Fluid and electrolyte imbalnce

FLUID AND ELECTROLYTE IMBALNCE .

INTRODUCTION

Fluid & electrolyte balance is a dynamic process i.e. crucial for life, as fluid & electrolyte help to maintain health & function in all body system. Water is found everywhere on earth including human body

In an adult 60% of the weight is water Two third of the body’s water is found in

the cell

FUNCTION OF WATER

DISTRIBUTION OF BODY FLUID

The body fluid is distributed into two compartment

1) Intracellular fluid 2) Extra cellular fluid

1)INTRACELLULAR FLUID It is found within the cells

of the body. It constitute of

approximately 2/3 of the total body fluid in adult i.e approx. 40% of body weight.

It is vital to normal cell functioning.

It contains solute such as O2, electrolyte, &glucose.

It provides a medium in which metabolic process of the cell take place.

EXTRACELLULAR FLUID It is found out side the cell & account for

about 1/3 of total body fluid. It is transport system that carries nutrients

& waste products from the cell .It is subdivided into three compartments 1) Interstitial fluid 2) Intravascular fluid 3) Tran cellular fluid

1) INTERSTITIAL FLUID:-- It contains lymph is a fluid between cells & outside the blood vessels.- Accounting for approximately 75% of ECF surrounds the cells. 2) INTRAVASCULAR FLUID- It accounts for approximately 20% of ECF & found within the vascular system.- It is blood plasma. 3) TRANSCELLULAR FLUID- It includes cerebrospinal fluid, pericardial, pancreatic, pleural, intraocular, biliary, peritoneal & synovial fluid.

COMPOSITIONS OF BODY FLUID

The fluid circulating throughout the body in extra cellular & intracellular fluid spaces contain:-

Electrolyte Mineral Cells.

DEFINITION OF ELECROLYTE An ELECTROLYTE is an element or compound that when

melted or dissolved in water or another solvent, dissociate into ions and carry electrical current.

There are positively charged ions & negatively charged ions. Positively charged ions Sodium ( Na+) Potassium ( K+ ) Calcium (Ca+) Negatively charged ions:- Chloride ( Cl-) Bicarbonate ( HCo3-) Sulfate ( So2-) Phosphate ( HPo4-)

MOVEMENT OF FLUID. The method by which electrolyte & other

solutes move are as follows. 1) Osmosis 2) Diffusion 3) Filtration 4) Active transport

1) OSMOSIS

It is themovement ofwater across cell membrane fromlow concentrated solution to moreConcentratedsolution.

2) DIFFUSION It is continual

intermingling of molecule in liquid , gases or solid brought about by random movement of molecule .

Eg. Two gases become mixed by the constant motion of their molecule

3) FILTRATION It is process where

by fluid & solutes move together across a membrane from one compartment to another compartment. The movement is from area of higher pressure to one of lower area.

4) ACTIVE TRANSPORT Substance can move across cell membrane

from less concentrated solution to more concentrated one by active transport.

REGULATION OF FLUID

The body fluid is regulated by:- 1) Fluid Intake 2) Fluid Output 1) Fluid intake:- The adult drinks about 1500 ml of fluid in a

day but need 2500ml/day. This remaining 1000 ml added from food & Oxidation of food from metabolic process

i.e. 750 ml &200 ml respectively

REGULATION OF WATER INTAKE The hypothalamic thirst center is

stimulated: By a decline in plasma volume of 10%–15% By increases in plasma osmolality of 1–2% Via baroreceptor ,osmoreceptors and other stimuli.

Feedback signals that inhibit the thirst centers include: Moistening of the mucosa of the mouth and throat Activation of stomach and intestinal stretch receptors

REGULATION OF OUTPUT. ANTI DIURETIC HORMONE.

ALDOSTERONE.

2) Fluid output :- Fluid losses from body 2500ml .There are

following routes of fluid output e.g.- urine, insensible loss through skin,

perspiration & through lungs & feces.

REGULATION OF ELECTROLYTES. SODIUM.

CALCIUM.

