Fluids, Electrolytes Sudqi Hamadah. Children are NOT simply small adults Age Weight

Fluids , Electrolytes

Sudqi Hamadah

Children are NOT simply small adults

AgeWeight

4

Total body water

Total body Water

Premature

Full Term

2 year old

0%

10%

20%

30%

40%

50%

60%

70%

80%

90%

Internal Distribution of Water


ECF - quantity

Age % BW

28-week fetus 55

Newborn 40

12 months 25

Adult 20

Age %BW

12-week fetus 90

Newborn 80

12 months 60

Adult 60

TBW


Fluids and Electrolytes• Fluid compartments are separated by membranes

that are freely permeable to water.

• Movement of fluids due to:

– hydrostatic pressure

– osmotic pressure

• Capillary filtration (hydrostatic) pressure

• Capillary colloid osmotic pressure

• Interstitial hydrostatic pressure

• Tissue colloid osmotic pressure

10

Fluids and Electrolytes

Transport of Water and Fluids

Transport of Water and Fluids• Osmosis:

– Movement of water across a membrane from a less concentrated solution to a more concentrated solution

• Diffusion: – The random movement of particles down a concentration

gradient. (high to low)• Active transport:

– movement of solutes across membranes; requires expenditure of energy

• Filtration: – Transfer of water and solutes through a membrane from a

region of high pressure to a region of low pressure

Solutes – dissolved particles

• Electrolytes – charged particles– Cations – positively charged ions

• Na+, K+ , Ca++, H+

– Anions – negatively charged ions

• Cl-, HCO3- , PO4

3-

• Non-electrolytes - Uncharged • Proteins, urea, glucose, O2, CO2

0

100

200

300

400

Protein

Organic Phos.

Inorganic Phos.

Bicarbonate

Chloride

Magnesium

Calcium

Potassium

Sodium

Summary of Ionic composition

InterstitialH2O

PlasmaH2O

CellH2O


ICF (mEq/L) ECF (mEq/L)Sodium 20 135-145Potassium 150 3-5 Chloride --- 98-110Bicarbonate 10 20-25Phosphate 110-115 5Protein 75 10

ECF and ICF Composition


Dehydration-Case 1

• A 5 month male old infant is brought to your ER with 4 day history of vomiting, diarrhea, and reduced oral intake. UOP is markedly reduced. On exam, the infant is fussy but consolable. He pushes you away when you try to examine him.

• Pre-illness Weight is 7 kg (cwt 6.3) (5-25th %ile), BP is 90/55 (50th %ile), HR is 190 (>95th %ile).

• The fontanelle is slightly sunken and his skin turgor is diminished. The cardiopulmonary, abdominal, and neurologic exams are normal.

• He has stopped vomiting but refuses to drink.

Na K Cl HCO3Gastric juice 20-80 15 125 0Small-intestinal juice 100-140 15 155 40Diarrhea 10-90 40 40 40Sweat normal 10-30 10 25 0Sweat CF 50-130 15 75 0

Electrolytes in Body Fluids (mEq/L)

Fluid and electrolytes requirements

Clinical assesment of dehydration

Clinical Observations

Examination 3-5% (mild) 10% (moderate) >10% (severe)Skin turgor Normal Tenting NoneSkin-touch Normal Dry DryBuccal mucosa/lips Moist Dry DryEyes Normal Deep set SunkenCrying/tears Present Reduced NoneFontanelle Flat Soft SunkenCNS Consolable Irritable LethargicPulse Regular Slight increase IncreasedUrine output Normal Decreased Anuric

Clinical assessment of dehydration

Urine specific gravityUrine electrolytesFractional excretion of Na+ (UNa/PNa)/(UCr/PCr)Serum electrolytesSerum osmolality

– 2(Na) + BUN/2.8 + glucose/18 Renal function

Lab assessment of dehydration

ECF and ICF Percentage of Loss

% fluid of deficit % fluid of deficitDuration of illness from ECF from ICF<3 days 80 20>3days 60 40



Maintenance requirements(metabolism, growth, excretion)

Deficit replacement

Continuing loss

Total requirements

Isonatremic dehydration:– Serum sodium: 130-150 mEq/L.

– 70-80%.

– No fluid shift between ECF and ICF.

Hypernatremic dehydration: – Serum sodium: >150.

