care of the child with disturbances in fluid

8/3/2019 Care of the Child With Disturbances in Fluid

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Care of the Child With Disturbances

in Fluid and Electrolytes


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Distribution of Body Fluids Total body water

Intracellular

Extracellar Intravascular

Interstitial

Transcellular


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AgeTBW as % of body weight

ECF as % of body weight ICF as % body weight

Premature 75-80

Newborn 70-75 50 35

1 Year Old 65 25 40-45

Adolescent Male 60 20 40-45

Adolescent Female 55 18 40

Total Body Weight (TBW)
http://family.georgetown.edu/welchjj/netscut/fen/fluids_acknowledgements.htmlhttp://family.georgetown.edu/welchjj/netscut/fen/fluids_acknowledgements.html


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Normal Blood Values

Electrolytes Potassium

Newborn - 3.0-6.0mEq/L

Thereafter 3.5-5.0mEq/L Sodium

Infant 139-146mEq/L

Child 138-145mEq/L

Chloride Newborn 97-110mEq/L

Thereafter 98-106mEq/L


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Normal Blood Values

Electrolytes Carbon dioxide

Newborn 13-22mEq/L

Infant, child 20-28mEq/L Calcium

Newborn 9.0-10.9mg/dL

Child 8.8-10.8mg/dL

Glucose Newborn >1 day-50-90mg/dL

Child 60-100mg/dL


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Developmental Differences

Acid-base Balance Infants

pH

Birth-7.11-7.36 1 day-7.29-7.45

PCO2 Newborn-27-40 Infant-27-41

HCO3 Infant-21-28 mEq/L

BE Newborn- -2 to -10

Infant- -1 to -7

Children pH

Child-7.35-7.45 PCO2

Girls-32-45 Boys-35-48

HCO3 Child-22-26 mEq/L

BE Child-+2 to -4 Thereafter-+3 to -3


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Dehydration Most common disturbance in infants and children

Occurs when output exceeds input

Usually from vomiting or diarrhea Diabetic ketoacidosis

Extensive burns

Three types Isotonic

Hypotonic

Hypertonic


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Degree of Dehydration How to reflect acute loss

Milliliters per kilogram of body weight

For each 1% weight loss=10 ml/kg of fluids

have been lost

Mild - 100 ml/kg


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Water Intoxication Water overload water excess = sodium

decrease

CNS symptoms:

Irritability, somnolence, headache, vomiting,

diarrhea, or generalized seizures


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Water Intoxication Occurs with:

Acute IV water overload, too rapid dialysis,

tap water enemas, feeding of incorrectly mixedformulas, excessive water ingestion, or withtoo rapid reduction of glucose levels indiabetic ketoacidosis

CNS infections, administration ofinappropriate hypotonic solutions ( i.e. 0.45%

NACL)


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Water Intoxication Why are infants especially vulnerable?

Thirst mechanism not well developed

Decreased glomerular filtration rate ADH levels levels not maximally reduced

Causes in infants

Inappropriately prepared formulas (most common) Vigorous hydration

Swimming lessons


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Edema Abnormal accumulation of fluid

Why develops?

Defect in normal cardiovascular circulation

Failure of lymphatic drainage to remove

increased amounts


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Mechanisms of Edema

Formation Increased venous pressure

Capillary permeability

Diminished plasma proteins

Lymphatic obstruction

Tissue tension Other


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Acid-Base Imbalances Alkalosis

Accumulation of base

Loss of acid

Acidosis

Accumulation of acid

Loss of base


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Acid-Base Imbalances Respiratory acidosis

Diminished or inadequate pulmonary ventilation

causes elevation in PCO2, increased HCO3 Compensated thru kidneys

Treatment Correct primary cause

Improve gas exchange remove CO2 Administer O2

Sodium bicarb not recommended


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Acid-Base Imbalances Respiratory alkalosis

