Week 5 Fluid Electrolyte imbalance PDF

Title Week 5 Fluid Electrolyte imbalance
Author Alysha
Course Nursing Care of Children
Institution West Coast University
Pages 20
File Size 606.3 KB
File Type PDF
Total Downloads 112
Total Views 146

Summary

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Week 5 Fluid Electrolyte imbalance, renal and genitourinary dysfunction, cerebral dysfunction and CNS malformations (Ball – 18, 26,27) (ATI 12,13,14, 24, 25, 26) Infants have a larger EXTRACELLULAR FLUID VOLUME than older children and adults  Increased risk for dehydration o Sensible loss  Measurable loss through urine or wound drainage o Insensible loss  Measurable loss such as through the skin and respiratory tract Kidneys immature in children under 2 years old o Ineffective secretion  Difficulty regulating electrolytes FLUID VOLUME IMBALANCES  Dehydration o Isotonic  Proportionate loss of fluid and sodium  Extracelluar loss  E.g vomiting and diarrhea o Hypotonic  Greater loss of sodium than water  Extracellular shift to intracellular to compensate  E.g prolonged vomiting, diarrhea, renal disease, burns o Hypertonic  Greater water loss than sodium  Intracellular shirt into extracellular to compensate  E.g diabetes insipidus, fluid volume overload DEHYDRATION  Occurs due to vomiting, diarrhea, burns, hemorrhage  Radiate warmers (overhead warmers or phototherapy) o Increased insensible loss through the skin.  Third spacing o Adrenal insufficiency  Accumulation of extracellular fluids in peritoneal cavity o Diuretic overuse  How does the patient look? 

LOC

Mild Alert, restless, thirsty

Moderate Irritable, lethargic

Severe Lethargic to comatose (infants)

BP

Normal for age

Pulse

Regular, strong

Skin Tugor Urine

Immediate Usual output

Respiration s Eyes

Regular, usual rate Normal

(infants) Alert, restless, thirsty (older kids) Normal or low Postural hypotension Rapid Poor Decreased output,>1mL/k g/hr, dark color, increased s.g Usual or rapid rate Slightly sunken, decreased tears

Often conscious, apprehensive (older children Low to undetectable

Rapid, weak to nonpalpable Very poor Very decreased or absent output

Changing rate and regularity Deeply sunken, absent tears

ORAL REHYDRATION THERAPY  Prevent dehydration if possible o Recover patient with IV fluid resuscitation, oral rehydration therapy, change environmental factors when applicable  Oral rehydration best for mild or moderate loss o See 18-6 o No diarrhea/dehydration  Minimal  Moderate  Severe  Rehydration complete o IV fluid resuscitation see 18-7  Complete calculations A. Up to 10kg 100mL/kg B. 11-20 kg 50mL/kg C. >20kg 20mL/kg FLUID VOLUME EXCESS  Too much fluid in vascular and interstitial compartment o Serum sodium normal o Due to aldosterone  Adrenal tumors  CHF  Liver cirrhosis  Chronic renal failure o May also be attributed to low socioeconomic families that over dilute formula and fluid overload children

EDEMA AND CARE MANAGEMENT  Assess for o Weight gain o Increased input vs output o Infusion rate and ensure patient is not being overloaded o Edema table 18-8  Pitting  Capillary leak  Third spacing  Nursing care management o Elevate for localized edema o Monitor for skin integrity o Provide diuretics and pharmacological interventions as appropriate o Psychosocial support ELECTROLYTE IMBALANCES Sodium pp 420-422 • Hypernatremia • Water deprivation OR Diabetes Insipidus • Thirsty, decreased UOP, ALOC, lethargy, seizures • Fluid resuscitation (hypotonic or isotonic), ORT • Hyponatremia • Excess water, dilution • Water intoxication forced or otherwise • ALOC, N/V, headache, muscle weakness, decreased DTR, seizures • Fluid restriction, hypertonic solutions Potassium pp 423-425 • Hyperkalemia • Increased intake through IV fluids, replacement, blood products • Abd cramping, diarrhea, LE weakness that ascends, flaccid paralysis, arrhythmias/dysrhythmias • PD, kayexalate, K-wasting diuretics • Hypokalemia • Increased K excretion • Decreased K intake • Muscle dysfunction; slow, unresponsive, progresses to flaccid paralysis, arrhythmias, polyuria • K replacement IV/oral Calcium pp 427-430 • Hypercalcemia • Increased intake or absorption • Chicken liver, mega-doses Vitamin A or D, calcium rich foods and antacids

