A. The Child with Nutrition – Elimination Patterns Alterations

1. Acid-Base Imbalances

1.1. Respiratory Acidosis and Alkalosis1.1.1. Respiratory Acidosis

a. Background Results from diminished or inadequate pulmonary ventilation Increase plasma PCO2 Increase concentration of carbonic acid Increase carbonic acid and hydrogen ion concentration Compensation: Through the kidneys increase plasma HCO3

- excrete hydrogen ionsb. Laboratory Finding: increase plasma HCO3

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c. Treatment: Correcting the underlying cause Improving gas exchange (provide more efficient removal of carbon dioxide) Oxygen therapy Mechanical ventilation Oral sodium bicarbonate = administered in children with chronic metabolic

acidosis IV sodium bicarbonate = administered in acute metabolic acidosis

1.1.2. Respiratory Alkalosisa. Background Increase in the rate and depth of pulmonary ventilation = large amounts of

carbon dioxide being exhaled decreased plasma PCO2

increased plasma pH Compensation: Performed by the kidneys Excretion of carbonic acid with sodium and potassium

conserve hydrogen ionsb. Laboratory Finding: increased plasma pH decreased plasma carbonic acid concentration increased plasma PCO2

c. Treatment: Treatment of underlying cause Preventions of lost anions and potassium deficit Rebreathing carbon dioxide

Oxygen therapy

1.2. Metabolic Acidosis and Alkalosis1.2.1. Metabolic Acidosis

a. Background Caused by gain of nonvolatile acids or loss of bicarbonate decreased plasma pH Compensation: Respiratory Kussmaul respiration = breathing is deep and rapid

b. Laboratory Finding: decreased plasma pH decreased plasma bicarbonate concentration Plasma AG = used in evaluating patients with metabolic acidosis

c. Treatment: Correcting the basic deficit Replacing the excessive losses of bicarbonate with sodium or potassium

bicarbonate or sodium lactate1.2.2. Metabolic Alkalosis

a. Background Occurs when there is reduction in hydrogen ion concentration and an

excess of bicarbonate Increased plasma pH Compensation: Theoretically: Respiratory Irregular and unpredictable Sodium, potassium and chloride loss kidney will attempt to

conserve sodium and potassium concentration elevated urine pH, plasma pH, plasma bicarbonate; reduced chloride concentration

b. Treatment Preventing further loss of acid Replacing lost electrolytes

**General Nursing ResponsibilitiesA. Assessment:

Observe general appearance Drawn expressions Dry mucous membranes and lips “Look sick” Loss of appetite Cry of infant Child is irritable

B. Diagnosis History taking

Taken from the parent or primary caregiver Amount and type of fluid intake and output are important.

o Number and consistency of stools the child passed in the past 24 hourso Number of times the child voidedo Type and amount of food and fluid ingested of vomitedo Number of wet diapers in the past 24 hourso History of normal or increased intake of an unusual fluid

History of gradual weight gain and observations of puffiness History of excessive water intake with diminished output

I/O MeasurementC. Care Management

Venous Access Device: Factors for VAD

o reason for placement of cathetero patient ageo length of therapyo risk of patient in placement of cathetero availability of resources

Types of central catheterso Peripheral Intermittent Infusion Deviceo Peripherally Inserted Central Cathetero Long-term Central Venous Access Device

1) Tunneled catheter2) Groshing Catheter3) Implanted Parts

Total Parenteral Nutrition and Total Nutrient Admixture: TPN – also known as alimentation

o Provides for the nutritional of infants or children who cannot consume an adequate amount of nutrients to support physical growth, positive nitrogen balance and water and electrolyte homeostasis.

Parenteral Nutrition – delivered into a large diameter vessel such as the subclavian vein.

Total Nutrient Admixture (TNA) - refers to the PN formula with carbohydrates, lipids, amino acids, vitamins, minerals, water, trace elements and other additives in a single container with lipids piggybacked into the administration setup.