Caused by increased rate and depth of

pulmonary ventilation, decreased PCO2,increased pH

Compensated in the kidney

Treatment Correction of the primary defect

Prevention of lost ions and K+ deficit

Rebreathing CO2 and O2 administration


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Acid-Base Imbalances Metabolic acidosis

Caused by any process that reduces HCO3

concentration thru gain of acids or loss ofHCO3

Compensation-respiratory

Treatment Correct the basic defect

Replace excess losses of HCO3 with sodium orpotassium bicarbonate


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Acid-Base Imbalances Metabolic alkalosis

Occurs when there is a reduction in H+ concentration

and an excess of HCO3 Compensation:

Respiratory (irregular and unpredictable);

Renal correction (complicated by losses of Na+, K+, & Cl-)

Treatment Prevent further losses of acid

Replace lost electrolytes


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Disturbances of Fluid and

Electrolyte Balance Potassium depletion (Hypokalemia)

Potassium excess (Hyperkalemia)

Cell permeability affected by changes inpH Lowered pH-K+moves from ICF to ECF

Serum K+ Levels increase with acidosis

Levels decrease with alkalosis


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Disturbances of Fluid and

Electrolyte Balance-Conditions Diarrhea

Vomiting

Sweating Fever

Disorders diabetes, renal disease, & cardiacanomalies

Administration of drugs diuretics & steroids

Trauma major surgery, burns, & other extensiveinjuries


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Nursing Management Assessment

General appearance

Loss of appetite/decreased activity level Cry

Irritable

Clinical observations

Tachycardia earliest sign of dehydration Dry skin and mucous membranes early

Capillary filling time

Strict I & O


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Nursing Management Oral fluid intake

Oral rehydration for mild to mod dehydration

Oral rehydration solution 75-90 mMol sodium & 111-139 mMol glucose

(WHO solution, PedialyteRS, Rehydrate) 1st 4-6 h

30-60 mMol sodium & 111-139 mMol glucose

(Pedialyte, Lytren, Resol, Infalyte) next 18-24 hrsNo longer recommended at onset of diarrhea

NPO for 24 hours BRAT diet (Behrman, Kliegman, Jenson, 2000)


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IV Therapy To deliver prescribed fluids and

medications without complications

Pediatric-most common-dextrose (5-10%) andNaCl (0.22-0.3%)

Calculate solution needs based on size and 24hour volume needs

To decrease complications use smallestcatheter (stainless steel needles increasedislodge and infiltration rate)


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IV Therapy Microdrip factor Buretrol or Solu-set

Continuous infusion pumps

Prep

Quiet private setting

Distract as able, allow parents to comfort

Select appropriate site


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Long Term Venous Access Intermittent intravenous devices (Central

venous catheters)

Short term Subclavian, femoral, jugular

Short term to moderate-term

Peripherally inserted central catheters Long term

Tunneled catheters and implanted ports


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Diarrhea Pathophysiology

Abnormal intestinal water and electrolyte

transport Secretory

Cytotoxic

Osmotic Dysenteric


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Diarrhea Etiology

Most spread by the fecal-oral route via

contaminated food or water or spread personto person thru close contact

In US, rotavirus is most common pathogen

Other causes- Concomitant with other diseases i.e. HIV

Ingestion of laxatives,or excess sorbitol, fructose

Antibiotics


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Diarrhea Clinical manifestations

Severity as well as frequency and consistency

of stools highly variable Most serious consequences

Dehydration

Electrolyte disturbances

Malnutrition

Metabolic rate of child high-predispose torapid depletion of nutritional reserves


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Diarrhea Diagnostic evaluations

History

Lab tests-only if moderately to severely

dehydrated Stool specimens persistent diarrhea and

internationally adopted


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Diarrhea Therapeutic management

Assessment of fluid and electrolyte imbalance

Rehydration Oral-safe, effective, less painful and less cost than

IV

IV if severe Maintenance fluid therapy

Reintroduction of adequate diet


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Diarrhea Nursing considerations