– 10-15%.

– Fluid shifts: from ICF to ECF.

– Signs of dehydration modified.

– Irritable and fussy.

– Fever; DI; concentrated formula or ORS;

Types of Dehydration

Hyponatremic dehydration:– Serum sodium: <130.

– 10-15%.

• Fluid shift from ECF to ICF.– Exacerbates volume depletion.

– Diuretics; water without sodium

Cell in a hypertonic solution

Cell in a hypotonic solution

• Isotonic Solutions No change in ICF • Hypertonic Solutions Decrease ICF• Hypotonic Increase ICF

SOLUTIONS USED FOR VOLUME REPLACEMENT THERAPY

0.9 NaCL 154 0 308

Ringers lactate 130 0 272

0.3 NaCl 3.3% dex 53 33 269

0.18 NaCl 5% dex 35 43 321

5% dex 0 50 252

3% NaCl 513 0 1027

Solution Na glucose osmolaritymmol/L gm/L mOsml/L

Osmolality and Tonicity of IV Fluids

0.9 NaCL 154 154 308 5.5

Ringers lactate 130 109 272 6.5

0.45 NaCl 77 77 154 5.5

0.2 NaCl 5% dex 35 35 321 4

5% dex 0 0 252 4

3% NaCl 513 513 1027 5.5

Na Cl Osmolality Solution mmol/L mmol/L mOsmol/L pH

Osmolality and tonicity of IV fluids

SOLUTIONCARBOHYDRATE (G/L)

SODIUM (MMOL/L)

POTASSIUM (MMOL/L)

CHLORIDE (MMOL/L)

BASE* (MMOL/L)

OSMOLARITY (MOSM/L)

ORS

World Health Organization (WHO) [2005]

13.5 75 20 65 10 245

WHO [2002] 13.5 75 20 65 30 245

WHO (1975) 20 90 20 80 30 311

European Society of Paediatric

Gastroenterology, Hepatology and Nutrition

16 60 20 60 30 240

Enfalyte† 30 50 25 45 34 200

Pedialyte§ 25 45 20 35 30 250

Rehydralyte¶ 25 75 20 65 30 305

CeraLyte** 40 50-90 20 NA†† 30 220

COMMONLY USED BEVERAGES (NOT APPROPRIATE FOR DIARRHEA TREATMENT)

Apple juice§§ 120 0.4 44 45 N/A 730

Coca-Cola¶¶ Classic 112 1.6 N/A N/A 13.4 650

Composition of ORS fluids

• Guideline for ORS, – 50mL/kg of the (ORS) within 4hr to in mild dehydration

and – 100mL/kg over 4hr in moderate dehydration

• Supplementary ORS is given to replace ongoing losses from diarrhea or emesis. 10mL/kg of ORS is given for each stool

• ORS is given in small amounts at short intervals (1tsp every 1-2min). Emesis usually lessens over time

ORS guidelines

Overview of IV Rehydration Strategy• Phase I (immediate): If the patient is hemodynamically

unstable or in shock, “one or more” boluses of 20 cc/kg isotonic fluid (0.9%NS or LR) should be given in the first 30 minutes

• Phase II (deficit, maintenance, ongoing fluid replacement):

1. Calculate fluid deficit

2. Calculate maintenance fluid

3. Give ½ of deficit therapy + maintenance over first 8 hours and remainder of deficit + maintenance over next 16 hours

4. Adjust above based on consideration of ongoing losses likely to be encountered

Fluid Management in Children-maintenance

simplified method for calculating caloric expenditure from body weight

Body weight (kg) Caloric expenditure

Up to 10 100 kcal/kg

11 to 20 1000 kcal + 50 kcal/kg for each kg >10 kg

above 20 1500 kcal + 20 kcal/kg for each kg >20 kg

Maintenance fluids and electrolytes: 100 ml water [35ml insensible water loss, 65ml urinary water loss] and 2-4 mmol Na and K for each 100 kcal expended

Nelson Textbook of Paediatrics WB Saunders Company


Body Surface Area MethodFor non-dehydrated patientsWater 1500 ml/M2/24 hrSodium 30-50 mEq/M2/24 hrPotassium 20-40 mEq/M2/24 hr