Home Parenteral Nutrition Before a home care program can be implemented, a thorough assessment is

made of the family and the home care situation. Technical Aspects of the procedure:

a) Psychosocial readiness of the familyo Family support systems

b) Availability of a pharmacy to prepare the parenteral alimentation solution.o A practitioner to handle a day-to-day emergency needs.

c) Cooperating insurance company or agencyo Major responsibilities for the child and family with HPN include assurance

that the proper solution is infusing, proper maintenance of the VAD, prevention of sepsis and other mechanical complications, monitoring of infusion rate, and assessment of the patient’s tolerance to the solution.

2. Acute Gastroenteritis a. Background

Gastroenteritis is an infection of the gut. Viruses that cause gastroenteritis include: rotavirus, noro virus, and hepatitis A. Bacteria that cause gastroenteritis include: salmonella, campylobacter, bacillus,

vibrio, and escherichia coli. Bacterial gastroenteritis is caused by food poisoning.

b. Assessment Assess recent change in weight Assess child of signs of dehydration

appears unwell altered responsiveness reduced urine output Pale or mottled skin Cold extremities Sunken eyes Dry mucous membranes reduced skin turgor

c. Signs and Symptoms Diarrhea Nausea and Vomiting Fever Abdominal pain

d. Diagnostic Procedure Stool Exam

e. Treatment Probiotics helps reduce the duration of diarrhea Analgesics for headache Antibiotics are not advisable because they cause diarrhea Pedialyte™ or Re-hydration formulas to prevent dehydration

f. Nursing Care Management

Encourage the child to increase oral fluid intake Provide comfort so that the child can recover easily Monitor urine output

3. Genitourinary Alterations

1. UTIa. Background Clinical condition that may involve the urethra and bladder (lower urinary tract)

and the ureters, renal pelvis, calyces, and renal parenchyma (upper urinary tract). Females have a 10 to 30 times greater risk for developing UTI than males. Escherichia Coli - most common causative agent. Proteus, Pseudomonas, Klebsiella, Staphylococcus Aureus - other organisms

associated with UTI.b. Clinical Manifestations

Depends on the child’s age. Newborn infants and children less than 2 years of age:

1) Characteristically nonspecific2) Nearly resemble gastrointestinal infection such as:

Failure to thrive Feeding problem Vomiting Diarrhea Abdominal distention Jaundice

3) Other evidence: Frequent and infrequent voiding Constant squirming and irritability Strong-smelling urine Abnormal stream Persistent diaper rash

Children more than 2 years of age:1) Often observable, such as:

Enuresis or daytime incontinence Fever Strong or foul-smelling urine Increased frequency of urination Dysuria or urgency Hematuria

2) May complain having abdominal pain. Adolescents:

1) Manifestations are MORE specific.

2) Lower Tract Infection symptoms: Frequency and painful urination Fever is usually absent Small amount of turbulent urine that may be glossy bloody

3) Upper Tract Infection symptoms: Fever Chills Flank pain Lower tract symptoms, which may appear 1 or 2 days after.

c. Diagnostic Procedure Bag Urine Specimen - commonly contaminated by perineal and perianal flora

and are usually considered inadequate for a definitive diagnosis. Suprapubic Aspiration - most accurate test of bacterial content for children less

than 2 years of age. Properly Performed Bladder Catheterization - most accurate test of bacterial

content as long as the first few millimeters are excluded from collection. Plastic Dipstick and Agar-coated Slide Test - quick and inexpensive methods for

detecting infection before obtaining final culture results. Specific test for the localization of the infection site:

Ureteral catheterization Bladder washout procedures Radioisotope renography Ultrasonography Dimercaptosuccinic Acid Scan

d. Treatment Antibiotic Therapy - guided by the laboratory culture and sensitivity tests. Empiric Therapy - may be necessary when fever or systemic illness complicates

UTI. Common anti-infective drugs:

1) Penicillins2) Sulfonamide (including trimethoporin and sulfamethoxazole in combination)3) Cephalosporins4) Nitrofurantoin5) Tetracyclines

Urine cultures - usually repeated at monthly intervals for 3 months and at 3-month intervals for another 6 months.

