Dyselectrolytemias

- CSN Vittal

Electrolyte disorders Definition

An electrolyte disorder is an imbalance of certain ionized salts in the blood.

e.g. bicarbonate, calcium, chloride, magnesium, phosphate, potassium, and sodium

ElectrolytesElectrolytes are ionized molecules found

throughout the blood, tissues, and cells of the body.

Cations +Anions -

Electrolytes – Functions

Sodium (Na) Helps to balance fluid levels in the body and Facilitates neuromuscular functioning.

Potassium (K) Main component of cellular fluid Helps to regulate neuromuscular function and osmotic

pressure. Calcium (Ca)

Affects neuromuscular performance and Contributes to skeletal growth Blood coagulation.

Magnesium (Mg) Influences muscle contractions and Intracellular activity

CationsCations:

Electrolytes – Functions

Chloride (CI-) Regulates blood pressure.

Phosphate (HPO4) Impacts metabolism and regulates acid-base balance and calcium levels.

Bicarbonate (HCO3) Assists in the regulation of blood pH levels

Anions:Anions:

ELECTROLYTE BALANCE The exchange of interstitial and intracellular

fluid is controlled mainly by the presence of the electrolytes sodium and potassium

NaNa++KK++

NaNa++KK++

NaNa++ KK++

NaNa++

KK++

Normal levels of electrolytes

Sodium Serum 135 - 145 mEq/L

Potassium Serum 3.5 - 5.5 mEq/L

Calcium (total) (Unbound)

Serum 8.8 - 10.4 mg/dL4.7 - 5.2 mg/dL

Magnesium Plasma 1.4 - 2.1 mEq/L

Chloride Serum 100 - 108 mEq/L

Phosphate Plasma 2.5 - 4.5 mEq/L

Electrolyte Disturbances Electrolyte Ionic formula Elevation disorder Depletion disorder

Sodium Na+ hypernatremia hyponatremia

Potassium K+ hyperkalemia hypokalemia

Calcium Ca2+ hypercalcemia hypocalcemia

Magnesium Mg2+ hypermagnesemia hypomagnesemia

Chloride Cl- hyperchloremia hypochloremia

Phosphate PO43- hyperphosphatemia hypophosphatemia

Bicarbonate HCO3- hyperbicarbonatemia hypobicarbonatemia

SodiumSodiumNormal = Normal = 135-145 mEq/L135-145 mEq/L

Sodium helps the kidneys to regulate the amount of water the body retains or excretes.

SODIUM PRINCIPLES

1) Sodium ions do not cross cell membranes as quickly as water does

Na+

H2O

H2O H2O

H2O

H2O

Na+

SODIUM PRINCIPLES

2) Cells pump sodium ions out of the cell by using sodium-potassium pumps

Na+

Na+

Na+

Na+

SODIUM PRINCIPLES 3) Increases in extracellular sodium ion

levels do not change intracellular sodium ion concentration

Na+Na+

Na+Na+

Na+

Na+

Na+

Na+

Na+

Na+

Na+

Na+

Na+

Na+

Na+

Na+

Na+

Na+

Na+

Na+

HYPERNATREMIA

Normal range for blood levels of sodium is app. 137 - 143 meq/liter

HypernatremiaHypernatremia refers to an elevated serum sodium level (145 -150 meq/liter)

Increased levels of sodium ions are the result of diffusion and osmosis

Na+

14

RESULTS OF HYPERNATREMIA 1) Water is osmotically drawn out of the

cells

Resulting in dehydration

2) Increase in extracellular fluid volume

Extracellular fluid

volume

Intracellular fluid

volume

15

CNS REACTION TO HYPERNATREMIA

In the CNS tight junctions exist between In the CNS tight junctions exist between endothelial cells of the capillary wallsendothelial cells of the capillary walls

These junctions restrict diffusion from These junctions restrict diffusion from capillaries to the interstitium of the braincapillaries to the interstitium of the brain blood-brain barrierblood-brain barrier

Increased levels of sodium ions in the Increased levels of sodium ions in the blood do not result in increased sodium blood do not result in increased sodium ions in brain interstitial fluidions in brain interstitial fluid

CNS REACTION TO HYPERNATREMIA As the result of an osmotic

gradient, water shifts from the interstitium and cells of the brain and enters the capillariesThe brain tends to shrink and the

capillaries dilate and possibly rupture

Result is cerebral hemorrhage, blood clots, and neurological dysfunction

H2O

CNS PROTECTIVE MECHANISM

There is an unknown mechanism that protects the brain from shrinkage

Within about 1 day

Intracellular osmolality of brain cells increases in response to extracellular hyperosmolality

