Alterations in Fluid, Alterations in Fluid, Electrolyte and Acid-Base Electrolyte and Acid-Base

Balance in ChildrenBalance in Children

Dr. Nataliya Haliyash, MD, BSN

Institute of Nursing, TSMU

Pediatric Differences

• ECF/ICF ratio varies with age• Neonates and infants have

proportionately larger ECF volume• Infants: high daily fluid

requirement with little fluid reserve; this makes the infant vulnerable to dehydration.

FIGURE 23–2 The newborn and infant have a high percentage of body weight comprised of water, especially extracellular fluid, which is lost from the body easily. Note the small stomach size which limits ability to rehydrate quickly.

Jane W. Ball and Ruth C. BindlerChild Health Nursing: Partnering with Children & Families

© 2006 by Pearson Education, Inc.Upper Saddle River, New Jersey 07458

All rights reserved.

Fluid Loss; Infants and <2yr.

• excretion is via the urine, feces, lungs and skin

• have greater daily fluid loss than older child• more dependent upon adequate intake• greater about of skin surface (BSA),

therefore greater insensible loss.• respiratory and metabolic rates are higher• therefore, dehydrate more rapidly

Mechanism to Restore balance

• kidney: conserves water, regulates electrolyte excretion• <2yr kidneys immature• less able to conserve or excrete water

and solutes effectively• greater risk for acid/base imbalances• Will use the SG norm: 1.005-1.015

Fluid Volume ImbalancesFluid Volume Imbalances• Dehydration: loss of ECF fluid and sodium.

• Caused by: vomiting, diarrhea, hemorrhage, burns, NG suctioning and drainage loss, adrenal insufficiency.

• Manifested by wt loss, poor skin turgor, dry mucous memb., VS changes, sunken fontanel

• Dehydration that is not corrected will lead to hypovolemic shock and death.

• Fluid overload: excess ECF fluid and excess interstitial fluid volume with edema. • Causes: fluid overload, CHF.• Manifested by wt.gain, puffy face and extremities, enlarged

liver.

Clinical Manifestations of Clinical Manifestations of DehydrationDehydration

Depend on the degree of dehydration. • Weight loss • Rapid-thready pulse • Hypotension • Decreased peripheral circulation• Decreased urinary output• Increased specific gravity • decreased skin turgor• dry mucous membranes• absence of tears• a sunken fontanel in infants.

Nursing ConsiderationsNursing Considerations

• How can the nurse determine if the child is mildly dehydrated vs moderately dehydrated?

Mild Dehydration:Mild Dehydration: by history.

• hard to detect because the child may be alert, have moist mucous membranes and normal skin turgor.

• Wt loss may be up to 5% of body weight.• The infant might be irritable; the older

child might be thirsty• vital signs will probably be normal• Capillary refill will most likely be normal• Urine output may be normal or sl less

Moderate DehydrationModerate Dehydration

• dry mucous membranes; delayed cap refill >2 sec; Wt loss 6-9% of body weight

• irritable, lethargic, unable to play, restless• decreased urinary output: <1ml/kg/hr; dark

urine with SG > 1.015 (in child >2yr)

• Sunken fontanel• HR increased, BP decreased. Postural vital

signs

Severe DehydrationSevere Dehydration

• wt loss > 10% body weight• lethargic/comatose• rapid weak pulse with BP low or

undetectable; RR variable and labored.• dry mucous membranes/parched;

sunken fontanel• decr or absent urinary output.• Cap refill >4sec

Types of Dehydration and Sodium Loss

• Sodium may be:• Low• High • Or normal

Isotonic Dehydration or Isotonic Dehydration or Isonatremic DehydrationIsonatremic Dehydration

• Loss of sodium and water are in proportion• Most of fluid lost is from extracellular

component• Serum sodium is normal (130-150mEq/L)

Harriet Lane Handbook, 2000.• Most practitioners consider below 135 and above

148 a more conservative parameter (138-148)• Most common form of dehydration in young

children from vomiting and diarrhea.

Hypotonic or Hyponatremic Hypotonic or Hyponatremic DehydrationDehydration

• Greater loss of sodium than water• Serum sodium below normal• Compensatory shift of fluids from

extracellular to intracellular makes extracellular dehydration worse.