POTTASSIUM

FACTORS AFFECTING FLUID AND ELECTROLYTE IMBALANCE.

FLIUD IMBALANCES The two types of fluid imbalances

that may occur are: fluid volume excess(FVE) fluid volume deficit(FVD)

1) EXTRACELULLAR FLUID VOLUME DEFICIT (HYPOVOLEMIA)

An ECFVD, commonly called as dehydration , is a decrease in intravascular and interstitial fluids

An ECFVD can result in cellular fluid loss if it is sudden or severe .

TYPES OF ECFVD

A) Hyperosmolar fluid volume deficit- water loss is greater than the electrolyte loss

B) Isosmolar fluid volume deficit – equal proportion of fluid and electrolyte loss

C) Hypotonic fluid volume deficit – electrolyte loss is greater than fluid loss

In Mild ECFVD, 1to 2 L of water or 2% of the body weight is lost

In Moderate ECFVD, 3 to 5L of water loss or 5%weight loss

IN Severe ECFVD , 5 to 10 L of water loss or 8% of weight loss

ETIOLOGY AND RISK FACTORS Lack of fluid intake.

Excess fluid loss.

CLINICAL MANIFESTATION Thirst Muscle weakness Dry mucus membrane; dry cracked lips or

furrowed tongue Eyeballs soft and sunken (severe deficit) Apprehension , restlessness, headache ,

confusion, coma in severe deficit Poor skin turgor. Fatigue. Elevated temperature Tachycardia, weak thready pulse

Peripheral vein filling> 5 seconds Postural systolic BP falls >25mm Hg and

diastolic fall > 20 mm Hg , with pulse increases > 30

Narrowed pulse pressure, decreased CVP&PCWP

Flattened neck veins in supine position Weight loss Oliguria(< 30 ml per hour)

LABORATORY FINDINGS Increased osmolality(> 295 m Osm/ kg) Increased or normal serum sodium level (>

145mEq/ L ) Increase BUN (>25 mg / L ) Hyperglycemia ( >120 mg /dl ) Elevated hematocrit (> 55%) Increased specific gravity ( > 1.030)

MANAGEMENT Mild fluid volume loss can be corrected with

oral fluid replacement -if tolerates solid foods -1200 ml to 1500ml of

oral fluids -if takes only fluids, increase the total intake to

2500 ml in 24 hours

Management of Hyperosmolar fluid volume deficit

Hypotonic IV solution, such as D5% in 0.2 %saline If the deficit has existed for more than 24 hours,

avoid rapid correction of fluid [sodium solution to be infused at the rate of 0.5 to 0.1m Eq/ L/ hr]

If hemorrhage is the cause -Packed red cells followed by hypotonic IV fluids is administered

In situations where the blood loss is less than 1 L normal saline or ringer lactate may be used

2) EXTRACELLULAR FLUID VOLUME EXCESS ECFVE is increased fluid retention in the intravasular and

interstitial spaces ETIOLOGY AND RISK FACTORS Heart failure Renal disorders Cirrhosis of liver Increased ingestion of high sodium foods Excessive amount of IV fluids containing sodium Electrolyte free IV fluids SIADH,Sepsis decreased colloid osmotic pressure lymphatic and venous obstruction Cushing’s syndrome & glucocorticoids

CLINICAL MANIFESTATION Constant irritating cough Dyspnea & crackles in lungs Cyanosis, pleural fffusion Neck vein obstruction Bounding pulse &elevated BP S3 gallop Pitting & sacral edema Weight gain Increased CVP& PCWP Change in level of consiousness

LAB INVESTIGATION serum osmolality <275mOsm/ kg Low , normal or high sodium Decreased hematocrit [ < 45%] Specific gravity below 1.010 Decreased BUN [< 8mg/ dl] MANAGEMENT Diuretics [combination of potassium

sparing and potassium depleting diuretics] In people with CHF, ACE inhibitors and low

dose of beta blockers are used A low sodium diet

ELECTROLYTE IMBALANCES.