Mild dehydrationWater 2000 ml/ M2/24 hr

Moderate dehydrationWater 2500 ml/ M2/24 hr


Modifications

Increase DecreaseFever (12% for each oC Renal failure

above 37 oC ) Heart failureHigh ambient temperature Inappropriate secretionDiabetes mellitus of ADHDiabetes insipidus High-humidity respiratoryVigorous exercise therapy


Renal failure: Oligo-anuric patients should receive fluid intake equal to their total output; output must include insensible losses

Neonates:Insensible losses in neonates vary with gestational age and

birth weight and may be dramatically increased by phototherapy or radiant warmers

Newborns cannot concentrate urine as well and GFR is lower so they are more prone to fluid overload


Deficit: Fluid• Definition: Amount of fluid lost before treatment is

begun

• Methods:– Weight loss due to acute illness

• Fluid deficit (L) = Preillness weight (kg) – current weight (kg)

– Estimation of % dehydration• Fluid deficit (L) = [% dehydration x Preillness

weight (kg)] / 100

Deficit: Electrolytes

• Sodium: usually in pediatrics, losses are gastrointestinal or due to a relatively short period of decreased oral intake– approximated by 0.45 NS

• Potassium: deficit replacement is based on rate of safe replacement and not amount since danger of hyperkalemia is greater than hypokalemia– Add 20 mEq potassium/L after UOP is established– Potassium infusion rate should not exceed 1

mEq/kg/hour unless in monitored setting

Case 1: Solution Combined Deficit/Maintenance

• Bolus: 140 cc (20 cc/kg) of NS given for hemodynamic instability

• Deficit Fluid:• Oliguria, tachycardia, no shock 10% dehydrated• Deficit = 10% x 7kg wt loss / 100*= 0.7L or 700cc

– (alternatively 10cc/kg weight loss x 7 kg = 700 cc)

• Maintenance Fluid:– Holliday-Segar: 4 cc/kg for first 10 kg = 7 kg x 4 cc/kg = 28

cc/hr

*Note: Should use preillness weight to calculate deficit = (6.3 kg x 100)/(100-10%) = 7 kg


• First 8 hours: – Maintenance:

• 28 cc/hr x 8 hours = 224 cc

• In theory: D5 0.2 NS + 20 mEq KCl/L

• In practice: D5 0.45 NS + 20 mEq KCl/L

– Half Deficit = 700/2 = 350 cc of 0.45 NS– Total Fluid = 574 cc/ 8 hour = 71.8 cc/hr

– IVF: 75 cc/hr of D5 0.3 NS + 20 mEq KCl/L• In practice, we would give D5 ½ NS + 20 K

– ADH is increased

– We usually choose between ¼ NS and ½ NS


• Next 16 hours: – Maintenance:

• 28 cc/hr x 16 hours = 448 cc

• In theory: D5 0.2 NS + 20 mEq KCl/L

• In practice: D5 0.45 NS + 20 mEq KCl/L

– Half Deficit = 700/2 = 350 cc of 0.45 NS– Total Fluid = 798 cc/ 16 hour = 49.9 cc/hr

– IVF: 50 cc/hr of D5 0.45 NS + 20 mEq KCl/L

Dehydration- Case 2

• A 12 year old male is found unresponsive at the bottom of a swimming pool. He is resuscitated in the field and on arrival to the ER is intubated and ventilated but has a spontaneous pulse. In the trauma room, he develops generalized tonic-clonic seizures. He is loaded with phenytoin.

• His weight is 45 kg, BP is 100/70 (normal), HR is 100 (normal). On exam, he is unresponsive and his right pupil is sluggish.

• His stat sodium then returns at 110 mmol/L.

Dehydration- Case 2

Hyponatremic Dehydration

Frequently seen in children with vomiting and diarrhea who have received tap water as an oral replacement

Shock is an early symptom

Physical exam findings usually exaggerate amount of dehydration

Correcting Na+ to quickly in adults can lead to central pontine myelinosis; ???children

Hyponatraemia - Na <130 mmol/L

Equals an expanded ICF

Is it water gain or salt loss?

Salt lossHypernatraemic urineGI tractSweat

Water gainIV fluidsoral fluidscardiac and renal failure


Acute or Chronic?

SymptomaticSymptomatic oror asymptomatic?asymptomatic?