Decreased neuromuscular excitability, constipation, anorexia, N/V, ALOC, polyuria, FTT • Causes increased Na and K excretion • Increase fluids, Lasix, glucocorticoids, phosphates (risky), dialysis • Hypocalcemia • Diet low in Vitamin D and calcium, no access to sunlight, very dark skin, uremic syndrome, chronic diarrhea, steatorrhea • Tetany/ muscle excitability, seizures, arrhythmias, CHF • Oral/IV calcium, magnesium replacement, calcium rich foods, vitamin D. Magnesium pp 430-431 • Hypermagnesemia • Increased intake, decreased excretion • Enemas, laxatives, antacids, IV fluids, Epsom salts (deadly in peds population) • Decreased muscle irritability, hypotension, bradycardia, lethargy, absent DTR, flaccid paralysis, respiratory depression, arrhythmias, cardiac arrest • Increase urinary excretion of magnesium, increased fluid intake, diuresis • Hypomagnesemia • Decreased intake, increased excretion, prolonged IV therapy without magnesium, chronic diarrhea, short bowel syndrome, malabsorption, steatorrhea • Tetany, hyperactive reflexes, cramps, arrhythmias, seizures • Administer magnesium ACID-BASE IMBALANCES Acidosis- too much acid Respiratory acidosis- too much carbonic acid Metabolic acidosis- too much metabolic acid Alkalosis- too little acid Respiratory alkalosis- too little carbonic acid Metabolic acidosis- too little metabolic acid •

EDEMA OCCURS  IF the balance of these four forces is altered in excess fluid o Increased blood hydrostatic pressure  Increased cap. Blood flow,venous congestion  Inflammation, local infection, extracellular FVE, R.Heart failure, venous thrombosis, muscle paralysis o Decreased blood colloid osmotic pressure  Increased albumin excretion  Decreased albumin synthesis  Nephrotic syndrome (albumin leaks into urine), proteinlosing enteropathies (excess albumin in feces),

Kwashiorkor (low-protein, high carb starvation diet provides too few amino acids for liver to make albumin), liver cirrhosis o Increased interstitial fluid osmotic pressure  Increased capillary permeability  Inflammation, toxins, hypersensitivity reactions, burns o Blocked lymphatic drainage  Venous congestion  Tumors, goiter, parasites that obstruct lymph nodes, surgery that removes lymph nodes

DEFINING THE GASES  Respiratory Acidosis o Accumulation of CO2 in blood o ALOC, lethargy, headache, INCREASED ICP  Respiratory Alkalosis o Too little CO2 o Hyperventilation, asthma, sepsis o No renal compensation in early stages o Parathesis, cramping, ALOC  Metabolic Acidosis o Increased acid or excess loss of HCO3 o Hyperventilation, Kussmaul respirations, PVR, arrhythmias, hypotension, pulmonary edema, ALOC  Metabolic Alkalosis o Decreased acid or increased HCO3 o Bradypnea, tetany, seizures, ALOC  Mixed imbalances o E.g. CF patient with respiratory acidosis due to lung dysfunction and metabolic alkalosis due to emesis/illness  Always treat ID and underlying cause an replace deficits

ALTERATION IN GENITOURINARY FUNCTION  URINARY TRACT INFECTION o Bacterial o Fungal o Viral o Site  Upper tract – pyelonephritis  Lower tract – cystitis  Common in children o More common in males in first 6 months of life, then females  Circumcision in males

Short urethra closer proximity to anus, risk for contamination in females Manifestations o Fever, foul smelling urine, pain, n/v Treatment o Abx therapy, hydration, education with non-structural defects, good hygiene 