Assessment

Nursing diagnosis

Planning

Implementation

Evaluation


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Vomiting Pathophysiology

Forceful ejection of gastric contents through

the mouth

Under CNS control

Usually accompanied by:

Nausea Retching


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Vomiting Etiology

Color and consistency vary Green, bilious bowel obstruction Curdled, mucus, or fatty foods -poor gastric emptying or

high intestinal obstruction

Gastric irritation (medicine, food, toxic)

Associated symptoms

Fever and diarrhea infection Constipation obstruction Pain appendicitis, pancreatitis, peptic ulcer Change in LOC CNS or metabolic disorder Forceful pyloric stenosis


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Vomiting Clinical manifestations-causes

Acute infectious diseases

Increased intracranial pressure Toxic ingestion

Food intolerances

Allergies

Mechanical obstruction of the GI tract

Metabolic disorders

Psychogenic problems


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Vomiting Diagnostic evaluations

Thorough history and physical exam

Urine analysis Serum electrolytes

Radiographic studies

Endoscopy Endoscopy

Psychiatric evaluation


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Vomiting Therapeutic management

Detection and treatment of cause

Prevention of complications

Antiemetic drugs Zofran (ondansetron) or Tigan (trimethobenzamide)

Reglan (metoclopramide) Phenergan (promethazine)

Dramamine (dimenhydrinate)


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Vomiting Nursing considerations

Determined by the cause

Accurate assessment

Maintain hydration or prevent dehydration

Monitor fluid and electrolyte status

Emphasis on brushing teeth or rinsing after

vomiting to dilute effects of hydrochloric acid


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Shock Pathophysiology-hypoperfusion

Alteration of myocardial, intravascular or

neuronal control mechanisms

Three types Hypovolemic

Distributive Cardiogenic


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Shock Etiology

Hypovolemic-most common in childhood

Cardiogenic

Distributive or vasogenicNeurogenic

Anaphylactic Septic


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Shock Clinical manifestations

Actually a form of compensation for

circulatory failure

Three stages or phases Compensated

Uncompensated or decompensated Irreversible


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Shock Diagnostic evaluations

History and physical exam

Vital signs Laboratory tests

ABGs

Liver function

Coagulation studies

Cultures

Renal function


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Shock Therapeutic management

Ventilatory support Lung is most sensitive to shock

Cardiac support Fluid administration

Vasopressor support (dopamine), vasodilators Improve the pumping action of the heart


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Shock Nursing considerations

Ensure adequate tissue oxygenation

Position client flat with feet elevated

Monitor closely

Family support


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Shock Disseminated intravascular coagulation

Develops from: Degeneration of tissue causing aggregation of

RBCs and sludging of blood

Bacterial toxins

Consumes the clotting factors Produces widespread hemorrhages


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Glomerulonephritis

Pathophysiology Speculative

Streptococcal infection occurs

Release of a membrane-like material

Antibodies formed

Immune complexes form

Become trapped in glomerular capillary loop

Reduction of glomerular filtration rate


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Glomerulonephritis

Etiology An immune complex disease

Latent period of 10-14 days

Multiple cases tend to occur in families

Second attacks are rare


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Glomerulonephritis

Diagnostic Evaluations Urinalysis

Electrolytes

ASO titer

Serum compartment level (C3)