Acute Hyponatraemia

Symptoms & signs

•Headache

•Nausea and vomiting

•Somnulence

•Convulsions

•Respiratory arrest

•Brain stem coning


Hyponatremia and the CNS

H2O

Acute (rapid) onset


Hyponatremia – Differential Dx

• Hypovolemic– Renal loss

– GI loss

– Sweat

– Third space

• Euvolemic– SIADH

– Glucocorticoid deficiency

– Hypothyroidism

– Water intoxication

• Hypervolemic– Edema forming states

– Renal failure

Hypotonic


Hyponatremia – Differential Diagnosis

• Isotonic Pseudohyponatremia (Osm 275-295)– Protein

– Lipids

• Hypertonic Hyponatremia (Osm > 295)– Glucose

– Mannitol



Correcting Na+ too quickly in can lead to central pontine myelinosis

Follow same steps as for isonatremic dehydrationAdditional Na+ neede = (D Na – S Na) X 0.6 x wt

Symptomatic: Hypertonic saline therapy (1 ml/k NaCL 3% increase serum Na by 1 mEq/L) so give 4-6 ml/k of 3% NaCLCorrect 1-2 mmol/L/hour x several hours if severly symptomaticTarget for increase in serum sodium of no more than 12 mmol/d to prevent osmotic demyelination


Case 2: Solution• Initial management is to prevent cerebral edema and

herniation; 45 kg

• Use NaCL 3%: 4-6* 45

• The goal of therapy is to increase the serum sodium by 4-6 mmol/L in 3 hours.

Dehydration- Case 3

• A 1 week old female neonate is admitted to the PICU after increasing lethargy and difficulty with breastfeeding. Her birthweight was 3.8 kg. Her admission weight is 3.3 kg.

• On exam, the infant is difficult to arouse. BP is 72/62 (75th %ile), HR is 120 (50th %ile), RR is increased at 60. The PE is unrevealing except for hypotonia and decreased level of consciousness.

• The nurse informs you the sodium is 165 mmol/liter.

Dehydration- Case 3

Serum Na > 150 mEq/L

Mortality can be high

Often iatrogenic

The circulating volume is preserved at the expense of the intracellular volume and circulatory disturbance is delayed

The patient looks better than you would expect based on fluid loss

Hypernatremic Dehydration

Hypernatremia: Clinical Manifestations

• Related to CNS dysfunction; sequelae are prominent when the increase in serum sodium is rapid or large

• Infants: hyperpnea, muscle weakness, restlessness, high-pitched cry, insomnia, lethargy, or coma. Seizures are uncommon.



• Slow Correction– Patients with hypernatremia of longer or unknown

duration– Correct sodium by 0.5 mmol/L/hr or 10 mmol/d with goal

of 145 mmol/L

• Rapid Correction– Improves prognosis in patients in whom hypernatremia

developed acutely (sodium loading)– Correct serum sodium by up to 1 mmol/L/hr

Hypernatremic Dehydration-management

• Always assume total fluid deficit of at least 10%• Aim of correction: 145-157 (24hrs), 158-170 (48hrs), 171-

183 (72hrs)

• You only want to correct half of the free water deficit in first 24 hours if Na+ < 175 mEq/L

• For Na+ > 175 mEq/L you do not want to correct faster than 1 mEq/L/hr because of risk of cerebral edema

• Use hypotonic fluids unless frank circulatory collapse exists

Hypernatremic Dehydration-management

Case 3: Solution A• Bolus?: no• Deficit Fluid:

– Deficit = 3.8 kg – 3.3 kg = 0.5 kg or 500 cc

• Maintenance Fluid:– Holliday-Segar: 4 cc/kg for first 10 kg: 3.8 kg x 4 cc/kg =

15.2 cc/hr

• 48 hours needs: – Deficit = 500 cc of 0.45 NS– Maintenance = 15 cc/hr x 48 hr = 720 cc of D5 0.2 NS + 20

mEq KCl/L– Total Fluid = 500 cc + 720 CC = 1200 cc/ 48 hour = 25 cc/h– IVF: 25 cc/hr of D5 0.3 NS + 20 mEq KCl/L

63

Regulation of fluid and electrolytesWater:

• ADH

• Aldosterone

• Thirst

K• Aldosterone• Insulin

Na• Aldosterone• Renin/angiotensin• Atrial Natriuretic Peptide (ANP)

