Genetourinary part 2
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Transcript Genetourinary part 2
Pediatric Nursing
Genitourinary Disorders
Lecture 15
Acute Post infections
Glomerulonephritis
Is an inflammation of the glomeruli of the kidneys. It
is most often a response of a group A beta-hemolytic
streptococcal infection of the skin or pharynx.
It can be caused by other organisms such as
Staphylococcus, Pnuemococcus.
Or it can be due to immunologic abnormalities,
effects of drugs or toxins, systematic diseases &
viruses.
It occur more often in children from 2-12 years of
age.
Pathophysiology
Antibody-antigen complexes become logged in the
glomerular. Leading to inflammation & obstruction.
The glomerular membranes are thickened & capillaries
in the glomeruli are obstructed by the damaged tissue
cells, leading to a decreased GFR.
Vascular permeability increases, allowing protein,
RBCs to be excreted. Sodium & water are retained,
expanding the intravascular & interstitial
compartments.
Low levels of proteins in serum will result in shifting
of fluid from intravascular to intracellular
compartment & resulting in the characteristic
findings of edema.
Clinical manifestations
Many children are asymptomatic, in other children
the onset abrupt with flank or midabdominal pain,
irritability, malaise & fever.
Hematurea is present in all cases,
Mild preorbital edema occurs early along with
dependent edema of the feet & ankles
Edema may progress to pulmonary effusion (dyspnea
& crackles), or ascites.
Acute hypertension may cause an encephalopathy that
includes headache, nausea, vomiting, irritability,
lethargy, & seizures.
Oligurea may or may not be present.
Diagnostic tests
BUN, Cr are elevated.
Serum protein is decreased due to mild or moderate
proteinurea.
WBC, ESR are elevated.
Serum lipid levels are increased in about 40% of
cases. (due to increase production of lipoprotein).
An elevated antistreptolysin O (ASO) titer, reflects
an the presence of antibody from a recent pharyngeal
streptococcal respiratory infections.
The anti-DNase B titer is used for detecting
antibodies in recent skin infection.
urine analyses reviles hematurea, proteinurea.
Anemia is common in the acute phase due to diluted
serum, as well as hemoglobin & hematocrit levels.
Clinical therapy.
Treatment is supportive & to relive symptoms.
Bed rest is a key component of treatment plan in the
acute phase.
Edema & mild to moderate hypertension should be
treated with sodium restriction (diet) & diuretics
such as Fursemide.
A course of antibiotic is given to ensure treatment of
the original infectious agent.
Fluid requirement are determined by monitoring of
urinary output, wt, B/P & serum electrolytes.
Low salt high protein diet.
Nursing interventions
1.
2.
3.
4.
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2.
3.
Monitor fluid status:
by monitoring V/Ss, electrolyte status, intake &
output.
Monitoring levels of ascites by measuring abdominal
girth.
Monitor urine specific gravity.
Educate parents, family & visitors about fluid
restriction as a therapy to prevent over intake.
Prevent infections:
Monitor signs of infection such as fever, increased
malaise, elevated WBC.
Instruct family about hygiene & hand washing.
Limit visitors & screen for infection.
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2.
3.
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2.
3.
Prevent skin breakdown:
Turn child frequently or at least every 2 hours.
Pad the bony prominence or susibtable area with
sheepskin.
Make sure the child’s bed is free from crumbs or
sharp toys or wrinkles of the sheets.
Meet nutritional needs:
Low salt diet, high protein diet.
Encourage parents to bring the child favored food
from home to over come the anorexia.
Allow the child to eat with other family members.
Provide emotional support
Nephrotic Syndrome
It is a clinical state characterized by edema, massive
proteinurea, hypoalbomemia, hypoproteinemia,
hyperlipidimia, & altered immunity.
It can be congenital: autosomal recessive disorder
(defect in the gene CNF on chromosome No.19.)
Or can be primary due to other diseases in kidneys
such as glomerulonephritis.
90% of cases have one of the primary nephrotic
syndrome types which is the minimal change nephrotic
syndrome (MCNS).
MCNS: drives its name from normal or minimally
changed appearance of glomeruli on light microscopic
evaluation.
Pathophysiology
The mechanism of increase the membrane
permeability is usually due to the releasing of the
permeability factors from abnormal circulating T
cells. And the loss of the negative charge of the
glomerular capillary wall.