Chest x-ray Renal biopsy - rare


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Glomerulonephritis

Therapeutic Management No specific treatment

Fluid balance

Hypertension

Nutrition

Antibiotics


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Glomerulonephritis

Nursing Considerations Careful assessment of diseased status

Regular assessment Vital signs especially B/P

Fluid balance

Behavior

Dietary restrictions Family education and support


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Nephrotic Syndrome

Pathophysiology


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Nephrotic Syndrome

Clinical Manifestations Previously well child

Gains weight, slowly progresses to generalized

edema (unnoticeably) Decreased urine output

Skin pallor, irritable, fatigues easily

Weight loss Nails - Muercke lines

Rare-hypertension, azotemia, hematuria


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Nephrotic Syndrome

Diagnostic Evaluations Made on history and clinical manifestations

Hyaline cast and few RBC in urine

Glomerular filtration rate is usually normal Low

Total protein

Serum sodium

High Serum cholesterol

Platelets

Hgb / hct or normal


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Nephrotic Syndrome

Therapeutic Management Diet

Corticosteroid therapy

Immunosuppressant therapy

Diuretics


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Nephrotic Syndrome

Nursing Considerations Daily I & O

Monitoring edema and vital signs

Protect from infection

Maintain nutrition

Family support Strain of hospitalizations

Social isolation


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Case Studies Glomerulonephritis

Nephrotic syndrome


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Burns Epidemiology & etiology

Third leading cause of unintentional injury related

death among children 14 and under Child abuse

Contact burns, flame burns

Ignition of clothing

Chemical, electrical

Causative agent guides treatment and prognosis


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Characteristics of Burn Wounds Extent

Expressed in percentage of total body surface

area (TBSA) Modified rule of nines

For each year of life after 2 1% deducted from the head

0.5% is added to each leg


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Characteristics of Burn Wounds Depth

First

Second Third

Fourth

Severity Minor

Moderate

Major


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Burns - Pathophysiology Local response

Edema formation

Fluid loss

Circulatory status

Burn wound


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Burns - Pathophysiology Systemic responses

Cardiovascular

Renal GI

Metabolism

Neuroendocrine Anemia and metabolic acidosis

Growth and development


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Burns - Therapeutic Management Emergency care

Stop the burning process

Assess condition Cover burn

Transport to medical aid

Provide reassurance

Management Minor

Major


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Burns - Management Prevention of infection

Decreased by early wound excision

Topical antimicrobial agents Removal of devitalized tissue

Excision

Debridement

Closure of the wound Skin coverings: biological, synthetic, artificial,

permanent, cultured epithelium


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Burns - Nursing Considerations Assessment

Nursing diagnosis

Planning

Implementation

Evaluation


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Burns - Prevention Responsibility of all members of

community

Nurses responsible for education Water heater temps

Adequate supervision

Potential risks decreased

Best cure is prevention


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Case StudyKenny, age 5 years old, is brought to the emergency department after his

clothes caught on fire while he was playing with matches in thefamily garage. He is burned on approximately 25% of the bodyincluding: partial thickness second degree burns and full thicknessthird degree burns of his anterior chest, anterior abdomen, upper rightarm, both shoulders, and right hand. There is singed nasal hairapparent on physical examination and some minor burns apparent onhis face. His height is 45 inches and weight is 40 pounds. A foleycatheter is inserted and a small amount of urine is obtained. Two IVroutes are established for fluid replacement. Morphine sulfate 30 mgIV is ordered for pain.

Kenny is stabilized and sent to the burn unit. He receives dailyhydrotherapy. Dressing changes are performed bid and is placed on

prophylactic antibiotics. He has weekly wound cultures obtained


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Poisonings Prevention

Poison control

Anticipatory guidance Bottle of ipecac per child

Selected poisons

Acetaminophen Aspirin

Lead


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Critical Thinking Exercise

Mrs. Berry, a neighbor calls you. She is veryupset because her 2 yo son has eaten several

chewable multivitamins with iron. She asks

you if she give syrup of ipecac. What shouldyou advise her to do first?

1. Call the poison control center

2. Give an antiemetic3. Dilute the poison with several glasses of water

4. Wait to see if the child develops symptoms


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Critical Thinking ExerciseThe clinic in which you practice has received funds to begin

a program to reduce lead poisoning in children. As a

member of the planning committee, which of the

following projects is effective and easy to implement?

1. Screening for blood lead levels by heel or finger in allchildren under 6.

2. Question parents about the age and condition of home since

childs birth including renovations

3. Screening for blood lead levels by venipuncture in allchildren under6 who are at risk

4. Question parents about hobbies, occupations and ethnic

remedies that may expose child to lead

care of the child with disturbances in fluid

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