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Most common bacterium E. coli Primarily due to urinary stasis o Neurogenic bladder due to paralysis or SCI o Infrequent voiding Poor hygiene Tight fitting underwear, irritated perineum Uncircumcised males Sexually active adolescent females Vesicoureteral reflux Hydronephrosis o Urine accumulation in renal pelvis

STRUCTURAL DEFECTS  Bladder exstrophy o Bladder outside of abdominal wall o Multiple stage surgery to reconstruction  Hypospadias/Epispadias o Congenital anomalies, urethral opening on ventral or dorsal surface of penis o Stent placement o Early intervention, image integrity  Vesicoureteral Reflux (VUR) o Retrograde flow of urine from bladder to ureters  Risk for recurrent UTI prophylactic abx therapy  Diagnosed with voiding cystourethrogram (VCUG) ENURESIS  Involuntary voiding by child old enough that bladder control is expected (5-6 years)  Occurs during the night, day, or both  Diagnostic tests  Assess for any neural tube defect  Requires bladder training, pharmacologic intervention  Education, psychosocial support, assess child’s readiness for treatment MILESTONES IN THE DEVELOPMENT OF BLADDER CONTROL  1.5 years o Child passes urine at regular intervals  2 years

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o Child announces when voiding 2.5 years o Child makes know the need to void; can hold urine 3 years o Child goes to the bathroom alone; holds urge if preoccupied with play 2.5 – 3.5 years o Child achieves nighttime control 4 years o Child shows great interest in going to bathrooms when away from home 5 years o Child voids 5-6 times a day, prefers privacy

NEPHROTIC SYNDROME  Congenital, secondary to glomerulonephritis, disease or toxin, or injury  Presents with ankle edema, resolving periorbital edema that descends, pallor, irritability, anorexia, hematuria, decreased UOP, proteinuria, hypoalbuminemia, hyperlipidemia, hypotensive/normal, altered immunity  Peaks 2-7 years of age  Management and assessments o UA, albumin, sodium, BUN, cholesterol, electrolyte panel o Course of steroids-taper dose o IV albumin o Diuretics o CCS or Cytoxan  Risk for infection with immunosuppressive therapies ACUTE GLOMERULONEPHRITIS  Most often post infectious – GABHS o Staph, pneumococcus, coxsackie virus o Usually due to tonsillitis  recovers develops APIGN/APSGN (Acute postinfectious glomerulonephritis)  Glomerular damage, edema (periorbital and dependent) o Flank/abdominal pain o Irritability o Fever o Hematuria o Proteinuria o Pulmonary congestion o Hypertension o N/V o Oliguria  Management and assessments

o BUN, creatinine, protein, WBC, ESR, ASO (antistreptolysin) titer, UA, H&H, throat culture, xray o Daily weights I/O, neuro assessment o Sodium restriction and diuretics hydralazine ( if hypertensive with neuro manifestations) o No salt, low protein diet, low potassium with oliguria, fluid restriction with edema RENAL FAILURE  AZOTEMIA o A medical condition characterized by abnormally high levels of nitrogen-containing compounds (such as urea, creatinine, various body waste compounds, and other nitrogen-rich compounds) in the blood.  OLIGURIA o Production of abnormally small amount of urine  ANURIA o Failure of the kidneys to produce urine  Acute o Prerenal, postrenal, kidney o Severe dehydration o Acute renal injury o Hemolytic uremic syndrome (caused by E.coli) o Acute glomerulonephritis o Sepsis o Poisoning o Nephrotoxic drugs o Hypovolemia o Obstructive uropathy o Complications in cardiac surgery o Decreased perfusion of hypovolemia, N/V, lethargy, edema, gross hematuria, oliguria, hypertension, electrolyte imbalance, uremia, fluid overload o Watch for hyperkalemia, hypo/hypernatremia  Assessment and management o BUN, creatinine, Na, K, Ca, osteodystrophy HYPERTHYROIDISM o Minimize/prevent permanent renal damage, balance fluids and electrolytes fluid replacement, albumin, diuretic therapy o Na, K, Phos may be restricted, maintain nutritional needs ( Kcals, fats, carbs, proteins) RENAL FAILURE  CHRONIC o Progressive, irreversible  18.1 million children



