1. Alterations in Fluid, Electrolyte and Acid-Base Balance in Children
Dr. Nataliya Haliyash, MD, BSN
Institute of Nursing, TSMU

2. 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.

3. FIGURE 23– 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. Bindler Child Health Nursing: Partnering with Children & Families
© 2006 by Pearson Education, Inc. Upper Saddle River, New Jersey All rights reserved.

4. 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

5. 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:

6. Fluid 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.

7. Clinical Manifestations of Dehydration
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.

8. Nursing Considerations
How can the nurse determine if the child is mildly dehydrated vs moderately dehydrated?

9. 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

10. Moderate 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 > (in child >2yr)
Sunken fontanel
HR increased, BP decreased. Postural vital signs

11. Severe 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

12. Types of Dehydration and Sodium Loss
Sodium may be:
Low
High
Or normal

13. Isotonic Dehydration or Isonatremic Dehydration
Loss of sodium and water are in proportion
Most of fluid lost is from extracellular component
Serum sodium is normal ( mEq/L) Harriet Lane Handbook, 2000.
Most practitioners consider below 135 and above 148 a more conservative parameter ( )
Most common form of dehydration in young children from vomiting and diarrhea.

14. Hypotonic or Hyponatremic Dehydration
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.

15. Hypertonic or Hypernatremic Dehydration
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.

16. Clinical Manifestations Associated with Degree of Dehydration

17. Dehydrated child
Before… and after treatment

18. 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.

19. 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.

20. 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.

21. Diarrhea
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.

22. 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.

23. Acute 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 days.

24. Etiology of acute diarrhea
Viral agents
Bacterial pathogens
Human rotavirus
Small round viruses:
Norwalk
Taunton
Snow Mountain
Astrovirus
Wollan
Enteric adenoviruses
Coronaviruses
Escherichia coli
Campylobacter
Salmonella
Shigella
Vibrio cholera
Yersinia enterocolitica
Clostridium difficile

25. Parasitic pathogens
Helmintic pathogens
Protozoa:
Giardia lamblia
Cryptosporidium
Entamoeba histolytica
Balantidium coli
Nematodes:
Ancylostoma duodenale
Strongyloides stercoralis
Necator americanus
Trichuris trichiura
Trematodes:
Schistosoma
Cestodes:
Taenia solium
Taenia saginata
Diphyllobothrium latum

26. Pathogenesis of Acute Diarrhea
Diarrhea results when the net intestinal fecal loss of fluid and salt exceeds the absorbed amount.
There are 5 pathogenic forms of diarrhea:
Toxigenic diarrhea
Osmotic diarrhea
Secretory diarrhea
Invasive diarrhea
Motility disorders

27. Toxigenic 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.

28. Osmotic 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.

29. Differential diagnosis of osmotic and secretory diarrhea
Stools
Osmotic diarrhea
Secretory 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

30. Secretory 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

31. Invasive diarrhea
Is caused by direct mucosal damage by the invasive organism
It is similar to colitis and is usually associated with blood and mucous.

32. Motility 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.

33. Clinical characteristics of infectious gastroenteritis in dependence on enteropathologic cause.
Organism
Characteristics
Comments
Rotavirus
Incubation period:2-3 d.
Abrupt onset
Fever (≥ 38°C) for 48 hh
Associated upper resp.tract infection
Incidence higher in cool weather
6- to 24-month-old infants are more vulnerable
Norwalk-like viruses
Inc.period:
1-2 days
Fever
Loss of appetite
Nausea/vomiting
Abdominal pain
Malaise
Source of infection: drinking water, food
Affects all ages
Self-limited

34. Pathogenic Escherichia coli
Incubation period: highly variable
Diarrhea with moist-green, watery stool with mucus; becomes explosive
Vomiting may be present from onset
Abdominal distension
Fever, intoxication
Incidence higher in summer
Usually interpersonal transmission, but may transmit via inanimate objects
Salmonella groups (nontyphoidae) – gram-negative, non-encapsulated, nonsporulating
Incubation period: 6 hh-21 day
Rapid onset
Variable symptoms – mild to severe
Nausea, vomiting, and colicky abdominal pain followed by diarrhea, occasionally with blood and mucus
Infants 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

35. Shigella groups – gram-negative, nonmotile, anaerobic bacilli
Incubation period: 1-7 days
Onset usually abrupt
Fever (to 40.5°C) and cramping abdominal pain initially
Febrile convulsions in 10 % cases
Headache, neck rigidity, delirium
Transmitted directly or indirectly from infected persons
Vibrio cholerae groups
Inc.period: 1-3 days
Sudden onset of profuse, watery diarrhea without cramping, tenesmus, or anal irritation
Stools are intermittemt at first, then almost continuous
Stools are whitish, almost clear, with flecks of mucus – “rice water stools”
Rare in infants
Mortality is high
Transmitted via contaminated food or water