• Caused by severe and prolonged vomiting and diarrhea, burns, renal disease. Also by treatment of dehydration with IV fluids without electrolytes.

Hypertonic or Hypernatremic Hypertonic or Hypernatremic DehydrationDehydration

• Greater loss of water than sodium• Serum sodium is elevated• Compensatory shift from intracellular

to extracellular which masks the severity of water loss (dehydration) delaying signs and symptoms until condition is quite serious.

• Caused by concentrated IV fluids or tube feedings.

Clinical Manifestations Clinical Manifestations Associated with Degree of Associated with Degree of

DehydrationDehydration

Dehydrated child

• Before… and after treatment

Nursing Diagnoses

• Nursing diagnoses appropriate for a child with dehydration may include:

1. Deficient fluid volume related to excessive fluid volume loss or inadequate fluid intake.

2. Risk for injury (fall) related to orthostatic (postural) hypotension.

3 . Deficient knowledge (caregiver) related to lack of exposure to information about preventing/detecting dehydration.

Outcome Identification

1. The child will receive sufficient fluids to replace losses.

2. The child will exhibit signs of adequate hydration.

3. The child will not fall or sustain other injuries while hypotensive or lethargic.

4. Caregivers will demonstrate understanding of conditions that can lead to dehydration and of the early signs and symptoms.

Planning/Implementation• Nursing interventions include:

• assessment of daily weight, vital signs, and maintenance of accurate intake and output records.

• Blood may be drawn to assess electrolytes, BUN and Creatinine levels

• administration of oral or IV fluids.• Injury due to falls can be prevented by making sure

that the side rails of the bed are raised, assessing level of consciousness, and monitoring the serum sodium level.

• An elevation in serum sodium will cause the brain cells to dehydrate and result in a loss of consciousness if not corrected quickly.

DiarrheaDiarrhea

•is increase in the number of stools and/or a decrease in their consistency as a result of malabsorption or alterations of water and electrolyte transport by the alimentary tract.•Diarrhea may be acute or chronic.

Grades of diarrhea

• Mild diarrhea – 4 to 7 loose stools each day as a rule without other evidence of illness

• Moderate diarrhea – 8 to 15 loose or watery stooles daily with elevated temperature, vomiting, irritability, mild dehydration

• Severe diarrhea – numerous (>15) to continuous stools, evident signs of moderate to severe dehydration, drawn, flaccid expression, high pitched cry, irritable or lethargic or even comatose.

Acute gastroenteritisAcute gastroenteritis

•is characterized by the passage of ≥3 loose or watery stools in an 24 hour period, or the passage of one or more bloody stools, with or without vomiting, nausea, fever, and abdominal pain.

•Acute gastroenteritis usually refers to as an illness lasting no longer than 10-14 days.

Etiology of acute Etiology of acute diarrheadiarrheaViral agentsViral agents Bacterial pathogensBacterial pathogens

Human rotavirusSmall round viruses:NorwalkTauntonSnow MountainAstrovirusWollanEnteric adenovirusesCoronaviruses

Escherichia coliCampylobacterSalmonellaShigellaVibrio choleraYersinia enterocoliticaClostridium difficile

Parasitic pathogensParasitic pathogens Helmintic pathogensHelmintic pathogens

Protozoa:Giardia lambliaCryptosporidiumEntamoeba histolyticaBalantidium coli

Nematodes:Ancylostoma duodenaleStrongyloides stercoralisNecator americanusTrichuris trichiuraTrematodes:SchistosomaCestodes:Taenia soliumTaenia saginataDiphyllobothrium latum

Pathogenesis of Acute Pathogenesis of Acute DiarrheaDiarrhea

• Diarrhea results when the net intestinal fecal loss of fluid and salt exceeds the absorbed amount.

• There are 5 pathogenic forms of diarrhea:1. Toxigenic diarrhea2. Osmotic diarrhea3. Secretory diarrhea4. Invasive diarrhea5. Motility disorders

Toxigenic diarrheaToxigenic diarrhea

• Toxins from bacteria, like enterotoxigenic E.coli or Vibrio cholerae, bind to specific receptors: labile toxin (LT) raises the level of cyclic guanosine

monophosphate (cGMP) in the intestinal mucosa, stable toxin (ST) increases the adenasine 3 ׳5:׳ -

cyclic monophosphate (cAMP)

• This leads to blocking the absorption of Na and Clˉ ions into the villous enterocytes.