o Due to developmental abnormalities of kidney or urinary tract, obstructed flow or reflux, hemolytic-uremic syndrome or unresolved AGN o Progresses to End Stage Renal Disease (ESRD)  Requires dialysis  Unmanaged fluid/electrolyte balance unable to produce vitamin D or excrete phosphorus resulting in hyperparathyroidism o Assessment and management  No initial symptoms, renal insufficiency, polyuria, HA, nausea, decreased alertness, anemia, tachycardia tachypnea, anorexia, hypertension  Monitor electrolytes, phosphate, BUN, creatinine, pH to confirm CRF, UA, GFR, renal bx  Irreversible but may be managed with medications, diet modification (table 26-9)  Dialysis: limit Phos, K, Na intake, increase Ca intake, protein, carbs ESRD o Progressive renal deterioration led to multi-system failure: N/V, uremic frost deposited on skin, HA, confusion, pulmonary edema, CHF o Dialysis imperative  Infections common and require hospitalization o Possible need for transplant; favorable in children vs adults

RENAL REPLACEMENT THERAPIES  Peritoneal dialysis o Waste products pass from blood into abdominal cavity o In ARD, temporary catheter placed; in CRF catheter surgically placed for long term use o Dialysate dwells in cavity then drained out to pull off fluid draw in by dialysate  Maybe ambulatory; continuous ambulatory PD (4-5 times daily and dwells 4-8 hours) or automated PD (5 times over 10 hours, usually overnight) o Complication of peritonitis, usually Staph; need sterile technique for therapy  Hemodialysis o Blood filtered through a machine to filter out waste and excess fluids o Intravascular volume decreased when dialysate pumped in opposite direction of blood return to promote extraction  Provided in ICU settings when other treatment modalities have failed or in outpatient setting



 Therapy 3 times weekly over 3-4 hours each day o Children over 20 kg get an AV fistula, or synthetic graft is placed for vascular access o Monitor for hypotension, N/V, disequilibrium syndrome caused from rapid changes in water/electrolyte balance o Nursing management to include Heparin education, monitor risk for bleeding, fluid balance, vital signs, weight neuro status Transplantation o Only alternative to long term dialysis o Good outcomes r/t effective pre- and post-transplant care, immunosuppression, and prevention/dx/treatment of infections o Risk for rejection and infection o Long term medication compliance imperative

STRUCTURAL DEFECTS OF THE REPRODUCTIVE SYSTEM  Phimosis o Foreskin over glans of penis  Skin must be retracted with steroid cream due to adhesions; of circumcision required  Cryptorchidism o Undescended testes (one or both)  Testosterone deficiency, complications of infertility and malignancy due to higher temps in abdomen  Orchiopexy surgery to pull down testes before 12 months to avoid damage and body image issues with development  Inguinal Hernia o Inguinal or scrotal swelling due to bowels extending into Inguinal canal  6:1 boys vs girls  More apparent with crying/straining  Surgical mesh correction  Hydrocele o Fluid filled mass in scrotum  Resolve spontaneously by 12 months  Testicular torsin o Testes rotate on spermatic cord, cutting off blood supply engorgement and ischemia  1:4000 before 25 y/o  Surgical emergency within 6 hours of occurrence o Psychosocial support for concerns about future fertility SEXUALLY TRANSMITTED INFECTIONS (STI) o Chlamydia  Leading cause of early pneumonia and conjunctivitis in newborns

o Genital herpes  C-section if herpes is present o Gonorrhea  Spread to the infant during childbirth and can result in serious health problems for the infant o Human papillomavirus  No cure, can lead to cervical cancer o Trichomoniasis o Syphilis  Risk of fetal death, pregnant woman should be tested 

PELVIC INFLAMMATORY DISEASE (PID) o Infection of upper genital tract by spread of organisms in cervix and vagina

ALTERATION IN NEUROLOGIC FUNCTION  focused assessment o LOC o Cranial nerves o Fontanels and sutures o Cognitive function o Pupils o VS o Neck stiffness o Pain o Family hx o LOCs  Confusion  Delirium  Lethargy  Stupor  Coma o Etiology  Injury  Infection  ICP o Posturing

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Decorticate a. Lesions above the brainstem Decerebrate b. Lesions of brainstem

Figure 27-3 Pupil findings in various neurologic conditions with altered consciousness. A, A unilateral dilated and reactive pupil is associated with an intracranial mass. B, A fixed and dilated pupil may be a sign of impending brainstem herniation. C, Bilateral fixed and dilated pupils are associated with brainstem herniation from increased intracranial pressure.