ELECTROLYTE IMBALANCE 1) HYPONATREMIA (SODIUM DEFICIT):- It means a plasma sodium level is less than 135 mEq/lit It is one of the most common electrolyte disorder in adult. It is usually associated with changes in fluid volume status. Type of Hyponatremia 1)Hypovolemic hyponatremia:- In this sodium loss is greater than water loss. 2)Euvolemic hypoatremia:- When total body water is moderately increased & the

total body sodium at normal level. 3)Hyervolemic hyponatremia:- Greater increased in total body water in total ody sodium. 4) Redistributed hyponatremia:- No changes in total body water or sodium,

water merely shifted between the Intracellular & extra cellular compartment relatively to the sodium concentration

ETIOLOGY:- Hypovolemic hyponatremia:-

Renal loss of sodium from diuretic use Diabetic glycosuria Aldostreron deficiency Intrinsic Vomiting Diarrhea Increased sweating Iliostomy

Euvolemic hyponatremia:- Increase secretion of ADH Pain ,Emotion ,Medication ,Some

cancer ,CNS disorder Hypervolemic hyponatremia:-

Edematous disorder such as Congestive heart failure Cirrhosis of liver Nephrotic syndrome Acute & chronic renal failure

Redistributive Hyponatremia:- Hyperglycemia Hyperlipidemia

OTHER CAUSES:- - Prolonged diuretic therapy - Excessive diaphoresis - Insufficient Na intake - GI losses – suctioning, laxatives,

vomiting - Administration of hypotonic fluids - Compulsive water drinking - Labor induction with oxytocin - Cystic fibrosis - alcoholism

CLINICAL MANIFESTATIONSClinical manifestation of hyponatremia vary with cause type &

rate of onset of sodium or fluid imbalance. CNS:- Confusion Lethargy Hallucination Seizures Muscles twitching/cramping Focal weakness Hemi paresis Papiledema Behavioral changes Convulsion Faintness Brain herniation Coma Death Headache

CVS: Decrease systolic & Diastolic BP Orthostatic hypotension Weak & thready pulse Tachycardia RS:- Crackles in lung. Tachypnea Dyspnea Orthopnea Cheyne stoke respiration Apneustic breathing Ataxic breathing GI:- Nausea Vomiting Hyper active bowel sound Abdominal cramping Diarrhea Other:- Dryness of skin, tongue, & mucous membrane

MANAGEMENT OF HYPONATREMIA. - Monitor for - Restrict fluids - Monitor Vital sign - Monitor serum Na levels - Oral intake of sodium - IV normal saline or Lactated Ringers - If Na is below 115, mEq/L hypertonic saline is ordered - May give a diuretic eg- Furosemide to prevent pulmonary fluid overload or increasing H2O loss - Encourage a balanced diet - I/O monitoring - Safety for weakness or confusion - Assist with ambulation if low B/P

2) Hypernatremia:-_ Plasma sodium

level is greater than 145mEq/ lit It occurs with

excess loss of H2O or excessive retention of Na Can lead to death if not treated

Type of Hypernatremia 1) Hypovolemic hypernatremia:- In it total body water(TBW) is greatly

decreased relatively to sodium (loss of hypotonic fluid)

2) Euvolemic hypernatremia:- In it TBW is decreased relative to the

normal total body sodi 3) Hypervolemic hypernatremia:- In it TBW is increased but the Na+ gains

exceed the water gain.

Etiology:-1) Hypovolemic hypernatremia:-

Renal lossOsmotic diauresisSev.hyperglycemiaProfuse diaphoresisDecrease thirstDiarrhea Inadequate fluid volume replacement Inadequete water intakeExcessive water loss due to fever, vomiting,

excess drainage, polyureaBurn

2) Evolumic hypernatremia:-Excess fluid loss from skin& lungsHypodipsia in older adult & infantDiabetic incipidus