• LT induce the secretion of Clˉ and HCO3ˉ ions by crypt cells.

Osmotic diarrheaOsmotic diarrhea

• Characterized by a positive osmotic gap of the stool

• Clinically, osmotic diarrhea is distinguished by the fact that the diarrhea diminishes when the patient fasts or stops eating the poorly ingested solute.

Differential diagnosis of Differential diagnosis of osmotic and secretory osmotic and secretory

diarrheadiarrheaStools Stools Osmotic diarrheaOsmotic diarrhea Secretory diarrheaSecretory diarrhea

Electrolytes Na<70 mEq/l Na>70 mEq/l

Osmolality >(Na + K)2 =(Na + K)2

pH <5 >6

Reducing substances

Positive Negative

Volume < 200 ml/day > 200 ml/day

Secretory diarrheaSecretory diarrhea

• There is no positive osmotic gap and the stool osmolality is equal to the ionic constituents: (Na + K)2 = stool osmolality

• Food ingestion does not usually affect the stool volume

• The stool is watery without blood or pus and is characterized by very high volume and ion output

Invasive diarrheaInvasive diarrhea

• Is caused by direct mucosal damage by the invasive organism

• It is similar to colitis and is usually associated with blood and mucous.

Motility disordersMotility disorders

• Hypermotility can cause diarrhea by reduction of contact time between intestinal mucosa and its contents, despite normal absorption function of the cell

• Hypomotility can be primary, as in idiopathic intestinal pseudo-obstruction syndrome, or secondary to neuronal disorders.

Clinical characteristics of infectious Clinical characteristics of infectious gastroenteritis in dependence on gastroenteritis in dependence on

enteropathologic cause.enteropathologic cause.Organism Organism Characteristics Characteristics Comments Comments

Rotavirus Incubation period:2-3 d.

Abrupt onsetFever (≥ 38°C) for 48 hhAssociated upper resp.tract infection

Incidence higher in cool weather6- to 24-month-old infants are more vulnerable

Norwalk-like virusesInc.period: 1-2 days

FeverLoss of appetiteNausea/vomitingAbdominal painMalaise

Source of infection: drinking water, foodAffects all agesSelf-limited

Pathogenic Pathogenic Escherichia Escherichia colicoliIncubation period: highly variable

Diarrhea with moist-green, watery stool with mucus; becomes explosiveVomiting may be present from onsetAbdominal distensionFever, intoxication

•Incidence higher in summer•Usually interpersonal transmission, but may transmit via inanimate objects

Salmonella Salmonella groups groups (nontyphoidae(nontyphoidae)) – gram-negative, non-encapsulated, nonsporulatingIncubation period: 6 hh-21 day

Rapid onsetVariable symptoms – mild to severeNausea, vomiting, and colicky abdominal pain followed by diarrhea, occasionally with blood and mucusInfants may be afebrile and nontoxic

•Highest incidence in children younger than 9 years, especially infants•Transmission – via contaminated food and drink, more commonly poultry and eggs

Shigella Shigella groupsgroups – gram-negative, nonmotile, anaerobic bacilliIncubation period: 1-7 days

Onset usually abruptFever (to 40.5°C) and cramping abdominal pain initiallyFebrile convulsions in 10 % casesHeadache, neck rigidity, delirium

Transmitted directly or indirectly from infected persons

Vibrio choleraeVibrio cholerae groupsgroupsInc.period: 1-3 days

Sudden onset of profuse, watery diarrhea without cramping, tenesmus, or anal irritationStools are intermittemt at first, then almost continuousStools are whitish, almost clear, with flecks of mucus – “rice water stools”

Rare in infantsMortality is highTransmitted via contaminated food or water

Food poisoning:Food poisoning:

StaphylococcusStaphylococcusIncub.period:4-6 hours

Nausea,vomitingSevere abdominal crampsProfuse diarrheaShock may occur in severe casesMay be a mild fever

•Transfered via contaminated food – inadequately cooked: custards, mayonnaise, cream-filled desserts•Self-limited (24-72 hours)•Exellent prognosis

BotulismBotulism

Clostridium Clostridium botulinumbotulinumIncub.period:12 hr – 3 days

Nausea,vomitingDiarrheaCNS symptoms with curare-like effectDry mouth, dysphagia

Transfered via contaminated foodVariable severity – mild symptoms to rapidly fatal within a few hoursAntitoxin administration

Diagnosis• Diagnosis is based on:• the history, physical exam, and laboratory

studies focused on evaluating the child's hydration status and identifying the causative agent.