CNS PROTECTIVE MECHANISM Idiogenic osmoles accumulate inside

brain cells K+, Mg+ from cellular binding sites and

amino acids from protein catabolism

These idiogenic osmoles create an osmotic force that draws water back into the brain and protects cells from dehydration

H2O

HYPERNATREMIA (Serum sodium > 150 mEq/L)(Serum sodium > 150 mEq/L)

Clinical Evaluation

Excessive Sodium Water Deficit Water & Na Deficit

Central DI Nephrogenic DI Increased

insensible losses Preterms Radiant warmer Phototherapy

Inadequate Intake Ineffective BF Child abuse Adipsia

GI Losses Diarrhoea Vomiting / NG suction Osmotic cathatrics

Cutaneous Losses Burns Excessive sweating

Renal Losses Osmotic diuretics DM Ch. Renal Disease Postobstructive

diuresis Polyuric phase of ATN

IV Hypertonic saline

Improper Formula Ingestion of sea

water Salt poisoning Hyperaldosteronism

HYPERNATREMIA (Serum sodium > 150 mEq/L)(Serum sodium > 150 mEq/L)

Check urine / plasma osmolarity >1 extrarenal loss mineralocorticoid = 1 osmotic diuresis <1 diabetes insipidus

HYPERNATREMIA - Symptoms

Typical signs of dehydration masked – fluid moves from ICF to ECF

Doughy feeling of skin Woody consistency of tongue - ICF loss

HYPERNATREMIA - Symptoms Without Dehydration

Irritability Fatigue Lethargy High pitched cry Hyperpnea Muscle twitching and/or seizures

With Dehydration Thirst Orthostatic hypotension Dry mouth and mucous membranes Tachycardia

Serious Consequence Brain Hemorrhage

HYPERNATREMIA - Management If patient is conscious:

ORS – correction spread over 4 – 6 hours Breast feeding Free water

If patient is with altered sensorium: Intravenous treatment Acute Hypernatremia : Sodium free fluids – All other conditions –

Slow correction (not more than 10 mEq / L / d) Infusate sodium conc. About 40 mEq/L

Salt Poisoning (serum Sodiu, >180 mEq/L) Urgent dialysis

Correct underlying problems (e.g. treat DI with ddAVP)

Elevated serum sodium should be lowered no faster than 10-15 mEq/L in 24 hours.

HYPERNATREMIA – Idiogenic OsmolesIdiogenic Osmoles

The production of extra osmoles

within the cell called

osmolytes which help preventing

disruption of enzyme function.

Rapid Fall in S. Sodium

Water

HYPONATREMIA(Serum sodium less than 130 mEq/L)(Serum sodium less than 130 mEq/L)

Up to 1% of all hospitalized patients Up to 1% of all hospitalized patients develop hyponatremia, making it develop hyponatremia, making it

one of the most common one of the most common electrolyte disorders. electrolyte disorders.

• Implies an increased ratio of water to sodium in extracellular fluid

CNS RESPONSE TO HYPONATREMIA Brain cells lose osmoles creating a higher

extracellular solute concentration Effect is to protect against cerebral edema by

drawing water out of the brain tissue

GENERAL RESPONSE TO HYPONATREMIA

Suppression of thirst

Suppression of ADH secretion

Both favor decreasing wateringestion and increasingurinary output

HYPONATREMIA (Serum sodium < 130 mEq/L)(Serum sodium < 130 mEq/L)

Plasma Osmolality

Hypovolemia HypervolemiaEuvolemia

SIADH Glucocorticoid

deficiency Hypothyroidism Water Intoxication

Iatrogenic Swimming lessons Tap water enema Psychogenic

polydypsia Diluted formula Child abuse

Cardiac failure Renal failure Cirrhosis Nephrotic Syndrome Capillary leak due to

sepsis Hypoalbuminemia –

GI disease

External LossUrine Na < 20 mmol/L GI Loss Skin Loss (burns)Renal LossUrine Na > 20 mmol/L Diuretics Minerelo corticoid

def. Salt losing nephritis Cerebral salt wasting Type II RTA Hypoaldosteronism

Pseudo HyponatremiaPseudo Hyponatremia Hyperglycemia Mannitol

POTASSIUM ION LOSS

KK++

NaNa++

KK++

KK++

KK++

PlasmaPlasmaInterstitial fluidInterstitial fluid

CellCell

KK++

KK++

NaNa++

NaNa++

Click

HYPONATREMIA - Symptoms

Nausea Abdominal cramping, Vomiting Headache Edema (swelling) Confusion Seizures Coma