Renal scarring - can develop during the initial infection, especially in younger children.

Aim of therapy:1) Prevent morbidity2) Reduce the chance of renal scarring

e. Nursing Care Management

Nurses should instruct parents to observe regularly for clues that suggest UTI. Careful history regarding voiding habits, stooling patterns, and episode of

unexplained irritability may assist in detecting less obvious cases of UTI. Children who are old enough to understand need an explanation of the

procedure, it purpose, and what they will experience. Patients should primarily drink clear liquids. Caffeinated or carbonated beverages are avoided because of their potentially

irrigative effect on the bladder mucosa.

2. Enuresisa. Background

A common and troublesome disorder that is defined as intentional or involuntary passage of urine into bed (usu. at night) or into clothes during the day the children who are beyond the age when voluntary bladder control should normally have been acquired.

This is more common in boys. Enuresis is an alteration of neuromuscular bladder function and is often benign and self-limiting.

b. Assessment compute for the normal child’s bladder capacity: Child’s age + 2 = Normal

Bladder Capacity

c. Signs and Symptoms urgency that is immediate and accompanied by acute discomfort, restlessness

and urinary frequency.d. Diagnostic Procedure

To diagnose as enuresis, the child must be at least 5 years and voiding of urine at least twice a week for at least 3 months.

e. Treatment1) Drugs

a) Imipramine (Tofranil) – inhibits urinationb) Oxybutynin – reduces uninhibited bladder contractions and may be helpful

for children with daytime urinary frequencyc) Desmopressin (DDAVP) – reduces nighttime urine output to a volume less

than functional bladder capacity2) Bladder Training3) Elimination of fluids after every evening meal4) Interruption of sleep to void

f. Nursing Care Management The nurse can both help the children and parent in understanding the problem,

the treatment plan and difficulties they may encounter in the process.

The nurse provides consistent support and encouragement to help sustain them And lastly, the children should develop feelings of confidence and hope that

they are helping themselves.

3. Structural Defects

A. Renal Tubular Disorders

Abnormalities of the following: Tubular Transport Tubular Reabsorption Glomerular Function

Key Points: Edema and hypertension are ABSENT. BUN level and routine urinalysis are NORMAL.

Function Proximal Tubules – reabsorption of substances from the glomerular filtrate

– sodium, potassium, chloride, bicarbonate, glucose, phosphate and amino acids

Distal Renal Tubules – acidification of urine; potassium secretion; selective and differential reabsorption of sodium, chloride, and water – determines the final urinary concentration.

1) Renal Tubular Acidosisa) Distal Tubular Acidosis (Type 1)

i. Etiology Kidneys inability to establish a normal pH gradient between tubular cells

and tubular contentsii. Characteristics

Inability to produce a pH below 6.0 despite the presence of severe metabolic acidosis Primary Disorder

Hereditary defect; greater penetrance in females Secondary Disorder

Rare**After the age of 2 = growth failure, history of vomiting, polyuria, dehydration, anorexia, failure to thrive, bone demineralization, with occasional formation of urinary calculi (urolithiasis) in older children.

b) Proximal Tubular Acidosis (Type 2)i. Etiology Impaired bicarbonate reabsorption of the proximal tubule

ii. Characteristics

Plasma concentration of bicarbonate stabilizes at a lower level than normal -> Hypercholerimic metabolic acidosis

*Fanconi syndrome – transport mechanisms are damaged by the accumulation of toxic metabolites; the tubular epithelium is damaged by – lead, cadmium or platinum

Secondary or idiopathiciii. Clinical manifestation Growth failure Tachypnea Dehydration Vomiting Episodic fever Nephrolithiasis secondary to hypercalciuria Muscle weakness Severe life-threatening academia

iv. Therapeutic Management For both proximal and distal disorders:

Administration of sufficient carbonate and citrate = to balance metabolically produced hydrogen ions; To maintain plasma bicarbonate levels in normal range; And to correct associated electrolyte disorders.