• The history should include the following data:• Recent exposure to infectious agents• Travel history• Exposure to contaminated food and water supplies• Exposure to turtles• Attendance at a day-care center

If no systemic manifestations are present:

• Diagnostic laboratory tests are not indicated.

• Stool cultures should be performed for:• children with a fever lasting more than 24

hours,• blood or mucus in the stool, • a family or household member with

similar symptoms, • or a positive stool white blood cell stain.

Treatment Treatment

The main treatment aims are:• To prevent dehydration –

restoration and maintenance of adequate hydration and electrolyte balance.

• Nutritional support, adequate to prevent protracted diarrhea and malnutrition.

What about antimicrobial What about antimicrobial therapy?therapy?

• In about 30 % of patients no specific agent can be found

• Most of the isolated pathogenic organisms are viral

• The majority of the bacterial pathogens are self-limited

• In some cases, antimicrobial therapy prolongs the infection duration

• Antibiotic therapy has no effect on fluid transport nor on nutritional support

When should antibiotics When should antibiotics be used?be used?

• In young infants• In immunocompromised patients• When a systemic bacteremia is

suspected.• In case of specific persisting infection

caused by Yersinia, Campylobacter, and Giardia

RehydrationRehydration

• In the majority of cases of acute diarrhea with mild or moderate dehydration, this aim can be achieved with oral rehydration solutions (ORS)• 1-3 tsp of ORS every 10-15min to start (even if

vomits some)• 50ml/Kg/Hr is the goal for rehydration.

• Severe dehydration requires immediate admission to hospital and intravenous replacement of fluid and electrolytes.

The rationale for the use The rationale for the use of ORSof ORS

1. During diarrhea, the normal mechanism for water and sodium absorption is impaired, so, the replacement of water or saline fluids alone will only lead to more diarrhea.

2. The sodium-glucose-coupled transport generally remains intact. This mechanism stimulates water transport by solvent drag.

The basic components of The basic components of ORSORS

• Glucose• Electrolytesin an isotonic solution.

In the World Health Organization formula the glucose concentration

is 2 %.

WHO recommendations for a WHO recommendations for a sodium concentrationsodium concentration

• 90 mEq/l, essentially for treatment of cholera

• 30-60 mEq/l for countries, where cholera is not a concern and the stool sodium concentration in diarrheal illness is much lower

• 30-40 mmol/l for neonates up to 2 mo whose kidneys have less capacity to excrete excess amounts of fluid and salt

Rehydration Fluids

• The World Health Organization recommends the following electrolyte concentrations for rehydration fluids:• 20 g glucose/L, • 90 mEq sodium/L, • 80 mEq chloride/L,• 20 mEq potassium/L, • and 30 mEq bicarbonate/L.

• Encourage caregivers to look at product labels and make sure that the rehydration fluid they are choosing has the above electrolyte concentrations.

Composition of oral Composition of oral electrolyte solutions (in electrolyte solutions (in

mEq/l)mEq/l)Na+ K+ Clˉ

Other anion

CHO(%)

WHO solution 90 20 80 30 2

Gastrolyte 90 20 80 30 2

Pedialyte 45 20 35 30 2.5

Rehydralyte 75 20 65 30 2.5

infalyte 50 20 40 30 2

Composition of Composition of “clear liquid” solutions “clear liquid” solutions

Na+ K+ CHO(%)

Pepsi Cola

1-2 0.1 10.9

Coca Cola

1-2 0.1 10

Root beer 6 0.6 10.6

Super-ORSSuper-ORS

• Recent studies demonstrate the advantage of short glucose polymers as the carbohydrate source in ORS

• Traditionally it is widely used rice water + 3-5 % sugar syrup.

• Or carrot decoction: 500 g of cleansed carrot boil in 1 l of water during 1 hour, then mash it to homogenous mass and add boiled water up to 1 l. Boil for 10 min. Add 3 tsf of lemon juice. Give 1-2 teaspoon every 5-10 min up to 400 ml/day.