CARE AND MANAGEMENT  Maintain airway o Monitor for secretions o Be alert for no-gag reflex o Suction PRN  Protect from seizures o Pad side rails o Be ready to time o Medication management  Eye and oral care  Nutrition NG, GT, TPN,IL  Sensory stimulation o Music therapy o Talk to the child as if they are responsive  Psychosocial support SEIZURE DISORDERS  Partial or Generalized  Record o Time, start, and stop o Aura? Triggers? o Tonic, clonic phases

o Hypoxia? o Postictal state







Staus Epilepticus o Seizure lasts more than 30 minutes o Give Rx meds slowly  Pp750-751 Nursing Care o Protect from injury o Document o Teaching  Meds  Restrictions  Triggers Diet o Ketogenic  High fat, low carb for one or more years  Body learns to metabolize fat for energy instead of carbs  Monitor for constipation, kidney, stones, slowed growth  Believed to produce anticonvulsant effects



BACTERIAL MENNIGITITS o Fever, lethargy, vomiting, headache o Nuchal rigidity o Sometimes fatal  Neisseria meningitidis, strep pneumoniae, E. coli, Group B strep Listeria common agents  Risk factors: immunosuppression, VP shunt, cochlear implant trauma, recent sinus/ear infection o Labs, LP for CSF collection, CT scan with increased ICP o Treated with abx 7-21 days  Ampicillin, cefotaxime, pen G, vanco o NPO, MIVF, monitor ICP and SIADH o Complications include severe neurologic complications/deficits



Viral o o o o o o

Meningitis (aseptic) Lesser severity of symptoms Fever, lethargy, irritability Malaise Maculopapular rash Increased blood cells and protein in CSF More common than bacterial due to vaccinations in US  Increased risk in peak season for enterovirus o Care and management

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Antipyretics, analgesics, dark room and decreased stimuli, IV or PO fluids, comfort care and positioning

ENCEPHALITIS o Generalized brain inflammation  Fever  Altered mental status  Caused by viruses transmitted by mosquito (west Nile) a. Usually in warm weather seasons o Starts with flu like symptoms, bulging fontanel, then altered mental status  Flaccid or spastic paralysis  + Kernig or Brudzinski signs  Risk for seizures, ICP, RF b. Monitor cardiorespiratory fx, airway, sats, vitals c. CPT to prevent pneumonia  As the child recovers, provide age-appropriate activities to promote recuperation To test for Kernig Sign o Raise the child’s leg with the knee flexed o Extend the child’s leg at the knee o Any resistance in noted or pain is felt- result is positive Brudzinski sign o Flex the child’s head while in a supine position o If this action makes the knees or hips flex involuntarily positive Reyes Syndrome o Acute encephalopathy cause by toxic, inflammatory insult or injury  Associated with aspirin use and influenza  N/V and mental status changes  Seizures, progressive unresponsiveness o Diagnosis based on change to LOC, labs, and WBCs in CSF o Care with ventilation, art line and CVP monitoring  Hypoglycemia managed with IV glucose, labs and electrolytes monitored  Neurological deficits greater in children under 2 years old

GUILLIAN-BARRE SYNDROME  Progressive muscular weakness, areflexia, RD o Ascending weakness 2 days to 4 weeks  Self-limiting  Autoimmune triggered by respiratory or gastrointestinal illness o EBV, cytomegalovirus, varicella, campylobacter most common agents

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Requires extensive PT/OT for recovery and reestablishing self-care measures o Psychosocial support and education on prognosis Treatment with immunoglobulin, mechanical ve...


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