For proximal disorders: Large volumes by carbonate = to compensate for urinary losses.

Best management: Mixture of sodium and potassium carbonate = prevent deficiencies of either

cation *Shohl solution – effective but uneasily prepared

v. Nursing care management: Intensive medical evaluation Providing and informing medication plants to parents Teaching of the importance of taking medications for long-term treatment

2) Nephrogenic Diabetic Insipidus

a) Etiology Defect in the ability to concentrate Distal tubules and collecting ducts – insensitive to ADH action Occurs primarily in males; females are carriers of the defective gene

May be related to Chronic obstructive renal disorders Sickle cell disease Renal tuberculosis Other renal disorders

b) Clinical manifestations Newborn

Vomiting Unexplained fever Failure to thrive Severe recurrent dehydration Dehydration with hypernatremia

Growth retardation related to diminished food intake and poor general health

c) Diagnosis Family history

d) Therapeutic management Provision of adequate volumes of water = compensate for urinary losses Low sodium, low solute diet Chlorothiazide or ethacrynic acid diuretics = increase reabsorption of

sodium and water Supplemental potassium = prevent hypokalemia as a result of thiazide

therapy

e) Nursing care management Assist family and children in coping with long-term convenience Teach family to administer medications and help with diet planning Avoid activities that contribute to dehydration Early recognition of disease Genetic counselling is recommended

4. Acute Glomerulonephritisa. Etiology

Pneumococcal, streptococcal and viral infections An immune-complex disease (a reaction that occurs as a by-product of an

antecedent streptococcal infection with certain strains of group A B-hemolytic streptococci

b. Clinical Manifestations Initial Signs

Edema of the face, especially around the eyes (periorbital edema) Anorexia Tea/Dark-colored urine

Reduced urinary output Pale

c. Diagnostic Evaluation Urinalysis shows hematuria and proteinuria

Hypertensiond. Therapeutic and Nursing Care Management

Record daily weight to assess fluid balance Sodium and water restriction is useful when the output is significantly reduced

(< 2 to 3 dl/24hr) Diuretics shouldn’t be used if renal failure is severe. However, if not severe,

diuretic therapy is helpful if edema and fluid overload are present. BP should be taken every 4-6 hours Limit sodium intake Note volume and character of urine

5. Nephrotic Syndromea. Definition

Most common presentation of glomerular injury in children Characterized by massive proteinuria, hypoalbuminemia, hyperlipidemia, and

edema A clinical manifestation of a large number of distinct glomerular disorders in

which increased glomerular permeability to plasma protein results in massive urine protein loss

b. Background Rare in children younger than 6 months of age Uncommon in infants younger than 1 year of age Unusual after the age of 8 years Occurs more in males than femals 2:1 In adolescence, the ratio is 1:1 Types of Nephrotic Syndrome

Primary Nephrotic Syndromeo Minimal Change Nephrotic Syndrome (MCNS)

Secondary Nephrotic Syndrome Congenital Nephrotic Syndrome

c. Assessment Assess for weight gain greater than previous patterns Assess for generalized edema

Abdomen Lower extremities

Assess for changes in the appearance of the nails White (muercke) lines parallel to the lunula

d. Signs and Symptoms Periorbital or ankle edema Wight gain greater than expected based on previous pattern Decreased urinary output Pallor

Fatiguee. Diagnostic Procedure

Urinalysis Renal biopsy

f. Therapeutic Management Objectives

Reduce the excretion of urinary protein and maintain protein-free urine Prevention or treatment of acute infection Control of edema Establishment of good nutrition Readjustment of any disturbed metabolic processes