3) Hypervolemic hypernatremia:-Administration of concentrated saline solutionHypertonic feeding (tube feeding)Accidental or intentional salt ingestionCommercially prepared soupRetention of sodium occur in heart ,renal, or

liver disease, Cushing syndrome,hyperaldesterone

Corticosteroid therapy Inadequate ADH

SIGN & SYMPTOMS CNS:-

RestlessnessAgitation IrritabilityMuscles weaknessConfusionSeizuresComaMuscles twitchingTremorsHyperflexiaHyperactive deep tendon reflexes

CVS:- Orthostatic hypotension in hypovolemic hypernatremia In hypervolemic hypernatremia Increase BP Jugular venous distention Prolong peripheral vein emptying S3 gallop sound Edema Weight gain Tachycardia

RS:- - Crackles - Plural effusion GI:-

Anorexia Nausea Vomiting Thirst increase

Renal:- Low UOP or Oliguria in hypovolemic hypernatremia Kidney excreta some of excess water in hypervolemic

hypernatremia Other:-

Dry & flushed skin Mucous membrane become dry & sticky Tongue furrows

Managment - Hypo-osmolar electrolyte solution -(o.2% or 0.4% NaCl)- D5W & furosemide – in hypernatremia

Encourage H2O consumption Low Na diet. Monitor fluid intake on patients with heart or renal disease. Monitor serum Na levels Assess respiratory for crackles Weigh daily Assess skin and mucus membranes Assist with oral hygiene Check neurological status. Safety precautions

POTASSIUM DISORDERS 1) Hypokalemia:- Serum potassium level is

less than 3.5 mEq/lit A serum K+ level below 2.5 or above 7.0 can

cause cardiac arrest

Causes Prolonged diuretic therapy Inadequate intake Restricted K+ diet Weight reduction diet Use of osmosis diuretics. Potassium wasting diuretics e.g.- Thiazide loop, & osmotic

diuretics, steroid, amino glycosides, amphotericine B , digital preparation, Beta adrenergic drug, Cisplastin & bicarbonate

Increase level of Na+ intake promotes K+ loss Alkalosis Healing phase of sev. Injury or burn – as a result of the

shifting of K+ into the cell.

Diuretic phase of renal failure Hyperaldosteronism.Severe diaphoresisNesogastric suctioning laxative use Vomiting Intestinal fistula or iliostemyDiarrhea.Excess stressAcute alcoholism

SIGNS AND SYMPTOMS GI:-

- Anorexia Abdominal distention Constipation

Musculoskeletal:- Muscles weakness may

progress paralysis Leg cramps Parasthesia Hyperreflexia

CNS:- increase conduction of

nerve impulses Fatigue Convulsion Areflexia Coma Drowsiness Lethargy Confusion Depression Dysphasia

CVS:- Decreased myocardial contraction leads Hypotension Slow , weakened pulse Cardiac dysrhythmias Ventricular fibrillation & cardiac arrest due to less K+

level i.e 2.5mEq/li RS:- - Shallow respiration - Shortness of breath - Apnea Renal:- Inhibit the ability of kidney to concentrate urine which leads to:-

Polyuria Nocturia Decrease plasma osmolality Extreme smooth muscles slowing leads to urinary

retention

Treatment & Managment To restore potassium level:- Administer high K+ food

- IV or PO replacement. Give K+ IV diluted in a large vein. Never push K+ as a bolus . Monitor site for infiltration Monitor patients at risk Monitor I/O Monitor EKG Monitor Serum K+ Watch urine out put

Watch patients who take Digitalis for toxicity because low K+ level increases sensitivity of myocardium to digitalis induce dysrhythmia.

Monitor for nausea, vomiting, anorexia, diarrhea, headache, weakness, blurring vision & change in cardiac rate in pt receiving digitalis.