Due to decrease in extracellular osmolality and movement of water into intracellular space

HYPONATREMIA - Treatment Principles : Depends on underlying cause. (e.g. fluid

restriction in SIADH) Rapid correction is only indicated in

symptomatic patients (e.g. convulsions) Avoid correcting s.sodium by more than 12

mEq/L each day

HYPONATREMIA - Treatment Diagnostic Criteria for SIADHAbsence of

Renal, adrenal or thyroid deficiency CHF, nephrotic syndrome, or cirrhosis Diuretic ingestion Dehydration Urine osmolality > 100 (usually > plasma) Serum osmolality < 280 and serum Na <135 Urine Na > 25

HYPONATREMIA - Management With Expansion of ECF & EdemaWith Expansion of ECF & Edema

Increased Total Body Water (+ ve Na and water balance)The progressive reduction of these two positive balances is the

aim of therapy. Intake of sodium chloride and water should be moderately

restricted and Their urinary excretion increased by loop diuretics

With Slight Expansion but No EdemaWith Slight Expansion but No Edema SIADH

The simplest way to correct hyponatremia is water restriction if the intake of sodium is adequate.

The underlying cause should be corrected if possible Furosemide with Na supplementation

With Decreased ECFWith Decreased ECF (Contraction and Na loss)(Contraction and Na loss) Sodium and water replacement Treat the cause

HYPONATREMIA - ManagementAcute (<3 days) – When symptomatic:

3% Hypertonic Saline - each ml increases S.Na by 1 mEq/L) No greater than 2mmol / L / hr,

do not raise Na >12mmol / 24hours Dose: 4 - 6 ml / Kg

Chronic (>3 days) No greater than 0.5mmol / L / hr, do not raise Na >12mmol/24hours

Important: 1. Where you are not sure whether hyponatremia has

developed acutely or chronically, assume it has developed chronically.

2. Correct Na slowly because of the risk of central pontine myelinolysis (CPM)

3. Plasma Na must be monitored closely.

HYPONATREMIA - Clinical tips If children and young people require intravenous fluids, they should initially receive

isotonic fluids that contain sodium in the range of 131 to 154 mmol/l such as Sodium chloride 0.9% Sodium chloride 0.9% and glucose 5% Ringer’s solution

During surgery, the majority of children may be given fluids without glucose; but blood glucose should be monitored if no glucose is being administered. Neonates in the first 48 hours of life and any infants already receiving glucose containing solutions should continue with them during surgery

Check the child’s weight before starting fluids and daily thereafter Measure the sodium, potassium, urea, and creatinine levels before

starting fluids (apart from prior to elective surgery) and regularly during intravenous infusion therapy

 

PotassiumPotassium

Normal S. Pot = 3.5-5.5 mEq/LNormal S. Pot = 3.5-5.5 mEq/L Intracellular Potassium > 150 m Eq/LIntracellular Potassium > 150 m Eq/L Less than 1% of total body potassium is in

plasma Normal daily requirement = 50-80 mEq/d Helps to regulate neuromuscular function

and osmotic pressure

Potassium Regulation - 1 Na+, K+ ATPase Na+, K+ ATPase

maintains high maintains high intracellular intracellular potassium potassium concentration concentration by pumping by pumping sodium out of sodium out of the cell and the cell and potassium into potassium into the cellthe cell

Na+ / K+ Pump Cells pump K+ ions in and Na+ ions out of the cell by using

sodium-potassium pumps

Na+

Na+

Na+

Na+

K+

K+

K+

K+

Potassium Regulation - 3 Acid – base balance:Acid – base balance:

Metabolic acidosis : increases S. potassium while alkalosis reduces it.

Glucose infusion : - pushed potassium inside the cell leading to low serum levels.