General Measures Diet Corticosteroid Therapy Immunosuppressant Therapy Diuretics

g. Nursing Care Management Daily monitoring of intake and output Examination of urine for albumin Monitor daily weight and measurement of abdominal girth Monitor vital signs Inform parents of possible relapses and side effects that may occur during the

course of treatment Reassure parents that relapses can occur but continuation of the drugs will

diminish side effects

6. Renal Failure Background

inability of the kidneys to excrete waste materials, concentrate urine, and conserve electrolytes.

can be acute or chronic and affects most systems in the body.A. Acute Renal Failure

a. Etiology result of a large number of related or unrelated clinical conditions: poor

renal perfusion; acute renal injury; or the final expression of chronic, irreversible renal disease.

b. Clinical Manifestations Oliguria Anuria

c. Signs and Symptoms Drowsiness circulatory congestion

cardiac arrhythmia from hyperkalemiad. Diagnostic Procedure

History Takinge. Nursing Care Management

treatment of the underlying cause management of the complication of renal failure provision of supportive therapy within the constraints imposed by the

renal failure

B. Chronic renal failure

a. Etiology congenital renal and urinary tract malformations: renal hypoplasia and

dysplasia and obstructive uropathy; and vesicoureteral reflux.b. Clinical Manifestations

loss of normal energy and increased fatigue on exertion pale growth retardation

c. Signs and Symptoms Evidence of difficulty

d. Diagnostic Procedure Observation

e. Nursing Care Management Children areencouraged to attend to school Regulation of diet

7. Bladder Exstophy Epispadia Complexa. Background

Bladder Exstrophy is a complex combination of disorders that occurs during fetal development.

involves many systems in the body, including the urinary tract, skeletal muscles and bones, and the digestive system

the bladder is essentially inside out and exposed on the outside of the abdomen urine constantly trickles onto the skin causing local irritation

b. Clinical Manifestations widened pubic bones outwardly rotated legs and feet triangle-shaped defect in the abdomen and visibility of the membrane of the

bladder which is usually bright pink abnormally-shaped abdominal muscles displacement of the umbilicus (belly button), usually above the defect

umbilical hernia may be present (section of intestine protrudes through a weakness in the abdominal muscles)

short, small penis with urethral opening along top of penis (epispadias) narrow vaginal opening, wide labia, and short urethra

c. Diagnostic ProcedureExstrophy of the bladder can usually be diagnosed by fetal ultrasound before an

infant is born. After the infant is born, exstrophy can be determined by physical examination. Other diagnostic procedures may include:

renal ultrasound - a non-invasive test in which a transducer is passed over the kidney producing sound waves which bounce off of the kidney, transmitting a picture of the organ on a video screen. The test is used to determine the size and shape of the kidney, and to detect a mass, kidney stone, cyst, or other obstruction or abnormalities.

renal scan - a specialized scan that may include injections of a radioactive substance. A scan is then performed at different intervals to determine the blood flow through the renal vessels and urine flow through the kidneys.

d. Treatment Modern therapy is aimed at surgical reconstruction of the bladder and genitalia.

TRINITY UNIVERSITY OF ASIASt. Luke’s College of Nursing

IN PARTIAL FULFILLMENT OF THE REQUIREMENTSin NURSING CARE MANAGEMENT (NCM) LEC

WRITTEN OUTPUTTHE CHILD WITH NUTRITION – ELIMINATION PATTERNS ALTERATIONS

SUBMITTED BY:2NU08

EXALERON

Obar, Jean Kathleen Aynn M.Ocampo, Rouzele Katherine L.Omampo, Jennider Andrei B.

Ong, Renz Andrew V.Oquendo, Rose Ann A.

Orellosa, Diane Emmille E.Otico, Joseph S.

Paat, Joden Ryan D.Pacis, Lea Therese R.

Pajaro, Barbrah Allana A.Palon, Dorelyn Jade P.

Panay, Jason V.

SUBMITTED TO:Ms. Julie Ann Gundran, RN

Professor