Teach family and patient dietary changes

2) Hyperkalemia K+ level is greater than 5.0mEq/lit Results form impaired renal function Metabolic acidosis Acts as myocardial depressant; decreased heart rate,

cardiac output Muscle weakness GI hyperactivity

Etiology Increased dietary intake

Excessive administration of K+ Excessive use of salt substitutes Excessive release of K+ from the cell during 1st 24-27

hrs after traumatic injury , cell damage, burns, trauma, acodosis

Administration of larger quantities of blood that is old Hyponatremia Renal failure

Signs and Symptoms:- - Tachycardia - Intestinal colic

Mild to moderate hyperkalemia(K+ near by 6mEq/l) cause nerve & Muscles irritability resulting in paresthesia,numbness, tingling

- Diarrhea - K+ 7MEq/l – Na+ channels become

inactivated & Cause disturbances in nerve & muscles

function - Impaired cardiac conduction - Ventricular contraction - Hypotension - Cardiac arrest

- Convulsion - Neuromuscular weakness progressing to

flaccid paralysis & Respiratory muscles paralysis may develop.

-Apathy -Confusion -Numbness/paresthesia ofextremities -Abdominal cramps -Nausea -Oliguria & anuria

Medical mg & Nursing managment:- I/V saline to improve urine output Calcium gluconate IV - to decrease the antagonistic

effect of K+ excess on myocardium Infusion of insulin & glucose or sodabicarb to promote

K+ uptake into the cell Beta-agonist albuterol (0.5mg iv) – it decrease K+ level

within 30 min. lasting for 6 hrs. Administer Kayexolate or sodium polystyrene sulfonate

(oral and rectal) – due to that K+ ion is exchanged for Na+ ion in the intestinal tract & K+ ion is excreted in the stool.

Dialysis .

Cardiac monitoring Monitor pulse, rate and rhythm, and B/P Lung sound Vital sing / apical pulse Urine output 1 hrly Watch for peripheral edema every 4-8 hr Assess for hyperactive bowel sounds Assess sensory and motor function Monitor neurological status ECG monitor

CALCIUM DISORDER 1) Hypocalcaemia :-

Ca++ level less than 8.5 mg/dL Common in older adult because of inadequate intake

ETIOLOGY Decrease intake for several days Dieting or weight reduction Open wound increase loss of Ca++ Renal failure, Inadequate vitamin D consumption. Excess Na+ e.g. in Cushing syndrome – promotes

the excretion of Ca+. Client receiving multiple transfusion of store blood

are at risk of binding of the preservatives citrate with the Ca++

Hyperparathyroidism

Vitamin D deficiency Inadequate exposure to ultraviolet lightAcute pancreatitishyperphosphatemia Medications like1) Magnesium sulphate, Colchicin, & Neomycin

inhibit PTH secretion2) Aspirin, Anticonvulsant & Estrogen after Vit D

metabolism3) Phosphate preparation impairs reabsorption

of Ca++ 4) Steroid increases Ca++ mobilization

5) Antacids & laxatives decreases Ca++ absorption from the intestine

Signs and Symptoms Muscle cramps Hyperactive deep tendon reflexes Hyper excitability Numbness & tingling of fingers, toes, lips and face Emotional labiality (e.g. irritability & anxiety) Tetany Positive Trousseau’s sign/Chvostek’s sign Laryngeal spasms Confusion Memory loss Cardiac insufficiency Cardiac dysrhythmias Hypotension Dysrhythmias Prolong QT interval

Trousseau’s & Chvostek’s sign

Prolong bleeding timeThese abnormalities progress to seizures,

laryngeal stridor, tetany, hemorrhage, cardiac collapse & eventual death

Cataract – with prolong hypocalemia because of increase uptake of Na+ & water by lens.

Dry, spare hair & rough skinSpontaneous fracture can occur when the bone

is depleted of calcium.Can cause skeletal and neuromuscular

abnormalities Impairs clotting mechanismsAffects membrane permeabilityDiagnostic findingsSerum Ca++ levels decrease

- Prolonged PT and PTT

Medical & Nursing managmet:- 1) Restore calcium balance: Asymptomatic hypocalemia is usually corrected with oral

calcium gluconate, calcium lactate or calcium chloride For increased calcium absorption it should be given with

milk & meal Vit D in the milk promotes calcium absorption Treat the cause. Seizure precautions Administer IV Ca++ slowly; watch for infiltration Keep calcium gluconate at bedside Assess nutritional intake of Ca++

2) Hypercalcemia Increased serum levels of Ca++ greater than 10.5 mg/dl.