ALKALOSIS >> Hypokalemia H+ ions are exchanged for KK++

(potassium moves into cells)Thus serum concentrations of KK++ are

decreased And alkalosis causes

hypokalemia

HCOHCO33--

HCOHCO33--

HCOHCO33--

HCOHCO33--

HCOHCO33--

HCOHCO33--

HH++

HH++ HH++

HH++ HH++

HH++

HH++ HH++

KK++KK++

KK++

KK++

KK++

KK++

KK++

KK++

41

Hypokalemia >> ALKALOSIS Conversely when K+ ions are lost from the

cellular and extracellular compartments Sodium and hydrogen ions enter cells

in a ratio of 2:1 as replacement This loss of extracellular H+

causes alkalosis HCOHCO33--

HH++

KK++HCOHCO33

--

HCOHCO33--

HCOHCO33--

HCOHCO33--

HCOHCO33--

HCOHCO33--

HH++

HH++HH++

HH++HH++

HH++

NaNa++

KK++

KK++

KK++

KK++

KK++KK++

KK++ NaNa++

NaNa++

NaNa++

NaNa++

NaNa++

NaNa++

42

KIDNEY FUNCTION Kidney function is altered by hypokalemia

NaNa++ ions are reabsorbed into the blood when KK++ ions are secreted into the urine by kidney tubules

K+

Tubular lumen

K+K+

K+

K+K+

K+

Na+Na+

Na+ Na+

Na+Na+

Na+

Peritubular fluidNORMAL

43

KIDNEY FUNCTION Kidney function is altered by hypokalemia

If adequate numbers of KK++ are not available for this exchange

HH++ ions are secreted instead

H+

Tubular lumen

K+H+

K+

H+K+

H+

Na+Na+

Na+ Na+

Na+Na+

Na+

Peritubular fluidHYPOKALEMIA

44

KIDNEY FUNCTION Hypokalemia promotes renal loss of HH++ ions and thus

results in alkalosis

HYPOKALEMIA (Serum K+ < 3.5 mEq/L)(Serum K+ < 3.5 mEq/L)1. Increased Potassium Loss:

Extrarenal – Diarrhoea, laxative abuse, sweating Renal – (Urinary K+ > 30 mEq/d)

RTA Polycystic kidneys Diuretic phase of ATN Tubular toxins : amphoterecin, aminoglycosides Endocrine – Cushing’s disease, hyperaldosteronism Magnesium deficiency Drugs: Diuretics, corticosteroids

2. Decreased Stores Malnutrition

3. Shift into intracellular compartment Alkalosis Hyperinsulinemia Hyopthermia Hypokalemic Periodic Paralysis Beta 2 agonists

4. Poor Intake Low dietary potassium; K+ free IV fluids

KK++

HYPOKALEMIA - Symptoms CVS –

ECG changes (flattening of T waves, ST depression, U waves, prolong QT)

Arrhythmia – SVT, VT, torsades

GI – ileus constipation

CNS – cramps parasthesia weakness tetany rhabdomyolysis

Others – glucose intolerance renal polyuria metabolic alkalosis • Hypomagnesemia produces similar

EKG changes

HYPOKALEMIA - Management

Deficit corrected over 24 hrs. Oral correction safer – if patient is

conscious IV Correction :

Pt. unable to take oral medicationSerum K + < or = 2.5 mEq/LCardiac rhythm disturbances +

HYPOKALEMIA - Management

Usual maximum concentration of potassium for peripheral infusion is 4 mEq per 100 ml of IV fluid

Rate of infusion should not be more than 0.6 mEq / kg / hr)

For most instances 2-3 mEq per 100 ml will suffice. In cases of hypokalemia higher levels can be used,

but the heart should be monitored. Before giving potassium be aware of the possible

existence of renal failure.

HYPOKALEMIA - Management

Which Preparation : Oral KCl

Soln. contains 20 mEq / 15 mlTabs. Contain 8 mEq / tablet

HYPOKALEMIA - ManagementIntravenous Potassium Therapy 1 ml of 15% KCl = 20 mEq of potassium1 ml of 15% KCl = 20 mEq of potassium

Always monitor S. Pot. Never give KCl directly IV Never add KCl to maintenance fluid Don’t use 5% dextrose as diluent Don’t give > 10 – 20 mEq / hour Don’t give > 40 mEq / L Don’t give > 240 mEq / day

Hypokalemia is safer than HyperkalemiaHypokalemia is safer than Hyperkalemia

HYPERKALEMIA S. Potassium > 5.5 m Eq/LS. Potassium > 5.5 m Eq/L

Hyperkalemia is an excess of serum potassium

One of the most alarming electrolyte disturbance – because of potential for lethal arrhythmias.

K+

HYPERKALEMIA - What Causes It?

