment
Therapy for basic disease Increase pulmonary dead space 5% CO2 added to the inspired air

Dangerous!!!

How to differentiate the four types of acid-base imbalance

Arterial blood gases test AB: actual bicarbonate(Both metabolism

and respiration) SB: Standard bicarbonate(Only metabolism) SB 38 760mmHg PCO2 40mmHg fully oxygenated Hb BE: Base excess

The four types of acid-base disturbances

AB = SB = Normal AB = SB < Normal AB = SB > Normal AB > SB AB < SB Normal Metabolic acidosis Metabolic alkalosis Respiratory acidosis Respiratory alkalosis

Case Studies

1. Found Down
45 yo WM, found down, presumed to be

assaulted, well known to ED for EtOH CT head - hygromas, small ICH labs:
Na = 118 K = 2.4 Cl = 74

What do you think? What do you do?

 Severe Hyponatremia Severe Hypokelamia Management Correct sodium to above 120 mEq/dl
NaCl + 40 mEq/L KCl 3% Saline furosemide diuresis (euvolemic) serial electrolytes be prepared to handle seizures

Replace potassium Cl should correct itself

2. JO
JO is a 58 year-old male with cirrhosis of the liver due to ethanol abuse. Physical examination reveal ascites. Baseline lab is as follows: Na 128, K 3.8, Cl 95, CO2 24 JO is to be started on TPN, Should we request additional sodium to correct his hyponatremia?

 JOs is in an edematous state. He has an

excess of TB water and sodium. The appropriate treatment is water and sodium restriction. He should also receive diuretic treatment. The drug of choice is Aldactone (spironolactone), an aldosterone antagonist.

3. Mrs Jones
Mrs Jones. is a 62 year-old female who is having an acute exacerbation of Crohns disease. She complains to you of severe and frequent diarrhea over the last four days. She experiences dizziness when she stands. Your physical examination reveals dry mucous membranes. In the supine position her BP=110/65 and in the upright position her BP=90/45 and her pulse=140. Your lab values are as follows: Na 132, K 2.9, Cl 92, CO2 31, BUN 25, Cr 1.0 Discuss Mrs. Ds fluid and electrolyte problems.

Mrs Jones has extracellular volume depletion due to prolonged diarrhea. The ECVD is supported by her physical assessment and postural hypotension and her BUN/Cr is > 20:1. The diarrhea has resulted in a loss of fluid and sodium chloride. Some potassium was lost directly in the stools, but the main cause of her hypokalemia is her ECVD which has induced a metabolic alkalosis (contraction alkalosis.) The alkalosis contributed to her hypokalemia by two mechanisms. Some potassium has moved to the intracellular compartment but much of it has been lost in the urine where potassium wasting occurs secondary to chloride deficit. Administration of Normal Saline with Potassium Chloride will correct her fluid and electrolyte problems (and alkalosis.)

4. M.T.
M.T. is a 55 year-old female with a history of chronic renal failure who is admitted to the SICU following a motor vehicle accident. She is started on a TPN solution with minimal K, no Mg and no Phos. She also receives Mylanta II 30 ml per NG tube every four hours. Although her baseline labs were normal on day six her labs are as follows: K 4.3, Mg 2.6, Phos 1.6

1.
2.

What role did the antacid play in her electrolyte abnormalities? What role did the TPN play?

M.Ts K is normal, but she has hypermagnesemia and hypophosphatemia. The antacid contributed to both of these abnormalities. It provided a significant source of Mg this patient with impaired excretion. Also the aluminum in the antacid acted a phosphate binder contributing to the hypophosphatemia. The TPN could have contributed to the hypophosphatemia by inducing an intracellular shift of phosphate (refeeding.) The potassium probably remained normal because some was being provided. Mg was being provided enterally.