36. Food poisoning:
Staphylococcus
Incub.period:
4-6 hours
Nausea,vomiting
Severe abdominal cramps
Profuse diarrhea
Shock may occur in severe cases
May be a mild fever
Transfered via contaminated food – inadequately cooked: custards, mayonnaise, cream-filled desserts
Self-limited (24-72 hours)
Exellent prognosis
Botulism
Clostridium botulinum
12 hr – 3 days
Diarrhea
CNS symptoms with curare-like effect
Dry mouth, dysphagia
Transfered via contaminated food
Variable severity – mild symptoms to rapidly fatal within a few hours
Antitoxin administration

37. 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

38. 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.

39. 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.

40. What about antimicrobial 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

41. When should antibiotics 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

42. Rehydration
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.

43. The rationale for the use of ORS
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.
The sodium-glucose-coupled transport generally remains intact. This mechanism stimulates water transport by solvent drag.

44. The basic components of ORS
Glucose
Electrolytes
in an isotonic solution.
In the World Health Organization formula the glucose concentration is 2 %.

45. WHO recommendations for a sodium 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

46. 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.

47. Composition of oral electrolyte solutions (in mEq/l)
Na+ K+
Clˉ
Other anion
CHO(%)
WHO solution 90 20 80 30 2
Gastrolyte
Pedialyte 45 35
2.5
Rehydralyte 75 65
infalyte 50 40

48. Composition of “clear liquid” solutions
Na+ K+
CHO(%)
Pepsi Cola
1-2
0.1
10.9
Coca Cola 10
Root beer 6
0.6
10.6

49. Super-ORS
Recent studies demonstrate the advantage of short glucose polymers as the carbohydrate source in ORS
Traditionally it is widely used rice water % 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.

50. 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.
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.

51. 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.

52. 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)

53. 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

54. 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
Potassium is only added to an IV after the patient has voided to avoid hyperkalemia in a child with little or no urinary output

55. Adding Potassium to Intravenous 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.

56. Which of the following IV solutions replaces Sodium?
D5 W
Lactated Ringers
Normal Saline
D5 ½ NS
Answer: All but D5 W

57. 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

58. 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: ml/Kg = 500ml
for the remaining 15 Kg (35-20Kg) , replace at 20 ml/Kg: 15 = 300ml
= 1800 ml/day.

59. 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

60. 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
9yr old wt 20 Kg = 1500ml/day
6 mo old wt 8Kg= 800ml/day
36mo old wt. 18 Kg= 1400ml/day
3yr old wt 28Kg=1660ml/day
18yr old wt 50Kg= 2100ml/day
Adult > 50Kg= 2-3L/day

61. 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

62. 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.

63. 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.

64. 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.

65. 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
Lab test: serum sodium
Treatment: hypotonic IV solution

66. 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.

67. 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:
Lab tests: serum sodium
Treatment: hypertonic solution.

68. 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

69. 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.

70. 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)

71. 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.

72. 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).

73. 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.

74. 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.

75. Hypocalcemia (cont)
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.
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: p 755 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.

76. Hypocalcemia (cont 2)
In children and adolescents, chronic hypocalcemia more common, manif. By spontaneous fractures. Lab tests: serum Ca; bone density study Rx: oral and/or IV Ca, Ca rich diet

77. 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.

78. Hypermagnesemia (cont)
Clinical Manif: decreased muscle irritability, hypotension, bradycardia, drowsiness, lethargy, weak or absent DTR’s.
Rx: increase fluids, diuretics, dialysis.

79. 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.

80. 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.

81. 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?
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.

82. 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.

83. Fluid and Electrolyte Worksheet
Use the fluid and electrolyte worksheet to help review some of the major concepts of fluid and electrolyte imbalance.

84. pH - Is the acidity or alkalinity of a solution.
- From French pouvoir 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+]

85. 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 1 7 14
Acidic
Alkaline

86. H+
HCO3-
Neutral
Acidic
Alkaline

87. 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)

88. 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

89. Management of Respiratory Acidosis
Incr ventilatory rate
give O2
intubate
adm NaHCO3

90. 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.

91. 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.

92. 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.

93. 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.

94. 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.

95. 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.

96. 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.

97. 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

98. 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

99. Examples of ABG: pH 7.35-7.43 PaCO2 35-45 HCO3 20-28 =Norm
Resp Acidosis
Resp Alkalosis
Metabolic Acidosis
Metabolic Alkalosis

100. That’s all, folks!