Inadequate Excretion : Renal failure Adrenal disease UT obstruction Hyporeninemic hypoaldosteronism

Excessive intake Diet high in potassium (bananas, oranges, tomatoes, high protein diets, salt

substitutes, potassium supplements) Shifting of potassium from tissues

Trauma, especially crush injuries or burns, tumor lysis Hemolysis Acidosis Insulin deficiency Malignant hyperthermia

Drugs Digoxin, succinyl choline, beta agonists, potassium sparing diuretics, NSAIDs,

Trimethoprim, ACE inhibitors

Ficticious: Hemolysis Tissue ischemia during drawing Thrombocytosis Leukocytosis

54

HYPERKALEMIA Hyperkalemia causes acidosis Acidosis causes hyperkalemia

HYPERKALEMIA

H+

H+

H+

H+

H+

H+

H+ H+

K+

K+

K+

K+

K+

K+

K+ K+

ACIDOSIS

55

HYPERKALEMIA Hyperkalemia causes acidosis Acidosis causes hyperkalemia

HYPERKALEMIA

H+

H+

H+

H+

H+

H+

H+ H+

K+

K+

K+

K+

K+

K+

K+ K+

ACIDOSIS

HYPERKALEMIA Signs and Symptoms

Fatigue Weakness Tingling, numbness,

or other unusual sensations

Paralysis Palpitations Difficulty breathing

ECG Changes : Tall T waves, flat P waves, prolonged PR interval, prolonged QRS, sine waves), Arrhythmia – VF

6 – 7 mEq / L

7 – 8 mEq / L

> 9 mEq / L

HYPERKALEMIA - Management

Basic goals:Basic goals:1. To stabilize the heart to

prevent life threatening arrhythmias

2. To remove potassium from body

HYPERKALEMIA - Management Principles:Principles:1. Antagonism of membrane

effects Calcium gluconate

2. K+ movement into cells Insulin and glucose Beta agonists Inj. Soda bicarb

3. K + removal from body Loop or thiazide diuretics Cation exchange resin Peritoneal / hemodialysi

CELLULAR-EXTRACELLULAR SHIFTSCELLULAR-EXTRACELLULAR SHIFTS

Insulin deficiency predisposes an individual to hyperkalemia

Cellular uptake of KK++ ions is enhanced by insulin, aldosterone and epinephrineinsulin, aldosterone and epinephrineProvides protection from extracellular KK++

overload

Insulin K+

K+

K+

K+

K+ K+

Click

HYPERKALEMIA - Management Mild: ((Serum K+ = 5.5 to 6.0 m Eq/L)Serum K+ = 5.5 to 6.0 m Eq/L)

Stop intake of potassium Stop offending drugs

Moderate: (in addition to above..)(Serum K+ = 6.0 to 8.0 m Eq/LSerum K+ = 6.0 to 8.0 m Eq/L or peaked T waves)

Glucose Insulin Infusion : (0.5g/kg with 0.3 U regular insulin / g of glucose) over 2 hours

Sodabicarb infusion (2 mEq/kg of NaHCO3 over 5 – 10 min)

Severe: (Serum K+ > 8.0 m Eq/L)(Serum K+ > 8.0 m Eq/L) IV Calcium gluconate 0.5 mEq/kg – to reverse cardiac effects Above measures IV or nebulized salbutamol Dialysis

Long term management Sodium polyesterene sulphate - ion exchange resin - oral – 15g Q6H ;

rectal – 30g Q12H

HYPERKALEMIA - Nutrition Eliminate high-potassium foods.

meat proteins and dairy products refined foods sugar saturated fats

Avoid alcohol, caffeine Drink more water (dehydration can make it worse) Small, frequent meals can help prevent

hypoglycemia. Magnesium (200 mg 2 to 3 times per day)

helps regulate potassium levels.

CALCIUM ((8.8 - 10.4 mg/dL)8.8 - 10.4 mg/dL)

PTH Renal

Increases Ca2+ reabsorption in DCT

Decreases PO4-  reabsorption in DCT

Increases 1-alpha-hydroxylase (which facilitates the production of 1,25-(OH)2-Vit D)

Bone Increases bone

resorption Facilitates bone

formation

CALCIUM ((8.8 - 10.4 mg/dL)8.8 - 10.4 mg/dL)

HYPOCALCEMIA (Serum Calcium < 8 mg/dL)(Serum Calcium < 8 mg/dL)

Ionized Ca is more physiological important than total calcium Adjusted Ca = (40 – albumin)/40 + measured Ca

Factitious (Reduction in ionized Ca with normal total

plasma calcium) Respiratory alkalosis Citrate toxicity

HYPOCALCEMIA (Serum Calcium < 8 mg/dL)(Serum Calcium < 8 mg/dL)