Cause Hyperthyroidism

Excessive intake of Ca++ supplement withVit D or calcium containing antacids

Excessive use of antacids with phosphate-binding Prolonged immobility – reabsorption of calcium in bone Metabolic acidosis – it promote hypercalcemia by two

mechanisms. Excessive vitamin D intake Thiazide diuretics therapy Renal failure.

Cancer – most common cause of hypercalcemia are malignancies

Thyrotoxicosis metastatic cancer are especially at risk Signs and Symptoms Anorexia Nausea Vomiting Polyuria it leads to dehydration & thirst & further

exacerbates the constipation Muscle weakness Fatigue Dehydration. Confusion impaired memory.

Weakness Depression Difficulty in concentration Osmotic diuresis Ca++ precipitation tends to urethral or kidney stones

which result in urinary blockage & sev. Colicky pain Excess Ca++ also impairs glomerular blood flow , which

can lead to renal failure Bone pain – often associated with Ca bone & is due to

pressure on nerve ending from the tumor cells Pathological # are due to decalcification of bony matrix &

can occur with Ca of bone or any condition that causes reabsorption of Ca++

Calcium deposit can also occur on the skin Progressive neurological depression from increase in

hypercalcemia & is manifested by Lethargy

Depressed sensoriumConfusionComaSev hypercalcemia may result in hypercacemia

crisis, Ca++ reach 7.1 mEq/lit or 15 mg/dlThe resultant increased conduction

transmission, shortened repolarization(shorten QT interval widen T waves

Sev. Cardiac depression can cause cardiac dysrhythmias, ECG changes & cardiac arrest

Personality changesCalcifications in the skin and cornea

Diagnostic Findings Serum Ca++ > 10.5 mg/dl ECG changes

Medical &Nursing Managment:- I/V NS given rapidly with furosimide. Antitumour antibiotics – that inhibit the action of PTH on

osteoclasts in bone tissue which reduce decalcification & the plasma calcium level

Calcitonin - decrease Ca++ level by inhibiting the effect of PTH on osteoclast & increases urinary calcium excretion

Corticosteroid drug decrease the Ca++ level by competing Vit D, resulting in decreased the intestinal absorption of Ca++ & by inhibiting prostaglandins , resulting in decreased bone reabsorption

Restrict calcium food

PHOSPHATE DISORDERS;(2.5-4.5MG/DL)

1) HYPOPHOSPETEMIA:- Phosphorus level is less than 2.5 mg/dl. It can occur from loss of phosphate ions in the

urine or intestine from decreased absorption from the intestine or from intracellular shift of phosphate ions.

Etiology:-Low intake of phosphorous containing foods

such as milk, meat, vegetables due to anorexia, starvation,vomiting, prolong diarrhea

Poor absorption from the GIT Increase renal excretion of phosphate .Excessive ingestion of phosphate-binding

antacids, such as magnesium-aluminium hydroxide(Amphogel,Gelusil, Maaloxetc)

SIGN & SYMPTOMS:CNS:-

Mental irritabilityApprehensionMalaiseParesthesias around the mouthDysarthriaConfusion seizuresComa.

Treatment:- Antacid containing aluminium or magnesium that bind

phosphate should be avoid Milk and other dietry suppliments. I/V phosphorous as a potassium phosphate or sodium

phosphate

2) HYPERPHOSPHATEMIA:-Phosphate level greater than 4.5 mg/dl. Etiology:-Excessive intake of high phosphate foodExcess vit D (especially with renal insufficiency) Impaired colonic motility causing increased

absorptionHypo parathyroidism.MenopauseAddisons diseaseRenal failure

Sign & symptoms:-TachycardiaPalpitationRestlessnessAnoresiaNauseaVomittingHyper-reflexiaTetany

Treatment:-Limit high phosphate food especially milk, ice

cream, cheese, large amount of meat & fish & carbonate beverages or giving calcium aluminium products that promotes the binding & excretion of phosphate

Dialysis for renal failure

MAGNESIUM DISORDER 1) Hypomagnesaemia

Magnesium level is less than 1.5 mEq/l or 1.8 mg/dl.