This will lead to ,proteinurea, hypoalbuminemia,
edema, loss of immunoglobulin resulting in altered
immunity.
loss of antithrombin III by urine along with reduced
levels of factors IX, XI< & XII leading to
hypercoagulability
Clinical Manifestations
Edema develops gradually over several weeks.
Other signs include snug fit of clothing & shoes.
Pallor, hypertension, irritability, anorexia, hematurea,
decreased urine output.
The urine is frothy or foamy.
In some cases, plural effusion occur & progress to
respiratory distress.
Massive edema resulting in a dramatic weight gain,
abdominal pain, with or without vomiting, depending on
amount of sodium ingestion.
Pale, shiny skin with prominent veins, & brittle (weak)
hair.
Diagnostic Tests
Urine analysis.
BUN, sodium.
Serum albumin: hypoalbuminemia (<25 g/l).
Cholesterol
Serum electrolytes.
Protein > 40 mg/m2/ hour proteinurea.
Microscopic hematurea is present.
renal ultrasound.
Clinical Therapy
Hospitalization in sever cases.
Treatment focuses in decreasing proteinurea,
relieving edema, improving nutrition preventing
infections.
A corticosteroid (Prednisone) is used to decrease
proteinurea.
Antihypertensive, diuretics & antibodies are given.
Intravenous albumen in sever hypoalbominea.
Low salt diet is recommended
Relapse occur frequently, mostly in the form of
respiratory infections.
Nursing Interventions
1.
2.
3.
4.
Administered medications:
Monitor side effects of corticosteroid such as
moon face, increased appetite, increased hair
growth, abdominal distension, mood swings,
hypertension, nausea, & hyperglycemia.
Evaluating fasting blood sugar is needed during
therapy.
If child on diuretics watch for shock signs
(hypotension).
If child on IV albumin, watch for overload signs
(crackles)
1.
2.
3.
4.
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2.
Prevent infections:
Child is at risk for infection due to corticosteroid
therapy & loss of immunoglobulins.
Educate parents about importance of hygiene &
hand washing.
Monitor both V/Ss & WBCs.
Decreased visitors (child’s social contact) during
immunosuppression treatment.
Prevent skin breakdown:
Turn the child frequently.
Keep skin dray & clean.
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2.
1.
2.
3.
Meet nutritional needs:
Present meal in attractive ways and in small portion,
to increase child appetite.
Fluid is not restricted unless sever edema.
Promote rest:
Educate families to provide child with quiet play
such as drawing, watching videos.
Monitor signs of fatigue after activity, such as
irritability, mood swings.
Limiting visitors in the acute phase is important, use
telephone as an alternative.
Renal Failure
1.
2.
3.
Renal failure may be acute or chronic, occurs when
the kidney can not excrete wastes & concentrate
urine.
Acute renal failure occurs over days or weeks & may
be reversible.
Chronic renal failure occur over months or years, &
permanent dysfunction.
Both types is characterized by:
Azotemia: accumulation of nitrogenous wastes in
the blood.
Uremia: excess of urea & other waste products in
blood.
Oligurea: urine out put is < 0.5-1 ml/kg/hr.
Acute renal failure
It caused by acute glomerulonephritis, poisoning,
sepsis, hypovolemia, obstructive uropathy,
complications of cardiac diseases or surgery.
The causes is classified into prerenal, postrenal &
actual kidney damage:
1- Prerenal factors: result of decreased perfusion to a
normal kidney in association with systematic
condition, cased by hypovolemia, septic shock, cardiac
failure.
2- Primary kidney damage: (intrinsic factors), results
from infections, ingestion of drugs or poisons.
3- Postrenal factors: results from obstruction of both
kidneys such as in posterior urethral valves.
Chronic renal failure
Is a progressive, irreversible reduction of the kidney
function.
It results from developmental abnormalities of the
kidneys or obstructed urine flow & reflux, heredity
disease, infections.
The progressive dysfunction of nephrons results in
end stage renal disease (ESRD). Which is
characterized by minimal (<10% of normal) or no renal
functioning, anemia, abnormal blood values, metabolic
acidosis, fluid & electrolytes imbalance; the child
needs dialysis.
Elevated B/P is due to water & sodium retention.
Continue…
Hypocalcaemia occur due to irresponsive parathyroid
gland in response to low calcium levels & vitamin D.
increasing the risk of fractures.
Kidney become unable to produce activated vitamin D
& to excrete phosphorus causing increased
phosphorus levels.
Growth retardation due to disturbances of calcium,
phosphorus & vitamin D; decreased caloric intake; &
metabolic acidosis.