Why are drinks high in glucose avoided during

rehydration?• Simple sugars increases the

osmotic effect in the intestine by pulling water into the colon, thereby increasing diarrhea and subsequent fluid/electrolyte loss

• Drinks high in glucose: apple juice, sodas, jello water.

Recommended foods during rehydration

progression:• In this question opinions differ:

“bowel rest” versus “early feeding” is still controversial.

• Generally, formula feeding should be introduced gradually by starting with dilute mixtures.

• In practice, refeeding can start gradually after 24 hr of only fluid intake, i.e.,”bowel rest”.

• An exception is made for nursing infants, who should continue their regular feeding.

• Children already on solid foods are easier to handle. Food with a high content of disaccharides and monosaccharides (fruits, sweets) should be withheld in the convalescent period.

• Foods with starch carbohydrates (cereal, rice, noodles, bananas, potatoes, carrot, cooked fruits & vegetables), soups, yogurt should be encouraged.

• It is important to give often small food-intakes (up to 8-10 times per day)

IV Therapy• Used for severe dehydration or in the

child who will not/cannot tolerate ORS• Half 24hr maintenance plus

replacement given within first 6-8hr (in ER) to rapidly expand the intravascular space. Usually a normal saline bolus.

• slower IV rate for the remainder of the first 24hrs

• nurse records IV vol infused hourly

Rehydration and IV solution

• Why is the child initially rehydrated with a normal saline bolus and not an IV solution with potassium?

• Potassium is only added to an IV after the patient has voided to avoid hyperkalemia in a child with little or no urinary output

Adding Potassium to Adding Potassium to Intravenous SolutionsIntravenous Solutions

• Be sure that the child is able to void (1 -2 ml/kg/hr) before adding potassium to the IV.

• Children who are dehydrated are oliguric and can become anuric. An anuric child will not be able to excrete electrolytes that are in the IV solution; therefore, if potassium is added to the IV, it would result in an elevated serum potassium. An elevated serum potassium can cause cardiac irritability and ventricular fibrillation.

• Always check the dose and dosage calculations prior to giving. Never give more than 40 mEq/L at a rate not to exceed 1 mEq/kg/hr.

• After adding potassium to an IV bag, shake it to make sure the potassium is equally distributed.

• Never give potassium by IV push.Never give potassium by IV push.

Which of the following IV solutions replaces Sodium?

• D5 W• Lactated Ringers• Normal Saline• D5 ½ NS

• Answer: All but D5 WAnswer: All but D5 W

Calculation of intravenous fluid needs: maintenance

• For the 1st 10 Kg, replace at 100ml/Kg

• for the second 10 Kg, replace at 50ml/Kg

• for >20kg, replace at 20ml/Kg

Example of Maintenance Fluid Calculation

• Your patient is a 10 yr old weighing 35 Kg. You want to determine this patient’s 24hr maintenance fluid needs:

• for the first 10 Kg give 100ml/Kg = 1000ml• for the second 10 Kg: 50ml/Kg = 500ml• for the remaining 15 Kg (35-20Kg) , replace

at 20 ml/Kg: 20 15 = 300ml • 1000 + 500 + 300= 1800 ml/day.

How much fluid should this patient get per hour?

• 1800 ml / 24 hrs = 75 ml/hr.• Therefore, if the patient was NPO and not

taking in fluids from any other source, the IV should be running at 75ml/hr.

• If there is a deficit that also needs to be replaced, the IV rate may be slightly higher for a defined period of time.

• If the patient is receiving fluids from other sources, these need to be accounted as well

Practice Problems for Calculating 24hr Fluid Maintenance and the

hourly IV rate for:

• A 9 yr old patient who weighs 20 Kg.

• A 6 mo old baby who weighs 8 Kg

• An 24mo old toddler who weighs 18 Kg

• A 3 yr old preschooler who weighs 28 Kg

• An 18 yr old who weighs 50 Kg

Answers for 24hr Fluid Calc.