Factitious (Reduction in ionized Ca with normal total

plasma calcium) Respiratory alkalosis Citrate toxicity

Others Critical illness (sepsis, burns) Pancreatitis Rhabdomyolyis Hyperphosphataemia

HYPOCALCEMIA - Symptoms Muscle cramps and spasms Tetany and/or convulsions Mood changes (depression,

irritability) Dry skin Brittle nails Facial twitching Latent Tetany

Trousseu’s sign Chvostek’s sign

HYPOCALCEMIA - Management Tetany, laryngospasm,

seizures2 ml/kg of 10 % Calcium

gluconate slow IV under cardiac monitoring

Later Oral calcium supplementation

– 40 to 80 mg/kg/dTreat Vit. D def.

HYPERCALCEMIA (Serum Ca++ > 12 mg/dL)(Serum Ca++ > 12 mg/dL)

Parathyroid excess Multiple myeloma, Vitamin D excess Sarcoidosis Subcutaneous fat necrosis William’s syndrome Thyrotoxicosis Prolonged immobilization Metastatic cancer, Multiple bone fractures, Milk-alkali syndrome, and Paget's disease. Drugs

Excessive use of calcium-containing supplements Certain over-the-counter medications (i.e., Antacids)

HYPERCALCEMIA - Symptoms Nonspecific

Fatigue, constipation, depression, confusion, muscle pain, nausea and vomiting, dehydration, increased urination

Irregular heartbeat (arrhythmia), QT shortening

Urinary stones Nephrocalcinosis Stupor & coma – S.Ca > 15 mg/dL)

HYPERCALCEMIA - Management

Forced saline diuresis with fruesemide

Peritoneal dialysis Treat primary cause

HYPERCALCEMIA - Management 1. General measures

• remove offending cause. Treat underlying cause.• dietary restriction• hydration (dilution effect)

2. increase Ca excretion• saline 2-3L over 3-6 hours

maintain urine output 200ml/hourfrusemide 10-40mg Q4H

• consider dialysis3. decrease bone resorption

calcitonin – onset 6-10hoursglucocorticoidsbiphosphonate, mithramycin

CSN VittalCSN Vittal

HYPERMAGNESEMIA

End-stage renal disease, Addison's disease, or An overdose of magnesium salts.

HYPERMAGNESEMIA

Lethargy Hypotension Decreased heart and respiratory rate Muscle weakness Diminished tendon reflexes

HYPOMAGNESEMIA Inadequate dietary intake

Chronic alcoholism Malnutrition

Malabsorption syndromes, Pancreatitis, Aldosteronism, Burns, Hyperparathyroidism, Digestive system disorders, and Diuretic use.

HYPOMAGNESEMIA Leg and foot cramps Weight loss Vomiting Muscle spasms, twitching, and tremors Seizures Muscle weakness Arrhythmia

HYPERCHLOREMIA Severe dehydration, Kidney failure, Hemodialysis, Traumatic brain injury, and Aldosteronism can also cause hyperchloremia. Drugs such as

Boric acid and ammonium chloride and the Intravenous (IV) infusion of sodium chloride can also

boost chloride levels, resulting in hyperchloremic metabolic acidosis.

HYPERCHLOREMIA - Symptoms

Weakness Headache Nausea Cardiac arrest

HYPOCHLOREMIA

Result of sodium and potassium depletion (i.e., Hyponatremia, hypokalemia).

Severe depletion of serum chloride levels causes metabolic alkalosis

HYPOCHLOREMIA - Symptoms

Mental confusion Slowed breathing Paralysis Muscle tension or spasm

HYPERPHOSPHATEMIA Skeletal fractures or disease, Kidney failure, Hypoparathyroidism, Hemodialysis, Diabetic ketoacidosis, Acromegaly, Systemic infection, and Intestinal obstruction can all cause phosphate retention

and build-up in the blood. The disorder occurs concurrently with hypocalcemia

HYPERPHOSPHATEMIA

Asymptomatic, Tingling in hands and fingers Muscle spasms and cramps Convulsions Cardiac arrest

HYPOPHOSPHATEMIA Serum phosphate levels of 2 mg/dl or below may be caused by Hypomagnesemia Hypokalemia Severe burns Alcoholism Diabetic ketoacidosis Kidney disease Hyperparathyroidism Hypothyroidism Cushing's syndrome Malnutrition Hemodialysis Vitamin d deficiency Prolonged diuretic therapy

HYPOPHOSPHATEMIA

Muscle weakness Weight loss Bone deformities (osteomalacia)