ETIOLOGY:-

Excess Mg loss from GI – Nasogastric suction , diarrhea, vomiting

Chronic Alcoholism Pancreatitis Burn Chronic malnutrition Malabsoption syndrome – crohn’s or celiac disease

or pancreatitis High volume iliostomy Fistulae Laxatives abuse. Diuretic therapy with loop or thiazide diuretics, or

ammonium chloride

alcoholismAdministration of fluids without MgStarvationUlcerative colitisHypercalcemia. HypoaldosteronismHigh dose steroid use Insufficient dietary intakeEssential for neuromuscular integration;

hypomagnesaemia increases muscle irritability and contractility

Causes decreased blood pressure and cardiac dysrhythmias

Often mistaken for hypokalemia, which can occur simultaneously

Cancer chemotherapy

Signs and Symptoms Anorexia Nausea Abdominal distention Depression Psychosis Confusion Agitation Hallusination Convulsion Increases reflexes, clonus , a positive babinski sign Tachycardia

AtaxiaNystagmusTetany with chvostek signMuscles fasciculationMuscles cramps Paresthesias of feet & legs Abnormal electrocephalogram.Vasomotor changes such as painful cold hands

& feet or increased perspiration, & nonspecific T wave changes in ECG

Dysphagia

Cardiac dysrhythmias TremorHyperactive deep tendon reflexesPositive Chvostek’s and Trousseau’s signsMemory lossEmotional liabilitySeizures

Diagnostic FindingsSerum Mg level < 1,5 mEq/literHypocalcaemiaHypokalemiaEKG changes

Medical & Nursing Management.Inj. Magnesium sulphate IM/IV/orallGreen vegetablesNutsBeansFruitslegumes

2) Hypermagnesemia Mg level greater than 2.5 mEq/lit .

Causes Renal failure Excessive use of Mg containing antacids Untreated diabetic ketoacidosis Hypoadrenalism Frequent magnesium sulphate enemas used in

congenital megacolon Hypocalcemia Many potassium sparing diuretics conserve

magnesium

Signs and Symptoms Lethargy and drowsiness Sev. Muscles weakness Loss of deep tendon reflexes respiratory paralysis Loss of conciousness Cardiac sign – wide QRS complex, elevated T wave Heart block Premature ventricular contraction Depress neuromuscular activity Depresses respirations Sensation of warmth throughout the body Hypotension BradycardiaCardiac arrest

Medical ManagmentSaline infusion with diuretics

increase the renal elimination of mgI/V calcium may be given to

antagonize the effect of hypermagnesemia

Albuterol also used to reduce mg level

In Respiratory distress require ventilator support

In renal failute hemodialysis.Avoid constant use of laxatives.

CHLORIDE. EQUILIBRIUM IN BODY.

HYPOCHLOREMIA. GI DRAINAGE. SALT RESTRICTED DIET. SEVERE DIARRHEA. VOMITING.

CLINICAL FEATURES. HYPER EXCITABILITY OF MUSCLES. TETANY. HYPERACTIVE DTR. WEAKNESS TWITCHING. MUSCLE CRAMPS.

MANAGEMENT. CORRECT THE CAUSE IV NS OF 0.45%. DIET. -TOMATO JUICE. -SALTY BROTH. -PROCESSED MEAT. -FRUITS.

HYPERCHLOREMIA. MORE THAN 106 Meq/ liter.Causes Increased intake Reduced elimination by urine.

CLINICAL FEATURES. Tachypnoea. Weakness. Lethargy. Deep rapid respirations. Reduced cognition.

TREATMENT. IVF RL. IV SODIUM BICARBONATE. DIURETIC SODIUM AND WATER RESTRICTION.

THANK YOU