• 9yr old wt 20 Kg = 1500 ml/day• 6mo old wt 8Kg= 800 ml/day• 36mo old wt 18 Kg= 1400 ml/day• 3yr old wt 28Kg=1660 ml/day• 18yr old wt 50Kg= 2100 ml/day• Adult > 50Kg= 2-3 L/day

Fluid Overload:Edema

capillary blood flow: inflammation, infection• venous congestion: ECF excess, R sided heart

failure, muscle paralysis. albumin excess: Nephrotic Syndrome albumin synthesis: Kwashiorkor, liver cirrhosis capillary permeability: inflam/ burns• blocked lymphatic drainage: tumors/surg.

Clinical Assessment / Management of Edema

• assess dependent limbs if ambu or sacrum if lying

• ascites; periorbital edema; rings too tight

• pitting edema for degree of swelling

• daily wt and strictly In and Out

• elevation/change position Q2hr/ protect skin against breakdown

• distraction to deal with discomfort and limitations

of edema.

Electrolyte Imbalances

• Electrolytes usually gained and lost in relatively equal amounts to maintain balance

• Imbalance caused by:• Abnormal route of loss

(vomiting/diarrhea) can disturb electrolyte balance

• Disproportionate IV supplementation• Disease states: renal dis.

Hypernatremia

• Excess serum sodium in relation to water• Causes:

• Too concentrated infant formula• Not enough water intake• Clinical manif.: thirst, lethargy, confusion• Seizures occur when rapid or is severe.• SG concentrated 1.020-1.030• Lab test: serum sodium• Treatment: hypotonic IV solution

Hyponatremia

• Excess water in relation to serum sodium

• Most common sodium imbalance in children

• Causes:• Infants vulnerable to water

intoxication:dilute form, excess pool water, poorly developed thirst mech so cont to drink and can’t excrete excess water.

Hyponatremia (cont)

• Clinical manif: decreased level of consciousness d/t swelling of brain cells.• Anorexia, headache, muscle weakness,

decreased DTR’s, lethargy, confusion or coma.

• Seizures occur when rapid or severe.• SG dilute: 1.000-1.0005• Lab tests: serum sodium

• Treatment: hypertonic solution.

Hyperkalemia

• Excess serum potassium• Causes:

• excess K intake from IV overload, blood transfusion, rapid cell death (hemolytic crisis, large tumor destruction from chemo rx, massive trauma, metabolic acidosis from prolonged diarrhea and in DM when insulin levels are low• Insulin drives K back into the cells

• decreased K loss from Renal insufficiency

Hyperkalemia (cont)

• Clinical manif: all are related to muscle dysfunction: hyperactivitiy of GI smooth muscle: intestinal cramping and diarrhea.• Weak skeletal muscles• Lethargy• Cardiac arrhythmias (tachycardia, prolonged QRS, peaked T

waves: also AV block and VTach).• Lab test: serum potassium• Treatment: correct underlying condition (take K out of the IV)• dialysis (peritoneal or hemo), Kayexalate (po or enema), K

wasting diuretics, IV calcium, bicarbonate, insulin and glucose.

• Low potassium diet.

Hypokalemia

• Decreased serum potassium• Causes: diarrhea and vomiting, ingestion

of large amts black licorice, diuretics, osmotic diuresis (glucose in urine as in DM), NPO without K replacement in IV, NG Sx, bulimia, insulin. • Also in nephrotic syndrome, cirrhosis,

Cushing Syndrome, CHF (to be covered elsewhere)

Hypokalemia (cont)

• Clinical manif: muscle dysfunction• Slowed GI smooth muscle resulting in

abdominal distention, constipation and paralytic ileus

• Skeletal muscles are weak; may effect respiratory muscles

• Cardiac arrhythmias: hypokalemia potentiates Digitoxin Toxicity.

• Lab test: serum potassium• Treatment: oral and/or IV potassium, diet

rich in K.

Hypercalcemia

• Excess calcium• Needs vit D for efficient absorption; most

of Ca is stored in the bones.• Causes: bone tumors that cause bone

destruction, chemo rx release Ca from the bones; immobilization causes loss from the bones (usually excreted) but if kidneys can’t clear it, hypercalcemia results, increased intake (milk-alkali syndrome).