Serum Osmolality• Calculated: (2 x (Na + K)) + (BUN / 2.8) + (glucose / 18) • Measured• Osmolar gap = Osmmeas – Osmcalc

• Methanol/Ethanol/Isopropanol• Mannitol• Ethylene glycol

• Normal: 275 – 295 mOsm/L Isotonic• < 275 mOsm/L = Hypotonic• > 295 mOsm/L = Hypertonic

Regulation of fluids

Normal water homeostasis

• Serum osmolality maintained at 275-295 mOsm/L

• AVP corrects for large variations in water intake

• Osmoreceptor location uncertain, probably anterolateral hypothalamus

• Primary stimulus: increase in plasma osmolality

– Hypoosmolality: ADH secretion suppressed

– Hyperosmolality: ADH level rises

AVP receptors• V1a receptors: vascular smooth muscle, affect vascular tone

• V2 receptors: Kidneys renal collecting duct cells when AVP binds it stimulates adenyl cyclase → cAMPAquaporin-2 (AQP-2) water channels are shuttled to apical plasma membraneIncreased water reabsorption

• V3 receptors: Anterior pituitary, regulate corticotropin release

• V1a receptors: vascular smooth muscle, affect vascular tone

• V2 receptors: Kidneys renal collecting duct cells when AVP binds it stimulates adenyl cyclase → cAMPAquaporin-2 (AQP-2) water channels are shuttled to apical plasma membraneIncreased water reabsorption

• V3 receptors: Anterior pituitary, regulate corticotropin release


• Osmotic threshold for thirst = 5-10 mOsm/L above that for AVP release

• Kidney regulates body water in response to early, small changes

• Thirst is activated by larger, more threatening disturbances

• Capacity of AVP to limit water loss is limited

– Obligatory minimum urine output (based on solute load) is 6-10 mL/kg/d


Osmolality : ADH level and Thirst

From:Berl T, Robertson GL. Pathophysiology of Water Metabolism. In: Brenner AM, ed. Brenner and Rector's The Kidney. 6th ed. Philadelphia: W.B. Saunders; 2000:873.


Non-osmotic stimulators of AVPHypotension, hypovolemia

•Exponential relationship to vasopressin level•Mediated by baroreceptors (atria, aorta, carotid sinus)Am J Physiol Regul Integr Comp Physiol 2000;278(2):R469-75.

Angiotensin II stimulates AVP releaseKeil LC. Endocrinology 1975;96(4):1063-5.

•CHF, Cirrhosis, Nephrotic syndrome


ADH response in humans

to changes in osmolality,

pressure and volume

Berl T, Robertson GL. Pathophysiology of Water Metabolism. In: Brenner AM, ed. Brenner and Rector's The Kidney. 6th ed. Philadelphia: W.B. Saunders; 2000:875.



Factors affecting ADH release

Pathway of RAAS

• Atrial natriuretic peptide

ABG INTERPRETATION

Sudqi Hamadah

What’s normal PH?• The definition of metabolic acidosis in preterm

infants has not been clearly established.

• A normal arterial blood pH in the term infant: pH 7.27- 7.43 at up to 24 hours post birth and 7.32 - 7.42 at seven days of age (Koch 1968).

• Normal BE in the first 28 days of life has been defined as - 5 to + 5 mmol/litre in the preterm infant (Rennie 1999).

• The Joint Working Group of the British Association of Perinatal Medicine recommended maintaining an arterial pH >7.25 [below this pH various physiological and cellular functions are compromised] (BAPM 1992).

• Compensation The lung: CO2 excretion, for Metabolic alkalosis –only

partial compensation (no hypoventilation) The kidney Never overcompensation

What’s normal PH?

ABG Interpretation

• Does the patient have an acidosis or an alkalosis• The primary problem – metabolic or respiratory• Is there any compensation by the patient –

respiratory compensation is immediate while renal compensation takes time

• Normal values– pH 7.35 to 7.45– paCO2 36 to 44 mm Hg– HCO3 22 to 26 meq/L

• For a primary respiratory problem, pH and paCO2 move in the opposite direction– For each deviation in paCO2 of 10 mm Hg in either

direction, 0. 08 pH units change in the opposite direction

• For a primary metabolic problem, pH and HCO3 are in the same direction, and paCO2 is also in the same direction

ABG Interpretation

Case 1

Hasan ingests many tablets of his dad’s barbiturates. He suffers a significant depression of mental status and respiration. You see him in the ER 3 hours after ingestion with a respiratory rate of 4.