Decreased production of erythropoietin leading to
decrease production of RBCs in bone marrow &
anemia.
Clinical manifestations
Type
Clinical manifestations
Acute
Dark urine or gross hematurea, headache,
edema, hypertension, lethargy, nausea,
vomiting, oligurea.
Mass in flank area, if cyst or tumor, or
obstructive lesion is present.
Fatigue, malaise, poor appetite, nausea,
vomiting, failure to thrive, headache,
decreased mental alertness, or ability to
concentrate, secondary enuresis, chronic
anemia, hypertension, edema,.
Fractures with minimal trauma, rickets, bone
deformities.
Chronic
Diagnostic tests
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2.
3.
4.
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2.
3.
Urine analysis:
pH: acidic urine.
Specific gravity: high in prerenal, low in intrinsic &
normal in postrenal.
Protein: positive.
hematurea
Blood chemistry:
potassium, phosphorus, Cr, & BUN are elevated.
calcium & pH are low.
Sodium: normal, high or low: according to amount of
water in body
Clinical therapy: ARF
Treat the underlying cause.
Fluid replacement in the acute stage by isotonic
solution (RL).
Diuretic therapy is needed in patients with pulmonary
edema as well as dialysis if poorly responded to
diuretics.
Fluid requirements must be calculated to meet (Zero
Water Balance) intake should be same output.
Low potassium diet, in case of sever hyperkalemia
give calcium gluconate to exchange sodium for
potassium.
antibiotic is prescribed for infection.
Give sodium bicarbonate to correct the metabolic
acidosis by exchange hydrogen for potassium.
Give calcium gluconate to correct hypocalcaemia.
Give nitroglycerin to control elevated blood pressure.
In CRF: diet need to be low in potassium, sodium &
phosphorus. With high calcium.
Dialysis is needed.
Kidney transplant.
Dialysis
It can be peritoneal
where a sterile solution
containing menials &
sugar is administered
into the peritoneal
cavity where it left for
a specific period of time
then irrigated carrying
wastes.
Fluid drained is clear
not cloudy. If cloudy it
is indication of
peritoneal infection
Patient needs fewer
dietary restriction.
Hemodialysis is the
second type, where
blood is drained from
artery into the dialzer
to be cleared from
waste and
electrolytes then
return into body
through vein.
Patients needs fluid &
food restrictions
Nursing Interventions
1.
1.
2.
1.
Prevent complications:
Ensure compliance with treatment by monitoring
V/S, intake & output, serum electrolytes, level of
consciousness.
Maintain fluid balance:
Estimate child status by monitoring of weight,
intake & output, B/P three to four times a day.
The aim of maintaining fluid balance is to achieve
sodium balance & decrease body weight by 0.5-1% a
day.
Administer medication:
Monitor adjusted doses of medication (increase
interval or decrease dose).
A.
B.
C.
D.
While performing daily peritoneal dialysis &
catheter exit site care with the mother of a child
with chronic renal failure, which of the following
would be an important step to stress to the mother?
Applying an occlusive dressing after cleaning the
site.
Changing the dressing when the peritoneal space is
dry.
Examining the site for signs of infection while
cleaning the area.
Pulling on the catheter to hold taut while cleaning
the skin.
A.
B.
C.
D.
The mother of a toddler with nephrotic syndrome
asks the nurse what can be done about the child’s
swollen eyes. Which of the following would the
nurse suggest?
Applying cool compresses.
Elevating the head of the child’s bed.
Applying eye drops every 8 hours.
Limiting the child’s television watching.
A.
B.
C.
D.
When developing the discharge teaching plan for a
child with chronic renal failure & the family, the
nurse would emphasize restriction of which of the
following nutrients?
Ascorbic acid.
Calcium.
Magnesium.
Phosphorus.
A.
B.
C.
D.
When developing the plan of care for school-aged
child with acute poststerptoccal glomerulonephritis
who has a fluid restriction of 1,000 ml/day; which
of the following fluids would the nurse consider as
most appropriate for the client’s condition &
effective for preventing excessive thirst?
Diet cola.
Ice chips.
Lemonade.
Tap water.
A.
B.
C.
D.
The nurse determines that interventions for
decreasing fluid retention have been effective
when the child which nephrotic syndrome
demonstrates evidence of which of the following?
Decreased abdominal girth.
Increased caloric intake.
Increased respiratory rate.
Decreased heart rate.