Hypercalcemia (cont)

• Clinical manif: Ca imbalances alter neuromuscular irritability with non-specific symptoms• Constipation, anorexia, N/V, fatigue, skeletal

muscle weakness, confusion, lethargy.• Renal calculi, cardiac arrhythmias• HyperCa increases Na and K excretion

leading to polyuria and polydipsia.• Rx: serum Ca, Ionized Ca, fluids, Lasix,

steroids, dialysis.

Hypocalcemia

• Decreased serum calcium• Causes: decreased intake of Ca and/or Vit D

(adolescents are vulnerable d/t fad diets and the deficit cannot be made up later, increasing risk for osteoporosis).• Limited exposure to sunlight, premature infants and

dark skinned people at increased risk to inadeq. Vit D and therefore decreased Ca absorption.

• Parathyroid dysfunction, multiple transfusion (Citrate binds Calcium), steatorrhea (as in pancreatitis and Cystic Fibrosis) binds Calcium in the stool.

Hypocalcemia (cont)

• Clinical Manif:acute situation related to increased muscular excitability: tetany. +Chvostek’s Sx, + Trousseau’s Sx.

• In children: Twitching, cramping, tingling around the mouth or fingers, carpal/pedal spasms.

• In infants: tremors, muscle twitches, brief tonic-clonic seizures, CHF.

• Laryngospasm, seizures and cardiac arrhythmias in severe situations.

Chvostek’s Sx: tap the skin lightly in front of the ear (over the facial nerve), if the corner of the mouth draws up, d/t muscular contraction = +Chvostek’s Sx.Trousseau’s Sx: + if carpal spasm after BP cuff inflated ~ 3min.

Hypocalcemia (cont 2)

• In children and adolescents, chronic hypocalcemia more common, manif. By spontaneous fractures.Lab tests: serum Ca; bone density studyRx: oral and/or IV Ca, Ca rich diet

Hypermagnesemia

• Excess in Mg.• Imbalances characterized by

neuromuscular irritability• Causes: impaired renal function, Mag

Sulfate given perinatally to treat eclampsia, increased use of laxatives, enemas, antacids, IV fluid additives.

Hypermagnesemia (cont)

• Clinical Manif: decreased muscle irritability, hypotension, bradycardia, drowsiness, lethargy, weak or absent DTR’s.

• Rx: increase fluids, diuretics, dialysis.

Hypomagnesemia

• Decreased serum Mg.• Stored in cells and bones• Causes: prolonged NPO without

replacement, chronic malnutrition, chronic diarrhea, short bowel syndrome, malabsorption syndromes, steatorrhea, multiple transfusions, prolonged NG Sx, some medications.

Hypomagnesemia (cont)

• Clinical manif: increased neuromuscular excitability (tetany). Hyperactive reflexes, skeletal muscle cramps, twitching, tremors, cardiac arrhythmias, seizures.

• Lab: serum Mg along with Ca and K. • Rx: po/IV Magnesium admin and

treating underlying cause of imbalance.

Critical Thinking: Clinical Evaluation of Fluid and Electrolyte Imbalance

• How can you evaluate children appropriately for fluid and electrolyte imbalance without thinking through the clinical manifestations of every possible disorder, one after the other?

Answer to Critical Thinking:

3 paragraphs of text that review this concept and pull the content together with clinical application:

• 1) risk factor assessment• 2) exam several body systems: cardiovascular,

respiratory, neurological• 3) look for factors that alter intake, retention, and loss

of fluids and electrolytes• 4) consider growth and development to realize

problems most common to the age group.• 5) clinical assessment: wt, fluid balance, vascular

volume (BP, HR), interstitial volume (edema?), mentation, DTR’s, muscle irritability, GI function, cardiac rhythm, assess electrolyte levels.

Fluid and Electrolyte Worksheet

• Use the fluid and electrolyte worksheet to help review some of the major concepts of fluid and electrolyte imbalance.

pH

- Is the acidity or alkalinity of a solution.- From French pouvoir hydrogènepouvoir hydrogène ("hydrogen power“) - pH is the Hydrogen ion concentration [H+] of a solution.- It is a measure of the solution's acidity.

• pH is defined as the negative logarithm of the concentration of H+ ions:

pH = -log10[H+]

• The greater the concentration of H+, the more acidic a solution is.

• The lower the concentration of H+, the more basic or alkaline a solution becomes.