A blood gas is obtained (after doing the ABC’s). It shows pH = 7.16, pCO2 = 70, HCO3 = 22

Case 1

What is the acid/base abnormality?

1. Uncompensated metabolic acidosis

2. Compensated respiratory acidosis

3. Uncompensated respiratory acidosis

4. Compensated metabolic alkalosis

Case 2

Suzie had vomiting and diarrhea for 3 days. In her mom’s words, “She can’t keep anything down and she’s runnin’ out.” She has had 1 wet diaper in the last 24 hours. She appears lethargic and cool to touch with a prolonged capillary refill time. After addressing her ABC’s, her blood gas reveals: pH=7.34, pCO2=26, HCO3=12

Case 2

What is the acid/base abnormality?

1. Uncompensated metabolic acidosis

2. Compensated respiratory alkalosis

3. Uncompensated respiratory acidosis

4. Compensated metabolic acidosis

Case 3

You are evaluating a 15 year old female in the ER who was brought in by EMS from school because of abdominal pain and vomiting. Review of system is negative except for a 10 lb. weight loss over the past 2 months and polyuria for the past 2 weeks.

On exam, she is alert and oriented, afebrile, HR 115, RR 26 and regular, BP 114/75, pulse ox 95% on RA. Exam is unremarkable except for mild abdominal tenderness on palpation ,capillary refill time of 3 seconds.

blood gas. pH = 7.21 pCO2= 24 pO2 = 45 HCO3 = 10

BE = -10 saturation = 72%

Case 3

What is the blood gas interpretation?• Uncompensated respiratory acidosis with severe hypoxia• Uncompensated metabolic alkalosis• Combined metabolic acidosis and respiratory acidosis

with severe hypoxia• Metabolic acidosis with respiratory compensation

Expected Compensation

Respiratory acidosis

• Acute –pH ↓0.008 for 1 mm Hg ↑ in paCO2

– HCO3 0.1-1 mEq/liter per 10 mm Hg paCO2

• Chronic –pH ↓ 0.003 for 1 mm Hg ↑ in paCO2;

– HCO3 1.1-3.5 mEq/liter per 10 mm Hg paCO2


Respiratory alkalosis

• Acute – the pH increases 0.008 units for every 1 mm Hg decrease in paCO2; HCO3 0-2 mEq/liter per 10 mm Hg paCO2

• Chronic - the pH increases 0.017 units for every 1 mm Hg decrease in paCO2; HCO3 2.1-5 mEq/liter per 10 mm Hg paCO2


Metabolic acidosis

• paCO2 = 1.5(HCO3) + 8 (2)

• paCO2 1-1.5 per 1 mEq/liter HCO3

Metabolic alkalosis

• paCO2 = 0.7(HCO3) + 20 (1.5)

• paCO2 0.5-1.0 per 1 mEq/liter HCO3

Elevated AG Metabolic Acidosis

• Causes– Ketoacidosis - diabetic, alcoholic, starvation– Lactic acidosis - hypoxia, shock, sepsis, seizures– Toxic ingestion - methanol, ethylene glycol, ethanol,

isopropyl alcohol, paraldehyde, toluene– Renal failure - uremia

Normal AG Metabolic Acidosis

• Causes– Renal tubular acidosis

– Post respiratory alkalosis

– Hypoaldosteronism

– Potassium sparing diuretics

– Pancreatic loss of bicarbonate

– Diarrhea

– Carbonic anhydrase inhibitors

– Acid administration (HCl, NH4Cl, arginine HCl)

– Sulfamylon

– Cholestyramine

– Ureteral diversions

Effectiveness of Oxygenation

• Further evaluation of the arterial blood gas requires assessment of the effectiveness of oxygenation of the blood

• Hypoxemia – decreased oxygen content of blood - paO2 less than 60 mm Hg and the saturation is less than 90%

• Hypoxia – inadequate amount of oxygen available to or used by tissues for metabolic needs

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Fluids, Electrolytes Sudqi Hamadah. Children are NOT simply small adults Age Weight