Neutral

Acidic Alkaline

71 14

Neutral

H+

HCO3-

Alkaline

Acidic

Acid Base Balance

• normal arterial blood pH: 7.35-7.43 (in general)

• Acidosis < 7.35 : too much acid• Alkalotic > 7.43 : too little acid• pCO2 reflects carbonic acid status:

• 40 mmHg (+- 5)

• HCO3- reflects metabolic acid status: • 24 mmol/l (+- 4)

Respiratory Acidosis

• caused by decr respir effort• build up of CO2 in the blood• pH decr or normal; pCO2 incr.• Symptoms manifested: confusion,

lethargy, HA, incr ICP, coma, tachycardia, arrhythmias

Management of Respiratory Acidosis

• Incr ventilatory rate• give O2• intubate• adm NaHCO3

Clinical Conditions that cause Respir Acidosis

• conditions associated with decreased respiratory drive, impaired gas exchange/air trapping, ie:

• head trauma, general anesthesia, drug overdose, brain tumor, sleep apnea, mechanical under ventilation, asthma, croup/epiglottitis, CF, atelectasis, MD, pneumothorax.

Respiratory Alkalosis

• caused by hyperventilation• CO2 is being blown off• pH incr : pCo2 decr• Symptoms: dizziness, confusion,

neuromuscular irritability, paresthesias in extremities and circumoral, muscle cramping, carpal or pedal spasms.

Management of Resp. Alkalosis

• First determine if oxygenation is adequate, if not, you don’t want to slow the RR.

• Determine the cause and correct it: • Causes of hypervent: hypoxemia, anxiety, pain,

fever, ASA toxicity, meningitis/encephalitis, Gram - sepsis, mechanical overventilation.

• Ipecac is no longer recommended for treatment of ingestions.

Metabolic Acidosis

• caused by a loss of bicarbonate (HCO3)• therefore, is an incr of acids in the blood• pH decr or moving towards normal• pCo2 decr ; HCO3 decr• Symptoms: Kussmaul respirations = incr

rate and depth as compensation (hyperventilation / acetone breath), confusion, hypotension, tissue hypoxia, cardiac arrhythmias, pulmonary edema.

Management of Metabolic Acidosis

• Identify and treat underlying cause• In severe case may give IV NaHCO3 to incr pH,

or insulin/glucose.• Causes of MA for gain of acid: ingestion of ASA,

antifreeze, oliguria, RF, HAL, DKA, starvation or ETOH KA, lactic acidosis (tissue hypoxia).

• Loss of HCO3: maple syrup urine disease, diarrhea, RF.

Metabolic Alkalosis

• caused by loss of H+ or HCO3 retention

• HCO3 incr with probable incr in pH, incr pCO2.

• Symptoms:weak, dizzy, muscle cramps, twitching, tremors, slow shallow resp., disorientation, seizures.

Management of Metabolic Alkalosis

• correct underlying cause; facilitate renal excretion of HCO3.

• admin NS, K+ if hypokalemic, replace loss of fluids, prec for Sz, monitor I and O and electrolytes

• Causes: prolonged vomiting, ingestion of lg quantities of bicarb, antacids, loss of NG fluids, hypokalemia from prolonged diuretic use, multiple blood transfusion with citrate.

ABG Basic (Uncompensated) Analysis

• Resp Acidosis: low pH and high PaCO2

• Resp Alkalosis: incr pH and low PaCO2

• Metab Acidosis: low pH and nl PaCo2; decr HCO3

• Metab Alkalosis: high pH; nl PaCO2 ; high HCO3

ABG Analysis with Compensation

• Resp Acidosis: HCO3 will incr, pH will approach nl; PaCO2 will still be increased

• Resp Alkalosis: HCO3 will decr, pH will approach nl; PaCO2 will still be decreased

• Metab Acidosis: PaCO2 will decr, pH will approach nl; HCO3 will still be decreased

• Metab Alkalosis: PaCO2 will incr, pH will approach nl; HCO3 will still be increased

Examples of ABG:

• pH 7.35-7.43 PaCO2 35-45 HCO3 20-28 =Norm

• pH 7.33 PaCO2 52 HCO3 26• pH 7.48 PaCO2 32 HCO3 24• pH 7.28 PaCO2 37 HCO3 18• pH 7. 45 PaCO2 38 HCO3 32

That’s all, folks!That’s all, folks!